Orthopedic Sports Medicine: Principles and Practice

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Author: Fabrizio Margheritini

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Orthopedic Sports Medicine

Fabrizio Margheritini · Roberto Rossi (Eds.)

Orthopedic Sports Medicine Principles and Practice

~ Springer

Editors Fabrizio Margheritini Department of Health Sciences Unit of Orthopedics and Sports Traumatology University of Rome “Foro Italico” Rome, Italy Roberto Rossi Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy The Editors gratefully acknowledge the very generous support and outstanding contribution of Bayer to the production and distribution of this educational book ISBN 978-88-470-1701-6

e-ISBN 978-88-470-1702-3

DOI 10.1007/978-88-470-1702-3 Springer Dordrecht Heidelberg London Milan New York Library of Congress Control Number: 2010931869 © Springer-Verlag Italia 2011 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the Italian Copyright Law in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the Italian Copyright Law. The use of general descriptive names, registered names, trademarks, 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. Product liability: The publishers cannot guarantee the accuracy of any information about dosage and application contained in this book. In every individual case the user must check such information by consulting the relevant literature. 9 8 7 6 5 4 3 2 1 Cover design: Ikona S.r.l., Milano Typesetting: C & G di Cerri e Galassi, Cremona Printing and binding: Arti Grafiche Nidasio, Assago (MI) Printed in Italy Springer-Verlag Italia S.r.l., Via Decembrio 28, I-20137 Milano Springer is part of Springer Science+Business Media (www.springer.com)

Foreword

Sports have become an important part of our civilization and of our social life. With the multitude of sports activities available to people of all ages, the number of injuries has increased dramatically, paralleled by modifications in their treatment. For example, in the field of knee surgery, when we started our careers some 30 years ago, treatment of a ligament injury usually consisted of rest and immobilization but the end of the sports activity was a frequent outcome. Nowadays, the athlete can choose between a wide variety of therapeutic approaches, which in many cases will allow a resumption of the sport, e.g., anatomic arthroscopic ligament reconstruction, a specific rehabilitation program, or biological stimulation via the delivery of growth factors. There is probably no other field in Orthopedics like Sports Medicine, in which the treatment options have so tremendously improved. This has been due not only to new medical technologies but also to better knowledge of the underlying science. Today, Sports Medicine is not limited to surgery, but rather is an ever-changing and evolving field that encompasses many subspecialties. As such, it requires knowledge of the basic principles of Cardiology, Nutrition, and – especially given the widespread problem of doping among athletes – Sports Pharmacology. In addition, the Sports Medicine specialist serving as team physician must be able to recognize and manage on-field emergencies and all the medical issues they encompass. This book is a state-of-the-art guide for those starting in the field of Orthopedic Sports Medicine, as well as for experienced specialists. The reader will become acquainted with many aspects of basic science that have improved the treatment of sports injuries and which have established a foundation for the operative management of orthopedic pathologies. Orthopedics is a fascinating area of medicine that will continue to grow. The Editors and contributors should be proud of their accomplishment in having provided an outstanding

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Foreword

compilation and reference for postgraduate researchers as well as practicing clinicians in the fields of Orthopedics and Sports Medicine. Rome and Turin, September 2010

Paolo Rossi Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Pier Paolo Mariani Department of Health Sciences Unit of Orthopedics and Sports Traumatology University of Rome “Foro Italico” Rome, Italy

Preface

Sports Medicine is a rapidly evolving interdisciplinary field that has benefited from recent scientific and clinical advances in many medical specialties, including Nutrition, Physiology, Biomechanics, and, of course, Orthopedics. The idea to create a text focused on the fields of Orthopedics and Sports Medicine with a specific orthopedics viewpoint that would present this wide range of information originated two years ago, while we were attending a conference on Sports Medicine. To realize this book, we invited orthopedic surgeons, medical fellows and residents, and researchers from Italy, Europe, and the USA to share their personal experiences regarding the main principles and practice of Orthopedic Sports Medicine. The text includes sections on the pathophysiology of musculoskeletal structures, injury prevention, and the related medical issues. The second part focuses on the upper and lower extremities and the spine. The goal of this book is to provide a novel global overview of sports-related pathologies and the many treatment options offered by the specialty of Sports Medicine. We are therefore pleased and honored to have assembled leading experts in the field and are indebted to them for their excellent contributions. We hope this book will allow established Sports Medicine specialists to further hone their skills, and novices in the field to improve their knowledge. We would like to thank each of the contributors and to join them in expressing appreciation and gratitude to the publisher for the opportunity to develop and realize this ambitious project. Rome and Turin, September 2010

Fabrizio Margheritini Roberto Rossi

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About the Editors

Fabrizio Margheritini (left). Roberto Rossi (right)

Fabrizio Margheritini was born in Rome, where he graduated from the University “La Sapienza” (1992). Honorary Observer in Orthopedics at Princess Elizabeth Orthopedic Hospital, Exeter, UK (1996); Clinical Research Fellow at the Cambridge Lea Hospital, Cambridge, UK (1997-1998); visiting physician at the Sports Medicine Department of the Cleveland Clinic Foundation, Cleveland, OH (1999); visiting physician at the Sports Medicine Department at the University of Pittsburgh, PA (2000), and post-doctoral research fellow in the the university’s Department of Orthopedics (2001). In 1998 he completed his residency program cum laude in orthopedics and traumatology. Selected in 2005 for the the ESSKA-AOSSM traveling fellowship in North America. He is currently Assistant Professor at the University of Rome “Foro Italico” and a member of scientific committees of different national and international professional societies. He has also served as Editorial Board Member of the Arthroscopy Journal and as a reviewer in several international journals. His main interest is in hip and knee surgery. Roberto Rossi was born in Genova in 1972 and attended school in Torino. He graduated from the University of Torino and finished his residency in Orthopedics and Traumatology in 2003. He has completed two fellowships in the USA (2002) and in the UK (2005). During his career, he received several national and international awards in joint replacement, arthroscopy and sports medicine. In June 2010, he became Associate Professor of the University of Torino. He has authored over 60 articles in peer-reviewed journals, 14 book chapters in internationally published books, and over 100 Abstracts. His research interests are in the fields of sports injuries, arthroscopy surgery, and knee joint replacement. ix

Acknowledgments

Editing this book would have been impossible without the help of many people before and during its compilation. Many thanks to all those involved and many apologies to those whom I forget to mention. Specifically, I would like to thank my mentors, both in Italy (Prof. Pier Paolo Mariani) and abroad (Prof. Chris Harner and Prof. Freddie Fu), who have encouraged and supported me throughout my professional career. Special thanks go to Dr. Richard Villar, who first introduced me to hip arthroscopy and thus allowed me to discover an exciting world, and to Prof. Savio Woo, who opened my narrow clinical mind to a wider biomechanical approach. Lastly, of course, I am grateful for the patience and tolerance of my family (Sabina, Filippo Maria, Tommaso Maria, and Costanza) who have long become accustomed to the locked study door and to the chaos on my desk, both meaning “Danger! Daddy is working”. F.M. This book is dedicated to my family: first and foremost to my mother and my father, who inspired me to enter Orthopedics and Sports Medicine, and then to my wife, Micaela, and two daughters, Francesca and Cecilia, for their constant support in all my endeavors. R.R.

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Contents

Section I

Special Issues

1

Present and Future of Sports Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kenneth D. Illingworth, Shail M. Vyas, Volker Musahl and Freddie H. Fu

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2

The Pathophysiology of Tendon Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nicola Maffulli, Umile Giuseppe Longo, Filippo Spiezia and Vincenzo Denaro

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3

Pathophysiology of Muscle Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pietro M. Tonino, Micah K. Sinclair

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4

Pathophysiology of Ligament Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Andrea Cereatti, Francesca R. Ripani and Fabrizio Margheritini

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Pathophysiology of Cartilage Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Giuseppe M. Peretti, Giuseppe Filardo, Antonio Gigante, Laura Mangiavini, Antongiulio Marmotti and Mario Ronga

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Prevention in Sports-related Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Leonardo Osti, Nicola Maffulli

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Stress Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Marco Conte, Francesco Caputo, Giuseppe Piu, Stefania Sechi, Francesco Isoni and Massimiliano Salvi

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Section II 8

Medical Issues

Cardiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fabio Pigozzi, Marta Rizzo and Paolo Borrione

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Contents

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Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 105 Attilio Parisi, Arrigo Giombini

10 Sports Pharmacology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117 Fabio Pigozzi, Paolo Borrione and Alessia Di Gianfrancesco 11 Thromboprophylaxis in Sports Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 Walter Ageno, Francesco Dentali and Alessandro Squizzato

Section III Emergencies on the Field 12 Management of On-The-Field Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . 137 Piero Volpi, Roberto Pozzoni, Gabriele Thiebat, Herbert Schönhuber and Laura de Girolamo

Section IV Upper Extremity 13 Biomechanics of the Shoulder and Elbow . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145 Ofer Levy, Ali Narvani 14 Physical Examination Tests for the Shoulder and the Elbow . . . . . . . . . . . . 159 Giuseppe Porcellini, Francesco Caranzano, Fabrizio Campi and Paolo Paladini 15 Shoulder Injuries in the Throwing Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . 173 Sunny Cheung, C. Benjamin Ma 16 Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185 Filippo Castoldi, Davide Blonna, Mattia Cravino and Marco Assom 17 Acromioclavicular Injuries of the Shoulder . . . . . . . . . . . . . . . . . . . . . . . . . . 199 Emilio Calvo, Diana Morcillo 18 Rotator Cuff Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 Thomas R. Duquin, John W. Sperling 19 Elbow Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227 Samuel A. Antuña, Raúl Barco Laakso 20 Wrist Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 Patrick R. Finkbone, Marco Rizzo 21 Rehabilitation of the Upper Extremity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 Willem J. Willems

Contents

Section V

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Lower Extremity

22 Anatomy and Pathophysiology of Hip Injuries . . . . . . . . . . . . . . . . . . . . . . . . 265 Karl F. Bowman Jr., Jon K. Sekiya 23 Hip Injuries in the Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 275 George P. Pappas, Marc R. Safran 24 Anatomy and Biomechanics of the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 Davide E. Bonasia, Paolo Rossi and Roberto Rossi 25 Clinical Examination of the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319 Roberto Rossi, Matteo Bruzzone, Federico Dettoni and Fabrizio Margheritini 26 Anterior Cruciate Ligament Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 Stefano Zaffagnini, Francesco Giron, Giovanni Giordano and Hakan Ozben 27 Collateral Ligament Injuries of the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . 359 Keith R. Reinhardt, Anil S. Ranawat 28 Posterior Cruciate Ligament Injuries: Rationale for Treatment . . . . . . . . . 375 Fabrizio Margheritini, Roberto Rossi, Francesco Frascari and Pier Paolo Mariani 29 Multiple-ligament Injuries of the Knee . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 383 Corey A. Gilbert, Christopher D. Harner 30 Meniscal Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 René Verdonk, Karl F. Almqvist and Peter Verdonk 31 Patellofemoral Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 417 Roland Becker, Christian Stärke 32 Lower Extremity-Articular Cartilage Injuries . . . . . . . . . . . . . . . . . . . . . . . . 447 Sarvottam Bajaj, Massimo O. Petrera and Brian J. Cole 33 Ankle Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465 Davide E. Bonasia, Annunziato Amendola 34 Lower Limb Rehabilitation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 485 João Espregueira-Mendes, Rogério Barbosa Pereira and Alberto Monteiro

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Section VI

Contents

Spine

35 Spinal Disorders in Sports Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 499 Alessio Maiello, Joseph D. Smucker Subject Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 521

List of Contributors

Walter Ageno Clinical Medicine University of Insubria Varese, Italy Karl F. Almqvist Department of Orthopedic Surgery and Traumatology Ghent University Hospital Gent, Belgium Annunziato Amendola Department of Orthopedic Surgery and Rehabilitation University of Iowa Sports Medicine University of Iowa Hospitals and Clinics Iowa City, Iowa, USA Samuel A. Antuña Shoulder and Elbow Unit Department of Orthopedics Hospital Universitario La Paz Universidad Autónoma de Madrid Madrid, Spain Marco Assom Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy

Sarvottam Bajaj Department of Orthopedics Division of Sports Medicine Midwest Orthopedics at Rush Rush University Medical Center Chicago, IL, USA Rogério Barbosa Pereira Health Sciences Faculty University Fernando Pessoa Saúde Atlântica Clinic Porto, Portugal Raúl Barco Laakso Shoulder and Elbow Unit Department of Orthopedics Hospital Universitario La Paz Universidad Autónoma de Madrid Madrid, Spain Roland Becker Department of Orthopedics and Traumatology Hospital Brandenburg Brandenburg/Havel, Germany Davide Blonna Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy xv

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Davide E. Bonasia University of Iowa Sports Medicine Fellow Turin, Italy Paolo Borrione Department of Health Sciences University of Rome “Foro Italico” Rome, Italy Karl F. Bowman Jr. Department of Orthopedic Surgery University of Michigan Ann Arbor, MI, USA Matteo Bruzzone Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Emilio Calvo Shoulder and Elbow Surgery Unit Department of Orthopedic Surgery and Traumatology Fundacion Jimenez Diaz - Capio Madrid, Spain Fabrizio Campi Unit of Shoulder and Elbow Surgery D. Cervesi Hospital Cattolica (RN), Italy Francesco Caputo Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy Francesco Caranzano Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy


Filippo Castoldi Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Andrea Cereatti Department of Biomedical Sciences University of Sassari Sassari, Italy Sunny Cheung Orthopedic Surgery, Sports Division University of California San Francisco, CA, USA Brian J. Cole Department of Orthopedics, Division of Sports Medicine, Midwest Orthopedics at Rush Rush University Medical Center Chicago, IL, USA Marco Conte Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy Mattia Cravino Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Laura de Girolamo Orthopedics Biotechnology Unit IRCCS Galeazzi Orthopedic Institute Milan, Italy Vincenzo Denaro Department of Orthopedic and Trauma Surgery Campus Bio-Medico University Rome, Italy


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Francesco Dentali Clinical Medicine University of Insubria Varese, Italy

Freddie H. Fu Department of Orthopedic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA, USA

Federico Dettoni Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy

Antonio Gigante Department of Molecular Pathology and Innovative Therapy Polytechnic University of Marche Ancona, Italy

Alessia Di Gianfrancesco CONI-NADO Italian National Olympic Committee National Antidoping Organization Stadio Olimpico - Curva Sud Rome, Italy Thomas R. Duquin Orthopedic Surgery Mayo Clinic Rochester, MN, USA João Espregueira-Mendes Minho University Saúde Atlântica Clinic Porto, Portugal Giuseppe Filardo Biomechanics Lab – IX Division Rizzoli Orthopedic Institute Bologna, Italy Patrick R. Finkbone Orthopedic Surgery Mayo Clinic Rochester, MN, USA Francesco Frascari Department of Health Sciences Unit of Sports Traumatology University of Rome “Foro Italico” Rome, Italy

Corey A. Gilbert UPMC Center for Sports Medicine Pittsburgh, PA, USA Arrigo Giombini University of Rome “Foro Italico” IUSM Italian University of Sport and Movement Rome, Italy Giovanni Giordano Biomechanics Laboratory Rizzoli Orthopedic Institute Bologna, Italy Francesco Giron I° Orthopedic Clinic University of Florence Florence, Italy Christopher D. Harner UPMC Center for Sports Medicine Pittsburgh, PA, USA Kenneth D. Illingworth Department of Orthopedic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA, USA Francesco Isoni Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy

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Ofer Levy Reading Shoulder Unit Royal Berkshire Hospital Reading, UK Umile Giuseppe Longo Department of Orthopedic and Trauma Surgery Campus Bio-Medico University Rome, Italy C. Benjamin Ma Orthopedic Surgery, Sports Division University of California San Francisco, CA, USA Nicola Maffulli Centre for Sports and Exercise Medicine Barts and The London School of Medicine and Dentistry Mile End Hospital London, UK Alessio Maiello Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Laura Mangiavini Residency Program in Orthopedics and Traumatology University Milano-Bicocca Monza, Italy Fabrizio Margheritini Department of Health Sciences Unit of Orthopedics and Sports Traumatology University of Rome “Foro Italico” Rome, Italy


Pier Paolo Mariani Department of Health Sciences Unit of Orthopedics and Sports Traumatology University of Rome “Foro Italico” Rome, Italy Antongiulio Marmotti Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Alberto Monteiro Saúde Atlântica Clinic Porto, Portugal Diana Morcillo Shoulder and Elbow Surgery Unit Department of Orthopedic Surgery and Traumatology Fundacion Jimenez Diaz - Capio Madrid, Spain Volker Musahl Department of Orthopedic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA, USA Ali Narvani Reading Shoulder Unit Royal Berkshire Hospital Reading, UK Leonardo Osti Arthroscopy and Sports Medicine Unit Hesperia Hospital Modena, Italy Hakan Ozben Department of Orthopedics and Traumatology Istanbul University Medical Faculty Istanbul, Marmara, Turkey


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Paolo Paladini Unit of Shoulder and Elbow Surgery D. Cervesi Hospital Cattolica (RN), Italy

Roberto Pozzoni Sports Traumatology and Arthroscopic Unit IRCCS Galeazzi Orthopedic Institute Milan, Italy

George P. Pappas Department of Orthopedic Surgery Stanford University Redwood City, CA, USA

Anil S. Ranawat Orthopedic Surgery Hospital for Special Surgery New York, NY, USA

Attilio Parisi University of Rome “Foro Italico” IUSM Italian University of Sport and Movement Rome, Italy

Keith R. Reinhardt Orthopedic Surgery Hospital for Special Surgery New York, NY, USA

Giuseppe M. Peretti Department of Orthopedics and Traumatology San Raffaele Scientific Institute Faculty of Exercise Sciences University of Milan Milan, Italy Massimo O. Petrera Department of Orthopedics, Division of Sports Medicine Mount Sinai Hospital Toronto, Ontario, Canada Fabio Pigozzi Department of Health Sciences University of Rome “Foro Italico” Rome, Italy Giuseppe Piu Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy Giuseppe Porcellini Unit of Shoulder and Elbow Surgery D. Cervesi Hospital Cattolica (RN), Italy

Francesca R. Ripani Department of Health Sciences Unit of Sports Traumatology University of Rome “Foro Italico” Rome, Italy Marco Rizzo Orthopedic Surgery Mayo Clinic Rochester, MN, USA Marta Rizzo Department of Health Sciences University of Rome “Foro Italico” Rome, Italy Mario Ronga Department of Orthopedics and Traumatology University of Insubria Varese, Italy Paolo Rossi Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy

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Roberto Rossi Department of Orthopedics and Traumatology Mauriziano “Umberto I” Hospital University of Turin Turin, Italy Marc R. Safran Department of Orthopedic Surgery Stanford University Redwood City, CA, USA Massimiliano Salvi Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy Herbert Schönhuber Sports Traumatology and Arthroscopic Unit IRCCS Galeazzi Orthopedic Institute Milan, Italy Stefania Sechi Joint Replacement and Sports Medicine Unit Lay Hospital Cagliari, Italy Jon K. Sekiya Department of Orthopedic Surgery University of Michigan Ann Arbor, MI, USA Micah K. Sinclair Department of Orthopedic Surgery Loyola University Medical Center Maywood, IL, USA Joseph D. Smucker Department of Orthopedics and Rehabilitation The University of Iowa Iowa City, Iowa, USA


John W. Sperling Orthopedic Surgery Mayo Clinic Rochester, MN, USA Filippo Spiezia Department of Orthopedic and Trauma Surgery Campus Bio-Medico University Rome, Italy Alessandro Squizzato Clinical Medicine University of Insubria Varese, Italy Christian Stärke Department of Orthopedic Surgery Otto-von-Guericke University Magdeburg Magdeburg, Germany Gabriele Thiebat Sports Traumatology and Arthroscopic Unit IRCCS Galeazzi Orthopedic Institute Milan, Italy Pietro M. Tonino Department of Orthopedic Surgery Loyola University Medical Center Maywood, IL, USA Peter Verdonk Department of Orthopedic Surgery and Traumatology Ghent University Hospital Gent, Belgium René Verdonk Department of Orthopedic Surgery and Traumatology Ghent University Hospital Gent, Belgium


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Piero Volpi Knee Surgery and Sport Traumatology Unit IRCCS Clinic Institute Humanitas Rozzano (MI), Italy

Willem J. Willems Department of Orthopedics Onze Lieve Vrouwe Gasthuis Hospital Amsterdam, The Netherlands

Shail M. Vyas Department of Orthopedic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA, USA

Stefano Zaffagnini Biomechanics Laboratory Rizzoli Orthopedic Institute Bologna, Italy

Section I Special Issues

Present and Future of Sports Medicine

1

K.D. Illingworth, S.M. Vyas, V. Musahl and F.H. Fu

Abstract Sports-related injuries are expected to increase with time and health-care professionals of all disciplines are becoming aware of common injuries and their treatment. Sports medicine is expanding in recognition of the fact that: (1) athletes participate in sport-specific training year round and often in multiple sports, (2) there has been a steady increase in “weekend warriors”, (3) the patient population is better educated and has higher performance expectations and a greater awareness of physical fitness, and (4) recreational activities for the general population have increased tremendously. This chapter provides a brief overview of the current state of management of common sport-related injuries, including injuries in the shoulder, elbow, hip, knee, foot and ankle, head and spine, and concussion. It also describes some of the current controversies existing in these areas. The topics of cartilage, soft tissue injury, stem cells in orthopedics, proprioception in sports, biologics and imaging are also addressed in terms of current issues and what the future holds for their application in orthopedic sports medicine.

1.1 Introduction In the USA, the first American Academy of Orthopedic Surgeons sub-committee on sports medicine was formed in 1967 with the first American Orthopedic Society for Sports Medicine (AOSSM) meeting held in New Orleans in 1975. Currently, there are over 2600 members in the AOSSM and 81 accredited fellowship programs. Sports-related injuries are expected to increase with time and health care professionals of all disciplines are becoming aware of common injuries and their treatment. Both the breadth and depth of sports medicine is expanding in response to the fact that: 1) athletes participate in sport-specific training year round and often in multiple sports, 2) there has been a steady increase in “weekend warriors”, 3) the patient population is better educated, has higher performance Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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K.D. Illingworth et al.

expectations, and an increased awareness of physical fitness, and 4) recreational activities for the general population have increased. Orthopedic sports physicians specialize in the operative and non-operative management of the active individual. Their patient population ranges from those in the general population who choose to live an active lifestyle to the care of dedicated professional athletes. Training in arthroscopic surgery is required to treat intra-articular derangements of the shoulder, elbow, wrist, hip, knee, and ankle. The orthopedic sports specialist is further qualified to manage acute on-field injuries and make decisions for the injured athlete that are in his or her best interest in the face of pressures from the team, fans, family, and even from the injured individuals themselves. The academic sports specialist is also involved in contributing to the vast field of sports research, whether it is on the cellular, biomechanical, or clinical level. Orthopedic sports specialists also help promote awareness of new methodologies and philosophies in sports-related care, two areas that are in constant flux and improvement, at the hundreds of centers of excellence worldwide. Sports medicine is one of the few orthopedic sub-specialties in which the surgeon is not simply treating the patients’ pain, but rather, has the added challenge of optimizing athletic function. This chapter provides a brief overview of the scope of sports medicine, including a description of current treatments and controversies as well as its future directions.

1.2 Rotator Cuff Pathology of the rotator cuff is one of the most common reasons for visits to the orthopedic sports specialist. In the last decade, treatment of rotator cuff injuries has significantly improved, with adjustments made to surgical indications, surgical techniques, surgical philosophy, and rehabilitation protocols. Whereas in the past, the results of arthroscopic rotator cuff surgery were questioned regarding the advantages over open or mini-open methods of repair, the recent literature has shown arthroscopic rotator cuff to be equal, if not superior to open techniques [1-4]. Current controversies in rotator cuff surgery include single- vs. double-row fixation, the utility of acromioplasty, the difficulties in treating massive cuff tears, and the incorporation of the dozens of constantly evolving surgical devices and biological agents that have continued to flood the industry. Several recent reviews of the literature have failed to show a clinical difference between double-row and single-row techniques of rotator cuff repair [5, 6]. A systematic review by Wall et al. showed that in three level-one studies and two level-two studies there was no clinical difference at one year in the single-row vs. double-row technique for rotator cuff repair [7]. However, Wall et al. also systematically reviewed the literature on the biomechanical strength of single- vs. double-row rotator cuff repair and concluded that the biomechanical properties of the double-row technique are superior to those of the single-row technique [8].

1 Present and Future of Sports Medicine

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1.3 Shoulder Instability The treatment of shoulder instability is one of the primary reasons for younger athletes to see the orthopedic sports specialist. Studies have characterized the risk for future recurrence and have found that those in their teens and twenties have a significantly higher risk of repeat episodes of instability than those in their thirties and forties [9-11]. Controversy remains regarding whether or not to immobilize the shoulder of a patient presenting with a dislocation for the first time, the position of the immobilization, and the considerations for early surgical repair of the capsulolabral structures. Patients with atraumatic multidirectional instability have generally been treated with shoulder rehabilitation, and in some cases surgical indications may be revised. Finally, those patients with recurrent instability are being more closely evaluated for the etiology of their pathology. Depending on whether the etiology is due to capsulolabral laxity, bony glenoid deficiency, humeral head morphology, etc., treatments can vary. Arthroscopic soft-tissue restoration has been the front-line treatment for recurrent instability. However, it is backed by open stabilizing procedures such as the open Bankart repair, Latarjet procedure, remplissage, and humeral head morphology restoration with allograft.

1.4 Superior Labrum/Biceps Anchor/Acromioclavicular Joint The diagnosis and treatment of superior labral and biceps anchor pathologies is a common challenge for the orthopedic sports physician. Conservative vs. operative treatment have had mixed results depending on the level of activity, type of superior labral tear, and concurrent pathology. Also, the debate over biceps tendon tenotomy vs. tenodesis remains an active issue for the orthopedic surgeon [12, 13]. The sports medicine literature is evolving in the development of an algorithm for the treatment of superior labral and biceps disease. Disorders of the acromioclavicular joint can be acute or chronic. Acute type I and type II acromioclavicular separations have traditionally been managed non-operatively, but controversy exists over early vs. delayed surgical reconstruction of the type III acromioclavicular disruption [14, 15]. Chronic end-stage acromioclavicular arthrosis, traditionally managed with an open distal clavicle resection, is increasingly being treated arthroscopically, with excellent results [15, 16]. Chondrosis of the shoulder continues to be a challenge for the sports specialist. Arthroscopic debridement of the arthritic shoulder is a short-lasting option with early promising results for added microfracture techniques [17]. Diffuse chondrosis refractory to alternative management has been treated with humeral hemi-arthroplasty or glenohumeral arthroplasty.

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1.5 Elbow The throwing athlete is particularly susceptible to ulnar collateral ligament injury and its associated sequelae [18, 19]. While the gripping athlete (e.g., tennis and golf) is predisposed to tendinopathies about the elbow [20], common elbow pathologies include lateral and medial epicondylitis, triceps rupture/tendinitis, olecranon bursitis, distal biceps rupture, ulnar collateral ligament injuries, valgus extension overload, osteochondritis dissecans (OCD), elbow arthritis, ulnar neuropathy, fractures, and dislocations. Arthroscopic treatment of intra-articular elbow pathology has advanced over the past decade, with indications expanding beyond simple diagnosis and loose-body removal. The arthroscope is being used to treat impingement, arthritis, contractures, OCD stabilization, and certain intra-articular fractures [21]. Techniques and procedures continue to evolve as surgeons gain more insight and skill in the indications for arthroscopic treatments of the elbow.

1.6 Hand and Wrist Hand injuries during athletic participation are common and the sports orthopedic specialist is often the front-line physician seeing these athletes. While many hand injuries are ultimately cared for by a hand surgeon, the sports orthopedist must be facile in the diagnosis and management of acute hand injuries. Common acute injuries include dislocations, fractures, and ligamentous injuries. Wrist arthroscopy has also benefited from advances in surgical technique and equipment advances. Current usage of wrist arthroscopy includes evaluation of chronic wrist pain, treatment of triangular fibrocartilage complex and ligament tears, resection of synovitis and joint-based ganglia, visualization for reduction and fixation of intra-articular fractures and acute carpal dislocations, treatment of ulnar styloid impaction syndrome, loose-body removal, and debridement and partial or complete ostectomy for arthritis [22].

1.7 Hip The approach and treatment of intra-articular hip pathology in the active individual has seen a dramatic change over the last five years. Disease of the labrum and femoroacetabular impingement (FAI) are diagnoses that are being made with more evidence and confidence. FAI has been shown to present in two varieties: cam-type impingement refers to the abnormal morphology of the femoral head/neck junction while pincer-type impingement refers to morphological abnormalities on the acetabular side, with many


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patients being affected by a combination of both. Ultimately, both have been shown to cause labral and chondral disease [23-26]. Concordantly, arthroscopic treatment of these conditions has also seen a dramatic rise, with demonstrated success for osteo-chondroplasty as well as labral debridement and repair [27-29]. With time, long-term data will become available regarding the efficacy of arthroscopic hip surgery in treating immediate symptoms and in the prevention of long-term degeneration. Other conditions currently being treated with hip arthroscopy include septic arthritis, intra-articular loose bodies, pigmented villonodular synovitis, synovial chondromatosis, and ruptured ligamentum teres. Expansion of the indications of hip arthroscopy is on the forefront of sports medicine.

1.8 Anterior Cruciate Ligament The anterior cruciate ligament (ACL) continues to be the most extensively researched and reconstructed of the ligaments. In 2008, there were approximately 105,000 ACL reconstructions in the USA [30]. Despite the extent of ACL research, many controversies remain, involving autograft vs. allograft [31-34], optimum allograft sterilization and processing [33, 35], location of tibial and femoral tunnel placement [36-39], single vs. double bundle technique [36, 40-44], transtibial vs. medial portal femoral tunnel drilling [45-47], fixation methods, and post-operative protocols. Indications for ACL reconstruction are debated. Most surgeons agree that athletic patients with a previously normal knee, with new-onset subjective instability with activity, benefit from ACL reconstruction. Thus far, the results of ACL reconstruction have largely been good to excellent, with a majority of patients able to return to pre-injury activity level [48]. However, the challenge of improving on a generally successful operation has been proposed. Currently, “anatomic” ACL reconstruction is receiving much attention as it is felt that reconstruction of the native anatomy of the athlete with respect to graft size, tunnel location, tunnel shape, and collagen orientation results in optimal return to preinjury function. The most common natural history of an ACL-deficient knee is chondral degeneration [49, 50]. The restoration of knee kinematics is hypothesized to be the most important factor in long-term outcomes and the prevention of early arthritis associated with current ACL reconstructions. As the anatomic technique and double-bundle concept continue to be investigated, long-term follow-up and biomechanical data will be crucial to make the necessary conclusions regading optimal reconstruction techniques. The use of an allograft vs. autograft in ACL reconstruction has long been debated. Autografts have the disadvantage of resulting in higher surgical morbidity. Allografts incorporation and healing take longer than is the case for autografts but have the advantage of no donor site morbidity and allowing the surgeon to choose a graft size that is not constrained, unlike in autografts. Recent reviews have shown no difference in clinical outcome between autograft and allograft in ACL reconstruction [32, 33, 51].

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1.9 Posterior Cruciate Ligament The posterior cruciate ligament (PCL) has received significant recent attention. Grade I and most grade II PCL injuries are treated non-operatively. Grade III PCL and combined PCL/PLC and PCL/MCL injuries continue to challenge the orthopedist with regard to management decision-making. The natural history of a grade III PCL injury has been shown to result in medial and patellofemoral compartment chondrosis and degeneration [52, 53]. Surgical intervention is influenced by age and activity level of the patient, subjective instability, and other concurrent ligamentous injuries. There is variation amongst surgeons with regard to the “inlay” technique vs. the transtibial approach to reconstruction [54, 55]. Furthermore, the utility of osteotomy to decrease the biomechanical demand on the PCL is an unanswered question outside the laboratory. Identification of simultaneous ligament injuries and their appropriate management has been shown to influence the outcome of PCL reconstruction [53]. The goal of PCL reconstruction should be the restoration of early stability and of knee kinematics to a near native state in order to prevent long-term complications, such as osteoarthritis. Clinical outcome studies involving PCL reconstruction are necessary to help address these unresolved issues.

1.10 Posterolateral Corner The anatomy of the posterolateral corner (PLC) has been well characterized and shown to contribute static and dynamic stability to the knee. The critical structures of the PLC are the lateral collateral ligament (varus stability), the popliteus tendon (rotational stability), and the popliteofibular ligament (rotational stability). The PLC is commonly injured concomitant with other ligamentous injuries, with the torn ACL being its most common partner [56]. The deficient PLC has been shown to be a primary cause of failed cruciate reconstruction surgery as it allows excessive stress on the reconstructed grafts [53, 56, 57]. Algorithms have been developed to include treatment of the PLC to avoid these disastrous consequences. Currently, it is believed that in acute high-grade injuries of the PLC in which a specific major PLC structure is obviously deficient, primary repair is effective within 2–3 weeks of the injury [58]. However, beyond this time frame, primary repair is difficult and reconstruction of the posterolateral stabilizing structures must be undertaken. Finally, with chronic PLC injuries, ligament reconstruction may not be enough and concurrent realignment osteotomy may be necessary to prevent further chondrosis of the knee joint.


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1.11 Medial Collateral Ligament The medial collateral ligament (MCL) is the most commonly injured of the knee ligaments; however, it has been shown to have good healing potential [59, 60]. Grade I and II injuries of the MCL most commonly improve with appropriate bracing and activity modification [61]. Grade III injuries are often given a non-operative trial, during which many also improve. A majority of MCL injuries occur in the mid-substance and femoral insertion site with a minority at the tibial insertion site. Tibial-sided grade III MCL injuries are the subset of MCL injuries associated with worse clinical outcome, and surgical repair is therefore more often advocated. Reconstruction of the MCL is less common, as repair is usually effective.

1.12 Meniscus The meniscus serves to provide joint stability, shock absorption, load distribution, and proprioception. Preservation of the meniscus has recently been in the spotlight as the primary goal for meniscal surgery. With menisectomy as one of the most commonly performed surgical procedures, physicians must be educated on the significance of meniscal preservation when there is potential for healing. Research into the use of biologics (e.g. fibrin clot, PRP, platelet-rich plasma) in meniscal repair has attempted to expand the indications of meniscal repair over subtotal meniscectomy [62-66]. Further, meniscal root tears are now increasingly being recognized as devastating injuries resulting in the alteration of knee contact forces [67, 68]. Surgical techniques are being developed to repair the meniscal root in an attempt to restore its function. For end-stage meniscal disease, meniscal transplantation is an option [69], but the indications are still a source of controversy. Superior surgical techniques, the use of biologics for meniscal healing, long-term data on root repair, indications for transplantation, and physician education on the critical role of the meniscus are at the frontier of meniscal surgery.

1.13 Patellofemoral Disorders Disease involving the patellofemoral joint is often the most difficult problem for the sports surgeon to address. Patellofemoral pathology can stem from instability, chondrosis, and tendonosis. In recent years, patellar instability has been shown to involve loss of the medial patellar stabilizing structures. In particular, the medial patellofemoral ligament (MPFL) has been identified as a primary stabilizing structure for the patellofemoral joint and has been an effective target for repair or reconstruction in the patient with chronic

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instability [70]. However, treatment algorithms have recently been developed that consider the etiology of the instability and focus on treatment to address a possible anatomic cause (such as patella alta, trochlear dysplasia, and atypical tubercle anatomy). In such cases, other procedures that address this anatomic variation may be added to MPFL repair or reconstruction.

1.14 Foot and Ankle Foot and ankle injuries are common to the athletic population. The nature of these injuries varies depending on the sport. Chronic overuse injuries are seen in endurance athletes such as long-distance runners while acute bone, ligament, tendon, or cartilage injuries are more seen in contact athletes. Ankle sprains are the most common ankle injury in athletes and are most often treated conservatively. First-line treatment of chronic conditions such as Achilles, peroneal, or posterior tibialis tendonitis as well as stress fractures of the feet continue to be managed non-operatively. Tibiotalar impingement as well as chondral or osteochondral lesions of the ankle joint are more readily being treated with ankle arthroscopy, with good evidence-based medicine [71]. The role of microfracture in acute ankle cartilaginous lesions and the benefits of autologous cartilage transplantation and open osteochondral transplantation are questions that are currently being investigated [72-74].

1.15 Head and Spine Although the head and spine are often left outside the surgical scope of a sports medicine practice, these injuries are the most crucial when evaluating acute on-the-field injuries. It is estimated that nearly 70% of all sport-related deaths can be attributed to head injuries. Recent sport-related rule changes and advances in equipment have been implemented as part of the greater emphasis being placed on protecting the head, neck, and spine for contact athletes. In the National Football League, spearing and leading with the head are examples of illegal forms of tackling that have helped decrease the incidence of head and neck injuries, not only in professional athletes but at all levels of football. There is continued emphasis on protecting athletes from these catastrophic injuries through education, equipment technology, and medical advances. In addition, identifying patients who are at risk of spine and spinal cord injuries is imperative and questions regarding the relationship between spinal stenosis and spinal injury continue to be debated.


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1.16 Concussion Over the past several years, significant knowledge has been gained in the area of concussion and the approach to return to play for athletes. The diagnosis and treatment of concussion has evolved from a rudimentary diagnosis and classification to a more sophisticated process that better protects athletes from devastating outcomes. The center for disease control estimates that there are more than 300,000 sport-related concussions each year [75]. The advent of Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT) has revolutionized the approach to concussion management, taking into consideration the somatic, cognitive, and neurobehavioral sequelae of concussion [76-78]. It has been shown that early return to play while still symptomatic from concussion-like symptoms predisposes the athlete to an increased risk of subsequent concussion and further neurological damage [76]. The future of concussion management includes better identifying athletes at risk of a second neural injury and protecting them from further longer-lasting consequences. In addition, the utility of neurologic therapy (e.g. psychological therapy, vestibular therapy) warrants further exploration.

1.17 Cartilage Much energy has been focused on the injury and repair of the articular cartilage; however, restoration of lost cartilage is not yet possible. Current research focuses on the use of smart polymers, stem cells, and gene therapy to deliver growth factors known to induce chondrogenesis. Biodegradable hydrogels are also being developed for use as an artificial matrix for tissue engineering and drug delivery. Tan et al. developed an injectable biodegradable hydrogel from chitosan and hyaluronic acid and demonstrated its in vitro potential by implanting bovine chondrocytes and showing their survival and proliferation [79]. Cartilage imaging has expanded to include optical coherence tomography (OCT) and multi-parametric quantitative magnetic resonance imaging (MRI), both of which attempt to detect early reversible articular cartilage damage [80-82]. The continued goals of basic science, radiographic, and clinical research in the field of cartilage are to help identify the etiology of cartilage loss, improve early visualization of cartilage damage, and devise effective means to restore lost cartilage to prevent and treat osteoarthritis. Current methods of treating articular cartilage injuries include chondroplasty, microfracture, autologous chondrocyte implantation, osteochondral grafting, osteotomy to redirect weightbearing forces, and arthroplasty.

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1.18 Soft-tissue Injury and Regeneration Athletes who sustain soft-tissue injuries, such as muscle strains and ligament sprains, lose a significant amount of time in the process of recovery. Treatments geared at minimizing time lost due to injury are constantly being evaluated. A key step in muscle injury is the role of fibrosis. Blocking fibrotic factors in vitro has been shown to increase the healing time in muscle injuries [83-85]. Losartan, an angiotensin 2 receptor blocker, has been demonstrated to decrease fibrosis and increase recovery from muscle injury. A study at the University of Pittsburgh is looking at the possible clinical role of losartan following muscle injury. Use of relaxin, a peptide hormone, and decorin has also been shown to improve muscle regeneration and reduce muscle fibrosis development [86-88]. Stem cells, gene therapy, and biological adjuncts to healing are being investigated with the aim of decreasing recovery time for muscle injury and all are likely to play a future role in the management of soft-tissue injury.

1.19 Proprioception/Neuromuscular Control Research in the area of neuromuscular control and proprioception is intended to better understand capsuloligamentous structures and the patho-etiology of joint injury. Biomechanical and neuromuscular assessments under sports-simulated environments continue to be used to determine the influence of weight distribution, muscle function, balance, flexibility, proprioception, gender, aging, and fatigue, as well as the effects of injury, surgery, and rehabilitation on joint stability. With a better understanding of the body’s mechanics and muscle function, better programs can be developed to improve performance and to minimize associated injuries [89]. Some areas that have benefited from this research include golf [90, 91], cycling [92], overhead-throwing athletes [93], ACL injuries in females [94, 95] and training of elite members of the military, including the USA’s 101st airborne and Navy Seals.

1.20 Biologics Biologic augmentation of physiological healing attempts to harness the body’s own complex healing pathways and stimulate them supra-physiologically. Emergent technologies target the activation of signal pathways that induce healing in the form of osteoinduction, angiogenesis, and stem-cell-related migration and proliferation. The global orthobiologics market was estimated by Espicom to be worth $4.2 billion in 2007 and accounted for 13% of the $33 billion total orthopedic market. With an annual growth rate of 17%, orthobiologics is one of the fastest growing orthopedic segments.


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1.21 Platelet-rich Plasma The platelet has been shown to represent an effective carrier for biologic delivery of growth factors to promote healing. For over two decades, fibrin clots have been used to aid in healing meniscal tears, with moderate success [62-66]. Platelet-rich plasma (PRP) has gained recent attention as a potentially more effective vehicle to accelerate healing, as it is hypothesized to activate higher levels of growth factors than achieved by the fibrin clot. Current clinical applications include elbow tendinopathy, Achilles tendinopathy, plantar fasciitis, patellar tendinopathy, osteoarthritis, acute ligamentous injuries, acute muscle injury, total knee arthroplasty, ACL reconstruction, acute Achilles tendon rupture, rotator cuff repair, and acute articular cartilage repair [96, 97]. However, a recent double-blind randomized control trial failed to find a difference between PRP and placebo saline injection in Achilles tendonitis [98]. Current drawbacks to the use of PRP is the limited basic science research devoted to its use and its cost. Further research is necessary to determine ideal levels of platelet activation, growth factor titers, and delivery methods, thus making the product more cost effective for regular use, as well as clinical studies that effectively evaluate PRP and other platelet-derived therapies. Other biologics, such as bone morphogenic protein, osteoprotegerin, and metalloproteinase inhibitors, are also being studied regarding their effective application in sports medicine.

1.22 Tissue Regeneration/Stem Cells The final frontier of tissue engineering is the use of stem cells and the induction of progenitor cell differentiation into the necessary tissue. Adult stem cells can be obtained from a variety of tissues, including adipose [99], periosteum [100], synovial membrane [101], pericytes [102], blood [103], bone marrow [104], and skeletal muscle [105, 106]. Although sensationalized by popular culture and the non-scientific media, stem cells are expected to play a role in the healing response to sports injuries. While most of the current research in stem cells is in its early stages, clinical studies have found good results in applications such as bone-tunnel healing in ACL surgery, healing of avascular necrosis lesions, and uniting fracture non-unions. The anticipated role of stem cells is to aid in the growth and repair of cartilage, improve the correction of bony defects as well as ligament and softtissue repair, and ultimately, to support regrowth of lost native tissue.

1.23 Imaging The use of plain radiographs and high-resolution MRI continue to be the primary means by which imaging aids in the diagnosis of sports-related injuries. Nuclear imaging is be-


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ing used to evaluate early arthritis that may not be appreciated on plain radiography and MRI. It can also serve to rule out atypical bony processes and thus to narrow the differential diagnosis for the surgeon. Three-dimensional CT scans can serve as a guide for bony landmarks and anatomic variation. The technique has been found useful in better delineating bone tunnels in revision cruciate ligament surgery, thereby providing a blueprint for the surgeon to plan and execute the operation. High speed bi-planar radiographs combined with MRI and/or CT scans have allowed for the determination of both contact paths of in vivo joint kinematics and cartilage thickness [107-111]. This technology is being used to study tibiofemoral contact patterns in lateral meniscus tears, contact paths in PCLdeficient knees, scapular kinematics, double-bundle vs. single-bundle ACL reconstruction kinematics, tibiofemoral joint congruency after medial meniscal root tears, and spinal fusions motion, and can be applied to many other situations. The ability to measure in vivo kinematics will allow us to better evaluate reconstruction techniques and result in a more precise evaluation of short- and long-term outcomes as well as a reduction in the incidence of post-traumatic arthritis.

1.24 Conclusions The practice and administration of sports medicine has significantly evolved over the last few decades. Advances in the non-operative and operative management of common injuries have increased our ability to care for patients, and active individuals of all ages are returning to their pre-injury activities at higher levels. Current controversy remains in diagnostic modalities, treatment algorithms, surgical techniques, surgical indications, biologic adjuncts, and return to play guidelines. The task for the sports orthopedic specialist is to answer these challenges and to resolve existing controversy through translational research and evidence based medicine in order to better serve our patients.

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3. 4. 5.

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30. Lyman S, Koulouvaris P, Sherman S et al (2009) Epidemiology of anterior cruciate ligament reconstruction: trends, readmissions, and subsequent knee surgery. J Bone Joint Surg Am 91:2321-2328 31. Krych AJ, Jackson JD, Hoskin TL et al (2008) A meta-analysis of patellar tendon autograft versus patellar tendon allograft in anterior cruciate ligament reconstruction. Arthroscopy 24:292-298 32. Baer GS, Harner CD (2007) Clinical outcomes of allograft versus autograft in anterior cruciate ligament reconstruction. Clin Sports Med 26:661-681 33. Carey JL, Dunn WR, Dahm DL et al (2009) A systematic review of anterior cruciate ligament reconstruction with autograft compared with allograft. J Bone Joint Surg Am 91:22422250 34. Fu F, Christel P, Miller MD et al (2009) Graft selection for anterior cruciate ligament reconstruction. Instr Course Lect 58:337-354 35. Harner CD, Lo MY (2009) Future of allografts in sports medicine. Clin Sports Med 28:327340, ix 36. Colvin AC, Shen W, Musahl V et al (2009) Avoiding pitfalls in anatomic ACL reconstruction. Knee Surg Sports Traumatol Arthrosc 17:956-963 37. Zantop T, Wellmann M, Fu FH et al (2008) Tunnel positioning of anteromedial and posterolateral bundles in anatomic anterior cruciate ligament reconstruction: anatomic and radiographic findings. Am J Sports Med 36:65-72 38. Kato Y, Ingham SJ, Kramer S et al (2010) Effect of tunnel position for anatomic single-bundle ACL reconstruction on knee biomechanics in a porcine model. Knee Surg Sports Traumatol Arthrosc 18:2-10 39. Kopf S, Musahl V, Tashman S et al (2009) A systematic review of the femoral origin and tibial insertion morphology of the ACL. Knee Surg Sports Traumatol Arthrosc 17:213219 40. Fu FH, Kowalchuk D (2009) Cost analysis comparing single-bundle and double-bundle anterior cruciate ligament (ACL) reconstruction. Am J Sports Med 37:e1; author reply e2 41. Tashman S, Kopf S, Fu FH (2008) The kinematic basis of ACL reconstruction. Oper Tech Sports Med 16:116-118 42. van Eck CF, Romanowski JR, Fu FH (2009) Anatomic single-bundle anterior cruciate ligament reconstruction. Arthroscopy 25:943-946; author reply 946-947 43. Irrgang JJ, Bost JE, Fu FH (2009) Re: Outcome of single-bundle versus double-bundle reconstruction of the anterior cruciate ligament: a meta-analysis. Am J Sports Med 37:421422; author reply 422 44. Kohen RB, Sekiya JK (2009) Single-bundle versus double-bundle posterior cruciate ligament reconstruction. Arthroscopy 25:1470-1477 45. van Eck CF, Morse KR, Fu FH (2009) The anteromedial portal for anterior cruciate ligament reconstruction. Arthroscopy 25:1062-4; author reply 1064-1065 46. Pombo MW, Shen W, Fu FH (2008) Anatomic double-bundle anterior cruciate ligament reconstruction: where are we today? Arthroscopy 24:1168-1177 47. Alentorn-Geli E, Lajara F, Samitier G et al (2010) The transtibial versus the anteromedial portal technique in the arthroscopic bone-patellar tendon-bone anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc 18:1013-1037 48. Meredick RB, Vance KJ, Appleby D et al (2008) Outcome of single-bundle versus doublebundle reconstruction of the anterior cruciate ligament: a meta-analysis. Am J Sports Med 36:1414-1421 49. Nebelung W, Wuschech H (2005) Thirty-five years of follow-up of anterior cruciate ligament-deficient knees in high-level athletes. Arthroscopy 21:696-702 50. Fithian DC, Paxton LW, Goltz DH (2002) Fate of the anterior cruciate ligament-injured knee. Orthop Clin North Am 33:621-636 51. Samuelsson K, Andersson D, Karlsson J (2009) Treatment of anterior cruciate ligament injuries with special reference to graft type and surgical technique: an assessment of randomized controlled trials. Arthroscopy 25:1139-1174


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52. Skyhar MJ, Warren RF, Ortiz GJ et al (1993) The effects of sectioning of the posterior cruciate ligament and the posterolateral complex on the articular contact pressures within the knee. J Bone Joint Surg Am 75:694-699 53. Harner CD, Vogrin TM, Hoher J et al (2000) Biomechanical analysis of a posterior cruciate ligament reconstruction. Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med 28:32-39 54. MacGillivray JD, Stein BE, Park M et al (2006) Comparison of tibial inlay versus transtibial techniques for isolated posterior cruciate ligament reconstruction: minimum 2-year follow-up. Arthroscopy 22:320-328 55. Seon JK, Song EK (2006) Reconstruction of isolated posterior cruciate ligament injuries: a clinical comparison of the transtibial and tibial inlay techniques. Arthroscopy 22:27-32 56. Ranawat A, Baker CL, 3rd, Henry S et al (2008) Posterolateral corner injury of the knee: evaluation and management. J Am Acad Orthop Surg 16:506-518 57. LaPrade RF, Resig S, Wentorf F et al (1999) The effects of grade III posterolateral knee complex injuries on anterior cruciate ligament graft force. A biomechanical analysis. Am J Sports Med 27:469-475 58. Swenson TM, Harner CD (1995) Knee ligament and meniscal injuries. Current concepts. Orthop Clin North Am 26:529-546 59. Frank C, Amiel D, Akeson WH (1983) Healing of the medial collateral ligament of the knee. A morphological and biochemical assessment in rabbits. Acta Orthop Scand 54:917-923 60. Frank C, Woo SL, Amiel D et al (1983) Medial collateral ligament healing. A multidisciplinary assessment in rabbits. Am J Sports Med 11:379-389 61. Lundberg M, Messner K (1996) Long-term prognosis of isolated partial medial collateral ligament ruptures. A ten-year clinical and radiographic evaluation of a prospectively observed group of patients. Am J Sports Med 24:160-163 62. Arnoczky SP, Warren RF, Spivak JM (1988) Meniscal repair using an exogenous fibrin clot. An experimental study in dogs. J Bone Joint Surg Am 70:1209-1217 63. Rodeo SA (2000) Arthroscopic meniscal repair with use of the outside-in technique. Instr Course Lect 49:195-206 64. McAndrews PT, Arnoczky SP (1996) Meniscal repair enhancement techniques. Clin Sports Med 15:499-510 65. Ishida K, Kuroda R, Miwa M et al (2007) The regenerative effects of platelet-rich plasma on meniscal cells in vitro and its in vivo application with biodegradable gelatin hydrogel. Tissue Eng 13:1103-1112 66. Tumia NS, Johnstone AJ (2009) Platelet derived growth factor-AB enhances knee meniscal cell activity in vitro. Knee 16:73-76 67. Harner CD, Mauro CS, Lesniak BP et al (2009) Biomechanical consequences of a tear of the posterior root of the medial meniscus. Surgical technique. J Bone Joint Surg Am 91 Suppl 2:257-270 68. Allaire R, Muriuki M, Gilbertson L et al (2008) Biomechanical consequences of a tear of the posterior root of the medial meniscus. Similar to total meniscectomy. J Bone Joint Surg Am 90:1922-1931 69. Sekiya JK, West RV, Groff YJ et al (2006) Clinical outcomes following isolated lateral meniscal allograft transplantation. Arthroscopy 22:771-780 70. Colvin AC, West RV (2008) Patellar instability. J Bone Joint Surg Am 90:2751-2762 71. Glazebrook MA, Ganapathy V, Bridge MA et al (2009) Evidence-based indications for ankle arthroscopy. Arthroscopy 25:1478-1490 72. Giannini S, Battaglia M, Buda R et al (2009) Surgical treatment of osteochondral lesions of the talus by open-field autologous chondrocyte implantation: a 10-year follow-up clinical and magnetic resonance imaging T2-mapping evaluation. Am J Sports Med 37 Suppl 1:112S-118S 73. Lee KB, Bai LB, Yoon TR et al (2009) Second-look arthroscopic findings and clinical outcomes after microfracture for osteochondral lesions of the talus. Am J Sports Med 37 Suppl 1:63S-70S

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74. Lee KB, Bai LB, Chung JY et al (2010) Arthroscopic microfracture for osteochondral lesions of the talus. Knee Surg Sports Traumatol Arthrosc 18:247-253 75. Theye F, Mueller KA (2004) “Heads up”: concussions in high school sports. Clin Med Res 2:165-171 76. Lovell M (2009) The management of sports-related concussion: current status and future trends. Clin Sports Med 28:95-111 77. Schatz P, Pardini JE, Lovell MR et al (2006) Sensitivity and specificity of the ImPACT Test Battery for concussion in athletes. Arch Clin Neuropsychol 21:91-99 78. Iverson GL, Lovell MR, Collins MW (2005) Validity of ImPACT for measuring processing speed following sports-related concussion. J Clin Exp Neuropsychol 27:683-689 79. Tan H, Chu CR, Payne KA et al (2009) Injectable in situ forming biodegradable chitosanhyaluronic acid based hydrogels for cartilage tissue engineering. Biomaterials 30:2499-2506 80. Bear DM, Williams A, Chu CT et al (2009) Optical coherence tomography grading correlates with MRI T2 mapping and extracellular matrix content. J Orthop Res 81. Chu CR, Izzo NJ, Irrgang JJ et al (2007) Clinical diagnosis of potentially treatable early articular cartilage degeneration using optical coherence tomography. J Biomed Opt 12:051703 82. Chu CR, Lin D, Geisler JL et al (2004) Arthroscopic microscopy of articular cartilage using optical coherence tomography. Am J Sports Med 32:699-709 83. Bedair HS, Karthikeyan T, Quintero A et al (2008) Angiotensin II receptor blockade administered after injury improves muscle regeneration and decreases fibrosis in normal skeletal muscle. Am J Sports Med 36:1548-1554 84. Zhu J, Li Y, Shen W et al (2007) Relationships between transforming growth factor-beta1, myostatin, and decorin: implications for skeletal muscle fibrosis. J Biol Chem 282:2585225863 85. Sato K, Li Y, Foster W et al (2003) Improvement of muscle healing through enhancement of muscle regeneration and prevention of fibrosis. Muscle Nerve 28:365-372 86. Negishi S, Li Y, Usas A et al (2005) The effect of relaxin treatment on skeletal muscle injuries. Am J Sports Med 33:1816-1824 87. Li Y, Negishi S, Sakamoto M et al (2005) The use of relaxin improves healing in injured muscle. Ann N Y Acad Sci 1041:395-397 88. Fukushima K, Badlani N, Usas A et al (2001) The use of an antifibrosis agent to improve muscle recovery after laceration. Am J Sports Med 29:394-402 89. Sell TC, Ferris CM, Abt JP et al (2006) The effect of direction and reaction on the neuromuscular and biomechanical characteristics of the knee during tasks that simulate the noncontact anterior cruciate ligament injury mechanism. Am J Sports Med 34:43-54 90. Myers J, Lephart S, Tsai YS et al (2008) The role of upper torso and pelvis rotation in driving performance during the golf swing. J Sports Sci 26:181-188 91. Lephart SM, Smoliga JM, Myers JB et al (2007) An eight-week golf-specific exercise program improves physical characteristics, swing mechanics, and golf performance in recreational golfers. J Strength Cond Res 21:860-869 92. Abt JP, Smoliga JM, Brick MJ et al (2007) Relationship between cycling mechanics and core stability. J Strength Cond Res 21:1300-1304 93. Myers JB, Oyama S, Wassinger CA et al (2007) Reliability, precision, accuracy, and validity of posterior shoulder tightness assessment in overhead athletes. Am J Sports Med 35:19221930 94. Lephart SM, Ferris CM, Fu FH (2002) Risk factors associated with noncontact anterior cruciate ligament injuries in female athletes. Instr Course Lect 51:307-310 95. Lephart SM, Abt JP, Ferris CM (2002) Neuromuscular contributions to anterior cruciate ligament injuries in females. Curr Opin Rheumatol 14:168-173 96. Hall MP, Band PA, Meislin RJ et al (2009) Platelet-rich plasma: current concepts and application in sports medicine. J Am Acad Orthop Surg 17:602-608 97. Alsousou J, Thompson M, Hulley P et al (2009) The biology of platelet-rich plasma and its application in trauma and orthopaedic surgery: a review of the literature. J Bone Joint Surg Br 91:987-996


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98. de Vos RJ, Weir A, van Schie HT et al (2010) Platelet-rich plasma injection for chronic Achilles tendinopathy: a randomized controlled trial. JAMA 303:144-149 99. Zuk PA, Zhu M, Mizuno H et al (2001) Multilineage cells from human adipose tissue: implications for cell-based therapies. Tissue Eng 7:211-228 100. Nakahara H, Goldberg VM, Caplan AI (1992) Culture-expanded periosteal-derived cells exhibit osteochondrogenic potential in porous calcium phosphate ceramics in vivo. Clin Orthop Relat Res 291-298 101. De Bari C, Dell'Accio F, Tylzanowski P et al (2001) Multipotent mesenchymal stem cells from adult human synovial membrane. Arthritis Rheum 44:1928-1942 102. Diefenderfer DL, Brighton CT (2000) Microvascular pericytes express aggrecan message which is regulated by BMP-2. Biochem Biophys Res Commun 269:172-178 103. Zvaifler NJ, Marinova-Mutafchieva L, Adams G et al (2000) Mesenchymal precursor cells in the blood of normal individuals. Arthritis Res 2:477-488 104. Pittenger MF, Mackay AM, Beck SC et al (1999) Multilineage potential of adult human mesenchymal stem cells. Science 284:143-147 105. Qu-Petersen Z, Deasy B, Jankowski R et al (2002) Identification of a novel population of muscle stem cells in mice: potential for muscle regeneration. J Cell Biol 157:851-864 106. Gussoni E, Soneoka Y, Strickland CD et al (1999) Dystrophin expression in the mdx mouse restored by stem cell transplantation. Nature 401:390-394 107. Bey MJ, Kline SK, Tashman S et al (2008) Accuracy of biplane x-ray imaging combined with model-based tracking for measuring in-vivo patellofemoral joint motion. J Orthop Surg Res 3:38 108. Anderst WJ, Tashman S (2009) The association between velocity of the center of closest proximity on subchondral bones and osteoarthritis progression. J Orthop Res 27:71-77 109. Anderst W, Zauel R, Bishop J et al (2009) Validation of three-dimensional model-based tibiofemoral tracking during running. Med Eng Phys 31:10-16 110. Tashman S, Collon D, Anderson K et al (2004) Abnormal rotational knee motion during running after anterior cruciate ligament reconstruction. Am J Sports Med 32:975-983 111. Bey MJ, Zauel R, Brock SK et al (2006) Validation of a new model-based tracking technique for measuring three-dimensional, in vivo glenohumeral joint kinematics. J Biomech Eng 128:604-609

The Pathophysiology of Tendon Injury

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N. Maffulli, U.G. Longo, F. Spiezia and V. Denaro

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Abstract The etiology of tendinopathy and tendon rupture is unclear. Tendon pathology is likely caused by intrinsic or extrinsic factors alone or in combination, but the evidence for most of these factors is limited or absent. The essence of tendinopathy is a failed healing response. In the last few decades, biomaterials have become critical components in the development of effective new medical therapies for wound care, with many new tissue-engineered materials recently introduced. Indeed, the principles of engineering and biology have been applied to the development of artificial polymers, biodegradable films, and biomaterials derived from animal or human sources. Preliminary studies support the use of biomaterials as an alternative to tendon augmentation, with enormous therapeutic potential. In animal models, growth factors are effective in increasing the cellularity and overall tissue volume of the repair site. Several interesting techniques are being developed to manage tendon injuries. Whilst these emerging technologies may substantially improve clinical treatment options, their full impact needs to be critically evaluated in an unbiased, scientific fashion.

2.1 Introduction Tendon injuries produce considerable morbidity, and the disability that they cause may last for several months. Tendon injuries can be acute or chronic and are caused by intrinsic or extrinsic factors, either alone or in combination. Extrinsic factors may predominate in acute trauma.

Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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2.1.1 Tendon Structure Healthy tendons are brilliant white with a fibroelastic texture. Tenoblasts and tenocytes constitute 90-95% of the cellular elements of tendons in the extracellular matrix (ECM). Tenoblasts are spindle-shaped, immature tendon cells with high metabolic activity. In their mature form they become elongated and are referred to as tenocytes. The remaining 5-10% of the cellular elements of tendons is made up of chondrocytes, which are found at bone attachment and insertion sites. In addition, there are synovial cells of the tendon sheath and vascular cells; the latter include capillary endothelial cells and the smooth muscle cells of arterioles [1]. Tenocytes are responsible for energy production, in addition to synthesizing collagen and all the components of the ECM. With aging, metabolic pathways shift from aerobic to increasingly anaerobic energy production. In fact, the oxygen consumption of tendons and ligaments is lower than that of muscles. This property explains the ability of tendons to sustain heavy loads and to maintain tension for long periods, without risking ischemia or necrosis. Unfortunately, metabolism is also low after injury. Water accounts for 70% of the tendon mass while the dry mass comprising the remaining 30% is a mixture of various types of collagen and elastin. A collagen fiber is the smallest tendon unit that can be tested mechanically and is visible under light microscopy. Collagen fibers are generally oriented longitudinally, but there are also fibers that run transversely and horizontally, in the shape of spirals and braids. Proteoglycans, glycosaminoglycans, glycoproteins, and other small molecules are present in a network of ECM ground substance that surrounds the collagen fibers and the tenocytes. Proteoglycans are strongly hydrophilic. Adhesive glycoproteins, such as fibronectin and thrombospondin, participate in tendon repair and regeneration processes. Tenascin-C, which is also present in the ECM, contains a number of repeating fibronectin type-III domains. In response to stress, these domains unfold, thus allowing tenascin-C to function as an elastic protein. The expression of tenascinC is regulated by mechanical strain and is up-regulated in tendinopathy. This protein may play a role in collagen fiber alignment and orientation. The epitenon is a fine, loose connective-tissue sheath containing the tendon’s vascular, lymphatic, and nerve supply. It covers the entire tendon and, as the endotenon, extends deep within it, between the tertiary bundles. Tendons receive their blood supply from three main sources: intrinsic systems at the myotendinous and osteotendinous junctions, and the extrinsic system, through either the paratenon or the synovial sheath.

2.1.2 Tendon Pathology The etiology of tendon rupture is unclear. In ruptures of the Achilles tendon, an acceleration-deceleration mechanism has been reported in up to 90% of sports-related traumas. Also, malfunction of the normal protective inhibitory pathway of the musculotendinous unit has been described. Advanced features indicative of a failed healing response are a

2 The Pathophysiology of Tendon Injury

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common histological finding in spontaneous tendon ruptures. In addition, tendon degeneration may decrease tensile strength, predisposing it to rupture. Tendon pathology is likely caused by intrinsic or extrinsic factors or by both. The evidence for most of these factors is limited or absent. Risk factors suggested in the literature are generally based on theories or assumptions arising from associations found between Achilles tendinopathy and variables identified in case-control or case-series studies. Postulated intrinsic factors include tendon vascularity or weakness, a lack of flexibility of the gastrocnemius-soleus, pes cavus, and lateral ankle instability. Excessive loading of tendons during vigorous physical training is considered the major causative factor in tendinopathy. Free radical damage, occurring on reperfusion after ischemia, as well as hypoxia, hyperthermia, and impaired tenocyte apoptosis have been linked to tendinopathy. Meta-analysis of the effects of corticosteroid has shown that published data are insufficient to predict the risk of rupture following corticosteroid injections. In a case-control study, subjects with chronic painful Achilles tendinopathy had a lipid profile characteristic of a dyslipidemia. Evidence from a large population-based case-control study suggested that Achilles tendon rupture is a common adverse reaction to management with fluoroquinolones. Based on the study’s findings, a single case would occur for every 5958 individuals treated with fluoroquinolones. The corresponding number needed to harm was 979 (95% CI 122, 9172) for patients who concomitantly use corticosteroids and 1638 (95% CI 351, 8843) for those aged > 60 years. The clinical impact of fluoroquinolone use on the onset of less severe forms of tendon disorders is actually unknown, but it is expected to be even higher. Clinicians should therefore be aware of this adverse effect and of potential concurrent corticosteroid use, especially in elderly patients. Evidence arising from an observational historic cohort-based study showed that quinolone-related Achilles tendinopathy is frequent among heart transplant patients, especially in those with renal dysfunction or lengthy post-transplantation survival. If no alternative anti-bacterial therapy is available for high-risk patients, close clinical surveillance is warranted. An association between the AB0 blood group and the incidence of Achilles tendinopathy ruptures or chronic Achilles tendinopathy is evident in Hungarian and Finnish populations with blood group 0, but not in other populations. The gene for the AB0 blood group on chromosome 9q34 encodes transferases, which, apart from determining the structure of glycoprotein antigens on red blood cells, may also determine the structure of some ECM proteins present in tendons. A single gene is unlikely to be involved in the pathogenesis of tendinopathy [2, 3]. Polymorphisms within the type V collagen (COL5A1) and tenascin-C (TNC) genes have been associated with Achilles tendon injuries in a physically active population, with the strongest association determined for the COL5A1 variant rs12722, BstUI RFLP. Type V collagen, a quantitatively minor fibrillar collagen that forms heterotypic fibrils with type I collagen, plays a role in the regulation of the size and configuration of fibrils of the much more abundant Achilles tendon component type I collagen. The COL5A1 and COL5A2 genes encode a heterotrimer composed, respectively, of two pro-a1(V) chains and a single pro-a2(V) chain. COL5A1 differs somewhat from the major fibrillar-collagen genes, in terms of intron-exon structure, and encodes a very large amino-terminal (N-) propeptide. Haploinsufficiency for type V collagen, caused by a nonfunctional COL5A1-allele, is responsible for approximately one-third of patients with clas-

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sic Ehlers-Danlos syndrome, a heterogeneous group of inherited disorders characterized by soft, hyperextensible skin, hypermobile joints, abnormal scarring, and other forms of systemic involvement. The exact role of COL5A1 and TNC genes in the pathogenesis of tendinopathy is still debated, and current evidence is insufficient to clarify whether or not these genes are the ideal markers of tendinopathy. A negative association of a particular gene with, e.g., the AB0 system does not necessarily imply that there is absolutely no association with that particular gene(s) at that locus. Instead, the fact that certain studies have found an association between the AB0 system and tendon injuries warrants further investigation at that particular locus. It is also possible that other genes, yet to be determined, contribute to the pathogenesis of tendinopathy, which may be a polygenic condition, given the multitude of genes involved in maintaining normal tendon homeostasis. Based on current evidence, it is difficult to conceive that only a single gene and not multiple genes are involved in the pathogenesis of tendinopathy. Thus, additional investigation are needed to identify these genes.

2.1.3 Metalloproteases in Tendinopathy The tendon matrix constantly remodels, with higher rates of turnover at sites exposed to high levels of strain. Matrix metalloproteases (MMPS), a family of zinc- and calcium-dependent endopeptidases active at neutral pH, are involved in the remodeling of ECM through their broad proteolytic capabilities. Collagen degradation in tendon ECM is initiated by MMPs, and the 23 human MMPs identified thus far have a wide range of extracellular substrates. MMPs can be subdivided into four main groups: collagenases, which cleave native collagen types I, II, and III; gelatinases, which cleave denatured collagens and type IV collagen; stromelysins, which degrade proteoglycans, fibronectin, casein, and collagen types III, IV, and V; and membrane type MMPs. The activity of MMPs is inhibited reversibly by TIMPs in a non-covalent fashion and with a 1:1 stoichiometry. There are, likewise, four types of inhibitory TIMPs (TIMP1-TIMP4). The balance between the activities of MMPs and TIMPs regulates tendon remodeling, with an imbalance producing collagen disturbances in tendons. Alteration of MMP and TIMP expression from basal levels leads to alteration of tendon homoeostasis. Tendinopathic tendons have an increased rate of matrix remodeling, leading to a mechanically less stable tendon that is more susceptible to damage. MMP3 may play a major role in the regulation of tendon ECM degradation and tissue remodeling. Increased expression of this enzyme may be necessary for appropriate tissue remodeling and the prevention of tendinopathic changes. The timing of MMP3 production is probably also critical in this process. As MMP3 and TIMP1-TIMP4 are down-regulated in tendinopathic tendons, decreased MMP3 expression may lead to tendinopathic changes in tendons. The expression of MMP2 can be up-regulated in Achilles tendinopathy. Physical exercise can influence local MMP and TIMP activities in human Achilles tendon, with a pronounced increase in local levels of pro-MMP9 and MMP9 after exercise, a probable result of the increased number of leukocytes in the circulation. MMP9 may well have a role in the inflammatory reaction induced in human Achilles tendon by intensive exercise.


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2.1.4 Histology The essence of tendinopathy is a failed healing response, with the haphazard proliferation of tenocytes, some evidence of degeneration in tendon cells and the disruption of collagen fibers, and a subsequent increase in non-collagenous matrix. Tendinopathic lesions affect both the collagen matrix and tenocytes. The parallel orientation of collagen fibers is lost and there is a decrease in collagen fiber diameter as well as the overall density of collagen [4-6]. Collagen microtears may also occur and may be surrounded by erythrocytes, fibrin, and fibronectin deposits. Normally, collagen fibers in tendons are tightly bundled in a parallel fashion. In tendinopathic samples, however, there is unequal and irregular crimping, loosening, and an increased waviness of collagen fibers, with an increase in type III (reparative) collagen. In tendinopathic tendons, tenocytes are abnormally plentiful in some areas. They have rounded nuclei, and there is ultrastructural evidence of increased proteoglycan and protein production, which gives these cells a chondroid appearance. Other areas may contain fewer tenocytes than normal. In addition, these cells have small, pyknotic nuclei and are associated with an occasional infiltration of lymphocyte- and macrophage-type cells, possibly part of a healing process associated with the proliferation of capillaries and arterioles.

2.2 Mechanobiology By transmitting muscle forces to bone, tendons allow locomotion and enhance joint stability. The functional and mechanical features of tendons are adapted to dynamic stresses and strains. Collagen, water, and interactions between collagenous and non-collagenous proteins (proteoglycans) determine the viscoelastic features of tendons that provide flexible links between muscles and bones. Viscous materials are deformable and resist shear flow as well as strain linearly with time when a stress is applied. Tendons are therefore more deformable at low strain rates, but they are less effective at transferring loads. Conversely, they are less deformable at high strain rates, with a high degree of stiffness, and thus more effective in moving large loads. The dynamic stresses and strains imposed on tendons determine their structural changes. Appropriate physical training increases the cross-sectional area and tensile strength of tendons, due in part to an increase in the production of type I collagen by tenocytes. However, inappropriate physical training leads to tendon overuse injuries and tendinopathy. Highintensity exercise was shown to cause greater matrix-collagen turnover in growing chickens, resulting in the reduced maturation of tendon collagen. In that study, the distribution of IGF-I (insulin-like growth factor I) immunoreactivity was mapped in normal Achilles and tibialis anterior tendons. Training the animals for 5 days on a treadmill for 20-60 min per day induced, after 3-5 days, an increase in IGF-I immunoreactivity throughout the cytoplasm of tendon and paratenon fibroblasts. IGF-I acts as a potent stimulator of mitogenesis and protein synthesis, therefore serving as a protein marker for remodeling activi-

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ties of the tendon. Microdialysis techniques were used to similarly study the effect of physical training on humans. Nineteen young males were evaluated before and after 4 and 11 weeks of physical training, using microdialysis catheters to measure interstitial concentrations of collagen propeptide and a collagen degradation product. The catheters were placed under ultrasound guidance in the peritendinous space ventral to the Achilles tendon in both legs. Physical training resulted in increased turnover of collagen type I in local connective tissue of the peritendinous Achilles region. Immobilization decreased the total weight, tensile strength, and stiffness of the tendons. Tendon overuse injuries affect millions of people in both occupational and athletic settings. Excessive mechanical loading is regarded as an important causative factor for tendinopathy. Repetitive strains below the failure threshold of tendons result in microinjuries to the tendon, with episodes of tendon inflammation. Increased levels of prostaglandin (PG)E2 are present in human tendons after repetitive mechanical loading. In vitro repetitive mechanical loading of human tendon fibroblasts increases the production of PGE2 and leukotriene (LT)B4. The local administration of PGE1 produces acute inflammation of the tendon and its surrounding tissues in animal tendons. Prolonged PGE1 administration causes peri- and intra-tendinous degeneration, providing a simple and reproducible model of Achilles tendinopathy. Repeated exposure of the rabbit patellar tendon to PGE2 causes degenerative changes within the tendon. Microdialysis was also used to study concentrations of substances in human tendons. In four patients with a painful nodule in the Achilles tendon and in five controls (mean age 37.2 years) with normal Achilles tendons, local concentrations of glutamate and PGE2 were measured under resting conditions. There were no significant differences in the mean concentrations of PGE2 between tendons with tendinopathy and normal tendons. Concentrations of the excitatory neurotransmitter glutamate in the Achilles tendons with a painful nodule were higher. Thus, repetitive submaximal strains below the failure threshold may be responsible for tendon microinjuries and episodes of PG-mediated tendon inflammation; however, by the time the microinjuries become clinically evident, PGs are no longer present in the tendon.

2.3 The Future 2.3.1 Biomaterials In the last few decades, biomaterials have become critical components in the development of effective new medical therapies for wound care, with many new tissue-engineered materials recently introduced. Indeed, the principles of engineering and biology have been applied to the development of artificial polymers, biodegradable films, and biomaterials derived from animal or human sources. As the limitations of previous generations of biologically derived materials are overcome, many new and impressive applications for biomaterials are being examined [6-9].


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Biological scaffolds are protein-based extracellular matrices usually derived from human or animal connective tissues. The advantages of biological scaffolds are their welldefined 3D surface protein microstructure (allowing host cell integration), and natural porosity (which provides a much larger space for host cell attachment, proliferation, migration, and gas and metabolite diffusion). These proprieties allow biological scaffolds to interact with host tissue and to induce new tissue formation faster than achieved with synthetic scaffolds. One of the advantages of biomaterials is that they can be used together with exogenous growth factors, gene therapy approaches, and cell delivery. However, the limitations of biological scaffolds relate to their mechanical properties (often resulting in failure of surgery), nonspecific induction ability, undefined degradation rate, and variation in biocompatibility depending on the source material, all of which can cause an inflammatory response and even implant rejection. By contrast, synthetic scaffolds are manufactured from chemical compounds, allowing better control of their chemical and physical properties and thus greater mechanical strength and consistency in quality. However, the biocompatibility of synthetic scaffolds is very poor, as they can never be absorbed or integrated into host tissue. High incidences of postoperative infection in addition to chronic immune response have been reported with the use of such materials. The ideal scaffold should induce host tissue ingrowth and tendon regeneration during the degradation process, but these features vary dramatically among the commercially available scaffolds. The capability of biological scaffolds to induce host tissue ingrowth is superior, even though this process may seem to be uncontrolled and nonspecific. The surface of biological scaffolds is mostly composed of natural type I collagen, which confers a higher affinity for host cells and therefore promotes cellular adhesion, proliferation, migration, and tissue induction. This is in contrast to the surfaces of synthetic scaffolds, which are composed of macromolecules lacking a well-defined structure that would allow host cells to strongly bind and thus initiate growth. Even though biological scaffolds are becoming more popular, well-conducted clinical studies are lacking, and the data describing complications or adverse events associated with the use of these products are scarce. ECMs fabricated in parallel with other cellular materials may improve the mechanical properties of biological scaffolds; for example, natural ECMs seeded with bone marrow stem cells or tenocytes. However, clinical evidence supporting this approach is still lacking. Major concerns about biological as well as synthetic scaffolds are their biocompatibility and the inflammatory response associated with a foreign-body rejection. To decrease the bio-burden and the risk of inflammatory or foreign-body reactions, all tissues, regardless of their origin, are extensively purified to remove proteins, cells, and lipids. Some graft options have been artificially cross-linked to decrease their antigenicity, by decreasing their sensitivity to collagenases. Although rare, aseptic, nonspecific inflammatory reactions and foreign-body-like reactions have been reported with certain xenografts. Aseptic reactions were reported in 16-22% of implantations, always with negative aspirates and cultures, destroyed xenografts, and histopathological evidence of inflamed granulation tissue with abundant neutrophils, but no foreign-body reaction, as documented by the absence of organisms, crystals, or giant cells. The use of biological scaffolds manufactured from human or animal tissue also carries the risk of disease transmission, which although not re-

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ported to date, remains a matter of concern. Obviously, there is no risk of disease transmission with the use of synthetic scaffolds. Several chemical cross-linking agents (glutaraldehyde, poly-epoxy compound, carbodiimide, genipin, isocyanate, and proanthocyanidin) have been used to stabilize the scaffold’s collagen structure, thus maintaining its mechanical properties. Clinical studies have not confirmed the expected beneficial effect of chemical cross-linking scaffolds. Further investigations are warranted to establish the in vivo benefits of chemical cross-linking of scaffolds in terms of their biocompatibility and mechanical properties. Another cause for concern is that currently available scaffolds are produced to mimic the extracellular microenvironment of the tendon or ligament in order to stimulate cell proliferation and tissue in-growth, largely ignoring the healing process at the enthesis. The repair procedure often involves reconstruction of the junction but the failure of surgery is frequently the result of osteolysis and scaffold pullout. Further investigations are required to better understand how to promote healing of the bone-tendon junction. In conclusion, preliminary studies support the use of biomaterials as an alternative to tendon augmentation, with enormous therapeutic potential. However, definitive conclusions on the use of biomaterials for tendon augmentation await the results of further studies. Additionally, the prevalence of postoperative complications encountered with their use varies within the different studies.

2.3.2 Gene Therapy Several strategies have recently emerged, including the use of growth factors and cytokines, gene therapy, and tissue engineering with mesenchymal stem cells, all aimed at enhancing tendon healing. They hold the promise of more successful outcomes in the management of patients with tendon pathology. Growth factors are signaling molecules involved in cell chemotaxis, proliferation, matrix synthesis, and cell differentiation. They also play an important role in regulating the phases of tendon healing. After their release from platelets, polymorphonuclear leukocytes, and macrophages at the wound site, growth factors bind to cell surface receptors that activate intracellular changes in DNA synthesis and the expression of genes involved in neovascularization, chemotaxis, fibroblast proliferation, and collagen synthesis. Although the use of growth factors is still largely experimental, their beneficial effect on tendon healing is well established. In animal models, growth factors are effective in increasing the cellularity and overall tissue volume of the repair site. These features usually result in increased failure loads on biomechanical testing. However, the differences in failure loads become less significant when they are normalized to the volume or cross-sectional area of the repaired tissue. This implies that growth factors are able to improve the strength of the repair by promoting the formation of more scar tissue (i.e., the structural properties are improved but the material properties are not). Excessive scar tissue at the healing attachment site may predispose patients to impingement postoperatively [9-15]. The ultimate outcome of the repair depends on both pullout strength and stiffness, with the latter, together with creep perhaps


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being more important. Ideally, biological therapies are able to induce the formation of tissues whose material properties are close to that of normal tissue. Platelet-derived growth factor (PDGF) and epidermal growth factor (EGF) were the first two growth factors applied in vitro to study the effect on tendon healing, with the results indicating the stimulation of tendon fibroblast proliferation. PDGF-BB acts as a mitogen and chemotactic cytokine that may enhance ligament and tendon healing, but improved healing with PDGF is dependent on the dosage, timing, and delivery vehicle used. There are currently several commercially available systems to produce a “platelet-rich plasma” or “platelet gel” from autologous blood. These systems involve spinning autologous blood in a centrifuge to form a dense, suturable fibrin matrix that can be easily placed directly at the tendon repair site. One technical problem with these systems is that many use human or bovine thrombin to form the platelet-rich plasma. Excess thrombin causes premature platelet activation and degranulation, with the immediate release of platelet-derived cytokines. Newer systems have addressed this problem by omitting the use of thrombin. Growth factors can be delivered to the injured area by direct application. This is the most straightforward method, with delivery achieved via local injection or the use of impregnated sutures or scaffolds. The latter options have the advantage of delivering the growth factor to the specific site of injury while avoiding the overflow loss normally associated with local injection. However, local injection is comparatively non-invasive, simple and quick. The main disadvantage of direct application is that the growth factors remain at the site only for a short duration of time, which, given the fact that tendon healing continues for months to years, may not be sufficient for effective repair. Nevertheless, several animal studies have demonstrated beneficial results from the local injection of growth factors. Gene transfer using vectors can be achieved through in vivo or ex vivo techniques. In vivo transfer involves direct application of the gene to the relevant tissue. In the ex vivo technique, target cells are removed from the body, transfected with the relevant gene in the laboratory, and then transferred back into the body. In vivo transfection is less invasive and technically easier, and treatment can be commenced during the acute phase of injury. The disadvantage of this approach is the non-specific infection of cells adjacent to the site of injury. Furthermore, the success of gene transfer cannot be confirmed, and in areas of relative cell paucity only a few cells may be transfected. Both the use of highly transgenic vectors and injection into areas with a high cell density will ensure transfection of a large number of cells. More time is required for ex vivo transfection, but this technique avoids the complication of non-specific transfection and allows successful transfection to be confirmed as well as the in vitro expansion of cells if required.

2.4 Conclusions Tendon injuries give rise to significant morbidity, but at present the number of scientifically proven management modalities is limited [13, 14]. A better understanding of tendon pathology [1-5] function, and healing will lead to innovative and specific treatment strate-

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gies. Several interesting techniques, including the optimization strategies discussed in this chapter, are being developed. Whilst these emerging technologies may substantially improve clinical treatment options, their full impact needs to be critically evaluated in an unbiased, scientific fashion.

References 1. Khanna A, Friel M, Gougoulias N et al (2009) Prevention of adhesions in surgery of the flexor tendons of the hand: what is the evidence? Br Med Bull 90:85-109 2. Lippi G, Longo UG, Maffulli N (2010) Genetics and sports. Br Med Bull 93:27-47 3. Longo UG, Fazio V, Poeta ML et al (2010) Bilateral consecutive rupture of the quadriceps tendon in a man with BstUI polymorphism of the COL5A1 gene. Knee Surg Sports Traumatol Arthrosc 18:514-518 4. Longo UG, Franceschi F, Ruzzini L et al (2009) Characteristics at haematoxylin and eosin staining of ruptures of the long head of the biceps tendon. Br J Sports Med 43:603-607 5. Longo UG, Franceschi F, Ruzzini L et al (2008) Histopathology of the supraspinatus tendon in rotator cuff tears. Am J Sports Med 36:533-538 6. Longo UG, Franceschi F, Ruzzini L et al (2007) Light microscopic histology of supraspinatus tendon ruptures. Knee Surg Sports Traumatol Arthrosc 15:1390-1394 7. Longo UG, Franceschi F, Ruzzini L et al (2009) Higher fasting plasma glucose levels within the normoglycaemic range and rotator cuff tears. Br J Sports Med 43:284-287 8. Longo UG, Franceschi F, Spiezia F et al (2009) Triglycerides and total serum cholesterol in rotator cuff tears: do they matter? Br J Sports Med 9. Longo UG, Lamberti A, Maffulli N et al (2010) Tendon augmentation grafts: a systematic review. Br Med Bull 94:165-188 10. Longo UG, Oliva F, Denaro V et al (2008) Oxygen species and overuse tendinopathy in athletes. Disabil Rehabil 30:1563-1571 11. Longo UG, Ramamurthy C, Denaro V et al (2008) Minimally invasive stripping for chronic Achilles tendinopathy. Disabil Rehabil 30:1709-1713 12. Longo UG, Rittweger J, Garau G et al (2009) No influence of age, gender, weight, height, and impact profile in achilles tendinopathy in masters track and field athletes. Am J Sports Med 37:1400-1405 13. Maffulli N, Longo UG (2008) Conservative management for tendinopathy: is there enough scientific evidence? Rheumatology (Oxford) 47:390-391 14. Maffulli N, Longo UG (2008) How do eccentric exercises work in tendinopathy? Rheumatology (Oxford) 47:1444-1445 15. Maffulli N, Longo UG, Franceschi F et al (2008) Movin and Bonar scores assess the same characteristics of tendon histology. Clin Orthop Relat Res 466:1605-1611

Pathophysiology of Muscle Injuries

3

P.M. Tonino, M.K. Sinclair

Abstract Muscle injuries, ranging from mild contusions to severe strains, are the most common sports-related injuries encountered today. Although they have received scant attention compared to other sports injuries, such as soft-tissue injuries of the knee and shoulder, they are often very disabling and result in prolonged recovery and significant absence from competition. Successful treatment for these injuries remains largely conservative, following an athlete-specific rehabilitation protocol. As our knowledge of the cellular pathophysiology involved in injury and subsequent repair increases, researchers continue to search for treatments that may allow for shortened recovery times and earlier return to sports participation.

3.1 Introduction Muscle injuries are the most common sports-related injuries, with an incidence of up to 90% being contusions or strains [1, 2]. They can occur in both contact and non-contact sports and unless they are incurred during a sporting event or practice with an informed coach or trainer accessible, many go unreported and untreated in the initial stages. Based upon the mechanism of action, muscle injuries can be classified into two categories: indirect, non-contact injuries and direct, contact injuries. Indirect injuries are most commonly muscle strains that occur due to tensile forces causing disruption of muscle fibers. Direct injuries include both muscle contusions, resulting from a direct blow causing disruption of muscle fibers with subsequent hematoma, and lacerations due to penetrating trauma, which are uncommon in sporting events [3].


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3.2 Muscle Strains Strains are the result of eccentric contractions in muscles that are unable to accommodate the degree of stretch imparted by the applied forces during activities such as sprinting and jumping. They most commonly occur at the myotendinous junction (MTJ) of muscles that are composed primarily of fast-twitch fibers, particularly those muscles that cross two joints, such as the hamstrings, rectus femoris, gastrocnemius, and biceps brachii [4].

3.3 Muscle Contusions Muscle contusions, the second most common cause of injury in athletes, are the result of blunt trauma and are seen most often in contact sports such as football, rugby, soccer, lacrosse, and racquetball.

3.4 Pathophysiology The healing injured muscle progresses through a common three-stage process irrespective of the mechanism of injury: destruction, repair, and remodeling [1, 2, 5, 6] (Fig. 3.1). At the time of initial insult, the myofibers and the involved microvasculature of the muscle are torn. The ensuing hematoma and myonecrosis immediately induces an inflammatory cascade that proceeds over the first few days following injury. Resident macrophages and fibroblasts phagocytose necrotic debris and produce proteins that both restore the connective tissue and release growth factors and cytokines, both of which are thought to stimulate myogenic precursor cells to proliferate and differentiate into regenerated myofibers [1, 2, 5, 7]. The repair process begins within the first few days following the initial injury, with the peak of activity at 2 weeks, which gradually tapers off. During this process, there is associated neovascularization at the injury site that helps support the reparative process. The remodeling phase is associated with the production of scar tissue and begins 2-3 weeks following injury. In this phase, as the myofibers mature, reorganization and contraction of the scar tissue occurs as type 3 collagen is slowly remodeled to type 1 collagen. The ends of the new myofibers are not reunited but rather form new MTJs with the scar tissue.

3 Pathophysiology of Muscle Injuries

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Fig. 3.1 Timeline of the three stages in the repair process of muscle injuries. Phase I, destruction, begins with injury and lasts up to 2 weeks. It includes inflammation, removal of cell debris, and the initiation of muscle regeneration. Phase II, repair, begins within the first few days of injury, peaks at 2 weeks, and lasts up to 4 weeks. It includes revascularization and the regeneration of myofibers. Phase III, remodeling, begins during the second week and increases in intensity through the fourth week. It includes production and remodeling of scar tissue (Adapted with permission from Huard J, Li Y, Fu FH (2002) Muscle injuries and repair: current trends in research. J Bone Joint Surg Am 84:822-832)

3.5 Clinical Presentation The diagnosis of a muscle injury is most often made on a clinical basis. A history of injury should be obtained and the patient or athlete should undergo a standard physical exam of the injured limb, which includes: inspection, palpation, and functional muscle testing with comparison to the uninjured contralateral limb [5]. The clinical picture will depend upon the severity of injury and on the nature of the resultant hematoma, which can be either intramuscular or intermuscular. In an intramuscular injury, the surrounding fascia limits the size of the hematoma. Although this may restrict the amount of bleeding and the size of the hematoma, it increases the intramuscular pressure, placing the patient at increased risk for compartment syndrome. Intermuscular hematoma has a much smaller risk for compartment syndrome but is often accompanied by a greater amount of blood loss [5].


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3.6 Classification A number of authors have defined a classification system of muscle injuries, all of which include a similar three-level system that incorporates clinical and microscopic findings [5, 8, 9]. The landmark study and subsequent update on West Point cadets with quadriceps contusions provided the most detailed clinical information about injury grading, and is based upon examination of the knee’s range of motion within 12-24 h following injury [8, 9]. Due to the pathophysiological similarities between muscle strains and contusions, this grading system is useful for all types of muscle injuries (Table 3.1).

3.7 Diagnosis and Imaging Studies Muscular injuries are typically diagnosed with a history and clinical examination [5]. However, imaging studies may be indicated in some patients, such as those with a vague, atraumatic history or with delayed recovery following injury. Ultrasound and magnetic resonance imaging (MRI) have been used to evaluate the location and extent of injury. Ultrasound was once considered the imaging modality of choice in muscle injuries because of its ease of accessibility, low cost, and ability to dynamically evaluate the injured muscle [5]. However, studies have shown that the results are heavily operator-dependent and it does not provide the detail afforded by MRI, in which axial images can detect changes in muscle volume and signal intensity, and coronal or sagittal images can help define the extent of the injury [5, 7, 10]. Additionally, post-injury MRI allows for the evaluation of recovery status, which aids in assessment of the vulnerability for re-injury despite clinical resolution of symptoms [10].

Table 3.1 Muscle injury classification system Grade

Quadriceps contusions [12, 13]

Muscle injuries [2]

1 (mild)

Active knee range of motion > 90° Localized tenderness No alteration of gait Deep knee bend achievable

Tear of few muscle fibers Minor swelling and discomfort Minimal loss of strength Minimal loss of range of motion

2 (moderate)

Active knee range of motion 45-90° Swollen, tender muscle mass Antalgic gait Unable to achieve deep knee bend

More muscle damage than grade I Clear loss of function

3 (severe)

Active knee range of motion < 45° Markedly swollen and tender muscle with loss of contour Severe limp

Complete muscle tear Near complete loss of function


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3.8 Non-operative Treatment For the majority of injuries, non-operative management will successfully return the athlete to his or her pre-injury condition. The essential treatment principles include RICE (see below), early mobilization, and rehabilitation guided by clinical symptoms [2, 5-9, 11-13].

3.8.1 Initial Treatment: The RICE Principle (Rest, Ice, Compression, Elevation) The RICE concept is widely used and generally accepted in the treatment of musculoskeletal injuries [3, 5, 6, 8, 9]. The concept of brief immobilization is intended to limit the amount of edema and inflammation occurring at the injury site. It also allows time for the formation of scar tissue with adequate strength to tolerate the initiation of a physical therapy regimen [2, 8, 9]. With muscle contusions, immobilization should take place with the knee splinted in flexion up to 120° the first 12-24 h following injury to limit intramuscular hematoma [9]. Studies of injured muscle treated with immediate mobilization have demonstrated larger connective tissue scars and more frequent re-rupture at the site of original trauma [5]. This period of immobilization should be brief, lasting only the first few days following injury, until there is minimal pain at rest. Early treatment may include limited weight-bearing, depending upon the location and severity of the injury [5, 9, 10]. Cryotherapy has been independently shown to be beneficial to the healing process. The decrease in intramuscular temperature results in a slowing of tissue metabolism, thereby minimizing secondary hypoxic injury, cell debris, and edema. Ice is also thought to be effective when combined with physical therapy due to its ability to alleviate pain by relieving muscle spasm and neural inhibition [13]. Compression in combination with cryotherapy has been shown to aid in this decrease of intramuscular blood flow, reducing edema to allow for improved tissue healing [5, 9, 13]. Elevation of the extremity augments this reduction of edema as well as subsequent tissue necrosis by preventing interstitial fluid from pooling.

3.8.2 Pharmacologic Therapy Non-steroidal anti-inflammatory medications (NSAIDs) decrease the inflammatory reaction in the immediate post-injury period and reduce early catabolic loss of muscle protein without adversely affecting the healing process, tensile strength of the repair tissue, or contractibility of injured muscle. However, over the long term, they may inhibit the normal muscle regeneration cascade [5, 6, 12]. Recently, topical administration of NSAIDs was shown to effectively provide analgesia and an anti-inflammatory effect without systemic complications [7]. Hydrocortisone topical creams, as well as locally injected corticosteroids, can cause delayed elimination of the hematoma and necrotic tissue, leading to slower rate of muscle regeneration [6, 14].


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3.8.3 Rehabilitation of Muscle Injuries The basic concept of therapy is to individualize the treatment for each patient through the following progression: limitation of hemorrhage and edema, restoration of range of motion, and restoration of limb strength and function. Current accepted therapy protocols for rehabilitation of muscle injuries follow the goal-oriented steps which were initially described, and subsequently modified, in the study of West Point cadets for the treatment of quadriceps hematoma [8, 9] (Table 3.2). The initiation of rehabilitation should begin once pain at rest has resolved, about 3-5 days following injury. In determining the tempo of progression through the rehabilitation protocol, the patient’s pain should be used as a guide. Once he or she is able to successfully complete the goals of each phase in a pain-free manner, the next level of intensity may be initiated. The role of early mobilization for the early treatment of muscle injuries was first described 60 years ago and continues to receive widespread support; however, mobilization should not be immediate [5, 9]. Studies comparing mobilization and immobilization have demonstrated improved histological and biological changes with early mobilization [5]. Early mobilization induces a more rapid and intensive capillary in-growth in healing muscle, allowing for complete regeneration of muscle fibers and with a more parallel orientation [2, 5]. Active mobilization should commence with isometric exercises, within the limits of the patient’s pain tolerance. When pain-free active range of motion of the joint has been achieved, isometric exercises with resistance can be instituted, progressing to isotonic training, initially without resistance and then with the gradual addition of resistance exercises. Isokinetic exercises are then performed until all activities are pain-free and the patient has full active range of motion of the injured limb, comparable to the contralateral extremity [5, 9]. Table 3.2 Treatment algorithm for muscle injuries [3, 5, 7] Phase

Patho-physiology [1, 2, 15]

1. Immobilization/ RICE

Goal

Therapy

Progression to next phase

Local hemorrhage Limit Myofibrillar hemorrhage retraction Edema due to increased capillary permeability

Rest Crutch use Compression Water-based therapy

Pain-free at rest

2. Early mobilization

Deposition of collagen Formation of new MTJ Capillary vessel formation

Restoration of pain-free range of motion

Isometric

Pain-free with range of motion Near-complete resolution of edema

3. Functional rehabilitation

Remodeling of fibrotic scar

Restoration Isotonic of strength Isokinteic and endurance

Pain-free with all activities


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Once these goals have been achieved, a decision to return to sport can then be made. Compression wraps are used for athletes returning to sports activities after muscle injuries, by providing more effective contraction of the muscle and helping to distribute impact forces [6]. Prevention of re-injury of the affected muscle is critical once the athlete is ready to return to competition. Warm-up prior to competition is recommended, as increased joint range of motion and elevated muscle temperature help improve the efficiency of muscle contractions [4]. The likelihood of re-injury of the affected muscle can be reduced with the use of padding for contact sports in addition to training athletes to tense muscles prior to impact in order to distribute the force of contact [4, 9].

3.9 Operative Treatment Although most muscle injuries will heal with appropriate non-operative management, specific surgical treatments are indicated for the most severe forms of each muscular injury type [1, 5, 7, 11]. Large intramuscular hematomas can be evacuated by ultrasound needle-guided aspiration followed by a compressive bandage if performed within 7-10 days of the traumatic event. In some cases, formal irrigation and thorough debridement of the hematoma and surrounding necrotic tissue may be required. Grade 3 or complete tears, particularly in muscles with few or no agonists, is also an indication for surgical repair. Menetrey recommended suturing with large absorbable sutures through the thick substance of the muscle, using a modified Kessler stitch technique. This decreases the distance between the lacerated edges, resulting in faster healing, decreased scar tissue production, and improved restoration of strength compared with immobilization [5, 11]. For patients with >50% of the muscle belly torn, suture repair of the overlying fascia is indicated. Lastly, patients who present with persistent extension pain (> 4-6 months following injury) accompanied by an extension deficit may have adhesions, which require lysis. Immediate post-operative management should include a compression dressing and immobilization of the operative muscle in a neutral position, including crutch use and nonweight-bearing status. The duration of immobilization is variable, depending upon the severity of the injury [5].

3.10 Complications of Muscle Injuries Myositis ossificans traumatica, a complication of hematoma most commonly associated with muscle injuries, is a heterotopic formation of bone and cartilage within muscle tissue. It is encountered in higher-grade muscle injuries occurring in adolescent and young adult males who sustain high-energy contact-sports-related injuries. It can also be seen in patients who sustain a re-injury after returning to sports following a significant muscle contusion. The muscles most commonly affected are the proximal limb muscles of the thigh (quadriceps) and upper arm (brachialis) [1, 5, 9].

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The diagnosis of myositis ossificans should be considered if pain and swelling after traumatic injury do not respond to conservative treatment within 10-14 days of the initial trauma or if symptoms worsen after 2-3 weeks. Clinical exam reveals that the region of the injured muscle has become increasingly tender and warm, with loss of range of motion of the affected joint. Radiographs will show evidence of this pathology but they tend to lag 2-4 weeks behind the presenting symptoms. Other imaging techniques, in addition to plain radiographs, that can be helpful in the diagnosis prior to evidence of disease include: MRI, CT, and bone scan. Laboratory values, including serum alkaline phosphatase and erythrocyte sedimentation rate can be elevated; however, these have not been proven to be specific in the diagnosis of myositis ossificans. Treatment is the same as that for muscle injury using the RICE technique followed by progressive rehabilitation guided by the patient’s symptoms – although the rehabilitation course will be significantly lengthened, with a delay in return to sports [5, 6, 9]. Despite their effectiveness in preventing heterotopic ossification following surgery, pharmacologic agents, including bisphosphonates and indomethacin, have not been shown to be effective in the prevention of myositis ossificans [5, 7]. Studies have shown that non-operative management allows most patients, regardless of degree of injury and the development of myositis ossificans, to return to their pre-injury level of activity [8, 9]. Surgical excision is indicated when the calcification mass limits the range of motion of the adjacent joint, leading to a functional disability. This should be delayed until the myositis ossificans mass has matured radiographically, which normally occurs between 12 and 24 months after the onset of symptoms [5]. A pseudocyst is a post-injury complication often occurring in muscle that is re-injured after return to activity. It is diagnosed using MRI and frequently requires surgical excision, with re-approximation of muscle fibers [7].

3.11 Innovations and Considerations As our knowledge of the cellular processes that occur after muscle injuries has increased, modern research has focused on treatments that attempt to intervene at the cellular level. This includes enhancing or accelerating the muscular healing process and/or diminishing the degree of fibrosis that occurs (Fig. 3.2).

3.11.1 Growth Factors Autologous platelet-rich plasma (PRP) has been used since the 1970s in an attempt to enhance the recruitment, proliferation, and differentiation of cells involved in tissue regeneration [15]. The goal of this therapy is not to hasten return to sport, but rather to increase muscle strength when athletes return to sports following these injuries [7]. Studies have shown a positive effect of PRP when used to treat grade III muscle strain, the most severe injury, with-


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Fig. 3.2 Muscle repair cycle at the cellular level. The cellular factors affecting each step of muscle repair serve as targets for potential interventional innovations to improve muscle healing (Adapted with permission from Huard J, Li Y, Fu FH (2002) Muscle injuries and repair: current trends in research. J Bone Joint Surg Am 84:822-832)

in the first 7 days of its occurrence. The administration of autologous PRP is performed in sterile fashion under ultrasound guidance, following aspiration of the hematoma [1, 7, 15]. Although successful, the World Anti-Doping Agency considers this therapy as illegal for elite athletes. Therefore, PRP has only been used in those who are not subject to the agency’s rules.

3.11.2 Gene Therapy Growth factors must be administered in high concentration in order to enhance the repair of skeletal muscle. Thus, gene therapy is currently being explored as a delivery method that would allow for sustained effective concentrations of growth factor to injured muscle [1, 5].

3.11.3 Anti-fibrotic Treatment Transforming growth factor β1 (TGF-β1) expression is elevated in animal models of injured skeletal muscle and can lead to the development of fibrosis in muscle tissue. Accordingly, TGF-β1 antagonists may be helpful in preventing fibrosis in healing skeletal muscle [1].

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References 1. Huard J, Li Y, Fu FH (2002) Muscle injuries and repair: current trends in research. J Bone Joint Surg Am 84:822-832 2. Crisco JJ, Jokl P, Heinen GT et al (1994) A muscle contusion injury model: biomechanics, physiology and histology. Am J Sports Med 22:702-710 3. Mair S, Royalty B (2009) Muscle injuries in OKU: sports medicine 4. AAOS Rosemont Illinois 4. Safran MR, Garrett WE Jr, Seaber AV et al (1988) The role of warmup in muscular injury prevention. Am J Sports Med 16:123-129 5. Järvinen TA, Järvinen TL, Kääriäinen M et al (2005) Muscle injuries: biology and treatment. Am J Sports Med 33:745-764 6. Beiner JM, Jokl P (2002) Muscle contusion injury and myositis ossificans traumatica. Clin Orthop Relat Res 403 suppl:S110-S119 7. Di Carli A, Volpi P, Pelosini I et al (2009) New therapeutic approaches for management of sport-induced muscle strains. Adv Ther 26:1072-1083 8. Jackson DW, Feagin JA (1973) Quadriceps contusions in young atheletes. Relation of severity of injury to treatment and prognosis. J Bone Joint Surg Am 55:95-105 9. Ryan JB, Wheeler JH, Hopkinson WJ et al (1991) Quadriceps contusions. West Point update. Am J Sports Med 19:209-304 10. Boutin RD, Fritz RC, Steinbach LS (2002) Imaging of sports-related muscle injuries. Radiol Clin North Am 40:333-362 11. Menetrey J, Kasemkijwattana C, Fu FH et al (1999) Suturing versus immobilization of a muscle laceration: a morphological and functional study in a mouse model. Am J Sports Med 27:222-229 12. Rahusen FT, Weinhold PS, Almekinders LC (2001) Non-steroidal anti-inflammatory drugs and acetaminophen in the treatment of acute muscle injury. Am J Sports Med 32:1856-1859 13. Bleakley C, McDonough S, MacAuley D (2004) The use of ice in the treatment of acute soft tissue injury: a systematic review of randomized controlled trials. Am J Sports Med 32:251261 14. Beiner JM, Jokl P, Cholewicki J, Panjabi MM (1999) The effect of anabolic steroids and corticosteroids on healing of muscle contusion injury. Am J Sports Med 27:2-9 15. Foster TE, Puskas BL, Mandelbaum BR et al (2009) Platelet-rich plasma: from basic science to clinical applications. Am J Sports Med 37:2259-2272

Pathophysiology of Ligament Injuries

4

A. Cereatti, F.R. Ripani and F. Margheritini

Abstract Ligaments are specialized connective tissues whose biomechanical properties allow them to adapt to and carry out the complex functions required of the body. While ligaments were once thought to be inert, it is now recognized that they are in fact responsive to many local and systemic factors which influence their performance within the organism. Injury to a ligament results in a drastic change in its structure and physiology and may resolve by the formation of scar tissue, which is biologically and biomechanically inferior to the ligament it replaces. This article briefly reviews the basic structure, physiology, and function of normal as well injured ligaments.

4.1 Anatomy Ligaments have been studied extensively because of their prevalent role in sports injuries as well as their importance in maintaining joint stability. Ligaments comprise dense bands of collagenous tissue (fibers) that span a joint, and they are anchored to the bone at either end. They vary in size, shape, orientation, and location. The ability of ligaments to stabilize the joints is based on the fact that they serve as a mechanical restraint against abnormal joint motion and provide sensory feedback in response to the relative position and orientation of the relevant adjacent bones that stimulate muscle contractions. Closer inspection reveals that ligaments are organized into groups of fiber bundles and are often covered by a membrane (an epiligament in the case of extra-articular ligaments and a synovium in the case of intra-articular ligaments). The ultrastructure of ligaments is similar to that of tendons, but the fibers are more variable and have a greater elastin content. Unlike tendons, ligaments have a homogeneous microvascularity, which starts at the insertion site; however, ligaments are hypovascular compared to surrounding tissues. Ligaments are composed of the following elements, which differ in their proportions as a function of anatomic location along the length of the ligament: Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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• • • • • • • • •

nerve cell processes; fibroblasts (relatively rare; they form and maintain the extracellular components); extracellular matrix; fluid (water contributes about 60% of ligament wet weight); macromolecules; collagens (primarily types I and III, contributing about 80% of the dry weight); elastin (< 1%); non-collagenous proteins; proteoglycans (glycosaminoglycans). Some of these components have been shown to change quantitatively during growth, maturation, and aging. Frank and colleagues [1] found a variation in the concentration of three matrix components (water, collagen, and glycosaminoglycans) along the length of the rabbit medial collateral ligament (MCL). Transmission electron microscopy studies have shown that collagen fibrils within each collagen fiber vary in size, from about 60 nm to about 4000 nm in diameter, and that elastin, proteoglycans, and minor collagens (e.g., type VI) are present within the interfibrillar spaces. The fibrils exhibit characteristic sinusoidal patterns or crimps and mostly run in parallel to each other but with some sites of interweaving. Collagen fibrils are grouped into fibers, which in turn constitute a subfasicular unit that is surrounded by an endotenon. The subfasciculi bind together to form fasciculi and are surrounded by an epitenon. The paratenon surrounds the entire group of fascicles that form the ligament. The collagen fibers and bundles are arranged along the ligament’s axis of tension. Unlike the fibrils, the fascicles are not connected by molecular bonds and thus are free to slide relative to each other. These unique properties of the crimped and sliding fascicles enable fiber recruitment in order to resist an increased load. The ligament elongates, allowing normal kinematics. Higher loads cause increased stiffness (resistance to deformation) thereby restricting excessive motion in the joint. Ligament insertions are either direct or indirect. Direct insertions display superficial and deep fibers. The latter attach to bone at an angle of 90° and contain four morphologically distinct zones: ligament, fibrocartilage, mineralized fibrocartilage, and bone. A typical example of this arrangement is the femoral insertion of the MCL. Conversely, in the more common indirect insertions, the superficial layer connects directly with the periosteum whereas the deeper layer is anchored to bone via Sharpey’s fibers, as seen in the tibial insertion of the MCL.

4.2 Biomechanics The tensile properties of ligaments can be divided into structural and material properties, which determine how the structure or the material reacts to forces that are applied in tension.

"

4 Pathophysiology of ligilment Injuri15 4.2.1

Structur.1 Properties Structural properties clw:racterize the behavior ofthe overall bone-Iigament-bone complex and depend on the mechanical properties and geometry of the l..igauwnt, as well as on the properties of the insertion sites. Stiffness can be derived from the load-elongation curve (Fig. 4.1), obtained from a uniaxial tensile test. The curve can be divided into three different regions. An initial low stiffDe911 region, called the toe region, is followed by a linear region with hi.g1wr stiffness. A :further increase of the load results in permanent deformation, and stiffness will continue to rise until failure, as seen in the yield and failure region. The maximum. load that can be sustained by a speciInen prior to failure dcImes its tensile strength. This behaviorof1igaments is attributOO to easy straightening ofthe collagen-fibril crimp and to the non-uniform recruitment of the individual fibers. Other :factors that influence the structural properties of ligaments arc: 1. Increases in ligament length: increased elongation to failure, decreased stiffue9ll, but no change in ligament strength. 2. Increases in the ligament's cross-sectional area: increased strength and stiffue911 but no change in elongation to failure.

LOAD (N)

Toe

region

Lineilr reg ion

ELONGATION (mm) flt.4.1 Load-elongatian curve

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4.2.2 Material Properties Material properties characterize the behavior of the ligament substance itself under tensile loading and their contribution can be derived from the stress-strain curve. Since both stress and strain are obtained by dividing the load and elongation by constant factors, the load-elongation curve will have the same shape as the engineering stress-strain curve. In particular, strain is defined as deformation per unit length and can be measured by noncontact methods, such as a video dimension analyzer, or by contact methods, such as strain gauges and transducers. Stress is the load per unit area and its measurement requires knowledge of the specimen’s cross-sectional area. Similar to the load-elongation curve, the modulus of elasticity is represented by the slope of the stress-strain curve in the linear region. The maximum strain that can be sustained by a specimen prior to failure is its ultimate strain. A ligament’s material properties are influenced by its collagen composition and fiber orientation as well as by the interactions between collagen and the surrounding ground substance.

4.3 Viscoelasticity In viscoelastic materials, the relationship between stress and strain depends on time. The viscoelastic characteristics of ligaments are described in term of creep, stress relaxation, and hysteresis. Creep is the increase in ligament length under constant load (e.g., increased knee laxity after exercise). Stress relaxation, which protects from fatigue failure, is the decrease in stress over time under a constant strain or deformation. Hysteresis refers to the amount of energy dissipated with continued loading and unloading (preconditioning). For example, during reconstruction of the anterior cruciate ligament (ACL), the initial force applied to tension the graft decreases over time as a result of stress relaxation. It has been shown that preconditioning a ligament can reduce the amount of stress relaxation by approximately 50% compared to a ligament with no preconditioning.

4.4 Factors Influencing Ligament Properties Several biological factors influence ligament properties. These include: Skeletal maturity. Ligament properties, specifically, linear stiffness, tensile strength, and energy absorbed at failure, increase during skeletal maturation. The ligament substance matures earlier than the insertion sites. Thus, ACL failures in immature rabbits occur at the insertions whereas with mature specimens failure occurs at the mid substance.

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Age. Aging is accompanied by decreasing water and collagen content, less metabolically active fibroblasts, and reduced mechanical properties. The tensile properties of ACL specimens obtained from young human donors are more than threefold greater than those from older donors [2]. However, the rate of decline of ligament properties with aging may not be the same for all ligaments. Immobilization, remobilization. Immobilization significantly compromises ligament properties. Immobilization of the rabbit MCL complex for 9 and 12 weeks was shown to result in ultimate loads that were 31% and 29% of the contralateral controls. Similarly, rat ACL strength decreases by 25% after 4 weeks of immobilization. However, with remobilization, ligament properties return to nearly normal [3]. Gender differences. According to some authors [4], female athletes who participate in jumping and cutting sports are four to six times more likely to sustain a serious knee injury than male athletes participating in the same sports. This phenomenon has been attributed to decreased neuromuscular strength and coordination or increased ligamentous laxity. Female sex hormones (estrogen, progesterone, and relaxin) fluctuate radically during the menstrual cycle and are reported to increase ligamentous laxity and decrease neuromuscular performance.

4.5 Ligament Injury and Healing 4.5.1 Ligament Injuries The most common mechanism of ligament failure is rupture of a sequential series of collagen fiber bundles distributed throughout the body of the ligament and not localized to one specific area. As ligaments do not plastically deform, a tear of the ligament can be defined as either partial or complete. Midsubstance tears are more common in the adults, while avulsion injuries are more often seen in children and occur between the unmineralized and mineralized fibrocartilage layers. Ligament injuries can be classified into three grades, as detailed in Table 4.1.

Table 4.1 Ligament injuries according to grade of severity Grade I

Grade II

Grade III

The ligament is tender to palpation and pain is induced when stress is applied. There is no laxity. Minimal rupture of some fibers is present. There are mild signal changes on MRI. Clinically, the prognosis is relatively good. Acute pain and swelling are reported along with painful stressing of the ligament (as with grade I). There is detectable joint laxity as well as disruption of some but not all ligament fibers. This partial integrity is noted on MRI. Clinically, the prognosis depends on the lesion as well as on the ligament type but usually is good. Pain, swelling, and tenderness are observed together with gross laxity. There is no fiber continuity; the torn ends and fluid-filled gap are seen on MRI. The prognosis is ligament-specific but usually stabilization is required.

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4.5.2 Ligament Inflammation and Healing Phase I: inflammation. In the complete rupture of a ligament, the torn ends retract, with the accompanying hematoma filling the gap. Inflammatory cells recruited to the site of injury release histamine, serotonin, bradykinins, and prostaglandins. The vasodilatation and increased capillary permeability allow fluid transudation and movement of inflammatory cells. Fibroblasts produce a matrix of proteoglycans and collagen, forming a rudimentary scar, and collagen remodeling ensues, beginning with type III and then later type I. Phase II: matrix and cellular proliferation. Over the next 6 weeks, there is increasing organization of the fibrin clot, and the original gap fills with granulation tissue. During this phase, fibroblasts predominate, although macrophages and mast cells play important roles in the healing process as well. The highly vascularized wound is also the site active collagen synthesis, with bridging fibrils seen as early as 2 weeks. Initially, the collagen concentration is relatively low, with type I predominating. There is also an increase in glycosaminoglycan content. Over time, the mechanical strength of the scar improves. Phases III and IV: remodeling and maturation. The relative decreases in vascularity and cellularity are accompanied by an increase in collagen density. In addition, the collagen becomes more organized, with alignment of the fibers and bundles along the ligament axis. As the collagen content reaches a plateau, tensile strength increases due to collagen reorganization and cross-linking. The healing ligament is slightly disorganized and hypercellular, with typically up to 12 months but sometimes even longer required to complete remodeling.

4.5.3 Modulation and Regulation of Ligament Healing In recent years, biochemical intervention in ligament healing has gained serious consideration. The most notable advances involve the use of growth factors and gene therapy methods. The abilities of epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), acidic-fibroblast growth factor (aFGF), and platelet-derived growth factor-BB (PDGF-BB) to enhance ligament fibroblast division have been examined in vitro using the rabbit model, with promising results [5]. For example, PDGF has been shown to enhance the in vivo healing of injured ligaments [6, 7]. Hildebrand and colleagues [8] demonstrated, in an in vivo rabbit MCL model, that the addition of PDGF increased the tensile strength (1.6-fold), energy absorbed (2.4-fold), and ultimate elongation (1.6-fold) of the healing ligament at 6 weeks compared to the control group. Menetrey and colleagues [9] studied the use of recently developed gene therapy techniques to improve ligament healing. The aim of their study was to investigate three different gene therapy approaches (direct, fibroblast-mediated, and myoblast-mediated) for gene transfer to the ACL. The subsequent detection of cells expressing the marker gene in the ACL opens up the possibility of delivering growth factors capable of improving

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ACL healing and graft maturation (i.e., PDGF, TGF-β, and EGF). Furthermore, engineered myoblasts may mediate and accelerate intra-ligament neovascularization. This study clearly demonstrated the potential of gene therapy and tissue engineering to enhance ACL healing following injury. Kuroda and colleagues [10] showed increased levels of three growth factors (bFGF, TGF-β1, and PDGF) in bone-patellar tendon-bone (B-PT-B) grafts during the early postoperative phase. The expression of all three growth factors was maximal 3 weeks after implantation, followed at 12 weeks postoperatively by a rapid decline to preoperative levels similar to those of the control ACL. The concept of biological healing has been pursued since the late 1990s as a “marrow stimulation technique” [11, 12] with promising in vivo results in animals and humans. However, complete ligament healing continues to be elusive and will remain the focus of future investigations.

References 1. Frank CB, Mcdonald D, Lieber R et al (1988) Biochemical heterogeneity within the maturing rabbit medial collateral ligament. Clin Orth 236:279-285 2. Woo SL-Y, Hollis JM, Adams DJ et al (1991) Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med 19:217-225 3. Noyes FR (1977) Functional properties of knee ligaments and alterations induced by immobilization: a correlative biomechanical and histological study in primates. Clin Orthop 123:210-242 4. Hewett TE (2000) Neuromuscular and hormonal factors associated with knee injuries in female athletes. Strategies for intervention. Sports Med 29:313-327 5. Schmidt CC, Georgescu HI, Kwoh CK et al (1995) Effect of growth factors on the proliferation of fibroblasts from the medial collateral and anterior cruciate ligaments. J Orthop Res 13:184-190 6. Letson AK, Dahners LE (1994) The effects of combination of growth factors on ligament healing. Clin Orthop 308:207-212 7. Weiss JA, Beck CL, Levine RE et al (1995) Effects of platelet-derived growth factor on early medial collateral ligament healing. Trans Orthop Res Soc 20:1959 8. Hildebrand MD, Woo SL-Y, Smith DW et al (1998) The effects of platelet-derived growth facto-BB on healing of the rabbit medial collateral ligament. An in vivo study. AJSM 26:549-554 9. Menetrey J, Kasemkijwattana C, Day CS et al (1999) Direct-, fibroblast- and myoblast-mediated gene transfer to the anterior cruciate ligament. Tissue Engineering 5:435-442 10. Kuroda R, Kurosaka M, Yoshiya S et al (2000) Localization of growth factors in the reconstructed anterior cruciate ligament: immunohistological study in dogs. Knee Surg Sports Traumatol Arthrosc 8:120-126 11. Rodkey WG, Arnoczky SP, Steadman JR(2006). Healing of a surgically created partial detachment of the posterior cruciate ligament using marrow stimulation: an experimental study in dogs. J Knee Surg 19:14-18 12. Steadman JR, Cameron-Donaldson ML, Briggs KK et al (2006) A minimally invasive technique (“healing response”) to treat proximal ACL injuries in skeletally immature athletes. J Knee Surg 19:8-13

Pathophysiology of Cartilage Injuries

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G.M. Peretti, G. Filardo, A. Gigante, L. Mangiavini, A. Marmotti and M. Ronga

Abstract Articular cartilage lesions represent one of the major unsolved problems in orthopedic surgery due to the limited capacity of articular cartilage for self-repair following trauma. The biological response of cartilage to injury varies depending on the extent of the traumatic event. When a lesion is confined to the superficial layer, the repair process is not initiated, as the inflammatory stimulus is too weak to stimulate the resident chondrocytes surrounding the lesion; consequently, the defect persists. However, when a full-thickness lesion occurs, reaching the vessels of the subchondral bone, the inflammatory stimulus is more important. Bleeding from the bone marrow occurs, allowing the access of growth factors and reparative cells to the lesion site. These cells are mainly fibroblasts in addition to a low percentage of mesenchymal stem cells. As a result, the newly formed reparative tissue differs from the normal hyaline cartilage in term of morphology, biochemical composition, and biomechanical properties. For these reasons it is called fibrocartilage. The aim of this chapter is to review the morphology, composition, and biomechanical function of normal cartilage and to present an analysis of the response of the cartilage tissue to the different traumas.

5.1 Introduction The repair of chondral or osteochondral lesions still represents a major challenge for the orthopedic surgeon. Many of the successful efforts have been incorporated into clinical programs and have stimulated further research. Articular cartilage plays an important role in characterizing and maintaining the delicate balance of the joint. It is therefore easy to understand how a chondral lesion can trigger the development of pathological mechanisms that alter the fragile articular balance, jeopardizing over time the function of the joint and thus causing pain as well as eventual progression to osteoarthritis. Accordingly, Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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it is evident that a chondral or osteochondral defect requires rapid treatment, with the main goal being a quick return to normal physical activity for young people and the prevention of the early implantation of a joint prosthesis in older patients. In both cases, the end result should be an improvement in the quality of life.

5.2 Normal Cartilage: Morphology and Biochemistry Articular cartilage is a hypocellular, aneural, avascular, and alymphatic connective tissue. In adults, articular cartilage comprises a small (1-5%) population of chondrocytes, a cell type unique to this tissue, and mostly (80-95%) extracellular matrix (ECM). The latter is composed of collagen, non-collagenous proteins, proteoglycans, and glycoproteins [1]. About 60-80% of the ECM’s wet weight consists of extracellular water, which is retained by the negatively charged proteoglycans. Chondrocytes from different cartilage zones differ in size, shape, and metabolic activity. Among the many functions of these cells is the synthesis and maintenance of the matrix structure. Chondrocytes receive nutrients from molecules of the synovial fluid, which must pass through a diffusion barrier, the ECM, before reaching the cells [2]. The nature of this barrier leaves chondrocytes with a low concentration of oxygen; therefore, they depend primarily on anaerobic metabolism. Collagens contribute about 60% of the dry weight of articular cartilage, with type II collagen being the principal component (90-95%). The organization of collagen fibrils into a tight meshwork gives cartilage its tensile stiffness and strength. Proteoglycans and non-collagenous proteins (25% and 15% of the dry weight, respectively) bind to the collagenous meshwork or become mechanically entrapped within it, providing articular cartilage with its compressive strength. Two major classes of proteoglycans are found in articular cartilage: large aggregating proteoglycan monomers, or aggrecans, and small proteoglycans, including decorin, biglycan, and fibromodulin. Proteoglycans consist of a core protein and one or more glycosaminoglycan chains made of negatively charged repeating disaccharides units. The main glycosaminoglycans found in cartilage are hyaluronic acid, chondroitin sulfate, and keratan sulfate. Chondrocytes organize collagens, proteoglycans, and non-collagenous proteins in three regions (Fig. 5.1). Directly adjacent to the cells is the pericellular region, delimited by the pericellular capsule. These two elements together with the enclosed chondrocytes define the “chondron”, the functional unit of cartilage. The surrounding territorial region forms the transition from the chondron toward the inter-territorial region. The morphological changes of articular cartilage from the surface to the subchondral bone, also known as the cortical endplate, define four zones according to cell distribution, cell morphology, and ECM organization: the superficial, transitional, radial, and calcified zones (Fig. 5.1). In the superficial zone, cells are flattened as a consequence of the shearing forces acting on the articular surface. Chondrocytes synthesize high concentrations of collagen and low concentrations of proteoglycans. This molecular pattern testifies to the fact that compressive stiffness is less important than tensile strength at the cartilage surface [3]. The superficial zone is covered by the “lamina splendens”, also known as lubricin, a lubricant se-

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Fig. 5.1 Schematic representation of the structure of articular cartilage. The superficial zone contains collagen fibrils (insets) with a diameter (20 nm) smaller than fibrils of the deeper zones (v100 nm)

creted by cells that is responsible for the special gliding features of articular cartilage. The morphology of the transitional zone is intermediate between the superficial and the radial zones. The cell density is lower, with predominantly spheroid shaped cells embedded in abundant ECM. The collagen fibers are randomly arranged and the proteoglycan concentration is higher in this zone. In the radial zone, cell density is at its lowest and the cells are arranged perpendicular to the surface and are spheroid in shape. This zone contains the largest-diameter collagen fibrils and the highest concentration of proteoglycans, in particular aggrecan. The compressive stiffness and the ability to dissipate load are provided by the middle and deep zones. The radial zone is separated from the calcified zone by a basophilic line termed the “tidemark”, which plays a crucial role in load transmission from the deep zone of the cartilage to the underlying calcified cartilage. The calcified zone contains, embedded in a calcified matrix, hypertrophic chondrocytes with a very low metabolic activity. This zone represents an important transition to the less resilient cortical endplate. The synthesis of collagen type X provides a shock absorber along with the subchondral bone.

5.3 Biomechanics Cartilage is able to sustain high stresses and strains over a lifetime. Far from a mere sliding surface, it acts as a load transmitter, surviving cyclic compressive stresses of up to 20 MPa in the joints of the lower limb due to its unique mechanical properties [4].

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In terms of material behavior, cartilage is comparable to a soft solid “sponge” of very low permeability. Water flows through the porous structure by matrix compaction, and the subsequent structural deformation increases with time under the constant compressive load until equilibrium is reached. This time-dependent behavior is described as viscoelastic. Moreover, the mechanical response to stresses differs depending on the direction of the loads applied, due to the inhomogeneous orientation of collagen fibers and other macromolecules. Consequently, cartilage is defined as anisotropic. Mechanical properties and fluid flow are also influenced by the negatively charged proteoglycans, which confer a negative electrical potential to the cartilage matrix. The complex deformational behavior of cartilage can be understood and measured with a theoretical model in which cartilage is considered as a “biphasic material”. The biphasic theory [5, 6] assumes that cartilage is composed of two phases: an interstitial incompressible fluid phase and a porous-permeable, elastic-solid matrix of collagen type II fibers and PG aggregates. The load support in the articular cartilage derives from fluid pressure in the interstitial fluid phase (flow-dependent viscoelasticity) and from elastic stress developed within the solid matrix during loading (flow-independent viscoelasticy from intermolecular friction). In normal articular cartilage, fluid pressure supports 95% of the applied load, whereas the remaining 5% is supported by the contacting collagen-proteoglycan matrix of the opposing articular surface. Under compression, the matrix is compacted and pressure in the interstitium rises, forcing water and soluble ions out of the tissue. Water efflux follows Darcy’s law of permeability: the rate of volume discharge is proportional to the applied pressure under a coefficient k of hydraulic permeability, ranging in normal cartilage from 10-15 to 10-16 m4/N. This permeability coefficient is inversely related to the frictional drag force between the solid-fluid interface and the porosity of cartilage. Porosity is defined as the ratio of the interstitial fluid volume to the total tissue volume and in cartilage ranges from 65% to 80%. A diffusive drag coefficient D can be calculated as directly proportional to porosity and inversely proportional to k. In normal cartilage, D ranges from 1014 to 1015 N/m4. Such a very large drag coefficient indicates low permeability, which means that very high pressures are required to move water through the tissue. As a consequence, in vivo, fluid pressure accounts for a significant component of total load support, dissipating and minimizing the stresses – a phenomenon called “stress shielding of the solid matrix”. Moreover, cartilage permeability decreases with compression as frictional drag force increases, due to the reduction in water content and the relative increase in the negative charges of the proteoglycans that hold water in the interstitium. This prevents rapid and excessive fluid exudation from the tissue and regulates the ability of cartilage to resist cyclic loading. For these mechanisms, flow-dependent viscoelasticity corresponds to the variations in frictional drag force resulting from interstitial fluid flow. However, under a constant load, deformation continues until fluid pressure dissipates and load support is gradually transferred from the fluid phase to the compressed collagen-proteoglycan solid phase, following a flow-independent viscoelastic behavior. In vitro, this equilibration process is reached within 2-6 h and the compressive strain is related linearly to the applied compressive stress under a proportionality constant called the “equilibrium compressive modulus”. In normal cartilage the equilibrium compressive modulus ranges from 0.4 to 1.5 MPa. In vivo, joints are always moving and there is no time


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for a constant load to allow an equilibrium state to be reached. Accordingly, in normal articular cartilage, fluid pressurization is always the dominant physiologic load-support mechanism of diarthrodial joints, in human osteoarthritic cartilage, the reduced proteoglycan concentration increases tissue permeability and water content, diminishing the fluid pressurization mechanism of load support. Consequently, the collagen-proteoglycan solid matrix starts to bear more of the compressive load. This excessive load in the solid matrix is detrimental for the long-term survival of the collagen network and is one of the factors involved in the development and progression of cartilage degeneration in arthritic joints. The collagen-proteoglycan matrix is also responsible for the flow-independent viscoelastic shear resistance of articular cartilage. Similar to compression, a pure shear in vitro generates a stretch related to the force applied under a proportionality constant called the “equilibrium shear modulus”, ranging from 0.05 to 0.30 MPa. In vivo, shear stresses are observed mostly during compression. In fact, a compression applied to an expandable tissue results in an expansion of the tissue itself, perpendicular to the direction of the load applied. Fortunately, cartilage compression results in stiffening of the tissue: the stiffer the matrix, the more energy is required to stretch the fibers. This leads to an increase in cartilage resistance to shear as compression is applied. Nevertheless a “pitfall” in this mechanism is created by the firm attachment of deep zone cartilage to the tidemark. Here, thick collagen fibers connect the deep zone to the calcified cartilage. In this area, the hard bony substrate prevents any expansion and energy dissipation and, during compression, shear forces attain their highest values. This explains why a hard, blunt impact may cause cartilage to be sheared off the bone, by the unbalanced peak stresses at the bone interface. The properties of the collagen-proteoglycan matrix can also be measured under tensile forces at equilibrium, when fluid pressure is completely dissipated. When cartilage is tested in tension, a typical stress (tensional force applied)-strain (deformation) curve can be observed, with an initial toe region (corresponding to collagen network realignment as it is pulled through the proteoglycan gel) followed by a linear response. The slope of the linear portion defines the stiffness of the collagen network in tension and is expressed by Young’s modulus, which for cartilage varies from 5 to 50 MPa. Superficial zones are stiffer than deeper zones because of a higher collagen concentration, whereas fibrillated osteoarthritic cartilage is less stiff because of the damaged collagen network. Tensile forces generated by the collagen network at equilibrium are also responsible for balancing the “swelling” of cartilage. Swelling is the ability of a material to gain in size or weight when soaked in a solution. In cartilage, swelling arises from the presence of negatively charged proteoglycans, constituting a fixed charge density. For normal articular cartilage, the total fixed charge density ranges from 0.1 to 0.5 mEq/ml at physiologic pH. In osteoarthritic cartilage, this density is reduced as a result of proteoglycan loss from the tissue. Each of these negative charges requires a mobile counter-ion (e.g. Na+, Ca2+) in the interstitial fluid to maintain electroneutrality within the interstitium. This gives rise to a relative excess of mobile ions in the interstitium compared to the external fluid space and the imbalance yields a swelling pressure known as the “Donnan osmotic pressure”. In normal cartilage, osmotic pressure is around 0.25 MPa. The collagen network resists the swelling pressure exerted by the proteoglycans, restricting its capacity to absorb

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water to only 20%, so that cartilage matrix is always in a state of “partial hydration”. In the early stages of osteoarthritis, the increased water content comes from collagen damage, as the latter reduces the tensile forces and increases tissue hydration. All these different biomechanical properties coexist during joint motion and they strongly interact with chondrocytes for cartilage matrix maintenance. Although the specific mechanisms by which joint loading influences chondrocyte metabolism is still unknown, it is thought that integrins play a fundamental role in mechano-electrochemical signal transmission. Future experimental studies will allow the fascinating non-linear, viscoelastic, anisotropic behaviors of articular cartilage to be better clarified and will integrate mechanoelectrochemical parameters into cellular metabolism pathways, allowing us to understand the mechanical regulation of chondrocyte function.

5.4 The Response of Articular Cartilage to Injuries: Blunt Traumas, Superficial Lesions, and Osteochondral Injuries Articular cartilage responds differently to injury than other tissues. In fact, cartilage has no direct blood supply, lymphatic drainage, or innervation. In addition, articular cartilage has a slow regeneration rate and chondrocytes have difficulty in migrating within the matrix to the injury site, as do cells in other tissues. The usual inflammatory response of hemorrhage, formation of the fibrin clot, cellular production, and migration of mesenchymal cells are absent in pure cartilage lesions, preventing cartilage from healing after even minor injuries. Other factors, such as the mechanism of the lesion, the depth and extension of the damage, patient age, associated instability, history of previous surgical treatments, and genetic condition, also affect the healing of cartilage. Articular injuries may result from open joint injuries or, more often, closed injuries such as prolonged repetitive joint loading or through a single high-shear load. The maintenance of an adequate concentration of matrix components and the preservation of a structurally intact matrix are crucial for articular cartilage to withstand compressive, tensile, and shear forces. Collagen fibrils are strong under tension, in contrast to proteoglycans, which resist compression due to their bulk compressive stiffness and the electrostatic repulsive interactions between glycosaminoglycan chains. Static and dynamic compressions have been demonstrated to differentially alter chondrocyte and matrix metabolism in cartilage explants. The induced biophysical phenomena are highly dependent on the amplitude and frequency of loading. Low-displacement/high-frequency dynamic compression of cartilage explants can stimulate matrix biosynthesis, perhaps by generating high hydrostatic pressure, high fluid velocity, and high streaming potential, but little deformation of cells and matrix. High amplitude and static compression can induce, however, immediate increases in tissue swelling as well as prolonged increases in the rate of release of matrix macromolecules. Such mechanical forces may act by disruption of the collagen meshwork, thereby leading to an increase in the diffusion of macromolecules within and out of the cartilage matrix [7]. The depth and degree of the lesion are two other factors that influence cartilage healing. In fact, surface defects that do not penetrate the subchondral bone have to rely on


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sparsely populated chondrocytes for matrix remodeling, whereas deeper lesions may count on bleeding to the lesion site from the well-vascularized subchondral bone. Joint trauma can damage both the macromolecular framework of the matrix and the cells without causing mechanical disruption of the tissue; alternatively, it can fracture or rupture the cartilage matrix, causing visible splints in the articular surface. Differences in the type of tissue damage separate mechanical injuries of the cartilage into three types, as discussed in the following.

5.4.1 Damage to Matrix and/or Cells without Visible Disruption of the Articular Surface (Blunt Trauma) Acute or repetitive blunt traumas are the most important causes of this type of lesion. Other causes include prolonged joint immobilization, synovial inflammation, some medications, and traumatic or surgical disruption of the synovial membrane. Experimental evidence shows that a loss of proteoglycans or an alteration of their organization occurs before other signs of significant matrix damage. Currently, there is no clinically applicable method of detecting alterations in cartilage matrix composition, such as decreased proteoglycan concentration or increased water content. Softening of the tissue, which can be probed by the surgeon and may result from alterations in the matrix, is not necessarily associated with the progression of matrix disruption. Available evidence suggests that, following a loss of proteglycans, chondrocytes increase their synthesis of these macromolecules, restoring the matrix concentration of proteoglycans toward normal. However, if the cells do not significantly repair abnormalities in the macromolecules that form the matrix or if the loss of matrix molecules progresses, the tissue will deteriorate. It is also the case that the death of chondrocytes may result from a single or repetitive blunt trauma, causing a crucial perturbance of matrix renovation. Currently, it is not clear at what point this type of injury becomes irreversible and leads to a progressive loss of articular cartilage. Finally, repetitive blunt traumas may also significantly alter the deep zone of the cartilage as well as the osteochondral area. In fact, these kinds of insults may result in a thickening of the cortical endplate, altering the fine mechanism of load transmission from the cartilage deep zone through the tidemark, the calcified cartilage, and the underlying subchondral bone.

5.4.2 Superficial Cartilage Disruption The resulting compression or shear forces of impact loading and twisting on an articular surface can produce chondral fissures, flaps, or fractures. A study of human articular cartilage showed that this tissue could withstand impact loads of up to 25 N/mm2 without apparent damage [8]. Impact loads exceeding this level cause chondrocyte death and matrix fissures. The clinical diagnosis of chondral fractures is difficult because cartilage lacks innervation, injuries that are limited to cartilage are not directly associated with pain. Therefore,

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the most common symptoms of chondral fractures include locking, catching, or joint effusion. The local response to injury depends entirely on the chondrocytes, due to the absence of blood vessels and the impossibility of undifferentiated mesenchymal cells to migrate to the site of injury and then proliferate, differentiate, and synthesize new matrix. Consequently, with the exception of sharp deep fissures in young patients, the superficial lacerations of articular cartilage generally do not show spontaneous repair.

5.4.3 Osteochondral Fractures Closed joint injuries can cause fractures that extend through the cartilage into the subchondral bone. This kind of lesion may cause mechanical symptoms, synovitis, and joint effusion. The reparative mechanism includes formation of a fibrin clot, inflammation and invasion of new cells, and production of new tissue. In fact, localized bleeding begins a cascade of events involving hematoma formation, stem cell migration, and the synthesis of collagen type I, which result in fibrocartilage repair, filling the defect with a matrix that is structurally weaker than native tissue. Native cartilage at the edge of the lesion shows an attempt at responding, by chondrocytes mitosis (Fig. 5.2). This does not lead, however, to the formation of functional new tissue. Age affects healing in part because adults have a lower concentration of mesenchymal stem cells in the subchondral bone than is the case in young people. Adults also have more co-morbidities that could influence cartilage metabolism and the repair process. Finally,

Fig. 5.2 Osteochondral lesion showing two clusters of chondrocytes (arrows) at the edge of the lesion site

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it must also be considered that focal chondral defects, if left untreated, may increase in size over time and induce concomitaot chaoges of the underlying subchondral bone plate and bone overgrowth or bone loss. Indeed, in large cartilage lesions the subchondral bone is involved in the degenerative process as well. The biomechanical perturbations caused by different osteochondral defects substaotially alter the pattern and maglitude of contact pressures and cartilage strains in the joint [9]. These alterations in tum affect the mechanical environment of the articular cartilage surrounding and opposing the lesion as well as the homeostatic balance of the entire knee joint. As such, they have the poteutial to contribute to the initiation and development of osteoarthritis. Therefore, the treatment goal of osteochondral cartilage defects should be to restore the physiological properties of the entire osteochondral unit, aiming to achieve a more predictable repair tissue that closely resembles the native articular surface and remains durable over time.

5.5

Conclusions When a cartilage lesion occurs, the human articular cartilage exhibits a poor or null regenerative potential, due to the inability to synthesize a new tissue having the staodard biochemical composition and hiomechanical properties typical of native cartilage tissue. Four reasons can be considered as an explanation of this behavior: frrst, the articular cartilage is not vascularized and does not have a nerve supply; second, it is of low cellularity; third, chondrocytes have a low proliferative potential and are unable to produce a functional exttacellular matrix following injury; fmally, the chondroeytes' capacity of responding to mechanical, chemical and pharmacological factors deereases with age. In order to modify the natoral evolution of these lesions, a valid therapeutic option is indicated in attempts at reducing the progression of joint damage as well as the patient's symptoms, and at limitiug the development of early osteoarthritis.

Acknowledgments. The authors acknowledge Elizaveta]{on, MD, Stefano Cecconi, MD, Marina Protasuni, Marcella Reguzzoni, and Alberto Passi for their contributions in the preparation of this chapter.

References I. 2.

3.

Buckwalter JA, Mankin HI (1998) Articular cartilage: tissue design and chondrocyt&-matrix interactions. Instr Course Leet 47:477-86 Fischer AE, Carpenter TA et al (1995) Visualisation of mass transport of sma1l mganic molecules and metal ions through articular cartilage by magnetic resonance imaging. Magn Re-

son Imaging 13:819-826 Kempson GE, Muir H et al (1973) The tensile properties of the cartilage ofhumao femoral condyles related to the content of collagen and giycosaminoglycans. Biochim Biophys Acta 297:456-472

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4.

Langworthy MJ, Nelson FRT, Coutts RD (2004) Basic science. In: Cole BJ and Malek MM (ed) Articular Cartilage Lesions: A Practical Guide to Assessment and Treatment. Springer, New York, pp 3-12 Mow VC, Guo XE (2002) Mechano-electrochemical properties of articular cartilage. Annu Rev Biomed Eng 4:175-209 Mankin HJ, Mow VC (2000) Articular cartilage structure, composition, and function. In: Buckwalter JA, Einhorn TA (ed) Orthopaedic Basic Science. Biology and Biomechanics of the Musculoskeletal System. 2nd ed. Rosemont, Illinois: American Academy of Orthopaedic Surgeons, pp 458-470 Greco F, Lorini G, Specchia N (1990) L’influenza del sovraccarico sulla cartilagine articolare del ginocchio. Giornale italiano di Ortopedia e Traumatologia Vol XVI N. 1 Repu RU, Finlay JB (1977) Survival of articular cartilage after controller impact. J Bone Joint Surg 59A:1068-1076 Shirazi R, Shirazi-Adl A (2009) Computational biomechanics of articular cartilage of human knee joint: Effect of osteochondral defects. J Biomech 42:2458-2465

5. 6.

7. 8. 9.

Prevention in Sports-related Injuries

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L. Osti, N. Maffulli

Abstract Sports activities have become a part of the modern lifestyle and the number of related injuries has therefore increased dramatically. This chapter provides a brief review of injury prevention in the light of scientific evidence focusing on the knee, ankle, shoulder, and spinal joints as well as the associated muscles. The results obtained through prevention programs in reducing anterior cruciate ligament and hamstring injuries are highlighted as a model of sports-related injury prevention. The role of brace and proprioception is investigated for both the knee and the ankle joints and aging is analyzed as a factor predisposing to injury. The prevention of running injuries is discussed based on biomechanical and clinical analysis.

6.1 Introduction Sports activities have become an important part of life in modern society, providing not only physical but also psychological benefits. Scientific studies have demonstrated positive effects of regular sports activities in preventing illnesses such as cardiovascular disease, diabetes, cancer, depression, and osteoporosis. However, with the growing number of athletes (amateur and professional), both the injury rate and the overall number of injuries have increased as well. A debate has arisen regarding the benefit of sports activities under all circumstances and has clearly demonstrated a need for strong injury prevention programs [1-3]. This chapter provides a brief review of injury prevention in the light of scientific evidence generated from analysis in the field of orthopedic sports medicine.


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6.2 The Prevention of Knee Injuries Knee injuries have become a dominant factor in sport injuries, accounting for up to 60% of all injuries according to some reports. Among the various types of knee injuries, those involving the anterior cruciate ligament (ACL) are of particular importance. Numerous prevention and rehabilitation programs as well as prophylactic braces have been developed in order to decrease the total number and relative percentage of ACL injuries [4, 5].

6.2.1 The Prevention of ACL Injuries Injuries involving the ACL are a common issue in orthopedic sports medicine, with the total number of these injuries growing exponentially each year [6]. Female athletes are more likely than males to suffer ACL injury, with a ratio as high as 8:1 in some reports. In addition, teenage athletes are more likely than older ones to suffer ACL tear. The prevention of ACL injuries and associated lesions (meniscal and chondral) is important not only to avoid the need for surgery but also to reduce the early onset of osteoarthritis [6] (Table 6.1). Anatomic and hormonal factors account for the higher rate of ACL injuries in female athletes. Anatomic factors include the shape of the intercondylar notch, limited knee and hip flexion angles, and increased valgus alignment and tibial rotation [6]. Ligamentous laxity is greater in females, independent of the changes associated with the menstrual cycle; however, data supporting a relationship between ligamentous laxity and sex hormones are not definitive, and epidemiological studies have not found a conclusive correlation between menstrual phase and injury rate [6].

6.2.2 Prophylactic Braces Prophylactic knee braces have become a common option in the conservative management of patients vulnerable to knee-ligament injuries, with contradictory reports on the benefits of bracing with respect to knee unloading effects and degree of safety provided [6, 7]. ACL knee braces can greatly reduce anterior translation of the joint, but their effectiveness is limited to lower load forces since higher load forces usually develop in the context of high-energy trauma. Moreover, Lam [8] demonstrated that an ACL brace activates the hamstring reflex but does not protect against fatigue effects on these muscles, and electromyogram (EMG) studies of the true effectiveness of knee braces in muscle function and proprioception have been inconclusive. Although some authors found that prophylactic knee braces decrease peak tension magnitudes and impulse responses on the knee ligament [9], others noted limited or no differences in either knee stability or absorption of impact compared with controls [10-12].

DB, VB, soccer, 6-..oks ProspectM: n=126 males ptCo"lSOll 000· 1F434fema1es;intervention, !IIIdotniud of the totIl: 1-,... 3661I1ined, monitoring, 463 ",,1DinCd 60-90 min/clay. foc3dayo1week

ProspectM: !IIIdotniud

j"""box and boIance

PI,."....,

j"""box

PI,."....,

Yes

No

Yes

No

No

No

Yes

No

Yes

BaiaDoc

thcintcm:ntion

._-wIgos

COIIIIDotioo

"'-.nng

andhme

smgIh,

t ..rncaI1eap. t-.nng

perturbation,

Vidcolapc. • peak landing f""""

sm&Il Noo·1DIioJni,.cd, ACLs rq>Ortod: low VB injury rates in onrolimen, fonaIes 0.43 motivational bias. in untrained vs. 0.12 l-cm.-l progrun in trained va. male in spcxt fadlity, con1rolll 0.9 over 6implementatioo """-progmn3.6not feasible in '" 4.8-fold bigher • large cohort rate of ACL injuries

ACL injuries was group

numbcrof

lUndomU.ed cliDi· 37% drop"" rate, Training did ca11ri11, sign. _ """"" "" ICdw:c risk of1nining; ofprimary M"" injuries in unknown if 1Iain- traumatic injury ing _ illan boI· '" lhc lower limb. control w. intcrvcntioo. "'" boazd ... 80% of ACL injuries the same; thc oocmrcd in

tive randomized intervention study. Knee Surg Sports Traumatol Artbrosc 8:356-363 b Hewett TE. Lindenfeld TN, Riccobene N et a1 (1999) The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study. Am J Sports Med 27:699-706 (cont. -»

BB, basketball; NM, Neuromuscular; VB, volleyball • SOderman K. Werner S. Pietili T et al (2000) Balance board training: prevention of traumatic injuries of the lower extremities in female soccer players? A prospec-

Hewett et at. (1999)'

of intcmIJ.tions and 78% oecontrols complotod thcswdy

only 51%

SOderman ct aI. Soccer fcmalcs, I-season n=121 (n=IOO intcrvcntion (2OO0r -.,Is); 10-15 min

Table 6.1 Summary of MedLiner (peer rewieved) papers focusing on ACL injury preveotion programs in the athlete population (from [20])

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ill'

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I

s·

Ig'

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(123 """'). 0=1837 piAJm (1 haruIball (1586 _... ....on). 251 mal..) 15 consccutivc

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(17-18_). 20-.

Randomized controlled cluster trial

Randomized -.l1cd cluster trial

Squall and power (bom!ding)

Balance board Yes (proprioceptive) at four lewIs

Wobble _ (Nopro). bolaru:e foam rna. (Allox)

'MlIDM

No

yes

No

Yeo

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withanklc

Boimce 1I1ining

RmuIomizcd cliDical trial

warm""

of injuries, s1ructuIcd

-d, -..

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injury Illes

Plyometric Proprio- Strength ceptiOD

Plmting, Knee om toe Balance cutting, proper ImdiDg IOIMty on NM oon1:roi technique single! double leg. rna. and boards

Equipment Strength Flexibility Agility

injuries in knccIan-

VB.

f"NM

Ankle injuries sig-

in anld. di!o 1I1ining oontro1 J!I1llIP (2.4 no! doo:ribed; vt. 0.21 ""'P"'ifioi WIIm.-up knee injuries not ClCIcises aIao per- significant; fewer in formoi by tninoi _ group (69 ". gro"" "" typo 0.6), 5 kooo sp!Iins not specified; and I knee "luxation" compliance with in control groop VB. all CItlCises 1knee sprain in IlllI noted _ gIOOp

SpecifIC Injury

typo IlllI .p.cifIod; niflClll< _

re-cducation at incon1rols mccbI!Ioccp1l!r 1",,1 Uncorflin which 129 _ m.. and auklc injmics prog!IlII CIYCl'Ill, 81 in con""'POIIO!! was effective; ..1(0.9.....n, malo and fomJlo 03 m.d, participants; 2.5 rnatcbod); results cannot be 80% reduction in ACL mjurioo "tnpoWod to other sports

-.. 3.1%

He; 2.4% in

Not statistically sigoificant; h"oks

--

Outcome

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BB, basketball; NM, Neuromuscular; VB, volleyball C Heidt RS Jr, Sweetennan LM, Carlonas RL et al (2000) Avoidance of soccer injuries with preseason conditioning. Am J Sports Med 28:659-662 d Olsen OE. Myklebust G, Engebretsen L et at (2005) Exercises to prevent lower limb injuries in youth sports: cluster randomised controlled trial. BMJ 330(7489):449. Epub 2005 Fob 7 'Wedderkopp N. Kaltoft M, Holm R et at (2003) Comparison of two intervention programmes in young female players in European bandball- with and without anklo disc. Scand J Med Sci Sports 13:371-375

u. (21J03r

Randomized

nonJlIC"".... intervention, raru!otni.:d l-Y'" monitoring. 3 dayiIwcck, (1 plyomcttic and 2 .....m.ill)

Duration

European team. 12-20 min

handboll

Sport

Wcddcrkopp ct Emopcan team. IO-monts handbolI, 263 females (ooc season)

2005d

0... ~ 01

0110'

Authors

Table 6.1 (continued)

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6 Prevention in Sports-related Injuries

63

The effect of prophylactic knee braces on preventing ACL injuries in particular is also debated in the literature [13-15]. In 2008, Pietrosimone et al. [16], in a systematic review of the published studies, examined the relative reduction in risk associated with prophylactic knee braces used to prevent knee injuries in college football players. The authors concluded that it was not possible to advocate or to discourage the use of prophylactic knee braces in preventing knee ligament injuries in this population, but they also highlighted the need for better-quality randomized controlled trials.

6.2.3 Injury Prevention Programs Prevention programs have been aimed at decreasing both the percentage of female athletes suffering ACL injures and the total number of ACL lesions, reporting overall reduction rates of 72-89%. For example, Caraffa et al. [17] investigated the use of proprioception balance training and were able to show an 87% reduction in the injury rate compared to the control group. Other studies examined the use of PEP (prevent injury, enhance performance) specifically directed at ACL injury prevention in a large group over two seasons, with subsequent reduction of the injury rate ranging from 75% to 88% [18]. In terms of risk factors, since there is extensive evidence that specific training can increase neuromuscular control and decrease ACL injury risk, it is reasonable to consider neuromuscular impairment as a risk factor in this type of injury [19, 20]. Training programs typically consist of one or more of the following components: plyometrics, isolated balance training, biofeedback techniques, and strength training. However, there are no specific data analyzing the single role of each one [20].

6.2.4 Patellar Injuries Knee pain is source of disability for athletes engaged in various sports. There are different causes of knee pain in athletes: patellofemoral arthritis, meniscal lesions, osteochondral lesions, patellar tendinopathy etc. In the anterior knee pain arising from patellar tendinopathy, there is tenderness at the attachment of the patellar tendon over the lower pole of the patella. The condition is commonly associated with overuse. The increased participation in recreational and competitive sporting activities over the last three decades has been accompanied by an increased incidence of tendinopathies [21]. Patellar tendinopathies are particularly common in track and field athletes, sprinters, and jumpers but the exact etiology is still unknown [22]. Changes in training pattern, poor technique, previous injuries, inappropriate footwear, and environmental factors such as training on hard, slippery, or slanting surfaces have been associated with patellar tendinopathy in the athletic population. The main pathological stimulus is thought to arise from vigorous physical training, which may expose tendons to excessive loads [22-24]. Professional and recreational athletes commonly use taping and bracing of the patella to prevent or ameliorate a wide range of pathologies, ranging from anterior knee pain to

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consistent patellar instability. The aim of taping is to tilt, glide, or rotate the patella. The external devices used in bracing influence the position of the patella as well. It is commonly believed that these treatments decrease pain by increasing the area of patellofemoral contact. The evidence supporting patellar taping and bracing in the management of chronic knee pain is not definitive [25] even though these measures are popular in athletes and are commonly prescribed. Moreover, taping and bracing may have different effects. A systematic review and meta-analysis carried out by Warden et al. [26] showed that patellar taping is beneficial whereas the benefits of patellar bracing are disputable and there is no evidence for either one in the management of chronic knee pain. However, these authors also stated that there is insufficient evidence defining the direction that forces should be applied to the patella to optimally reduce pain (medially or laterally) or establishing the efficacy of patellar bracing. There is also insufficient evidence from quality studies directly comparing patellar taping and bracing effects in the management of chronic knee pain.

6.3 Ankle Ankle sprains are the most common sports injury, with the incidence varying from 10 to 30% of all musculoskeletal injuries [27, 28]. Usually, ankle supports are used in the acute stage of the injury to manage swelling, and in the chronic stage to provide support or to improve the stability of the joint. Taping and bracing may stimulate neuromuscular mechanisms through proprioceptive stimulation that protect against injurious movement [29]. Athletes and coaches consider taping and bracing of the ankle to be important in the management of acute and chronic ankle injury. Furthermore, many athletes believe these devices to be essential for the success of their performance. Different taping techniques and braces are used in the prevention and management of acute and chronic ankle injuries, with the choice guided by factors such as cost, comfort, ease of application, personal preference, age, and the type of sport [30]. Both the mechanical and the functional stability of the ankle can be improved with taping [27-29]. The advantages of ankle braces are that they can be self applied, are easily removed, and are washable. They are made of various materials and shapes and most are commercially available. The role of taping and braces in the prevention of acute ankle injuries has been studied by several groups [31-35]. Garrick et al. [31] evaluated the effect of taping on 2563 basketball players with previous ankle sprains over two successive seasons and concluded that taping may prevent ankle sprains. Ankle braces may also reduce the incidence and severity of acute ankle sprains [32]. Another study compared traditional taping techniques and ankle braces in the prevention of acute ankle sprain [34]. The use of a non-rigid laceup ankle brace halved the risk of ankle sprain. In acute ankle sprain, taping and bracing are also used to manage edema [30, 31] but there are few studies evaluating the efficacy of taping to achieve limb or joint compression. Capasso et al. compared the effect of adhesive and non-adhesive tape on swelling and measured the compressive forces for the different kinds of taping [34]. They concluded that non-adhesive tape should be renewed after 3 days and adhesive tape after 5 days because of diminished compression.


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Taping and bracing have been used to manage ankle instability in the chronic setting, i.e., when the athlete, after acute injury, returns to his or her sport [35, 36]. Both forms of support are believed to limit the range of movement and thus to reduce abnormal movements of the ankle [37]. However, the restricting effects of ankle tapes and braces are lost after periods of exercise [35]. Studies investigating the role of taping and bracing in chronic injury [37-38] found that the more unstable the ankle, the greater the improvement.

6.4 Shoulder: Prevention Program for Overhead Athletes Overhead sports activities can involve repetitive microtrauma stress forces to the shoulder, resulting in specific injuries to the joint. The basic principles underlying programs aimed at the prevention and treatment of shoulder injuries have been identified through evidence-based studies, with adequate ROM (range of motion) being the primary goal [38]. In the thrower’s shoulder, joint stress laxity allows increased external rotation but internal rotation is decreased and total motion reduced compared to the non-dominant arm [38]. A statistical correlation between throwing-motion reduction and injury rate was reported in two independent studies [39, 40]. ROM equal to that of the non-dominant shoulder should be maintained through a constant and gentle stretching program [41, 42]. According to the kinetic chain concept, any imbalance regarding strength, flexibility, endurance, or stability can affect fatigue and the biomechanical function of the throwing shoulder, leading to compensation. Accordingly, this imbalance acts as a predisposing factor for shoulder injuries [43, 44]. A SICK scapula (scapular malposition, inferior medial border prominence, coracoid pain and malposition, dyskinesia of scapular movement) refers to an overuse muscular fatigue and imbalance syndrome that can result in altered shoulder kinematics associated with persistent shoulder pain and increased risk of labral pathologies [41-43]. The gleno-humeral and scapulo-thoracic muscles are the overall dynamic stabilizing structures of the shoulder and their maintained strength is essential to reduce the stresses directed into the shoulder joint during the throwing action. Improved neuromuscular control, and therefore a reduced risk of injury, of the gleno-humeral joint and scapulo-thoracic joint can be enhanced via specific rehabilitation programs that include closed kinetic chain exercises, plyometric exercises, and rhythmic stabilization [38, 43]. Similarly, core stabilization increases the lower body’s neuromuscular strength and endurance and thereby reduces the forces acting on the upper body during throwing activities.

6.5 Muscle Injuries and Their Prevention Sports-related muscle injuries have also increased, according to the most recent reports. Two common mechanisms of muscle trauma are described: direct (contusion) and in-

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direct (strain or distension). Hamstring strains are the most common form of muscle injury, arising from sports requiring sprints and acceleration. Quadriceps lesions are frequent in sport such as soccer. The majority of them are caused by direct contusion trauma, with the player commonly injured by a direct blow to the lateral aspect of the thigh [44, 45].

6.5.1 Hamstring Injuries The hamstring comprises three distinct muscles, the semimembranosus, semitendinosus, and biceps femoris. Together, they build a muscular bridge between the hip and the knee (lower leg). Hamstring function is evaluated in terms of peak force, the ratio between hamstring quadriceps muscle, and side to side balance, as several studies have shown a role for each one in the risk of injury. The majority of hamstring injuries occur in distance runners and sprinters and involve the myotendinous junction but it is unclear during which component of the running phase they occur. While most reports cite evidence supporting the late swing phase, others maintain that injury occurs during the push-off phase [44-46]. Predisposing factors for hamstring injuries include reduced ROM, increased age, previous injury, and poor hamstring condition/strength. A history of previous trauma increases the chance of further injury due to: (1) the increased area of scarred tissue within the muscular and tendon complex, (2) decreased ROM, and (3) decreased strength of the previously injured muscle. Age is also a predisposing factor, in terms of the effect of the aging process on tendon and muscle strength and the number of previous injuries. Other predisposing factors have been pointed out, such as improper running technique, low back pain, muscle fatigue, and increased stress in training and peak performance [44-46].

6.5.2 The Prevention of Hamstring Injuries Programs aimed at preventing hamstring injuries have been developed, taking into account the risk factors highlighted in related studies. They should be used in routine training to reduce the rate and overall numbers of hamstring injuries during the sport season. Eccentric training has been demonstrated to be the training method of choice based on low hamstring strength as a risk factor for hamstring strain, EMG studies showing the highest peak at the end of the eccentric phase entering the concentric phase, and the fact that the majority of hamstring strains occur during the eccentric phase [46]. Clinical support for this approach comes from data collected in a Scandinavian study showing that the use of eccentric training can reduce the risk of hamstring injuries [47]. Furthermore, a simple exercise, the Nordic lower hamstring exercise, has been shown to be effective in boosting eccentric hamstring performance [48, 49]. The effect of flexibility has not been investigated in elite athletes, with controversial evidence in a military training series [44, 45].


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6.6 The Prevention of Spinal Injuries Core stability depends on the group of trunk muscles surrounding the spine and abdominal viscera, and improved stability has been identified as an important aspect of improved athletic performance and injury prevention. Core stability programs can be used for therapeutic and prevention purposes [50, 51]. Indeed, increasing attention is being paid to spinal exercise programs aimed at reducing spinal injuries and increasing core stability [50]. In addition, core stability programs with increasing levels of difficulty have been integrated into many sports programs. The goals of these programs are to optimize the recovery of the injured athlete and to improve aerobic condition as well as athletic performance. Quadriceps exercises, wall slides, stabilization exercises with the green gymnastic ball integrated with upper extremity postural exercises have been shown to be beneficial in preventing injury and in enhancing sports-specific performance in the athlete [51]. Prospective randomized studies conducted in golfers have shown that focus on the transversus abdominus and multifidus muscles is a necessary part of physical therapy for lowback pain. For other sports, such as volleyball, specific programs have been designed but no randomized studies have been conducted to date [52, 53].

6.7 Aging and Sports Injuries: The Older Athlete The increased number of older people practicing sports activities has created the emerging issue of specific musculoskeletal injuries in this population. The effects imposed on the body by the aging process include those involving the musculoskeletal system, with decreased muscle mass, muscle strength, bone mass, ligament and tendon tensile strength and increased stiffness in muscle, tendons, and ligaments. Musculoskeletal injuries, changes in sports competition motivation, and medical conditions (such as cardiovascular disease) can affect the sports performance and practice of the older athlete [54, 55]. Stretching, adequate strength, and muscle condition as well as a proper warm up have been recommended in the literature, with no specific studies investigating the real preventive role in decreasing injury rate in the older athlete [54]. In addition general conditions such as decreased hearing and visual performance can enhance the risk of musculoskeletal injuries as a predisposing factor [56]. There is no conclusive evidence regarding the relationship between the aging process, sports, and osteoarthritis. Although repetitive load-impact activities can increase the risk of developing osteoarthritis and acute chondral damage, especially in individuals with lower limb malalignment, there is no evidence that in individuals with normal alignment either sport or exercise can increase the risk of osteoarthritis with documented changes into the joint structures [57, 58].

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6.8 The Prevention of Running Injuries Running injuries are increasing as the numbers of runners, both competitive and amateur, have increased as well. The principles of prevention, however, are quite similar for both groups, and are based on intrinsic and extrinsic factors [59]. The most important of these, evaluated through evidence-based studies are: training methods, leg malalignment, running shoes, muscle strength, and flexibility. Studies of injury prevention and risk factors have been inconclusive. Yeung and Yeung analyzed randomized and non-randomized studies on injury prevention and concluded that an optimal training load has yet to be determined [60]. In their systematic review, these authors noted that military recruits who used shock-absorbing insoles in their training boots did not have fewer soft-tissue injuries [60]. Macera et al. investigated running distance as an injury prognostic factor, concluding that lowering the weekly running distance 20%, below 64 km, reduced the injury risk by 15% [61]. McKenzie et al. studied the difference between the foot arch type, identifying three principal types, and found that the pronated and supinated types were linked to higher stress forces transmitted in the upper leg [62]. The relationship between running-shoe quality and the potential for injury has also been examined. Running in improper or overused running shoes affects limb alignment, increasing the risk of injury. Running shoes should be replaced every 500-700 km to prevent injuries. Stretching has been advocated as important habit to reduce the risk of injury; however, according to review by Shrier, stretching before running does not lower the risk [63]. Nonetheless, other authors found that muscle imbalance and reduced flexibility are associated with a higher injury rate and that stretching should therefore be performed after any form of exercise [63-65]. Medial tibial stress syndrome has been widely studied but the data on prevention and treatment guidelines are inconclusive. The most consistent preventive device reportedly was the cushioned sole support [66].

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7. Wright RW, Fetzer GB (2007) Bracing after ACL reconstruction: a systematic review. Clin Orthop Relat Res 455:162-168 8. Lam RY, Ng GY, Chien EP (2002) Does wearing a functional knee brace affect hamstring reflex time in subjects with anterior cruciate ligament deficiency during muscle fatigue? Arch Phys Med Rehabil 83:1009-1012 9. Patterson PE, Eason J (1996) The effects of prophylactic brace construction materials on the reactive responses of the MCL during repetitive impacts. J Athl Train 31:329-333 10. Baker BE, Van Hanswyk E, Bogosian St et al (1987) A biomechanical study of the static stabilizing effect of knee braces on medial stability. Am J Sports Med 15:566-570 11. Salvaterra GF, Wang M, Morehouse CA, Buckley WE (1993) An in vitro biomechanical study of the static stabilizing effect of lateral prophylactic knee bracing on medial stability. J Athl Train 28:113-119 12. Cawley PW, France EP, Paulos LE (1991) The current state of functional knee bracing research. A review of the literature. Am J Sports Med 19:226-233 13. Erickson AR, Yasuda K, Beynnon B et al (1993) An in vitro dynamic evaluation of prophylactic knee braces during lateral impact loading. Am J Sports Med 21:26-35 14. France EP, Paulos LE (1990) In vitro assessment of prophylactic knee brace function. Clin Sports Med 9:823-841 15. Paulos LE, Cawley PW, France EP (1991) Impact biomechanics of lateral knee bracing. The anterior cruciate ligament. Am J Sports Med 19:337-342 16. Pietrosimone BG, Grindstaff TL, Linens SW et al (2008) A systematic review of prophylactic braces in the prevention of knee ligament injuries in collegiate football players. J Athl Train 43:409-415 17. Caraffa A, Cerulli G, Projetti M et al (1996) Prevention of anterior cruciate ligament injuries in soccer. A prospective controlled study of proprioceptive training. Knee Surg Sports Traumatol Arthrosc 4:19-21 18. Yoo JH, Lim BO, Ha M et al (2009) A meta-analysis of the effect of neuromuscular training on the prevention of the anterior cruciate ligament injury in female athletes. Knee Surg Sports Traumatol Arthrosc 18:824-833 19. Brophy RH, Silvers HJ, Mandelbaum BR (2010) Anterior cruciate ligament injuries: etiology and prevention. Sports Med Arthrosc 18:2-11 20. Silvers H (2009) Components of prevention program. In: Hewitt TH, Shultz S, Griffin LY (eds) Understanding and preventing noncontact ACL injury. Human Kinetics, Champaign, IL 21. Blazina ME, Kerlan RK, Jobe FW et al (1973) Jumper’s knee. Orthop Clin North Am 4:665678 22. King JB, Perry DJ, Mourad K et al (1990) Lesions of the patellar ligament. J Bone Joint Surg Br 72:46-48 23. Renstrom P, Johnson RJ (1985) Overuse injuries in sports. A review. Sports Med 2:316-333 24. Dixit S, DiFiori JP, Burton M et al (2007) Management of patellofemoral pain syndrome. Am Fam Physician 75:194-202 25. Fulkerson JP (2002) Diagnosis and treatment of patients with patellofemoral pain. Am J Sports Med 30:447-456 26. Warden SJ, Hinman RS, Watson MA Jr et al (2008) Patellar taping and bracing for the treatment of chronic knee pain: a systematic review and meta-analysis. Arthritis Rheum 59:73-83 27. Miller EA, Hergenroeder AC (1990) Prophylactic ankle bracing. Pediatr Clin North Am 37:1175-1185 28. Hollis JM, Blasier RD, Flahiff CM (1995) Simulated lateral ankle ligamentous injury. Change in ankle stability. Am J Sports Med 23:672-677 29. McCluskey GM, Blackburn TA Jr, Lewis T (1976) Prevention of ankle sprains. Am J Sports Med 4:151-157 30. McCluskey GM, Blackburn TA Jr, Lewis T (1976) A treatment for ankle sprains. Am J Sports Med 4:158-161 31. Garrick JG, Requa RK (1973) Role of external support in the prevention of ankle sprains. Med Sci Sports 5:200-203

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32. Laughman RK, Carr TA, Chao EY et al (1980) Three-dimensional kinematics of the taped ankle before and after exercise. Am J Sports Med 8:425-431 33. Rovere GD, Clarke TJ, Yates CS et al (1988) Retrospective comparison of taping and ankle stabilizers in preventing ankle injuries. Am J Sports Med 16:228-233 34. Capasso G, Maffulli N, Testa V (1989) Ankle taping: support given by different materials. Br J Sports Med 23:239-240 35. Rarick GL, Bigley G, Karst R et al (1962) The measurable support of the ankle joint by conventional methods of taping. J Bone Joint Surg Am 44(A):1183-1190 36. Sitler M, Ryan J, Wheeler B et al (1994) The efficacy of a semi rigid ankle stabilizer to reduce acute ankle injuries in basketball. A randomized clinical study at West Point. Am J Sports Med 22:454-461 37. Jerosch J, Hoffstetter I, Bork H et al (1995) The influence of orthoses on the proprioception of the ankle joint. Knee Surg Sports Traumatol Arthrosc 3:39-46 38. Seroyer S, Nho Sm, Bach B et al (2010) The kinetic chain in overhead pitching: its potential role for performance enhancement and injury prevention. Sports Health 2:135-145 39. Ruotolo C, Penna J, Namkoong S et al (2003) Shoulder pain and the overhand athlete Am J Orthop 32:248-258 40. Meyers JB, Laudner KG, Pasquale MR et al (2005) Scapular position and orientation in throwing athletes. Am J Sports Med 33:263-271 41. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder. Spectrum of pathology. Part I Pathoanatomy and biomechanics. Arthroscopy 19:404-420 42. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder. Spectrum of pathology: Part III The SICK scapula dyskinesis and the kinetic chain and rehabilitation. Arthroscopy 19:641-661 43. Akuthota V, Ferreiro A, Moore T et al (2008) Core stability exercise principles. Curr Sports Med Rep 7:39-44 44. Zachazewski LE, Magee DJ, Quillens WS (eds) (1996) Athletic injuries and rehabilitation. WB Saunders, Philadelphia, pp 599-622 45. Tomberlin JP, Saunders HD (1994) Evaluation treatment and prevention of musculoskeletal disorders. Saunders Group, Chaska, MN, vol. 2 (3rd ed) 23:187-215 46. Heiderscheit BC, Sherry MA, Silder A et al (2010) Hamstring strain injuries: recommendations for diagnosis, rehabilitation, and injury prevention. J Orthop Sports Phys Ther 40:67-81 47. Askling C, Karlsson J, Thorstensson A (2003) Hamstring injury occurrence in elite soccer players after preseason strength training with eccentric overload. Scand J Med Sci Sports 13:244-250 48. Kraemer R, Knobloch K (2009) A soccer-specific balance training program for hamstring muscle and patellar and Achilles tendon injuries: an intervention study in premier league female soccer. Am J Sports Med 37:1384-1393 49. Croisier JL, Ganteaume S, Binet J et al (2008) Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am J Sports Med A 36:14691475 50. Zazulak B, Cholewicki J, Reeves NP (2008) Neuromuscular control of trunk stability: clinical implications for sports injury prevention. J Am Acad Orthop Surg 16:497-505 51. Akuthota V, Ferreiro A, Moore T et al (2008) Core stability exercise principles. Curr Sports Med Rep 7:39-44 52. Gluck GS, Bendo JA, Spivak JM (2008) The lumbar spine and low back pain in golf: a literature review of swing biomechanics and injury prevention. The Spine J 8:778-788 53. Smith CE, Nyland J, Caudill P et al (2008) Dynamic trunk stabilization: a conceptual back injury prevention program for volleyball athletes. J Orthop Sports Phys Ther 38:703-720 54. Galloway MT, Jokl P (2000) Aging successfully: the importance of physical activities in maintaining health function. J Am Acad Orthop Surg 8:37-44 55. Brown (1996) Limitation of sports participation in elderly. Sports Med Arthroscopy Rev 4:235242 56. Marabhan LG, Bauman PA, Kalman D et al (1998) Masters athletes: factors affecting performance. Sports Med 28:283-285


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57. Kallinen M, Markku A (1995) Aging, physical activities and sports injuries. Sports Med 20:4152 58. Buckwalter JA, Woo SL-Y (1996) Age related changes in ligaments and joint capsules: implication for participation in sports. Sports Med Arthroscopy Rev pp 250-262 59. Johnston CA, Taunton JE, Lloyd Smith DR, McKenzie DC (2003) Preventing running injuries. Canadian Family Physician 49:1101-1109 60. Yeung EW, Yeung SS (2001) A systematic review of interventions to prevent lower limb soft tissues injuries. Br J Sports Med 35:383-389 61. Macera CA, Pate RR, Powell KE et al (1989) Predicting lower extremity lower limb injury among habitual runners. Arch Int Med 149:2565-2568 62. Mc Kenzie DC, Clement DB, Tauntoin JE (1985) Running shoes, orthotics and injuries. Sports Med 2:2334-2347 63. Shrier (1999) Stretching before exercise does not reduce the risk of local muscle injury. A critical review of basic science literature. Clin J Sports Med 9:221-927 64. Wen DY, Puffer JC, Shmalzried TP (1997) Lower extremity alignment and risk of overuse injuries in runners. Med Sci Sport Exc 29:1291-1298 65. Wen DY, Puffer JC, Shmalzried TP (1998) Injuries in runners. A prospective study of alignment. Clin Sports Med 8:187-194 66. Craig DI (2008) Medial tibial stress syndrome: evidence-based prevention. J Athl Train 43:316318

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M. Conte, F. Caputo, G. Piu, S. Sechi, F. Isoni and M. Salvi

Abstract Stress fractures (SFs), or fatigue fractures, are common overuse injuries of bone often suffered by elite and recreational athletes. They may occur anywhere in the body since all bones, but especially those of the lower limbs, are involved in most sports-related activities. Extrinsic and intrinsic factors influence the probability of SF development, some of these factors, such as physical conditioning, are well known, but others are still a matter of debate, such as anatomical conformation, gender, nutrition and equipment. The literature consists mostly of case series, with only a few analyses providing generally applicable evidence concerning risks and treatment. Pain is related to the particular activity. The clinical diagnosis of SFs is not always apparent from the patient’s history and physical examination, such that imaging (MRI, bone scan and CT scan) is crucial. In most patients, non-surgical treatment – consisting of rest and NSAIDs followed by a gradual return to sports activity once clinical symptoms are no longer present and there is radiographic evidence of recovery of bone fracture – is successful after 12 weeks. The timing of surgical treatment is not yet well established and depends on the SF site, symptoms duration, and activity level. Surgeons specializing in sports medicine should strive to recognize SFs as early as possible to achieve the best results for these patients and to reduce inactivity for elite and recreational athletes. Further studies are needed to prevent this common overuse injury and to establish a treatment algorithm aimed at allowing the athlete to return to his or her activity as quickly as possible and at reducing the risk of refracture.

7.1 Introduction Stress fractures (SFs), or fatigue fractures, are common overuse bone injuries that can be very painful and debilitating. SFs occur typically in professional endurance athletes, but Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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they are also observed in many recreationally active individuals, especially in the “weekend warrior,” as well as in soldiers and the osteoporotic elderly [1]. They are more frequent in weight-bearing bones, such as the lower limbs. The pathophysiological mechanism is quite different from that of acute bone trauma [2]. Repetitive stress to the bone by compressive, tensile, and rotational forces overloads its strength, producing deformation of the trabeculae until a microfracture or fracture occurs. An increase in sports-related activity among people of any age and a sudden change in the intensity of training increase the likelihood of overuse injury. Modern imaging techniques allow a fast and precise diagnosis. A visible line of fracture on standard radiographs confirms a SF, but bone scan or magnetic resonance imaging (MRI) can further demonstrate bone remodeling prior to fracture occurrence. In some cases, SFs do not progress to healing, resulting in delayed union or non-union.

7.2 Epidemiology To our knowledge, the first SF described in the literature was a metatarsal SF, reported by Breithaupt in 1855 in Russian military recruits. Devas, in 1958, was the first to report this injury in athletes. Based on the recent SF literature, stratification and statistical analysis are almost impossible as there are only a few epidemiological studies but many case series [2]. Moreover, many SFs are often misdiagnosed and repair spontaneously, without a remarkable clinical course. Consequently, the true incidence of SF is not known [3]. It has been estimated that SFs represent 10% of sports injuries, with an annual rate in athletes and military recruits in the USA of 5-30%. This broad range is explained by the method of imaging used for SF diagnosis and by the extremely variable clinical course of these fractures. As noted above, SFs are more common in the lower limbs, in people undergoing military training, and in athletes, particularly long-distance runners. Niemeyer et al. described a series of 27 SFs, 48% of which were in the tibia, followed by the metatarsal bones. In 26 of their cases, the fractures were treated conservatively, with an average treatment period of 8.9 weeks. In 63% of SF patients, a return to full athletic activity without restrictions was achieved within 3 months of the diagnosis, while 33% returned to their previous activity within 12 months [4]. In a review of 3198 SFs, 82% involved the lower extremities, 17% the trunk and pelvis, and 1% the upper extremities. In the Matheson review of 320 SFs, the locations were: tibia (49.1%), tarsal bone (25.3%), metatarsal (8.8%), femur (7.2%), fibula (6.6%), pelvis (1.6%), sesamoids (0.9%), and spine (0.6%). Bilateral SF occurred in 16.6% of these cases [5]. However, a more-detailed analysis of SF distribution shows differences among military recruits, athletes, and ballet dancers [6] (Table 7.1).

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Table 7.1 Distribution of stress fractures (from [6]) Fracture site Tibia Tarsus Femur Metatarsus Fibula Ribs Spine Pelvis Ulna Radius Medial malleolus Patella

Athletes

Military recruits

Ballet dancers

42.9 19.8 9.0 8.2 8.0 3.9 3.9 2.4 1.0 0.6 0.2 0.2

53.4 2.9 31.6 9.2 1.5 – – 1.5 – – – –

22.0 – – 63.0 – – 7.0 – – – – –

7.3 Etiology and Pathophysiology Bone is a living and dynamic tissue, with a cellular and molecular remodeling response to applied mechanical stress in accordance with Wolff’s law. Previous concepts of SF emphasized fatigue in the muscles surrounding the bone preceding fatigue failure within the bone in response to excessive forces. Currently, however, the most widely held view regarding the pathogenesis of SF is that repetitive stress of bone causes a periosteal resorption that outstrips the rate of bone remodeling, weakening the cortex and resulting in fracture [3]. The etiology of SF is multifactorial [2]. Many studies have shown that bone elasticity and geometry are as important as bone mineral density in predicting fracture risk. Abnormal gait could also play a role in SFs of the lower limbs. Brief daily vibration may positively stimulate bone. Genetic factors may contribute to bone quality as well, affecting bone strength and providing new insights into fracture healing and tissue reengineering [7]. Biomechanical, compressive, tensile, and shearing forces contribute to SF formation. A simple cylinder model does not clarify the dynamic nature of either bone or the muscles, tendons, and ligaments that act on it, as evidenced by the occurrence of SFs in non-weight-bearing bones in addition to those in the expected sites such as the tibia or metatarsal. According to the most recent research, repeated cyclical stress induces remodeling through increased osteonal activity and increases the likelihood of a SF. Anatomic conformation and specific repetitive sport-related movements may produce a focal area of bone stress [3]. The pathomechanics of SF can arise from two modalities: (1) direct mechanical damage, arising from the sudden application of a repetitive load, thus exceeding the mechanical resistances of bone; (2) repetitive microtrauma, which shifts bone remodeling from osteoblastic to osteoclastic activity. However, it is probable that a continuum between these two mechanisms exists [8] (Fig. 7.1):

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Normal/accelerated remodelling (in response to exercise) Trabecular weakening of trabeculae

Microfracture

Macrofracture (if activity is not modified)

Fig. 7.1 Pathomechanics of stress fracture

7.4 Extrinsic and Intrinsic Risk Factors The etiologic factors contributing to the risk of SF formation are numerous and can be classified as extrinsic or intrinsic. Extrinsic factors are related to the environment while intrinsic factors involve the athlete directly. Nonetheless, many of the factors that promote fracture development remain to be identified, while many others are interrelated and thus methodologically difficult to analyze independently. Large prospective studies will better identify the risk factors and their relative importance in determining SFs [9].

7.4.1 Extrinsic Factors Physical conditioning. Physical conditioning and training are quite important in the prevention/development of sports-related injuries. High-level training is a major risk factor; a higher weekly running mileage correlates with an increased incidence of SF. Ballet dancers who train for more than 5 h per day have a significantly higher risk of SF [2]. Fatigue compromises muscle function and attention and is a prelude to injury. This could explain the high incidence of SF in military recruits, who are suddenly introduced to intensive exercise regimens, or in athletes who suddenly increase their training schedules [9]. Athletes who refrain from sports activity for several days and then re-start their training with overly intensive loads are at risk, as is an out-of shape athlete.

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Table 7.2 Stress fracture development in different sports Location

Sport

Tibia Peroneal Navicular Sesamoids Humerus Clavicle Acromion and scapular Radius Femoral neck Medial malleolus Metatarsal Jones fracture Lumbar spine Rib

Running, basket, soccer Running and skating Hurdles, basket, soccer Running and jumping Throwing athletes, baseball, tennis, cricket, javelin Shooting at a target, weightlifters, throwing athletes Gymnastics Gymnastics and weight training Older athletes, military recruits, runners Basketball, long-distance running, football Military recruits, ballet, running, aerobic dance, skating, hockey Basketball, football, dance Gymnastics, dance, weight-lifters, rowing Lifting and rowing

Equipment. The incidence of calcaneal SF in military recruits seems to correlate with the use of combat boots. Other risk factors are the use of heavy machines and the type of ground or surface (see below). Shoe damage has been shown to be a better indicator of shock-absorbing quality than shoe cost. Training surface. Training on uneven surfaces may increase the risk of SF by causing increased muscle fatigue and redistributing the load to bone. Type of sport. The location of a SF in athletes seems to correlate with the specific sport activity and the required athletic movements (Table 7.2). Goldberg et al. quantified the rate of SF in men and women in different sports: softball 6.3%, track 3.7%, basketball 2.9%, tennis 2.8%, gymnastics 2.8%, lacrosse 2.7%, baseball 2.6%, volleyball 2.4%, crew 2.2%, and field hockey 2.2%. Knowledge of the sport practiced by the patient and the site of the SF can improve the diagnosis and management of these injuries [1].

7.4.2 Intrinsic Factors Anatomic conformation. The pathogenesis of SF involves two very important intrinsic factors: bone shape and muscle action. There is good evidence that tall and lean people have a lower incidence of SF, while muscle hypertrophy leads to a higher incidence of SF. Valgus alignment of the lower limbs, flatfoot or hyperpronation, cavus foot, loss of extrarotation of the hip, thin corticals, limb-length discrepancy, and muscular force have been implicated as factors predisposing a person to SF formation [5], but there is controversy in the literature. The surrounding muscles seem to have a bone-protective whereas mus-

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cle fatigue can contribute to overloading. The nature of a SF differs depending on the anatomic site: in the convex zone of the bone, they have a transverse course, and in the concave zone an oblique course. Some SFs may arise from excessive, direct, repetitive muscular traction at one point (e.g., the triceps for the olecranum or the peroneus brevis in the proximal 5th metatarsal). Gender. Women have a higher incidence of SF than men (12:1 in military recruits, 55% in sports activities) for many reasons. Women with a history of menstrual disorders, eating disorders (quality and quantity) and patholaxity are at greater risk. Protein intake is also an important factor for bone and, ultimately, bone strength [10]. Due to insufficient estrogen levels, oligomenorrheic or amenorrheic female athletes have a reduced ability to maintain bone density, which alters the normal balance between osteoclast and osteoblast activity via a lack of inhibition of interleukin-6, which stimulates osteoclast production. Smoking lowers serum estrogen levels and therefore reduces bone mineral density, both in a dose-related manner. It has also been shown that athletes weighing < 75% of their ideal body weight have a higher incidence of SF than those with an ideal body weight [1]. Nutrition. Bone strength may be reduced by insufficient intake of calcium, vitamin D, and proteins, consistent with the increased risk of SF by a reduced bone mineral density.

7.5 Classification Stress fractures can be classified according to their topography and prognosis.

7.5.1 Topographic Classification Stress fractures can occur in any bones, as summarized in Table 7.3. Femoral SFs are uncommon but very serious injuries involving endurance athletes and soldiers. In military recruits, about 34% of femoral SFs are located at the neck, 27% at the subtrochanteric area, 27% in the distal diaphysis, and 11% in the medial femoral condyle. Usually, non-surgical management, such as rest and restricted weight-bearing, yields excellent outcomes. Some femoral SFs require surgical treatment to prevent catastrophic displacement or to reduce a displaced fracture. Cannulated screws or intramedullary nailing is required, depending on the location and the type of SF. Spinal and sacral SFs have to be considered in the differential diagnosis of general low back pain in children or adolescent athletes. The risk is higher in young gymnast females, in whom the posterior arch of the 5th lumbar vertebrae is overstressed in

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Table 7.3 The topography of stress fracture Upper extremity

Pelvis

Femur Knee Ankle Foot

Clavicle, acromion, and coracoid process Scapula Humerus Ulna (shaft and olecranon) Radius Metacarpus Spine and sacrum Rib Ala of the ilium Pubic ramus Lower limbs Superior and inferior aspect of the neck Shaft Tibia and fibula Patella Medial malleolus Distal fibula Metatarsal shaft fracture Proximal fifth metatarsal (Jones’s fracture) Navicular Cuboid Cuneiform Sesamoids Calcaneus

repetitive extension movements. SFs of the sacrum are more common, especially in long-distance runners and military recruits as well as volleyball and basketball players. Sacral SFs should be considered in female athletes suffering low back pain, particularly when it is associated with eating disorders or menstrual irregularity. Diagnostic imaging with radiographs, bone scans, CT scans, and MRI are quite important in the differential diagnosis and treatment of these fractures in adolescent athletes. Pelvic SFs occur in the pubic branch and simulate groin pain. They are usually seen in runners and military recruits. Tibial SFs are very common (50-75% of the overall SF) and often difficult to treat. Devas, in 1958, was the first to report the clinical pattern and radiographic findings of this type of fracture. Non-operative treatment is the gold standard, but surgical intervention may be necessary in some cases. Fibular SFs occur more frequently in athletes and in 55% of the cases involve the proximal fibula. SFs of the medial and lateral malleolus are seen in runners and likely result from axial and torsional forces, muscular contractions, and alignment abnormalities. Usually, the fracture is of the transverse type. The preferred approach to treatment is non-surgical management with restriction of activity using a cast or splint. If there is no evidence of displacement, internal fixation with a small lag screw is recommended. Navicular SFs were described for the first time in 1970 and represent up to 35% of all SFs and 80% of all tarsal SFs. Non-surgical treatment is the strategy of choice.

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Metatarsal SFs are relatively common in athletes, military recruits (9% of all SFs), and ballet dancers. Of particular importance is SF of the proximal fifth metatarsal (Jones fracture), as it frequently requires surgical intervention in patients who do not accept cast immobilization. Upper-extremity SFs are less common (10% of SF) than lower-extremity SFs but are becoming ever more frequent in throwing athletes and rowers. Since they seem to be caused by overuse and fatigue of the surrounding musculature, they may be prevented by appropriate training and conditioning. Clavicular SFs occur mainly in rowers, in athletes involved in throwing events, such as baseball, and in gymnasts and divers who must bear their weight on their upper limbs. Acromial SFs have been described in weight-lifters, golfers, car mechanics, and following the repetitive use of a screwdriver [6]. Most humeral SFs are diaphyseal and have been documented in baseball pitchers, swimmer, weightlifters, and throwing athletes. Ulnar SFs are seen in weight-lifters, throwing athletes (baseball players, tennis players), and, occasionally, with the use of crutches. Olecranon SFs often are associated with complications, such as non-union. Here, it is very important to immobilize the fractured area at an early stage and to urge the patient to avoid using the triceps. In some cases internal fixation is necessary. Premature physeal closure of the distal radius has been reported among young gymnasts with SF of the growth plate. Dancers often suffer overuse injuries of the lower extremities because of the high performance and flexibility demanded and the need to hold extreme positions for long periods of time. Treatment is essentially symptomatic, with restriction of activities until union of the fracture is achieved. Rib SFs are common and are mainly associated with rowing (6-12% of high-level rowers). Prisk et al. described five case series of SF, involving the first rib and simulating a shoulder problem, in dancers who suddenly began a weight-training program. Both the trapezius squeeze test and the radiographs were positive, but the dancers were able to return to their activity after 5 weeks. Upper-rib SFs are mainly typical of weight lifters and baseball pitchers, whereas SFs of the lower rib seem to be more frequent in golfers and tennis players [11].

7.5.2 Prognostic Classification Stress factors can be divided into two groups according to the prognosis: high-risk SF and low-risk SF. This classification is based on the biomechanical environment and the natural history of the fracture. High-risk SFs occur in the supero-lateral femoral neck, patella, anterior tibial shaft, medial malleolus, talus, tarsal navicular, proximal 5th metatarsal, talar neck and sesamoids. Low-risk SFs present in the femoral shaft, medial tibia, ribs, ulnar shaft, lateral malleolus, calcaneus, and 2nd, 3rd, and 4th metatarsals. This classification is very useful in decision-making regarding treatment and return to full activity. Most SFs heal with relative rest and activity modification [1].

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7.6 Clinical Diagnosis While the history and physical examination are very helpful in making the diagnosis, they do not always reveal the typical characteristics and reproducible signs of SF. In most cases, an athlete with a SF will have a history of an increase in the amount of activity or a substantial change in training or footwear. In the early stages, localized pain is noted at the conclusion of activity. Rest from the offending activity usually relieves the pain completely, whereas continuation of the same activity not only increases pain severity but also causes it to begin earlier in the activity. Most patients do not have a history of severe trauma. As the history frequently reveals recent changes in routine, the athlete must be questioned as to a change in his or her training regimen, including an increase in distance or duration of training, training on a harder playing surface or track, or the use of new or poor-quality footwear. In female athletes, menstrual status, history of smoking, and nutritional irregularities must be noted [1]. Very often, the history reveals a period of selftreatment by the patient to relieve pain and to allow continuation of the sports activity. There are no typical clinical signs or tests to rule out other possible causes of the patient’s symptoms and thus to obtain an accurate clinically based diagnosis. However, symptoms are correlated with the location and stage of the SF. Local tenderness is the most consistent finding correlating with activity. Pain may lead to claudication if the lower limbs are affected. A local tenderness is palpable only on superficial bone, such as the tibia or 5th metatarsal. Sometimes, there is associated edema, redness, and muscle contracture. When a SF is located at the tibial shaft, the differential diagnosis should include medial tibial stress syndrome (MTSS), shin splints, exertional compartment syndrome, and popliteal artery entrapment syndrome. MTSS results from stressful forces applied to the tibia that are not sufficient to cause a fracture but do stimulate remodeling. Shin splints result from repetitive running on a hard surface and excessive use of the foot dorsi-flexors; they consist of musculo-cutaneous inflammations of the leg but fracture or ischemic disorders must be excluded. In exertional compartment syndrome, the pain does not restrict impact-loading activity and the patient may describe paresthesias or anesthesia [1]. In Matheson’s series of 320 SF [5], the average time from symptoms to diagnosis and average recovery time from diagnosis to full activity were, respectively, 5.5 and 7.5 weeks for the femur, 9.9 and 7.7 weeks for the fibula, 12.6 and 11.7 weeks for the tibia, 12.6 and 7.9 weeks for the metatarsal, and 16.2 and 17.3 weeks for the tarsal (with an overall average for the latter indicator of 12.8 weeks).

7.7 Imaging Modern imaging techniques are crucial in the diagnosis of SF. Radiographs, however, are not very sensitive, with 70% of X-rays being initially negative in the early stage of SF and only half of these revealing a radiolucent line later (Figs. 7.2, 7.3). The findings

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Fig. 7.2 Fibular stress fracture as seen on X-ray

Fig. 7.3 Proximal 5th metatarsal, as seen on X-ray, in an elite soccer player

are best revealed on standard antero-posterior and lateral views. When present, radiographic findings include periosteal new bone formation and endosteal thickening or a radiolucent line. Nuclear bone scan allows the depiction of areas of even subtle osseous turnover and stress remodeling. The sensitivity of bone scan is reportedly quite high

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Fig. 7.4 Calcaneal stress fracture, as revealed by MRI

(84-100%) [1]. Radionuclide uptake can reveal a SF very early on, within 2-8 days after symptoms begin. Ultrasound provides a limited evaluation of the superficial osseous structures and is best reserved for those cases in which MRI is not suitable for patient reasons. CT scan and MRI represent the gold standards in the diagnostic protocol of SF. CT scan provides exquisitely fine osseous detail in multiple planes, often demonstrates endosteal remodeling or a fracture line, and can be used to monitor the healing process. At present, MRI provides the most complete evaluation of SF, revealing both functional and morphological information on bone [12]. Its sensitivity and specificity approach 100% [2] (Fig. 7.4). In localized bone pain in children, the differential diagnosis must include infectious diseases, osteoid osteoma, or tumor. In case of negative imaging but no improvement in the patient’s symptoms, a new imaging study should be repeated 2-3 weeks after the initial one.

7.8 Treatment An algorithm for the treatment and management of SF is shown in Fig. 7.5. However, the treatment of SF is discussed controversially in the literature. Prognostic classification seems to be the major difficulty in SF management. Surgeons should take into consideration the injury site (low- vs high-risk), the grade of the lesion, the individual’s athletic level and age, and the time point in the competitive season. In high-level competitive athletes, SFs

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History and physical examination

7

Rx – (Persistents symptoms)

RX –

TREATMENT

MRI

BONE SCAN

+ with pain

+ without pain

+ without pain

+ with pain

TREATMENT

Biomechanical evaluation

Biomechanical evaluation

CT SCAN

– with pain

Repeat imaging after 2-4 weeks

– with pain

Repeat imaging after 2-4 weeks

Fig. 7.5 Algorithm for the management of stress fracture

pose a frustrating problem as they require a long time away from the sports activity. The physical and psychological integrity of the athlete after a SF largely depends on rapid diagnosis and correct treatment. Communication between the athlete and his or her physician about the risks and benefits of full activity rather than relative or absolute rest is mandatory [2]. Treatment may be non-surgical or surgical. Firstly, and in most cases, non-surgical treatment is the strategy of choice even in competitive high-level athletes, since success is usually achieved within 12 weeks. In order to minimize the risk of non-union, activity should be reduced below the threshold of symptoms or even stopped completely, depending on the pain and the stage of the SF. Active rest, activity modification, pain control, crutches and non-weight-bearing for lower limbs and even immobilization should be considered as options in a non-surgical protocol. Alternative training activity can be used to maintain cardiovascular fitness, skills, and muscle tone and to prevent psychological problems such as depression. Rowing machines, stationary bicycles, pool-running, and swimming are useful. Ice applications several times per day, NSAIDs, and stretching and strengthening exercises are also recommended. The use of an orthosis device, such as pneumatic lower leg braces, or specific footwear devices should be considered. Particular attention must be given to strength deficits and muscle tightness. Different therapeutic modalities, including daily pulsed low-intensity ultrasound and electrical bone stimulators, can be employed. Extracorporeal shock wave therapy (ESWT) seems to be effective in relieving recalcitrant pain in SF [13]. Low-risk SFs usually heal spontaneously simply by limiting full activity to pain-free activity for 4-8 weeks. A gradual increase in activity should begin when the athlete is pain-free. High-risk SFs are more difficult to treat and a return to full activity should be recommended only after

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proper treatment and demonstration of complete healing of the SF at imaging. Usually, absolute rest and surgical intervention for high-risk SFs are recommended to improve healing and to allow early return to competition, as this approach minimizes the risk of dislocation of the fracture or refracture and related sequelae [2]. In case of an adverse outcome of non-surgical treatment after 12 weeks, surgery should be considered. Surgical treatment options are, however, not well-established in the literature. As is the case for traumatic fractures, the surgical repair of a SF depends on its location and stage and on the displacement. Cortical bone drilling, excision in the case of sesamoid SF, and internal fixation by nailing, plate, or screw are recommended depending on the parameters mentioned above. Some SFs tend spontaneously to delayed union or non-union, such as those of the 5th metatarsal, sesamoids, and olecranon. These fractures sites usually need surgery. Successful treatment of SF generally implies a long period of activity restriction. The under-treatment of a high-risk SF can lead to a prolonged loss of activity, but the over-treatment of a low-risk SF can result in unnecessary deconditioning and loss of activity time [2]. These two opposing strategic problems have to be considered in the management of SF in elite athletes. In general, SFs should be adequately treated until all symptoms have disappeared. A variety of medications have been investigated in animal studies regarding their effects on fracture healing. In the future, parathyroid hormone and the bisphosphonates may represent satisfactory options to prevent and treat sports-related SFs as well as acute fractures. Nevertheless, large randomized clinical trials are required to evaluate the many approaches to SF treatment and their relative success.

7.9 Prevention Greater efforts and emphasis must be devoted to the prevention of SFs. Physicians, athletes, and trainers should be aware of the risk factors that predispose athletes to these injuries as well as the appropriate training and nutritional regimens to avoid them. Indeed, SFs can be considered as a failure of the progressive training program developed by the coach and carried out by the athlete. Similarly, for individuals who are not physically fit, a very important step in SF prevention is a gradual increase in training loads. There is evidence indicating that a gentle introduction to exercise is associated with a dramatic reduction in the incidence of SF, probably due to the effect of muscle conditioning. Communication between the physician, athlete, and coach regarding diet, training, and psychological problems must be encouraged. In female athletes, the use of oral contraceptives or a decrease in the activity intensity or the frequency of workouts allows a return of menses, reducing the risk of SF [14]. Severe eating disorders are considered medical emergencies and often require a multidisciplinary approach [2]. Measures to prevent SFs include modifications to footwear and changes in training schedules. The use of shock-absorbing inserts in footwear would probably reduce the incidence of SF in military personnel. Although there is insufficient data to determine the best design of these inserts, comfort and tolerability should obviously be kept in mind. While rehabilitation after tibial SF may be aided by the use of pneumatic bracing, confirmation

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awaits further evidence [14]. Worn-out and outdated shoes must be avoided because of their reduced shock-absorbing qualities. A favorite aphorism of some coaches is: “save money on all equipment, but not on shoes.” Snyder et al. [15], in a review of the literature, found good results in SF prevention by the use of insoles in high-risk military recruits whereas in competitive athletes the findings were less clear. The AAOS guidelines to prevent SFs [16] are: 1. Maintain a healthful diet, including foods rich in calcium and vitamin D, to help build bone strength. 2. Use proper sports equipment, avoiding old or worn-out running shoes. 3. Alternate your activities; for example, substituting jogging with swimming or cycling. 4. Start any new sports activity slowly, with a gradual increase, e.g., 10% per week, in time, speed, and distance. 5. Strength training can help prevent early muscle fatigue and prevent the loss of bone density associated with aging. 6. If pain or swelling returns, stop the activity and rest for a few days; if the pain continues, see your doctor.

7.10 Conclusions Both for the active population and competitive athletes, SFs are a frequent and frustrating pathology that should be well recognized by sport physicians. The education of coaches and athletes in SF avoidance is also important. Evaluation of potential extrinsic and intrinsic risk factors, early diagnosis, and appropriate treatment are crucial to reduce loss of competition time and to allow a quicker return to full activity. Further research on SFs, particularly related to athletes, is mandatory to identify effective methods in the prevention and treatment of these overuse injuries.

References 1. Shell D (1999) Stress fractures. Sports medicine secrets. 2nd edn. Hanley & Belfus, Philadelphia, pp 331-337 2. Kaeding CC (2006) Stress fractures. Clinics Sports Med Jan, pp 1-174 3. Reid DC (1992) Stress fracture. In: Bone a specialized connective tissue. Sports injuries: assessment and rehabilitation. Churchill Livingstone, pp 120-127 4. Niemeyer P, Weinberg A et al (2006) Stress fractures in the juvenile skeletal system. Int J Sports Med 27:242-249 5. Matheson GO, Clement DB, McKenzie DC et al (1987) Stress fractures in athletes. Sports A J Sports Med 15:46 6. Brown CC, McQueen M, Tornetta P (2006) Trauma. Stress fractures. Lippincott Williams & Wilkins, pp 32-41 7. Friedl KE, Evans RK, Moran DS (2008) Stress fracture and military medical readiness: bridging basic and applied research. Med Sci Sports Exerc 40:s609-s622

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8. Wang WG (1963) Stress lesions of the tibia in athletes. China J Sports Sci 120:121 9. Goldberg B, Pecora C (1994) Stress fractures: a risk of increased training in freshman. Phys Sports Med 22:68-78 10. Bennel KL, Malcolm SA, Thomas S et al (1996) Risk factors for stress fractures in track and field athletes: a twelve-month prospective study. Am J Sports Med 24:810-818 11. Prisk VR, Hamilton WG (2008) Stress fracture of the first rib in weight-trained dancers. Am J Sports Med 36:2444-2447 12. Sofka CM (2006) Imaging of stress fractures. Clin Sports Med 25:53-62 13. Taki M, Iwata O, Shiono M et al (2007) Extracorporeal shock wave therapy for resistant stress fracture in atletes. A report of 5 cases. Am J Sport Med 35:1188-1192 14. Rome K, Handoll HHG, Ashford RL (2009) Interventions for preventing and treating stress fractures and stress reactions of bone of the lower limbs in young adults. Cochrane Database of Systematic Reviews 2005 Issue 2. Art. No: CD000450.DOI: 10.1002/14651858. CD000450.pub2. 15. Snyder RA, Deangelis JP, Koester MC et al (2009) Does shoe insole modification prevent stress fractures? A systematic review. HSS J 5:92-98 16. AAOS (2007) Stress fractures. Your orthopaedic connection. http://orthoinfo.aaos.org/topic. cfm?topic=A00112. Last update July

Section II Medical Issues

Cardiology

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F. Pigozzi, M. Rizzo and P. Borrione

Abstract An athlete’s cardiologic assessment is the basis for his or her safe participation in vigorous training and competition. However, athletes represent an interesting study sample for the cardiologist, both in terms of diagnosis and management because of the peculiarity of the clinical and instrumental findings that frequently characterize their evaluation. Well-trained athletes very often present with significant morphological, functional, and electrophysiological alterations that comprise a physiological clinical picture known as the “athlete’s heart”. Cardiologists who evaluate athletes should have a deep knowledge of this clinical picture in order to correctly interpret the findings of these patients. Moreover, they must bear in mind that the consequences of an erroneous diagnosis are potentially devastating, leading to the death of the athlete or to the end of his or her sports career. In this chapter, the authors provide an overview of the main issues contributing to a deeper knowledge of the athlete’s heart and suggest specific further readings.

8.1 “Athlete’s Heart” The most important factor in sustained vigorous physical activity is the capability of the cardiovascular system to supply oxygen to exercising muscles. In trained individuals, the heart undergoes profound morphological and functional changes that represent the physiological adaptation to athletic training. The term “athlete’s heart” (AH) refers to this collection of changes, which predominantly includes increases in left ventricular cavity dimension and wall thickness, improved diastolic filling, and a decreased heart rate. The changes that occur in AH are related to the gender, age, and race of the athlete, as well as to the type, duration, and intensity of the sport performed. They have a beneficial effect, allowing the heart to function as a more efficient and powerful pump. Over the last three decades a vast body of literature has been collected on AH such that, nowadays, the condition is a very well characterized entity. Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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For sports cardiologists, distinguishing the physiological, adaptive changes characteristic of AH from structural diseases associated with an increased risk of sudden death is obviously of extreme importance. The diagnosis of structural heart disease may result in recommendations to stop athletic participation in order to reduce the risk of sudden death, whereas correct identification of physiological cardiac adaptations will prevent the unwarranted withdrawal of healthy athletes from training and competition.

8.1.1 Morphological Features of “Athlete’s Heart” A large number of echocardiographic studies have provided a clear and detailed picture of AH. The main modifications occur on the left side of the heart and include an increase in left ventricular end-diastolic cavity dimension and volume, with a proportional increase in septal and free-wall thickness, associated with normal systolic and diastolic function (physiological cardiac hypertrophy), as well as an increase in left atrial size. The increases in cardiac dimensions are generally small (about 10-20%), with values remaining within the normal limits in most athletes. However, in a significantly large subgroup of highly trained athletes (about 15%) marked enlargement of the left ventricular cavity (v 60 mm) and/or an increase in wall thickness up to the accepted normal limits (13-16 mm) is observed. Echocardiographic studies on elite athletes (perhaps the most important of which was performed by Pelliccia and colleagues) have demonstrated that the response of the heart to athletic training is not uniform: evidence of cardiac remodeling, in fact, is observed in about the 50% of athletes, and the degree of remodeling depends on age, body surface area, gender, race, in addition to the type and intensity of training. In particular, the most extreme increases in cardiac dimensions occur in male athletes engaged in rowing, cross-country skiing, cycling, or swimming. By contrast, in sports requiring a high degree of skill, such as fencing, equestrian events, and yachting, modifications of the cardiac morphology are usually minimal, consisting of a mild increase of left ventricular end-diastolic internal diameter. Another important factor modulating training-induced cardiac remodeling is the athlete’s gender. In female athletes, left ventricular cavity dimensions are smaller (10%) than in male athletes matched for age and type of sport. The same holds true for wall thickness (20%) and cardiac mass (30%). This different response of-women’s hearts to athletic training is probably due to a number of factors, including smaller body surface area and lean body mass, lower cardiac output, and lower plasma levels of androgenic hormones.

8.1.2 Differential Diagnosis of Athlete’s Heart and Pathological Cardiac Hypertrophy The picture of AH is generally recognized without difficulties by an accurate echocardiographic exam. However, in those athletes who present with marked cardiac remodeling, the differential diagnosis with congenital cardiomyopathies (hypertrophic or dilated), associated with increased risk of sudden death, becomes a critical issue. Actually, a mor-

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phological “gray zone” between AH and pathological cardiac hypertrophy has been described, including a markedly increased wall thickness of 13-16 mm (about 2%) and a markedly enlarged left ventricle of 60-70 mm (about 14%). In particular, in athletes presenting with a markedly enlarged left ventricular cavity, clinical suspicion of dilated cardiomyopathy may arise. However, the differential diagnosis is generally easy because of the absence of left ventricular dysfunction in AH. On the other hand, in athletes presenting with markedly increased left ventricular wall thickness, hypertrophic cardiomyopathy (HCM), the primary cause of sudden cardiac death in young athletes, may be suspected. In most of these cases a differential diagnosis is possible based on a careful evaluation of both echocardiographic and clinical data. Specifically, the criteria for differential diagnosis are: 1. Echocardiographic parameters – Pattern of hypertrophy. AH presents as a symmetric hypertrophy, different from HCM in which the pattern of hypertrophy is typically heterogeneous and asymmetric. – Left ventricular cavity dimension. In AH, increased wall thickness is associated with a dilated left ventricular cavity (> 55 mm); in HCM, the left ventricular cavity is typically reduced (< 45 mm) (Fig. 8.1).

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13 Fig. 8.1 Left ventricular dimension in a male elite rower: increased septal and posterior wall thickness is associated with a dilated cavity

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– Diastolic function. Doppler analysis of trans-mitral flow is invariably normal in AH whereas it is one of the first functional parameters that is altered in HCM, reflecting the reduced ventricular compliance due to parietal fibrosis. 2. Clinical parameters – ECG alterations. Individuals with HCM always show characteristic ECG alterations, including increased voltages of R and S waves, deep negative T waves, and deep Q waves. However, healthy highly trained athletes may present an ECG pattern with marked alterations, overlapping those of HCM but representing the extreme expression of AH. In those athletes, ECG alone is not useful for the differential diagnosis and the results must be evaluated in the light of all the other parameters. – Family screening. HCM is a genetic cardiac disease with autosomal dominant transmission; so, in most cases, the disease is present in one or more first-degree relatives. However, some cases of disease are sporadic, as a result of de novo mutations. – Reversibility. Physiological cardiac hypertrophy is a response to athletic training and is thus completely reversible after a period of detraining, unlike the pathological condition. If all the other parameters do not allow an assured differential diagnosis, a 3-month period of detraining should be the definitive choice. What To Keep in Mind. The differential diagnosis between AH and potentially lethal cardiac disease has particularly important clinical implications since the identification of a structural cardiac disease (especially HCM) in an athlete may be the basis for disqualification from training, in the effort to minimize the risk of athletic field death. This problem arises in a relative small but significant number of individuals who fall in the above-mentioned “gray zone” between physiological and pathological hypertrophy (left ventricular wall thickness of 13-16 mm for HCM, end diastolic internal diameter > 60 mm for dilated cardiomyopathy). Careful analysis of several echocardiographic and clinical features allows diagnostic differentiation in most cases. When, despite these investigations, doubt persists, a short period of detraining is suggested because while physiological hypertrophy regresses, pathological hypertrophy does not.

8.2 Cardiologic Evaluation of Trained Athletes 8.2.1 Clinical and Instrumental Findings 8.2.1.1 Medical History and Physical Examination The medical history of the athlete includes both the familial and the personal history. The former should investigate the presence of hereditable cardiac diseases and history of premature sudden cardiac death (< 40 years) among first-degree relatives. The latter should aim in particular to ascertain the presence of cardiac symptoms, such as palpitation, chest

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pain, dizziness, syncope or pre-syncope, and the possible relation between such symptoms and physical activity. The physical examination reveals a normal or slow pulse. Arterial blood pressure is within normal limits. The left ventricle may be prominent to feel and displaced laterally. Third and fourth sounds are permissible, as is a soft mid-systolic flow murmur (“innocent murmur”).

8.2.1.2 Resting, Dynamic, and Exercise ECG In most trained athletes, the resting 12-lead ECG is normal or shows minor modifications that are part of the AH picture, such as incomplete right bundle branch block, early repolarization, and mild increased R or S wave voltage (Fig. 8.2). Sinus bradycardia is the most common finding in athletes, particularly those engaged in endurance disciplines (present in up to 85%). Resting heart rates are as low as 40 bpm and usually associated with sinus dysrhythmia and/or sinus pauses lasting v2 s; the latter are present in about 30% of athletes examined. Moreover, athletes have a higher prevalence (37%) of first-degree and second-degree (Mobitz type 1, 23%) atrioventricular (A-V) block than is found in the general population (14 and 6%, respectively). The degree of sinus dysrhythmia and A-V block appears to be related to the extent of athletic conditioning, as these alterations become less prominent or even disappear upon cessation of regular exercise training. Pathophysiologically, the changes have been attributed to an altered neural input to the heart, with (relatively) increased vagal and reduced sympathetic tone. In addition, functional changes are postulated to occur in the sinus node, partially explaining the slower intrinsic heart rate. Apart from these physiological changes, highly trained athletes frequently have a number of other ECG alterations. Specifically, in a study by Pelliccia and colleagues, 40% of

Fig. 8.2 Early repolarization pattern and sinus bradycardia (40 bpm) in a male elite rower

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a large group of elite athletes showed abnormal ECGs raising clinical suspicion of structural heart disease, including 15% with distinctly abnormal patterns (Fig. 8.3). However, cardiac diseases were rarely responsible for the abnormal ECGs in those athletes; in fact, a cardiac abnormality was identified in only 5%. Instead, the most important determinant of ECG pattern appeared to be the extent of physiological hypertrophy, the type of sport performed, and gender. Those athletes with the most marked ECG abnormalities showed the greatest dimensional increase in the left ventricular cavity and in wall thickness and cardiac mass. Overall, athletes engaged in endurance sports, such as cycling, rowing, canoeing, and cross-country skiing, present with ECG alterations more frequently than those engaged in largely technical disciplines, such as yachting, equestrian events, and shooting. Finally, the prevalence of abnormal ECG is higher in male than in female athletes, most likely as a consequence of the more marked cardiac remodeling associated with athletic conditioning. Interestingly, in unselected athletic populations the prevalence of markedly abnormal ECG patterns suggestive of structural cardiac disease is much lower (5%) than that reported in highly trained athletes, confirming that the intensity of conditioning and the extent of physiological cardiac remodeling represent the major determinants. What To Keep in Mind. ECG alterations in highly trained athletes are usually an expression of AH and are sometimes the extreme expression of this physiological picture. However, long-term follow-up studies have demonstrated that ECG changes may represent the initial expression of underlying cardiomyopathies that may not be evident until many years later. Accordingly, when ECG alterations are identified, echocardiographic and clinical surveillance of the athlete is needed to clarify their significance.

Fig. 8.3 Markedly abnormal ECG of a healthy male athlete. Note the deep, negative T waves in the precordial leads, mimicking a HCM pattern

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8.3 Arrhythmias in Athletes Due to the heightened vagal tone that accompanies physical conditioning, trained athletes frequently show arrhythmias and conduction alterations, such as sinus bradyarrhythmia, junctional rhythm, and first-degree A-V block. In athletes, 24-h ECG Holter monitoring is commonly used to better evaluate arrhythmias and conduction disturbances. This technology is particularly important because it provides a means to monitor and record the electrical activity of the heart during athletic training. Moreover, it is able to document the arrhythmic cause of cardiac arrest (ventricular fibrillation) in individuals, including athletes, who died suddenly. Holter ECG can detect a number of cardiac rhythm alterations in healthy athletes. These include sinus bradycardia of 30-45 bpm, sinus arrhythmia, atrial ectopy, and atrial couplets, as well as ventricular ectopy and couplets. Brief periods of supraventricular rhythm and idioventricular rhythm may also occur and are seen on Holter monitoring. Interestingly, ventricular arrhythmias are a quite common finding in asymptomatic trained athletes, both as isolated premature beats and, even rarely, as complex tachyarrhythmias (including couplets and bursts of nonsustained ventricular tachycardia, Fig. 8.4). These disturbances in cardiac rhythm are not associated with adverse clinical events and usually cease or are substantially reduced after a brief period of deconditioning but also during physical training sessions and exercise testing. Collectively, these findings suggest that some arrhythmias are part of the AH spectrum. What To Keep in Mind. When dealing with arrhythmias it is important to know that they are a common finding in athletes, a fact that sometimes may cause difficulties in their interpretation. Based on their extensive experience, Furlanello and colleagues classified arrhythmias in athletes into three categories: benign, paraphysiological, and pathological. Benign arrhythmias consist of asymptomatic ventricular or atrial premature complexes that occur in the absence of structural heart disease and are similar to those found in the untrained population. Paraphysiological arrhythmias, such as sinus pauses and Mobitz type 1 second-degree A-V block, may result from intensive training and do not require withdrawal from sports activity whereas pathological arrhythmias are characterized by their adverse hemodynamic effects on athletic performance and/or by their association with a structural cardiac disease. To assess with certainty the nature of the arrhythmia, a careful evaluation of the athlete is needed that basically includes medical history, physical examination, echocardiography, maximal exercise ECG test, and 24-h Holter ECG. Moreover, in unresolved cases, further exams must be undertaken, such as signal-averaged ECG (SAECG), electrophysiological study (EPS), and cardiac magnetic resonance imaging (MRI).

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Fig. 8.4 Run of non-sustained TV during Holter monitoring in a male asymptomatic elite athlete with a normal heart

8.3.1 Exercise ECG Test This test is usually performed with using a cycle ergometer or treadmill with increasing load (generally with steps of 2-min duration) up to the maximum heart rate, with simultaneous monitoring of ECG and blood pressure. Trained athletes usually show an outstanding exercise capacity, with rapid recovery of heart rate and blood pressure at the end of the test. The heart rate response is slower than in untrained people, but the maximum rate that is reached is the same. This test is commonly used in the functional evaluation of professional athletes and of athletes with known cardiac alterations or arrhythmias. In particular, during exercise testing, certain arrhythmias resolve with increasing heart rate while others may increase in frequency and severity. These changes may be helpful in recognizing the nature of the arrhythmia (benign or potentially threatening) as well as the he-

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modynamic impact of the rhythm disturbance. The exercise test is also recommended for the evaluation of athletes > 35 years of age, independent of their level of conditioning and resting evaluation findings. In addition, this test represents the first step in the identification of exercise-induced myocardial ischemia, the main cause of sudden death among elite athletes. What To Keep in Mind. The ECG of the athlete reflects the extremes of normality more than any other method for cardiovascular evaluation. This single test is often used in the evaluation of a trained athlete. In doing so, wave forms, heart rate, and rhythm recorded by the ECG must be evaluated in the context of other findings in the athlete’s history, physical examination, and other tests to avoid an incorrect diagnosis of a cardiac abnormality in a very healthy individual.

8.4 Sudden Cardiac Death in Athletes 8.4.1 Demographics, Causes, and Mechanisms Sudden cardiac death (SCD) in an apparently healthy athlete typically occurs on the athletic field during competition (more rarely, during a training session) or immediately after the end of the athletic activity, in the absence of prior symptoms. These tragic events are not as uncommon as previously thought, considering that in the USA a young athlete dies every 3-4 days, with an annual average of about 110 cases. Obviously, these deaths are numerically insignificant compared to those due to other causes; however, because they occur in a group of people considered the healthiest in society, almost invulnerable, they have a particularly dramatic impact on the community. Moreover, exercise-related SCDs are often considered “tragic fatalities” but, in most cases, they are preventable. These deaths, in fact, occur in individuals with underlying cardiac diseases, usually unknown and asymptomatic, the vast majority of which could have been identified with an accurate cardiologic evaluation. In SCD, structural cardiac diseases are often recognized at autopsy. While in older athletes (> 35 years) the main cause of SCD is atherosclerotic coronary artery disease, in the young athlete a broad spectrum of congenital (prevalently) cardiac abnormalities have been described, the most important of which are hypertrophic cardiomyopathy (HCM, the most common cause in the USA), arrythmogenic right ventricular cardiomyopathy (ARVC, the most common cause in Italy), and congenital arterial anomalies, followed by valvular heart disease, Marfan syndrome (with aortic dissection or rupture), dilated cardiomyopathy, premature atherosclerotic coronary artery diseases, and myocarditis. Nonetheless, in about 2% of young athletes who died suddenly, no structural cardiac abnormalities could be detected on standard autopsy examination. However, most of these previously unexplained cases were likely due to ion-channel disorders, Wolf Parkinson-White syndrome, or coronary vasospasm (Fig. 8.5).

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USA (Maron et al. JAMA 1996) miscellaneous

CAD 2% ARVD 3%

CCA 13%

HCM 36%

LVM 10%

ITALY (Corrado et al. NEJM 1998) miscellaneous

HCM 2%

ARVD 22%

CCA 12%

CAD 18%

Fig. 8.5 Causes of SCD (sudden cardiac death) in young athletes in American and Italian series. HCM, hypertrophic cardiomyopathy; LVM, left ventricular mass; ARVD, arrhythmogenic rigth ventricular dysplasia; CCA, congenital coronary anomalies; CAD, coronary artery diseases

8.4.2 Pathogenesis Sudden cardiac death occurs much more frequently in male athletes (9 of 10), usually in the late afternoon or early evening (corresponding largely to the time of competitions), and in most cases in people who had never experienced prior symptoms. Prodromal complaints (chest pain, palpitation, dizziness) have, however, been described in some cases. Independent of the underlying cause, in most cases the final common pathway of SCD is the development of an electrical instability resulting in a fatal arrhythmia (ventricular fibrillation in > 90% of cases) and cardiac arrest (Fig. 8.6). The marked arrhythmogenicity is, in fact, the common denominator among most of the pathological substrates of sports-related SCD, in which the physical activity (and thus increased sympathetic drive) acts as a trigger for the development of a lethal arrhythmia. Therefore, withdrawal of the athlete from sports activity may significantly reduce his or her overall risk. Conversely, vigorous exercise causes a 2.5-fold increase in the risk of SCD. Since the mechanism of athletic field deaths is generally a sudden cardiac arrest due to ventricular fibrillation, all athletic staff (including team physicians, trainers, and coaches) should receive specific training in cardiopulmonary resuscitation as well as in the use of automatic external defibrillators. The presence of these devices is warranted at all sites of athletic competition; unfortunately, this is currently not the case. What To Keep in Mind. Sport-related SCD does not occur in healthy individuals but in athletes with underlying cardiac disease. While in older athletes (>35 years) the leading cause is coronary artery disease, in young athletes a number of congenital cardiac alterations have been described, primarily primitive cardiomyopathies (HCM and ARVC). An accurate cardiovascular evaluation of all athletes would identify high-risk subjects and, consequently, disqualify them from participation in sports. Since the mechanism of death in athletes is usually sudden cardiac arrest due to ventricular fibrillation (independent of

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Fig. 8.6 Ventricular fibrillation leading to cardiac arrest

the underlying substrate), prompt cardiopulmonary resuscitation, and thus the availability of an automatic external defibrillator on the athletic field, represents the only effective means to save a life.

8.5 Pre-participation Screening of the Competitive Athlete The prevention of SCD in athletes is the main challenge of sports cardiology and the rational basis for the implementation of large-scale pre-participation screening (PPS) for all competitive athletes. The PPS applied in Italy since 1982 represents a unique model for the entire medical community and is a source of pride for the country. This national medical program, established by the Italian government 30 years ago, is mandatory for all competitive athletes and consists of an annual evaluation that routinely includes a 12lead ECG, a medical history, and a physical examination. Suspicion of cardiac disease based on the screening examination is followed in most cases by second- and third-level instrumental tests (echocardiography, maximal exercise test, 24-h ECG monitoring, cardiac MRI, EPS, and endomyocardial biopsy) to obtain a specific diagnosis. When a definitive diagnosis of heart disease is made, the Italian Cardiologic Guidelines for Competitive Sports Eligibility (COCIS) are used to formulate specific recommendations for either continued participation in the sport or disqualification (temporary or permanent) from competitive sports. The various analyses of this model confirm the use of ECG as the strength of screening. The American experience is proof that screening based only on medical history and physical examination has limited potential to detect (or raise the suspicion of) potentially lethal cardiovascular abnormalities in young athletes. The Italian approach, by contrast, has demonstrated that ECG is a practical and cost-effective method of population-based screening. Indeed, ECG has a high negative predictive value: a normal test is associated

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with a structurally normal heart in 95% of the cases whereas ECG abnormalities are commonly found in individuals with potentially lethal cardiac diseases. The fact that highly trained athletes may present with markedly altered ECG patterns is not a serious limitation for the use of this test, as the integrated evaluation of clinical and instrumental findings (including echocardiographic evaluation) allow the significance of those alterations to be determined. The most important evidence for the efficacy of the Italian PPS was provided in a critically important study by Corrado and colleagues, consisting of a retrospective analysis of trends in SCD in athletic and non-athletic young individuals in Italy in the first 25 years of the application of the national screening program. During this period, the rate of SCD among young athletes (screened population) decreased by 90%, while there was no change in the incidence of SCD among non-athletic individuals (unscreened population) of the same age-range. Indeed, the Italian PPS appears to be the best currently available method for detecting cardiovascular conditions that may predispose athletes to sudden death. The program, in fact, has been designated by both the European Society of Cardiology and the International Olympic Committee as the only one that is effective in preventing athletic field deaths, and consequently, it is the only one that has been recommended to all European countries. What To Keep in Mind. The goal of pre-participation cardiovascular screening of competitive athletes is to identify those with cardiac alterations that may render their athletic activity unsafe and, consequently, to disqualify these individuals from training and competition, to reduce the risk of athletic-field catastrophes. The Italian model of screening based on the ECG together, with medical history and physical examination, has proven to be the only really effective approach to preventing SCD.

Suggested Reading Athlete’s Heart Maron BJ, Pelliccia A (2006) The heart of trained athletes. Cardiac remodelling and the risks of sports, including sudden death. Circulation 114:1633-1644 Pelliccia A, Maron BJ, Spataro A et al (1991) The upper limit of physiologic cardiac hypertrophy in highly trained elite athletes. N Engl J Med 324:295-301 Pelliccia A, Culasso F, Di Paolo F, Maron BJ (1999) Physiologic left ventricular cavity dilatation in élite athletes. Ann Inter Med 130:23-31 Pelliccia A, Maron BJ, Culasso F et al (1996) Athlete’s heart in women: echocardiographic characterization of highly trained elite female athletes. JAMA 276:211-215

Differential Diagnosis of Athlete’s Heart Spataro A, Pisicchio C, Rizzo M et al (2005) Athlete’s heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, the “grey zone”. J Sports Cardiol 2:102-108

Cardiologic Evaluation Fletcher GF (1999) The athlete’s electrocardiogram. In: Williams RA (ed) The athlete and heart disease: diagnosis, evaluation & management Lippincott Williams & Wilkins, Philadelphia

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Pelliccia A, Maron BJ, Culasso F et al (2000) Clinical significance of abnormal electrocardiographic patterns in trained athletes. Circulation 102:278-284 Pelliccia A, Di Paolo F, Quattrini FM et al (2008) Outcomes in athletes with marked ECG repolarization abnormalities. N Engl J Med 358:152-161

Arrhythmias in Athletes Zeppilli Paolo (2007) Cardiologia dello Sport, 4th edn. CESI, Italy Fletcher GF (1999) The athlete’s electrocardiogram. In: Williams RA (ed) The athlete and heart disease: diagnosis, evaluation & management. Lippincott Williams & Wilkins, Philadelphia Maron BJ, Pelliccia A (2006) The heart of trained athletes. Cardiac remodelling and the risks of sports, including sudden death. Circulation 114:1633-644

Sudden Cardiac Death in Athletes Pigozzi F and Rizzo M (2008) Sudden death in competitive athletes. Clin Sports Med 27:153-181 Maron BJ (2003) Sudden death in young athletes. N Engl J Med 349:1064-1075 Pigozzi F and Rizzo M (2010) Cardiac emergencies on athletic fields. In: McDonagh D, FIMS sports medicine event manual. Lippincott Williams & Wilkins, in press

Pre-participation Screening Pigozzi F, Rizzo M, Maffulli N (2009) Pre-participation screening of young athletes to prevent sudden cardiac death. Intl Sport Med J 10:101-115 Corrado D, Basso C, Pavei A et al (2006) Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening. JAMA 296:1593-1601 Corrado D, Pelliccia A, Bjornstad HH et al (2005) Cardiovascular pre-participation screening of young competitive athletes for prevention of sudden death: proposal for a common European protocol. Consensus Statement of the Study group of Sport Cardiology of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of myocardial and pericardial Diseases of the European Society of Cardiology. Eur Heart J 26:516-524

Nutrition

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A. Parisi, A. Giombini

Abstract Training as well as physical and technical abilities are fundamental for the high-level athlete, but of equal importance is adequate and proper nutrition. While intake of the correct proportion of carbohydrate, proteins, lipids, and fluid is essential, so are dietary strategies related to timing of intake, type of nutrient, its source, and the need to add other nutrients, as these considerations will optimize the performance capacity of the athlete. A normal diet, if balanced, is sufficient for the athlete although it may sometimes (short recovery period, adverse environmental conditions, etc.) be necessary to add supplements or ergogenic aids to improve athletic performance. The most commonly consumed ergogenic products are: creatine, β-hydroxy-β-methybutyrate, proteins and amino acids, pyruvate, caffeine, carnitine, and bicarbonate. Although legal, these products need a medical prescription in order to avoid performance withdrawal symptoms, atopic reactions, side effects, overdosage, and organ damage. Supplements have a particularly important role in the diets of athletes who are vegetarians, especially female athletes. The exact composition of these supplements will depend upon the specific type of vegetarian diet.

9.1 Introduction Athletes use a wide range of strategies to gain a competitive advantage before or during competition. In this regard, nutritional intervention may have the biggest impact, supporting consistent intensive training and promoting the physiological and biochemical adaptations that will lead to improved performance. While the correct food choices will not make a champion out of the athlete who is neither talented nor motivated, a meager or inadequate diet can prevent the talented athlete from reaching his or her peak. Becoming an elite athlete requires good genes, good training and conditioning, and a sensible diet. Optimal nutrition is essential for high-level performance whereas nutritional Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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misinformation can do severe harm to the ambitious athlete. The goal of the nutritionist involved in advising competitive athletes is first to identify the nutritional needs of the athlete and then translate them into dietary strategies that take into account individual circumstances. Any form of sport activity will increase the rate of energy expenditure; therefore, energy intake must be increased accordingly. Of course, the energy demands of men vs. those of women vary greatly depending primarily on body mass and on the training load.

9.2 Macronutrients 9.2.1 Role of Carbohydrates Athletes benefit most from carbohydrates stored in the body, as carbohydrates yield more energy per unit of oxygen consumed than fats. The rate of blood glucose and muscle glycogen use depends on exercise intensity and on exercise duration. It is also influenced by the availability of other fuel sources, mainly plasma free fatty acids. If carbohydrate stores were the sole fuel source available during exercise, they would provide only enough energy to complete a 32-km run. As the exercise intensity increases linearly, muscle glycogen use increases exponentially. Saltin and Gollnick found that the rate of muscle glycogen use was 0.7, 1.4, and 3.4 mmol/kg/min at exercise intensities of 50, 75, and 100% of VO2max, respectively [1]. Studies of nutrition prior to exercise have traditionally examined the administration of carbohydrates to maximize endogenous glycogen stores and to maintain serum glucose levels during endurance demands [2]. As with muscle glycogen, a linear increase in exercise intensity results in an exponential increase in muscle glucose uptake [1]. Bjorkman and Wahren reported that, after 40 min of exercise at exercise intensities of 25% and 75% VO2max, leg glucose uptake was 0.4 and 1.8 mmol/min, respectively [3]. The daily ingestion of high-carbohydrate meals (~65%) is recommended to maintain muscle glycogen, while increased ingestion rates are needed (~70% carbohydrates) in the 5-7 days leading up to competition, as a means of maximizing muscle and liver glycogen stores and in order to sustain blood glucose during exercise [4]. Maximal levels of glycogen storage, however, may be achieved after just 1-3 days of consuming a highcarbohydrate diet while minimizing physical activity [4]. A study by Bussau et al. [2] found that eating a highly glycemic carbohydrate (10 g/kg/day) diet for as little as one day could significantly increase muscle glycogen levels. In that particular study, muscle glycogen levels increased from baseline levels of 95±5 mmol/kg/wet weight to 180±15 mmol/kg/wet weight after one day, and remained at those levels for three subsequent days. Research involving the ingestion of single high-carbohydrate feedings has also demonstrated the promotion of higher levels of muscle glycogen and an improvement of blood glucose maintenance (euglycemia), although changes in performance have been equivo-

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cal [5]. Indeed, carbohydrate ingestion within an hour prior to exercise generally yielded equivocal results regarding changes in performance, but studies have routinely shown the ability of carbohydrate ingestion to maximize glycogen utilization and promote carbohydrate oxidation [6]. For the rapid restoration of muscle glycogen, some authors recommend that 1.0-1.5 g carbohydrate/kg/body weight be consumed immediately after exercise. The continued intake of carbohydrate supplementation every 2 h, or smaller supplements taken more frequently, will maintain a maximal rate of storage for as long as 6 h after exercise [6]. Supplements composed of glucose or glucose polymers are more effective than those based on fructose for the restoration of muscle glycogen; however, the addition of some fructose to the supplement is recommended because it is more effective than glucose in the restoration of liver glycogen. The addition of protein to the supplement may also be of benefit because it has been found to increase the pancreatic insulin response and the rate of muscle glycogen synthesis. In conclusion, there is wide evidence that adequate carbohydrate intake is important for the restoration of muscle glycogen stores, and that other dietary strategies, related to the timing of intake, type of carbohydrate source, and the addition of other nutrients, may directly enhance the rate of glycogen recovery and/or improve the practical achievement of carbohydrate intake targets.

9.2.2 Role of Proteins Proteins and amino acids are an important part of athletes’ diets and as such have been the subject of a great deal of discussion and controversy, especially among strength athletes. After carbohydrates and fats, proteins provide energy for the body. Exercise may increase an athlete’s need for protein depending on the type and frequency of exercise. Extra protein is stored as fat. In the fully grown athlete, it is training that builds muscle, not protein per se. Most authorities recommend that endurance athletes eat 1.2-1.4 g protein per kg body weight (bw) per day; resistance and strength-trained athletes may need as much as 1.6-1.7 g protein per kg bw. A varied diet will provide more than enough protein as caloric intake increases. Indeed, excess protein can deprive the athlete of more efficient fuel and can lead to dehydration as high-protein diets increase the water requirement necessary to eliminate nitrogen through the urine. Also, an increase in the metabolic rate can occur and therefore an increase in oxygen consumption. Both the synthesis and the degradation of muscle protein are increased as a result of resistance exercise, with a greater increase in synthesis allowing a net accretion of body protein. Evidence shows that protein intake in the range of 1.2-1.8 g/kg bw/day is optimal for maintaining body protein and allowing maximal muscle protein synthesis [7]. Novices beginning a resistance-training program should use the upper end of this range. Long-term consumption of protein at levels higher than this range has not been shown to have any benefit. Preliminary research suggests that consumption of carbohydrate with protein mixtures after resistance exercise enhances protein accretion and metabolic recovery.

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More recently, protein-hydrolysate-containing products specifically formulated for postexercise recovery have gained popularity. Protein hydrolysates are produced from purified protein sources by heating with acid or, preferably, by the addition of proteolytic enzymes, followed by purification procedures. Each protein hydrolysate is a complex mixture of peptides of different chain length together with free amino acids, and they can be classified by a global value referring to the degree of hydrolysis (DH). The DH is the fraction of peptide bonds that have been cleaved in the starter protein [8]. It is generally accepted that protein hydrolysates containing mostly di- and tripeptides are absorbed faster than intact proteins. Certainly, hydrolysis can facilitate the absorption of casein protein (the main component of whole-milk protein), which in its intact form is slowly absorbed. In a recent study by Koopman et al., subjects received a 350-ml beverage containing 35 g of either intact or extensively hydrolyzed casein. The results showed that the ingestion of casein hydrolysate induced plasma amino acid peaks 25-50% higher than those obtained following intact casein ingestion [9]. Although carbohydrates and lipids supply most energy needs during exercise, human skeletal muscle can also oxidize at least seven amino acids, namely, leucine, isoleucine, valine, glutamate, asparagine, aspartate, and alanine, which thus provide additional free energy to fuel muscle contraction. Rapidly absorbed protein hydrolysates may be especially suitable for intra-exercise consumption. A well designed study by Beelen et al. examined the effect of protein hydrolysate co-ingestion with carbohydrate on muscle protein anabolism during resistance-type exercise. Importantly, the subjects in their study were investigated in a postprandial state, reflecting a real-life situation. The mixed muscle protein fractional synthetic rate was found to be substantially higher after protein hydrolysate co-ingestion [8]. As far as sports nutrition is concerned, protein hydrolysates, usually produced from whey or casein protein, are generally not used as meal replacements. Rather, athletes use these products to induce rapid increases in plasma amino acids around the time of their workouts, with the aim of maximizing muscle protein anabolism and facilitating recovery. However, there are no studies comparing the effects of whey or casein protein hydrolysates and intact proteins on skeletal muscle anabolism in healthy athletes. It is our opinion that an adequate protein intake, in the range of 1.2-1.8 g/kg bw, can help a person who is active in aerobic or resistance training to reach their potential by preserving muscle tissue and possibly enhancing recovery after strenuous exercise. Protein intake > 2 g/kg bw has not been shown to be beneficial and may have negative effects on overall dietary quality.

9.2.3 Role of Fats Even though maximal performance is impossible without muscle glycogen, fat also provides energy for exercise. Fat is the most concentrated source of food energy and supplies more than twice as many calories (9 kcal/g) by weight as either protein (4 kcal/g) or carbohydrate (4 kcal/g) [6].

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Plasma triacylglycerols (TGs) and free fatty acid (FFAs) as well as muscle TGs are important, oxidizable lipid fuel sources for skeletal muscle metabolism during prolonged exercise. The rate of plasma FFA use by muscle is a function of several factors, including availability, transport from the plasma to the mitochondria, and intracellular metabolism. FFA mobilization from adipose tissue is the first committed step in FFA metabolism, and it depends on the rate of adipose tissue lipolysis. Fat is the major fuel for light- to moderate-intensity exercise. However, although fat is a valuable metabolic fuel for muscle activity during longer-term aerobic exercise and performs many important functions in the body, no attempt should be made to consume more fat. High lipid availability can be achieved by short-term or long-term exposure to highfat diets but the value of eating a high-fat diet in preparation for competition is still a matter of debate. There is evidence both for and against the hypothesis that training on a highfat diet for a few weeks before competition improves performance by promoting fat utilization and sparing glycogen stores [6]. Nonetheless, a low-fat, high-carbohydrate diet is preferable for general health reasons because a high-fat diet has been associated with cardiovascular disease, obesity, diabetes, and some kinds of cancer.

9.3 Supplements and Ergogenic Aids Recreational and elites athletes make use of products aimed at improving performance. The value of these products, which is claimed by the manufacturers in numerous magazine advertisements, is generally not supported by sport nutrition experts, except in those cases in which scientific trials have documented a significant ergogenic effect [6].

9.3.1 Creatine Creatine is a naturally occurring compound made from the amino acids glycine, arginine, and methionine. Nowadays it is the most widely used nutritional supplement. The basis for creatine supplementation is its role in the rapid resynthesis of ATP during short-duration maximal sessions of anaerobic exercise. Harris et al., in 1992 [10], showed that the effect of oral creatine supplementation is a significant increase, reaching 50%, in the total creatine content of muscles. Further studies carried out by Balsom et al. [11] indicated that creatine supplementation decreases anaerobic glycolysis during brief maximal exercise. These mechanisms may enhance anaerobic training, leading to strength and performance gains. Human performance with creatine supplementation has been studied extensively. A summary statement on these studies would be that creatine can be an effective ergogenic supplement when used for simple, short-duration, maximal-effort anaerobic events. Another effect of creatine supplementation is an increase in weight and lean body mass after a shortterm supplementation cycle. The long-term effects of creatine supplement on the kidneys

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are not known, nor are there appropriate data on its possible effects on other creatine-containing tissues, such as the brain and cardiac muscle. Furthermore, several authors have stated that long-term administration of creatine will likely lead to down-regulation of the creatine transporter protein, thus increasing resistance to the compound. A daily dose of approximately 0.03 g/kg was reported to be sufficient to restore the normal breakdown of creatine and to preserve elevated creatine stores [12, 13]. A recent study stated that muscle strength is sigoificantly higher after creatine supplementation during recovery from a muscle-damaging exercise session; in fact, there is faster muscle growth during the recovery petiod and significantly lower plasma creatine kinase activity in the days after injury, which is indicative ofless muscle damage [14]. Many reservations remain concerning creatine supplementation, such as regimens to maximize creatine accumulation in muscle, doses needed to load muscle and to maintain elevated creatine stores, tintiog of intake, and factors regulating the creatine receptor on muscle. To date, none of the studies published in the literature bave reported adverse effects in athletes following long-term creatine supplementation.

9.3.2 ~-Hydroxy-~-M.thylb.tyr.t.

Supplements containing the leucine metabolite ~-hydroxy-~-methylbutyrate (lIMB) are aimed at increasing strength and lean body mass by preventing muscle breakdown. lIMB is metabolized to hydroxymethylglutaryl coenzyme A. Since cholesterol synthesis is need-

ed in membrane repair, HMB supplementation has been suggested to decrease muscle damage and enhance the process of recovery. Despite the popularity and intense marketing of lIMB, the basis for its use bas yet to be proven and studies on its ergogenic effect are controversial [13]. The study cartied out by Knitter et aI. [15] on untrained individuals supplemented with 3 g lIMB /day for 6 weeks showed that the lIMB group had a lower increase in creatine phosphokinase and lactate dehydrogenase after a 20-km run, supporting a role for lIMB in preventing muscle damage. By contrast, Gallagher et aI. [16] studied untrained college men duting 8 weeks of resistance training, supplementing one experimental group (n ~12) with 3 g lIMB/day and another(n ~ 11) with 6 g HMB/day. The results were mixed, making it difficult to draw conclusions. In another study, lowko et aI. [17] examined the effects of supplementation with 3 g lIMB/day on resistance training in nine untrained individuals and found beneficial results in 6 of 7 strength tests compared with placebo, but no significant changes in body fat or lean body mass. The benefits of HMB on trained individuals are less prontising. Recently, Slater and colleagues [18] found that lIMB supplementation for 6 weeks did not affect strength or body com-

petition in trained men, explaining these results by the training-induced suppression of protein breakdown. Nissen et al. [19] examined the safety of lIMB and did not f'md untoward effects, although the longest study was only 8 weeks. Thus, while lIMB may have

an ergogenic role in untrained but not necessarily in trained individuals, further research is needed not only on performance effects but also on the potential role ofHMB in exercise and muscle breakdown [6].

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9.3.3 Proteins and Amino Acids It is generally accepted that athletes have a greater daily protein requirement than sedentary people. Nevertheless, athletes eating a proper diet take in adequate amounts of protein such that protein supplements are not necessary to enhance performance. Williams et al. [20] monitored seven untrained individuals receiving a glucose/amino supplement for 10 weeks, studying the same individuals trained on successive days in order to minimize inter-individual variability. The researchers found no strength benefits conferred by the supplement. In another study, Jentjens et al. [21] found that the addition of protein and amino acids to a carbohydrate diet did not enhance post-exercise muscle glycogen synthesis. In 1992, Lemon et al. [22] demonstrated that supplemental protein intake did not increase muscle mass or strength in novice bodybuilders. The branched chain amino acids (BCAA) leucine, isoluecine, and valine have also been advocated as a supplement but data supporting their ergogenic effects are not convincing. In fact, Davis et al. [23] did not find a beneficial effect of BCAA administration in individuals who performed intermittent, high-intensity running. According to some studies, which did not address performance, BCAA may reduce exercise-induced muscle damage, as reflected in creatine phosphokinase and lactate dehydrogenase levels. Instead, Wagenmakers [24] reported that BCAA may have an ergolytic effect (detrimental to performance) due to the impedance of aerobic oxygenation. A recent study carried out by Matsumoto demonstrated that BCAA supplementation may be effective in increasing the endurance exercise capacity in trained individuals [25]. In summary, while protein and amino acids are essential dietary components, studies on the benefits of supplemental protein are not convincing. It is important to emphasize that a proper diet is sufficient to ensure that athletes receive adequate amounts of protein.

9.3.4 Pyruvate Pyruvate is a carboxylic acid produced by the metabolism of glucose. In 1990, Stanko et al. [26] published two studies examining upper- and lower-extremity endurance capacity in individuals who consumed pyruvate. The unproven mechanism was that pyruvate enhances glucose oxidation, but the study was limited by its very small sample size (8-10 individuals) and the fact that pyruvate/dihydroxyacetone rather than pyruvate alone was used, with the dose of pyruvate (25 g) being very high. In a recent study [27], Morrison and colleagues found that the intake of 7 g of pyruvate for 7 days did not improve cycling performance time (approximately 90 min of cycling) [6]. Equally important, blood pyruvate levels did not increase despite the supplementation. In a separate study carried out by Morrison, published in the same paper, nine recreationally active individuals ingested 7, 15, and 25 g of pyruvate, but again no effect was found on either blood pyruvate or glucose or lipid metabolism. These results are of particular interest because pyruvate is also marketed as a weight-loss and cholesterol-lowering agent, neither of which has been proven [6].

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9.3.5 Caffeine Caffeine is an adenosine-receptor antagonist and a stimulant belonging to the dimethylxanthine class. The proposed mechanism behind caffeine’s ergogenic effect is the stimulation of adrenaline secretion, resulting in the mobilization of FFA. This mechanism increases fat utilization and decreases carbohydrate consumption, thus delaying glycogen depletion. However, this claim failed to gain support in a recent study [6]. Nonetheless, the strength of evidence of caffeine’s ergogenic potential is strong, particularly in aerobic activities. Even for sprint activities, caffeine has shown ergogenic potential in one-time cycling and swimming sprints. By contrast [28], Paton et al. demonstrated, in a double-blind, crossover study, that caffeine is not ergogenic for repetitive bouts of sprinting, although it is commonly used for this purpose in team sport workouts. In these studies, the doses of caffeine used range from 2 to 9 mg/kg (about 250-700 mg caffeine), taken 1 h or less prior to the event. Clearly, an ergogenic effect was demonstrated in doses that would not reach the disqualifying levels of NCAA and IOC sports, i.e., 9 mg/kg, determining a urinary concentration of 12 μg/ml.

9.3.6 Carnitine Carnitine combines with acyl-CoA and allows fatty acid to enter the mitochondrion, where carnitine also functions to regulate the acetyl-CoA and free CoA concentration. Thus, it plays a major role in the integration of fat and carbohydrate oxidation, stimulating oxidative metabolism and improving exercise performance Barnett et al. [29] and Vukovic et al. [30] reported that short-term supplementation with carnitine (4-6 g/day for 7-14 days) had no effect on muscle carnitine concentrations or on the metabolic response to exercise. Despite these negative findings, there are published reports suggesting that carnitine supplementation increases the contribution of fatty acids to oxidative metabolism and thus promotes the use of body fat stores.

9.3.7 Bicarbonate and Other Buffers When taken before exercise, NAHCO3 can reduce the metabolic acidosis that accompanies glycolysis and increase both the muscle-buffering capacity and the rate of efflux of H+ from active muscles, potentially delaying the attainment of a critically low intracellular pH. Improvements in performance are usually seen in exercise lasting from about 30s to a few minutes; but achieving this result requires large doses of bicarbonate (0.3 g/kg body mass), which can be associated with side effects such as vomiting and diarrhea. McNaughton [31] investigated the potential of sodium citrate as an exogenous buffer since it might be associated with less gastrointestinal discomfort [6]. The ingestion of sodium citrate was found to have a positive effect on work output but not on performance.

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9.4 The Vegetarian Athlete Vegetarianism in athletes is a controversial topic. A vegetarian diet surely has positive effects, including reducing the risk for obesity, type 2 diabetes, hypertension, cardiovascular disease, and some type of cancers. In addition, it was observed that vegetarians are usually more physically active, do not smoke, and do not abuse alcohol [32]. However, health problems may arise from the avoidance of all animal-derived foods, especially in individuals following radical vegetarian regimens, such as the vegan diet or the fruitarian diet; in the latter, only what can be obtained without killing plants is consumed. For example, non-heme iron absorption in vegetarians is 70% lower and total iron absorption is approximately one-sixth. Consequently, whereas the iron RDA for omnivorous adult men and premenopausal women is 8 and 18 mg/day, respectively, for vegetarians the recommendations are 14 and 32 mg/day. In addition, adolescents requiring zinc for growth but who maintain a vegetarian diet may have suboptimal zinc status and a reduction in muscle creatine concentration [33]. Hormonal alterations are also seen in vegetarians, and a significant proportion of female athletes with amenorrhea are vegetarians. Hanne et al. [34] observed that when vegetarian female athletes are properly nourished, their menstrual cycle function is normal compared with that of matched non-vegetarian control subjects. Another important matter is performance in the vegetarian athlete. Many studies found no differences between vegetarian and non-vegetarian athletes in running performance, aerobic and anaerobic capacities, arm and leg circumferences, hand grip and back strength, hemoglobin, and total serum protein. Therefore, it is reasonable to conclude that if energetic balance and diet are adequate, a vegetarian diet is neither beneficial nor detrimental to athletic performance.

9.5 Conclusions The influence on performance of correct and balanced nutrition cannot be emphasized enough. The use of supplements is very common in sports but these preparations are frequently ineffective. Few of them have confirmed ergogenic effects, which are nonetheless limited by the variability among individuals taking these supplements and in the type of exercise performed. It is essential for athletes to maintain an adequate and balanced diet and to know that supplements mainly have a role when the diet is not adequate or when there is a verified deficiency syndrome. The full range of supplements’ potential side effects is not known, because pharmaceutical industries do not investigate them. Another important aspect that athletes must be aware of is the risk of a positive drug test resulting from the use of sports supplements contaminated with prohibited substances. Accordingly, extreme caution with these products is strongly recommended.

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References 1. Saltin B, Gollnik PD (1988) Fuel for muscular exercise, role of carbohydrate. In: Horton ES, Terjung RL (eds) Exercise nutrition and energy metabolism. New York, McMillan Library Reference, pp 45-71 2. Bussau VA, Fairchild TJ, Rao A et al (2002) Carbohydrate loading in human muscle: an improved 1 day protocol. Eur J Appl Physiol 87:290-295 3. Björkman O, Wahren J (1998) Glucose homeostatis during and after exercise. In: Horton ES, Terjung RL (eds) Exercise, nutrition, and energy metabolism. New York, Macmillan 4. Kavouras SA, Troup JP, Berning JR (2004) The influence of low versus high carbohydrate diet on a 45-min strenuous cycling exercise. Int J Sport Nutr Exerc Metab 14:62-72 5. Earnest CP, Lancaster SL, Rasmussen CJ et al (2004) Low vs. high glycemic index carbohydrate gel ingestion during simulated 64-km cycling time trial performance. J Strength Cond Res 18:466-472 6. Pigozzi F, Giombini A, Fagnani F et al (2007) The role of diet and nutritional supplements. In: Frontera WR, Herring SA, Micheli LJ, Silver JK (eds) Clinical sports medicine- medical management and rehabilitation. Saunders Elsevier, Philadelphia 7. Rankin JW (1999) Nutritional aspects of exercise: Role of protein in exercise. In: Wheeler KB, Lombardo JA (eds) Clinics in sports medicine: nutritional aspects of exercise. WB Saunders, Philadelphia, pp 499-512 8. Beelen M, Koopman R, Gijsen AP et al (2008) Protein coingestion stimulates muscle protein synthesis during resistance-type exercise. Am J Physiol Endocrinol Metab 295:E70-E77 9. Koopman R, Crombach N, Gijsen AP et al (2009) Ingestion of a protein hydrolysate is accompanied by an accelerated in vivo digestion and absorption rate when compared with its intact protein. Am J Clin Nutr 90:106-115 10. Harris RC, Söderlund K, Hultman E (1992) Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci 83:367-374 11. Balsom PD, Ekblom B, Söderlund K et al (1993) Creatine supplementation and dynamic highintensity intermittent exercise. Scand J Med Sci Sports 3:143-149 12. Green AL, Hultman E, MacDonald IA et al (1996) Carbohydrate ingestion augments skeletal muscle creatine accumulation during creatine supplementation in humans. Am J Physiol 271:E821-E826 13. Slater GJ, Jenkins D (2000) β-hydroxy-β-methylbutyrate (HMB) supplementation and the promotion of muscle growth and strength. Sport Med 30:105-116 14. Cooke MB, Rybalka E, William AD et al (2009) Creatine supplementation enhances muscle force recovery after eccentrically-induced muscle damage in healthy individuals. J Intl Soc Sports Nutr 6:13 15. Knitter AE, Panton L, Rathmacher JA et al (2000) Effects of beta-hydroxy-beta-rnethylbutyrate on muscle damage after a prolonged run. J Appl Physiol 89:1340-1344 16. Gallagher PM, Carrithers JA, Godard MP et al (2000) Beta-hydroxy-beta-metbylbutyrate ingestion. Par I: effects on strength and fat free mass. Med Sci Sports Exerc 32:2109-2115 17. Jowko E, Ostaszewski P, Jank M et al (2001) Creatine and beta-hydroxy-beta-rnethylbutyrate (HMB) additively increase lean body mass and muscle strength during a weight-training program. Nutrition 17:558-66 18. Slater G, Jenkins D, Logan P et al (2001) Beta-hydroxy-beta-methylbutyrate (HMB) supplementation does not affect changes in strength or body composition during resistance training in trained men. Int J Sport Nutr Exerc Metab 11:384-396 19. Nissen S, Sharp RL, Panton L et al (2000) Beta-hydroxy-beta-metbylbutyrate (HMB) supplementation in humans is safe and may decrease cardiovascular risk factors. J Nutr 130:19371945 20. Williams MH (1999) Facts and fallacies of purported ergogenic amino acid supplements. Clin Sports Med 18:633-649

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21. Jentjens RL, Van Loon LJ, Mann CH et al (2001) Addition of protein and amino acids to carbohydrates does not enhance post exercise muscle glycogen synthesis. J Appl Physiol 91:839-846 22. Lemon PW, Tarnopolsky MA, MacDougall JD et al (1992) Protein requirements and muscle mass/strength changes during intensive training in novice bodybuilders. J Appl Physiol 73:767775 23. Davis JM, Welsh RS, De Volve KL et al (1999) Effects of branched-chain amino acids and carbohydrate on fatigue during intermittent, high-intensity running. Int J Sports Med 20:309314 24. Wagenmakers AJ (1999) Amino acid supplements to improve athletic performance. Curr Opin Clin Nutr Metab Care 2:539-544 25. Matsumoto K, Koba T, Hamada K et al (2009) Branched-chain amino acid supplementation increases the lactate threshold during an incremental exercise test in trained individuals. J Nutr Sci Vitaminol 55:52-58 26. Stanko RT, Robertson RJ, Galbreath RW et al (1990) Enhanced leg exercise endurance with a high-carbohydrate diet and dihydroxyacetone and pyruvate. J Appl Physiol 69:1651-1665 27. Morrison MA, Spriet LL, Dyck DJ (2000) Pyruvate ingestion for 7 days does not improve aerobic performance in well-trained individuals. J Appl Physiol 89:549-556 28. O’Rourke MP, O’Brien BJ, Knez WL et al (2008) Caffeine has a small effect on 5-km running performance of well-trained and recreational runners. J Sci Med Sport 11:231-233 29. Barnett C, Costill DL, Vukovic D et al (1994) Effect of L-carnitine supplementation on muscle and blood carnitine content and lactate accumulation during high-intensity sprint cycling. Int Journal of Sport Nutr 4:280-288 30. Vukovic MD, Costill DL, Fink WJ (1994) Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise. Med Science Sports and Exerc 26:1122-1129 31. McNaughton LR (2000) Bicarbonate and citrate. In: Nutrition in Sport. Maughan RJ editor. Blackwell Science, Oxford 32. Key TJ, Fraser GE, Thorogood M et al (1999) Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr 70 (3 Suppl):516S 33. Barr SI, Rideout CA (2004) Nutritional considerations for vegetarian athletes. Nutrition 20:696703 34. Hanne N, Dlin R, Rotstein A (1986) Physical fitness, anthropometric and metabolic parameters in vegetarian athletes. J Sports Med Phys Fitness 26:180-185

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F. Pigozzi, P. Borrione and A. Di Gianfrancesco

Abstract It is widely accepted that growth factors play a central role in healing processes, by modulating cellular recruitment, duplication, activation, and differentiation. This observation underlies the use of plateletrich plasma (PRP) in several orthopedic circumstances, all of them characterized by the need to activate, modulate, speed up, and/or ameliorate tissue repair. There is extensive documentation in both animal and human studies, with widespread applications, demonstrating the safety and efficacy of PRP. Unfortunately, the precise biological efficacy and a lack of long-term side effects have yet to be clearly demonstrated. Indeed, not all studies on autologous growth factors have shown favorable results when considering the promotion of bone formation and healing, tissue grafting, and wound repair. In sports medicine, doping-related issues are still a matter of debate when considering of the therapeutic use of PRP in sportsrelated injuries. In this chapter, PRP applications in orthopedic medicine are described. The limitations of this therapeutic approach are discussed as are issues related to PRP and anti-doping regulations.

10.1 Introduction Continuous progress in the fields of pharmacology and sports medicine has resulted in a wide variety of new substances and methods artificially enhancing performance which, in turn, have necessitated dynamic yet flexible antidoping legislation. The list of prohibited substances established by the World Anti-Doping Agency (WADA) is annually revised and both athletes and their physicians must be aware of the list’s contents and amendments. A summary of the 2010 list of prohibited substances and methods is presented in Table 10.1. The list also identifies substances that are vulnerable to unintentional anti-doping rule violations because of their general availability in medical products or their common use in medical practice. In accordance with WADA Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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Table 10.1 Summary of the prohibited substances and methods according to the WADA 2010 Substances and Methods Prohibited at All Times (In- and Out-of-Competition) S1. S2. S3. S4. S5. M1. M2. M3.

Anabolic agents Peptide hormones, growth factors and related substances Beta-2 agonists Hormone antagonists and modulators Diuretics and other masking agents Enhancement of oxygen transfer Chemical and physical manipulation Gene doping Substances and Methods Prohibited In-Competition In addition to categories S1-S5 and M1-M3 defined above, the following categories are prohibited in competition

S6. S7. S8. S9.

Stimulants Narcotics Cannabinoids Glucocorticosteroids

International Standards, the administration of a prohibited substance for a documented medical condition requires the submission of a therapeutic use exemption (TUE) to the relevant committee. Moreover, the list identifies some substances that are not prohibited but in the case of their use the athlete is required to fill out a declaration of use (DUT). To satisfy DUT requirements, the athlete must declare the use of the substance on the doping control form and complete the DUT through the WADA’s ADAMS system. The use of glucocorticosteroids and narcotics in the orthopedic medicine setting may therefore lead to adverse analytical findings after doping controls. All narcotics are prohibited in competition and the adverse analytical finding, in the absence of a TUE submission, is considered as an antidoping rule violation. In the case of glucocorticosteroids treatments, the route of administration is essential for defining adherence to antidoping regulations. Glucocorticosteroids are prohibited when administered by oral, intravenous, intramuscular, or rectal routes whereas a DUT must be completed by the athlete for glucocorticosteroids administered by intrarticular, periarticular, peritendinous, epidural, intradermal, and inhalation routes. The most important modification of the WADA criteria occurred in the 2010 version of the prohibited list and the new rules have specific implications for orthopedic medicine. Specifically, the list refers to the use of growth factors affecting muscle, tendon, or ligament protein synthesis/degradation, vascularization, energy utilization, regenerative capacity, or fiber-type switching, and to platelet-derived preparations. After a review of the healing process and its critical growth factors, this chapter analyzes the therapeutic use of platelet-rich plasma (PRP) in orthopedic medicine as well as the controversy surrounding this form of treatment, including in light of the updated antidoping regulations.

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10.2 The Healing Process Healing is classically defined as a complex and dynamic process resulting in the restoration of anatomic continuity and function. The cascade of events triggered by tissue injury initiate a healing process that progresses in a sequence of overlapping phases consisting of hemostasis, an acute inflammatory phase, an intermediate (repair) phase, and an advanced (remodeling) phase. The first phase usually starts with the formation of a blood clot and the subsequent degranulation of platelets, which locally release their granules’ constituents, some of which are present at high concentrations. The inflammatory phase can last up to 72 h, involves a number of inflammatory responses, and is usually characterized by pain, swelling, redness, and increased local temperature. During the repair phase, which lasts from 48 h up to 6 weeks, anatomic structures are restored and tissue regeneration occurs. Several cell types are involved in the repair phase, especially fibroblasts, which synthesize scar tissue simultaneously with capillary neoformation aimed at transporting nutrients to the injury site. This phase ends with the beginning of wound contracture. The remodeling phase lasts from 3 weeks up to 12 months and is characterized by collagen remodeling, leading to an increase in the functional capabilities of the injured tissues. Throughout these phases of the healing process, complex and dynamic molecular mechanisms involving local and systemic factors direct the function of the many different cell types recruited to the injury site from the surrounding tissues and/or circulation. These factors therefore act as signaling molecules and they can be categorized within three different groups: pro-inflammatory cytokines, transforming growth factor-β superfamily members, and angiogenic factors. Each of these molecules shows different biological activities, but all of them promote the interactions among different cell populations at different stages of maturation, thereby modulating the recruitment, duplication, activation, and differentiation of cells involved in boneand soft-tissue repair [1, 2]. The growth factors and cytokines relevant to platelet-rich plasma are examined in greater detail below.

10.3 Growth Factors Growth factors are proteins secreted by cells acting through specific cell-surface receptors on the appropriate target cell. The effect of each growth factor is, usually, related to its concentration and to the sensitivity of its receptor, although some experimental studies have shown that at higher concentration the growth-factor’s effect may be reversed [1]. Classically, three types of action are described: (1) autocrine, in which the growth factor influences its cell of origin or a cell of identical phenotype, (2) paracrine, in which the growth factor influences neighboring cells of different phenotype, and (3) endocrine, in which the growth factor influences a cell of different origin and phenotype, perhaps at a remote anatomic site. Growth factor activity can also be divided into three groups: mitogenic, chemo-attractant, and transforming factors. Mitogens can be further divided into

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two groups, competence and progression factors. The former stimulates cells to exit the resting phase (G0) of the cell cycle and enter the G1 phase while progression factors, as their name implies, stimulate cells to enter S (DNA synthesis) phase. Although the roles of all growth factors involved in the healing process are only partially known, the efficacy of many of them has been extensively demonstrated. For instance, platelet-derived growth factor (PDGF) has a mitogenic effect on connective tissue cells; transforming growth factor-β (TGF-β) has morphogenetic properties and has been implicated in the synthesis of collagen; insulin like growth factor-1 (IGF-1) is critical for cell survival, growth, and metabolism; and vascular endothelial growth factor (VEGF) induces endothelial cell proliferation and migration, thus initiating the angiogenic response [3, 4].

10.4 Platelet-rich Plasma Platelets are small, non-nucleated cell fragments in the peripheral blood known primarily for their hemostatic role. The normal platelet count ranges from 150,000/μl to 400,000/μl. Three specific platelets granule populations store different types of molecules. Dense granules contain small non-protein molecules (adenine nucleotides, ionized calcium, histamine, serotonin, and epinephrine) which are mainly secreted to recruit and activate other platelets. Lysosomes contain a wide variety of hydrolases that digest endocytosed materials. Alpha granules are storage units within platelets and they contain pre-packaged growth factors in an inactive form. The main growth factors stored in alpha granules are: PDGF, TGF-β, fibroblast growth factor (FGF), IGF-I and IGF-II, VEGF, and epidermal growth factor (EGF) (Table 10.2) [1]. The demonstrated efficacy of growth factors in modulating the recruitment, duplication, activation and differentiation of cells involved in bone and soft-tissue healing underlies the use of PRP to activate, modulate, speed up, or ameliorate the process of tissue repair and accounts for the interest in its therapeutic applications. PRP is an autologous thrombocyte concentrate produced from whole blood with a platelet concentration of at least 1,000,000/μl. In most therapeutic settings, PRP should be considered as highly safe, autologous hemocomponents for non-transfusional use. A particular value of PRP is represented by the fact that native cytokines are present in physiologic ratios, whereas exogenous cytokines, singularly administered, have several limitations in improving the highly complex process of tissue healing. Several commercially available methods to obtain PRP concentrate are currently used in the clinical setting and many types of kits, centrifuges, and vials are available [5]. Briefly, venous blood is drawn into a tube containing citrate and then centrifuged to separate the different blood components. The first centrifugation is called the “soft spin” and it separates whole blood into three layers: a lower layer of red blood cells, the topmost acellular plasma layer, and an intermediate platelet-rich plasma layer. The latter is transferred into another tube and submitted to a second centrifugation that is longer and faster than the first one, called the “hard spin”. In this step, the platelets settle at the bottom of the tube, allowing most of the acellular plasma to be removed. The remaining, platelet-rich layer is mixed with bovine thrombin, or batroxobin, and calcium chloride to activate fibrinogen,


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Table 10.2 Growth factors contained in platelet α-granules and their function Growth factor

Function

STGF-β

– – – – –

FGF

– Promotes the growth and the differentiation of chondrocytes and osteoblasts – Stimulates the mitogenesis of mesenchymal cells, chondrocytes, and osteoblasts

PDGF

– – – – –

EGF

– Stimulates endothelial chemotaxis and angiogenesis – Regulates collagenase secretion – Stimulates epithelial and mesenchymal cell mitogenesis

VEGF

– Increases angiogenesis and vascular permeability – Stimulates endothelial cell mitogenesis

IGF-1

– – – – –

Stimulates the proliferation of undifferentiated mesenchymal cell Regulates endothelial cell, fibroblast, and osteoblast mitogenesis Regulates collagen synthesis and collagenase secretion Stimulates endothelial chemotaxis and angiogenesis Inhibits macrophage and lymphocyte proliferation

Stimulates mesenchymal cell and osteoblast mitogenesis Stimulates chemotaxis and fibroblast mitogenesis Regulates collagenase secretion and collagen synthesis Stimulates macrophage and neutrophil chemotaxis Stimulates muscle satellite cell activation

Promotes mesenchymal cell mitogenesis Promotes collagen synthesis Promotes fibroblast proliferation Stimulates myoblast proliferation and differentiation Inhibits apoptosis

which is converted to fibrin and cross-linked. This procedure yields a platelet concentrate. Most protocols (except that of Sanchez et al. [6]) for the manufacturing of PRP produce such thrombocyte concentrates.

10.5 Platelet-rich Plasma Therapies in Orthopedic Medicine According to the World Health Organization (WHO), musculoskeletal injuries are the most common cause of severe long-term pain and physical disability, affecting hundreds of millions of people around the world and connected in many cases to sports-related injuries. In the therapeutic administration of growth factors, the need to target different signaling pathways demands the use of a “physiologically balanced” combination of mediators, rather than a single growth factor. The simple protocols and the safety of platelet-derived preparations have stimulated the interest of orthopedic surgeons and sports physicians in their therapeutic applications. The following examples represent some of the most interesting current approaches in the field of orthopedic medicine.

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10.5.1 Tendon Tendons usually undergo slow and difficult healing after injury. However, it has been shown that several growth factors may stimulate tendon repair, positively affecting both gene expression and matrix synthesis. In vitro studies demonstrated that tenocyte proliferation and collagen production are increased in the presence of PRP and that the pool of growth factors released from an autologous PRP preparation stimulates tendon cells to produce growth factors such as VEGF and hepatocyte growth factor (HGF). In vivo, a platelet concentrate injected percutaneously into a hematoma 6 h after the creation of a defect in a rat Achilles tendon resulted in increased tendon callus strength. Further research, carried out in animal models, showed that PRP injection into the Achilles tendon triggered a healing response characterized by increased cell number and angiogenesis, without provoking fibrosis [6, 7]. It was also reported that tendon healing may be enhanced by PRP application during surgery for serious structural damage, such as partial or complete tendon tears, and that functional recovery after the surgical repair of a ruptured Achilles tendon is significantly accelerated. Other researchers reported that injections of PRP 1 week postoperatively significantly increased tendon regeneration and strength [7]. Another common problem in orthopedic medicine is tendinopathies, a syndrome characterized by tendon pain, localized tenderness, swelling, and impaired functional ability. The rationale of using PRP in this context is the need to restore the normal tissue composition, avoiding concomitant further degeneration. In this context, ultrasound-guided PRP injection may offer an alternative to palliative or operative treatments. Indeed, several authors reported that PRP treatment reduced the pain in chronic severe elbow tendinosis and severe medial epicondylitis, with a success rate ranging from 60 to 80% and no recurrences reported. Other authors reported positive effects of PRP treatment on chronic refractory plantar fasciitis in almost 80% of patients, with a complete resolution in 1 year [7]. Since the inflammatory response seems to be a crucial component in the increased healing processes mediated by platelet-derived growth factors, several authors suggested that patients should undergo a “washout” period prior to PRP injection, in which nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroid injection are prohibited [6, 7].

10.5.2 Muscle With the exception of muscle complete rupture and persistent symptoms from myositis ossificans, almost all muscle injuries are usually treated non-surgically. Standard therapeutic approaches include rest, ice, compression, elevation, and NSAIDs, but there is no clear consensus on either the treatment of muscle injuries or how to accelerate recovery. Experimental and clinical studies demonstrated that myogenesis is not restricted to the prenatal period but may also occur during the regeneration of injured muscle tissue. Accordingly, it has been shown that IGF-1 stimulates the proliferation and differentiation of myoblasts, FGF enhances the number and diameter of regenerating muscle fiber, HGF activates resting satellite cells, and TGF supports the activity of other growth factors, especially PDGF, in stimulating satellite


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cell activation [8]. In one clinical study, PRP treatment of the injured muscles of high-level professional athletes resulted in restoration of full functional capabilities in half the expected recovery time [6]. Despite these and other successes in muscle healing, concerns have been raised regarding that PRP treatment may induce a fibrotic healing response in muscle tissues. This hypothesis is based on the observed elevation of TGF-β levels following PRP injection into muscle. Indeed, experimental data demonstrated that TGF-β stimulates fibrosis in cultured muscle tissue. If this were the case, then a fibrotic healing following muscular injury could lead to an increased risk of re-injury [8, 9]. Additional concerns have been voiced with respect to the presence of neutrophils in PRP preparations, since proinflammatory proteases and acid hydrolases released from leukocytes may act as cytotoxic agents, causing secondary damage of the muscle tissue. In addition, the release of reactive oxygen species by neutrophils may act as an aggravating contributing factor [8].

10.5.3 Bone The vast majority of fractures heal by a combination of intramembranous and endochondral ossification. Endochondral bone formation occurs external to the periosteum lying immediately near the fracture site, and intramembranous ossification internal to the periosteum, at the proximal and distal edges of the callus, resulting in the formation of a hard callus. The first inflammatory phase, i.e., immediately following the fracture, leads to the recruitment of mesenchymal stem cells that will differentiate into chondrocytes producing cartilage and osteoblasts producing bone matrix. At this stage, interleukins (IL)-1 and IL6 as well as TNF-β play central roles in the recruitment of other inflammatory cells, enhancing the synthesis of extracellular matrix and stimulating angiogenesis [10]. In addition to these growth factors, the presence and activity of others have been demonstrated: TNFβ promotes the recruitment of mesenchymal stem cells; VEGF is involved in endothelial cell proliferation and migration and stimulates the chemotaxis and activity of osteoclasts; PDGF enhances osteoblast migration and proliferation, both of which are essential to subsequent bone remodeling [9-11]. However, controversies persist in the literature regarding the clinical applications of these findings, despite the small size of the samples reported and the lack of proper control groups. Indeed, some authors reported significant increases in bone formation and maturation rates with the use of PRP while other authors did not observe any improvement [8-11]. Actually, aside from the applications of PRP in dentistry, platelet-derived growth factors seem to be effective in improving cellular proliferation and the strength of the healing bone in fractures in diabetic subjects, in improving pain control and blood loss in knee surgery, and in improving the outcome of bone grafts [9-11].

10.5.4 Cartilage Cartilage repair remains a major challenge for clinicians and numerous research efforts have been devoted to re-establishing a structurally and functionally competent repair tissue.

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In this regard, growth factor therapy has received considerable attention due to the potential ability of different mediators to induce and/or facilitate the synthesis and repair of cartilage matrix. Indeed, FGF has been shown to stimulate chondrocyte mitogenesis, growth, and differentiation, whereas IGF-1 exerts both paracrine and autocrine activities to stimulate matrix synthesis and inhibit matrix degradation, the latter by down-regulating matrix metalloproteinases and inflammatory cytokine production [12]. Experimental data suggest that IGF-1 also promotes chondrocyte survival and that the response to IGF-1 is influenced both by age and by disease severity. Finally, cultured mesenchymal stem cells were shown to produce significantly more proteoglycans and type II collagen when treated with TGF-β, with IGF-I exerting a synergistic effect with TGF-β in promoting mesenchymal stem cell chondrogenesis [9]. In animal models, the ability of PRP to support the healing of meniscal defects was demonstrated. Clinical studies showed that PRP preparations enhance the grafting of inactive scaffolds, thus providing the scaffold structure with the biological stimulation necessary for its transformation into a functional tissue [6-12]. These results are promising, particularly in light of the fact that avascular cartilage and meniscus have limited, if any, chances for proper repair. Other authors described the use of PRP in the treatment of chondral defects in athletes, reporting that this approach was effective for the recovery of articular cartilage. PRP treatment was also shown to induce the secretion of hyaluronic acid, providing a better homeostatic environment for tissue repair inside the joint [6]. Taken together, these observations indicate an important role for PRP in cartilage regeneration, by regulating cell proliferation and differentiation as well as protein synthesis. Unfortunately, discrepancies exist in the literature, as some authors failed to observe any effect of PRP treatment on cartilage repair and even the worsening of pain immediately following treatment.

10.5.5 Limitations Even if experimental data and clinical observations support the use of PRP to enhance tissue healing, and concerns of immunogenic reactions or disease transfer have been clearly eliminated by using PRP preparations from autologous blood, several limitations of this approach should be noted. First of all, a survey of the literature reveals a lack of standardization of PRP preparations, which may explain the inconsistent clinical and experimental results obtained in different studies. Conceivably, even if all PRP preparations contain a basic set of growth factors, the relative concentration of each factor can differ among preparations. Moreover, proteases in the preparations may degrade some of the growth factors, thereby reducing their availability and changing the composition of the PRP, with a modification of its clinical effectiveness. Second, PRP must be prepared in accordance with the international and national laws regulating the manipulation collection, and control of blood products, and the sterility of the entire procedure ensured. Moreover, controversy concerns the use of local anesthetics and NSAIDs in conjunction with PRP therapy, as well as the white blood cell content within PRP preparations [6]. This author’s position is that the use of local anesthetics should be avoided in order not to modify the local pH, which is essential for the stability of several growth factors. In addition, NSAIDs reduce


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the initial inflammatory response to injury, which is an essential step in the healing process. Regarding the white blood cell count, the number of granulocytes in the PRP preparation should be minimized, particularly when treating muscle injuries. Third, the small sample size in the majority of human studies reported in the literature do not have enough statistical power to support the acceptance of PRP therapy into clinical routine. In particular, the mechanism of action and the clinical effect on each tissue should be further studied in prospective, randomized, controlled trials. Even if PRP preparations are deemed to be highly safe autologous hemocomponents, the use of bovine thrombin as activating factor may lead to complications associated with the formation of antibodies to this protein. This is a rare but potentially life-threatening complication that may result in an immune-mediated coagulopathy [4]. Other potential limitations associated with the use of PRP have been pointed out. For example, even if PRP treatment enhances the migration and proliferation of mesenchymal stem cells, an overexposure of cells to growth factors may, in theory, limit their differentiation, possibly inducing cancerous effects. However, there are no data supporting this theoretical concern. Finally, the lack of long-term side effects has yet to be clearly demonstrated and the possibility of long-term muscle fibrosis following repeated treatment with growth factors has not been ruled out.

10.6 Sports Medicine Implications of PRP Particular attention has been focused on PRP treatment in sports medicine based on its positive effects on tissue repair processes. Nonetheless, doping-related issues should be considered if amateur or professional athletes are to be treated with PRP. Certainly, PRP used in the treatment of bone, tendon, cartilage, and ligament injuries cannot be considered as performance-enhancing but the effects of intramuscular injection are still a matter of debate. For instance, in section S2 (Peptide hormones, growth factors and related substances), point 5, of the 2010 WADA’s prohibited list, the following molecules are included: growth hormone (GH), IGF-1, mechano growth factors (MGFs), PDGF, FGFs, VEGF, and HGF “as well as any other growth factor affecting muscle, tendon or ligament protein synthesis/degradation, vascularisation, energy utilization, regenerative capacity or fibre type switching”. Point 6 clearly indicates that “Platelet-derived preparations (e.g. Platelet Rich Plasma, “blood spinning”) administered by intramuscular route” are prohibited and that “other routes of administration require a declaration of use in accordance with the International Standard for Therapeutic Use Exemptions” [13]. Moreover, according to the United States Antidoping Agency (Usada), the injection of platelet-derived preparations should be considered equivalent to an injection of growth factors. In summary, when considering PRP treatment of athletes, physicians must first clarify several issues. Assuming that this technique is indeed able to ameliorate the repair of muscle tissue, it is still unclear whether the concentrated amount of growth factors injected into the skeletal muscles affects the performance of the treated tissues. In addition, one study suggested that local treatment with PRP has systemic effects, probably influencing growth factor and inflammatory cytokine homoeostasis – as well as antidoping evaluations [14]. Another study

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concluded that PRP is unlikely to provide a significant athletic advantage because the halflife of the small amount of unbound IGF-I is too short to produce systemic anabolic effects [15]. Clearly, further studies are required to obtain scientific evidence strong enough to support a definitive conclusion. Until then, PRP preparations for the treatment of athletes injuries must be used in accordance with the above-mentioned WADA standards.

References 1. Frechette JP, Martineau I, Gagnon G (2005) Platelet-rich plasmas: growth factor content and roles in wound healing. J Dent Res 84:434-439 2. Lynch SE, Colvin RB, Antoniades HN (1989) Growth factors in wound healing. J Clin Invest 84:640-646 3. Mehta S, Watson JT (2008) Platelet rich concentrate: basic science and current clinical applications. J Orthop Trauma 22:432-428 4. Foster TE, Puskas BL, Mandelbaum BR et al (2009) Platelet-rich plasma: from basic science to clinical applications. Am J Sports Med 37:2259-2272 5. Appel TR, Potzsch B, Müller J et al (2002) Comparison of three different preparations of platelet concentrates for growth factors enrichment. Clin Oral Implants Res 13:522-528 6. Sanchez M, Anitua E, Orive G et al (2009) Platelet-rich therapies in the treatment of orthopaedic sport injuries. Sports Med 39:345-354 7. Alsousou J, Thompson M, Hulley P et al (2009) The biology of platelet-rich plasma and its application in trauma and orthopaedic surgery: a review of the literature. J Bone Joint Surg Br 91:987-996 8. Hammond JW, Hinton RY, Curl LA et al (2009) Use of autologous platelet-rich plasma to treat muscle strain injuries. Am J Sports Med 37:1135-1142 9. Sampson S, Gerhardt M, Mandelbaum B (2008) Platelet rich plasma injection grafts for musculoskeletal injuries: a review. Curr Rev Musculoskelet Med 1:165-174 10. Al-Aql ZS, Alagl AS, Graves DT et al (2008) Molecular mechanisms controlling bone formation during fracture healing and distraction osteogenesis. J Dent Res 87:107-118 11. Lieberman JR, Daluiski A, Einhom TA (2002) The role of growth factors in the repair of bone: biology and clinical applications. J Bone Joint Surg Am 84:1032-1044 12. Martinez-Zapata MJ, Marti-Carvajal A, Sola I et al (2009) Efficacy and safety of the use of autologous plasma rich in platelets for tissue regeneration: a systematic review. Transfusion 49:44-56 13. The World Anti-Doping Code, the 2010 Prohibited list, International Standard (2009) http://www.wada-ama.org/Documents/World_Anti-Doping_Program/WADP-Prohibitedlist/WADA_Prohibited_List_2010_EN.pdf. Accessed 25 Nov 2009 14. Banfi G, Corsi MM, Volpi P (2006) Could platelet rich plasma have effects on systemic circulating growth factors and cytokine release in orthopaedic applications? Br J Sports Med 40:816 15. Creaney L, Hamilton B (2008) Growth factor delivery methods in the management of sport injuries: the state of play. Br J Sports Med 42:314-320

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Abstract Patients undergoing major orthopedic surgery face an increased risk of venous thromboembolism (VTE) in the days and weeks after surgery. In recent years, the routine use of anticoagulants has played a significant role in reducing the morbidity and mortality associated with VTE after major orthopedic surgery. Currently recommended prophylactic strategies include low-molecular-weight heparins at usual high-risk doses, fondaparinux, and adjusted-dose vitamin K antagonists such as warfarin. New oral anticoagulants have been developed and are now approved for the prevention of VTE in patients undergoing elective hip or knee replacement surgery. Few studies have evaluated the efficacy and safety of thromboprophylaxis in patients undergoing minimally invasive surgical procedures, such as knee arthroscopy, or in patients with fractures of the lower extremities or soft-tissue injuries. In general, these conditions, which may occur as a consequence of sports injuries, are defined as of low to moderate risk for VTE and routine use of thromboprophylaxis is not warranted. However, it becomes crucial to carefully assess VTE risk factors in each patient in order to identify higher-risk situations and to prescribe adequate prophylactic strategies.

11.1 The Burden of Venous Thromboembolism in Major Orthopedic Surgery Venous thromboembolism (VTE) is associated with substantial morbidity and mortality that places an enormous burden on healthcare resources [1]. Patients undergoing major orthopedic surgery, including total hip replacement (THR) surgery, total knee replacement (TKR) surgery, and hip fracture surgery (HFS), face an increased risk of VTE, including deep-vein thrombosis (DVT) and pulmonary embolism (PE), in the days and weeks after surgery. According to the results of clinical trials in which venography was routinely performed in all patients undergoing major orthopedic surgery, DVT occurs in 40-60% of paOrthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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tients who receive no prophylaxis, with a rate of proximal DVT ranging between 10 and 30% [2]. Although most of these thrombi remain asymptomatic and tend to resolve spontaneously, in some patients they can either propagate or recur thus causing venous occlusion or embolization to the lungs. The reported rate of PE following major orthopedic surgery ranges between 1% and 28% in patients not receiving prophylaxis [2]. Commonly, symptomatic VTE presents after patients are discharged from the hospital, and it may occur some weeks after the surgical procedure [2].

11.2 Current Strategies To Prevent VTE in Major Orthopedic Surgery In recent years, the routine use of anticoagulants has played a significant role in reducing the morbidity and mortality associated with VTE after major orthopedic surgery [2]. Based on the results of clinical trials, the most effective agents include fondaparinux, low molecular weight heparin (LMWH), and vitamin K antagonists such as warfarin. Fondaparinux is a synthetic pentasaccharide that inhibits factor Xa indirectly by binding to antithrombin with high affinity. Four phase III trials of thromboprophylaxis after major orthopedic surgery demonstrated the efficacy and safety of fondaparinux, with an overall risk reduction of VTE >50% over the LMWH enoxaparin [3]. Although major bleeding occurred more frequently with fondaparinux, the incidence of clinically relevant bleeding did not differ between groups. LMWHs are more effective than warfarin, with a similar safety profile [4]. Overall, a slightly increased risk of surgical site bleeding and of wound hematoma with the use of all such effective prophylactic strategies is to be expected. Because the risk of VTE is sustained over time, clinical trials have also assessed the efficacy and safety of extended thromboprophylaxis. The results of a meta-analysis confirmed that the administration of pharmacologic prophylaxis for up to 35 days following surgery is associated with a significant reduction in the risk of both asymptomatic and symptomatic VTE as compared to short-term prophylaxis [5]. Based on the results of several clinical trials and meta-analyses, the 2008 guidelines of the American College of Chest Physicians (ACCP) consensus conference on antithrombotic and thrombolytic therapies [2] recommend the routine use of either LMWH, fondaparinux, or warfarin for patients undergoing THR, TKR, or HFS (Table 11.1). LMWH is to be given either pre-operatively, that is, started 12 h before surgery according to the European standard of practice, or post-operatively, that is, started 12-24 h after surgery according to the North American standard (Table 11.2). Fondaparinux should be started 6-24 h after surgery, whereas warfarin can be started either pre-operatively or the evening of the surgical day (Table 11.2). LMWHs and fondaparinux are administered subcutaneously at fixed prophylactic doses; warfarin is administered orally at adjusted doses according to the International Normalized Ratio (INR) values (Table 11.2). Finally, prophylaxis for a minimum of 10 days is recommended in all patients, with an extension of up to 35 days for patients undergoing THR and HFS, although, in this latter group, with lower levels of evidence [2].

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Tillie 11.1 Brief summary of the American College of Chest Physicians 2008 recommeodation for venous thromboembolism prophylaxis Indication

Recommendation

Elective hip replacement

Routine use of LMWH, fondaparinux, adjusted dose VKA Aspirin, dextran, LDUH, VFP and GCS not recommended as the only method In case of high risk of bleeding, optimal use of mechanical thromboprohy1asis (IPC,VFP); pharmacological thrombopro· phylaxis when bleeding risk decreases

Elective knee replacement

Routine use of IMWH, fondaparinux, adjusted dose VKA Optimal use of IPC is an alterative Aspirin, LDUH and VFP not recommended as the only method In case of high risk of bleeding, optimal use of mechanical thromboprohy1asis (IPC,VFP); pharmacological thromboprophylaxis when bleeding risk decreases No routine use of thromboprophylasis, other than early mohilization, in patients without risk factors LMWH in case of additional risk factors or complicated procedures Rootine use offondaparinux, LMWH, a4justed dose VKA, LDUH Aspirin not recommended In case of high risk ofbleeding, optimal use of mechanical thromboprohy1asis; pharmacological thromboprophy1asis when bleeding risk deereases No routine use of thromboprophylaxis. Individual assessment suggested

Knee arthroscopy

Hip fracture surgery

Isolated lower·extremity injuries distal to the knee

GCS, gradusted compressive stockings; lPC, intermittent poeumatic compreasion; WUH, low-dose uofractiousted heparin; IMWH, low-molecular-weight heparin; VFP, venous foot pomp; VKA, vitamin K antagonist

Tallie 11.2 Brief summary of general recommendations for major orthopedic surgery LMWH

High-risk dose, started 12 h before surgery or 12-24 h after surgery, or 4-6 h after surgery at half the usual high-riak dose and then increasing to the usual high-risk dose the following day

Fondaparinux

2.5 mg started 6-24 h after surgery

VKA

Started preoperatively or the evening of the surgical day (INR target, 2.5; 1NR range, 2.0-3.0)

Duration of thromboprophylaxis

For at least 10 days For hip surgery: thromboprophylaxis extended beyond 10 days and up to 35 days after surgery For knee surgery: thromboprophy1asis extended beyond 10 days and up to 35 days after surgery For hip fracture surgery: extended beyond 10 days and op to 35 days after surgery

INR, international normalized ratio; LMWH, low-molecular-weight heparin; VKA, vitamin K an-

tagonist

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11.2.1 New Anticoagulant Drugs for the Prevention of VTE in Major Orthopedic Surgery The approach to the development of new anticoagulants as alternatives to heparins and vitamin K antagonists has been guided by the requirement for convenient administration with predictable pharmacokinetics (PK), pharmacodynamics (PD), and a wide therapeutic window that permits fixed dosing without the need for coagulation monitoring. Research has in particular focused on targeting thrombin (factor IIa) and factor Xa, which are common to the intrinsic and extrinsic coagulation pathways. Direct thrombin inhibitors act to prevent fibrin formation, as well as inhibiting thrombin-mediated activation of factors V, VIII, XI, and XIII and platelets. Direct inhibitors of factor Xa act at an earlier stage in the coagulation cascade. Following the development of parenteral direct thrombin inhibitors, such as lepirudin or bivalirudin, ximelagatran was the first oral direct thrombin inhibitor to become available for clinical use in the EU, but it was withdrawn in 2006 after concerns over liver toxicity. The oral direct thrombin inhibitor dabigatran etexilate was recently approved for use in the EU and Canada for thromboprophylaxis after THR and TKR and is currently in development for other indications. Dabigatran has a rapid onset of anticoagulant activity, with peak plasma levels at 2 h and a half-life between 12 and 17 h [6]. Dabigatran produces a predictable anticoagulant effect, requires no coagulation monitoring, and can be given once daily. At least 80% of dabigatran is excreted unchanged via the kidneys; therefore, the drug is contraindicated in patients with severe renal failure, with a creatinine clearance < 30 ml/min. The results of three phase III randomized controlled trials for VTE prevention in orthopedic surgery have been published: RE-MODEL, RE-NOVATE, and REMOBILIZE [7-9]. All trials were designed to show the non-inferiority of dabigatran compared to enoxaparin. The efficacy and safety of two doses of dabigatran etexilate, 150 mg and 220 mg once daily, and of enoxaparin, 40 mg once daily started pre-operatively, was observed in the RE-MODEL and RE-NOVATE trials. On the basis of these results, the recommended dose for clinical use in Europe is 220 mg once daily [10]. The first dose should be administered 1-4 h post-operatively at a half dose (110 mg). In patients with moderate renal insufficiency (creatinine clearence between 30 and 50 ml/min) and in the elderly (age 75 or more), the recommended dose is 150 mg once daily (first dose, 75 mg) [10]. A dose reduction is also recommended for patients on amiodarone treatment. Several oral factor Xa inhibitors are under investigation for the prevention and treatment of thromboembolic disorders, of which rivaroxaban is at the most advanced stage of development. Rivaroxaban has recently been approved in the EU, Canada, and several other countries for the prevention of VTE after elective THR or TKR surgery. The onset of action of rivaroxaban is 2-4 h, and the elimination from plasma following a 10 mg oral dose occurs with a mean terminal half-life of 7-11 h [11, 12]. Due to its predictable anticoagulant effect, rivaroxaban requires no coagulation monitoring and can be given once daily. Since the drug is mainly excreted unchanged via the kidneys, creatinine clearance should be calculated to rule out severe renal insufficiency before starting treatment. The RECORD program assessed rivaroxaban in patients undergoing major orthopedic surgery and comprised four randomized controlled phase III clinical trials. Two were carried out in patients undergoing THR (RECORD 1 and 2) [13, 14], and two in patients undergoing

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TKR (RECORD 3 and 4) [15, 16]. In all four trials, rivaroxaban was administered at a fixed 10 mg once daily dose and was started post-operatively. In THR patients, the RECORD 1 and 2 trials showed that: (1) extended prophylaxis with rivaroxaban is superior to short-term prophylaxis with enoxaparin, with a similar safety profile and, (2) extended prophylaxis with rivaroxaban is more effective than extended prophylaxis with enoxaparin. Again, this greater superiority was achieved with a risk of major bleeding similar to enoxaparin. In TKR patients, RECORD 3 and RECORD 4 trials have also demonstrated that rivaroxaban is superior to both the European and the North American enoxaparin regimens for VTE prevention, significantly reducing the risk of VTE, again with a similar risk of major bleeding. The recommended dose for clinical use in THR and TKR is 10 mg once daily. The first dose should be administered 6-10 h postoperatively, with no dose adjustments for special populations required.

11.3 Thromboprophylaxis in Patients Undergoing Knee Arthroscopy As opposed to major orthopedic surgery, the risk of VTE following minor orthopedic procedures is less defined. Moreover, few prospective studies have assessed the efficacy and safety of antithrombotic prophylaxis in this setting. Based on available data, the risk of VTE after knee arthroscopy varies between 0.6% and 17.9% [2]. This wide range is explained by the heterogeneity of study designs and diagnostic approaches for the diagnosis of DVT. For patients undergoing knee arthroscopy who do not have additional thromboembolic risk factors, the 2008 ACCP panel suggested that clinicians do not routinely use thromboprophylaxis other than during early mobilization (grade 2B) [2] (Table 11.1). This recommendation is substantially based on the results of two clinical trials that assessed the efficacy and safety of LMWH in this setting [17, 18]. Compared to placebo, the use of LMWH was associated with a non-significant reduction of DVT rates in one study [17], and with a statistically significant reduction in the incidence of DVT in the second study [18]. However, more robust data were recently reported from the KANT study, which randomized almost 1800 low-risk patients to nadroparin (3,800 anti-Xa IU) or to elastic stockings for 7 days [19]. The 3-month cumulative incidence of asymptomatic proximal DVT, symptomatic VTE, and all cause-mortality in this study was significantly reduced by nadroparin, from 3.2% to 0.9%, with no significant difference in the rate of major or clinically relevant bleeding events (0.9% with nadroparin and 0.3% in the comparator group). These finding may support a broader use of pharmacologic prophylaxis in this setting.

11.3.1 Thromboprophylaxis in Patients with Lower Extremity Fractures Distal to the Knee Lower-extremity fractures distal to the knee are common and can occur in people of all ages. The rates of asymptomatic DVT detected by routine examination vary between 6% and 45%, with the wide range partially explained by the different methodologies used to detect DVT [2]. In addition to the presence of patient-specific risk factors, the risk of VTE

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can be increased by a more proximal location of the fracture and by the need for surgical repair. Fractures appear to be associated with a higher risk for DVT than soft-tissues injuries, whereas for Achilles tendon ruptures the risk is similar. The efficacy and safety of thromboprophylaxis in this setting was addressed by five clinical trials, all of which compared LMWH with either no treatment or placebo. The results of these studies are quite inconsistent, mainly because of the different designs and strategies used to alleviate DVT [2]. Based on the available evidence, no clear cut recommendations can be made (Table 11.1). Thus, physicians should decide on a patient to patient basis, according to the presence of additional risk factors for VTE, whether to avoid or prescribe thromboprophylaxis. The duration of prophylaxis, if prescribed, should be based on the degree of mobility.

11.4 Thromboprophylaxis in Sports Injury The incidence of sports injury requiring immobilization is increasing, probably because of the increasing popularity of recreational sports. Although the data are not compelling, the risk of VTE in these patients does not appear to be negligible. Unfortunately, evidence of the efficacy of antithrombotic prophylaxis in these patients and in patients with other minor sport injuries that require immobilization in an ambulant setting (ligament, cartilage, and other soft-tissues injuries) are extremely limited. Recent ACCP guidelines do not recommend routine prophylaxis in Achilles tendon rupture and do not provide any recommendation about the use of prophylaxis in the other minor sport injuries requiring immobilization [2]. In a subgroup analysis of a randomized controlled trial, the LMWH reviparin appeared to be effective in reducing VTE in patients with Achilles tendon rupture [20]. However, these results were not confirmed by a more recent study in which the incidence of VTE was similar in patients randomized to prophylactic doses of dalteparin or placebo [21]. In a Cochrane systematic review of the literature, Testroote and colleagues evaluated the efficacy of antithrombotic prophylaxis in patients with lower-leg immobilization, including patients with soft-tissue injuries [22]. In this subgroup, LMWH prophylaxis appeared to be effective in reducing DVT incidence. However, these results should be interpreted with extreme caution since they were only based on five studies comprising a total of 650 patients and included studies with different inclusion and exclusion criteria, duration of prophylaxis, and methods of DVT assessment. Thus, many questions remain, including the risk to benefit ratio for each subgroup of patients. Further methodologically adequate trials are needed to address these concerns.

11.5 Guide to Individual Assessment of the Patient at Risk for VTE Patients with minor trauma or undergoing minor surgical procedures are at substantially low risk of VTE. However, prolonged immobilization and the concomitant presence of risk

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TIllie 11.3 Major risk factors for VTE -

Age Obesity lDunobility (bed rest >4 days) Plaster cast

- Varicose veins

- TI8llII1Il - Inherited or acquired thrombophilia (tcndcocy to thrombosis)

- Active cancer

- High-dose es1rogen therapy - Pregnancy - Puerperium - Smgical or invasive procedure

- Increased blood viscosity

- Inflsmmstory disorders

factors for VTE may modilY individual risk profiles. Due to the paucity of high-quality clinical trials, there are no guidelines or definitive recommendations, and a coroplete evaluation of the individual patient therefore becomes crucial to identify higher risk situations.

The individual risk of VTE varies as a result of a complex interaction between congenital and either transient or permanent acquired risk factors. Risk factors can be either intrinaic or disease-related (Table 11.3). The presence or absence of specific risk factors may play an important role in decisions about the type and duration of thrombopropbylaxis to be used. Individual risk factors include advanced age, obesity, persoual history of VTE, known thrombophilia, or the ongoing use of oral contraceptives or other bormoual therapies. Disease-related risk factors include the need for surgical repair, the type of surgery

(invasive vs. minimally invasive, duration of the procedure), the concomitant presence of medica! disorders (e.g., sepsis or acute rheumatic disease), and cancer. Knowledge of specific risk factors forms the basis for the appropriate use of prophylaxis.

References I. Cohen AT, Agnelli G, Anderson FA et a! (2007) Venous thromboembolism (VTE) in Europe. T1uomb Haemost 98:756-764 2. Geerts WH, Bergqvist D, Pineo GF ct a! (2008) Prevention of venous thromboembolism: American College of Chest Physiciaus evidence-based clinica! practice guidelines (8th edn). Chest 133:381-453 3. Turpie AG, Bauer](A, Eriksson BI ct a! (2002) Fondaparinux vs enoxaparin for the prevention of venous thromboembolism in major orthopedic smgery: a meta-analysis of 4 randomized doubl...blind studies. Arch Intern Med 162:1833-1840 4. Mismetti P, Laporte S, Zulferey Petal (2004) Prevention of venous thrombembolism in orthopedic smgery with vitamin K antsgonists: a meta-analysis. IThromb Haemost 2: 1058-1070 5. Eikelboom IW, Quin1an OJ, Douketis ID (2001) Extended durstion prophylaxis against venous thromboembolism after total hip or knee replacement: a meta-analysis of the randomized trials. Lancet 358:9-15

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6. Weitz JI, Hirsh J, Samama MM (2008) New antithrombotic drugs: American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 133:234-256 7. Eriksson BI, Dahl OE, Rosencher N et al (2007) Oral dabigatran etexilate versus subcutaneous enoxaparin for the prevention of venous thromboembolism after total knee replacement: the RE-MODEL randomized trial. J Thromb Haemost 5:2178-2185 8. Eriksson BI, Dahl OE, Rosencher N et al (2007) RE-NOVATE Study Group. Dabigatran etexilate versus enoxaparin for prevention of venous thromboembolism after total hip replacement: a randomized, double-blind, non-inferiority trial. Lancet 370:949-956 9. RE-MOBILIZE Writing Committee, Ginsberg JS, Davidson BL, Comp PC et al (2009) The oral thrombin inhibitor dabigatran etexilate vs the north american enoxaparin regimen for the prevention of venous thromboembolism after knee arthroplasty surgery. J Arthroplasty 2:1-9 10. European Medicines Agency (EMEA). European public assessment report: Pradaxa [online]. http://www.emea.europa.eu 11. Perzborn E, Strassburger J, Wilmen A et al (2005) In vitro and in vivo studies of the novel antithrombotic agent BAY 59-7939 – an oral, direct Factor Xa inhibitor. J Thromb Haemost 3:514-521 12. Mueck W, Eriksson BI, Bauer KA et al (2008) Population pharmacokinetics and pharmacodynamics of rivaroxaban – an oral, direct factor Xa inhibitor – in patients undergoing major orthopaedic surgery. Clin Pharmacokinet 47:203-216 13. Eriksson BI, Borris LC, Friedman RJ et al (2008) Rivaroxaban versus enoxaparin for thromboprophylaxis after hip arthroplasty. N Engl J Med 358:2765-2775 14. Kakkar AK, Brenner B, Dahl OE et al (2008) Extended duration rivaroxaban versus shortterm enoxaparin for the prevention of venous thromboembolism after total hip arthroplasty: a double-blind, randomised controlled trial. Lancet 372:31-39 15. Lassen MR, Ageno W, Borris LC et al (2008) Rivaroxaban for thromboprophylaxis after total knee arthroplasty. N Engl J Med 358:2776-2785 16. Turpie AGG, Bauer KA, Davidson B et al (2009) Once-daily oral rivaroxaban compared with subcutaneous enoxaparin every 12 hours for thromboprophylaxis after total knee replacement: RECORD4. Lancet 373:1673-180 17. Wirth T, Schneider B, Misselwitz F et al (2001) Prevention of venous thromboembolism after knee arthroscopy with low molecular weight heparin (Reviparin): results of a randomized controlled trial. Arthroscopy 17:393-399 18. Michot M, Conen D, Holtz D et al (2002) Prevention of deep vein thrombosis in ambulatory arthroscopic knee surgery: a randomized trial of prophylaxis with low molecular weight heparin. Arthroscopy 18:257-263 19. Camporese G, Bernardi E, Prandoni P et al (2008) Low-molecular-weight heparin versus compression stockings for thromboprophylaxis after knee arthroscopy: a randomized trial. Ann Intern Med 149:73-82 20. Lapidus LJ, Rosfors S, Ponzer S et al (2007) Prolonged thromboprophylaxis with dalteparin after surgical treatment of Achilles tendon rupture: a randomized, placebo-controlled study. J Orthop Trauma 21:52-57 21. Lassen MR, Borris LC, Nakov RL (2002) Use of the low-molecular-weight heparin reviparin to prevent deep-vein thrombosis after leg injury requiring immobilization. N Engl J Med 347:726-730 22. Testroote M, Stigter W, de Visser DC et al (2008) Low molecular weight heparin for prevention of venous thromboembolism in patients with lower-leg immobilization. Cochrane Database Syst Rev (4):CD006681

Section III Emergencies on the Field

Management of On-The-Field Emergencies

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P. Volpi, R. Pozzoni, G. Thiebat, H. Schönhuber and L. de Girolamo

Abstract In recent years, the interaction and collaboration between sports activities and medicine has strongly increased, above all in terms of organizational, regulatory, and health aspects. Indeed, most sports teams now include specialists and consultants in sports-related medicine, who thus constitute a team within a team. The team physician has many difficult tasks relating to both the normal and the emergency management of the athletes. Very severe emergencies that occur on the field, which are fortunately very rare, can involve cardiovascular and neurological lesions, including head and spinal traumas. In these cases, the team physician has to promptly recognize and understand the severity of the accident, in order to safely transport the athlete to a facility equipped for treating critical situations.

12.1 Introduction Watching the kick-off from the sidelines or the bench and sharing the mounting tension during a sports match are exciting experiences for the sports physician. But behind a spectator’s emotions must lie the physician’s preparedness to respond to emergencies: to enter the field, quickly define the clinical picture, and rapidly make the necessary decisions. Indeed, prompt action is of utmost importance. It is much easier to reduce a shoulder dislocation or to diagnose an anterior cruciate ligament rupture immediately after trauma, before the onset of pain contractures that can complicate evaluation of the lesion. Moreover, by observing the traumatic event, the sports physician can draw on previous experience to confidently suggest a diagnosis. In many countries, the law mandates that a physician be present at competitive sports events in order to provide players with first aid in case of accidents. In Italy, a physician must be on hand at professional games. In some types of sports, such as soccer, standard practice is to have a sports and intensive care physician accompany the team, whereas in Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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others the physician need not be specialized in sports medicine. It is thus very often the case that sports injuries are treated by orthopedists, and emergency situations requiring another specialist are, fortunately, rare. What precisely constitutes a sports emergency is elusive; however, it is clear that an urgent event refers to a situation in which the player’s vital functions are unstable or at risk of worsening such that he or she requires prompt medical attention. Although they occur rarely, cardiocirculatory collapse and/or neurological emergencies, such as myocardial infarct and cerebral stroke, are on-field risks that cannot be completely excluded. Nevertheless, to be prepared for all the potential risks associated with sports would require the establishment of a field hospital at every stadium or arena. Instead, to be able to respond to an injury or emergency, professional sports organizations provide for medical assistance by assembling a staff comprising a “field” physician, physiotherapists, osteopaths, and chiropractors, as well as external consultants ready to intervene off-field by working in synergy with the team’s medical staff. This degree of readiness and the ability to evaluate priorities has thus far achieved very good results. One example of this model in Italy is in professional soccer [1]. The medical staff includes a sports physician with expertise in orthopedics and traumatology, coordinating a staff of specialists. In addition, there are masseurs, physiotherapists, and chiropractors, all of whom work under the medical staff. Besides the internal medical staff, there are external consultants and access to specialist facilities. To prevent emergencies not directly related to on-field accidents, competition athletes undergo sports medicine examinations during which functional and diagnostic tests are conducted to ensure that the players are fit for training and competition. As required by the Italian law, every year all professional athletes undergo a mandatory examination at authorized sports medicine centers, with updates every 6 months. For instance, in professional soccer the players annually receive a general clinical examination and cardiologic assessment, including echocardiography (every 2 years). In addition, at the first mandated examination, a chest X-ray is obtained. Every 6 months, the athletes must undergo spirometry, laboratory exams (blood and urine), and eye and audiometric assessments. All clinical data obtained from the athlete are kept in the team’s archives in order to verify that the clinical evaluation is complete and that the player is able to participate. These mandatory examinations can be accompanied by further evaluations that provide more detailed information about the clinical history and physical condition of the athlete. For instance, during the pre-season, an athlete might undergo a complete clinical examination, comprising an orthopedic assessment of the musculoskeletal system, diagnostic-instrumental tests (X-ray, magnetic resonance imaging, ultrasound, ECG, EEG), a postural examination, and a dental examination. Other tests include biomechanical evaluation of the lower limbs by means of isokinetic tests and explosive force and coordination tests. Simpler, less expensive, and less invasive examinations are performed in young athletes. The sports medicine examination is of fundamental importance for detecting underlying conditions that may result in field emergencies. The field physician needs to know the player’s medical history in order to understand situations that may occur on the field and to be in a position to distinguish between an acute, potentially life-threatening event and a chronic condition that can be treated over time.

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Furthermore, a good working relationship between the field physician and the managing staff, and the team trainer in particular, is highly important so that medical decisionmaking can be shared on a basis of mutual trust. The physician needs to be able to promptly decide whether an injured player can continue a game or not; indeed, an injured player on a team can adversely affect overall team performance, in addition to worsening his or her clinical condition. Since prevention is considered the most important goal, the sports physician assists the coach and the athletic trainer in determining the kind of training for the team, including whether protective equipment, such as helmets, braces, and taping, is needed. The sports physician must also verify the pertinence of the work spaces (e.g., gymnasium, changing room) and the sports fields. Another important area of input is the proper frequency of sports competitions, in order to avoid the negative effects of over-competition on the athletes’ physical condition. The medical staff, present at the field side along with the team physician, manages major emergencies but also minor, routine injuries. The former include rare instances of cardiovascular and neurological events as well as traumatic brain and spinal injuries. Under such circumstances, the field physician must be able to immediately recognize the severity of the injury so that the player can be safely transported to a facility equipped for treating critical situations. Emergencies should be handled as such, without attempting invasive procedures, but rather establishing a stable condition for transport. Extreme situations aside, the most common injuries can be classified as: • fractures; • luxations; • sprains; • contusions and wounds; • musculotendinous lesions. Injury rates depend on the type of sport and athletic movement. Figures 12.1 and 12.2 illustrate the occurrence of injuries recorded for the Italian downhill skiing team over the past 20 years (source: Medical Commission of the Italian Winter Sports Federation, FISI). Nonetheless, the field physician should avoid being influenced by the context of the sports event; instead, it is important to concentrate on establishing a prompt diagnosis while determining clinical priorities. Often, minor injuries resulting from low-impact incidents are misleading and therefore underestimated. Field or slope environments differ vastly from a hospital setting with respect to intervention time, medical equipment, and external and weather conditions (especially in winter sports), all of which render emergency management highly dependent on the resources at hand. By organizing first-aid operations based on the specialists present (as is routine in some high-impact sports), the field physician will be better equipped to identify a pathology and then refer the problem to the appropriate specialist. Of equal importance is the prompt identification of any complications arising from the injury and their immediate stabilization, in order to ensure safe transport of the injured athlete.

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Fig. 12.1 Injury site (downhill skiing, FISI database)

Fig. 12.2 Injury type (downhill skiing, FISI database)

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12.2 Common Field Injuries 12.2.1 Fractures Since fractured bone ends may be sharp, the injured athlete should not be moved unnecessarily, to prevent further damage. Trauma management following bone fractures involves: • stopping bleeding; • supporting the injured body area; • checking skin sensitivity, color, and temperature; • immobilizing the limb above and below the joint with a makeshift splint or bandage, taking care not that it is not too tight or placed over the fracture. In cases of open fracture, the exposed bone should be covered with a sterile gauze or clean cloth. If the wound is bleeding, pressure should be applied upstream. The emergency medical services should be called and the injured athlete kept still. Attempts to reduce the fracture on-field may lead to vascular complications or locoregional infection.

12.2.2 Luxations Luxations, or displacement of a bone entering a joint, can lead to severe complications in some cases. Identifying a displaced joint is usually simple as there is typically a deranged anatomic relation of bone and joint, with loss of joint function. The most common luxations involve the shoulder joint and are usually caused by falling onto the hands with the arm in abduction and extrarotation. Luxations should not be reduced on the field; instead, the limb should be immobilized with stiff bandages (braces) to relieve the pain and to prevent vascular and/or nerve complications until the athlete can be transported to the hospital.

12.2.3 Sprains Sprains are probably the most common sports injury. Since the pathogenetic mechanisms, sites, and severity vary widely, an exact diagnosis is often difficult. To prevent further damage to the sprained site, the specialist needs to decide whether the athlete should be withdrawn from the competition or allowed to continue with a brace. Generally, rest, immobilization of the limb, and local application of an ice pack and a compression bandage are the best form of treatment. Since distinguishing a distortion from more serious injuries such as fractures may be difficult, the athlete should be removed from the field until further examinations have been made.

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12.2.4 Wounds and Contusions Of fundamental importance is an evaluation of the severity of a wound or contusion. Superficial wounds, or even deep wounds in some cases, may only require medication or suturing, such that the player can return to the field. However, penetrating and internal wounds should prompt the suspicion of more serious injuries, with immediate withdrawal of the injured athlete and referral for clinico-diagnostic examinations.

12.2.5 Tendinous or Muscle Injuries Also in these injuries, prompt diagnosis by the field physician can make a difference in preventing the development of more severe problem. Generally, the first step is to apply an ice pack – as cold reduces bloodflow to damaged vessels – and then a compression bandage, followed by resting of the affected body part. In general, in case of musculoskeletal traumatic lesions involving the limbs, hemorrhage control, fracture stabilization, dislocation reduction, and wound treatment are essential. Lesions of tendons, ligaments, and nerves must also be promptly and expertly addressed. Particular attention has to be paid to injuries in adolescents, in which case, for instance, an ankle distortion can hide a chondro-epiphyseal detachment. Often, the diagnosis and related decisions need to be made quickly, under stress and in suboptimal situations. The physician is called upon to evaluate the severity of the trauma and to define the priorities. Furthermore, as a member of the technical staff, the physician will need to judge whether immediate return to the field may carry implications for sports performance, while taking into account that the health of the athlete is the most important goal.

References 1.

Volpi P (2006) Football traumatology. Organisation of a professional team’s medical staff and the physician’s role. Springer Italia, Milan, pp 67-73

Section IV Upper Extremity

Biomechanics of the Shoulder and Elbow

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Ofer Levy, Ali Narvani

aaa

Abstract This chapter describes the applied biomechanics of the shoulder and elbow. Special emphasis is given to the biomechanics of common pathological conditions, including shoulder instability, rotator cuff disease, adhesive capsulitis, acromioclavicular joint conditions, scapular dyskinesia, elbow instability, and the shoulder/elbow conditions encountered by throwing athletes.

13.1 Shoulder Biomechanics 13.1.1 Basic Anatomy and Biomechanics The shoulder complex consists of the glenohumeral, acromioclavicular, sternoclavicular, scapulothoracic, and subdeltoid joints in addition to many ligaments and muscles (approximately 30 in number). Together, these components provide the fine integration, coordination, and working synergy that are vital to achieve the fine balance between stability and mobility that characterizes the shoulder complex. The glenohumeral joint (GHJ), the central component of the shoulder complex, has a ball and socket configuration with a minimum contact area in order to facilitate motion, albeit at the expense of stability (see below). The acromioclavicular joint (ACJ) is a synovial joint that contains an incomplete, variably sized intra-articular disc that hangs down into the upper part of the joint cavity. Rotation at the ACJ is thought to occur in three planes: anterior/posterior rotation of the clavicle on the scapula, superior/inferior rotation, and axial rotation. The importance of ACJ rotation is evidenced by the fact that full abduction of the upper limb is only possible with rotation of the scapula, which, in turn, is dependent on movement at both the ACJ and the sternoclavicular joint (SCJ). Like the ACJ, the SCJ is a synovial joint with an intra-articular disc. Motion capabilities at the SCJ consist of elevation, depression, protrusion, retraction, and upwards and downwards rotation. The limited motion here facilitates rotation of the glenoid during abduction of the upOrthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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per limb (see above). The scapulothoracic joint allows scapular rotation, which is of vital importance as it allows maximum abduction of the upper limb, provides a stable platform for the humerus during elevation, decreases the risk of mechanical impingement, and maximizes deltoid efficiency by preserving deltoid muscle fiber length. In addition to the upward rotation of the scapula (see below), arm elevation is accompanied by an arc of about 15° of anterior/posterior rotation and approximately 20° of forward tilt with respect to the thorax [1]. Arm elevation (humerothoracic elevation), i.e., elevation between the humeral shaft axis and the thoracic axis, is a combination of glenohumeral (also referred to humeroscapular motion) and scapulothoracic motion. Maximum humerothoracic elevation is dependent on the plane of elevation. This appears to be highest in the 60° plane (approximately 20-30° anterior to the plane of the scapula) [2]. In the first 30° of elevation, glenohumeral motion is greater than scapular thoracic motion whereas in the last 60° of motion glenohumeral and scapulothoracic motions contribute equally. Overall the ratio of glenohumeral to scapulothoracic motion is approximately 2:1. Maximum elevation is also accompanied by external rotation of the humerus, which is necessary to minimize impingement by the greater tuberosity on the coracoacromial arch.

13.1.2 Biomechanics of Shoulder Conditions 13.1.2.1 Instability Stability of the GHJ is dependent on both dynamic and static factors, the fine balance of which is crucial. Static factors include: Bony anatomy. The ratio of the surface area of the humeral head to that of the glenoid fossa is generally agreed to be 3:1, resulting in minimal bony covering and contact area and thus limited inherent stability. There are, however, bony factors that play a crucial role, for example, version of both the humerus and the glenoid. In cases in which stability is accompanied by excessive glenoid retroversion or the humerus is retroverted by < 30°, osteotomies of the glenoid or humerus may be indicated in the presence of an instability. Similarly, if the instability is accompanied by significant bone loss, either from the glenoid or the humerus, an isolated Bankart’s repair may be contraindicated and either bone grafting or a “Laterjet” type procedure may be indicated. Another significant factor is the congruency of the joint, the absence of which results in greater translation. Labrum. This structure plays an important role in enhancing the stability of the GHJ by: increasing the contact area of the glenoid and the depth of the glenoid, resisting glenohumeral translation by functioning as a chock block, and acting as a site of insertion for the glenohumeral ligament (see below). Detachment of the anterior/inferior labrum from the glenoid rim (accompanied by the inferior glenohumeral ligament complex) may lead to anterior translation of the head, with abduction and external rotation. Similarly, there may be increased translation of the posterior and inferior humeral head, with detachment of the posterior/inferior labrum from the glenoid.

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Capsule and glenohumeral ligaments. Localized thickenings of the capsule form the superior, middle, and inferior glenohumeral ligaments (respectively, SGHL, MGHL, and IGHL). The SGHL limits anterior and posterior translation of the adducted humerus, while excessive anterior translation between 60 and 90° of abduction is prevented by the MGHL. The IGHL is the strongest of the three ligaments and is formed by the anterior and posterior bands and the axillary pouch. It functions as a hammock that restrains anterior, posterior, and inferior translation as the humerus is abducted > 45°. Capsular lesions, such as tears, reluctant pockets, or stretched tissues, may result in instability. Dysfunction of the GHL may be secondary to a labrum tear (see above) or to a capsular lesion. Vacuum effect. This is produced by negative intra-articular pressure. The shoulder musculature provide the dynamic instability of the GHJ. Rotator cuff muscles. Functional rotator cuff muscle contribute to stability by compressing the humeral head into the glenoid cavity during motion. Scapular rotator muscles. These enhance stability by positioning the glenoid such that it is maintained in an anteverted and superior position thus remaining congruent with a retroverted humeral head. Long head of the biceps. This resists external rotation forces during external rotation and abduction of the arm thus contributing to anterior GHJ stability at these positions. Muscular dysfunction may be secondary to muscular pathologies or to tendon, peripheral, or central nervous system lesions. It is of vital importance that dysfunction is recognized and appropriately addressed; otherwise, the outcome of any surgical intervention may be very disappointing. Similarly, proprioception dysfunction results in inadequate feedback information and therefore compromised stability due to insufficient muscle activation and coordination.

13.1.2.2 Rotator Cuff Pathology Impingement syndrome is a clinical entity with a complex and multifactorial pathophysiology. It is thought to arise either from mechanical impingement of the rotator cuff muscle (supraspinatus, infraspinatus, subscapularis, and teres minor), via an extrinsic mechanism, or from a pathology in the tendon itself (tendinopathy), i.e., an intrinsic mechanism (Fig. 13.1) [3]. It is important to emphasize that these two mechanisms are interlinked and can lead to a vicious cycle. Tendinopathy may cause secondary impingement as result of tendon swelling in the subacromial bursa. Additionally, rotator cuff dysfunction can lead to migration of the humeral head and thus secondary mechanical impingement. Similarly, mechanical impingement of the rotator cuff tendons may damage and worsen a tendinopathy. An understanding of the biomechanics of rotator cuff tears must be based on detailed knowledge of the functions of the rotator cuff muscles. These functions are [4]: (1) compression of the humeral head into the glenoid cavity (see above), (2) rotation of the humerus, and (3) establishment of muscular balance. Muscular balance is of critical importance in a fully func-

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Primary Impingement – mechanical impingement of coracoacromial arch into supraspinatus

Instability causing excessive load on rotator cuff

Secondary Impingement Overuse

– inadequate muscular stabilization of the scapula – chronic glenohumeral instability

Impingement

Rotator Cuff Tendinopathy

Advancing Age

– imbalance between deltoid & rotator cuff muscles causing – posterior capsule tightness (obligatory translation)

Internal Impingement – impingement of under surface of rotator cuff against posterosuperior glenoid

Acute Trauma

Clinical Features of Impingement/ Rotator Cuff + Bursitis Tendinopathy

Calcific Tendinopathy Partial Rotator Cuff Tears

Coracoid Impingement – impingement of lesser tuberosity with coracoid process

Full Thickness Rotator Cuff Tears

Biceps Tendinopathy OA of Glenohumeral Joint

Fig. 13.1 Pathophysiology of rotator cuff tendinopathy/impingement. OA, Osteoarthritis (From [3])

tional shoulder as activation of any specific muscle around the shoulder results in a number of rotational movements. Accordingly, other muscles must be activated at the same time in order to prevent unwanted rotation. An example of this is during elevation, whereby activation of the anterior deltoid also leads to internal rotation of the humerus (in addition to elevation). In order to prevent this internal rotation, the infraspinatus (an external rotator) and posterior deltoid are simultaneously activated with the anterior deltoid. Hence, the rotator cuff muscles play a vital role in balancing the coupled forces around the GHJ [4], which, in turn, may explain why some very large rotator cuff tears remain symptomatic whereas small tears can be very troublesome, and why an incomplete repair may be sufficient to achieve good results (see below). Rotator cuff tears may present following an acute traumatic event, or more commonly in a chronic setting, with slow creeping tears of degenerative tissue. They may also manifest as an acute episode against a chronic background. With advancing age, intrinsic changes in rotator cuff tendons result in the deterioration of cuff quality such that less force is required to tear the tendon. Furthermore, with age the healing capacity gradually becomes compromised. The end result is the inability of the rotator cuff to tolerate complex loading situations, failure of the tendon to heal once torn, and progression of the tear [2].


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The initial lesion involves the articular surface of the anterior supraspinatus, close to its insertion to the tuberosity and to the long head of the biceps. This is where the load is greatest and the tendon is intrinsically weakest, with compromised healing potential. As the initial fibers fail, the load on the neighboring fibers increases and the tear propagates. This is referred to as the “zipper phenomenon”. With tear propagation, the disturbed anatomy of the tendon further compromises its blood supply, such that along with exposure to lytic enzymes in the synovial fluid, any healing potential is significantly compromised. Tear propagation is in the posterior direction, starting from the suprapsinatus and extending into the infraspinatus. With progressive cuff failure, the humeral head subluxes superiorly, stressing the long head of the biceps and eventually damaging it. With further propagation, the subscapularis also becomes involved. Elevation of the head as the result of unopposed deltoid pull increases the damage to the rotator cuff muscle, impinging on the coracoacromial arch and establishing a vicious cycle. Eventually, there is erosion of the superior glenoid as a result of contact with the elevated humeral head. With superior glenoid erosion and wear, the glenoid loses its ability to prevent excessive elevation of the humeral head such that the humoral head migrates superiorly even further. Elevation is also enhanced by failing cuff muscles sliding down the humeral head to the extent that they act as elevators rather than as compressors of the head (boutonniere’s effect) [2]. At some point in this process, the humerus undergoes secondary degenerative changes as it comes into contact with the coracoacromial arch (cuff arthropathy). The degree to which the above-described process results in clinical manifestations is dependent on a number of factors. As noted above, a relatively large tear may remain clinically silent whereas a small partial-thickness tear can be very troublesome. Pain, even in the absence of a significant tear, can lead to rotator cuff dysfunction by causing inhibition of the muscle. In the presence of a large full-thickness tear, patients may remain asymptomatic as long as there is still adequate coupling and the muscles remain balanced (see above). The principles of force coupling must also be appreciated in the repair of massive rotator cuff tears. The shoulder may achieve reasonable function even when complete repair is not possible, as long as the repair “balances” the coupled forces in all planes (e.g., in the transverse plane, the anterior cuff muscle with the posterior cuff). Similarly, the rotator cuff cable must be re-established. This cable is a cord-like structure that extends from its anterior attachment to the greater tuberosity to its posterior insertion to the greater tuberosity. It plays a protective role by shielding the inner thinner avasular cuff tissue from stress, analogous to a suspension bridge [5]. A large tear may also remain clinically silent if there is adequate compensation from other muscles. This forms the basis of the anterior deltoid exercise regime for non-surgical management of massive cuff repairs [6]. 13.1.2.3 ACJ Conditions Through the ACJ and its interconnecting ligaments with the scapula, the clavicle acts as a strut between the axial skeleton and the upper limb [7]. The ACJ and interconnecting ligaments – primarily, the acromioclavicular and the coracoclavicular ligaments – therefore link scapularhumeral and scapulothoracic motion. The acromioclavicular ligament is divided into anterior, posterior, superior and inferior components, with the posterior and

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superior parts restricting posterior motion whereas anterior motion is limited by the inferior part of the ligament. The coracoclavicular ligament comprises the conoid and trapezoid ligaments. The trapezoid contributes to posterior restraint and together with the conoid forms provides superior stability [7]. The trapezoid contributes to the posterior restraint and together with conoid provides superior stability. The conoid and trapezoid ligament configuration is analogous to the cruciate ligaments of the knee. Damage to the trapezoid or conoid individually does not appear to compromise the overall strength of the coracoclavicular ligament whereas damage to both may result in ACJ dislocation. In an ACJ excision arthroplasty, attention must be paid to the insertion sites of the coracoclavicular and acromioclavicular ligaments as their sacrifice will lead to clavicular instability. It has been shown that resection lengths (from the end of the distal clavicle) of less than 11 and 24 mm do not result in sacrifice of the trapezoid and conoid ligaments, respectively, in 98% of males or females [7]. Excision of more than 7.6 mm in males and 5.2 mm in females, however, will damage the superior acromioclavicular ligaments [7]. We recommend routine excision of 4 mm from the distal clavicle and acromion when performing an ACJ excision for osteoarthritis. With this technique as well as the resection of 8 mm of bone (4 mm from each side), the coracoclavicular ligaments are not violated and the degenerative changes on the acromion side of the ACJ joint are addressed as well. As mentioned above, the ACJ consists of an intra-articular disc that contributes to load distribution and joint instability. Degenerative changes in the disc begin around age 30 onwards but this is variable. In young people, however, injury of the disc may cause symptoms without any ACJ instability or ACJ osteoarthritis. Disc tears may also be seen in whiplash injuries of the shoulder [8]. These usually occur as a result of indirect trauma in traffic accidents, as the clavicle and body are restrained by the seatbelt and there is a whiplash movement of the shoulder. In addition to disc tears, other injuries may be sustained, such as ACJ subluxation, rotator cuff tears, labral lesions, and in extreme cases fracture or fracture dislocations around the shoulder [8]. Motion at the ACJ is important to coupling of the clavicle and scapula during elevation of the upper limb (see above). Accordingly, any device that prevents motion in this joint, such as a screw or plate, will either compromise upper-limb elevation or result in metalwork cut out and failure or fracture.

13.1.2.4 Adhesive Capsulitis Frozen shoulder is an idiopathic condition characterized by global reduction of the GHJ as a result of contracture, either generalized or localized [2], and loss of compliance of the GHJ capsule. Localized posterior/inferior capsular tightness results in limitations in elevation in anterior planes and in the adduction and internal rotation of the elevated arm. Similarly, external rotation of the elevated arm is limited by a tight anterior inferior capsule, and external rotation at the side by anterior/superior tightness. Localized capsular tightness may also result in “obligate translation” [2], which refers to a localized tightness in the area of the capsule such that application of a rotational torque may result in displacement of the humeral head in the opposite direction. Therefore, external rotation


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in the presence of a tight anterior capsule can lead to posterior subluxation of the humeral head and consequently in posterior glenoid wear. An isolated tight anterior capsule may also be secondary to osteoarthritis (a tight capsule will result in posterior glenoid wear, causing a vicious cycle) or to previous surgical stabilizations (excessively tight repairs). The link between instability, surgical stabilization, and osteoarthritis remains unresolved. In a similar manner, obligate translation may result in anterior and superior translation of the humeral head towards the coracoacromial arch during elevation in the presence of a tight posterior-inferior capsule. As this translation can lead to subacromial impingement (see below), posterior/inferior capsular tightness must be recognized and addressed as part of the management of patients with impingement syndrome. Manipulation under anesthesia (MUA) is a popular technique used to manage adhesive capsulitis. We apply the principles of Codman’s Paradox, regarding the order of the serial angular motions, when carrying out MUA, i.e., 90° of rotation around the z axis followed by 90° of rotation around the x axis gives rise to a different final position than obtained if x axis rotation precedes z axis rotation. Furthermore, flexing or abducting the arm and then bringing it back in the plane of the scapula, or vice versa, leads to a change in the axial rotation position even though the humerus itself has never been formally axially rotated. This paradox is useful in MUA as external rotation can be achieved without the need for external rotation forces, therefore minimizing the risk of fracture.

13.1.2.5 Scapular Dyskinesia The scapula’s main functions are to facilitate arm elevation (see above) and to provide a stable base for rotator cuff function. Furthermore, during arm elevation, through its synchronized motion, the scapula maintains a congruent socket for the head of the humerus [9]. In order for the scapula to function efficiently, its positioning and motion must be correct and accurate. Furthermore, the scapula must be adequately stabilized. Abnormal scapular positioning, motion, and stability are referred to as scapular dyskinesia. Scapular dyskinesia may occur secondary to pathology in the neuromuscular chain, resulting in compromised muscle power, balance, coordination, and proprioception. Muscles that are particularly important in positioning, stability, and motion of the scapula are the upper and lower fibers of the trapezius, rhomboids, and serratus anterior. Scapular dyskinesia may also follow claviclular fractures or GHJ/ACJ pathology. The clavicle and ACJ are integral components of the strut that suspends the scapula on the axial skeleton. A significantly displaced, angulated, or shortened fractures of the clavicle, by disturbing the strut mechanism, compromise scapular positioning and motion. Similarly, in significant ACJ injuries, scapular positioning is suboptimal as the scapula becomes protracted and internally rotated. Irrespective of the cause, dyskinesia may lead to secondary rotator cuff and GHJ dysfunction as well as secondary ACJ symptoms. The presence of an impingement syndrome may reflect the abnormal motion of the scapula with arm elevation (loss of upward rotation, excessive internal rotation, and anterior tilt), leading to a reduction in the subacromial space. The efficiency of the rotator cuff muscles may likewise be significantly com-

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promised with abnormal positioning of the scapula, resulting in a suboptimal base. Scapular dyskinesia can also contribute to multidirectional GHJ instability (see above) and place excessive stress on the anterior structure, thus predisposing the patient to labral lesions [9]. Scapular malposition can also lead to ACJ pain as a result of a “discongruous” distal clavicle in relation to the acromion [10]. Although rare, scapula malpositioning and anterior inferior drop of the lateral clavicle may cause brachial plexus impingement and thoracic outlet syndrome [10]. The SICK syndrome (Scapular malposition, Inferior medial border prominence, Coracoid pain and malposition, and scapular dyKinesis), a concept popularized in the USA, is an extreme form of scapular dyskinesia seen in throwing athletes in which the scapula is displaced inferiorly (secondary to forward tilting and protraction) and abducted and displaced laterally [10]. The malpositioning and abnormal movement that make up this syndrome lead to coracoid tenderness (secondary to tightness in the pectoralis minor and short head of the biceps, with an anterior/inferior tilt and lateral displacement of the coracoid), impingement-like symptoms (secondary to scapular protraction causing anterior/inferior angulation of the acromium), and marked tenderness at the scapular superomedial angle (secondary to scapular tilt, resulting in traction, pain, and spasm of the levator scapula). This syndrome may also be accompanied by the scapular complications described above. Winging of the scapula, a general term referring to an abnormal position of the scapula such that it takes on a wing-like appearance, is a rare condition that can be primary, secondary, or voluntary. Causes of primary winging include serratus anterior, trapezius, and rhomboid palsy as well as facioscapulohumeral dystrophy. Secondary winging is usually the result of GHJ pathology (see above) whereas voluntary winging is associated with psychological factors. The main role of the serratus anterior is to rotate and protract the scapula; consequently, palsy of this muscle results in medial scapular winging in which in addition to lifting of the medial border there is superior and medial translation of the scapula when examined from behind. In a trapezius palsy, by contrast, along with winging (which is minimal) there is lateral displacement of the scapula and neckline “drooping” of the affected shoulder (the function of the trapezius includes scapular elevation, retraction, and rotation). Facioscapulohumeral dystrophy, a rare autosomal dominant type of muscular dystrophy, can result in weakness and winging of the scapular muscles. In these patients scapular fusion can improve function dramatically by allowing the deltoid muscle a stable post [11]. To ensure a good outcome in the treatment of different shoulder pathologies, it is important to detect and manage scapular dyskinesia. Furthermore, the primary pathology causing the dykinesia must be addressed.

13.1.2.6 Overhead Athlete, Superior Labrum Anterior/posterior Lesion, and Restriction of Internal Impingement A relationship between shoulder symptoms in overhead-throwing athletes, superior labrum anterior/posterior lesions (SLAP), and restriction of internal rotation has been established (Fig. 13.2) [5]. Burkhart referred to this lack of internal rotation as “glenohumeral internal


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Repetitive abduction & external rotation

Tight posterior inferior capsule Posterior pull of biceps

Posterior/superior shift of the GHJ contact point in abduction & external rotation

Delayed internal impingement of the greater tuberosity on glenoid

Less restriction of anterior inferior capsule to external rotation (cam effect)

Excessive external rotation

Excessive torsional/shear forces on superior labrum and rotator cuff muscle

SLAP lesions

Articular side rotator cuff damage

Fig. 13.2 Link between GIRD, SLAP lesions, and rotator cuff damage

rotation deficit”, or GIRD for short. Furthermore, it has also been shown that minimizing GIRD with a posterior inferior capsular stretching program provides symptomatic relief in the majority of overhead-throwing athletes with shoulder symptoms [5]. It therefore has been suggested that the primary problem in these athletes is tightening of the posterior inferior capsule. The tightness is associated with repetitive abduction and external rotation and may result in a posterior/superior shift of the GHJ contact point during abduction and external rotation. This is thought to occur because in abduction and external rotation, the posterior inferior glenohumeral ligament moves beneath the humeral head and its excessive tightness will lead to posterior/inferior shift of the GHJ contact point. It has also been argued that this shift is further enhanced by alterations in the direction of the biceps’ pull (to a posterior direction). The shift in the GHJ contact point, in turn, leads to greater external rotation, as impingement of the greater tuberosity against the glenoid rim occurs (internal impingement) at a later stage. Additionally, with this shift, there is less obstruction to external rotation by the anterior capsule (also referred

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to as the “cam effect”) [5]. This excessive external rotation leads to elevated torsional and shear forces on both the superior labrum and the rotator cuff muscles, resulting in a SLAP lesion and damage to the articular portion of the rotator cuff. There is also delayed internal impingement as the greater tuberosity impinges on the posterior/superior quadrant of the glenoid.

13.2 Elbow Biomechanics The elbow joint complex consists of three distinct joints and its primary function is the placement of the hand in a variety of positions around the body and space. This, in turn, requires the absolute mobility and stability of the elbow. The humero-ulnar joint acts as a hinge and is formed by the articulation between the trochlea and the trochleal notch on the proximal ulna. In the humero-radial joint, there is articulation between the hemispherically shaped capitulum and the radial head. The complex rotational movement is enhanced by the shape of this articulation. The articulation between the radial notch on the proximal ulna and the radial head form the proximal radio-ulnar joint. This is a pivot joint with the principle motion of pronation and supination (together with the distal radio-ulnar joint) around an axis formed by an imaginary line drawn from the center of the radial head fovea to the head of the ulna distally. Although hugely variable, the normal range of motion of the elbow complex in the sagittal plane is thought to be 0-5° extension/hyperextension and 135-140° flexion. The range of motion required for the normal activities of daily living is generally agreed to be 30-130° of flexion. The normal rotation range is 85° supination to 75° pronation. The functional requirement for the activities of daily living ranges from 50° supination to 50° pronation. The stability of the elbow complex is provided by statistic as well as dynamic elements. Forearm position also influences stability, as pronation reduces valgus laxity. Static components include the articular surfaces, lateral collateral and medial collateral ligaments (LCL and MCL, respectively), and the capsule. Muscles around the elbow complex provide dynamic stability. The biceps, triceps, brachioradialis, and brachialis all contribute to posterolateral stability. These muscles, together with flexor pronator muscles, also provide dynamic valgus stabilization. The articular surface components that contribute to static stability are ulno-humeral articulation, the coronoid, and the radio-humeral joint. The ulno-humeral joint is the primary stabilizer of the complex to varus stress in both flexion and extension. It also contributes to stability to valgus stress in both flexion and extension (although the primary stabilizer to valgus stress is probably the medial collateral ligament; see below). It is important to note that up to 50% of the olecranon can be excised before joint stability becomes compromised [12]. The coronoid functions as a major stabilizer of the ulnohumeral joint by resisting posterior motion. This requires the presence of at least 50% of the coronoid. The LCL complex consists of the lateral ulnar collateral ligament (LUCL), the radial collateral ligament (RCL), the annular ligament, and the accessory lateral collateral liga-


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ment (Fig. 13.3). The LUCL is thought to be the primary stabilizer to postero-lateral instability (see below). The annular ligament also contributes to varus/valgus stability (although not as a primary stabilizer). The MCL complex, consisting of the anterior oblique, posterior oblique, and transverse ligaments, is the primary stabilizer to valgus stress (Fig. 13.4). The contribution of the anterior oblique ligament seems to be the most important, with the anterior capsule as another critical valgus stabilizer, particularly in extension. The radial head, a component of the radio-humeral joint, contributes to valgus stability of the complex. This contribution, however, only becomes significant if the MCL is not functional or the interosseous membrane is damaged. It is therefore of crucial importance that the radial head is not excised if there is damage to the MCL or interosseous membrane, as this would result in valgus instability or superior migration of the radius (resulting in pain and instability at the distal radio-ulna joint), respectively. In summary, the primary valgus stabilizer comprises the anterior oblique ligament of the MCL complex and the anterior capsule in extension, whereas the secondary valgus

Fig. 13.3 Anatomy of the LCL complex. (© American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 12(6), pp 405-415 with permission)

Fig. 13.4 Anatomy of the MCL complex. (© American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 12(6), pp 405-415 with permission)

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stabilizers are the humero-radial and humero-ulnar joints. The latter joint plays the role of primary varus stabilizer but secondary support is provided by the LCL. Lateral ulnar collateral ligament acts as the primary stabilizer to posterolateral rotatory intstability; however, this instability has been suggested to result from injury to other anatomical structures along with the LUCL [13].

13.2.1 Medial Elbow Instability As mentioned above, the MCL is the main valgus stabilizer. It may become damaged by posterior elbow dislocation, repetitive valgus stress as a result of throwing motion in athletes (see below), or an acute valgus injury resulting in its isolated acute rupture [14]. MCL injuries that occur in association with posterior elbow dislocation are commonly accompanied by fracture (particularly of the radial head) or LCL ligament damage. Occasionally, the dislocation occurs in combination with radial head and coronoid fractures (as well as damage to both the MCL and LCL). This is referred to as “terrible triad of the elbow” and it is best managed with fracture fixation of both the coronoid process and the radial head (or a radial head prosthesis if reconstruction is not possible) as well as bilateral ligament repair/reconstruction. If the coronoid is not fractured (dislocation + LCL damage + MCL damage + radial head fracture), radial fixation/prosthesis and LCL repair/reconstruction are sufficient in all cases except in the highly demanding patient requiring MCL repair/reconstruction. In the majority of patients in whom dislocation is associated with MCL or bilateral ligament injury but no fracture, the outcomes are good when treated by close reduction and a short period of immobilization followed by intense active mobilization. MCL reconstruction may be indicated in patients who do not respond to 3-6 months of non-surgical management [14].

13.2.2 Posterolateral Rotatory Instability Posterolateral rotatory instability (PLRI), first described by O’Driscoll, usually occurs as a consequence of a previous elbow dislocation that was reduced either spontaneously or by close reduction [13]. A combination of axial compression and valgus and external rotation force to the elbow is thought to give rise to a staged disruption of the elbow’s soft tissues. Initially, the LUCL (the primary posterolateral rotatory stabilizer) is damaged, followed by anterior and posterior capsule disruption. Eventually, with force progression, the MCL is disrupted [13]. The elbow is reduced, but the lateral ligament complex is unable to heal in its anatomical position, resulting in PLRI. This reflects the excessive external rotation of the ulna on the humerus and subluxation of the radial head posterior to the capitellum, leading to a recurrent painful clicking, snapping, or locking of the elbow. As mentioned above, although LUCL is the primary posterolateral stabilizer, it is thought that PLRI only arises in the presence of damage to other anatomical structures in addition to the LUCL [13].


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13.2.3 Elbow Throwing Injuries Throwing athletes expose their elbow to tremendous valgus forces. In the late cocking and early acceleration phases of throwing, the compressive forces at the humero-radial articulation may be as high as 500 N. These forces can lead to damage of all compartments of the elbow complex, as illustrated in Fig. 13.5 [15].

THROWING (Late Cocking & Early Acceleration)

Excessive Valgus Forces & Rapid Extension

Large Tensile

Shear Stress on

Compression Forces

Strain on Medial

Posterior

on the Lateral

Compartment

Compartment

Compartment

Ulnar Collateral Ligament Injuries

Posterior Olecranon Impingement

Medial

Osteochondritis

Epicondylitis /

Dissecans of

Pronator-Flexor Mass

Capitellum

Olecranon Stress Fracture

Tendinopathy

Ulnar Nerve

Loose Bodies

Dysfunction

Medial Epicondyle Apophysitis “Little Leaguer’s Elbow”

Fig. 13.5 Elbow conditions in throwing athletes. (From [15])

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References 1. Itoi E, Morrey BF (2009) Biomechanics of the shoulder. In: Rockwood CA, Matsen FA, Wirth MA et al (eds) The shoulder, fourth edition. Saunders Elsevier, Philadelphia, pp 213-250 2. Matsen FA, Lippitt SB, Sidles JA et al (eds) (1994) Practical evaluation and management of the shoulder. WB Saunders Company, Philadelphia London Toronto Montreal Sydney Tokyo 3. Narvani AA (2006) Shoulder-impingement syndrome/rotator cuff disease. In: Narvani AA, Thomas P, Lynn B (eds) Key topics in sports medicine. Routledge, London New York, pp 253-258 4. Matsen FA, Fehringer EV, Lippitt SB et al (2009) Rotator Cuff. In: Rockwood CA, Matsen FA, Wirth MA et al (eds) The shoulder, 4th edn. Saunders Elsevier, Philadelphia, pp 771-819 5. Burkhart SS, Lo IKY, Brady PC (eds) (2006) A cowboy’s guide to advanced shoulder arthroscopy. Lippincott Williams & Wilkins, Philadelphia 6. Levy O, Mullett H, Roberts S et al (2008) The role of anterior deltoid re-education in patients with massive irreparable degenerative rotator cuff tears. J Shoulder Elbow Surg 17:863870 7. Collins DN (2009) Disorders of the acromioclavicular joint. In: Rockwood CA, Matsen FA, Wirth MA et al (eds) The shoulder, fourth edition. Saunders Elsevier, Philadelphia, pp 453-514 8. Levy O, Rath E (2002) Traumatic soft tissue injuries of the shoulder girdle. Trauma 4:1-13 9. Kibler WB, Sciascia A (2009) Scapular Dyskinesis: current concepts. Br J Sports Med published online December 2008 10. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder: spectrum of pathology part III: the SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19:641-661 11. Copeland SA, Levy O, Warner GC et al (1999) Management of shoulder problems in Muscular dystrophy. Clin Orthop Relat Res 368:80-91 12. Mansat P (2009) Elbow stability: anatomical and biomechanical principles. In: 22nd Congress of the European Society for Surgery of the Shoulder and the Elbow Abstract book, pp 6-7 13. Mehta JA, Bains GI (2004) Posterolateral rotatory instability of the elbow. J Am Acad Orthop Surg 12:405-415 14. Olsen BS (2009) Medial elbow instability. In 22nd Congress of the European Society for Surgery of the Shoulder and the Elbow Abstract book, pp 7-8 15. Narvani AA (2006) Elbow- throwing injuries. In: Narvani AA, Thomas P, Lynn B (eds) Key topics in sports medicine. Routledge, London New York, pp 95-101

Physical Examination Tests for the Shoulder and the Elbow

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G. Porcellini, F. Caranzano, F. Campi and P. Paladini

aaa

Abstract A successful outcome in shoulder or elbow surgery is related to the accuracy of diagnosis, which in turn requires a well reproducible model of clinical examination, including thorough inspection of the injured area, the completion of all the steps in the examination, the choice of the most accurate tests, and sound judgment based on experience. In the detection of shoulder and elbow pathologies, the history is very important and accurate data collection is mandatory. This information together forms the basis for carrying out specific tests. The first part of this chapter focuses on clinical examination of the shoulder. Anterior and posterior instability must be well distinguished from joint laxity, as the latter is often a physiological condition while the former is a pathological condition that must be treated. This is followed by an analysis of the long head of the biceps and a discussion of SLAP tests, tendon integrity tests to examine the superior, posterior, and anterior components of the rotator cuff in impingement cases, and acromio-clavicular joint tests. In the second part of the chapter, clinical examination of the elbow is reviewed, emphasizing accurate inspection and the palpation of anatomic landmarks. Finally, the proper use of range of movement and muscular strength tests, stability tests, and specifics tests for medial and lateral epicondylitis and for the distal biceps is described.

14.1 Introduction The shoulder girdle is composed of four articulations and 30 muscles that together contribute to maintaining the balance between shoulder mobility and stability. Thus, knowledge of the shoulder’s anatomy and physiology is mandatory to perform a complete clinical examination. Successful treatment is related to the accuracy of diagnosis. In the scientific literature, more than 110 clinical tests for the shoulder are described – an overwhelming Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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number of options that inevitably generates confusion. It is therefore critical that the clinician acquires a well reproducible system of clinical examination, one that is thorough and includes the most accurate tests, whose reliability has been validated with experience. The first step in the clinical examination is accurate data collection, starting with the two most important facts: age and type of symptoms. Participation in sports activities must be well investigated, focusing on the athletic movement and when the symptom appears – sometime an on-field visit may even be necessary to better evaluate the situation. The nature of the pain and the exact time of its onset can help in the diagnostic process. In amateur athletes, the type of work in which the patient is employed is an important parameter. The unstable shoulder must be completely evaluated, including the number of dislocation-subluxation episodes and their presentation, the reduction maneuvers used thus far, the age at onset of the first episode, and the frequency of re-dislocation. Present or past illnesses, comorbidity, surgical and non-surgical treatment (e.g., physiotherapy or physical therapy), and broad medical vs. local treatment (including type and number of corticosteroid injections) must be thoroughly determined.

14.1.1 Inspection and Palpation The thorax must be completely uncovered and the patient inspected both anteriorly and posteriorly, including conformation, aspect, and muscle features. The injured and non-injured sides should be compared, looking for deformity, scar from trauma or past surgery, and hematoma. A skilled inspection can diagnose hypotrophy of the infraspinatus and supraspinatus caused by tendon injury or suprascapular nerve entrapment, tendon ruptures (e.g., that of the long head of the biceps or distal biceps), dislocation of the acromio-clavicular joint (ACJ) or sterno-clavicular joint, muscle palsy, and post-traumatic gleno-humeral dislocation. In addition, deltoid strength and aspect and skin sensitivity must be well evaluated as these features will reveal an axillary nerve palsy or dysfunction. Scapulothoracic rhythm must always be evaluated, as scapular dyskinesia can generate false-positive results during cuff examination. The physical examination of patients with shoulder injuries not involving actual rotator cuff tears frequently demonstrates decreased rotator cuff strength on manual muscle testing. In many cases, this finding is incorrectly attributed to supraspinatus muscle weakness [1], perhaps owing to alterations in scapular position or weakness of the scapular stabilizers muscle. A “wall push up” or elevation against resistance at 30° of forward flexion reveals scapular winging, usually generated by a palsy of the anterior serratus (long thoracic nerve, migration in a proximal-medial direction of the scapula) or trapezius (spinal accessory nerve, scapula migration in a distal-lateral direction). Palpation is often used in specific tests, as described later in this chapter. Good knowledge of the anatomic landmarks and their variation in different shoulder positions is mandatory to correctly correlate physical findings with pathology. During palpation, several factors are considered: tenderness, swelling, temperature variation from the contralateral side, evident or hidden deformities, muscle features and the relationship between structures. Regarding the latter, the main landmarks are the sterno-clavicular joint, ACJ, clavicle, acromion, great tuberosity, bicipital groove, and coracoid.

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14.1.2 Evaluation of Joint Motion The physician must accurately evaluate not only the motion of the shoulder joint, but also its quality of movement, analyzing the contribution of both the gleno-humeral joint and the scapulo-thoracic joint to shoulder elevation. At this stage of the examination, comparison with the contralateral side, if not damaged, is very important. Joint motions are measured from a “zero starting position”, i.e., with the patient erect and arm at the side of the body in neutral rotation with palms facing the thighs. Both active and passive motion must be accurately reported, if different. According to the American Shoulder and Elbow Surgeons (ASES), active and passive motion in anterior forward elevation (FE), abduction (AB), internal rotation (IR) at 0°and 90° of abduction, and external rotation (ER) at 0° and 90° of abduction should be evaluated. Sometime it is useful, in order to avoid compensatory actions of the spine and pelvis, to examine AB and IR with the patient in sitting position, and elevation and ER in supine position. A large reduction in movement is observed in adhesive capsulitis and in untreated anterior and posterior dislocations, but in sports medicine slight reductions of movement must be searched for as well; for example, a limitation in IR at 90° AB is observed in pitchers and overhead-throwing athletes and is due to posterior capsular retraction subsequent to chronic stresses in forced ER. In these athletes, increased ER reflects adaptive mechanisms to obtain the required athletic movement. This is already evaluable in young athletes, after 1 year of practice. When comparing the dominant and non-dominant sides, the examining physician must keep in mind the physiological variations in the range of movement (ROM) that are seen in healthy people. In fact, a statistically relevant limitation in all movements in the dominant arm has been reported.

14.1.3 Specific Tests: Instability Test 14.1.3.1 Anterior Instability Tests The apprehension test can be performed with the patient in either supine or upright position. With the patient’s arm is in AB-ER, the examiner gently externally rotates the humerus, with the fingers of his or her hand used to control dislocation of the humeral head. If the patient reports apprehension and discomfort but not pain, this is diagnostic of anterior instability. The test can be performed at different degrees of AB in order to provide more precise information about the direction of the instability: anterior (90°), antero-superior (60°), or antero-inferior (120°). The bony apprehension test is performed at 45° of AB and 45° of ER and is positive in patients with significant glenoid bone loss. The Jobe relocation test is performed with the patient in the supine position: it, is positive if the patient’s apprehension in ER is reduced by applying a posteriorly directed force at the humeral head, relocating it at the glenoid. This test is immediately followed by the surprise or release test, in which a posteriorly directed force is suddenly withdrawn; the test is positive if apprehension reappears.

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14.1.3.2 Minor Instability Test In the Castagna test for minor instability [2], the patient is positioned supinely, with 45° of gleno-humeral AB. The arm is maximally externally rotated. Posterior/superior pain is associated with a loose anterior joint capsule and middle gleno-humeral ligament. If pain is relieved with relocation, the test is positive. The Castagna test is similar to the Jobe relocation test except that the latter is performed with the arm at 90° AB.

14.1.3.3 Posterior Instability Test A posterior apprehension test is performed with the patient supine, with the arm in 90° of FE. A positive test is defined if an impending feeling of posterior dislocation is produced by IR of the arm. The examiner can reproduce and amplify the symptoms by applying a posteriorly directed force on the humerus. The Kim test [3] requires that the patient is in a sitting position, with the arm in 90° AB (Fig. 14.1). Holding the patient’s elbow and lateral aspect of the proximal arm, the examiner applies a simultaneous axial loading force and 45° upward diagonal elevation to the distal arm, and an inferior and posterior force to the proximal arm. A sudden onset of posterior shoulder pain is considered a positive test result, regardless of the accompanying posterior clunk of the humeral head. During the test, it is important to apply a firm axial compression force to the glenoid surface by the humeral head. Having the patient sit against the back of a chair rather than on a stool, or with an assistant stabilizing the patient, provides good counter-support during axial loading of the examined arm.

Fig. 14.1 Kim test for posterior instability


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The jerk test is performed with the patient in a sitting position. While the examiner holds the scapula with one hand, the patient’s arm is abducted 90° and internally rotated 90°. An axial force is loaded with the examiner’s other hand holding the patient’s elbow, and a simultaneous horizontal adduction force is applied. A sharp pain with or without posterior clunk or click indicates a positive test result.

14.1.4 Laxity Tests Joint laxity is often a physiological condition and must not be confused with instability, which is a pathological condition and must be treated. The sulcus test evaluates laxity, especially of the superior part of the capsulo-labral and ligament complex: a downward traction on the arm produces inferior subluxation of the humeral head. The test is positive if a depression is observed between the lateral part of the acromion and the humeral head. Translation is classified as: grade 1: < 2 mm; grade 2: 25 mm; grade 3: > 5 mm. The test is performed at 0° and 30° of ER. Positivity at 30° of ER is a pathological sign of laxity at the rotator interval and is indicative of the lack of a coraco-humeral ligament. A load and shift test evaluates the anterior and posterior parts of the capsule and ligaments by translating the humeral head anteriorly and posteriorly . The examiner can appreciate the translation of the humeral head sliding off the glenoid. Anterior and posterior translation is classified as: grade 0: no appreciable translation; grade 1: 0-1 cm; grade 2: 1-2 cm; grade 3: subluxation or sustained dislocation. The Gagey test [4] assesses laxity of the anterior and posterior portions of the inferior glenohumeral ligament and inferior capsule. It is performed by fixing the scapula and reaching maximal AB. In the healthy shoulder, maximal AB is 90-95° whereas AB > 115° is pathologic and indicative of lengthening or laxity of the ligament.

14.1.5 Tests of the Long Head of the Biceps In the speed test, the patient anteriorly elevates the humerus against resistance, with the elbow extended and the forearm supine. The tendon is twisted and stressed during this maneuver. If pain is present in the bicipital groove during flexion, the test is considered positive. In the Yergason test, the long head of the biceps is tensioned by supination of the forearm against resistance, with the arm in adduction and mild ER. The test is positive if palpation of the bicipital groove causes pain.

14.1.6 SLAP Tests The diagnosis of a superior labrum anterior/posterior (SLAP) lesion is difficult as it is often associated with other lesions. In such cases, an accurate history and investigation are useful to suspect and even to diagnose this condition, which in fact is very common in

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overhead-throwing athletes with postero-superior impingement due to the “peel back” mechanism. The O’Brien test correlates well with type 2 SLAP lesions [5], the most common type. The arm is at 90° of forward flexion, with the thumb down, and the patient is asked to resist a force directed downwards. The test is positive if pain is present and decreases when the thumb is pointed up; pain limited to deep in the shoulder is regarded as positive for a SLAP tear. All other pain (posterior shoulder, over the ACJ) is considered evidence of a negative test. In the Crank test [6], the patient is placed in a supine or seated position with the affected arm elevated 160° in the scapular plane. An axial load is applied to the gleno-humeral joint as the humerus is internally and externally rotated. The test is considered positive if the patient notes pain with or without a mechanical click or during reproduction of the patient’s activity-related symptoms (usually pain or catching). In the resisted supination ER test, the patient is placed in the supine position on the examination table with the scapula near the edge of the table. The examiner stands at the patient’s side, supporting the affected arm at the elbow and hand. The limb is placed in the starting position with the shoulder abducted to 90°, the elbow flexed 65-70°, and the forearm in neutral or slight pronation. The patient must forcefully supinate the hand against resistance as the shoulder is gently externally rotated to the maximal point. At maximum ER, he or she is asked to describe the symptoms. The test is positive if the patient reports anterior or deep shoulder pain, clicking or catching in the shoulder, or the reproduction of symptoms that occur during throwing. The test is negative if the patient has posterior shoulder pain, apprehension, or if no pain is elicited.

14.1.7 Tendon Integrity Tests 14.1.7.1 Supraspinatus Tendon The Jobe test, or supraspinatus test, is performed with the arm at 90° AB, angled 30° on the axial plane (aligned with the scapular plane). The test can be performed both in IR and ER, with similar sensitivity and specificity. When performed in IR, with the thumb pointed down, the major axis of the supraspinatus is in line with the humerus, such that the musculo-tendinous unit is in the most favorable position to work. The test is positive if the patient cannot resist a downward force applied by the examiner. Unfortunately, this test is often biased by pain and there is a high rate of false-positive results. In this case, the xylotest is useful, in which 4-10 ml of xylocaine or lidocaine is injected into the subacromial space, eliminating pain and allowing the evaluation of tendon integrity only. In athletes with muscle hypertrophy, the Whipple test is performed to override deltoid strength in order to unmask a supraspinatus tear. From the same position as used in the Jobe test, the forearm is pronated, and strength in elevation is tested. If the patient cannot resist a downward force, the test is considered positive.


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14.1.7.2 Infraspinatus and Teres Minor The drop sign assesses the function of the posterior part of the cuff. The examiner holds the patient’s arm at 90° of elevation and almost full ER, which in this position is maintained by the infraspinatus and teres minor. The test is positive if the patient cannot maintain the position against resistance. The ER lag sign evaluates the integrity of the supraspinatus and infraspinatus tendons [7] by minimizing both the synergistic effect of all other muscles and the pain due to subacromial impingement. The examiner holds the patient’s arm in AB, with the elbow flexed at 90°; full ER is reached and the forearm then released. The patient should maintain the position; if in doing so the he or she internally rotates the forearm, the test is positive. The amount of IR correlates with the size of the tear. If the elbow is placed at 20° FE and 20° AB in the scapular plane, the supraspinatus moves posteriorly and acts as an external rotator. In this case, positivity of the test indicates a supraspinatus tear.

14.1.7.3 Subscapularis The lift-off test is used to evaluate the integrity of the subscapularis. The examiner places his or her hand on the patient’s back, at the mid-lumbar spine; a positive test is indicated if the patient cannot lift off the hand. The belly press test is performed with both of the patient’s arms at his or her sides and the elbows flexed at 90°. The patient presses his or her hands on the belly by internally rotating both shoulders. If weakness is demonstrated at the affected side or if the elbow falls backwards, the test is positive. The bear-hug test (Fig. 14.2) has the best sensitivity and specificity for a subscapularis tear [8] and better evaluates the intra-articular portion of the tendon, which is the

Fig. 14.2 Correct position for the bear-hug test

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one most frequently involved in tears. The patient places his or her hand on the opposite shoulder, with the fingers extended. The examiner tries to pull the hand away using an ER force. The test is positive if the patient cannot maintain the hand on the opposite shoulder.

14.1.8 Acromio-clavicular Joint Tests In the detection of ACJ pathology, the cross-arm test has high sensitivity but low specificity. The patient’s arm is placed at 90° of FE and the examiner forces the arm in adduction. If the latter results in pain during forced adduction, the test is positive. The Paxinos test is positive when pain is generated by direct palpation of the ACJ by the examiner’s thumb. In case of doubt due to concomitant intra-articular or extra-articular gleno-humeral pathology, the xylotest should be performed, with 1-2 ml of xylocaine or lidocaine injected into the ACJ.

14.1.9 Impingement Tests The following tests are positive in case of pain, which is caused by the conflict between the great tuberosity and the acromion. In the Hawkins test, the humerus is at 90° of forward flexion, the shoulder internally rotated, and the hand placed on the opposite shoulder. The patient must then elevate the elbow against resistance. In the Yocum test, the arm is placed at 90° of forward flexion and 30° of abduction. The examiner then maximally internally rotates the shoulder. The Neer test is performed with the elbow fully extended; after stabilizing the scapula, the arm is full forward elevated with the thumb down.

14.2 Elbow Examination 14.2.1 Introduction The elbow complex is made up of three separate articulations, i.e., the humero-ulnar, humero-radial (radio-capitellar), and superior radio-ulnar joints, all of which are covered by the same capsule. Elbow injuries in athlete are not common and may be difficult to diagnose. This difficulty may be resolved or simplified to some extent by a full and systematic clinical examination. The joint is superficial and hence readily accessible to clinical examination. As previously stated for the shoulder, accurate diagnosis requires that the examiner be thoroughly familiar with the anatomy of the joint and with the abnormal


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conditions that may be encountered. In addition to the standard orthopedic history, information should be collected regarding the type of sport, number of years of practice, and duration of the complaint. The dominant side needs to be ascertained. Pain is usually the most common symptom of elbow dysfunction, in terms of inflammatory pathology and instability. The patient should be questioned about locking, pain and/or instability during throwing movements, joint swelling, and fleeting inability to extend the elbow, which would suggest a joint effusion. Paresthesia of the hand may, in some cases, be related to ulnar nerve compromise at the level of the elbow. Particular attention must be paid to any previous treatment: medical or injective (intra- or extra-articular steroid injections), non-surgical (physiotherapy or physical therapy), and/or surgical.

14.2.2 Inspection and Palpation As noted above, due to the elbow’s superficial position, many of its disorders can be readily detected by simple inspection or by directed palpation. When the forearm is in full extension and supination, there is a physiological valgus (“carrying angle”) of 9-14° in men, while in women the angle is 2-3° greater. In the dominant arm of throwing athletes, this angle is 10-15° greater. However, the angle varies from valgus in extension to varus in flexion, and its measurement is not of any practical importance. Sometimes, on the side of the elbow, bulging in the para-olecranon groove is seen; this swelling is produced by an effusion or by synovial tissue proliferation. Bursitis is also a frequently encountered pathology. In addition, inspection may show skin atrophy at the site of multiple steroid injection, or scars from previous surgery. These features must be noted and accurately reported since they may affect the surgical approach. Palpation starts at the posterior aspect, with the patient standing with his or her shoulder braced backwards. The three palpation landmarks – the two epicondyles and the apex of the olecranon – form an equilateral triangle when the elbow is flexed 90° (Huter’s triangle) and a straight line when the elbow is in extension. Mild elbow flexion brings the olecranon out of the olecranon fossa, in which it lodges in extension; in this position, the proximal portion of the fossa on either side of the triceps tendon may be palpated. In overhead-throwing athletes, repetitive combined hyperextension, valgus, and supination of the elbow results in a mechanical abutment of bony or soft tissues in the posterior fossa of the elbow. The resultant soft-tissue swelling, loose bodies, osteophyte formation, or combinations of these, together with abutment, may produce symptoms in the posterior side of the elbow. The athlete complains of pain posteriorly, joint effusion, locking, crepitus, and a decrease in the range of motion, most notably an extension deficit. Posterior impingement can also be associated with ligamentous instability of the elbow, especially insufficiency of the ulnar collateral ligament. On the lateral side, the main landmarks are the supra-condylar ridge, the lateral epicondyle proximally and the radial head distally. The latter is palpated with the thumb while pronating and supinating the patient’s forearm. Pain at this site in young throwers or athletes is often related to osteochondritis (Panner’s disease). Inside the triangle formed by the lateral epicondyle, radial head, and olecranon, the joint itself is palpated, allowing the detection of even very minor effusions or low-grade synovitis. The muscles on the lateral

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side may be palpated individually. The anconeus may be palpated behind the radial head, on the side of the olecranon. Palpation of the arcade of Frohse, 2 cm anterior and 3 cm distal to the epicondyle, allows evaluation of the posterior interosseus nerve. Pain at compression in this site is related to radial tunnel syndrome and must be differentiated from epicondylitis, in which pain is felt in a more proximal location. From the medial side, the joint is not very accessible to palpation and the small amount of synovial tissue on the medial border of the olecranon makes joint palpation difficult. Behind the septum, the ulnar nerve may be palpated; in patients with a very mobile nerve, it can be seen rolling on the medial condyle. Ulnar nerve instability is more easily tested with the arm in slight AB and ER, with the elbow flexed between 20° and 70° [9]. Subluxation of the nerve should be distinguished from a hypertrophic part of the medial head of the triceps snapping over the medial epicondyle during flexion. In the throwing athlete, the initial presentation of ulnar neuritis may be pain along the medial joint line associated with dysesthesias, paresthesias, or even anesthesia in the little finger and the ulnar half of the ring finger. The ulnar nerve is well evaluated by execution of Tinel’s test proximally, and the cubital tunnel with the test performed distally. In the young patient, the medial epicondyle can be avulsed by trauma, while in young throwers the repetitive traction of this structure by flexor-pronator muscles (Little Leaguer’s elbow) can cause a lesion; in this case, directed palpation evokes pain. The medial collateral ligament is the main elbow stabilizer against valgus forces and is easily palpable by maintaining elbow flexed between 30° and 60°. Anteriorly, the bulk of the flexor-pronator group restricts the extent of joint palpation; anterolaterally, the brachio-radialis is felt, and in the middle, the biceps tendon is readily accessible if the patient flexes the forearm against resistance. The lacertus fibrosus is palpated medial to the biceps tendon, with the pulse of the brachial artery felt deep to this aponeurosis.

14.2.3 ROM Evaluation The investigation of elbow ROM (range of motion) is an important part of the examination process. The normal flexion-extension range is 0-140° (±10°). It is important to measure the mobility with a goniometer placed on the side of the arm and forearm. The measurement thus obtained will be reliable to within 5° of accuracy. The useful arc of motion is between 30° and 130°and most activities of daily living require an arc of only 60-120°. Loss of extension provides a very sensitive clue to intra-articular elbow pathology since with respect to ROM extension it is the first to be affected and the last to recover. At the end of flexion, there will be a soft end-point as the movement is blocked by the bulk of the arm and forearm muscles, in contrast to the rigid end-point present at the end of the normal extension movement, as the olecranon locks into the olecranon fossa. In examining pronation and supination, the integrity of both the proximal and the distal radio-ulnar joint, the normal length relative to the ulna and radius, and the interosseous membrane all must be kept in mind. The arc of motion varies widely in different individuals, with mean values of 70° pronation and 85° supination. At the end of pronation and supination, a capsular end-feel is noted.


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14.2.4 Muscular Strength Test Evaluation of strength in flexion and extension is assessed with the forearm in neutral rotation and the elbow flexed at 90°. Strength in extension is usually 70% of strength in flexion, strength in supination is 15% greater than strength in pronation. The dominant arm is usually 5-15% stronger than the contralateral arm.

14.2.5 Stability Tests The medial collateral ligament (MCL) complex is evaluated by the valgus stress test, with the arm in full ER and at 15° of elbow flexion to unlock the olecranon from its fossa. To obtain greater specificity for the MCL, the forearm is pronated and the examiner gently applies a valgus force on the elbow, avoiding shoulder rotation. No laxity is assessed in the healthy patient. A valgus opening with the forearm pronated should raise suspicion of a lesion involving the anterior MCL. If the elbow opening is assessed with the forearm supinated, a lesion of either the anterior MCL or the ulnar part of the radial collateral ligament (rotatory instability) may be detected. In the modified milking maneuver [10], the patient’s elbow is flexed to 70° and the examiner uses one hand to palpate the MCL and the medial joint line (Fig. 14.3), and the other to apply a valgus stress to the patient’s elbow by pulling down on his or her thumb. Opening of the medial joint line indicates a positive test. The integrity of the lateral collateral ligament complex is assessed with the varus stress test. The arm is in IR and a gently varus force is applied by the examiner; the test is pos-

Fig. 14.3 The modified milking maneuver


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itive if a lateral opening is determined. Both varus and valgus stress tests result in pain to the patient and should thus be performed gently. Bilateral examination better reveals slight differences and establishes if the laxity is truly of a pathologic nature. The lateral pivot shift test [11] assesses postero-lateral rotatory instability. It is performed at the head of the table, with the patient in the supine position and the shoulder elevated so that the arm is overhead (Fig. 14.4a). Some authors have advocated seated, lateral, and prone positions for the patient in order to improve control of the upper extremity. The shoulder is maximally externally rotated so that one hand of the examiner can control valgus moments. The examination begins with the humerus stabilized and the elbow in flexion. With one hand on the patient’s wrist, the forearm is supinated while the other hand is used to apply a valgus moment with a slight axial load to the elbow joint. Slow extension of the elbow may result in an apprehension response (a sense of instability) or guarding by the patient; with flexion > 40°, reduction of the ulna and the radial head occurs, sometimes with a sudden, visible, and palpable clunk. Joint reduction may also be achieved by forearm pronation. The test is difficult to elicit in patients who are not anesthetized. Guarding and apprehension constitute a positive response in an awake patient. In the postero-lateral rotatory drawer test [12], the patient is supine, with the affected limb overhead and the elbow flexed 40°. Antero-posterior force is applied to the radius and ulna with the forearm in ER. The examiner tries to detach the forearm away from the humerus on the lateral side, pivoting on the intact medial ligaments. Under general anesthesia, the radial head dislocates, whereas with the patient awake there is apprehension. The table-top relocation test [13] is carried out with the patient performing a press-up on the edge of a table using one arm, with the forearm in supination. In the presence of instability, apprehension occurs at about 40° flexion. The maneuver is repeated while the examiner’s thumb presses on the radial head, preventing subluxation. The test is positive if thumb pressure relieves apprehension.

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Fig. 14.4 Lateral pivot shift test (a) and chair sign (b) for posterolateral rotatory instability


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In the active floor push-up test [14], the patient attempts to push up from a prone position with both forearms maximally supinated, and then repeats this with both forearms maximally pronated. The test is positive if symptoms occur with the forearms supinated but not pronated. In the chair sign [14], the patient is seated with elbows flexed 90°, forearms supinated, and arms abducted. He or she then tries to rise from the chair, pushing down only with the arms (Fig. 14.4b). The test is positive if apprehension or radial head dislocation occurs with elbow extension.

14.2.6 Specific Tests The hook test is performed to assess the integrity of the distal biceps tendon [15]. The elbow is flexed 90° and the forearm fully supinated actively to the end-point of supination. If the biceps tendon is intact, it is possible to fully insert the finger under its lateral edge for about 1 cm or more depending on the relative size of the patient’s muscles and the examiner’s finger. The finger passes between the biceps tendon and underlying brachialis muscle. With complete avulsion of the distal biceps tendon, the hook test is abnormal, as indicated by the absence of a cord-like structure spanning the antecubital fossa behind which the examiner’s finger is otherwise hooked. Physical examination of patients with lateral epicondylitis (tennis elbow) reveals local tenderness at the origin of the extensor muscles at the lateral epicondyle, specifically, the tendinous origins of the extensor carpi radialis brevis and extensor digitorum communis. The maximum point of tenderness is usually located within a finger’s breadth anterior and distal to the lateral epicondyle. Pain can be elicited in the region of the lateral epicondyle and the proximal extensor on resisted wrist extension (Cozen test), resisted extension of the long finger, and resisted supination of the forearm (Mill’s test). Grasping in a position of elbow extension usually elicits pain. In the chair test, the patient is asked to lift a chair with one hand in a position of forearm pronation and wrist palmar flexion. Severe pain in the region of the lateral epicondyle is experienced by all those with tennis elbow. Patients with medial epicondylitis present with tenderness to palpation over the anterior aspect of the medial epicondyle. Some may have tenderness just distal to the medial epicondyle over the flexor-pronator tendinous bands. Pain over the medial epicondyle should be worse with resisted wrist flexion and pronation. In the medial epicondylitis test, the patient holds the elbow at 30° flexion with the wrist flexed. The examiner asks the patient to maintain the wrist in flexion and push against the palm of the hand. The test is positive if pain is elicited. In addition, the neurological examination is very important. The detection or exclusion of an ulnar neuropathy requires that the examiner determine the presence of Tinel’s sign between the olecranon and medial epicondyle.

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References 1. Kibler WB, Uhl TL, Maddux JWQ et al (2002) Qualitative clinical evaluation of scapular dysfunction: a reliability study. J Shoulder Elbow Surg 6:550-556 2. Castagna A, Nordenson U, Garofalo R, Karlsson J (2007) Minor shoulder instability. Arthroscopy 23:211-215 3. Kim SH, Park JS, Jeong WK et al (2005) The Kim test a novel test for posteroinferior labral lesion of the shoulder – a comparison to the jerk test. Am J Sports Med 33:1188-1192 4. Gagey O, Gagey N (2001) The hyperabduction test: an assessment of the laxity of the inferior glenohumeral ligament. J Bone Joint Surg Br 83:69-74 5. O’Brien SJ, Pagnani MJ, Fealy S et al (1998) The active compression test: a new and effective test for diagnosing labral tears and acromioclavicular joint abnormality. Am J Sport Med 26:610-613 6. Myers TH, Zemanovic JR, Andrews JR (2005) The resisted supination external rotation test: A new test for the diagnosis of superior labral anterior posterior lesions. Am J Sports Med 33:1315-1320 7. Castoldi F, Blonna D, Hertel R (2009) External rotation lag sign revisited: accuracy for diagnosis of full thickness supraspinatus tear. J Shoulder Elbow Surg 18:529-534 8. Barth J, Burkhart SS, De Beer J (2006) The bear-hug test: a new and sensitive test for diagnosing a subscapularis tear. Arthroscopy 22:1076-1084 9. Spinner R, Goldner R (1998) Snapping of the medial head of the triceps and recurrent dislocation of the ulnar nerve. J Bone Joint Surg 80:239-247 10. Safran MR, McGarry MH, Shin S (2005) Effects of elbow flexion and forearm rotation on valgus laxity of the elbow. J Bone Joint Surg Am 87:2065-2074 11. O’Driscoll SW, Bell DF, Morrey BF (1991) Postero-lateral rotatory instability of the elbow. J Bone Joint Surg Am 73:440-446 12. O’Driscoll SW, Jupiter JB, King GJW et al (2000) The unstable elbow. J Bone Joint Surg Am 82:724-737 13. Arvind CH, Hargreaves DG (2006) Tabletop relocation test: a new clinical test for posterolateral rotatory instability of the elbow. J Shoulder Elbow Surg 15:707-708 14. Regan W, Lapner PC (2006) Prospective evaluation of two diagnostic apprehension signs for postero-lateral instability of the elbow. J Shoulder Elbow Surg 15:344-346 15. O’Driscoll SW, Goncalves LBJ, Dietz P (2007) The hook test for distal biceps tendon avulsion. Am J Sports Med 35:1865-1869

Shoulder Injuries in the Throwing Athlete

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S. Cheung, C.B. Ma

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Abstract An understanding of the fundamentals of the throwing motion is essential in order to accurately diagnose and treat shoulder disorders of overhead-throwing athletes. Improper throwing technique or fatigue of any muscles along the kinetic chain leads to muscular imbalance and injury over time. In particular, fatigue of the shoulder-girdle stabilizers can lead to scapular dyskinesia and thus to impingement. Anterior shoulder pain during cocking and acceleration is associated with anterior shoulder instability or impingement, whereas pain during deceleration and follow-through suggests posterior shoulder pathology. Microinstability and repetitive shear stresses often result in pathologic anterior capsule laxity and posterior capsule contracture, all of which contribute to secondary and internal impingement, and subsequently to SLAP tears and partialthickness articular-sided rotator cuff tears. In the pediatric population, the growth plate is comparatively weaker and thus vulnerable to injury from repetitive microtrauma.

15.1 Introduction Elite pitchers and throwers experience a tremendous amount of repetitive stress in the shoulder, leading to unique pathologies that are associated with overhead throwing. The high angular velocity and large forces that are generated require coordinated muscle control to maintain stability and prevent injury. It is important that the clinician understand the fundamental biomechanics of throwing in order to recognize and address the pathologic states that bring a throwing athlete to medical attention. This chapter covers the basics of the throwing motion, anatomic adaptations to the repetitive stress, prevention and rehabilitation, as well as common pathologies and their management, including glenohumeral internal rotation deficit, scapular dyskinesia, SLAP tears, impingement, rotator cuff tears, and Little League shoulder. Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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15.2 Biomechanics of Throwing The kinematics of baseball pitching has been studied extensively and serves as a model for basic throwing mechanics. The act of throwing is a coordinated total body activity designed to transmit energy sequentially from the lower body to the upper body and ultimately to the ball. It can be conceptualized as a kinetic chain from the toes to the fingertips. The leg and trunk provide a stable base for arm motion and generate 50-55% of the force. Inflexibility or weakness in the hip or trunk may lead to increased lumbar lordosis during acceleration, thus placing the throwing arm “behind” the body and to increased posterior compression loads on the shoulder [1]. Throwing requires precise control of the dynamic stabilizers (rotator cuff, scapulothoracic muscles, long head of the biceps) in conjunction with the static restraints (glenoid curvature, labrum, capular ligaments) in order to generate a tremendous amount of force over the short time span required for throwing. Thus, even small alterations in any component along the kinetic chain (including the trunk and lower limb girdle) can lead to a significant and cumulative effect on the shoulder and, consequently, to injury and loss of maximal throwing velocity. The throwing motion can be divided into six phases, and usually takes < 2 s to complete (Fig. 15.1). The first phase is the wind-up phase, which can vary between individuals. In general, the stride foot (left for right-handed throwers) coils backward and weight is shifted onto the pivot (right) foot. This phase ends as the body is balanced on the pivot foot. The second phase is the early cocking phase. The pivot leg extends (pushes off), driving the stride leg, trunk, and non-dominant upper extremity forward. Meanwhile, the dominant upper extremity lags behind temporarily, but the trapezius muscle rotates the scapula, placing it in a stable position for the abducted humeral head. This phase ends when the stride foot hits the ground. Very few pathological conditions arise during the first two phases [2, 3]. In the third phase, or late cocking phase, the scapula protracts and rotates upward to allow the humerus to reach maximal external rotation. Anterior shoulder instability and elbow

Fig. 15.1 The six phases of throwing: wind-up, early cocking, late cocking, acceleration, deceleration, and follow-through

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medial instability may sometimes manifest during this phase [4]. The first three phases take approximately 1.5 s. The fourth phase, acceleration, takes only 0.05 s but the greatest torque is generated, accounting for most of the shoulder (and elbow) injuries. During this phase, the pectoralis major, latissimus dorsi, and subscapularis muscles all concentrically contract, internally rotating the shoulder at an angular velocity between 6100 and 7000°/s in elite pitchers, with a torque of 14,000 inch-pounds [5]. Anterior subluxation of the shoulder may occur during the acceleration phase. At ball release, professional pitches may experience distractive forces of up to 950 N [6]. Acceleration ends as the ball is released. In the fifth phase, deceleration, the remaining kinetic energy must be absorbed by the arm and body. The angular deceleration is about 500,000°/s, with an external rotation torque of about 15,000 inch-pounds [5, 7]. The rotator cuff and deltoid muscle generate compressive forces around 1090 N and posterior shear forces of 400 N [6]. As a result, the posterior shoulder stabilizers are more commonly injured during this phase. In the last phase, follow-through, the body rebalances until motion stops. These final two phases last approximately 0.35 s.

15.3 Adaptations and Maladaptations to Throwing As the body experiences repetitive stresses from throwing, the bones and soft tissues react to the increased load. An increased sulcus sign is often present, with the skin dimpling underneath the acromion with increased inferior traction [8]. Bone mineral density increases [9] and the humeral head becomes more retroverted by about 10° (36° in the dominant arm vs. 26° in the non-dominant arm). The increased retroversion and soft-tissue remodeling increase the maximum external rotation by about 10°, while the maximum internal rotation decreases; however, the total arc of motion remains the same (usually 180°) [10, 11]. This is known as glenohumeral internal rotation deficit (GIRD). Contractures develop in the posterior capsule and in the posterior band of the inferior glenohumeral ligament [12]. As the posterior capsule contracts, it acts as a checkrein during external rotation, and the humeral head’s center of rotation shifts posterior/superior, which may lead to the “peel-back” mechanism of a SLAP tear [13]. In addition, it is believed that forward flexion with a contracted posterior capsule causes obligate anterior/superior translation of the humeral head and thus “non-outlet” impingement of the rotator cuff despite normal acromial morphology [12]. GIRD is considered to be clinically relevant when the loss of internal rotation on the dominant arm is greater than 25° compared to the non-dominant side. In most cases, 90% of athletes will respond to a 2-week course of stretching, including the “sleeper stretch” and “cross body stretch” (Fig. 15.2) [14, 15]. A recent study shows that the cross-body stretch yields greater improvements in internal rotation than the sleeper stretch [16]. The minority 10% of throwers with GIRD who do not respond to stretching are usually older elite pitchers who have been throwing for years and have chronic symptoms, including type 2 posterior SLAP tears. These patients may benefit from arthroscopic posterior capsule release. Typical findings at surgery include a severely contracted posterior band of the inferior glenohumeral ligament, which is usually 6 mm thick or more. Release will increase the internal rotation to about 65° [1].

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a

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Fig. 15.2 a Cross-body adduction stretch; b the sleeper stretch

15.4 SICK Scapula Other maladaptations to the stress of throwing may occur in the scapula and the different steps of the kinetic chain. Burkhart and Kibler coined the acronym SICK syndrome (scapular malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis of scapular movement) in reference to the overuse muscular fatigue syndrome seen in throwing athletes with dead arm complaints. As the name implies, the main feature of this syndrome is a malposition of the scapula, which shifts such that it is more inferior than the other shoulder. This results in a dynamic imbalance during the throwing motion, causing labral pathology, impingement, and rotator cuff lesions. The scapula is protracted, and the inferior medial border becomes prominent. The coracoid tilts inferiorly and shifts laterally, tightening the pectoralis minor and causing tenderness at its insertion on the coracoid. Although patients may present with a variety of pain symptoms, the most common is anterior shoulder pain near the coracoid; the next most common is posterior/superior scapular pain with or without radiation to the paraspinous neck. The scapular retraction test is positive if the patient is able to achieve full forward flexion without coracoid pain when the examiner manually places the scapula in retraction and posterior tilt. Treatment of the SICK scapula focuses on strengthening the scapular stabilizers and stretching the tight structures, namely, the pectoralis minor and the posterior capsule associated with GIRD [1].

15.5 Rehabilitation The vast majority of shoulder injuries in throwers can be successfully treated non-surgically, with proper conditioning and rehabilitation to include the entire kinetic chain. This


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can be achieved with a phased protocol [17]. The first phase, or the acute phase, concentrates on decreasing pain and inflammation, normalizing range-of-motion deficits, and allowing injured tissues to heal. Nonsteroidal anti-inflammatories, passive range of motion, active-assisted exercises, and various modalities may be employed. The second phase consists of strengthening and specific stretching regimens to restore the patient’s pre-injury range of motion. Once the patient has regained rotator cuff and scapular strength, as well as motion, in the absence of pain, apprehension, or other clinical signs, then he/she may advance to the third phase. This includes intensive strengthening, endurance, plyometrics, and an interval throwing program (varying the distances, intensities, rest periods, and throwing on or off the baseball mound) [18]. In NCAA division I baseball players, an 8-week plyometric program was shown to yield higher throwing velocities than obtained with general shoulder conditioning [19]. The fourth phase is an advanced interval throwing program with position-specific throwing, while maintaining strength and neuromuscular control. If there is no improvement after 3 months or an inability to play competitively after 6 months, then an additional work-up or surgical intervention should be considered [3].

15.6 Conditioning and Injury Prevention A proper year-round conditioning program can help prevent injuries. Numerous programs exist; a good sample program in the off-season includes throwing 5 days per week at half speed and resting the other 2 days, with a maximum of 120 pitches per day. During the season, a sample 4-day program would start on day 1 with the pitcher pitching the game. On day 2, he rests but is allowed some light exercises and gentle throwing. On day 3, he throws the ball lightly, 40 feet at half speed. On day 4, he throws from the mound no more than 15 min and does conditioning exercises for the whole body in preparation for the next day’s game [2, 20].

15.7 Microinstability Microinstability refers to an acquired excess laxity in the shoulder due to the repetitive shear stresses generated during cocking and acceleration In contrast to shoulder instability, patients do not complain of frank subluxation or apprehension; however, the pathologic laxity leads to abnormal joint translation and rotation. As a result, the acquired anterior capsular laxity and posterior contractures shift the humeral head from its center of rotation, causing pain and injury during the throwing motion, including articular-sided partial rotator cuff tears, internal and non-outlet impingements, and SLAP lesions [3].

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15.8 Superior Labrum Anterior/Posterior (SLAP) Tear Injuries to the superior labrum and biceps tendon are often experienced by throwing athletes. The current model of injury leading to SLAP tears is the “peel-back” mechanism. During late cocking, at abduction and maximum external rotation, posterior rotation of the humeral head “peels” the biceps anchor and superior labrum off of the superior glenoid (Fig. 15.3) [21]. Snyder et al. first classified these injuries into four types (Fig. 15.4).

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Fig. 15.3 a Superior view of resting position of biceps-labral complex. b Superior view of bicepslabral complex in abducted-externally rotated position, showing peel-back mechanism as the biceps vector rotates posteriorly. (Reprinted from [21] with permission from Elsevier)

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Fig. 15.4 Four basic SLAP lesions. a Type I: the superior labrum is degenerative and frayed, but the peripheral edge and biceps anchor is attached to the glenoid. b Type II: an unstable superior labrum and biceps anchor is detached from the underlying glenoid. c Type III: an unstable bucket-handle tear of the superior labrum in which the central portion displaces into the joint, but the peripheral labrum and biceps anchor remain attached to the glenoid. d Type IV: an unstable bucket-handle tear similar to a type III lesion, but the tear extends into the biceps anchor. (Reprinted from [22] with permission from Elsevier)


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A type I tear is a marked fraying and degeneration of the superior labrum, but the peripheral labral edge and biceps anchor remain intact. In a type II tear, the superior labrum and biceps anchor are completely detached from the glenoid. A type III tear consists of a bucket-handle tear in which the central portion displaces into the joint, while the periphery remains attached. A type IV tear consists of a type III tear extending partially into the biceps tendon, which displaces along with the torn superior labrum into the joint [22]. Since Snyder’s original classification, several modifications have been proposed. Morgan et al. described three type II SLAP variants, anterosuperior, posterosuperior, and a combined anterior and posterior lesion, and noted that partial or full articular-sided rotator cuff tears occurred in 31% of shoulders with type II SLAP lesions [23]. Maffet et al. added three additional SLAP grades. A type V SLAP is an anterior-inferior Bankart lesion that continues superiorly to include separation of the biceps tendon and superior labrum. A type VI SLAP is an unstable flap tear of the labrum in addition to the biceps tendon separation. A type VII SLAP tear is a separation of the superior labrum and biceps that extends anteriorly beneath the middle glenohumeral ligament. These authors also found that 43% of SLAP tears had, in addition, increased humeral head translation and glenohumeral instability [24]. Symptoms of SLAP tears include pain in the posterosuperior joint line, locking, snapping, pain during late cocking, and decreased pitch velocity. A positive Speed’s test and bicipital groove pain together have a high sensitivity for anterior SLAP lesions (100%), while the Jobe relocation test has a high sensitivity for posterior SLAP lesions (85%), and the O’Brien’s test a high sensitivity for combined anterior/posterior SLAP lesions (85%) [23]. Standard magnetic resonance imaging (MRI) without contrast is helpful in the diagnosis of labral tears but the sensitivity varies between 62 and 95%. The addition of gadolinium intra-articular contrast can enhance the diagnostic accuracy of SLAP tears to 100% sensitivity and 88% specificity [25]. Surgical intervention is indicated if the patient fails conservative management. Type I SLAP tears can be simply debrided. Type II SLAP tears should include debridement and securing the biceps-labral complex to the glenoid. Type III tears can be debrided, and acute type IV tears repaired. Type IV tears with significant degeneration may be debrided and the biceps tenodesed.

15.9 Sublabral Variants It is important to realize that normal anatomic variations are commonly seen in the 11to 3-o’clock positions (viewing the glenoid as a clock face, with the 3-o’clock position anterior by convention). Attempting to “repair” these otherwise normal variants will cause excess tightening and pain in the shoulder. These include the sublabral recess (or sulcus), located between the 11- to 1-o’clock position. This is a recess between the biceps-labral complex and the superior glenoid cartilage, with a prevalence of 73%. In a cadaveric study of shoulders with this recess, only 17% were less than 20 years old, 50% were 20 years or older, and 95% were ages 70-89. The sublabral foramen, found at the 1- to 3-o’clock position, is a space between the anterosuperior labrum and adjacent glenoid cartilage, with

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a prevalence estimated between 11 and 15%. The Buford complex is a rare absent anterosuperior labrum with an associated cordlike middle glenohumeral ligament, with a prevalence of 1.5% [26]. A relatively simple rule of thumb regarding MRI to determine whether a labral lesion is pathologic or a normal variant is to look at the level of the coracoid on the axial view. If the anterior labrum appears detached on an axial view above the level of the coracoid, this is most often a normal variant.

15.10 Impingement Throwers may experience impingement from a variety of sources. “Classic” subacromial impingement, between the hooked coracoacromial arch and the humeral head, tends to occur in older athletes, who do not have the increase in external rotation arc seen in GIRD [27]. Treatment for throwers with this type of impingement is no different than for any other patient. Failure of physical therapy is an indication for surgical decompression. While in most non-throwers the results after this procedure alone are highly satisfactory (92-95%), throwing athletes and pitchers have lower satisfaction rates of 68% and 50%, respectively [28]. This suggests that only rarely is “classic” subacromial impingement the sole cause of pathology in a throwing athlete’s shoulder; rather, the surgeon should diligently rule out other causes of pathology that might have been overlooked in the initial work-up. Secondary impingement, or “non-outlet” impingement, most often occurs due to a tight posterior capsule (GIRD) that alters the center of rotation, causing obligate anterior-superior translation of the humeral head against a normal acromion [12]. The treatment is similar to that of GIRD, involving physical therapy for posterior capsular stretching and surgical release if that fails. Another cause of secondary impingement can be due to the SICK scapula syndrome, as excess scapular protraction leads to an inability to “clear” the acromion away from the humeral head during overhead motion [1]. Treatment should focus on physical therapy to rehabilitate the shoulder dyskinesia. Finally, “internal impingement” occurs as the undersurface of the rotator cuff is pinched between the posterior glenoid labrum and the humeral head as the shoulder is abducted and excessively externally rotated in the late cocking phase. It is believed that, during the acceleration phase of throwing, fatigue of the shoulder girdle muscles allows the humeral head to drift out of alignment with the scapula, causing tensile stress on the anterior capsule and hence pathologic anterior translation. Over time, the repetitive microtrauma gives rise to a variety of other problems, including SLAP tears and partial-thickness articular rotator cuff tears [3, 28-30]. Treatment focuses on scapula rehabilitation, proper throwing technique, and surgical intervention as warranted for any labral or rotator cuff tears.

15.11 Rotator Cuff Tears As noted in the section on impingement, tensile overload and repetitive stresses can lead to eccentric failure of the dynamic stabilizers. Throwers may incur partial-thickness ar-


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ticular-sided tears, usually at the junction of the supraspinatus and infraspinatus insertions [31]. MR-arthrograms can demonstrate delamination of the posterior/superior rotator cuff tendons. Partial tears of the superior subscapularis may also lead to biceps subluxation and anterior shoulder pain. As in the treatment of non-throwers, initial management of partial tears includes physical therapy, stretching, and strengthening the rotator cuff. Results of arthroscopic debridement and bursectomy for partial rotator cuff tears have been mixed for throwing athletes under age 40. Andrews et al. reported 85% good/excellent results in the short term, with an average of 13.1 months of follow-up in a cohort of competitive athletes (64% of whom were baseball pitchers). However, of the failures, 60% (3 of 5 patients) were professional pitchers [32]. Payne et al. reported similar results; although patients with acute injures tended to fare better (86% satisfaction and 64% returning to pre-injury sports). Those with chronic symptoms had worse outcomes, with only 66% satisfaction and 45% returning to pre-injury sports [33]. Professional and college pitchers treated with an open approach fared even worse; only 32% of patients with partial tears had good outcomes (defined as returning to competition with minimal pain) while 56% of the patients with repaired full-thickness tears had good results [34]. Full-thickness tears in professional baseball players are rare but devastating injuries. In a series of 16 such cases, Mazoué and Andrews performed a mini-open double row repair with an average follow-up of 67 months. Only 8% of the pitchers returned to full professional pitching without symptoms, and 50% did not play longer than a half season professionally. Although they regained good pitch velocity and control, they cited early fatigue and prolonged recovery between games as the primary reason for retiring. Not surprisingly, position players undergoing repair in the dominant arm fared better, with 50% returning to competition. The best results were observed in position players with a repair in their non-dominant shoulder, of whom 100% returned to competition [35]. Based on these studies, repair of full-thickness rotator cuffs in the elite overhead athlete should be approached with caution, as it is difficult to precisely restore the shoulder’s set point and hence throwing mechanics. Fortunately, the 2-year results following the repair of full-thickness tears in older recreational and amateur overhead athletes are much better and comparable to those of the general population. In a comparison of single-row repairs in this cohort (average age: 58.9) vs. in a similar cohort of non-overhead throwing athletes, Liem et al. noted an improvement in the constant score from 54.9 to 84.2 and in the re-tear rate (23.8%), both of which were similar to the results in the non-overhead cohort. All 21 of the overheadthrowing athletes returned to sporting activity at an average of 6.3 months. At the time of final follow-up, their overall activity level was 91.9% of the original healthy condition. In contrast to professional athletes, favorable prognostic factors included surgery on the dominant arm. Interestingly, of the overhead-throwing athletes who had re-tear on repeat MRI, 60% of them returned to full sporting activity (swimming, golf, and volleyball), but the remaining 40%, both tennis players, were only able to return to 50 and 60%, respectively, of their pre-injury level. Still, the re-tear group overall did not have a significant difference in sporting activity levels compared to the intact repair group [36]. Although these short-term results are encouraging, the long-term results of recreational overhead-throwing athletes who have re-torn their rotator cuff repair remain to be determined.

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15.12 Baseball Injuries in the Pediatric Population Shoulder injuries in children and teenagers may include tendonitis of the rotator cuff, glenohumeral instability and subluxation, and growth plate injuries, also known as “Little League shoulder”. Other nomenclatures for “Little League shoulder” include osteochondrosis of the proximal humeral epiphysis, proximal humeral epiphysiolysis, or rotational stress fracture of the proximal humeral epiphyseal plate. First recognized in 1953, this injury to the growth plate often presents as pain during throwing in the proximal humerus, with 70% of patients having lateral proximal humerus tenderness. Plain radiographs show widening of the proximal humeral epiphysis, with possible demineralization, sclerosis, or fragmentation of the proximal humeral metaphysis. Biomechanical studies suggest that repetitive rotational torque on the epiphysis, rather than distractive force, is the underlying cause [37]. Treatment with rest from baseball for 3 months followed by a gradual return to throwing once asymptomatic yields a 91% success rate of returning to competitive play [38].

15.13 Conclusions In the pediatric population, the growth plate is comparatively weaker and thus vulnerable to injury with repetitive microtrauma. In these situations, activity modification is all that is required for resolution of symptoms. For adults, it is essential to understand the fundamentals of the throwing motion in order to accurately diagnose and treat shoulder disorders of overhead-throwing athletes. Improper throwing technique or fatigue of any muscles along the kinetic chain leads to muscular imbalance and thus to injury over time. In particular, fatigue of the shoulder-girdle stabilizers can result in scapular dyskinesia and thus to impingement. Fortunately, rehabilitation of the scapula stabilizers and attention to proper throwing mechanics can yield excellent results. Microinstability and repetitive shear stresses from throwing often cause pathologic anterior capsule laxity and posterior capsule contracture. This can result in anterior shoulder pain during cocking and acceleration (due to anterior shoulder instability or impingement). Microinstability may also be the source of pain during deceleration and follow-through (usually associated with posterior shoulder pathology). Consequently, microinstability is an underlying cause of secondary and internal impingement, and thus potentially of SLAP tears and partial-thickness articular-sided rotator cuff tears. Physical therapy, including capsular stretching and strengthening of the rotator cuff muscles, should be the mainstay of treatment in these conditions as it addresses the underlying pathology. Surgical management should be considered in symptomatic SLAP lesions and rotator cuff tears that have failed conservative management. Although uncommon, full-thickness rotator cuff tears are devastating injuries for overhead-throwing athletes and most elite players are unable to return to their pre-injury level after repair. Fortunately, older recreational overhead-throwing athletes have a much better prognosis with a repair of full-thickness rotator cuff tear.


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References 1. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder: spectrum of pathology part III: the SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19:641-661 2. Petrie RS, Klimkeweicz JJ, Harner CD (2001) Baseball injuries. In: Fu F, Stone Da (eds) Sports injuries, 2nd edn. Lippincott, Philadelphia, pp 279-300 3. Braun S, Kokmeyer D, Millett PJ (2009) Shoulder injuries in the throwing athlete. J Bone Joint Surg Am 91:966-978 4. Jobe F, Bradley J (1988) Rotator cuff injuries in baseball: prevention and rehabilitation. Sports Med 6:337-387 5. Gainor BJ, Piotrowski G, Puhl J et al (1980) The throw: biomechanics and acute injury. Am J Sports Med 8:114-118 6. Kuhn JE, Lindholm SR, Huston LJ (2000) Failure of the biceps-superior labral complex (SLAP lesion) in the throwing athlete: a biomechanical model comparing maximal cocking to early deceleration. J Shoulder Elbow Surg 9:463 7. Pappas A, Zawack R, Sullivan T (1985) Biomechanics of baseball pitching. Am J Sports Med 13:216-222 8. Neer CS, Foster CR (1980) Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J Bone Joint Surg Am 62:897-908 9. Calbet JA, Diaz Herrera P, Rodriguez LP (1999) High bone mineral density in male elite professional volleyball players. Osteoporosis Int 10:468-474 10. Reagan KM, Meister K, Horodyski MB et al (2002) Humeral retroversion and its relationship to glenohumeral rotation in the shoulder of college baseball players. Am J Sports Med 30:354-360 11. Sethi PM, Tibone JE, Lee TQ (2004) Quantitative assessment of glenohumeral translation in baseball players. Am J Sports Med 32:1711-1715 12. Ticker JB, Beim GM, Warner JJ (2000) Recognition and treatment of refractory posterior capsular contracture of the shoulder. Arthroscopy 16:27-34 13. Grossman MG, Tibone JE, McGarry MH et al (2005) A cadaveric model of the throwing shoulder: a possible etiology of superior labrum anterior-to-posterior lesions. J Bone Joint Surg Am 87:824-831 14. Lintner D, Mayol M, Uzodinma O et al (2007) Glenohumeral internal rotation deficits in professional pitchers enrolled in an internal rotation stretching program. Am J Sports Med 35:617-621 15. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder: spectrum of pathology. Part I: pathoanatomy and biomechanics. Arthroscopy 19:404-420 16. Balaicuis J, Heiland D, Broersma ME et al (2007) A randomized controlled comparison of stretching procedures for posterior shoulder tightness. J Orthop Sports Phys Ther 37:108114 17. Ellenbecker TS (ed) (2006) Shoulder rehabilitation. Non-operative treatment. Thieme, NewYork 18. Wilk KE, Meister K, Andrews JR (2002) Current concepts in the rehabilitation of the overhead throwing athlete. Am J Sports Med 30:136-151 19. Carter AB, Kaminski TW, Douex AT Jr et al (2007) Effects of high volume upper extremity plyometric training on throwing velocity and functional strength ratios of the shoulder rotators in collegiate baseball players. J Strength Cond Res 21:208-215 20. McConnell ME (1960) How to play Little League baseball. Ronald, New York 21. Burkhart SS, Morgan CD (1998) The peel-back mechanism: its role in producing and extending posterior type II SLAP lesions and its effect on SLAP repair rehabilitation. Arthroscopy 14:637-640 22. Snyder SJ, Karzel RP, Del Pizzo W et al (1990) SLAP lesions of the shoulder. Arthroscopy 6:274-279

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23. Morgan CD, Burkhart SS, Palmeri M et al (1998) Type II SLAP Lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14:553-565 24. Maffet MW, Gartsman GM, Moseley B (1995) Superior labrum-biceps tendon complex lesions of the shoulder. Am J Sports Med 23:93-98 25. Applegate GR, Hewitt M, Snyder SJ et al (2004) Chronic labral tears: value of magnetic resonance arthrography in evaluating the glenoid labrum and labral-bicipital complex. Arthroscopy 20:959-963 26. Mohana-Borges AVR, Chung CB, Resnick D (2003) Superior labral anteroposterior tear: classification and diagnosis on MRI and MR arthrography. Am J Roentgenol 181:1449-1462 27. Roye RP, Grana WA, Yates CK (1995) Arthroscopic subacromial decompression: two to seven-year follow-up. Arthroscopy 11:301-306 28. Jobe CM (1995) Posterior superior glenoid impingement: expanded spectrum. Arthroscopy 11:530-536 29. Paley KJ, Jobe FW, Pink MM et al (2000) Arthroscopic findings in the overhand throwing athlete: evidence for posterior internal impingement of the rotator cuff. Arthroscopy 16:35-40 30. Jobe CM, Pink MM, Jobe FW et al (1996) Anterior shoulder instability, impingement, and rotator cuff tear: theories and concepts. In: Jobe FW (ed) Operative techniques in upper extremity sports injuries. Mosby, St. Louis, pp 164-176 31. Walch G, Boileau P, Noel E et al (1992) Impingement of the deep surface of the supraspinatus tendon on the posterosuperior glenoid rim: an arthroscopic study. J Shoulder Elbow Surg 1:238-245 32. Andrews JR, Broussard TS, Carson WG (1985) Arthroscopy of the shoulder in the management of partial tears of the rotator cuff: a preliminary report. Arthroscopy 1:117-122 33. Payne LZ, Altchek DW, Craig EV et al (1997) Arthroscopic treatment of partial rotator cuff tears in young athletes. A preliminary report. Am J Sports Med 25:299-305 34. Tibone JE, Elrod B, Jobe FW et al (1986) Surgical treatment of tears of the rotator cuff in athletes. J Bone Joint Surg Am 68:887-891 35. Mazoué CG, Andrews JR (2006) Repair of full-thickness rotator cuff tears in professional baseball players. Am J Sports Med 34:182-189 36. Liem D, Lichtenberg S, Magosch P et al (2008) Arthroscopic rotator cuff repair in overheadthrowing athletes. Am J Sports Med 36:1317-1322 37. Sabick MB, Kim Y-K, Torry MR et al (2005) Biomechanics of the shoulder in youth baseball pitchers: implications for the development of proximal humeral epiphysiolysis and humeral retrotorsion. Am J Sports Med 33:1716-1722 38. Carson WG, Gasser SI (1998) Little Leaguer’s shoulder. A report of 23 cases. Am J Sports Med 26:575-580

Shoulder Instability

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F. Castoldi, D. Blonna, M. Cravino and M. Assom

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Abstract Glenohumeral instability accounts for a significant proportion of shoulder diseases and depends on osseous and ligamentous deficiencies. Many different classifications have been proposed for glenohumeral joint instability, based on direction, etiology, degree of instability, number of episodes, or a combination of any of these features. The treatment of choice should depend on the results of a careful physical examination and a complete imaging study and includes both rehabilitative and surgical programs. This chapter focuses on the different types of instability, anterior, posterior, multidirectional, and minor, and evaluates their etiologies, pathological findings, and appropriate treatment.

16.1 Introduction Instability of the shoulder comprises a wide spectrum of pathologies. In the past, the literature focused on anterior instability but over time attention has been increasingly paid to recurrent subluxation as well as to posterior and multidirectional instabilities. A careful history, complete physical examination, and correct imaging are the keys to an accurate diagnosis. Glenohumeral stability is the result of static and dynamic forces that maintain the articulation of the humeral head with the glenoid while simultaneously providing for a large range of motion (ROM). The static stabilizers include the labrum, glenohumeral ligaments, coracohumeral ligament, and rotator interval capsule. Dynamic stability is guaranteed by the rotator cuff, deltoid, and biceps tendon through a concavity compression effect on the humeral head within the glenoid socket [1]. Instability of the shoulder is the result of a dysfunction or rupture of one or more of these structures leading to symptomatic conditions such as dislocation, subluxation, pain, and decreased performance. Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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Fig. 16.1 The capsule and the glenohumeral ligaments. PC, Posterior capsule; SGHL, superior glenohumeral ligament; MGHL, middle glenohumeral ligament; IGHL, inferior glenohumeral ligament (anterior band, posterior band)

Articulation is guaranteed by several mechanisms, such as the maintenance of negative intra-articular pressure and concavity compression, both of which contribute to glenohumeral stability. The strength of the rotator cuff is such that it compresses the humeral head into the glenoid, maintaining stability particularly in the mid-ranges of motion. The labrum increases the concavity of the glenoid; if it is excised, the concavity-compression force is reduced by 50%. The capsule and the glenohumeral ligaments are the most effective stabilizers of the glenohumeral joint at the end ranges of motion. In rotator cuff disorders, the concavity compression mechanism is insufficient and the ligament complexes become the most important stabilizers. The anterior band of the inferior glenohumeral ligament (IGHL) limits anterior translation of the humeral head at 90° of abduction. When the degree of abduction decreases, the role of the anterior band of this ligament becomes less important while the middle glenohumeral ligament (MGHL) takes on a more important role as an anterior restraint. The MGHL is recognized as an important secondary restraint to both inferior and anterior translations [2]. Another important area that contributes significantly to shoulder stability is the anterior-superior quadrant of the glenohumeral joint, which includes the MGHL, superior glenohumeral ligament (SGHL), coracohumeral ligament, and the rotator interval capsule [3]. The SGHL resists anterior and superior translation of the humeral head in shoulder flexion and lesser degrees of abduction and it also has an important function in posterior and inferior stability (Fig. 16.1).

16.2 Classification In evaluations of shoulder pathology, laxity must be distinguished from instability. The term instability is generally reserved for symptomatic shoulders. The condition is defined as a pathological joint translation that can cause symptoms such as dislocation, discomfort, pain, and reduced performance. An exception to this definition is the pathological

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displacement of the humeral head, which becomes fixed superiorly, anteriorly, or posteriorly relative to its normal position on the glenoid. Displacement in any of these positions may be asymptomatic. Laxity is defined as asymptomatic excessive translation (or hypermobility) of the humeral head. Individuals may have significant laxity and yet remain asymptomatic. Conversely, others with only a minimal degree of mobility of the shoulder may have significant symptoms of instability. Many different classifications of glenohumeral joint instability have been proposed based on direction, etiology, degree of instability (subluxation/ dislocation), number of episodes, or a combination of any of these features. Before the introduction of the term multidirectional instability, by Neer and Foster [4, 5], instability usually was considered to be either anterior or posterior. Multidirectional instability was then described as a problem caused, presumably, by enlargement of the capsule due to genetic factors and/or microtrauma. Traditional classification systems define three distinct groups of instabilities based on their etiology and treatment: (1) TUBS: traumatic, unidirectional, associated with a Bankart lesion that frequently requires surgical treatment; (2) AMBRI: atraumatic, multidirectional, usually bilateral and requiring rehabilitation or, when it fails, a surgical inferior capsular shift; (3) AIOS: an acquired instability caused by overstress of the shoulder, such as in the case of throwing athletes, and usually requiring surgical treatment. This simple classification, however, does not cover all the pathological conditions related to shoulder instability. A more complex and complete classification is that described by Gerber and Nyffeler, which divides shoulder instabilities into three groups: static, dynamic, and voluntary [6]. Static instability (class A) is characterized by the absence of classic symptoms; the humeral head is displaced and fixed superiorly, anteriorly, or posteriorly relative to its normal position on the glenoid. The diagnosis is radiological, not clinical (e.g., posterior subluxation in concentric arthritis). Static instability may remain asymptomatic for a long period. The cause of the migration seems to be a combination of tears and fatty degeneration of the tendons on the rotator cuff. Dynamic instabilities (class B) are characterized by the subjective loss of normal glenohumeral joint stability and a temporary but restorable loss of joint congruency. Dynamic instabilities are always initiated by trauma, either repetitive microtrauma or a single macrotraumatic event. A typical patho-anatomy is associated with each of the dynamic instabilities. All of them can be associated with major bony defects of the glenoid fossa. Individuals in the last group, voluntary dislocation (class C), can dislocate or reduce their shoulder at will. These patients should not be treated by an orthopedic surgeon, but by a psychiatrist and a physiotherapist.

16.3 History A detailed report of the symptoms is the main step in the diagnosis of glenohumeral instability. A major trauma could lead to the first episode of instability and it should be

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noted, but a relatively minor trauma or no trauma at all could be at the origin of the history of the affected shoulder. In any case, it is helpful to know the position of the arm at the moment of the dislocation in order to understand and classify the direction of the instability. Information about the first reduction is also very important: Was it carried out by someone with experience in the treatment of shoulder trauma, or was the shoulder reduced by itself, as in a transient subluxation? This information is generally helpful in distinguishing between TUBS and AMBRI. A first episode of dislocation is rarely associated with a classical Bankart lesion if the dislocation or, more likely, subluxation reduced spontaneously. It is also essential to ask the patient about the energy involved in the dislocation. Highenergy trauma, such as in motor vehicle accidents, is more likely than a dislocation that occurred during day-to-day activity to be the cause of severe shoulder-joint lesions (bony Bankart fracture of the glenoid). A history of laxity of many joints or other ligament problems may be the key to the diagnosis. Prior treatment, type and time of immobilization, number of recurring episodes, rehabilitative program, and prior surgical procedures are other important details to collect. The type and severity of the symptoms are also indicative of the pathology. Symptoms can vary from a benign feeling of discomfort to motion-inhibiting dislocation and severe pain. Apprehension during a particular activity is one of the most frequently reported symptoms. Details about the position of the arm or the motion that elicits apprehension and pain should be collected with care. By contrast, the location of the pain does not, by itself, increase the examiner’s ability to diagnose shoulder instability nor does it allow instability subgroups to be distinguished. However, the location of the pain can be useful in the diagnosis of associated pathological conditions, such as tendonitis of the long head of the biceps or subacromial bursitis, as both can complicate shoulder instability, especially in chronic phase.

16.4 Physical Examination As usual, the physical examination begins with the evaluation of both shoulders starting with the asymptomatic one. Inspection and palpation are mandatory. ROM and strength are investigated. Shoulder laxity in all the directions is assessed, testing the sulcus sign and load and shift maneuvers; other signs of generalized ligamentous laxity are sought as well. Provocative tests (apprehension) should be done at least to determine any patient contracture or defensive responses [7]. Sometimes, the direction of instability remains uncertain, especially when the patient is unable to relax during the exam. For this reason, it is very important to examine the shoulder under anesthesia, just before surgical stabilization (Fig. 16.2). In every case, this should be done using anatomic landmarks (coracoid and posterolateral acromion) for orientation, with the humeral head centered on the glenoid.


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Fig. 16.2 Examination of shoulder stability under anesthesia just before the surgical procedure is mandatory

16.5 Imaging While the diagnosis of shoulder instability is usually made through history and physical examination, a complete imaging study is mandatory in order to diagnose the soft-tissue and bone lesions that usually accompany shoulder instability. Standard shoulder radiographs are the starting point: a plain anteroposterior radiograph in the scapular plane in neutral, internal, and external rotations and an auxiliary view are the main tools in shoulder imaging [7] (Fig. 16.3). The aims of these radiographic examinations are to evaluate: (1) the relationship between the humeral head and the glenoid, (2) the presence of any bone defect, either anterior, inferior, or posterior, in the glenoid (Fig. 16.4), (3) impaction fracture posterior (Hill-Sachs) or anterior (McLaughlin) to the humeral head. Magnetic resonance imaging (MRI) is mandatory to detect soft-tissue lesions involved in the instability, searching for the following: 1. A classical anterior labrum avulsion with or without a glenoid rim fracture (Bankart or bony Bankart lesion). 2. Stretched and insufficient capsule. 3. A particular lesion of the anterior labrum avulsed with the anterior scapular periosteum (ALPSA lesion), displaced and healed medially on the scapular neck. 4. A capsulo-ligamentous avulsion at the side of the anterior or posterior humerus (HAGL or RHAGL lesion). 5. A superficial tear of the anteroinferior labrum associated with an adjacent articular cartilage injury (GLAD lesion). Other soft-tissue lesions can be found in an unstable shoulder but they are concomitant lesions such as SLAP or a cuff tear. Direct MR-arthrography with intra-articular injection of a dilute gadolinium solution has gained popularity during the last decade because of its ability to distend the joint and to outline labral and capsular structures as well as the undersurface of the rotator cuff. However, this exam is not always required. The indications are: multidirectional instability,

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Fig. 16.3 Plain anteroposterior radiographs in the scapular plane and an axillary view are the basic exams for investigating shoulder instability

a

b

Fig. 16.4 a Normal axillary view; b anterior bone defect in the glenoid surface

instability diagnosis not clear, suspected concomitant rotator cuff pathology, biceps tendon disorders, SLAP lesions, and isolated ligamentous or capsular injuries. In acute classic post-traumatic instability (TUBS), MR-arthrography may be not required. In the presence of intra-articular joint fluid (hemarthrosis or effusion), the diagnosis can be easily made using standard MRI.


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Fig. 16.5 An en face view of the glenoid of both shoulders is obtained in order to calculate the eroded area of the anterior part of the glenoid. The defect is calculated as the ratio between the areas of the inferior circle of both glenoids. If the difference between the two areas exceeds 15-20%, an arthroscopic stabilization is contraindicated

When a bone defect on the glenoid or on the humeral surface is suspected, computed tomography (CT) scan is the recommended study, especially when surgical treatment is planned. A CT scan with 3D reconstructions of both shoulders is indicated in order to define the percentage of glenoid affected by the fracture. An en face view of the glenoid allows calculation of its anterior part. Several methods have been described to measure the defect, determining the ratio between the areas of the inferior circle of both glenoids. These studies have important repercussions in the decision-making protocol since if the difference between the two areas exceeds 15-20% an arthroscopic stabilization is contraindicated (Fig. 16.5). The most common defect of the humeral surface is the Hill-Sachs lesion. CT study allows definition of the lesion’s depth, direction, and distance from the articular surface and consequently whether it is an engaging or non-engaging lesion with respect to the anterior rim of the glenoid (Fig. 16.6).

16.6 Anterior Instability Anterior instability of the glenohumeral joint accounts for 95% of shoulder instabilities and the incidence is highest in patients < 30 years of age. The etiology is primarily traumatic, but subluxations may occur due to sports-related repetitive microtrauma.

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a

b

Fig. 16.6 Posterior view of the humeral surface: Hill-Sachs lesion (white line). a Non-engaging lesion; b engaging lesion

The anterior band of the IGHL is the main anterior stabilizer in the 90° abducted position. The most frequent lesion associated with anterior shoulder dislocation is detachment of the anterior caspulolabral complex, the so-called Bankart lesion. Some biomechanical studies have demonstrated that detachment of the anteroinferior labrum alone does not result in anterior recurrence instability. In fact, intrasubstance capsular tear, redundancy of the IGHL complex, and increased capsular volume are common findings associated with the Bankart lesion [8]. Closed reduction followed by a period of immobilization and then rehabilitation is the typical non-surgical treatment of an anterior shoulder dislocation. Immobilization with the arm in internal rotation in a conventional sling or in external rotation does not seem to reduce the recurrence rate after a first dislocation. Non-surgical treatment, such as progressive range-of-motion (ROM) exercises and shoulder strengthening, is best suited for low-demand patients or patients with significant comorbidities. Recurrence is the most common complication and occurs in 55-66% of young athletic patients [9, 10], but some studies have reported that a restriction from sports participation for at least 6 weeks reduces this rate significantly. Given the high rate of recurrence in young athletic patients, some authors have advocated arthroscopic stabilization following the first episode of dislocation. However, there is as yet no long-term follow-up examining the success of this aggressive treatment. In our opinion, surgical treatment after the first episode of dislocation should be limited to high-demand young patients involved in sports, such as rugby, in which high-energy trauma is likely. Recurrent instability and failed non-operative treatment are the main indications for open or arthroscopic surgery. The outcomes of these kinds of treatment are directly related


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b

Fig. 16.7 a Arthroscopic view from the anterosuperior portal of a Bankart lesion. b The repaired lesion

to the ability of the surgeon to identify and address all the lesions contributing to the recurrence. Advances in technology have led to the development of multiple arthroscopic techniques to repair Bankart lesions and capsulo-labral deficits (Fig. 16.7). The proposed advantages of an arthroscopic procedure instead of an open one are less surgical morbidity, better cosmetic results, and a better overall range of both motion and function. Nonetheless, recurrent instability and recurrent dislocation after arthroscopic treatment are 18% and 12%, respectively, as opposed to 8% and 5% after traditional open surgery [11]. In our opinion, the main indications for open-shoulder stabilization are a significant bone defect of the glenoid (> 20% of the articular surface) and an engaging Hill-Sachs lesion, especially if it involves the humeral articular surface. Relative indications are HAGL lesion, failure of previous stabilization procedures, capsular insufficiency, and instability in a collision athlete < 20 years of age, with four or more episodes of recurrence. In these cases, an open bone block procedure (Latarjet or Bristow procedure) may be recommended [12].

16.7 Posterior Instability Posterior glenohumeral instability is not as common as the anterior type, representing only 2-5% of all shoulder instabilities. Accordingly, it may be a difficult condition to recognize [13]. There are two clinical presentations: posterior locked dislocation and posterior/posteroinferior instability. An acute posterior locked dislocation is a rare and often misdiagnosed condition that can occur during a seizure or traumatic event, when the arm is in an at-risk position (e.g., forward flexion, adduction, and internal rotation). Several lesions can be found associated with the dislocation but the most frequent one is a defect in the anteromedial head or

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an impression fracture (McLaughlin lesion). The main detail that must be clinically observed is the limited external rotation, which together with the imaging findings helps with the diagnosis. Posterior subluxation is the most common form of recurrent posterior/posteroinferior instability. Repetitive stresses on the posterior capsule, as in overhead sports, the backhand stroke in racket sports, the pull-through phase of swimming, and the follow-through phases in a throwing activity or golf, may lead to an acquired posterior instability. In addition, a posterior subluxation may be the main symptom in a multidirectional instability. A voluntary subluxator may develop a painful involuntary posterior instability if control of the scapula is lost (Fig. 16.8). The physical findings of patients with posterior instability often are more subtle than those of patients with anterior instability. Active and passive ROM are usually normal and symmetric. The posterior joint line may be tender to palpation. Strength testing is usually symmetric, except in rare cases of posterior rotator cuff muscle deficiency or nerve injury with external rotation weakness. In these cases, atrophy of the posterior rotator cuff muscles may be apparent on inspection. Patients should be assessed for generalized ligamentous laxity; load and shift and sulcus testing should be performed. Standard imaging plain radiographs are obtained to verify where the joint is located, to evaluate the morphology of the posterior glenoid rim, and to look for impaction fractures of the anterior portion of the humeral head (McLaughlin fracture). Dynamic radiographs could be performed in those patients with voluntary instability. CT or MRI is essential to assess the version and morphology of the glenoid as well as other pathological elements of the shoulder’s components. Laxity develops in the posterior-inferior capsular ligaments and in the anterosuperior corner of the capsule. Common findings are an enlarged posteroinferior capsule, tears or detachments of the posterior labrum, and chondral changes in chronic cases. Anterior labral tears, SLAP lesions, and enlarged rotator capsular intervals can also be found. The treatment of posterior shoulder instability is considered to be as difficult as the diagnosis. Operative management has a failure rate ranging from 30 to 72%. The absence of a single main lesion responsible for this disorder is the greatest reason for failure. Thus, for the great majority of patients non-surgical treatment is chosen. The focus should be

Fig. 16.8 Posteriror subluxation of the humeral head (black arrow) is visible during elevation and adduction of the arm


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on exercises that strengthen the posterior deltoid, external rotators, and periscapular muscles. This approach is successful in approximately 65-80% of patients. If it fails, surgery may be indicated. During the past decade, the arthroscopic treatment of posterior shoulder instability has attracted increasing interest as a means of restoring stability but without the morbidity of open surgery. However, there is no statistical difference in clinical outcomes for patients treated with either open vs. arthroscopic surgery [14]. A variety of arthroscopic techniques have been described to manage posterior glenohumeral instability in relation to posterior capsulo-labral injury and redundancy. The perceived advantages of the arthroscopic approach include less morbidity, shorter surgery time, improved cosmesis, and less post-operative pain. Relative contraindications to arthroscopic treatment of recurrent posterior instability include failed prior arthroscopic stabilization procedure, RHAGL lesions, or gross symptomatic bi- or multidirectional instability from excessive generalized laxity and bony defect. Before any surgical procedure, an examination under anesthesia must be performed. Arthroscopic treatment can be performed with the patient in either the lateral decubitus or beach-chair position. For the lateral position, the arm is placed in a traction device with 20° of abduction and 20° of extension. Three or four portal techniques can be used, with one or two posterior portals and two anterior portals. A significant capsulo-labral injury (posterior Bankart lesion) can be repaired with suture anchors; otherwise, the capsular redundancy, which is more typically encountered, can be reduced with a posterior capsular shift. The shift begins in the 6 o’clock position. The capsule is grasped 10-15 mm lateral to the glenoid rim and shifted to the labrum with three to five sutures, depending on the size of the shoulder, the degree of laxity, and the amount of retention desired. When a significant inferior laxity is present, a rotator interval closure is performed to gain additional stability against inferior translation. Closure of the MGHL to the SGHL defines rotator interval placation. However, these procedures are not indicated when shoulder instability is associated with a bone defect, such as glenoid dysplasia or retroversion (>20°), or a focal acquired glenoid defect, such as a reverse bony Bankart lesion. For these patients, respectively, an open wedge posterior glenoid osteotomy or an open glenoid reconstruction with an iliac bone graft is indicated [13].

16.8 Multidirectional Instability Multidirectional instability is a symptomatic glenohumeral subluxation or dislocation in more than one direction. The etiology is multifactorial and thus not always clear. There are some lax asymptomatic shoulders that become symptomatic after a minor or major trauma, a repetitive microtrauma, or a proprioceptive deficit. The condition can occur in young sedentary patients with an atraumatic history of multidirectional instability and generalized ligamentous laxity, or in athletes with a history of injury. There may also be labrum defects and/or a humeral head impression lesion [15]. The symptoms may be vague and difficult to sort out. Varying degrees of instability, pain, transient neurological symptoms, and discomfort at the shoulder may be typical. They

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are usually noted in the mid-range position of glenohumeral motion during the activities of daily life, thus causing the patient to avoid the extreme ROM. During the physical examination, it is possible to observe the possibility of dislocation or to subluxate the glenohumeral joint in three directions, thereby reproducing the symptoms. A careful history that investigates specific activities and the arm position that cause symptoms will suggest the direction of the instability. Clinically, all the signs of laxity are present: ROM is normal or excessive, and provocative tests may be positive. The scapulothoracic joint should be accurately evaluated for a potential dyskinesis. A hyperlaxity secondary to a connective tissue syndrome, such as Marfan’s or Ehlers-Danlos, must be recognized because this is indicative of the need for surgical treatment. The most important patho-anatomic findings are enlargement of the capsule, especially in the inferior pouch, enlarged glenohumeral joint space, and enlargement of the rotator interval. During arthroscopy, the presence of an abnormally increased space in the glenohumeral joint will allow the arthroscope to easily pass from the posterior to the anterior aspect of the joint; this is called the “drive-through” sign. The preferred treatment is conservative and consists of education of the patient and a specific rehabilitative program. Exercises are continued for a minimum of 6 months. Not only the patient but also his or her physician, therapist, and surgeon must recognize that recovery is a long process. The rate of satisfaction is 90%. If the shoulder remains symptomatic, surgery is the next option. Several open and closed surgical procedures have been proposed with the aim of shifting the inferior capsule, closing the rotator interval, and repairing any associated lesions.

16.9 Minor/Microinstability In recent years, numerous forms of instability have been observed that cannot be classified as simply anterior, posterior, or multidirectional. There is a group of symptomatic shoulders without evidence of either dislocation or major anatomic lesions affecting the stabilizing structures of the joint. In these minor instabilities, an alteration of the biomechanics of the shoulder, usually related to overuse, is probably the origin of the disease. However, even if complete knowledge of the etiology of minor instabilities is still lacking, there are data supporting the traumatic and atraumatic origins of this condition. Traumas that can lead to minor instability are usually those of medium-low energy. These so-called microtraumas consist of a series of abduction/external rotation movements. Repetitive microtraumas are typical of some overhead workers and throwing athletes. A deficit in the internal rotation at 90° of abduction is frequently noted. The normal kinematics of the shoulder is altered because of the retracted posterior-inferior capsule, resulting in a superior translation of the humeral head and insertional stress of the supraspinatus. Atraumatic minor shoulder instability is a rare and subtle condition. The key to the problem is the unbalanced muscular control resulting from scapular-humeral or scapular-


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thoracic dyskinesia. In those cases characterized by overstressed capsulo-labral structures, a proprioceptive deficit can amplify the effect of muscular hypotrophy on joint movement control. Occasionally, some capsule ligamentous anatomic variants are present, such as the absence of the anterior superior labrum, a cord-like MGHL, or an insertion of the anteriorsuperior labrum just above the glenoid notch. The patho-anatomic findings may involve the superior half of the ligamentous-tendinous glenohumeral labrum complex. It is possible to find a partial lesion of the supraspinatous tendon, superior labrum (SLAP lesion), rotator interval, MGHL, anterior-posterior labrum, IGHL, and posterior-inferior capsule. All these various lesions can be isolated, or they may be variously associated, according to the etiopathogenesis of the minor instability [15]. Often, active ROM is limited by pain. Provocative tests such as the Jobe test and Neer test are positive, as are laxity tests such as the sulcus sign and Rowe test. Low- and middle-energy traumas do not cause bony lesions; therefore, conventional radiographic and CT findings are negative. MRI is more significant with gadolinium because the contrast material can better define the anatomic variants of this kind of instability. The preferred treatment is physical rehabilitation of the larger muscles of the shoulder. Due to the multifactorial nature of minor instability and the lack of a major single lesion determining the symptoms, there is an elevated rate of failure after surgical treatment (> 50%). Therefore, surgery should be considered only in patients who have persistent symptoms after a long period of rehabilitation. The surgical procedure depends on the pathology. Labral detachment and SLAP lesion are reattached and rotator interval lesions are repaired by placation. In cases of internal impingement, the rotator cuff and posterosuperior labrum are most often addressed by a simple debridement. If the cuff tear involves > 50% of the tendon’s thickness, a repair is performed.

16.10 Conclusions Glenohumeral instability accounts for a significant proportion of shoulder diseases. The etiology, direction, and symptoms may be different, such that a precise diagnosis is essential to determine appropriate treatment options. A careful history, complete physical examination (perhaps under general anesthesia), and complete imaging study will provide the information needed to understand and treat every kind of instability. Treatment includes both rehabilitative programs and surgical procedures. If the choice is a surgical one, several points must be clear: Is it really glenohumeral instability? Is the anatomic/mechanical problem of the instability clearly identified? Is it possible to solve it surgically? Furthermore, it must be kept in mind that positive signs of laxity are not synonymous with instability. Finally, soft-tissue reattachment or repair may be sufficient when the capsulo-labral complex is compromised; however, when an osseous deficit is present, a repair relying on soft tissue cannot restore compressive load-bearing as well as one achieved with bone.

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References 1. Lee SB, An KN (2002) Dynamic glenohumeral stability provided by three heads of the deltoid muscles. Clin Orthop Relat Res 400:40-47 2. Savoie FH, Papendik L, Field LD et al (2001) Straight anterior instability: lesion of the middle glenohumeral ligament. Arthroscopy 17:229-235 3. Harryman D, Sidles J, Matsen F (1992) The role of the rotator interval capsule in passive motion and stability of the shoulder. J Bone Joint Surg Am 74A:53-66 4. Neer CS (1985) Involuntary inferior and multidirectionl instability of the shoulder: etiology, recognition and treatment. Instr Course Lect 34:232-238 5. Neer CS, Foster CR (1998) Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder: A preliminary report. J Bone Joint Surg 62A:897-908 6. Gerber C, Nyffeler RW (2002) Classification of glenohumeral joint instability. Clin Orthop Relat Research 400:65-76 7. Pollock RG, Bigliani LU (1993) Glenohumeral instability: evaluation and treatment. J Am Acad Orthop Surg 1:24-32 8. Lennart K, Hovelius L, Rösmark DL et al (2001) Long results with the Bankart and Bristow-Latarjet procedures: Recurrent shoulder instability and arthropathy. J Shoulder Elbow Surg 10:445-452 9. Hovelius L, Olofsson A, Sandström B et al (2008) Nonoperative treatment of primary anterior shoulder dislocation in patients forty years of age and younger. a prospective twentyfive-year follow-up. J Bone Joint Surg Am 90:945-52 10. Simonet WT, Cofield RH (1994) Prognosis in anterior shoulder dislocation. Am J Sports Med 12:19-24 11. Letters TR, Franta AK, Wolf FM (2007) Arthroscopic compared with open repairs for recurrent anterior shoulder instability. A sistematic review and Meta-Analisis of the literature. J Bone Joint Surg Am 89:244-254 12. Itoi E, Lee SB, Berglund LL et al (2000) The effect of a glenoid defect on anteroinferior stability of the shoulder after Bankart repair: a cadaveric study. J Bone Joint Surg Am 82:35-46 13. Millet PJ, Clavert P, Hatch GF III et al (2006) Recurrent posterior shoulder instability. J Am Acad Orthop Surg 14:464-476 14. Kakar S, Voloshin I, Kaye EK et al (2007) Posterior shoulder instability: comprehensive analysis of open and arthroscopic approaches. Am J Orthop 36:655-659 15. Schenk TJ, Brems JJ (1998) Multidirectional instability of the shoulder: pathophysiology, diagnosis, and management. J Am Acad Orthop Surg 6:65-72

Acromioclavicular Injuries of the Shoulder

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E. Calvo, D. Morcillo

Abstract Acromioclavicular joint injuries represent nearly half of all athletic shoulder injuries. Stability of this joint depends on the integrity of the acromioclavicular and coracoclavicular ligaments. Classification is based on the structures injured and joint stability. The majority of injuries are type II incomplete acromioclavicular separations and can be successfully treated non-surgically. Acute types IV, V, and VI are less common and surgical treatment is recommended. The treatment of type III injuries is controversial, but comparative studies and meta-analysis clearly favor a non-surgical approach, even in overhead-throwing athletes. Surgery in the repair of type III AC joint injuries should be reserved for athletes who remain symptomatic after conservative treatment. The goal of surgical intervention is to reconstruct the coracoclavicular ligaments, thereby furnishing joint stability in all planes.

17.1 Introduction The acromioclavicular (AC) joint is a robust articulation that anchors the scapula and the upper extremity to the clavicle. AC joint injuries represent half of the athletic shoulder injuries. Most are minor sprains, with the incidence of subluxations approximately twice as high as that of dislocations; therefore, the true incidence of AC joint injuries is likely underestimated. However, they occur five times more frequently in men than in women, with the highest incidence in the 20-30 years age group (43.5%) [1]. Depending on the magnitude of the injury, the treatment options range from non-surgical measures allowing quick return to athletic activity to various forms of surgical reconstruction of the joint. This chapter reviews the anatomy and biomechanics of the AC joint and describes the evaluation, diagnosis, and non-surgical and surgical treatment of various injuries involving the joint.


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17.2 Anatomy and Biomechanics of the Acromioclavicular Joint The AC joint is a diarthrodial articulation formed between the lateral end of the clavicle and the medial end of the acromion. It is surrounded by a joint capsule with synovium and contains an intra-articular fibrocartilaginous meniscus-type structure. With age, this meniscus undergoes degeneration and disintegration. Both static and dynamic stabilizers ensure the stability of the AC joint. The static stabilizers include the AC joint capsule reinforced with the AC ligaments (superior, inferior, anterior, and posterior) and the coracoclavicular (CC) ligaments. The AC joint capsule and ligaments are the primary restraints to anterior to posterior translation. The CC ligaments include the conoid ligament medially and the trapezoid ligament laterally, both of which provide vertical stability by preventing superior and inferior displacement of the clavicle [2]. The CC ligaments span a distance of 1.1-1.3 cm between the coracoid and the clavicle [3]. Complete sectioning of the CC ligaments is necessary for complete AC joint dislocation with either superior or inferior displacement of the entire scapulohumeral complex. Dynamic stabilizers of the AC joint rely on the origin of the anterior deltoid from the clavicle and on the trapezius muscle, through its fascial insertion over the acromion. During shoulder motion, the clavicle can move anteriorly to posteriorly and displace upward and backward, with its center of rotation in the sternoclavicular joint [4]; however, the clavicle also rotates approximately 40-45º with full shoulder elevation, but the magnitude of rotation does not exceed 5-8º relative to the acromion because of synchronous scapuloclavicular motion.

17.3 Mechanisms of Injury Acromioclavicular injuries are most commonly the result of direct trauma. For the athlete, the injury is usually due to a direct hit, either by another player or by contact with the ground. Direct injury is the consequence of a direct force on the acromion with the shoulder adducted, resulting in movement of the acromion while the clavicle remains stabilized by the sternoclavicular ligaments. Since the sternoclavicular joint is highly stable, the energy of impact is sequentially absorbed by the AC ligaments, CC ligaments, and deltotrapezoidal fascia. The severity of injury is determined by the magnitude of the force. AC joint injuries are more common in collision sports, such rugby or football, as well as in sports in which falls occur with the shoulder adducted, as in cycling. Indirect injuries are less frequent and are due to a fall on an outstretched arm or elbow with a superiorly directed force.

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17.4 Classification Acromioclavicular joint injuries are classified in six groups based on the extent of ligament and deltotrapezoid fascia injury, AC joint position on radiographs, and whether the AC joint can be reduced on physical examination [1, 3] (Table 17.1, Fig. 17.1). Type I injury represents a sprain of the AC ligaments. In type II injury, the AC ligaments are torn while the CC ligaments remain intact; the distal clavicle is unstable horizontally. In type III injury, both AC and CC ligaments are torn and the clavicle is dislocated and unstable horizontally and vertically. In type IV injury, there is complete AC joint dislocation, with the clavicle displaced posteriorly into or through the trapezius. A type V injury is a com-

Table 17.1 Classification of acromioclavicular (AC) joint injuries Type

AC CC Deltopectoral Radiographic ligaments ligaments fascia CC distance increase

Radiographic AC appearance

AC joint reducible

I II III IV

Sprained Disrupted Disrupted Disrupted

Intact Sprained Disrupted Disrupted

Intact Intact Disrupted Disrupted

Normal < 25% 25-100% Increased

N/A Yes Yes No

V VI

Disrupted Disrupted

Disrupted Intact

Disrupted Disrupted

100-300% Decreased

Normal Widened Widened Posterior clavicle displacement Widened Clavicle under coracoid

CC, Coracoclavicular; N/A, not applicable

I

II

III

IV

V

VI

Fig. 17.1 Classification of acromioclavicular joint injury

No No

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Fig. 17.2 Type V acromioclavicular joint injury of the left shoulder

plete AC dislocation with significant superior displacement of the clavicle; the joint is irreducible, in contrast to type III injury (Fig. 17.2). In the exceedingly rare type VI injury, the clavicle is displaced inferiorly into a subacromial or subcoracoid position. This type represents a high-energy variant of AC joint injury and is commonly associated with fractures and brachial plexus or vascular injury. “Pseudodislocation” is an unusual injury seen in children and adolescents. The joint is dislocated but the CC ligaments remain intact, attached to the periosteal sleeve, which is stripped off the distal clavicle [1]. Another variant of AC joint injury is a dislocation of the joint in which the CC ligaments remain intact but are avulsed from the coracoid process.

17.5 Diagnosis and Physical Examination The index of suspicion for injury to the AC joint should be high in any athlete complaining of anterior-superior shoulder pain after shoulder trauma. On physical examination, findings such as local swelling, deformity, abrasion, or bruising may be noted. The AC joint is tender on palpation. In types I and II AC joint injury a large deformity or gross instability is not present. In type III AC joint injury, the distal end of the clavicle protrudes; while the shoulder drops downward. It is important to examine the patient in the standing or sitting position without support for the injured extremity. The weight of the arm will make the deformity apparent. Inspection of the superior aspect of the shoulder is very useful to identify type IV AC joint dislocations. The clavicle is displaced posteriorly and may tent the posterior skin as it is displaced into the trapezius muscle. Type V AC injury shows more marked deformity than type III injury, and the clavicle frequently tents the


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skin since the deltoid and trapezius fascia have been stripped from the clavicle. Type VI AC joint injury is very rare, is often secondary to extreme trauma, and can be associated with brachial plexus injuries. Stabilizing the clavicle with one hand and placing an upward force under the ipsilateral elbow cannot reduce AC joint injuries of types V and VI.

17.6 Imaging Conventional anteroposterior radiographs of the shoulder are inadequate for thorough evaluation of the AC joint. This area requires lower penetration than is the case for the glenohumeral joint; thus, these views are often over-penetrated. Standardized projections are essential to diagnose and classify AC joint injuries. Routine radiographs for AC joint evaluation include a true anteroposterior and axillary view of the shoulder, as well as a Zanca view (10-15º cephalic tilt) taken with the patient in the upright position and without support of the injured arm. Comparison views of the opposite shoulder can be useful to obtain information regarding the CC distance and relative posterior displacement of the clavicle, but they are seldom necessary. Stress views are primarily used to differentiate between type II and type III AC separations. However, rarely is this difference clinically significant, and the information provided does not justify the added time, cost, and discomfort to the patient. Ultrasound and magnetic resonance imaging are not usually necessary but can be used to detect effusions, assess the extent of injury of the ligaments and deltotrapezius aponeurosis, and determine the degree of degenerative alterations in patients who develop late symptoms [5]. Coracoid process fractures should be suspected when radiographs reveal AC dislocation with normal CC distance. Computed tomography can be useful in these cases.

17.7 Treatment 17.7.1 Conservative Treatment 17.7.1.1 Type I and Type II AC Joint Injuries Conservative treatment is universally recommended for type I and type II AC joint injuries. The most common form of non-surgical treatment consists of simple analgesia, topical ice therapy, and rest in a sling to relieve symptoms. A broad sling is clearly preferred to a collar and cuff because it supports the elbow and tends to minimize sagging of the shoulder. The sling is removed after 7-14 days, once the acute symptoms and pain have

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subsided. Numerous techniques of external support, such as commercially manufactured braces, are available but none of them has proven to be particularly effective. In addition, they may give rise to local skin problems, shoulder stiffness, or non-compliance. The goal for athletes with these injuries should be to return to full sport activity within 1-4 weeks depending on the amount of contact involved in their sport and the amount of overhead activity it entails. Gladstone et al. described a four-phase rehabilitative program for athletes after an AC joint injury [6]. The first phase consists of ice and immobilization with a sling for up to 2 weeks to decrease pain and inflammation. Active-assisted motion is gradually increased as long as it is relatively pain-free. Elevation in pure abduction is avoided as this stresses the AC ligaments. The athlete advances to phase 2 when 75% motion is gained, there is minimal pain with palpation of the AC joint, and manual muscle testing is 4/5 for the deltoid and upper trapezius. Phase 2 involves advancing to full pain-free motion and increased isotonic strength focused on the trapezius, deltoid, and rotator cuff. Advancement to phase 3 is allowed when the athlete has full range of motion without pain, no tenderness at the AC joint, and strength that is 75% of the contralateral side. The aim of phase 3 is to strengthen the shoulder and increase power and endurance. Plyometric drills and isotonic exercise are used. When the phase 3 criteria have been met and the athlete has isokinetic strength equal to the opposite side, phase 4 is initiated, in which specific drills are practiced in order to allow full return to play.

17.7.1.2 The False Dilemma of Type III AC Joint Injury Although the treatment of type III AC joint injuries has been controversial, a conservative approach is the preferred initial mode of management. Comparative studies have reported similar results for conservative and surgical treatment, and meta-analysis failed to find any significant benefit in a surgical approach [7]. Moreover, the incidence of complications in terms of infection, revision surgery, osteoarthritis, and unsightly scars is clearly higher in surgically treated patients [8]. Type III injuries that are managed conservatively follow the same four-phase protocol for return to sports as outlined above. Although the majority of athletes are initially treated conservatively, some authors recommend surgical treatment in the overhead-throwing athlete. The evidence for acute surgical treatment in these athletes is not established; however, a survey of orthopedic surgeons treating professional overheadthrowing athletes in the USA revealed an overall preference for conservative management for type III AC joint injury [9]. Our personal approach is to treat a type III AC injury conservatively, with surgical stabilization considered only if the athlete specifically requests it.

17.7.2 Surgical Treatment Acute injury types IV, V, and VI generally require surgical treatment due to the morbidity associated with the severe soft-tissue disruption and a persistently dislocated, highly unstable joint. There is some literature to support reduction of the clavicle in types IV, V, and VI injuries, converting them into a type III injury and then treating them conservatively.


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17.7.2.1 Timing of Surgical Reconstruction: Acute or Delayed? Accurate reduction of the AC joint is easier when surgery is performed within the first 2 weeks after injury, with excision of the lateral end of the clavicle performed before reduction in most delayed reconstructions, and stability restored by ligament substitution. In spite of these data, acute reconstruction is usually reserved for type IV, V, and VI injuries, double disruptions of the superior shoulder suspensory complex, or when there are associated soft-tissue or neurovascular injuries. Surgical treatment for type III injuries is usually considered only for those patients with persistent symptoms after a trial of conservative treatment for at least 3 months. However, secondary reconstructive surgery in type III AC joint injuries is seldom needed [8]. 17.7.2.2 Which Surgical Technique? A wide variety of surgical techniques has been described to repair AC joint dislocations, but none has been demonstrated to be significantly superior to the others. Fraser-Moodie et al. pointed out the general principles to be addressed in every surgical technique [10]: First, anatomic reduction of the AC joint must be achieved, correcting the inferior drop of the shoulder and reducing the anteroposterior translation of the joint surfaces. Second, once the joint is reduced, the ligaments must be repaired or substituted, either using autografts or allografts. Third, ligament reconstruction must be stable enough to prevent postoperative redisplacement or the ligament should be protected with transient fixation until the repair heals. Finally, if rigid implants are used for transient stabilization of a ligament reconstruction, they must be removed when the repair is consolidated; otherwise they may break, loosen, or produce osteolysis or shoulder stiffness. Although all surgical techniques have these goals, they can be categorized in four main groups [3]: Primary Repair of the CC Ligaments. Primary repair of the ruptured ligaments can be attempted in the first 2 weeks after injury. The repair must be temporarily protected with some type of stabilization. Historically, Kirschner wires were transfixed through the AC joint but this procedure has since been abandoned due to the complications derived from the use of wires [8]. Instead, in recent years, a hooked-plate has been used in Europe to stabilize the repair (Synthes, Solothurn, Switzerland). The hook is inserted on the under-surface of the acromion, and the plate is secured to the clavicle with screws. While this osteosynthesis closely reproduces the stability of the intact joint, its prolonged retention can cause shoulder stiffness, clavicle osteolysis, or peri-implant fractures, while early removal is associated with new dislocation of the AC joint [10]. Other techniques obtain transient stability of the AC joint by fixating the clavicle to the coracoid process by coracoclavicular screws, or cerclage with wires. These techniques require in many cases staged removal of the fixation. Synthetic sutures or bands sutures (PDS, Dacron, or Mersilene tapes) as loops are advocated by some authors, their main advantage being that they do not require later removal. However, foreign-body reaction, clavicle osteolysis, and suture cutout have been reported with this technique [3].

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In our experience, direct repair of the ligament, even in the acute setting, is difficult to achieve because ligaments are usually torn in the midsubstance, and the outcome of the repair is uncertain regarding the structural integrity, due to poor tissue quality. On the other hand, we do not recommend fixation without ligament repair because of the high incidence of recurrence of AC joint separation. Ligament Reconstruction. Since direct repair of CC ligaments is difficult, even in the acute setting, techniques focused on their reconstruction have been developed. These can be used in acute as well as in chronic cases. The classic Weaver-Dunn procedure involves excision of the distal clavicle and transfer of the CA ligament to the distal end of the clavicle so that it becomes the newly reconstructed CC ligament [11]. It has been demonstrated that a transferred CA ligament has only 30% of the strength and 10% of the stiffness of intact ligaments, with no effect on horizontal instability. Augmentation of this reconstruction with various suture loops and suture anchors can increase the construct’s strength and ultimate load to failure while reducing primary and coupled translation [3]. An alternative technique for ligament reconstruction is based on the use of free tendon autografts. These permit placement of the tendon in a more anatomic position, attempting to reproduce the CC ligaments, restore comparable strength to the native ligaments, and provide a biological scaffold for revascularization. The semitendinosus is the tendon most frequently used, but other tendons, such as gracilis, toe extensors, and peroneus brevis, have also been proposed [10]. The technique usually is combined with distal clavicle resection. Initially, some authors described the use of a looped semitendinosus graft around the coracoid process. Mazzocca et al. modified this technique, incorporating a double semitendinosus graft inserted in a coracoid bone tunnel and secured in two separate clavicle bone tunnels [12]. Interference screws were used to approximate the anatomic location of the trapezoid ligaments. Biomechanical testing of this construct has been favorable and it has been shown to provide anterior, posterior, and superior stability not statistically different from the intact state. Compared with the arthroscopic suture loop, the graft offers the additional advantage of a scaffold for revascularization, but the technique has raised some concerns that the two interference screws could weaken the clavicle. Dynamic Muscle Transfer. Transfer of the short head of the biceps tendon with or without the coracobrachialis has usually yielded acceptable results. Although biomechanical studies suggest that the conjoined tendon has better consistency than CA ligament transfer, the operation carries the risk of over-tightening the coracoclavicular space [10]. Distal Clavicle Resection. This approach (also known as Mumford’s procedure) may be performed as a salvage procedure for persistent pain after AC joint injury, especially type I and type II, or as a treatment of post-traumatic AC osteoarthritis or osteolysis. When horizontal or vertical instability exists, distal clavicle resection must be accompanied by CC ligament reconstruction.


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17.7.2.3 Is There a Role for Arthroscopy? All the techniques to repair AC joint separations were initially described in the setting of an open exposure. A “bra-strap” incision remains the most common surgical approach, permits direct visualization and reduction of the joint, and facilitates ligament reconstruction. In addition, the deltotrapezius fascia can be repaired when injured. Wolf et al. and Lafosse et al. described an all-arthroscopic technique for CA ligament transfer in the setting of acute or chronic AC dislocations [13, 14]. Advances in instrumentation, implants, and techniques have disseminated the treatment of AC joint injuries with minimally invasive techniques [12]. Many of these techniques are similar to those used for ligamentous reconstruction of the knee, and reduction of the AC joint can be maintained with either a synthetic loop or a single-bundle tendon graft (Arthrex, Naples, Fl, USA). The accuracy of reduction is more difficult to evaluate and requires a steeper learning curve, but results are promising (Fig. 17.3). 17.7.2.4 Postoperative Treatment After surgery, the patient’s arm and shoulder are placed in a sling for at least 6 weeks. The patient must understand the importance of compliance with the sling and is only allowed to remove it for supervised physical therapy. Gentle pendulum exercises can be initiated immediately. At 2 weeks, passive and active assisted range of motion (ROM) is started, but must be restricted to beneath the shoulder level. The sling is discontinued between 6 and 12 weeks. At 12 weeks, strengthening is begun. The athlete can return to sports when full mobility and strength have been obtained. Contact sports are not allowed until 6 months postoperatively; however, peak strength may not be fully recovered until 9-12 months. If the clavicle was transitorily fixed to the coracoid with a screw, full ROM is not allowed until the fixation is removed, usually at 8 weeks. After AC joint reconstruction with an autogenous or allografted ligament, active and passive ROM are encouraged, with further graft maturation at approximately 8 weeks.

Fig. 17.3 Acute arthroscopic reconstruction of a type V acromioclavicular joint injury. See the endobutton corresponding to the tightrope system under the coracoid process maintaining the reduction. (Arthrex, Naples, Fl, USA)

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17.8 Complications Both conservative and surgical treatment can result in complications. After conservative management, the most common complications are osteoarthritis and clavicular osteolysis in type I and type II AC joint injuries, and symptomatic instability in type III AC joint injury. Surgical treatment by resection of the distal end of the clavicle is indicated in the first situations, with surgical stabilization by CC ligament reconstruction performed in the case of symptomatic instability. Some patients with AC joint injury managed conservatively complain of dysesthesia or arm weakness; these symptoms have been attributed to brachial plexus irritation due to separation of the AC joint. Surgical stabilization is also recommended in these cases. Complications following surgical treatment are more varied. Hardware failure and migration has been described in all techniques, but especially with fixations using Kirschner wires. Post-operative superficial wound infection is not uncommon and usually responds to conservative therapy with antibiotics. Deep sepsis can also occur. The superficial location of the joint, the necessity of extensive soft-tissue dissection to restore the anatomy, the use of metallic implants, non-absorbable sutures or tapes, or allografts to stabilize the joint are potential reasons for this complication. Extensive debridement, with soft-tissue removal, removal of artificial implants, and prolonged antibiotic therapy are recommended in this situation. Keloids and unsightly scars are common in this area. Recurrence of the dislocation or partial subluxation of the AC joint is frequent, mainly when the procedure involved direct reconstruction of the ligaments and transient immobilization of the joint with coracoclavicular screws, Kirschner wires, or plates, all of which necessitate later removal. The deformity usually becomes evident after implant removal but does not need surgical revision in the majority of patients [8]. If re-dislocation results in residual symptoms, surgical revision has in some cases been successful [15]. Any surgical technique carries a risk of injuring the brachial plexus, especially the musculocutaneous nerve, or the subclavian vessels, but the probability of this complication is higher with those techniques in which a graft is passed under the coracoid. Ossification of the CC ligaments is frequent after conservative or surgical treatment but has not been shown to have any effect on outcome.

17.9 Conclusions Injuries of the AC joint are frequent, particularly in the contact athlete. Significant recent advances have been made in understanding and treating AC joint injuries. Acute injuries types I and II are treated conservatively, whereas types IV, V, and VI should be managed surgically. Conservative treatment is the preferred approach for type III injuries, as studies have not shown a clear advantage of surgical treatment. Surgical intervention should be considered only when the athlete remains symptomatic after completing a conserva-


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tive course of treatment. Those patients involved in overhead-throwing sports might be more prone to develop pain and mechanical symptoms, which has led some authors to recommend a surgical approach. Further research is needed to define the treatment of type III AC joint injuries in this subpopulation of patients. Many techniques have been proposed to treat AC joint injuries. Direct ligament repair is difficult even in the acute setting, and techniques of ligament reconstruction are preferred. Transient fixation of the AC joint with Kirschner wires is to be avoided due to the risk of pin migration and loss of reduction. Recent biomechanical and anatomic studies have shown that procedures involving double-bundle reconstruction of the CC ligaments with tendon autograft restores the original anatomy and tensile strength, but additional studies are warranted to demonstrate clinical superiority.

References 1. Rockwood CA, Williams GR, Young DC (2004) Disorders of the acromioclavicular joint. In: Rockwood CR, Matsen FA, Wirth MA, Lippitt SB (eds) Saunders Philadelphia, pp 597-646 2. Fukuda K, Craig EV, An KN et al (1989) Biomechanical study of the ligamentous system of the acromioclavicular joint. J Bone Joint Surg Am 30:434-440 3. Simovitch R, Sanders B, Ozbaydar M et al (2009) Acromioclavicular joint injuries: diagnosis and management. J Am Acad Orthop Surg 17:207-219 4. Calvo E, Fernández-Yruegas D, Alvarez L et al (1995) Bilateral stress fracture of the clavicle. Skeletal Radiol 24:613-616 5. Ernberg LA, Potter HG (2003) Radiographic evaluation of the acromiocavicular and sternoclavicular joints. Clin Sports Med 22:493-506 6. Gladstone J, Wilk K, Andrews J (1997) Nonoperative treatment of AC Joint injuries. Oper Tech Sports Med 5:78-87 7. Phillips AM, Smart C, Groom AFG (1998) Acromioclavicular dislocation. Conservative or surgical therapy. Clin Orthop 353:10-17 8. Calvo E, López-Franco M, Arribas Leal IM (2006) Surgical treatment of type III acromioclavicular joint dislocation results in osteoarthritis. J Shoulder Elbow Surg 15:300-305 9. McFarland EG, Blivin SJ, Doehring CB et al (1997) Treatment of grade III acromioclavicular separations in professional throwing athletes: results of a survey. Am J Orthop 26:771-774 10. Fraser-Moodie JA, Shortt NL, Robinson CM (2008) Injuries of the acromioclavicular joint. J Bone Joint Surg Br 90:697-707 11. Weaver JK, Dunn HK (1972) Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg Am 54:1187-1194 12. Mazzocca AD, Santangelo SA, Johnson ST et al (2006) A biomechanical evaluation of an anatomical coracoclavicular ligamento reconstruction. Am J Sports Med 34:236-246 13. Wolf EM, Pennington WT (2001) Arthroscopic reconstruction for acromioclavicular joint dislocation. Arthroscopy 17:558-563 14. Lafosse L, Baier GP, Leuzinger J (2005) Arthroscopic treatment of acute and chronic acromioclavicular joint dislocation. Arthroscopy 21:1017 15. Tauber M, Eppel M, Resch H (2007) Acromioclavicular reconstruction using autogenous semitendinous graft: results of revision surgery in chronic cases. J Shoulder Elbow Surg 16:429-433

Rotator Cuff Disorders

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T.R. Duquin, J.W. Sperling

Abstract Rotator cuff disorders are common injuries among athletes of all ages and activity levels. Their etiology involves both intrinsic tendon degeneration and extrinsic impingement. The diagnosis can often be made based on the history and physical examination, but magnetic resonance imaging is a useful tool for characterizing the severity of the injury. Treatment in most cases involves non-operative modalities, with a high level of success in patients without full-thickness rotator cuff tears. The surgical treatment of rotator cuff disorders continues to be successful at relieving pain in most individuals, with results of tendon healing and functional improvement being less consistent.

18.1 Introduction Rotator cuff disorders are common causes of shoulder pain in athletes of all ages and activity levels. Their incidence has increased with the greater activity level and demands of the aging population. This chapter focuses on the basic principles of rotator cuff biomechanics as well as the diagnosis and management of common rotator cuff disorders.

18.2 Rotator Cuff Anatomy and Biomechanics The rotator cuff consists of four muscles (supraspinatus, infraspinatus, teres minor, and subscapularis) that originate on the scapula and insert at the greater and lesser tuberosities of the humerus. Although the rotator cuff contributes to rotational movement of the shoulder, the primary function is compression and stabilization of the glenohumeral joint. The relatively small cross-sectional area and short lever arm of the rotator cuff muscles Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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result in their limited ability to generate large rotational forces; however, their position and orientation are ideal for generating compression across the glenohumeral joint. The dynamic stabilizing effect of the rotator cuff is essential to allow the large muscle groups (pectoralis major, latissimus dorsi, and deltoid) to move the shoulder through an arc of motion that approximates ball and socket mechanics with limited translation or shearing of the joint (Fig. 18.1). In addition to its function as a dynamic stabilizer and secondary rotator of the shoulder, the rotator cuff also depresses the head of the humerus due to a dynamic force couple between the infraspinatus and teres minor posteriorly and the subscapularis anteriorly. This depression effect of the rotator cuff helps counteract the large superior forces generated by the deltoid and prevents impingement of the humeral head on the undersurface of the acromion (Fig. 18.2). An in-depth examination of the anatomy and biomechanics of the shoulder is beyond the scope of this chapter and has been discussed in other chapters of this book. However, the reader should be aware that a basic understanding of the functional anatomy of the rotator cuff is essential to understanding the associated pathology that results in rotator cuff disorders.

Fig. 18.1 Coronal plane force couple of rotator cuff resulting in dynamic stabilization of the humeral head

Fig. 18.2 Axial plane force couple of rotator cuff resulting in dynamic stabilization of the humeral head

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18.2.1 Etiology of Rotator Cuff Disorders Similar to tendinopathies in other areas of the body (tennis elbow, Achilles tendon), the true pathology of rotator cuff disorders involves little to no inflammatory component in the tendon itself and therefore is most accurately described as a tendinosis rather than as a tendonitis. The exact etiology of tendinosis of the rotator cuff has yet to be determined; but several intrinsic and extrinsic factors have been implicated in the disease process.

18.2.1.1 Intrinsic Factors Intrinsic factors affect the tendon itself and include degenerative changes associated with aging, poor vascularity, and mechanical properties. In 1934, Codman described a critical zone for injury approximately 1 cm medial to the supraspinatus insertion. This zone has subsequently been correlated with an area of relative hypovascularity of the tendon. The rotator cuff of elderly patients has decreased healing and regenerative properties in addition to increased rates of apoptosis, both of which contribute to the development of rotator cuff pathology. Tension overload and differential strain patterns within areas of the tendon’s insertion are also involved in the development and progression of rotator cuff tears.

18.2.1.2 Extrinsic Factors Extrinsic factors are the result of impingement of the rotator cuff tendon on the acromion, coracoid, or glenoid rim. External impingement, in which there is compression of the rotator cuff under the acromial arch, has been recognized since the early 1900s. However, it was Neer who described the essential lesion at the anterior aspect of the acromion, and Bigliani [1, 2] who subsequently classified the degree of impingement based on acromial morphology, with type I being flat, type II curved, and type III hooked. Several other factors contribute to the development of external impingement, mainly, intra-articular pathology, such as instability, labral tears, and biceps injury, and extra-articular factors, such as rotator cuff weakness or periscapular muscular imbalance (Fig. 18.3). Internal impingement is a common source of rotator cuff and labral pathologies in overhead athletes. In the late-cocking and early-acceleration phases of throwing, the greater tuberosity contacts the posterior and superior aspects of the glenoid rim. Capsular changes associated with throwing often result in anterior laxity, increased external rotation, and decreased internal rotation, which increases compression of the greater tuberosity against the glenoid rim. The end result over time is tearing of the rotator cuff and superior labrum. Recently, impingement between the lesser tuberosity and the coracoid and anterior glenoid

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Fig. 18.3 External impingement of the greater tuberosity on the undersurface of the acromion

Fig. 18.4 Internal impingement of the greater tuberosity on the posterosuperior aspect of the glenoid labrum resulting in tearing of the articular side of the rotator cuff and posterosuperior labrum

rim with the arm in a position of forward flexion, adduction, and internal rotation has been recognized as a cause of subscapularis tendon injury (Fig. 18.4). Disruption of the dynamic stabilization and depression functions of the rotator cuff by either intrinsic or extrinsic factors leads to the development of internal and external impingement. The result is a negative feedback loop that causes further cuff injury and dysfunction, by increasing impingement and tearing the rotator cuff tendon (Fig. 18.5).


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Fig. 18.5 Negative-feedback loop of rotator cuff disorders resulting in disease progression

18.2.2 Natural History of Rotator Cuff Disorders Rotator cuff disease comprises a spectrum of disorders ranging from bursitis and tendinopathy to full-thickness rotator cuff tears and rotator cuff arthropathy. As noted above, the etiology of rotator cuff pathology is a complex interaction of many factors. To further complicate matters, the presence of rotator cuff pathology does not always correlate with symptoms or physical findings. An individual with a relatively normal rotator cuff can have significant pain and limitation of activity, while a patient with a large rotator cuff tear may be asymptomatic. Magnetic resonance imaging (MRI) of the shoulders of asymptomatic volunteers showed rotator cuff tearing in 20-35% of participants [3]. Similar studies looking at full-thickness tears using ultrasound have shown a prevalence of 13% in asymptomatic 50- to 59-year-olds and > 50% in those over 80 [4]. It is currently not understood why some individuals with rotator cuff pathology experience pain and loss of function while others do not. Most orthopedic surgeons agree that, if left untreated, rotator cuff pathology is likely to progress and will eventually become symptomatic; however, there is only limited evidence supporting this theory. A recent longitudinal study of patients with asymptomatic rotator cuff tears seen on ultrasound found that > 50% became symptomatic at their 5year follow up [5]. Repeat ultrasound revealed that 50% of those who developed symptoms had tear progression compared to only 20% of the asymptomatic group. This suggests that tear progression often results in the development of symptoms, but some tears remain asymptomatic despite progression. A greater understanding of the natural history of rotator cuff disorders and the factors that lead to progression is needed to guide treatment of patients with asymptomatic rotator cuff tears.

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18.2.3 Clinical Evaluation 18.2.3.1 History The presenting symptoms of rotator cuff pathology often include lateral shoulder pain that is worse with lifting or overhead activity and pain at night that disturbs sleep. Athletes who are involved in repetitive overhead activities will often complain of stiffness, warmup pain, and pain that persists for several hours after activity. Occasionally, they will notice a loss of strength or range of motion that impairs performance. Minor trauma or an episode of overuse is often associated with the onset of symptoms, but acute traumatic injuries also occur in contact sports and subsequent to higher-energy collisions. A careful assessment of the rotator cuff is necessary in patients who sustain a shoulder dislocation. This is especially true in those over the age of 50, as the rates of associated traumatic rotator cuff tear have been shown to increase with age and are higher in females. Patients often present after symptoms have persisted for several months and many have already undergone a trial of physical therapy or other non-operative treatments. Knowledge of the duration of symptoms and of previous shoulder function is important especially in younger patients in order to assess whether there has been an acute traumatic tear that may benefit from early surgical management.

18.2.3.2 Physical Examination Physical examination of the bare shoulder region is necessary to assess the presence of muscle atrophy as well as scapular kinematics. A determination of active and passive ranges of motion in both the affected and contralateral shoulder is important. Isometric strength assessment of the individual rotator cuff muscles with comparison to the normal shoulder will often generate insight into the extent of the rotator cuff pathology. The supraspinatus is tested by resisted elevation in 90° of abduction, 30° of flexion, and maximal internal rotation. Resisted external rotation of the arm in an adducted and neutral position with the elbow flexed tests the infraspinatus, while resisted external rotation in 90° of abduction tests the teres minor. Many methods of assessing subscapularis strength have been reported, including the lift-off, belly-press, and bear-hug tests. Assessment of shoulder stability using an anterior and posterior drawer test and an apprehension test with relocation maneuvers is an important component in the evaluation of the young athlete. Throwing athletes should also be examined for excessive external rotation with an associated lack of internal rotation. This finding, termed glenohumeral internal rotation deficit (GIRD), is associated with posterior capsular tightness and subtle anterior instability that contribute to internal impingement and rotator cuff and labral tears in athletes. Pain with the impingement signs described by Neer and Hawkins [1, 6] are diagnostic for external impingement. The Neer impingement sign involves passive forward elevation of the arm in an internally rotated position, while the Hawkins impingement sign is tested


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by internally rotating the shoulder with the arm in 90° of flexion and 30° of adduction. A Neer impingement test involves the injection of lidocaine into the subacromial space and repeat evaluation; an improvement of pain, strength, and range of motion indicates symptomatic subacromial impingement. Other sources of pain in the shoulder must also be determined in patients who present with complaints consistent with rotator cuff pathology. Common conditions that can mimic the pain of rotator cuff include cervical spine radiculopathy, adhesive capsulitis, glenohumeral or acromioclavicular arthritis, labral tears, biceps tendinopathy, scapular dyskinesis, and suprascapular nerve entrapment. Careful examination of these areas is required even in the patient who has documented rotator cuff pathology.

18.2.4 Imaging 18.2.4.1 Radiographs Plain radiographs of the shoulder should include anteroposterior, scapular-Y, and axillary views. The morphology of the acromion should be assessed on the scapular-Y lateral view, with rotator cuff impingement suspected in those with a type III acromion. Subtle or nonspecific findings are often noted in patients with rotator cuff impingement, including sclerosis of the greater tuberosity and the undersurface of the acromion. Radiographic signs of large or massive tears include superior migration of the humeral head, which results in loss of continuity of the gothic arch formed by the medial neck of the proximal humerus and the inferior aspect of the glenoid neck as well as a decrease of the acromiohumeral distance (normal > 6 mm) (Figs. 18.6, 18.7).

a

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Fig. 18.6 Acromial morphology on scapular-Y radiographs. Flat type I (a), curved type II (b), hooked type III (c)

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Fig. 18.7 Radiographic signs of rotator cuff tear. Sclerosis and cystic change of the greater tuberosity and acromion (arrows); subtle superior migration of the humeral head is indicated by a loss of the “gothic arch” (white lines)

18.2.4.2 Magnetic Resonance Imaging The gold standard for assessment of rotator cuff disorders is MRI. In young athletes, the use of intra-articular contrast can increase sensitivity in the diagnosis of partial-thickness rotator cuff tears and associated labral pathology. It is important to include the entire scapula on the MRI so that both the rotator cuff muscles atrophy and fatty infiltration can be assessed. Supraspinatus atrophy has been identified as a negative prognostic indicator for rotator cuff healing, and the tangent sign described by Zanetti can be used to quantify the degree of supraspinatus atrophy [7, 8]. The degree of fatty infiltration of the supraspinatus muscle on axial CT scans has been shown to influence tendon healing [9]. However, while it has become common practice to assess fatty infiltration with an MRI, the accuracy of this practice has not been confirmed (Fig. 18.8).

18.2.4.3 Ultrasound Ultrasound has become an accepted alternative to MRI for assessment of rotator cuff pathology and is useful in patients with metal implants from prior surgeries. The sensitivity and specificity of ultrasound approach that of MRI scans, with the benefit of enabling dynamic examination [10]. However, ultrasound examination is extremely operator-dependent and requires someone with experience in performing and reading musculoskeletal ultrasound to ensure accurate results.


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Fig. 18.8 Sagittal MRI showing severe to atrophy of the supraspinatus with a positive tangent sign of Zanetti (white line) and fatty infiltration of the infraspinatus (white arrow)

18.2.5 Non-operative Management The initial management of rotator cuff pathology should be non-operative in all patients, with the exception of a full thickness tear in a young active patient. Non-operative modalities, including activity modification, NSAIDs, corticosteroid injections and physical therapy, are successful in 70-80% of patients without full-thickness tears. The outcomes of these measures in patients with full-thickness rotator cuff tears are less successful. Stretching of the posterior capsule and modification of throwing mechanics have been successful in throwing athletes with GIRD. NSAIDs and corticosteroid injections are successful for improvement in pain and function, with multiple studies failing to show significant superiority of one over the other. Corticosteroid injections have been demonstrated to compromise the quality of tendon tissue in animal models [11]. Tendon changes are unlikely to occur with a single injection, but there is concern regarding the effect of multiple injections on the quality of rotator cuff tissue. The efficacy of other non-operative modalities commonly used in rotator cuff disorders, such as ultrasound, phonophoresis, or iontophoresis, has not been established. The duration of non-operative management before proceeding to surgical treatment is influenced by age, activity level, and the degree of rotator cuff pathology. Non-operative management of tendinopathy or partial-thickness tears is unlikely to alter the results of future surgery. Similarly, the outcome of large or massive tears with fatty atrophy will not change with attempts of non-operative management. In these individuals, prolonged non-operative treatment is appropriate. However, small or medium-

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Fig. 18.9 Decision-tree diagram for the treatment of rotator cuff disorders

sized full-thickness tears are at risk of progression that may affect the outcome of eventual surgical repair since successful healing after rotator cuff repair occurs in > 90% of small tears compared to f 60% in large and massive tears. Therefore, prolonged non-operative management or the use of multiple injections is not advisable (Fig. 18.9). Our preferred practice is to obtain an MRI if a patient has failure of at least 6 weeks of non-operative management with NSAIDs and therapeutic exercises. We will perform subacromial injections at least once and up to three times before considering surgical intervention in patients with partial-thickness tears or elderly patients with large or massive tears. In younger patients with full-thickness tears, we consider early surgical repair and will not perform more than one subacromial injection. If non-operative treatment is successful in these patients, we advise follow-up on a yearly basis, or sooner if they become symptomatic or notice any development of weakness.


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18.2.6 Surgical Management 18.2.6.1 Subacromial Impingement Arthroscopic debridement with subacromial decompression is used for patients who, after thorough evaluation for other sources of pain in the shoulder, fail to improve with several months of non-operative management. Arthroscopic acromioplasty has produced good and excellent outcomes in 70-90% of patients in most reported series [12, 13]. However, the ability of subacromial decompression to prevent progression is less clear, with some studies showing development of tears in 20% of patients with long-term follow up [14].

18.2.6.2 Partial-thickness Rotator Cuff Tears The depth of a partial-thickness tear is the most important factor in determining whether debridement or repair should be performed. General consensus exists for debridement of tears involving < 50% of the tendon, and repair if the tear involves > 50% of the tendon. However, there is little to no evidence in the literature to support the 50% rule, and other factors should be considered in the decision for repair, including patient age and activity, tear location, and quality of the remaining tendon. The tear should be carefully evaluated on the articular and bursal surfaces since occasionally there will be partial tears on both sides of the tendon. During arthroscopic evaluation, the use of a suture to mark the location of an articular-sided tear allows for easy localization in the subacromial space, and the decision to repair should be made based on the total amount of tearing on both sides of the tendon (Fig. 18.10). The role of subacromial decompression and acromioplasty in the treatment of partialthickness tears has also been debated. The patient with classic external impingement with a bursal-sided tear will respond well to subacromial decompression in 75-85% of cases. However, long-term follow up reveals increased rates of re-operation for recurrent pain and progression of disease [15]. The ability of a subacromial decompression to alter the natural history has been questioned, as some studies have reported enlargement or progression to full-thickness tear in up to 80% of partial tears treated with debridement and acromioplasty alone. In addition, the results of subacromial decompression for articularsided tears are less predictable. Further controversy exists as to the best method of repair for a partial-thickness tear. Partial bursal-sided tears can easily be repaired, leaving the remaining tendon intact. Transtendinous arthroscopic repair techniques have been described that allow the repair of a partial articular supraspinatus tendon avulsion. However, there is some concern that the remaining tendon is not normal and leaving it as such may result in problems in the future. Our preference for the treatment of partial-thickness tears involves debridement of tears involving < 50% of the tendon, with subacromial decompression for bursal-sided tears or if evidence of subacromial impingement exists in articular tears. In tears > 50% of the


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Fig. 18.10 a MRI showing partial-thickness tear of the articular and bursal sides of the tendon. b Articular partial-thickness tear marked with PDS suture. c Bursal-sided partial-thickness tear marked with PDS suture, individually the tear is < 50% but its combined total size is > 50%

tendon, our preferred method of repair is to take down the remaining intact fibers, with debridement of the tendon down to healthy tissue followed by repair using a single- or double-row technique based on tear size and configuration. We perform these repairs both open and arthroscopically, with no long-term difference in outcome between the two.

18.2.6.3 Full-thickness Rotator Cuff Tears Repair of full-thickness rotator cuff tears is indicated in patients with persistent pain despite non-operative management. Recently, there has been an interest in early fixation in patients younger than 60 to prevent tear progression or atrophy of the rotator cuff musculature. The current available evidence is limited but it does suggest that most tears in a young, active person will progress over time. However, we cannot predict which tears will progress or become symptomatic and which remain stable, so the decision as to when to proceed to surgical treatment is challenging and should be made on an individual basis.


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There has been a rapid explosion in the popularity and techniques for arthroscopic rotator cuff repair, with a recent survey showing > 60% of surgeons performing arthroscopic rotator cuff repairs [16]. The indications for open and arthroscopic repair are identical and patients should not be misled into believing that arthroscopic repair is a lesser operation or that there is more rapid recovery, since the rate-limiting step following rotator cuff repair is the healing of the tendon, not the skin incisions. The benefits of arthroscopic repair are that the deltoid insertion is left intact and, in the hands of a skilled arthroscopic surgeon, the ability to view and access all areas of the rotator cuff are improved. However, in the hands of surgeons inexperienced in arthroscopic repair, mobilization and fixation of the tendon can be challenging. The long-term results of arthroscopic and open repairs have shown no difference in clinical outcomes or tendon healing, and surgeons should use whatever approach allows them to perform the best repair. Rotator cuff repair results in pain relief in 85-90% of patients, but the functional improvements are less predictable [17]. Strength and range of motion following rotator cuff repair depends on tendon healing, while pain relief and overall patient satisfaction occurs even in patients with failed repairs [18]. The reason for this is unclear, but it is fortunate because failure of tendon healing has been reported to be > 80% in some series of large and massive tears. Tendon healing is the primary objective of repair despite the fact that overall good results can be obtained even if it does not occur. Double-row repair techniques have become popular due to improved biomechanical strength and the ability to re-establish the footprint area and contact pressure. A recent systematic review of healing rates following double- and single-row repairs revealed higher re-tear rates with single-row repairs for all tears > 1 cm [19]. However, multiple clinical trials have failed to show a difference in clinical outcome measures between single- and double-row repair methods with short-term follow-up. It is likely that the improved healing rates with double-row repairs will result in improved clinical outcomes with longer-term follow up, but there is currently no evidence to confirm this theory. Interest in the use of biological methods to stimulate healing of rotator cuff repairs has increased recently. Platelet-rich plasma (PRP) has been injected to stimulate healing of partial-thickness tears and to augment the repair of full-thickness tears, but a significant improvement in healing rates or clinical outcomes has yet to be confirmed. There is enthusiasm in the use of biologics, and it is likely that the next significant improvement in the treatment of rotator cuff disorders will be to improve the biology of tendon healing by either direct or indirect means. Our current treatment of symptomatic full-thickness rotator cuff tears is to perform either open or arthroscopic repair using a suture bridge technique. A simple sling is employed following repair, and passive range of motion performed by a family member is started on the first day after surgery and continued for 4 weeks. Range of motion exercises with a pulley and wand are begun at 4 weeks, and active assisted exercises are started at 6 weeks. We discontinue the sling and allow use of the arm for activities of daily living without lifting at 6 weeks. Strengthening is started at 3 months, and full return to activity is allowed between 4 and 6 months, depending on recovery of strength and range of motion.

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18.3 Conclusions Rotator cuff disorders are common and include a spectrum of disease in a variety of patients, from the competitive athlete to the elderly individual who is still active in recreational sports. The underlying etiology involves an interaction between intrinsic and extrinsic factors, and progression of disease is common if intervention is not performed. It is important to note that clinical presentation does not always correlate with the degree of tendon pathology, and each patient must be treated on an individual basis. Despite recent enthusiasm for early surgical repair, an initial trial of non-operative management is still indicated in most patients. There has been rapid advancement in the surgical techniques for the treatment of rotator cuff pathology, such that currently there is little evidence to support the use of any one technique over another. Therefore, the orthopedic surgeon must use clinical judgment and experience to arrive at the best treatment for each patient.

References 1. Neer CS (1972) Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J Bone Joint Surg Am 54:41-50 2. Bigliani LU, Morrison DS, April EW (1986) The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 10:228 3. Sher JS, Uribe JW, Posada A et al (1995) Abnormal findings on magnetic resonance images of asymptomatic shoulders. J Bone Joint Surg Am 77:10-15 4. Tempelhof S, Rupp S, Seil R (1999) Age-related prevalence of rotator cuff tears in asymptomatic shoulders. J Shoulder Elbow Surg 8:296-299 5. Yamaguchi K, Tetro AM, Blam O et al (2001) Natural history of asymptomatic rotator cuff tears: A longitudinal analysis of asymptomatic tears detected sonographically. J Shoulder Elbow Surg 10:199-203 6. Hawkins RJ, Kennedy JC (1980) Impingement syndrome in athletes. Am J Sports Med 8:151158 7. Thomazeau H, Boukobza E, Morcet N et al (1997) Prediction of rotator cuff repair results by magnetic resonance imaging. Clin Orthop 344:275-283 8. Zanetti M, Gerber C, Hodler J (1998) Quantitative assessment of the muscles of the rotator cuff with magnetic resonance imaging. Invest Radiol 33:163-170 9. Goutallier D, Postel J, Bernageau J et al (1994) Fatty muscle degeneration in cuff ruptures. Pre- and postoperative evaluation by CT scan. Clin Orthop 304:78-83 10. Teefey SA, Hasan SA, Middleton WD et al (2000) Ultrasonography of the rotator cuff. A comparison of ultrasonographic and arthroscopic findings in one-hundred consecutive cases. J Bone Joint Surg Am 82:498-504 11. Tillander B, Franzen LE, Karlsson MH et al (1999) Effect of steroid injections on the rotator cuff: an experimental study in rats. J Shoulder Elbow Surg 8:271-274 12. Gartsman GM (1995) Arthroscopic treatment of rotator cuff disease. J Shoulder Elbow Surg 4:228-241 13. Odenbring S, Wagner P, Atroshi I (2008) Long-term outcomes of arthroscopic acromioplasty for chronic shoulder impingement syndrome: a prospective cohort study with minimum 12 years’ follow-up. Arthroscopy 10:1092-1098


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14. Hyvonen P, Lohi S, Jalovaara P (1998) Open acromioplasty does not prevent the progression of an impingement syndrome to a tear. Nine-year follow-up of 96 cases. J Bone Joint Surg Br 80:813-816 15. Weber SC (1999) Arthroscopic debridement and acromioplasty versus mini-open repair in the treatment of significant partial-thickness rotator cuff tears. Arthroscopy 15:126-131 16. Vitale MA, Kleweno CP, Jacir AM et al (2007) Training resources in arthroscopic rotator cuff repair. J Bone Joint Surg Am 89:1393-1398 17. Cofield RH, Parvizi J, Hoffmeyer PJ et al (2001) Surgical repair of chronic rotator cuff tears: A prospective long-term study. J Bone Joint Surg Am 83:71-77 18. Harryman DT II, Mack LA, Wang KY et al (1991) Repairs of the rotator cuff. Correlation of functional results with integrity of the cuff. J Bone Joint Surg Am 73:982-989 19. Duquin TR, Buyea C, Bisson LJ (2010) Which method of rotator cuff repair leads to the highest rate of structural healing? A systematic review. Am J Sports Med 38:835-841

Elbow Injuries

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S.A. Antuña, R. Barco Laakso

Abstract Elbow injuries in athletes are becoming more frequent, especially in those involved in racket and throwing sports. Correct diagnosis of a painful elbow requires a thoughtful understanding of the anatomy and complex kinetics of this joint. Although elbow problems may present acutely, they are more commonly seen as chronic overuse syndromes. Elbow tendinopathy is caused by tendinous microtearing followed by an incomplete reparative response. Lateral and medial epicondylitis are more common in the amateur athlete and usually respond to conservative measures. Participants in overhead sports are subjected to tremendous valgus and extension overload, generating medial tensile forces with compression on the lateral compartment and shear stresses posteriorly. This may lead to chronic injury to the elbow, the so-called valgus extension overload syndrome. This spectrum of pathology includes insufficiency of the medial collateral ligament, osteochondritis dissecans of the capitellum (in young athletes), and posterior olecranon impingement syndrome. In patients who fail to respond to conservative measures, surgical reconstruction of the medial ligament, or arthroscopic debridement of capitellar or olecranon lesions may be required. Lateral elbow pain may be due to posterolateral instability, usually found in the context of previous trauma or surgical treatment of radial head fractures or epicondylitis. Radiohumeral synovial plicae must be also considered in the differential diagnosis of pain on the lateral aspect of the elbow. Tendon ruptures, affecting the biceps and triceps, occur more often in weight lifters and should be treated surgically by re-attaching the torn tendon to bone.

19.1 Introduction Athletic injuries of the elbow are becoming more common as more people participate in throwing and racquet sports. Elbow injuries may involve any of the anatomic structures in the region, and the evaluation of elbow pain can be challenging. Diagnosing the injury Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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SA. Antul\a. R. Balm Laakso

correctly requires an understanding of the anatomy of the elbow, which consists of three articulations, two 1igammrt: complexes, four muscle groups, and three major nerves. Elbow injuries in athletes may be acute or chronic. This chapter will focus on the most common chronic overuse injuries. The type of injury that is encountered depends, to SODW extent. on the athletic pursuit, but the injuries can be roughly grouped into entbcsopatbies (lateral and medial epicondylitis), tendinopatbics (biceps and triceps), valgus extension overload syndrome, latexal instability, nerve compression syndromes, and osteochondritis dissecans. Some of these injuries, such as those involving the medial coUateralligament (MCL), occur much mmc frequently in the athlete; however, many ofthescproblems, such as lateral epicondylitis and biceps tendon ruptures, arc more often seen in individuals who do not participate in high school, collegiate, or professional sports. Regardless of w1wther these injuries occur in the professional or amateur athlete, it is the sports medicine physician who is usually called upon to manage elbow injuries.

19.2

Anatomy Ind Biomechanics The elbow contains three separate articulations. The ulnobllmeraljoint is a modified hinge jOOnt that allows flexion and extension. The radiohumeral joint is a combined 1ringc and pivot joint that permits flexion and extension as well as rotation of the head of the radius on the capitellum ofthc humerus. The proximal radioulnar joint facili.tates rotation during supination and pronation. Osseous stability is reinforced by the medial and lateral collatcxalligamcnt (LCL) complexes (Fig. 19.1). The MeL complcx comprises anterior, posterior, and transverse

•

AHCL

•

fig. ",1 The medial collateral ligament complex provides valgus stability, (a) with the anterior band (AMCL) being the most:important protection against valgus stress. The lateral ligament complex (b) resists varus and posterolateral rotatory displaccment. The lateral uInar collateral band

(LUCL) is the most importmrt in preventing rotatory instability. AL, annular ligament; ALGL, accessory lateral oollateralligamcnt; LCL, lateral collatmLlligamcnt; PMCL, posterior mcdial coliatcral.ligamcnt; roB, tnnsvcnc obliquc band

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bundles and, especially the anterior bundle, provides valgus stability. The LCL complex confers rotational and varus stability. Four muscle groups act on the elbow. The major flexors are the biceps brachii (which also supinates the forearm when the elbow is flexed), brachioradialis, and brachialis muscles while the extensors are the triceps and anconeus muscles. The supinators consist of the supinator and biceps brachii muscles. Pronation is accomplished by the pronator quadratus, pronator teres, and flexor carpi radialis muscles. The elbow also has a complex innervation. The median nerve crosses the elbow medially and passes through the two heads of the pronator teres, a potential site of entrapment. The ulnar nerve passes along the medial arm and posterior to the medial epicondyle through the cubital tunnel, a likely site of compression. The radial nerve descends the arm laterally, dividing into superficial (sensory) and deep (motor, or posterior interosseous) branches. The deep branch must then pass through the arcade of Frohse, a fibrous arch formed by the proximal margin of the superficial head of the supinator muscle, where it is most susceptible to injury. The functional range of motion of the elbow for activities of daily living is 30-130° of flexion and 50° of supination and pronation. This arc of motion allows independent function but would be very limiting for many athletic pursuits. The most appropriate range of motion varies with the type of sport. Additionally, although the elbow joint bears fewer loads than the hip or knee, it has been estimated that, at 90° of flexion, a force three times the body’s weight can be transmitted through the elbow [1]. The movement of the elbow is extremely complex in all athletic activities. Although the exact details differ in other overhead sports, the pitcher’s elbow movement can be used as a model of the stresses that are applied during strenuous activity. The throwing motion can be divided into six phases: wind up, stride, arm cocking, arm acceleration, arm deceleration, and follow-through. Minimal muscle activity and elbow kinetics are present during the wind up and stride phases [2]. At the conclusion of the arm cocking phase, the shoulder is abducted, extended, and externally rotated to about 130° and the elbow is flexed to about 90°. In this position, the elbow is subjected to severe valgus stress. The arm acceleration phase is the short time from maximum external rotation until ball release. During arm acceleration, the need to resist valgus stress at the elbow can result in wedging of the olecranon against the medial aspect of the trochlear groove and the olecranon fossa. This impingement leads to osteophyte formation at the posterior and posteromedial aspects of the olecranon tip and can cause chondromalacia and loose body formation. The arm deceleration phase lasts from ball release until the point at which the arm reaches its maximum internal rotation. The follow-through phase begins at maximum internal rotation and ends when the pitcher attains a balanced fielding position. When a patient presents with elbow pain, one should seek information about the quality of activities involving a repetitive load that could initiate a cycle of microtrauma, chronic inflammation, and tissue degeneration. In addition to the type of sport performed, it is quite useful to differentiate elbow problems in the athlete according to the location of the pain (Table 19.1).


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Table 19.1 Causes of elbow pain according to anatomic location Anterior elbow

Biceps tendinosis Pronator syndrome Musculocutaneous nerve compression

Posterior elbow

Posterior impingement Triceps tendinosis

Medial elbow

Medial epicondylitis MCL insufficiency Ulnar nerve entrapment

Lateral elbow

Lateral epicondylitis Osteochondritis dissecans Posterolateral rotatory instability Radial tunnel syndrome

MCL, medial collateral ligament

19.3 Elbow Disorders Pain on the medial aspect of the elbow is one of the commonest complaints in the throwing athlete. The source of pain can be ligamentous, muscular, or neurologic.

19.3.1 Valgus Instability The act of throwing depends on a stable elbow joint. Considerable emphasis has been placed on the role of the anterior bundle of the MCL in the stability of the elbow to valgus stress [1]. This ligament may be ruptured acutely, during a sudden valgus injury. However, more commonly, patients present with an insidious onset of vague medial elbow pain that worsens with activity. The pain is typically relieved with rest but returns on resumption of throwing. The cause of the pain is the subtle attenuation of the anterior band of the MCL due to repetitive microtrauma caused by excessive tension on the medial part of the joint. This entity is part of what has been called the “valgus extension overload syndrome.” Baseball players are the athletes most commonly affected; indeed, medial elbow symptoms account for up to 97% of elbow complaints in pitchers. However, athletes who participate in other sports that require similar overhead motion, such as football, volleyball, handball, tennis, and javelin throwing, can be likewise affected. Along with the history, physical examination will help to make the final diagnosis. Pain on palpation of the site of the MCL’s anterior band, with reproduction of the pain when a valgus stress force is applied with the elbow slightly flexed, is very suggestive of this entity. Testing of the anterior bundle can also be accomplished by the milking maneuver, which is performed by pulling on the patient’s thumb with the patient´s forearm supinated, shoulder extended, and elbow flexed beyond 90°.

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Fig. 19.2 Anteroposterior radiograph of a patient with clinical evidence of medial instability. There is an obvious calcification medially, suggestive of an old injury to the ulnar collateral ligament

Routine radiographs may show changes consistent with chronic instability, such as calcification and occasionally ossification of the ligament (Fig. 19.2). Stress radiographs can be used to confirm instability, especially in apprehensive patients and in patients in whom the clinical findings are equivocal. A medial joint opening greater than 3 mm is consistent with instability. Magnetic resonance imaging (MRI) is useful in evaluating ligamentous avulsions, partial ligamentous injuries, mid-substance tears, and the status of the surrounding soft tissues. The treatment of athletes with medial instability should start with conservative measures aimed at pain relief and, if possible, modification of the throwing mechanism. If the patient does not respond to conservative treatment or there is a high grade tear of the MCL, surgical intervention is warranted. Reconstruction of the MCL with a tendinous graft is the procedure of choice. The results of this technique using different grafts and various modifications of the original technique have been uniformly good [3].

19.3.2 Medial Epicondylitis Medial epicondylitis accounts for only 10-20% of all diagnoses of enthesopathies and is usually found in the dominant elbow of a golfer. Tennis players who hit their forehand with a heavy topspin are also at increased risk for developing medial epicondylitis. In general, it may be caused by training errors, improper technique, or inadequate equipment. Immunohistologic studies have shown that long-standing epicondylitis is associated with

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a degenerative state rather than a traditional inflammatory process. Ulnar nerve symptoms are associated in up to 20% of athletes with medial epicondylitis [4]. On physical examination, the athlete experiences pain with resisted wrist flexion, and there is palpable tenderness over the medial epicondyle. Pain is also frequently found with resisted forearm pronation. The Tinel sign should be checked over the ulnar nerve to rule out ulnar neuropathy. Plain radiographs may show calcification adjacent to the medial epicondyle, but radiography is not usually needed in the initial workup of this condition. Although in most cases MRI is not necessary, it should be considered in individuals with atypical symptoms or in patients who are not responsive to conservative measures. Treatment begins with rest, ice, compression, and bracing, to decrease pain and inflammation. The goal of physical therapy in the treatment of acute medial epicondylitis is to maintain the athlete’s range of motion. Modalities such as electrical stimulation, iontophoresis, phonophoresis, and ultrasonography are sometimes used to treat medial epicondylitis but few studies have demonstrated the long-term benefits of these methods [5]. When conservative treatment fails after 6-12 months, surgical treatment should be considered for medial epicondylitis. Various techniques have been described, most of which consist of release of the flexor origin and excision of the pathologic tissue. In general, good results are reported in over 80% of patients. Full return to sporting activity usually occurs within 4-6 months.

19.3.3 Ulnar Neuritis The presenting symptom of ulnar nerve entrapment is medial elbow pain, but the disorder is also characterized by distal paresthesias along the ulnar aspect of the forearm and into the ring and little fingers. The patient may complain of a weak grip, hand fatigue, and clumsiness. Ulnar nerve entrapment often occurs in throwing sports, as well as in racquet sports, weight lifting, and skiing. Tenderness or a positive Tinel’s sign is present over the ulnar nerve within the groove of the medial epicondyle. Other possible physical findings include hypothenar atrophy and index pinch weakness. Electrodiagnostic tests may be positive, but false-negative test results are common. Radiographs are often normal but may show olecranon hypertrophy, osteophytes, medial calcifications, or loose bodies. Once the diagnosis is made, a trial of conservative treatment is warranted, including rest, night splinting to avoid elbow flexion, and anti-neuritic and anti-inflammatory medications. When non-surgical treatment fails, surgical decompression of the nerve may be needed. Whether simple release or transposition is the preferred procedure is controversial [6], but it seems logical to move the nerve when there is severe valgus deformity of the forearm or when there are medial osteophytes in the cubital tunnel. The results of nerve decompression are usually good, and the prognosis is more closely related to the pre-operative status of the nerve.

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19.4 Lateral Elbow Disorders The source of pain on the lateral aspect of the elbow can be ligamentous, muscular, intraarticular, or neurologic.

19.4.1 Posterolateral Instability The cause of posterolateral rotatory instability of the elbow is the insufficiency of the ulnar part of the LCL complex [7]. This is more commonly seen as sequelae of elbow trauma affecting the ligament, with subsequent elbow dislocation with or without associated fractures. In athletes, it may be also diagnosed as failed surgical treatment of lateral epicondylitis, with secondary iatrogenic injury to the ligament. Clinically, these patients present with lateral elbow pain that is more intense with the elbow in extension and supination. Clicking and loss of strength are other common complaints. Physical examination shows apprehension with the lateral pivot shift test. Slight subluxation can be elicited with the drawer test. Radiographs may be normal but may also show posterolateral instability when performed under stress (Fig. 19.3). Surgical treatment is almost always indicated. Reconstruction of the lateral ulnar collateral ligaments with tendon grafts yields good results in the majority of cases, especially in those patients complaining of instability more than pain.

Fig. 19.3 Lateral stress radiographs of a golfer who had undergone a surgical procedure for lateral epicondylitis with secondary posterolateral instability. Note the posterior displacement of the radial head and ulnohumeral joint with extension and supination

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19.4.2 Lateral Epicondylitis The most common elbow problem in non-professional athletes is lateral epicondylitis. It is well known in tennis players but it also affects athletes participating in other racquet sports as well as in throwing athletes and golfers. It is associated with repetitive and excessive use of the wrist extensors, e.g., as a result of incorrect production of the single arm backhand stroke. Pathologically, there is degeneration of the origin of the extensor carpi radialis brevis (ECRB) at the common extensor origin. Clinically, patients complain of lateral elbow pain reproduced by forceful gripping. The pain is also reproduced by palpation of the ECRB origin and by resisted extension of the wrist with the arm extended. Simple radiographic studies are usually normal. Doppler ultrasound and MRI, although seldom required, may show increased vascularity at the common extensor origin and tendon degeneration, respectively. Most athletes respond to non-surgical methods of treatment. This includes activity modification, physiotherapy, and, occasionally, local steroid injection. Several randomized studies and meta-analyses have shown poor evidence of any long-term benefit of all forms of non-surgical treatments compared with the natural course of the disease [8]. Knowing that the great majority of patients improve over time, there are limited indications for surgery. Surgical release of the ECRB attachment is the procedure of choice, but there is no evidence of any benefit of one procedure over the other, including open, percutaneous, or arthroscopic techniques [9]. Therefore, it seems reasonable to conclude that the best procedure is the one with which the surgeon is most comfortable.

19.4.3 Intra-articular Pathology Although there may be several potential intra-articular sources of elbow pain, including loose bodies, radiohumeral arthritis, and synovitis, the two most commonly diagnosed entities causing lateral elbow pain are osteochondritis dissecans and radiohumeral plica. Osteochondritis dissecans presents as a localized injury of the cartilage and subchondral bone of the humeral condyle. The etiology is unknown, but ischemia and repetitive microtrauma are thought to be involved. It occurs almost only in the young athlete practicing throwing sports or gymnastics. Patients present with pain in the lateral elbow over the posterior capitellum, with synovial effusion. Locking and catching are also common when loose bodies are present. Physical examination often reveals reduced mobility, especially in extension. Diagnosis can be confirmed with simple radiographs, which initially show a radiolucent area in the capitellum progressing to fragmentation and detachment over time (Fig.19.4). Patients in the early stages of the disease, with stable lesions and open physes, do well with conservative treatment. When the physis is closed or there are loose bodies or unstable fragments, surgical treatment is indicated. The success of arthroscopic debridement depends on the size of the defect. Excellent results have been reported with osteocartilage grafts, but longer follow-up may be required to validate this option as the gold standard [10].

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An inflamed and thickened synovial fold entrapped between the radial head and capitellum is also a common source of lateral elbow pain [11]. It presents in patients of any age, usually those with a history of minor trauma, and may be encountered in combination with lateral tendinosis or minor intra-articular injury. On clinical examination, there is no pain at the tendinous insertion. Pain can be elicited by palpation of the radiocapitellar joint and is reproduced with pronation and extension. A click may sometimes be perceived by patients. If conservative measures fail to correct this problem, arthroscopic removal of the thickened tissue is the procedure of choice, with good results expected assuming that the correct diagnosis was made (Fig. 19.5).

a

b

Fig. 19.4 Anteroposterior radiographs of two patients with osteochondritis dissecans. During the initial phase, radiolucency on the capitellum can be detected (a). As the disease progresses, fragmentation, with intra-articular loose bodies, is seen (b)

Fig. 19.5 Arthroscopic view from the anteromedial portal of a synovial plica entrapped in the radiohumeral joint

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19.4.4 Radial Tunnel Syndrome Radial tunnel syndrome caused by a compression of the posterior interosseous nerve (PIN) is uncommon, but it is important because it may be confused with lateral epicondylitis [12]. It is more commonly due to entrapment of the PIN at its entrance on the supinator muscle (arcade of Frohse). This overuse syndrome is produced by repeated pronation and supination. Patients have pain on palpation of the proximal aspect of the supinator muscle, with possible irradiation to the proximal forearm. There is no motor deficit, no tendinosis on ECRB, and no articular pain. This entity usually resolves with rest and conservative measures. Surgical decompression of the nerve is rarely required.

19.5 Anterior Elbow Disorders Anterior elbow pain is an uncommon complaint among athletes. It may be caused by compression of the musculocutaneous or median nerves as they cross the elbow. However, the most frequent diagnosis is distal biceps tendinosis or rupture.

19.5.1 Distal Biceps Pathology Inflammation with subsequent degeneration of the distal biceps tendon is usually found in athletes involved in weight lifting [13]. It is necessary to be aware that, as in any other tendinous injuries in an athlete, anabolic steroid ingestion may be a contributing factor. Clinically, patients initially complain of deep anterior elbow pain that is clearly reproduced with resisted flexion and supination. MRI may show mucinous degeneration of the tendon attachment on the radial tuberosity. During the initial stages of the disease, conservative measures, including rest, non-steroid anti-inflammatories, and modification of activities, may reverse the degeneration process. However, when the problem has become chronic, surgical intervention is warranted. Distal biceps tendinosis and partial tears are best treated by detachment of the tendon, resection of the damaged tissue, and reattachment in the radial tuberosity. Distal biceps rupture is the final stage of biceps tendon degeneration and is caused by a sudden eccentric flexion force. Clinically, it presents as acute elbow pain, with proximal migration of the muscle belly and weakness in flexion and, especially, in supination. Once diagnosed, the rupture should be surgically treated by re-attaching the tendon to the radius. This can be done through different approaches (one vs. two incisions) and different fixation methods (bone tunnels, suture anchors, or endobutton technique) but there are no clinical differences among them; however, the endobutton seems to have better pullout strength [13].

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19.6 Posterior Elbow Disorders Pain over the posterior aspect of the elbow is fairly common among athletes. Although several anatomic structures may be involved, the two most frequent sources of pain are posterior olecranon impingement and triceps tendinopathy.

19.6.1 Valgus Extension Overload Syndrome Athletes involved in throwing sports are subjected to high valgus and extension stresses, which may lead to repetitive overload of the posterior compartment of the elbow joint and thus to olecranon impingement of the distal humerus [14]. Continuous microtrauma causes chronic synovitis and the formation of osteophytes (Fig. 19.6). Patients complain of posterior elbow pain during the terminal extension movement, limiting their ability to throw. Baseball, basketball, and javelin throwers are more commonly affected. On physical examination, pain can be reproduced by forceful extension of the elbow and by palpation of the posteromedial aspect of the olecranon. Concomitant ulnar nerve symptoms or medial instability may be present. Some patients have a mild extension contracture that should also be addressed at the time of surgery. Imaging studies, including simple radiographs and three-dimensional computed tomography scans, show osteophytes on the posteromedial aspect of the olecranon and related posterior area of the distal humerus. Once the diagnosis is made correctly, arthroscopic removal of the bone spurs and the synovitis yields satisfactory pain relief, and the great majority of patients are able to resume their previous level of activity.

a

b

Fig. 19.6 Lateral radiograph (a) and MRI view (b) of the elbow of a judo expert who complained of posterior elbow pain secondary to impingement. There is a fractured osteophyte posteriorly. His symptoms resolved after arthroscopic debridement

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19.6.2 Distal Triceps Pathology Tendinosis of the distal attachment of the triceps tendon may be found in the weight lifter. The pathology is also common to other enthesopathies, with tendon degeneration and inability to achieve adequate biological repair of the damaged tissue. Patients complain of posterior elbow pain, which can be reproduced with resisted extension. Sometimes, a discrete zone of tendon weakness may be palpated, coincident with the area of maximum pain. Treatment by conservative measures is often effective in relieving pain and recovering full elbow function. However, some patients may progress to chronic discomfort, which limits their level of performance. In these cases, surgical debridement of the affected tendon and repair of the remaining defect very commonly result in good outcomes [15].

19.7 Conclusions Sport medicine physicians should be aware of the increasing incidence of elbow problems among athletes and amateurs involved in overhead activities. The majority of these injuries are chronic, and can be easily diagnosed with an adequate physical examination. It is very useful to categorize the different entities according to the location of pain, although some patients may have concomitant pathologies, especially those with valgus extension overload syndrome. A trial of conservative measures is usually indicated and is often effective in relieving symptoms. Surgical options have become more popular recently with the advent of arthroscopic techniques. Patients should be informed of the nature of their injury and the necessity of adapting their limitations to their level of performance while they are recovering.

References 1. An KN, Morrey BF (1993) Biomechanics of the elbow In: Morrey BF (ed) The elbow and its disorders. WB Saunders, Philadelphia, pp 53-72 2. Frostick SP, Mohammad M, Ritchie DA (1999) Sport injuries of the elbow. Br J Sports Med 33:301-311 3. Ahmad CS, Elattrache NS (2006) Elbow valgus instability in the throwing athlete. J Am Acad Orthop Surg 14:693-700 4. Ciccotti MG, Ramani MN (2003) Medial epicondylitis. Tech Hand Up Extrem Surg 7:190196 5. Rineer CA, Ruch DS (2009) Elbow tendinopathy and tendon ruptures: epicondylitis, biceps and triceps ruptures. J Hand Surg 34A:566-576 6. Charles YP, Coulet B, Rouzard JC et al (2009) Comparative clinical outcomes of submuscular and subcutaneous transposition of the ulnar nerve for cubital tunnel syndrome. J Hand Surg 34A:866-874 7. Cheung EV (2008) Chronic lateral elbow instability. Orthop Clin North Am 39:221-228

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8. Kohia M, Brackle J, Byrd K et al (2008) Effectiveness of physical therapy treatments on lateral epicondylitis. J Sport Rehabil 17:119-136 9. Cohen MS, Romeo AA (2009) Open and arthroscopic management of lateral epicondylitis in the athlete. Hand Clinics 25:331-338 10. Takahara M, Mura N, Sasaki J et al (2007) Classification, treatment, and outcome of osteochondritis dissecans of the humeral capitellum. J Bone Joint Surg Am 89:1205-1214 11. Antuna SA, O’Driscoll SW (2001) Snapping plicae associated with radiocapitellar chondromalacia. Arthroscopy 17:491-495 12. Henry M, Stutz C (2006) A unified approach to radial tunnel syndrome and lateral tendinosis. Tech Hand Up Extrem Surg 10:200-205 13. Kokkakis ZT, Sotereanos DG (2009) Biceps tendon injuries in athletes. Hand Clinics 25:347357 14. Eygendaal D, Safran MR (2006) Postero-medial elbow problems in the adult athlete. Br J Sports Med 40:430-434 15. Mair SD, Isbell WM, Gill TJ et al (2004) Triceps tendon ruptures in professional football players. Am J Sports Med 32:431-434

Wrist Injuries

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P.R. Finkbone, M. Rizzo

Abstract The wrist is one of the most vulnerable and unprotected joints during athletic activity. When injured, it can significantly hinder an athlete’s success. Improper diagnosis and treatment of wrist injuries can lead to chronic pain and disability. Fractures of the wrist occur frequently in sports, with the scaphoid, distal radius, and triquetrum as commonly involved bones. The wrist is also prone to several varieties of ligamentous injury that can be challenging to diagnose and treat. Tendons can develop tenosynovitis and tendinitis secondary to overuse during training. Athletes are also susceptible to the development of nerve compression syndromes about the wrist. This chapter reviews the presentation, physical exam findings, diagnostic studies, and current recommended treatments for common wrist injuries and causes of wrist pain in athletes. It should serve as an aid to the sports medicine physician when evaluating athletes with wrist complaints.

20.1 Introduction The wrist is one of the least protected joints in the body and in the vast majority of sports there is no protective equipment dedicated to the wrist. However, the hand and wrist are often the most vulnerable to injury and are the first part of the body to sustain impact during a collision, fall, or impact through the use of a bat or club. The wrist is also vital to successful performance in several sports and wrist pain or dysfunction can greatly impact an athlete’s success. Wrist injuries require appropriate diagnosis and treatment for successful return to play and to decrease the athlete’s risk of chronic pain and disability. It is important that physicians who care for athletes have a basic understanding of wrist injuries and know when referral to a specialist is necessary. This chapter provides a brief overview of the common wrist injuries and causes of wrist pain in athletes. It should serve as a general reference and aid to the sports medicine physician when evaluating athletes with wrist complaints. Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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20.2 Fractures of the Wrist 20.2.1 Scaphoid Fracture The scaphoid is the most commonly fractured carpal bone and is the second most common wrist fracture. The reported incidence in college football players is 1 in 100 per year [1]. It often occurs secondarily to a fall on an outstretched hand although it may also result from axial loading or twisting injuries. Patients present with radially sided wrist pain and swelling. On physical exam, there will be anatomic snuffbox tenderness, pain with attempted scaphoid shift test, and pain with resisted pronation. The radiographic diagnosis can be elusive at times (early X-rays may be negative); however, the patient with snuffbox tenderness should initially be treated in a thumb spica splint. Recently, magnetic resonance imaging (MRI) has been gaining favor as a tool to diagnose occult scaphoid fractures. This may be worth the cost as it could save the athlete unnecessary immobilization or lead to earlier diagnosis and possible timely operative treatment. In addition, MRI may identify other lesions, such as non-displaced distal radius fractures or scapholunate ligament injuries. Computed tomography (CT) has also been shown to have utility in the diagnosis of occult fractures and has the added benefit of better demonstrating the bony architecture of the scaphoid. Proper diagnosis is vital, as patients who do not receive proper treatment can develop nonunion, avascular necrosis (AVN), and eventually advanced collapse. Scaphoid fractures are treated based on their risk of non-union and AVN. Displaced fractures, unstable fracture patterns, and fractures of the proximal pole require open reduction internal fixation (ORIF) to prevent AVN and non-union (Fig. 20.1). Arthroscopically assisted percutaneous reduction and screw fixation of displaced scaphoid fractures

a

b

Fig. 20.1 Computed tomography scan showing a proximal pole fracture of the scaphoid in a 21year-old football player (a). The fracture was treated with a percutaneously inserted compression screw (b)

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has had good preliminary results [2]. Arthroscopic techniques provide the benefit of less risk to the already tenuous blood supply of the scaphoid and less ligamentous injury than is associated with the exposure during open reduction. Fractures that are amenable to nonoperative treatment include non-displaced, stable waist, and distal pole fractures. There is controversy regarding whether a short-arm or long-arm cast is necessary. In the majority of studies, long-arm thumb spica casts have had slightly better results (rates of union); however, most compliant patients can be treated successfully with a short-arm thumb spica. The duration of immobilization is dependent on the fracture’s location. Waist fractures may require up to 3 months for union while distal pole fractures generally require 6 weeks. Some authors have advocated percutaneous screw fixation even in the case of stable, nondisplaced fractures. Studies have shown a significant reduction in time to union and return to activity, although long-term outcomes are likely similar to non-operative management [3]. The risk of such percutaneous techniques includes the possibility of displacing the fracture; therefore, the surgeon should be prepared for the possibility of performing an open reduction. The treatment of scaphoid non-union requires ORIF with bone graft. Return to play (RTP) should be decided on a case-by-case basis, taking into consideration the location of the fracture (time needed for union), the sport the athlete plays, and the method of treatment. In athletes involved in non-contact sports who are being managed non-operatively, the RTP is relatively soon thereafter, with the treated wrist in a protective cast. However, athletes involved in sports that require manual dexterity will not benefit from this treatment strategy, as prolonged immobilization may lead to stiffness and muscle wasting, a long period of rehabilitation, and a significant portion of the season missed. Instead, these athletes likely benefit from early percutaneous fixation as opposed to non-operative treatment. RTP as early as 6 weeks has been reported in this patient population [4]. The RTP for athletes in contact sports is controversial and often depends on the preference of the treating physician. Riester et al. reported good rates of union while allowing contact athletes to resume play immediately with a playing cast. Athletes were immobilized in a short-arm thumb spica cast which during play was exchanged for a silastic playing cast that complied with NCAA and high school regulations for games. Due to the possibility of returning contact athletes directly back to play, non-operative treatment may be preferred for non-displaced mid-third fractures [1]. Nonetheless, some experts now recommend a more conservative approach to RTP in contact athletes, suggesting that RTP should be delayed for 6 weeks followed by a CT to confirm fracture healing, with RTP in a playing cast at that time. If internal fixation is used in contact athletes, the earliest RTP may be 2-3 weeks with a playing cast [5] although some physicians prefer to wait for radiographic union.

20.2.2 Distal Radius Fracture Distal radius fractures are the most common wrist fracture and represent one out of six fractures that present to the emergency department. They most often occur secondarily to a fall on an outstretched hand. Patients present with wrist pain, swelling, bony tenderness, and deformity (if there is significant angulation or displacement). The diagnosis is readily confirmed with a radiograph of the wrist.

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The approach to treatment in athletes is similar to that used in the general population; however, small changes in radial height, inclination, and volar tilt may be more noticeable to dexterous athletes. Generally accepted parameters for non-operative treatment in a young active patient include neutral volar tilt, < 5-10° loss of radial inclination, < 2-3 mm loss of radial height, and < 1-2 mm of intra-articular step-off. Small articular splits without step-off are acceptable and can be expected to heal in with fibrocartilage. A better approach to treatment involves distinguishing low-energy injuries (stable, extra-articular metaphyseal fractures) from high-energy injuries (more common in athletes). Highenergy fractures often have a significant amount of comminution and articular involvement [6]. There also may be an axial compression component in these injuries, which causes articular comminution and die-punch lesions. CT can be a valuable tool to assess the fracture fragments and articular surface in more complex fractures. Non-operative management includes a long- or short-arm cast for approximately 6 weeks or until radiographic evidence of union. For fractures that do not meet acceptable criteria or in athletes that require anatomic reduction, treatment options include ORIF, percutaneous pin fixation, and/or external fixation. High-energy fractures generally have less favorable results when treated non-operatively (too unstable secondary to comminution) and usually require surgery. In some patients with distal radius fractures, there is a concomitant ligamentous injury of the wrist [7]. These injuries are often not diagnosed at the time of initial injury but can be just as important to treat as the fracture. Radiographic evidence of associated ligamentous injury includes widening of the scapholunate interval and abnormal lunate position on lateral (DISI and VISI deformity, see “Wrist Ligamentous Injuries”, below) or dorsal subluxation of the ulna. Some surgeons have advocated the use of arthroscopically assisted reduction and internal fixation (ARIF) to aid in the diagnosis of ligamentous injuries. Using this technique, the articular surface can be reduced under direct visualization and the fixation can be done percutaneously with K-wires, while any ligamentous injuries can be adequately diagnosed and treated as well. Fractures of the ulnar styloid may indicate avulsion or detachment of the ulnar insertion of the triangular fibrocartilage complex (TFCC). The distal radioulnar joint (DRUJ) should be assessed for instability after fixation of the distal radius and, if unstable, fractures involving the base of the styloid or the fovea should be fixed. In addition, DRUJ instability may exist without ulnar styloid fracture and can be treated with immobilization of the DRUJ in a reduced position and/or TFCC repair. RTP is achieved when the fracture is stable and the athlete is pain free. The determination of fracture stability is at the discretion of the treating physician but in the majority of cases radiographic evidence of union is necessary. Athletes involved in sports in which manual dexterity is necessary will require a rehabilitation program to regain their previous level of performance.

20.2.3 Hamate Hook Fractures Hamate hook fractures can occur during a fall but more often are a sport-specific injury, typically racquet sports, baseball, or golf. The primary mechanism of injury is direct com-

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pression over the hypothenar eminence; however, tension from the pull of the hypothenar muscles and shearing from the adjacent flexor tendons may contribute as well. In baseball and golf, the injury most commonly occurs on the non-dominant hand, and in racquet sports on the dominant hand. Patients present with a history of ulnar-sided wrist pain. They may occasionally have paresthesias in the ulnar nerve distribution or mild carpal tunnel syndrome. Grip strength is usually decreased secondary to pain, compression of the ulnar nerve motor branch, and/or from disturbance of the adjacent flexor tendons. In acute cases, all patients will have tenderness over the hamate. On physical exam, there may be pain with resisted ring- and small-finger flexion which is worst with the wrist in ulnar deviation and improves with radial deviation. Radiographic diagnosis is challenging and requires special views that include a carpal tunnel view, oblique view with the wrist partially supinated and radially deviated, or a lateral view with the thumb abducted. Alternatively, a CT scan can be used to identify the fracture. The treatment of choice for athletes is fragment excision [8]. This allows early mobilization of the wrist and quicker RTP. While an ORIF can be performed as well, it can be very challenging and there is no significant benefit over excision. At the time of excision, release of Guyon’s canal or the carpal tunnel can be performed when indicated. The flexor tendons should also be examined for fraying, rupture, or tenosynovitis, which is most common in chronic presenters and can be seen in up to 25% of cases [9]. Non-operative treatment is an option for non-displaced fractures presenting acutely (within 7 days of injury). The wrist needs to be immobilized in slight flexion with the small- and ring-finger metacarpophalangeal joints in flexion. Immobilization of the thumb may also minimize the pull from the thenar muscles through attachments to the transverse carpal ligament. Duration of immobilization is usually 8-12 weeks and the fracture should be followed closely with radiographs in case displacement occurs. If this indeed happens, fragment excision is likely the best option as the hook of the hamate has a very poor blood supply and limited capacity for healing. Immobilization of chronic hamate hook fractures is associated with a high rate of non-union [8]. For those treated with excision, RTP is relatively quick. Grip strengthening and light workouts (dry swings, chipping) with a protective glove may be allowed after sutures are removed at 10-14 days. At 3 weeks, athletes may progress to hitting a ball off of a tee (baseball), light volleying (racquet sports), or full swings off of a mat (golf). Players can return to full activity at 4-6 weeks.

20.2.4 Other Carpal Bone Fractures Less common carpal fractures that occur in athletes include fractures of the triquetrum, hamate body, and trapezium. Triquetral fractures can be divided into dorsal chip fractures and body fractures. Dorsal chip fractures can be treated symptomatically with short-term splinting followed by RTP with wrist protection. Triquetral body fractures occur in the context of greater arc perilunate fracture dislocations and have significant associated injuries. If the fracture is displaced or if there is associated perilunate instability, then ORIF or pinning is indicated. Hamate body fractures may be classified as either coronal or transverse

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and should be managed with ORIF if displaced, especially if there is associated carpometacarpal dislocation. Trapezial body fractures are treated with a thumb spica cast unless there is displacement and articular involvement, which requires ORIF. Trapezial ridge fractures are divided into type I fractures (base), which can be treated with cast immobilization, and type II fractures (tip avulsion), which have a high rate of non-union and require excision. Fractures of the capitate, trapezoid, and lunate are even rarer injuries [10].

20.3 Wrist Ligamentous Injuries 20.3.1 Scapholunate Injuries Scapholunate injuries typically occur due to a fall on an outstretched, pronated hand with forced hyperextension, ulnar deviation, and intercarpal supination. The patient may present acutely or with a chronic history of wrist pain following the initial injury. Pain is present on the radial and dorsal sides of the wrist. Exam will reveal tenderness at the scapholunate interval and anatomic snuffbox, as well as a positive (or painful) scaphoid shift test (Watson test). This test is performed by applying a volar force on the distal tubercle of the scaphoid (to prevent flexion of the scaphoid) and bringing the wrist from ulnar to radial deviation. In scapholunate dissociation, there will be dorsal subluxation of the proximal pole at the radiocarpal joint. As the volar pressure is released, the scaphoid reduces and there is a painful clunk. The scapholunate interosseus ligament is an important structure for maintenance of the arched configuration of the proximal row. It consists of a thick, transverse dorsal component, a thin oblique palmar ligament, and a proximal region composed of fibrocartilage. The scaphoid tends to naturally fall into flexion while the triquetrum tends to extend. Through interosseus connections with the lunate, the scaphoid and triquetrum resist each other, but when the scapholunate ligament is torn (particularly the dorsal component) this restraint can be lost, allowing the scaphoid to flex and the lunate and triquetrum to extend [11]. This can be seen on the lateral radiograph as a DISI (dorsal intercalated segmental instability) deformity of the lunate, which means the longitudinal axis of the lunate tilts dorsally. Additional radiographic findings suggestive of the injury include a flexed and foreshortened scaphoid (cortical ring sign) and an increase in the distance between the scaphoid and lunate (< 2 mm is normal). Stress views (grip views) can be useful to accentuate the scapholunate diastasis. The angle between the longitudinal orientation of the scaphoid and lunate on lateral radiograph has also been used to diagnose the injury, with normal being 30-60°. In acute or partial injuries, these changes may only be dynamic in nature and will be harder to pick up on radiographs. Of the advanced imaging options, CT arthrography may be better than MRI; however, overall detection is still suboptimal. If clinical suspicion is high enough but the diagnosis cannot be confirmed with imaging, diagnostic arthroscopy is required. In the acute setting, dynamic instability can be treated non-operatively with a shortarm cast although many surgeons prefer to treat these patients surgically. Arthroscopy can

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be beneficial to confirm dynamic instability, to perform debridement (of partial injuries), or for arthroscopic reduction and pinning of an unstable dynamic injury. For athletes who have acute scapholunate instability with DISI, repair of the scapholunate interosseous ligament is advocated. The goal is to reduce symptoms, stabilize the scapholunate joint, and delay the progression of carpal arthritis. The ligament may be directly repaired and augmented with dorsal capsule. In the subacute or chronic setting, ligament tissue is often insufficient for primary repair. Alternative options include dorsal capsulodesis, ligament reconstructions using tendon grafts, bone-ligament-bone graft, fixation of the scapholunate interval with a Herbert screw, or other intercarpal arthrodeses [12]. Patients treated accordingly usually have symptomatic relief and can return to high-level competition; however, there can be significant loss of wrist motion with these procedures and this may affect performance in certain athletes. Additionally, long-term follow-up has shown a high rate of recurrence as well as eventual development of degenerative arthritis and collapse [13]. Due to these poor results, some have suggested a role for non-operative management in chronic scapholunate dissociation, with the understanding that a salvage procedure will eventually be necessary [14]. Regardless of the choice of treatment, a discussion needs to be held with the athlete concerning realistic expectations and possible outcomes. Once arthritis has developed, salvage procedures include radial styloidectomy, proximal row carpectomy, PIN (posterior interosseus nerve) neurectomy, or scaphoid excision with fourcorner arthodesis.

20.3.2 Other Patterns of Carpal Instability Lunotriquetral instability is the second most common carpal instability but has an incidence six times less than that of scapholunate instability. The lunotriquetral joint is supported by the intercarpal ligament and by the dorsal radiolunotriquetral (RLT) ligament. In order for instability to be present, there has to be some degree of disruption in the RLT ligament and in the interosseus ligament. The mechanism of injury is a fall on the extended wrist in radial deviation with forced intercarpal pronation. These instabilities can also occur in conjunction with TFCC tears or perilunate injuries. They occasionally cause a VISI (volar intercalated segmental instability) deformity, analogous to the DISI deformity resulting from scapholunate dissociation; however, in this case, the longitudinal axis of the lunate tilts volarly. On physical exam, the injury can be detected with the lunotriquetral shear or compression test. Initial treatment includes immobilization, which is sufficient in approximately 80% of patients. In those who continue to have ulnar-sided wrist pain, diagnostic arthroscopy and debridement is the most appropriate surgical treatment. Those who fail arthroscopic treatment may benefit from an ulnar shortening osteotomy [15]. Ligament reconstructions and lunotriquetral fusion procedures are also being tried by some surgeons in the treatment of subacute and chronic lunotriquetral instabilities. Midcarpal instability involves disruption in the kinematic relationship between the proximal and distal carpal rows. Patients may complain of a “clunk” when moving the wrist in ulnar deviation and pronation. The proximal row normally moves from a flexed to extended position when going from radial to ulnar deviation; this motion is usually a smooth

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one. Instead, with midcarpal instability, the proximal row “sags” in flexion and as the wrist is ulnarly deviated the proximal row experiences a “catch up clunk” to snap back into an extended position. The disruption in this condition is due to an insufficiency of the ulnar portion of the volar arcuate ligament. Initial treatments should be conservative, with an emphasis on activity modification. Surgical efforts have been described in which reinforcement of the ligamentous complex or fusion of the midcarpal joint in a reduced position is attempted. Perilunate injuries involve instability within the proximal carpal row as well as between the proximal and distal rows. Mayfield described these injuries in stages, starting with scapholunate dissociation (stage 1) and progressing around the lunate to eventually result in lunate dislocation (stage 4). Injuries that occur through bone (fracture dislocations) are termed “greater arc” injuries while those that are purely ligamentous are termed “lesser arc” injuries. These are high-energy injuries that occur with the wrist in hyperextension and ulnar deviation. Perilunate and lunate dislocations are best seen on the lateral radiograph. The radius, lunate, and capitate should be fairly co-linear, with the lunate sitting on the radius and the capitate on the lunate. Posteroanterior radiographs may show disruption of Gilula’s arcs and excessive gaps between the carpal bones. Prompt diagnosis and reduction is important as the injury usually becomes irreducible after 3-4 days. Patients often present with median nerve distribution numbness. If this progressively worsens, then an emergent carpal tunnel release is needed. Definitive treatment involves open reduction, ligament repair, and internal fixation. Surgery is ideally timed 3-4 days after the injury, to allow swelling to subside, but may need to be done sooner if the closed reduction cannot be maintained in the splint or if there is acute carpal tunnel syndrome [16]. If surgery is delayed beyond 6 weeks, then results decline and the patient will likely require a salvage procedure. These injuries are severe and can be expected to be seasonending at a minimum.

20.3.3 Triangular Fibrocartilage Complex Tears and Distal Radioulnar Joint Instability The TFCC is the primary stabilizing structure of the DRUJ and comprises several anatomic structures, including the dorsal and volar radioulnar ligaments, the extensor carpi ulnaris (ECU) tendon subsheath, meniscus homologue, volar ulnar extrinsic ligaments, and triangular fibrocartilage, which have attachments to the radius, ulna, and carpus. The periphery of the TFCC has a vascular supply while the central portion is avascular. Deep fibers of the TFCC insert into the fovea at the base of the ulnar styloid. Injuries of the TFCC commonly present as ulnar-sided pain, with a popping or clicking sensation. There may or may not be a history of traumatic injury in which an axial load was applied to an ulnar-deviated wrist while in extreme supination or pronation. Clicking can often be reproduced on physical examination by holding the wrist in ulnar deviation, applying an axial load, and then moving the wrist in supination and pronation. The “press test” can also be useful for diagnosis but it may be very non-specific. This test consists of having the patient apply an axial load by using the affected wrist to push his or her own weight up from a chair. If this reproduces the wrist pain, then the test is consid-

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ered positive [17]. Patients often have tenderness at the foveal insertion of the TFCC, which is at the soft spot between the ulnar styloid and the flexor carpi ulnaris (FCU) tendon; this has been termed the “ulnar fovea sign”. MRI and arthrography have variable sensitivity and arthroscopy is often necessary to confirm the diagnosis. Radiographs are useful to show ulnar positive variance or associated DRUJ instability. The classification system developed by Palmer categorizes TFCC injuries into acute traumatic injuries (type 1) and chronic degenerative injuries (type 2) and subcategorizes injuries based on which structures are damaged (Table 20.1) [18]. Initial treatment for TFCC tears with no associated fractures or DRUJ instability is nonoperative and consists of immobilization, corticosteroid injections, oral anti-inflammatories, and physical therapy. If conservative measures fail then surgical options are offered, including TFCC repair (peripheral lesions) or debridement (central lesions). Patients with arthroscopic evidence of chronic lesions and ulnar positive variance require an ulnar-shortening procedure (ulnar-shortening osteotomy vs. wafer resection) or they will likely have recurrence of symptoms. TFCC injuries with associated DRUJ instability can be initially treated conservatively or with repair. If conservative treatment is chosen, the forearm is immobilized in supination for 4 weeks followed by wrist immobilization for an additional 2 weeks. Beyond 6 weeks, any attempt at repair may need to be augmented with a free tendon graft (usually the palmaris longus). The stability of the DRUJ in the volar and dorsal directions is primarily maintained by the respective radioulnar ligaments but support is also provided by the articulation between the radius and ulna at the sigmoid notch [19]. DRUJ instability can occur secondarily to solitary injuries to the TFCC or in relation to fractures of the radius or ulna. The DRUJ can be tested by stabilizing the radius with one hand and translating the ulna in volar and dorsal directions, assessing for excess laxity, subluxation, and firmness of endpoint. Distal radius fractures may have associated DRUJ instability, especially when there is an additional fracture involving the fovea (base) of the ulnar styloid or when the distal radius fracture has associated displacement at the margin of the sigmoid notch. If DRUJ instability is present after ORIF of a distal radius fracture, the ulnar styloid should be sur-

Table 20.1 Classification of triangular fibrocartilage complex (TFCC) lesions Type 1

Traumatic lesions

A B C D

Central lesion, near radial attachment Ulnar avulsion (with or without fracture of ulnar styloid) Distal avulsion from attachment to lunate Radial avulsion (with or without sigmoid notch fracture)

Type 2

Degenerative lesions (ulnocarpal abutment)

A B C D E

TFCC wear (horizontal portion) Wear with chondromalacia of lunate and/or ulna Wear, chondromalacia, and TFCC perforation Wear, chondromalacia, perforation, and disruption of the lunotriquetral ligament Ulnocarpal ± degenerative arthritis in the distal radioulnar joint, TFCC and lunotriquetral ligament may be completely disrupted

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gically fixed. Displaced sigmoid-notch marginal fragments should be reduced and fixed with a K-wire or screw – this can be done arthroscopically or open. DRUJ instability is also commonly seen in fractures of the distal radial diaphysis (Galleazi fracture). Fractures of the radial head can be associated with disruption of the interosseus membrane and DRUJ dislocation (Essex Lopresti fracture). As a general rule of thumb, it is always good to assess the DRUJ intra-operatively, after fixation of all radius fractures. If the DRUJ is reducible, it should be splinted in the most stable position (usually supination). If necessary for stability, the DRUJ may need to be pinned.

20.3.4 Ulnar Impaction Syndrome In ulnar impaction syndrome there is ulnar positive variance, central tears of the TFCC, and chondromalacia of the adjacent articular surfaces of the lunate, triquetrum, and ulnar head. Patients will present with ulnar-sided wrist pain and tenderness at the ulnocarpal space dorsally. A positive ulnar impaction test consists of reproducing the patient’s pain with passive, forceful ulnar deviation and wrist extension. Characteristic imaging findings for the condition include radiographs (with the wrist in neutral pronosupination) that show ulnar positive variance and subchondral lucency of the proximal lunate and triquetrum. An MRI will exhibit signal changes in the distal ulna, proximal lunate, and TFCC (the central region). If conservative treatments fail to provide relief, then surgical treatment addressing the ulnar positive variance and TFCC pathology is necessary. Arthroscopic debridement of the TFCC tear and ulnar wafer resection can be performed with good results, whereas peripheral tears of the TFCC should be treated with an open procedure as they may be amenable to repair [20]. Ulnar-shortening osteotomy can be performed as an alternative to wafer resection (Fig. 20.2). If there is significant arthritis, ulnar-head resection (Darrach), ulnarhead replacement, and interpositional arthroplasty are treatment options.

20.4 Tendon Disorders Repetitive motions of the wrist make athletes very susceptible to overuse injuries of the tendons and soft-tissue supporting structures. Tennis players are particularly at risk for such injuries but other athletes can sustain them as well. Tendonitis generally has a chronic waxing and waning nature and the majority of treatments involve conservative management. Rarely, athletes can sustain tendon ruptures, which require prompt diagnosis and repair. Stenosing tenosynovitis of the first dorsal compartment, also known as De Quervain’s tenosynovitis, is the most common wrist tendinitis seen in athletes. It occurs secondarily to thickening of the extensor tendons and extensor retinaculum of the first dorsal compartment. This thickening causes relative narrowing of the fibro-osseus tunnel that houses the abductor pollicis longus (APL) and extensor pollicis brevis (EPB) tendons. The incidence is much higher in women, but among athletes the most susceptible include wrestlers,

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a

b

c

Fig. 20.2 Radiographs of a patient with persistent ulnar sided wrist pain after a fall, showing ulnar positive variance (a). The magnetic resonance image showed a “kissing lesion” of the lunate from ulnar impaction (b). Arthroscopy revealed chondromalacia of the lunate and a central triangular fibrocartilage complex tear with fraying. The patient was successfully treated with arthroscopic debridement of the tear and an ulnar shortening osteotomy (c)

bowlers, rowers, golfers, and racquet sport players. Onset of pain is gradual and motions that exacerbate symptoms include grasping, lifting objects with the wrist in neutral position, and thumb abduction or extension. On physical exam, patients will have tenderness of the first dorsal compartment (over the radial styloid), pain with ulnar deviation with the thumb in the palm (Finkelstein test or Eichoff maneuver), or pain with resisted thumb abduction while the wrist is in radial deviation. Imaging is usually not necessary to make the diagnosis but may be useful to eliminate other possible conditions (i.e., carpometacarpal arthritis). The mainstay of treatment consists of corticosteroid injections and splinting (forearm-based thumb spica splint). Rest and/or oral anti-inflammatories are also recommended but are not as effective at achieving cure when used as a sole treatment. Corticosteroid injection alone can provide relief in over 80% of patients. Results from splinting following injection are actually lower (61%), and splinting alone provides cure in only 14% of

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patients [21]. An injection can be repeated in 4-8 weeks in patients who initially have a partial response. If the patient continues to have symptoms despite receiving 2-3 corticosteroid injections, surgical release of the first dorsal compartment can be helpful. Anatomic variation is very common and proper identification of accessory slips, compartments, and subsheaths is necessary in order to adequately decompress the APL and EPB tendons. Additionally, care must be taken to avoid damage to the sensory branch of the radial nerve, which can lead to paresthesias or neuroma formation. Intersection syndrome is another cause of forearm and wrist pain that needs to be distinguished from DeQuervain’s tenosynovitis. Symptoms involve pain and crepitation at the intersection of the tendons of the first dorsal compartment (EPB and APL) and the second dorsal compartment (extensor carpi radialis longus and brevis), which is located 4-8 cm proximally to the radial styloid. Patients may present after an episode of vigorous use of the wrist and forearm or with more chronic complaints. Swelling over the area of pain and tenderness are also common. Conservative treatment is usually successful and involves rest, non-steroidal anti-inflammatory drugs (NSAIDs), and immobilization with a thumb spica or wrist splint (in slight extension) [22]. If the patient is still symptomatic after 23 weeks then a steroid injection at the point of maximal tenderness should be offered. Rarely, surgical decompression and debridement is necessary. The ECU tendon occupies the sixth dorsal compartment of the wrist. It is stabilized in an osteofibrous sheath over the distal ulna and is susceptible to tenosynovitis, dislocation, and subluxation. The primary symptom with these lesions is dorsoulnar wrist pain worsened by supination, flexion, and ulnar deviation. Reproducible clicking can be elicited during ulnar deviation in supination (subluxation of tendon) and pronation (tendon reduces). Conservative measures are usually effective and include immobilization, anti-inflammatories, injections, equipment modification, adjustments in training or technique, and activity modification. Occasionally, refractory cases require surgical treatment, which consists of surgical debridement of the sixth dorsal compartment and, in the case of ECU subluxation or dislocation, imbrication or reconstruction of the osteofibrous sheath and tunnel [23]. Isolated disorders of the ECU tendon are rare and, depending on clinical suspicion or the results of advanced imaging, and/or arthroscopy, may be indicated to assess for concomitant injuries prior to surgical treatment for the presumed isolated ECU tendon disorder. Common associated injuries include TFCC tear, lunotriquetral ligament injury, ulnar styloid non-union, and ulnocarpal impingement. Tendinitis of the flexor carpi radialis (FCR) is a rare disorder that causes volar radialsided wrist pain in athletes. The FCR is susceptible to tendinitis because it runs in a tunnel (adjacent to the carpal tunnel) that narrows at the distal aspect, where it is bound by the trapezial ridge and transverse carpal ligament. Tendinitis can occur primarily due to overuse or secondarily due to neighboring pathology (most commonly scaphotrapeziotrapezoid synovitis or arthritis). Pain is elicited during resisted wrist flexion and radial deviation. The diagnosis is difficult to make and a diagnostic injection into the FCR subsheath may be necessary. Treatment involves immobilization, physiotherapy, NSAIDs, or injection of corticosteroids. In refractory cases, surgical release of the tunnel and treatment of any local lesions (i.e., osteophytes) is indicated [24]. The strongest wrist flexor, the FCU, has a unique anatomy in that it does not have a synovial sheath and it contains a sesamoid (the pisiform). Patients with FCU tendinitis

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will present with ulnar-sided wrist pain, tenderness near the insertion of the FCU, and pain with resisted wrist flexion and ulnar deviation. Pisotriquetral arthritis can also cause ulnar-sided wrist pain and can be difficult to distinguish from tendinitis. Diagnostic injections and radiographs may be helpful to distinguish the two conditions. Occasionally, the FCU tendon will have calcifications, which can be seen on X-ray. Initial treatment for FCU tendinitis is conservative. Operative treatment in recalcitrant cases involves tendon debridement and/or Z-plasty lengthening of the tendon proximal to the insertion on the pisiform. If the pathology is primarily from the pisiform, then excision of the pisiform with repair of the defect in the FCU is the treatment of choice [25].

20.5 Nerve Compression Syndromes Athletes are at risk for nerve compression syndromes at the wrist secondary to repetitive motions, chronic external compression, or traumatic insults from activities related to their sport. They are also just as likely as the general population to have space-occupying lesions, such as ganglion cysts or anomalous muscles, which may accentuate these compressive syndromes. By in large, treatment for these conditions is conservative, consisting of splinting and injections; however, in refractory cases the compression about the nerve needs to be relieved. The affected nerve can usually be diagnosed fairly easily by a thorough neurologic examination although referred pain and double crush phenomenon can be present as well. Carpal tunnel syndrome is the most frequently seen nerve compression syndrome in athletes. Cyclists, throwing athletes, gymnasts, and racquet sport athletes are the most commonly affected. It is characterized by pain in the wrist with pain and numbness in the radial three and one-half digits. There also may be referred pain to the forearm, elbow, or shoulder. Symptoms may be worst at night or with certain activities. The diagnosis can be made using several described provocative tests, including Phalen’s, Tinel’s, and the carpal tunnel compression tests. Thenar weakness and atrophy may be present in long-standing cases. Semme-Weinstein monofilament testing and two-point discrimination testing can detect sensory deficits. Electromyography (EMG) and nerve conduction studies (NCV) studies can help confirm the diagnosis. Initial management includes night splints, corticosteroid injections, and activity modification (if an offending activity can be identified). Carpal tunnel release should be performed in those who continue to have symptoms or evidence of denervation. Endoscopic carpal tunnel release has been shown in some studies to allow an earlier return than achieved with open release, but there is a higher risk of an incomplete release. Acute carpal tunnel syndrome in a traumatic setting may require immediate carpal tunnel release. The ulnar nerve is located superficially at the wrist and has several sites at which it can be compressed. It provides sensation to the ulnar one and one-half digits and motor supply to the hypothenar muscles, ulnar two lumbricals, interossei, adductor pollicis, and deep head of the flexor pollicis brevis. It is at risk for compression in athletes secondary to repetitive compressive forces and inflammation in Guyon’s canal. It is also prone to

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distinct compressive lesions, with the site of compression determining whether there are sensory deficits, motor deficits, or both. Motor deficits may be evident by weak grip strength (intrinsics) and the presence of Froment’s sign (compensatory flexion at the interphalangeal joint of the thumb during key pinch secondary to adductor pollicis weakness). Lunotriquetral ganglion is the most common cause of ulnar tunnel syndrome secondary to a spaceoccupying lesion. Other lesions include a non-nunited hamate hook fracture (which can sometimes cause motor only deficits), ulnar artery thrombosis (ulnar hammer syndrome), anomalous muscle, palmaris brevis hypertrophy, or tumor (lipoma). Diagnostic workup may be catered to the suspected pathology and includes EMG/NCV, CT (hamate hook fracture), MRI (suspected ganglion or mass), or angiography (ulnar hammer syndrome). Initial management is conservative, but patients with persistent symptoms, evidence of denervation, or space-occupying lesions will require surgical decompression. The dorsal sensory branch of the ulnar nerve can also be irritated by the extensor tendons to the small finger, which can lead to neuroma formation or dorsoulnar pain in the hand. Other nerve compression syndromes about the wrist include Wartenberg’s syndrome and distal PIN compression. Wartenberg’s syndrome (also known as cheiralgia paresthetica) is characterized by pain and numbness in the distribution of the superficial branch of the radial nerve. It is caused by compression of the nerve from things worn around the wrist (watches, wrist bands, etc.) or by scissoring of the nerve between the brachioradialis and extensor carpi radialis longus tendons during supination and pronation. The PIN can also be compressed distally at the wrist due to hyperextension and can be associated with pain. This is commonly seen in weightlifters and gymnasts [26].

References 1. Riester JN, Baker BE, Mosher JF et al (1985) A review of scaphoid fracture healing in competitive athletes. Am J Sports Med 13:159-161 2. Slade JF, Lozano-Calderón S, Merrell G et al (2008) Arthroscopic-assisted percutaneous reduction and screw fixation of displaced scaphoid fractures. J Hand Surg Eur Vol 33:350354 3. Dias JJ, Wildin CJ, Bhowal B et al (2005) Should acute scaphoid fractures be fixed? A randomized controlled trial. J Bone Joint Surg Am 87:2160-2168 4. Rettig AC, Kollias SC (1996) Internal fixation of acute stable scaphoid fractures in the athlete. Am J Sports Med 24:182-186 5. Kovacic J, Bergfeld J (2005) Return to play issues in upper extremity injuries. Clin J Sport Med 15:448-452 6. Rettig ME, Dassa GL, Raskin KB et al (1998) Wrist fractures in the athlete. Distal radius and carpal fractures. Clin Sports Med 17:469-489 7. Hanker GJ (2001) Radius fractures in the athlete. Clin Sports Med 20:189-201 8. Hirano K, Inoue G (2005) Classification and treatment of hamate fractures. Hand Surg 10:151157 9. Bishop AT, Beckenbaugh RD (1988) Fracture of the hamate hook. J Hand Surg Am 13:135139 10. Marchessault J, Conti M, Baratz ME (2009) Carpal fractures in athletes excluding the scaphoid. Hand Clinics 25:371-388 11. Berger RA, Imeada T, Berglund L et al (1999) Constraint and material properties of the subregions of the scapholunate interosseous ligament, J Hand Surg 24A:953-962

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12. Lewis DM, Osterman AL (2001) Scapholunate instability in athletes. Clin Sports Med 20:131140 13. Moran SL, Ford KS, Wulf CA et al (2006) Outcomes of dorsal capsulodesis and tenodesis for treatment of scapholunate instability. J Hand Surg 31A:1438-1446 14. Kalainov DM, Cohen MS (2009) Treatment of traumatic scapholunate dissociation. J Hand Surg Am 34:1317-1319 15. Slade JF 3rd, Milewski MD (2009) Management of carpal instability in athletes. Hand Clin 25:395-408 16. Budoff JE (2008) Treatment of acute lunate and perilunate dislocations. J Hand Surg Am 33:1424-1432 17. Nagle DJ (2001) Triangular fibrocartilage complex tears in the athlete. Clin Sports Med 20:155166 18. Palmer AK (1989) Triangular fibrocartilage complex lesions: a classification. J Hand Surg Am 14:594-606 19. Henry MH (2008) Management of acute triangular fibrocartilage complex injury of the wrist. J Am Acad Orthop Surg 16:320-329 20. Bickel KD (2008) Arthroscopic treatment of ulnar impaction syndrome. J Hand Surg Am 33:1420-1423 21. Richie CA 3rd, Briner WW Jr (2003) Corticosteroid injection for treatment of de Quervain’s tenosynovitis: a pooled quantitative literature evaluation. J Am Board Fam Pract 16:102-106 22. Hanlon DP, Luellen JR (1999) Intersection syndrome: a case report and review of the literature. J Emerg Med 17:969-971 23. Allende C, Le Viet D (2005) Extensor carpi ulnaris problems at the wrist-classification, surgical treatment and results. J Hand Surg Br 30:265-272 24. Gabel G, Bishop AT, Wood MB (1994) Flexor carpi radialis tendinitis. Part II: Results of operative treatment. J Bone Joint Surg Am 76:1015-1018 25. Shin AY, Deitch MA, Sachar K et al (2004) Ulnar-sided wrist pain: diagnosis and treatment. J Bone Joint Surg Am 86A:1560-1574 26. Izzi J, Dennison D, Noerdlinger M et al (2001) Nerve injuries of the elbow, wrist, and hand in athletes. Clin Sports Med 20:203-217

Rehabilitation of the Upper Extremity

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W.J. Willems

Abstract Rehabilitation of the upper extremity is a very important element in the treatment of complaints of the shoulder and elbow in athletes, with or without concomitant surgery. Thus far, however, there is very little evidence supporting conservative treatment or rehabilitation as the best approach to the various upper-extremity pathologies in athletes. This chapter describes what evidence we have regarding the success of this strategy and, if no evidence is available, what is the best protocol, mostly based on experience, that the physician can follow when choosing a training program for the athlete under treatment.

21.1 Shoulder 21.1.1 Introduction Physiotherapy is usually the first choice in treating patients with shoulder pathology; however, there is a lack of evidence regarding its efficacy. A Cochrane report [1] reviewing physiotherapy intervention for shoulder pain, stiffness, and/or disability concluded that there is little overall evidence to guide treatment. Many studies examining the efficacy of physiotherapy have evaluated this approach in the context of a wide spectrum of pathologies but they were generally too heterogeneous with respect to treatment modalities. Consequently, their findings are of limited use in guiding clinical practice.

21.1.2 Instability Shoulder instability is a great challenge for the physiotherapist, beginning with its classification, as several classification systems have been developed. One of the oldest is that Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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of Matsen [2], in which a distinction is made between traumatic and atraumatic instabilities: TUBS (Traumatic, Unidirectional instability with Bankart lesion requiring Surgery) vs. AMBRII (Atraumatic Multidirectional Bilateral instability responding to Rehabilitation, and if surgery is chosen, then an Inferior capsular shift and closing the rotator Interval is performed). Another classification system was developed by Gerber et al. [3], who distinguished between static, dynamic, and voluntary instabilities. Static instability is defined by the absence of classic symptoms of instability, with the humeral head displaced and fixed in any direction relative to its normal position. Dynamic instability is diagnosed when glenohumeral joint stability is lost and temporary but reducible loss of joint congruency is present. Dynamic instability is always initiated by trauma. Table 21.1 provides an overview of this classification system. The third classification system is that of Bailey [4] and it divides instabilities into three groups: (1) traumatic structural, (2) atraumatic structural, and (3) habitual non-structural. In general practice, the Gerber classification is the most useful, as it provides an important distinction between hyperlaxity (which is always multidirectional and not pathological) and the very rare entity of multidirectional instability (MDI). However, thus far, none of the classification systems has been validated. Barden et al. [5] showed that patients with MDI may have a reduced capacity to use proprioception in the control of motor output of the upper limb, as a consequence of proprioceptive deficits. The presence of such deficits in patients following traumatic dislocation is well documented [6]. In a systematic review of non-operative management of shoulder instability, Gibson [7] showed that the quantity and quality of evidence regarding non-operative management of shoulder instability is very poor. For example, a period of immobilization of 3-4 weeks followed by a structured rehabilitation program of 12 weeks duration reportedly maximized return to the pre-morbid activity level in traumatic dislocations; this was, however, supported by weak evidence. Handoll et al. [8] concluded, in their Cochrane review, that there is limited evidence in favor of primary surgery after a first-time dislocation in young adults engaged in highly demanding physical activities. Moreover, current evidence suggests that non-surgical treatment should remain the primary therapeutic option for other categories of dislocation patients. In traumatic instability, rehabilitation generally does not lead to satisfactory results,

Table 21.1 Classification according to Gerber A Static instability

A1 Static superior instability A2 Static anterior instability A3 Static posterior instability A4 Static inferior instability

B Dynamic instability

B1 Chronic locked dislocation B2 Unidirectional instability without hyperlaxity B3 Unidirectional instability with hyperlaxity B4 Multidirectional instability without hyperlaxity B5 Multidirectional instability with Hyperlaxity

C Voluntary

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while muscle-strengthening programs have been shown to be quite successful in atraumatic shoulder instability [9-11]. Reinold et al. [12] described an extensive training scheme that is based on a biomechanical understanding of the pathology. Nonetheless, in patients with shoulder instability, further studies are needed with well designed trials, including comparisons of different rehabilitation protocols as well as surgery vs. rehabilitation. After repair of an unstable shoulder, either open or arthroscopically, a rehabilitation protocol is generally recommended. It includes immobilization and exercises in a restricted range of motion over a period of 6 weeks, especially concerning external rotation. This is based on the presumption that soft tissue heals to bone in about this period of time. A level II study with a mean follow-up of 31 months compared a group of patients who underwent arthroscopic instability repair and who post-operatively were treated with either immobilization or accelerated rehabilitation. The results showed that an accelerated program consisting of immediate staged exercises and strengthening does not improve outcome [13].

21.1.3 Disabled Throwing Shoulder Burkhart et al. [14] described the disabled throwing shoulder in throwing athletes, but it can also occur in other sports in which extreme abduction and external rotation are needed. The condition comprises several different pathologies. The most important causative factors are: 1. A tight posterior-inferior capsule causing GIRD (glenohumeral internal rotation deficit) and a posterosuperior shift in the glenohumeral rotation point, with a resultant increase in the shear stress applied to the posterosuperior glenoid labrum 2. Peel-back forces in the late cocking phase of throwing that add to the already-increased labral shear stress, thus causing a SLAP lesion 3. Hyperexternal rotation of the humerus relative to the scapula caused by the shift in the glenohumeral rotation point, such that clearance of the greater tuberosity over the glenoid is increased and the humeral head’s cam effect on the anterior capsule is reduced 4. Scapular dyskinesia sometimes leading to SICK scapula syndrome. Scapular dyskinesia is an alteration of the normal position or motion of the scapula during coupled scapulohumeral movements. It occurs after a large number of injuries involving the shoulder joint and is often a cause of shoulder pain [15]. These dyskinetic patterns fall into three categories, distinguished by the prominence of the inferomedial border of the scapula (type I), the entire medial border (type II), or the superomedial border (type III). Recently, Burkhart et al. [14] related the disabled throwing shoulder to a particular overuse muscle fatigue syndrome: the SICK scapula. The acronym SICK stands for Scapular malposition, Inferior medial border prominence, Coracoid pain and malposition, and dysKinesis of scapular movement. The main feature of this syndrome is the malposition of the scapula in the dominant throwing shoulder, which appears to be lower than the contralateral shoulder. Symptomatic patients may complain of anterior shoulder pain in the

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region of the coracoid, posterosuperior scapular pain with or without radiation to the paraspinous neck region or proximal lateral arm, superior (acromio-clavicular joint) shoulder pain, or radicular symptoms. Two types of tightness accompany the SICK syndrome, involving the pectoralis minor muscle and the posterior shoulder capsule. There are several protocols for treating scapulothoracic dyskinesis. The protocol described by Kibler et al. [16] for rehabilitation of scapular dyskinesis emphasizes the achievement of full and appropriate scapular motion and the coordination of that motion with complementary trunk and hip movements. The protocol of Burkhart et al. for patients with SICK scapula syndrome includes exercises to regain control of scapular protraction, retraction, depression, elevation, and rotation. Closed-chain exercises without weight are initiated to regain scapular control. Open-chain forward and lateral lunges and diagonal pulls are added, first without weights and then with 2- to 3-lb wrist weights or dumb-bells. The two areas of tightness are addressed by stretching both structures (pectoralis muscle and posterior capsule).

21.2 Elbow 21.2.1 Introduction In several throwing sports, excessive loads are transmitted through the elbow. Strain can lead to injuries of the cartilage and the ligaments, and continuous strain on the ligaments to micro-ruptures and, eventually, instability. A severe varus or valgus trauma of the elbow may be the cause of instability, sometimes necessitating surgery. Damage to cartilage can explain the early onset of arthritis, which subsequently reduces the strength and the mobility of the elbow.

21.2.2 Instability Instability, either lateral or medial, can be caused by a trauma, with or without dislocation of the elbow. O’Driscoll [17] graded lateral instability in four stages of severity. In stage I, only the lateral ulnar collateral ligament is injured. This results in posterolateral ulnohumeral rotatory subluxation. In stage II, both the anterior and posterior capsule fail, resulting in a rotatory instability with varus and valgus instability. In stage IIIA, the injury progresses through the medial collateral ligament and a complete dislocation occurs. Finally, in stage IIIB, complete disruption of the medial ligament creates a complex instability. Depending on the surgeon’s choice, either a conservative or operative approach is followed, with surgery mostly limited to severe cases. For conservative management and for postoperative rehabilitation, generally the same exercise program is followed [18].

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Early treatment, during the inflammation phase (0-3 weeks), is directed at maintaining stability and achieving a limited arc of motion, while the injured structures are healing. Protected range of motion (ROM) exercises are performed to prevent joint stiffness and augment healing. It is well-documented that early motion nourishes the cartilage and enhances soft-tissue healing. In the second phase, fibroblastic healing (3-6 weeks), active and assisted active ROM exercises are started, avoiding any subluxation or instability. In the third phase (6-12 weeks) of scar maturation, full active ROM exercises with increasing strength are performed and normal activities resumed. Throwing can start after 12 weeks. During shoulder strengthening, particularly external rotation, exercises are important to avoid posturing in internal rotation and abduction, thus adding stress to the lateral ligament complex.

21.2.3 Lateral Elbow Tendinopathy Although lateral elbow tendinopathy has a benign natural history, refractory cases are seen and are, as such, a therapeutic challenge. Several conservative treatments have been proposed, including therapeutic ultrasound, friction massage, acupuncture, extracorporeal shock-wave therapy, corticosteroid injections, strengthening, and eccentric training. However, some of these interventions are based more on tradition rather than on scientific rationale, and current evidence supporting their use is limited [19]. In a recent review on eccentric training, Malliaras [20] demonstrated promising results in the management of lateral elbow tendinopathy, although current data are limited.

21.2.4 Overuse Injuries Overuse leads to strain on cartilage and ligaments and the diagnosis is often very difficult. The most prominent sign is pain. For example, in handball goalkeepers there is frequently pain at hyperextension [21]. Good results have been described with strength training in this group of patients.

21.2.5 Little League Elbow (Osteochondritis of the Capitellum) In young athletes who participate in throwing sports, a rather high incidence of osteochondritis of the capitellum has been observed [22]. The prognosis depends on the severity of the cartilage lesion, which is diagnosed either with MRI or arthroscopy. In some cases, surgery is needed. If the cartilage is still intact, a more conservative approach is warranted, starting with exercises when pain has subsided and MRI shows that the lesion has healed.

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References 1. Green S, Buchbinder R, Hetrick SE (2003) Physiotherapy interventions for shoulder pain. Cochrane Database of Systematic Reviews, Issue 2 2. Matsen FA 3rd, Thomas SC, Rockwood CA, Wirth MA (1998) Glenohumeral instability. In: Rockwood CA Jr, Matsen FA 3rd (eds) The shoulder. 2nd edn. Saunders WB, Philadelphia, pp 611-754 3. Gerber C, Nyffeler RW (2002) Classification of glenohumeral joint instability. Clin Orthop Relat Res 400:65-76 4. Lewis A, Kitamura T, Bayley JIL (2004) The classification of shoulder instability: new light through old windows. Curr Orthop 18:97-108 5. Barden JM, Balyk R, Vaso RJ et al (2004) Dynamic upper limb proprioception in multidirectional shoulder instability. Clin Orthop 420:181-189 6. Myers JB, Lephart SM (2002) Sensorimotor deficits contributing to glenohumeral instability. Clin Orthop Relat Res 400:98-104 7. Gibson K, Growse A, Korda L et al (2004) The effectiveness of rehabilitation for non-operative management of shoulder instability: a systematic review. J Hand Therap 17:229-242 8. Handoll HGG, Almaiyah MA, Rangan A (2004) Surgical versus non-surgical treatment for acute anterior shoulder dislocation (review). The Cochrane Database of Systematic Reviews 9. Burkhead WZ, Rockwood CA (1992) Treatment of instability of the shoulder with an exercise programme. J Bone Joint Surg 74(A):890-896 10. Kiss J, Damrel D, Mackie A et al (2001) Non-operative treatment of multidirectional instability. Int Orthop 24:354-357 11. Takwale VJ, Calvert P, Rattue H (2000) Involuntary positional instability of the shoulder in adolescents. Is there any benefit from treatment? Am J Sports Med 82:719-723 12. Reinold MM, Escamilla R, Wilk KE (2009) Current concepts in the scientific and clinical rationale behind exercises for glenohumeral and scapulothoracic musculature. J Orthop Sports Phys Ther 39:105-117 13. Kim SH, Ha KI, Jung MW et al (2003) Accelerated rehabilitation after arthroscopic Bankart repair for selected cases: a prospective randomized clinical study. Arthroscopy 19:722-731 14. Burkhart SS, Morgan CD, Kibler WB (2003) The disabled throwing shoulder: spectrum of pathology. Part III: The SICK scapula, scapular dyskinesis, the kinetic chain, and rehabilitation. Arthroscopy 19:641-661 15. Kibler WB (1998) The role of the scapula in athletic shoulder function. Am J Sports Med 26:325-337 16. Kibler WB, McMullen J (2003) Scapular dyskinesis and its relation to shoulder pain. J Am Acad Orthop Surg 11:142-151 17. O’Driscoll SW, Morrey BF, Korineck S et al (1992) Elbow subluxation and dislocation: a spectrum of instability. Clin Orthop 280:186-197 18. Wolff AL, Hotchkiss RN (2006) Lateral elbow instability: nonoperative, operative, and postoperative management. J Hand Ther 19:238-244 19. Buchbinder R, Green S, Struijs P (2007) Tennis elbow. Am Fam Physician 75:701-702 20. Malliaras P, Maffulli N, Garau G (2008) Eccentric training programmes in the management of lateral elbow tendinopathy. Disab Rehabil 30:1590-1596 21. Tyrdal S, Pettersen OJ (1998) The effect of strength training on ‘handball goalie’s elbow’ – a prospective uncontrolled clinical trial. Scand J Med Sci Sports 8:33-41 22. Krijnen MR, Willems WJ (2003) Arthroscopic treatment of osteochondritis of the capitellum. Report of 5 female athletes. Arthroscopy 19:210-214

Section V Lower Extremity

Anatomy and Pathophysiology of Hip Injuries

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K.F. Bowman Jr., J.K. Sekiya

Abstract The diagnosis and management of hip injuries in the athlete has gained significant clinical interest due to the improved ability to diagnose and manage these problems. The clinical evaluation of hip pathology can be difficult due to the complex local anatomy and frequently vague symptoms. A greater understanding of the clinically relevant anatomy and pathophysiology of intra-articular causes of hip pain can help the treating physician to successfully manage these injuries. These causes include skeletal deficiency, femoroacetabular impingement (FAI), labral tear, capsular laxity, hip instability, and articular cartilage injuries. The clinical goal of treatment is to alleviate symptoms of pain and prevent the development or progression of degenerative changes in the hip.

22.1 Introduction The evaluation and management of hip injury and pain in the young athletic patient has recently become a subject of intense interest in the practice of sports medicine. This is a trend that can be attributed to the increasing recognition and success in managing the symptoms associated with intra-articular and peri-articular pathology, such as labral tears, femoroacetabular impingement (FAI), capsular laxity, developmental dysplasia, and articular cartilage injury. The long-term outcomes of these interventions are not fully known, and there remains a paucity of studies evaluating the biomechanical implications of these disorders. Alterations in the anatomy of the hip through acute injury, chronic degeneration, or surgery can significantly impact the function of the hip during activities. The clinical goal of treatment is to alleviate symptoms of pain and prevent the development or progression of degenerative changes in the hip.


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22.2 Anatomy The hip effectively acts as a multi-axial ball and socket joint upon which the upper body is balanced during stance and gait. Stability of this joint is critical to allow motion while supporting the forces encountered during daily activity. Nearly all motion between the femoral head and acetabulum is rotational, with minimal translation due to the congruency of the articular surfaces. The range of motion required in the hip during everyday tasks can be described with three rotational axes. The high degree of articular congruency is provided by the bony architecture of the joint, the acetabular labrum, articular cartilage, joint capsule, and the surrounding musculature. The articular surfaces are covered by multiple highly organized layers of hyaline cartilage arranged in a specific distribution to appropriately handle the forces placed across the hip joint. It functions as a gliding surface and to dissipate the high forces experienced across the joint. Interestingly, the compressive abilities of the articular cartilage vary according to their location on the hip surface, and a mismatch in structural properties during certain motions or activities may predispose the hip to frequently observed patterns of injury or degeneration. The acetabular labrum is a complex structure consisting of a fibrocartilaginous rim composed of circumferential collagen fibers spanning the entirety of the acetabulum and becoming contiguous with the transverse acetabular ligament [1]. The complete physiological function of the labrum is not entirely defined, but it appears to serve multiple purposes, including a limitation of extreme range of motion and deepening the acetabulum to enhance the stability of the hip joint. The labrum contributes approximately 22% of the articulating surface of the hip and increases the volume of the acetabulum by 33% [2]. The labrum also provides a sealing rim around the joint, enabling increased hydrostatic fluid pressure to facilitate synovial lubrication and resistance to joint distraction [3]. Continuity with the transverse acetabular ligament provides conformity with the articular surfaces during range of motion while compensating for minor joint incongruities. This allows the labrum to function in its most important role of dissipating the high potential contact forces encountered by the hip joint during activity and weight-bearing at any flexion angle. The dynamic stability of the hip is further augmented by the strong surrounding capsule and ligaments. The capsule is divided into three distinct bands. These include the medial iliofemoral ligament, or the Y-ligament of Bigelow, originating from the area between the anterior inferior iliac spine and the acetabular rim and inserting on intertrochanteric line. Its role is to limit extension and external rotation of the hip and to assist in the maintenance of a static erect posture with minimal muscular activity. The ischiofemoral ligament originates from the ischial rim of the acetabulum and follows the iliofemoral ligament as it twists around the femoral head and inserts onto the posterior aspect of the femoral neck, limiting internal rotation and hip adduction with flexion. The femoral arcuate ligament is confluent with the posterior hip capsule and tensions the capsular tissue with extreme range of motion [4]. The ligamentum teres does not appear to contribute a significant amount of restraint to the femoral head when com-

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pared to the capsular ligaments and the osseous anatomy but does attain a state of mild tension during extreme hip adduction to function as a secondary contributor to hip stability [4]. Due to the complexity of the hip anatomy and varied clinical presentation of intra-articular pathology identification and management of hip pathology remains a clinical challenge. After identifying potential sources of pathology, further diagnostic testing and treatment including diagnostic injection and MR arthrogram can be employed for further clinical assessment [5]. This may help the orthopedic surgeon target the individual pathologies responsible for the patient’s symptoms and appropriately direct the orthopedic care. Understanding the potential future implications of injury to the hip and possible treatment effects can also help in predicting the future prognosis for development of recurrent symptoms or osteoarthritis.

22.3 Pathophysiology of Hip Injury 22.3.1 Osseous Anatomy The inherent stability of the hip is attributed to the depth of the acetabulum and the high level of anatomic congruity between the articular surfaces. Alteration of this important relationship can have significant consequences on the forces and contact areas experienced at the joint surface. In dysplastic conditions in which there is insufficient coverage of the femoral head by the acetabulum, contact between articular surfaces is concentrated on a small area of articular cartilage on the lateral aspect of the acetabulum. This focal area of increased contact forces has been implicated in the clinical development of early hip degeneration and painful arthritis. Coxa valga places the abductor muscles in a less-ideal position by medializing the trochanter with respect to the center of rotation of the femoral head, increasing their required pull to maintain the pelvis in a level state and thereby increasing the forces in the hip. Coxa vara, in contrast, places the abductor muscles in a more advantageous location for the maintenance of pelvic tilt. Surgical management for correction of the osseous anatomy in order to correct or optimize the biomechanics of the hip can be performed on the acetabulum, proximal femur, or both. Pelvic osteotomy for restoring coverage of the femoral head is a powerful tool to redirect the orientation of hip articulation, with the possibility to change the morphology of the acetabulum [6]. Intertrochanteric osteotomy can be employed to redirect the femoral head into the acetabulum, optimizing the contact surfaces between the joint, centering joint forces within the acetabulum, and redirecting the muscular balance of the gluteus medius and minimus.

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22.3.2 Femoroacetabular Impingement Femoroacetabular impingement is a condition that results in the abnormal contact between the bone of the proximal femur and the acetabulum due to variations or alterations in the osseous morphology of the hip. This creates a force on the acetabular labrum producing injury, pain, and tearing that can initiate a cascade of chondral injury and potential degenerative changes. Two distinct types of FAI have been described in the literature, cam-type and pincer-type. Cam-type FAI results from the decreased offset between the femoral head and neck, leading to impingement of a prominence on the femoral neck against the acetabular rim during specific hip motions such as flexion, adduction, and internal rotation. This contact generates an outside-in abrasion/compression of the acetabular labrum, resulting in tearing or avulsion of the cartilaginous tissue from its origin at the acetabular rim. Pincer impingement results from linear contact between the acetabular rim and the femoral head/neck junction due to abnormalities of the acetabular morphology. These acetabular abnormalities include retroversion, coxa profunda, and increased anterior or superior acetabular coverage. FAI creates a scenario in which the acetabular labrum is vulnerable to both acute and chronic injuries that can lead to symptomatic hip pain and degenerative changes in the labral and articular tissues [7]. The presence of cam- or pincer-type FAI can be managed through open or arthroscopic surgery. A femoral neck osteoplasty can be performed to remove any osseous impingement from the femoral head/neck junction and eliminate the source of impingement (Fig. 22.1). Management of pincer-type FAI involves elevating the acetabular labrum from its insertion on the acetabular margin followed by debridement of the underlying bone to correct the acetabular morphology and relieve the compression placed upon the labrum.

22.3.3 Labral Injury The acetabular labrum, or injury thereof, has been identified as a source of hip pain, mechanical symptoms, and biomechanical changes within the hip that may ultimately lead to osteoarthritis [8]. Absence of the labrum transfers the contact area of the femoroacetabular cartilage posteriorly and laterally towards the acetabular margin, with associated translational motion of the femoral head within the articulation [1, 9]. A significant association between the presence of labral lesions and degenerative changes of the articular cartilage of the femoral head and acetabulum has been observed arthroscopically [10]. Integral to the successful surgical management of labral pathology is the identification and management of the etiology of the labral injury. After concurrent hip pathology has been evaluated and managed, treatment options for the management of labral tears include debridement, repair, and reconstruction. Tears that are not amenable to repair include fraying, radial tears, and degenerative tears in which the blood supply is not amenable for healing or the disruption of the longitudi-


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a

b

c

d

e

Fig. 22.1 a Arthroscopic image of a large prominence on the anterior femoral neck of a right hip causing impingement against the acetabular labrum consistent with cam-type FAI. b Radiographic image demonstrating this lesion at the junction of the femoral head and neck. c, d Arthroscopic femoral neck osteoplasty is performed with a motorized burr to remove the bump, with confirmation that it no longer impinges against the labrum (e)

nal fibers prohibits adequate repair (Fig. 22.2). The goal of labral debridement is to create a stable base and minimize the discomfort associated with unstable flap tears. Primary labral repair is appropriate with certain tears of the labrum that do not significantly violate the longitudinal fibers of the structure, or with avulsion of the labral base from the


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a

b

Fig. 22.2 a Arthroscopic image of a complex labral tear viewed through a standard lateral portal. The femoral head can be visualized on the left of the image, with the acetabulum and frayed labral tear to the right. An arthroscopic probe demonstrates the significant fraying of the labral substance and multiple planes of the tear. The tear was managed with debridement to a stable rim (b) while preserving as much labral tissue as possible

acetabular margin. Intrasubstance splits may also be amenable to primary repair if the base has remained well fixed to the acetabular rim and there exists a stable outer rim [11]. Studies evaluating the results of arthroscopic labral repair versus debridement associated with FAI have demonstrated significantly improved outcomes with repair [12]. These early improved clinical outcomes following labral repair in the setting of FAI are encouraging, and future investigations may prove the benefit of labral preservation surgery in the delay or alteration of the natural course of degenerative hip arthritis.

22.3.4 Capsular Laxity and Hip Instability Hip instability and capsular laxity have recently emerged as identifiable and potentially correctable causes of hip pain and disability [7]. The origin of hip instability can be divided into traumatic and atraumatic causes, with traumatic hip instability generally the result of traumatic subluxation or dislocation of the hip. This may be associated with a highenergy trauma, such as a motor vehicle accident, or from a low-energy injury such as commonly occurs during athletic activities. These events may be associated with bony injuries to the femoral head and acetabulum, or shearing injuries to the articular cartilage. The onset of atraumatic hip instability is less distinct and may be due to repetitive microtrauma, generalized ligamentous laxity, iatrogenic causes, and connective tissue disorders [13]. It has been hypothesized that atraumatic instability is the result of repeated forceful hip abduction and external rotation, causing subclinical injury to the iliofemoral ligament and resulting in the development of capsular laxity. Once the static stabilizers of the hip, including the capsule and labrum, are compromised, there is an increased reliance on the


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dynamic stabilizers of the hip to maintain the joint surfaces during activity, with the development of overuse injury and associated symptoms of the surrounding musculature [13]. Recurrent instability may lead to arthritis, avascular necrosis of the femoral head, and heterotopic ossification. Instability of the hip may also be an underlying cause of painful coxa saltans, or snapping hip. Increased mobility of the hip allows the iliopsoas tendon to glide abnormally over the proximal femur and pubic ramus, or the iliotibial band to “snap” over the greater trochanter, resulting in clinical symptoms of painful and sometimes audible snapping in the hip upon provocative maneuvers [7]. Surgical management for capsular laxity includes suture plication and thermal capsulorrhaphy with the goal of restoring the native capsular stability and the pre-elongation length of the iliofemoral ligament (Fig. 22.3). This potentially decreases the translational

a

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d

Fig. 22.3 a Fluoroscopic view of a patient with capsular laxity, demonstrating significant joint distraction with minimal traction placed on the extremity pre-operatively. Arthroscopic view of a suture-based capsular plication performed following a femoral neck osteoplasty. A shuttling monofilament suture is placed (b) in the two limbs of the iliofemoral ligament and used to pass a braided suture (c). This is then used to close the capsular defect to reduce the intra-articular volume of the hip and restore the native length of the capsular tissue (d)

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motion of the femoroacetabular joint and protects the labrum from increased shear forces. There have not been any formal biomechanical studies to evaluate the effects of capsular plication of thermal shrinkage on the stability of the hip, but clinical outcomes appear to be favorable in successfully decreasing the preoperative symptoms of hip instability when performed in conjunction with surgical management of concomitant hip pathology.

22.3.5 Articular Cartilage Injury to the articular cartilage may be due to direct injury or a consequence of altered mechanical loading of the joint surface due to pathology in surrounding structures such as the bone or acetabular labrum [14]. After the development of articular cartilage injury, it can be very difficult to restore the native function of the joint and the usual result is progressive degenerative changes leading to symptomatic osteoarthritis. Focal chondral defects may be due to a direct blow injury or from delamination as a result of FAI and labral injury. Acute injury has frequently been attributed to the subcutaneous location of the trochanter, in which a lateral impact force is directly transferred through the dense cortical bone to the joint surface resulting in chondral lesions of the femoral head or acetabular surface without associated osseus injury [15]. Chondral defects are also frequently associated with labral lesions, with clinical series reporting a correlation as high as 73% with arthroscopically diagnosed labral injury and concomitant chondral lesions, suggesting that labral injury and articular surface lesions are a continuum in the development of degeneration osteoarthritis [10]. Surgical treatment to restore or repair articular cartilage injuries have included microfracture, primary repair, autologous cartilage transplantation, osteoarticular autograft, focal arthroplasty, and total hip arthroplasty. Significant controversy exists about which option is more appropriate in an individual patient, underlining the fact that there is no consensus on the optimal strategy to preserve or restore the articular surface. Microfracture has been advocated in treating full-thickness chondral defects of the articular surface measuring between 2 and 4cm in size. Tissue that is stimulated with microfracture has been demonstrated to consist mainly of fibrocartilage, which has differing characteristics from native hyaline cartilage. Primary repair of large delaminated lesions of articular cartilage with a suture technique has been reported in young patients in whom other options would be less optimal [16]. The use of autologous chondrocyte implantation for treatment of osteochondral lesions of the hip is experimental at this time, with case reports demonstrating moderate outcomes. Mosaicplasty applies the idea of harvesting autogenous osteochondral grafts from non-weight-bearing portions of adjacent joints and transplanting them into a focal cartilage defect in an attempt to restore the integrity of the articular surface. Partial resurfacing hemiarthroplasty for focal chondral defects and osteochondral allograft reconstruction of the proximal femur have yielded modest clinical success in young patients with femoral head collapse due to avascular necrosis. Currently, the best recommendation is the prevention of articular cartilage lesions with conservative and surgical treatments aimed at restoring the native biomechanics, kinematics, and biology of the hip.

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22.4 Conclusions The hip is a complex anatomical structure composed of osseous, ligamentous, and muscular structures responsible for transferring the weight of the body from the axial slrele-

too into the lower extremities. Due to this complex interplay between structures, the evaluation of hip pain and injury can be difficult because of the multiples etiologies that may be responsible for similar symptoms. A detailed understanding of the complex anatomy

and biomechanics of the hip in conjunction with a focused physical examination, diagnostic injection, and appropriate radiographic stodies can help the orthopedic surgeon to successfully diagnose and treat complex pathologies of the hip.

References I. Konrath GA, Hamel AI, Olson SA et al (1998) The role of the acetabular labrum and the transverse acetabular ligament in load 1Iansmission in the hip. J Bone Joint Swg Am 80: 17811788 2. Simon SRAH, An K, Cosgarea A, Fischer R et al (2000) Kinesiology. In: Bockwalter JA, Einhorn TA, Simon SR (ed) Orthopaedic basic science: biology and biomecbaoics of the musculoslreleta1 system. Vol 7, 2nd edn. American Academy of Orthopaedic Swgeons, Rosemont, IL 3. Crawford MI, Dy CJ, Alexander JW et al (2007) The biomecbaoics of the hip labrum and the stability of the hip. Clin Orthop Relat Res 465:16-22 4. Foss FK, Bacher A (1991) New aspects of the morphology and funetion of the human hip joint ligsments. Am J Anst 192:1-13 5. Martin RL, Sekiya JK (2008) The intcrrater reliability of 4 clinical tests used to assess individna1s with musculoslreleta1 hip pain. J Orthop Sports Phys Ther 38:71-77 6. Armiger RS, Armand M, Tallroth Ketal (2009) Three-dimensional mocbaoical evalustion ofjoint contact pressure in 12 periacetabular osteotomy patients with IO-year follow-up. Acta Orthop 80-2:155-61 7. Tihor LM, Sekiya JK (2008) Differential diagnosis ofpain around the hip joint. Arthroscopy 24:1407-1421 8. Harris WH, Bourne RB, Oh I (1979) Intra-articular acetabular labrum: a possible etiological factor in certain cases of osteoarthritis of the hip. J Bone Joim Swg Am 61:510-514 9. Fergnson SJ, Bryant IT, Ganz R ct al (2000) The influence of the acetabular labrum on hip joint cartilage consolidation: a poroelastic ,mite element model. J Biomech 33:953-960 10. McCarthy JC, Noble PC, Schuck MR et al (2001) The Otto E. AufrancAward: The role of labral lesions to development of early degenerative hip disease. Clin Orthop Relat Res 393:25-37 11. Kelly BT, Weiland DE, Schenker ML et al (2005) Arthroscopic labra1 repair in the hip: surgical technique and review of the literature. Arthroscopy 21:1496-504 12. Philippon MI, Briggs KK, Yen YM et al (2009) Outcomes following hip arthroscopy for femoroacetabular impingement with associated chondrolabral dysfunction: minimum twoyear follow-up. J Bone Joint Swg Br 91:16-23 13. Shindle MK, Ranawat AS, Kelly BT (2006) Diagnosis and management of traumatic and atraumatic hip instability in the athletic patient. Clin Sports Med 25:309-26, pp ix-x 14. Buckwalter JA (1998) Articular cartilage: injuries and potential for healing. J Orthop Sports Phys Tber 28: 192-202

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15. Byrd JW (2001) Lateral impact injury. A source of occult hip pathology. Clin Sports Med 20:801-815 16. Sekiya JK, Martin RL, Lesniak BP (2009) Arthroscopic repair of delaminated acetabular articular cartilage in femoroacetabular impingement. Orthopedics 32:692

Hip Injuries in the Athlete

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G.P. Pappas, M.R. Safran

aaa

Abstract There has been a recent explosion of interest in the evaluation and management of the athlete with non-arthritic hip pain as a result of enhanced technology to diagnose and treat non-arthritic sources of hip pain. This has resulted in increasing awareness of various pathologies involving the hip in the athlete. Evaluation of the athlete with hip pain must include differentiating between intra-articular and extra-articular causes, as well ruling out referred pain from other sources. Furthermore, bony and soft-tissue sources of pain must be evaluated. This chapter reviews the clinical presentation, physical examination, associated imaging, and treatments of many sources of hip pain and injury in athletes. These pathologies include bony injuries of the hip and pelvis, such as pelvic avulsion fractures (ischial tuberosity, anterior superior iliac spine, anterior inferior iliac spine, iliac crest and lesser trochanter), osteitis pubis, stress fractures (pelvis, sacrum, acetabulum and proximal femur), and hip dislocations. The soft-tissue injuries about the hip and pelvis reviewed herein include pelvic contusions and hip pointers, muscle strains and contusions, bursitis (trochanteric and iliopsoas), the different sources of snapping hip syndrome, gluteus medius syndrome, piriformis syndrome, and athletic pubalgia. Finally, intra-articular sources of hip pain are discussed, including labral tears, chondral lesions, femoroacetabular impingement, and hip instability. This chapter, while not meant to be comprehensive, provides an overview of these increasingly commonly diagnosed sources of hip pain in athletes.

23.1 Introduction Injuries of the hip and pelvis comprise approximately 2.5% of all sports-related injuries, with the number increasing to 59% in high school athletes [1]. In professional athletes, hip injuries are most commonly reported in ice hockey, soccer (football everywhere except America), and American football. The diagnosis and treatment of hip and pelvis injuries Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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can be challenging because of the complex pelvic anatomy and hip joint biomechanics, the relative lack of understanding of function and dysfunction in the non-arthritic hip, the difficulty of examining the hip due to its structure and location, as well as the overlap of hip joint pain with other sources of pain, such as the back, genitourinary system, gastrointestinal structures, and other musculoskeletal structures. In the past, sports-related injuries of the hip often went unrecognized and untreated. However, our understanding of these injuries has improved significantly in recent years, with advances in diagnostic imaging and arthroscopic surgical techniques [2, 3]. The examination and diagnosis of hip and groin pain is seldom straightforward because of coexisting pathology, secondary dysfunction, and coincidental findings. For example, intra-articular hip pain may present in the setting of coexisting lumbar spine pathology. Alternatively, patients with intra-articular pathology of the hip may initially be diagnosed and treated for intra-abdominal and gynecological disorders, such as hernia or endometriosis. As many as 60% of athletes who undergo hip arthroscopy for treatment of intra-articular injuries are initially misdiagnosed for an average of 7 months before the hip is considered a potential contributing source [4]. Secondary dysfunction that occurs with hip injuries may also confound diagnosis. For example, the pain from an intra-articular pathology, such as femoroacetabular impingement (FAI), can lead to extra-articular dysfunction and pathology such as abductor weakness and greater trochanteric bursitis. Finally, hip and pelvis injuries may have a multi-factorial etiology. For example, the term “sports hip triad” has been used to describe an intra-articular lesion (e.g., labral tear) with associated abnormalities of the surrounding soft tissue (e.g., adductor and rectus abdominis strains) [5]. When approaching the diagnosis of hip injuries in the athlete, it is critical to determine whether the pathology is intra-articular or extra-articular. Intra-articular pathology includes labral tears, chondral lesions, loose bodies, and ligamentum teres pathology that may be associated with FAI or hip instability. Furthermore, it is helpful to distinguish between bony and soft-tissue injuries. Bony injuries include avulsion fractures, stress fractures, hip dislocations, and osteitis pubis while common soft-tissue injuries include muscle strains and bursitis, snapping hip, piriformis syndrome, and athletic pubalgia. This chapter provides an overview of bony injuries, soft-tissue problems, and intra-articular joint pathology to aid the clinician in approaching the diagnosis and treatment of hip and pelvic injuries in the athlete.

23.2 Bony Injuries 23.2.1 Avulsion Fractures Avulsion fractures of the pelvis typically occur in adolescent or young athletes between the ages of 14 and 25 years during activities such as kicking or running. The injury is the result of a forceful concentric or eccentric contraction that acts through a muscle attachment to overload the apophysis, as the physis is the weakest link in the skeletally immature musculoskeletal system. This forceful contraction, combined with the muscle in a lengthened

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position, such as when the joint the muscle crosses is flexed or extended when the contraction begins to occur, places the pelvis at greatest risk for avulsion. An avulsion fracture in an adult, in the absence of external trauma, should raise the suspicion of a pathologic fracture. Anteroposterior (AP) pelvic radiographs show both sides, so that the physes of the injured and non-injured sides can be readily assessed. Most of these injuries are treated non-operatively. The immature pelvis consists of three primary ossification centers: the ileum, ischium, and pubis. The secondary ossification centers include the iliac crest, anterior superior iliac spine (ASIS), anterior inferior iliac spine (AIIS), pubic tubercle, and ischial tuberosity. The average ages for the appearance and fusion of several secondary ossification centers are listed in Table 23.1. The sartorius originates at the ASIS, the direct head of the rectus femoris at the AIIS, the hamstrings and adductors at the ischial tuberosity, and the iliopsoas inserts on the lesser trochanter (Fig. 23.1). The approximate distribution of pelvic avulsion fractures is 50% ischial, 23% ASIS, 22% AIIS, 3% lesser trochanter, and 2% iliac apophysis [6-8].

Table 23.1 Average ages of the appearance and fusion of several of the secondary ossification centers of the hips and pelvis. AIIS, Anterior inferior iliac spine; ASIS, anterior superior iliac spine Ossification center Iliac crest ASIS AIIS Ischial tuberosity Greater trochanter Lesser trochanter

Appearance (average age in years)

Fusion (average age in years)

13-15 13-15 13-15 15-17 2-5 8-12

15-17 21-25 16-18 19-25 16-18 16-18

Sartorius Rectus Femoris Gluteus Iliopsoas

Hamstrings Adductors

Fig. 23.1 Locations of several major muscle origins and insertions of the pelvis and proximal femur. (Reproduced with permission from [14])

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23.2.1.1 Ischial Tuberosity Avulsion injury of the ischial tuberosity is relatively common as bony union may occur as late as early adulthood (25 years). The usual mechanism of injury involves a maximal hamstring contraction with the knee in extension and the hip in flexion, during activities such as hurdling or gymnastics. Physical examination reveals point tenderness, and occasional palpable defect, at the origin of the proximal hamstrings on the ischial tuberosity. Provocative testing involving hip flexion and knee extension places the hamstrings under tension and thus reproduces symptoms. Ecchymosis may be present. Excellent results can be achieved with conservative treatment, i.e., rest, ice, and non-steroidal anti-inflammatory drugs (NSAIDs). Surgical intervention has been recommended for fractures displaced greater than 2 cm, as conservative treatment may lead to fibrous union, chronic pain, and disability. Most sources agree surgical excision is indicated in the setting of exuberant callus formation with chronic pain or dysfunction [6, 7]. 23.2.1.2 Anterior Superior and Inferior Iliac Spine (ASIS and AIIS) Avulsion of the ASIS can occur with strong contraction of the sartorius with hip extension and knee flexion during running or sprinting. Radiographs may reveal a displaced bony fragment in the setting of acute injury; however, displacement may be limited by the inguinal ligament and tensor fasciae latae. In chronic injuries, radiography may be negative or reveal chronic changes such as callus formation. Forceful contraction of the straight head of the rectus femoris during activities such as kicking may cause injury to the AIIS and is common in soccer players. Radiographs are often normal as displacement is limited by the intact reflected head and conjoined tendon. Treatment of ASIS and AIIS avulsions consists of rest, protected weight-bearing, and rehabilitation; indications for operative treatment are not well defined [6]. 23.2.1.3 Lesser Trochanter Avulsion of the lesser trochanter results from excessive traction of the iliopsoas muscle. A typical presentation involves the acute onset of anterior hip or groin pain in a runner or soccer player, which can be elicited by resisted hip flexion while the athlete is seated. Radiographs show superior migration of the lesser trochanter fragment. Management is usually conservative; however, surgical fixation may be considered if displacement is greater than 2 cm in an elite athlete. Most athletes are able to return to sports within 6-8 weeks with conservative treatment [6, 8]. 23.2.1.4 Iliac Crest Apophyseal injuries of the iliac crest may result from forceful contraction of the abdominal musculature or from direct trauma. Pain is exacerbated by resisted abdominal contraction or hip abduction. Radiographs that include the contralateral iliac crest may be helpful to dis-


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tinguish injuries from the normal ossification process, which progresses in a lateral-to-medial fashion. Iliac apophysitis is a related entity usually seen in adolescent long-distance runners; the etiology is postulated to be a traction apophysitis. Iliac avulsions and apophysitis are both treated conservatively, with rest and progressive rehabilitation for 4-6 weeks. 23.2.1.5 Osteitis Pubis Osteitis pubis is an uncommon injury most often reported in runners and soccer and American football players. Osteitis pubis is an inflammation of the pubic symphysis that usually involves the joint and adjacent pubic bone(s). The precise etiology of osteitis pubis is unclear but may be overtraining of the rectus abdominis and adductor muscles, a mechanical imbalance that results in shear across the pubic symphysis, or a muscle traction stress syndrome of the gracilis or adductor brevis or longus [6]. An association with hip impingement anatomy is possible. The patient often complains of groin or pubic pain that is more insidious in onset. Physical examination may elicit tenderness directly over the pubic symphysis, pain with adductor stretch, and limited range of motion (ROM) for hip abduction. Radiographs are initially negative, but may show sclerosis or cystic change on one or both sides of the symphysis after several weeks. Magnetic resonance imaging (MRI) and bone scintigraphy are positive early in the process. Treatment includes rest, anti-inflammatory medications, and core strengthening. Corticosteroid injection (often fluoroscopically or ultrasound guided) into the symphysis may serve as a therapeutic adjunct [6]. Debridement or arthrodesis of the pubic symphysis has been performed for chronic or recalcitrant cases.

23.2.2 Stress Fractures A stress fracture is a partial or complete bone fracture that results from the repeated application of stress exceeding the physiological remodeling adaptability of bone. Runners and track-and-field athletes have the highest incidence of stress fractures, with injury risk associated with biomechanical predisposition, training methods, and other factors such as diet and muscle strength and fatigue [9]. The topic of “stress fractures” is discussed in more detail elsewhere in this volume. 23.2.2.1 Stress Fractures of the Pelvis Stress fractures of the pelvis are relatively uncommon entities but may be seen in the ischiopubic ramus, sacrum, or acetabulum. Stress fractures of the inferior pubic ramus adjacent to the pubic symphysis can be mistaken for adductor strain or osteitis pubis. These patients present with groin pain that is exacerbated by weight-bearing and alleviated with rest. Inability to stand unsupported on the affected lower extremity may be a clue to the diagnosis. MRI or radionuclide scanning may confirm the diagnosis, as radiographs are typically negative. Conservative treatment with cessation of the offending activity yields excellent results; occasionally, a short period of crutch ambulation may be necessary.


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Stress fractures can also occur in the sacrum and typically present with unilateral pelvic pain localized to the sacroiliac joint area, mimicking sacroiliitis. These fractures are often reported in female distance runners, many of whom have a history of amenorrhea, suggesting that bone insufficiency is a contributing factor. Diagnosis is confirmed with MRI, as plain films are usually negative. Sacral stress fractures are typically localized to the anterior aspect of the sacral ala. Treatment includes a period of rest and protected weightbearing with crutches if there is any pain with ambulation. Gradual return to running activity can typically be accomplished by 10-12 weeks [9], although athlete triad and bone density evaluation should also be initiated. The term “acetabular rim syndrome” has been proposed to describe fatigue fractures of the anterolateral acetabular rim in dysplatic hips, even though stress fractures of the superolateral acetabulum may occur as a consequence of abnormal shear stress caused by cam-type FAI (Fig. 23.2; see section on FAI). MRI and computed tomography (CT) a

b

c

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Fig. 23.2 Stress fracture of the acetabular rim. a Coronal magnetic resonance image and (b) computed tomography reconstruction demonstrating an anterolateral fragment (arrow), which measures 30 × 17 mm. c Intraoperative arthroscopic image of the rim fracture. d Post-operative anteroposterior radiograph demonstrating anatomic reduction of the acetabular rim fracture with use of two 4.5-mm cannulated cancellous screws. (Used with permission from Marc R. Safran, MD)


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with three-dimensional reconstructions may be useful for defining the anatomy of the fragment. Treatment includes relative rest in an attempt to allow fracture healing. In patients with non-union or persistent pain, FAI should be treated, along with open or arthroscopic excision of the fragment (if it does not reduce the center-edge angle to < 25°) or internal fixation (if fragment removal compromises coverage of the femoral head) [10].

23.2.2.2 Stress Fractures of the Femoral Neck Early diagnosis of femoral neck stress fractures is essential given their potential for serious complications such as avascular necrosis or progression to a complete displaced fracture. This injury tends to occur in distance runners and results in groin pain that is worse with weight-bearing. Pain may be elicited by axial loading or log rolling of the extremity and maneuvers such as resisted straight leg raise. However, limited ROM, usually internal rotation, of the hip may be the only finding on clinical examination. Radiographs are usually negative initially, with the development of a visible fracture line or sclerosis at 2-4 weeks. MRI is commonly used for early detection of femoral neck stress fractures and can help differentiate from other causes of hip pain, such as intra-articular pathology, muscle injury and tendinopathy, and avascular necrosis. Management of femoral neck stress fractures depends on whether the fracture is on the compression-side, tension-side, or is complete and displaced [11]. Compression fractures, along the mid or inferior portion of the medial cortex, are more commonly seen in younger athletic patients. Early radiographs may reveal subtle endosteal lysis or sclerosis along the inferior cortex of the femoral neck that may progress to sclerosis, or the appearance of a fracture line. MRI can detect marrow edema and possibly the presence of a fracture line [9]. Healing of this fracture type tends to be more reliable due to its relative biomechanical stability. Treatment involves 6-weeks of non-weight-bearing using crutches and 3 months or longer for complete healing. Return to sports is based on asymptomatic full weightbearing, pain-free passive hip ROM, and signs of healing on follow-up imaging. Patients should be followed closely, with a low threshold for surgical intervention if symptoms worsen or displacement is seen on radiographs. Tension-side stress fractures are more common in older patients and characteristically begin as cortical defects along the lateral cortex of the femoral neck (Fig. 23.3). These fractures present a higher risk for progression to complete fracture and displacement, which may lead to complications such as malunion or avascular necrosis. While undisplaced tension-type fractures may be treated with bed rest, until passive movements of the hip are pain free and radiographs show evidence of callus formation [9], most clinicians recommend cannulated screw fixation to reduce the risks associated with fracture displacement or prolonged bed rest, with its inherent associated potential morbidities. A displaced fracture is considered a surgical emergency necessitating open reduction and internal fixation.


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a

b

Fig. 23.3 Tension-side femoral neck stress fracture at presentation in a 26-year-old female (a), and after surgical fixation (b). (Reproduced with permission from Marc R. Safran, MD)

23.2.3 Hip Dislocation Hip dislocation is an orthopedic emergency that requires immediate attention. Posterior hip dislocations account for 90-95% of traumatic and athletic dislocations of the hip. The mechanism usually involves an impact to the knee resulting in a longitudinal force directed along the femur with the hip flexed and adducted. In sports, it may occur in American football or rugby as a result of an athlete landing on the knee with the hip flexed or other players jumping on the athlete’s back when the knee is already on the ground and the hip is flexed. Anterior dislocations occur less frequently, as the result of traumatic hip abduction and external rotation. Clinically, the extremity is shortened, and in posterior dislocations there is hip flexion, adduction, and internal rotation, whereas anterior dislocations exhibit hip extension and external rotation. Pain will limit the patient’s ability to move the hip or bear weight. Awareness must be maintained for associated injuries such as femoral or acetabular fractures, and knee injuries. In addition, a careful neurological examination must be performed, as the sciatic and superior gluteal nerve may be injured – with a posterior hip dislocation. Radiographs should be obtained immediately to rule out fracture-dislocation. Reduction of the hip joint is advocated within 6 h to minimize the risk of osteonecrosis [12, 13]. The indications for surgical treatment include irreducible dislocations and non-concentric reductions. Irreducible dislocations should be treated emergently with open reduction from the direction that the hip dislocated (e.g., posterior approach for posterior dislocation). Non-concentric reductions should be treated on an urgent basis after assessment with


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CT or MRI to identify bony blocks (e.g., loose osteocartilaginous fragments) or soft-tissue interposition (e.g., labrum) preventing the hip from being reduced concentrically [12, 13]. Prognosis for a hip joint that has been dislocated is related to the presence of associated fractures and the timing of reduction. If a simple dislocation is reduced within 6 h, the risk of avascular necrosis (AVN) is less than 10%, but increases dramatically for reduction delayed beyond 6 h. Post-traumatic arthritis is the most common complication and has been reported in approximately 20% of cases. Redislocation occurs uncommonly (1%). Finally, there is controversy regarding treatment after reduction. Protected weight-bearing for 8-12 weeks has been advised in patients at high risk for AVN (e.g., those with fracture-dislocations or reduction delayed > 6 h). For lower risk patients, partial weight-bearing can be advanced as tolerated to full weight-bearing usually within 2-4 weeks [12]. Extremes of hip ROM should be avoided for 4-6 weeks to allow soft-tissue healing.

23.3 Soft-tissue Injuries Soft-tissue injuries of the hip and pelvis may be insidious in nature or may be the result of acute injury or trauma. This section will review muscle contusions and strains, bursitis, snapping hip syndrome, and complex entities such as piriformis and gluteus medius syndromes and sports hernia.

23.3.1 Neurological Injuries Hip and groin pain may be neurological in nature. Referred pain from the lower lumbar and sacral nerves frequently causes gluteal or posterior thigh symptoms. The femoral nerve stretch test may cause anterior hip pain with upper lumbar nerve (L1-L3) involvement. Cyclists may develop pudendal or genitofemoral neuropathy from direct compression. Obturator nerve entrapment has been described in skaters in association with adductor muscle overdevelopment. Meralgia paraesthetica produces pain and parasthesias over the anterolateral thigh as a result of compression of the lateral femoral cutaneous nerve. Etiologies include compression, blunt trauma, and prolonged hip flexion. Sciatic neuropathy can occur with piriformis or gluteus medius syndromes or hamstring muscle stretch [14].

23.3.2 Contusions Contusions to the hip or thigh are common in athletes due to direct trauma. A hip pointer, which is a contusion of the greater trochanter or iliac crest, is caused by a direct blow such as a football tackle or fall. Subsequent hemorrhage can be subcutaneous, intramuscular, or subperiosteal. Unresolving hematoma may be drained to decrease the duration

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of symptoms. Increasing swelling and uncontrolled pain should raise suspicion for arterial injury and the development of compartment syndrome. Treatments such as compression and cryotherapy are used to help control bleeding. NSAIDs should be used with caution as they may exacerbate hematoma formation. Complications of hip pointers include femoral or lateral femoral cutaneous nerve palsy, chronic bursitis, and post-traumatic myositis ossificans [15].

23.3.3 Muscle Strains Muscle strains are a frequent cause of hip and groin pain in athletes, especially those participating in sports that involve explosive movements, such as sprinting and soccer. Highrisk muscles include the hamstrings (particularly the biceps femoris), rectus femoris, sartorius, iliopsoas, and adductor magnus and longus [16, 17]. Clinical examination relies on ROM and muscle strength testing as well as palpation, especially near the origin, insertion, and musculotendinous junction, to localize tenderness or appreciate any defects. Rupture or strain of the iliopsoas near the insertion onto the lesser trochanter can mimic intra-articular hip pathology, whereas injury of the muscle belly may cause femoral nerve irritation [18]. Radiography can be used to rule out bony avulsions, which are more likely in the adolescent athlete. MRI is useful for assessing the severity of muscle strain and often for predicting prognosis, particularly for hamstring strains, as in these cases time to recovery has been correlated with MRI findings [17]. The initial treatment of muscle strains involves control of hemorrhage with rest, cold therapy, and compressive wrapping. Early, gentle ROM should be implemented with physical therapy. The use of NSAIDs and cortisone injections is controversial as they may delay the healing response and slow the rate of recovery of tensile strength of the muscletendon unit [18]. However, earlier return to American football following localized hamstring strains injected with corticosteroid within a day or two of injury has been reported [19]. Despite the common clinical impression that the average muscle strain will resolve with an appropriate rehabilitation program in 2-3 weeks, evidence suggests that there is a prolonged recovery period with increased susceptibility to re-injury for up to 2 months [1618]. Return to sports is generally allowed when full strength and ROM have been restored and functional activities can be performed without pain or obvious limitation [17]. Risk factors for the recurrence of muscle strains include strength imbalance as well as strength and flexibility deficits.

23.3.4 Bursitis Bursal inflammation, or bursitis, typically results from direct trauma, overuse, or repetitive microtrauma from an overlying tendon. The two most common forms of bursitis of the hip in athletes are greater trochanteric bursitis and iliopsoas bursitis [15, 20]. Ischial tuberosity bursitis is uncommon but may be initiated by a direct trauma, such as a fall.


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23.3.4.1 Greater Trochanteric Bursitis Disorders of the peritrochanteric space, such as recalcitrant trochanteric bursitis, external snapping of the iliotibial band, and gluteus medius or minimus tendonitis or tears, are often grouped into the greater trochanteric pain syndrome (GTPS). This syndrome describes chronic lateral hip pain that is accompanied by tenderness to palpation [20, 21]. There is a higher incidence in women and those with leg length discrepancies [21]. Runners who run on banked surfaces or adduct beyond the midline are also at increased risk. Trochanteric bursitis typically presents as a chronic, persistent pain in the lateral hip that may extend down the lateral aspect of the thigh. Pain is worse when lying on the affected side, climbing stairs, or sitting with the affected leg crossed. Examination reveals point tenderness along the lateral or posterior aspect of the greater trochanter and pain with resisted hip abduction. Symptoms may also be elicited by placing the hip in flexion, abduction, and external rotation (FABER). A positive Ober test indicates a tight iliotibial band is a contributing factor. A positive Trendelenberg sign suggests gluteus medius muscle dysfunction, tendinopathy, or tearing. Routine imaging is often unnecessary, although plain radiography may demonstrate calcifications adjacent to the greater trochanter. MRI may reveal bursitis or pathology of the gluteus medius tendon. The mainstay of treatment for hip bursitis is conservative and includes relative rest, NSAIDs, and a rehabilitation program that includes stretching of the iliotibial band and strengthening of the hip abductors. Bursal injections of local anesthetics and corticosteroid provide diagnostic information and pain relief [21]. Corticosteroid injections are beneficial as an adjunct to rehabilitation. In refractory cases, satisfactory results have been obtained with open or arthroscopic bursectomy, bony prominence resection, or partial resection or release of the iliotibial band [15, 20].

23.3.4.2 Iliopsoas Bursitis The iliopectineal bursa is a large synovial bursa that lies between the pelvic rim and the muscle and tendon of the iliopsoas. It may become inflamed from mechanical irritation of the iliopsoas tendon during activities that involve extensive hip flexion, such as sprinting, uphill running, soccer, and dancing. Athletes with iliopsoas syndrome report anterior hip or groin pain that is exacerbated by activity or resisted hip flexion. Deep palpation within the femoral triangle is painful distal to the midpoint of the inguinal ligament, on either side of the femoral artery [15]. Limping, weak hip internal or external rotation, restricted hip extension, or a shortened stride may be noted on physical examination [20]. Pain may be elicited by testing the iliopsoas; resisted hip flexion is performed with the hip at 15°, the knee flexed to 90°, and the examiner pushing down on the anterior aspect of the lower thigh [22]. Ultrasound can be used to guide a diagnostic anesthetic injection or to demonstrate subluxation of the iliopsoas tendon. MRI and CT are typically reserved for cases in which conservative management has failed or the diagnosis is uncertain. MRI can reveal tendinopathy of the iliopsoas or a fluid-filled bursa while CT may reveal osteophytes or bony promi-


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nences. Management includes stretching and strengthening of the iliopsoas tendon and ultrasound-guided corticosteroid injection in cases in which oral NSAIDs are ineffective. In refractory cases, open or arthroscopic surgical excision of the bursa can alleviate symptoms, with iliopsoas lengthening recommended by some authors [15].

23.3.5 Snapping Hip Syndrome (Coxa Saltans) Coxa saltans, or snapping hip syndrome, is characterized by an audible or palpable snapping sensation that may or may not be associated with pain. Snapping hip syndrome is usually subdivided into three main types: intra-articular, internal, and external. Intra-articular causes of snapping hip include synovial chondromatosis, osteochondral injury, loose bodies, acetabular labrum tears, or subluxation of the hip. The two most common causes of coxa saltans are the internal and external types. Other uncommon causes of the extraarticular type include snapping of the long head tendon of the biceps femoris posteriorly and snapping of the iliofemoral ligament over the femoral head or joint capsule medially, and snapping associated with ischiofemoral impingement [15, 20, 23, 24].

23.3.5.1 Internal Snapping Hip (Iliopsoas Tendon) Internal snapping of the iliopsoas tendon occurs over the iliopectineal eminence, femoral head, or lesser trochanter (Fig. 23.4). Painless snapping of the iliopsoas tendon has been reported in 5-10% of the general population. A higher incidence of painless snapping has

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Fig. 23.4 Internal snapping hip. Illustration of the iliopsoas tendon flipping back and forth across the anterior hip and pectineal eminence. a With hip flexion, the iliopsoas tendon lies lateral to the center of the femoral head. b With hip extension, the iliopsoas shifts medial to the center of the femoral head. (Reproduced with permission from Marc R. Safran MD)


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been noted in ballet dancers [23]. A painful internal snapping hip may be caused by either acute inflammatory changes associated with iliopsoas tendonitis or bursitis, or a more chronic degenerative change or tendinopathy. Due to the fact that the psoas originates on the lumbar spine, iliopsoas tendonitis may present as low back pain. Tenderness to deep palpation in the femoral triangle or pain with resisted hip flexion or external rotation may be found on physical examination. Moving the affected hip from the FABER position into extension, adduction, and internal rotation may elicit a painful snapping (this is known as the “snapping hip sign” or “extension test”). The snapping is often audible. The Thomas test may be positive for a hip flexion contracture on the affected side [21, 22]. Ultrasonography may show tendinopathy or bursitis. Dynamic ultrasonography or bursography may demonstrate tendon subluxation during snapping maneuvers. Initial management includes rest, NSAIDs, and a physical therapy program comprised of iliopsoas stretching and strengthening of the hip flexors, extensors, abductors, and rotators. In patients with continued pain, ultrasound-guided injection of anesthetic and corticosteroid can provide therapeutic benefit [23]. For recalcitrant cases, surgery consists of bursectomy and partial or complete iliopsoas tendon release to relax the iliopsoas muscle-tendon complex and eliminate snapping. In recent years, these procedures have been performed endoscopically as a continuation of hip arthroscopy, with minimal morbidity and preliminary results that are at least comparable, and possibly superior, to those reported for open methods [25, 26].

23.3.5.2 External Snapping Hip (Iliotibial Band) The movement of a thickened iliotibial band, tensor fasciae latae, or gluteus maximus tendon over the greater trochanter generates the external type of coxa saltans. Although external snapping is generally asymptomatic, pain can be generated as a result of secondary trochanteric bursitis. External snapping hip can occur in dancers, cyclists, and runners, i.e., those who undergo repetitive hip and knee flexion. Physical examination reveals tenderness with direct compression over the greater trochanter. Patients are often able to voluntarily reproduce the snapping [23]. Hip abductor tightness and tensor fasciae latae contracture should be assessed [22]. Patients often are able to voluntarily reproduce the snapping, which can be quite dramatic visually. Plain radiographs are usually negative, but may reveal peri-trochanteric calcification. Dynamic ultrasound can demonstrate iliotibial band snapping over the trochanter, but is usually unnecessary. Initial treatment includes avoidance of activities that cause snapping and a physical therapy regimen that emphasizes iliotibial band stretching using cross leg adduction or a foam roller [15]. Corticosteroid injection in the trochanteric bursa does not resolve the snapping, but may improve pain symptoms. Multiple operative techniques have been described for recalcitrant snapping hip, with mixed results. These techniques rely on Zplasty lengthening, the use of relaxing incisions, or excision of an elliptical portion of the iliotibial band at the greater trochanter, to eliminate snapping of the band. Excision of a central portion of the band or an incision in a thickened posterior portion may be accomplished arthroscopically [27, 28].

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23.3.6 Gluteus Medius Syndrome Hip abductor syndrome, or gluteus medius syndrome, is associated with pathology of the gluteus medius (and minimus). Buttock or lateral hip pain may result from direct trauma, overuse strain, or tendinopathy of the abductors, or inflammation of the nearby sciatic nerve. Tendinosis or tearing of the gluteus medius or minimus tendons may be present in as many as 14% of patients with lateral hip, buttock, or groin pain [15]. Physical examination reveals tenderness at the gluteal muscles lateral to the posterior superior iliac spine or the superolateral aspect of the greater trochanter. Trendelenberg testing is positive and muscle testing usually reveals weakness of hip abduction with the hip extended, which isolates the gluteus medius. Conservative treatment includes stretching and strengthening of the piriformis and gluteal muscles. MRI can confirm the presence of abductor tendinopathy. Recently, endoscopic techniques have been used to repair isolated tears of the gluteus medius and minimus with encouraging initial results [28, 29]. Injections of cortisone and/or platelet-rich plasma as an adjunct to conservative treatment have been used as well.

23.3.7 Piriformis Syndrome Piriformis syndrome is a constellation of symptoms that includes low back or buttock pain referred to the leg. It is often underdiagnosed and mistaken for more common lower back conditions. Piriformis syndrome has been attributed to: (1) anatomic variations in the muscle or nerve, (2) hypertrophy, inflammation, or spasm of the piriformis muscle, and (3) muscular fibrosis or myositis ossificans following trauma to the ischial spine and gluteal area. The sciatic nerve emerges from the greater sciatic notch below the piriformis; however, anatomic variants include the nerve passing through the muscle [15, 23, 30, 31]. Athletes with piriformis syndrome present with aching pain or cramping in the buttocks that frequently radiates down the posterior thigh and leg in a sciatic nerve distribution. The patient may also describe a feeling of tightness in the hamstring muscle. Prolonged sitting on hard surfaces may be difficult. A history of blunt buttock trauma (such as a fall onto the buttocks) with vague hip and buttock pain aggravated by activities that involve hip flexion, adduction, and internal rotation should raise suspicion of piriformis syndrome. Deep palpation reveals tenderness at the sciatic notch or greater trochanter and possibly a gluteal mass. The Lasegue sign may be positive with the straightened leg raised to 45°. Symptoms may be reproduced with the piriformis test, which stretches the muscle by placing the affected hip in flexion, adduction, and internal rotation (FADIR) [22]. The piriformis is mainly an external rotator with the hip extended and an abductor with the hip flexed. Therefore, pain may also be elicited by resisted abduction of the flexed hip (Pace maneuver) or passive internal rotation of the extended hip (Freiberg maneuver). Physical examination should also include gait assessment as excessive foot pronation and internal rotation can lead to compensation by the hip external rotators and lead to piriformis syndrome [15].


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Diagnostic modalities such as MRI, electromyography, and nerve conduction studies, are useful primarily for excluding other conditions rather than confirming a diagnosis of piriformis syndrome. MRI may identify anatomic anomalies such as accessory piriformis muscle fibers that can lead to sciatic or lumbosacral nerve root compression, and can assess the piriformis muscle itself, including its associated tendons, bursae, and surrounding structures. Electromyography and nerve conduction studies are usually normal [30]. Treatment for piriformis syndrome usually consists of physical therapy focused on muscle and connective tissue stretching, and a combination of local anesthetic and corticosteroid injections into the piriformis muscle belly, muscle-tendon sheath, or sciatic nerve sheath. Favorable initial results have been obtained with botulinum toxin injections to relax the piriformis [30]. Surgical techniques, such as sciatic nerve decompression or piriformis release, have yielded good results in refractory cases. Should release be undertaken, evaluation to assure that the nerve is not running through the muscle is necessary, as symptoms may be exacerbated if the tendon is released while the nerve is still entrapped within the muscle.

23.3.8 Athletic Pubalgia (“Sports Hernia”) Significant controversy surrounds the etiology of groin pain in athletes. Terms such as athletic pubalgia, sports hernias, sportsman’s groin, and Gilmore’s groin have been used to describe multiple syndromes with overlapping pathologies [32-35]. Athletic pubalgia or “sports hernia” is a condition of chronic inguinal or pubic exertional pain but without a palpable hernia; it usually affects high-performance male athletes. The term “sports hernia” is a misnomer because no hernia is present [32-34]. While the exact definition and etiology of this condition are unclear, a broad spectrum of injuries has been described. Most patients report the insidious onset of unilateral groin pain that radiates into adductor, rectus, inguinal ligament, or testicular areas. However, some athletes describe an acute tearing sensation. The proposed mechanism of injury involves pivoting around the pubic symphysis with trunk hyperextension and thigh hyperabduction, as frequently seen in hockey and soccer players. There is no palpable hernia on physical examination, but the superficial inguinal ring may feel dilated or tender [14, 23, 32]. Tenderness around the pubic tubercle may be exacerbated by a resisted sit-up or Valsalva maneuver. Adductor weakness on the affected side may be noted. One series found that 88% of patients had pain with resisted adduction but only 22% had pubic tenderness [35]. Athletic pubalgia is a clinical diagnosis with a limited role for imaging. However, MRI is helpful for ruling out alternate causes of groin pain and may also identify pathology of the pubic symphysis, abdominal wall, or adductor musculature. MRI cannot confirm or exclude the diagnosis of athletic pubalgia, but occasionally demonstrates thinning of the transversalis fascia and shear injuries of the muscles off the pubis [32]. Clinicians should be aware that athletic pubalgia has been reported to co-exist with intra-articular pathology, such as labral tears, in as many as 27% of hockey or football players [5, 34]. Initial treatment of athletic pubalgia consists of relative rest, NSAIDs, and physical therapy focusing on hip and pelvic imbalances. Surgery is indicated after failure of 6-8 weeks of targeted non-operative therapy [14, 23]. Multiple surgical techniques have been described

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for sports hernia, including exploration and repair of the weak posterior inguinal wall and repair of the distal edge of the rectus abdominis. Meyers et al. [35] described unilateral or bilateral reattachment of the rectus abdominis muscle, with the addition of adductor release in patients with a history of adductor pain or weakness on physical examination. In this series, 152 of 157 athletes (97%) were able to return to their previous level of performance [35]. Although the timing of postoperative rehabilitation protocols is variable, each begins with a period of relative rest (e.g., 4 weeks) with progression to strength training, running, and a return to sports at 6-12 weeks.

23.4 Intra-articular Lesions Intra-articular causes of hip pain in athletes include pathology of the acetabular labrum, articular cartilage, or ligamentum teres. Labral tears are the most common intra-articular cause of disabling hip pain in the athletic population. Labral tears are frequently associated with either FAI or acetabular dysplasia and hip instability [20, 23, 36]. The majority of these intra-articular hip pathologies can be addressed arthroscopically. A key goal of the patient history and physical examination is to determine if hip pain is intra-articular or extra-articular in origin [37]. However, diagnosis may be complicated by the co-existence of both intra- and extra-articular pathology. The history should include a description of mechanical symptoms, such as clicking or instability, and any history of trauma or developmental abnormality, as well as any risk factors for avascular necrosis or stress fractures [33]. A systematic approach to physical examination of the hip includes inspection, palpation, ROM, strength, and special tests [38]. Intra-articular pathologies rarely exhibit palpable areas of tenderness, although compensation for long-standing intra-articular problems may result in tenderness of muscles or bursae [22]. Routine radiographs should be obtained in all patients with hip pain. A plain hip radiographic series includes an AP view of the pelvis and either a cross-table or frog lateral of the affected hip. For those with suspected acetabular pathology, Judet or false profile views are helpful, whereas other pelvic pathology may be better assessed with inlet, outlet, and standard AP pelvis views. Plain radiographs will help exclude degenerative joint changes, osteonecrosis, loose bodies, stress fractures, or other osseous pathology [22]. Osseous abnormalities are also seen in the majority (up to 87%) of patients with labral tears [36]. The center-edge (CE) angle is measured from an AP pelvis radiograph (Fig. 23.5). The CE angle is normally between 25 and 40°. A CE angle < 20° is consistent with significant acetabular dysplasia, with 20-25° considered borderline. A CE angle of > 40° is consistent with over-coverage of the femoral head. AP radiographs should also be examined for a “cross-over sign”, indicative of a retroverted acetabulum. Coxa profunda is present when the floor of the acetabular fossa reaches the ilioischial line. Protrusio acetabuli is present when the femoral head reaches the ilioischial line medially. MRI is useful for the assessment of soft-tissue injuries such as labral tears, bursitis, and tendinopathy, as well as the early detection of osteonecrosis and stress fractures. In addition, MRI has proved important for screening the pelvis for other etiologies of pain


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Fig. 23.5 Anteroposterior radiograph of the pelvis. The center-edge (CE) angle is determined by drawing a line from the center of the femoral head to the most lateral margin of the acetabulum referenced to a vertical line (that is perpendicular to the ischial tuberosity tangent line). This radiograph shows bilateral cross-over signs that indicate a retroverted acetabulum, in which case the anterior acetabular rim (solid line) crosses over the posterior acetabular rim (dashed line). (Reproduced with permission from Marc R. Safran, MD)

as well as intra-articular pathology such as pigmented villonodular synovitis and synovial chondromatosis. Newer MRI techniques and higher field-strength magnets have increased the ability to detect isolated chondral defects of the femoral head and acetabulum. MR arthrography, with intra-articular injection of gadolinium, has 90% sensitivity and 91% specificity for detecting lesions of the acetabular labrum [39]. Fluoroscopically guided intra-articular injection of local anesthetic (along with gadolinium) during MR arthrography provides additional information. Pain relief with intra-articular anesthetic has 90% accuracy for detecting the presence of an intra-articular abnormality and is important when considering whether hip arthroscopy may be of benefit [22, 40]. Difficulty entering the joint with multiple attempts at injection as well as extravasation of anesthetic precludes intra-articular injection from being 100% specific for an intra-articular etiology of the pain.

23.4.1 Labral Tears The acetabular labrum is a fibrocartilaginous structure that is a seal for the joint and contributes to smooth gliding function, articular cartilage nutrition, proprioception and hip stability. Labral injuries are the most common pathology seen in athletes undergoing hip arthroscopy [41]. Common etiologies of labral tears include trauma, atraumatic instability, acetabular dysplasia, FAI, and psoas impingement [14, 20, 23, 36, 40, 42], although tears may occur as part of the degenerative process. Athletes involved in sports that require repetitive pivoting or hip flexion (e.g., football, soccer, gymnastics, golf, running, or ballet) appear to have an increased risk of labral tears. Patients with labral tears often present with insidious onset of groin, anterior thigh, lateral hip, or buttock pain. Athletes may describe the acute onset of pain after a twisting injury or slip. Pain is usually activity-related (walking, pivoting, impact activities) and patients have difficulty with prolonged sitting. Approximately 50% of patients report mechanical symptoms, such as snapping, popping, or locking [42]. Labral tears in the athletic population typically occur in the anterior and superior quadrants; these athletes may have bony predisposition for mechanical overload (e.g., FAI) that increases the likelihood of


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intra-articular injury with aggressive sporting activities. Direct anterior labral pathology has also been attributed to compression by the psoas tendon as it cross the anterior acetabular rim [36]. Labral injuries (Fig. 23.6) may consist of tears at the labral chondral junction (type 1 tear) or within its substance (type 2) [43, 44]. Tears are observed in association with FAI; type 1 labral-chondral separations are commonly seen in cam-type impingement and type 2 crush injuries are often associated with pincer lesions [36]. Patients with labral pathology may present with limited hip ROM, especially when there is concomitant FAI or hip arthritis. The Trendelenberg test is often positive for hip abductor weakness, and the hip impingement position of hip flexion, adduction, and internal rotation may be painful. Labral stress testing reproduces pain and/or a clunk in the presence of an anterior or posterior labral tear. Radiographs may reveal bony abnormalities of hip dysplasia, FAI, or arthritis [45]. Magnetic resonance arthrography using intraarticular gadolinium has excellent sensitivity and specificity for detecting labral tears [39]. The addition of intra-articular injection of anesthetic in conjunction with MR arthrography helps confirm the diagnosis of intra-articular pathology [14, 22, 40]. It may be possible to heal a clinically-symptomatic acute tear with protected weightbearing or through surgical fixation of the torn labrum to the bony acetabulum [43]. Appropriate treatment of acute labral tears should begin with partial weight-bearing for 4 weeks [14]. Physical therapy has no proven role in the treatment of labral injuries [20]. Hip arthroscopy is indicated for patients with suspected labral tears based on clinical examination, MR arthrography, and persistent hip pain for more than 4 weeks [23, 41, 42]. Good short-term results have been described for both arthroscopic labral debridement and labral repair [14, 23, 42, 45]. The goal of surgical treatment of labral tears is the elimination of unstable tissue by debridement or repair. Ideally, healthy labral tissue should be preserved to maintain the suction seal mechanism and secondary joint stability and to decrease stress on articular

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g f h a c b d

Type 2 Type 1

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Fig. 23.6 Illustration of the histological appearance of the labrum attachment site (a). The labrum is indicated by (a); articular hyaline cartilage (b), articular cartilage-labrum transition zone (c), bony acetabulum (d), tidemark (e), hip capsule (cut, f), capsular recess (g), group of vessels (h). 1, Capsular recess; 2, thickness of labrum; 3, width of labrum. b Illustration of type 1 and type 2 labral tears. Type 1 tears consists of labral detachment from the articular cartilage surface, which occurs at the transition zone (c in a) between the fibrocartilaginous labrum (a in a) and articular hyaline cartilage (b in a). Type 2 tears occur within the substance of the labrum, extend perpendicular to the surface of the labrum, and may be associated with endochondral ossification within the labrum. (Reproduced with permission from [43])


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cartilage [45]. When possible, labral tears at the articular margin should be repaired with suture anchors to the acetabular rim; degenerative labral tears should be debrided to stable edges [36, 44, 45]. Patients with bony abnormalities should undergo the appropriate corrective procedure such as femoral neck osteoplasty and/or acetabuloplasty for FAI or pelvic osteotomy for significant acetabular dysplasia [23, 41, 42, 45].

23.4.2 Chondral Lesions Chondral damage in the hip may be either traumatic or atraumatic in origin. It may be associated with either instability or impingement and has been noted to occur frequently in conjunction with labral tears [46]. Different patterns of cartilage injury have been correlated with FAI. Pincer-type FAI (see section on FAI) tends to cause shallow chondral lesions around the periphery of the acetabular rim whereas cam-type FAI results primarily in deep, focal anterolateral chondral injury [3]. The symptoms of chondral damage in the hip are often non-specific, as the articular cartilage is aneural. Patients may present with generalized hip or groin pain, stiffness, or mechanical symptoms. Pain with passive motion or decreased ROM may be demonstrated on examination. Although useful in detecting labral tears, MR arthrography has only moderate sensitivity for detecting articular cartilage pathology in the hip [3, 47, 48]. Arthroscopy is the gold standard for assessing acetabular cartilage pathology. Chondral flaps are managed with debridement to a stable edge using an arthroscopic shaver and a curette. Microfracture is considered for focal and contained, full-thickness chondral defects of the acetabulum, typically less than 2-4 cm in diameter [47, 48]. Contraindications for microfracture include partial-thickness defects, chondral lesions with associated bony defects, kissing lesions (chondral lesions on opposing surfaces) or an inability of the patient to comply with postoperative protocols. Postoperative rehabilitation protocols are based on the same principles as knee microfracture. Weight-bearing is restricted to toetouch for 6-8 weeks, with continuous passive motion used to stimulate fibrocartilaginous healing. Physical therapy focuses on regaining ROM in the immediate postoperative period and progresses to strengthening. Impact sports are delayed until at least 4-6 months postoperatively, when strength and ROM have been restored [47, 48].

23.4.3 Ligamentum Teres While the ligamentum teres supports the main blood supply to the femoral head in skeletally immature individuals, its function in adults is unclear. The ligament tightens during adduction, flexion, and external rotation, and may have a secondary stabilizing effect on the hip joint. Ligamentum teres pathology has been observed in 8% of hip arthroscopies, the third most common intra-articular pathology in athletes [49]. The injuries have been classified into three groups: (1) complete ruptures associated with major trauma and labral tears, (2) partial ruptures associated with chronic, ill-defined hip pain, and (3) degener-

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ative tearing associated with osteoarthritis. Traumatic, complete rupture of the ligamentum teres is often associated with an attached bone fragment from either the acetabulum or the femoral head. A sporting injury involving a rotational or twisting mechanism may result in partial disruption of the ligamentum [49]. Hypertrophic changes in the ligamentum have been observed in athletes and may be associated with chronic instability and/or acetabular dysplasia [3]. Patients with ligamentum pathology may report non-specific groin and thigh pain, painful clicking of the hip joint, or mechanical symptoms of locking or giving way. Physical examination may reveal an antalgic gait, decreased hip extension, or pain with hip log roll or straight leg raise. Injury to the ligamentum teres may be visualized on MRI. Osteochondral bone fragments are usually identified as loose bodies on CT or MRI. Ligamentum teres pathology is easily recognized on arthroscopy. The ruptured or hypertrophic ligamentum should be debrided with a curved arthroscopic shaver or radiofrequency probe; associated pathology such as loose bodies and labral tears should also be addressed [23, 49].

23.4.4 Femoroacetabular Impingement Femoroacetabular impingement is a cause of hip pain in athletes that may also be associated with early degenerative joint disease [50-53]. FAI describes a condition arising from repetitive microtrauma of the femoral neck against the acetabular rim, leading to labral and acetabular cartilage damage. Ganz et al. [50] described two distinct types of FAI: cam and pincer, each with a unique pattern of labral and chondral injury (Fig. 23.7). Cam impingement results when an abnormally-shaped femoral head-neck junction is forced into a spherical acetabulum, typically during hip internal rotation (although the more the hip is flexed, the less internal rotation that is necessary to result in the impingement) [50]. This predominantly shear mechanism can result in acetabular chondral injury and delamination, chondrolabral separation, and detachment of the labrum from the acetabular rim, primarily at the anterolateral acetabulum [23, 50-53]. Pincer impingement results from abutment of the femoral head-neck junction on the acetabular rim due to acetabular overcoverage or retroversion. This linear mechanism results in crush injury to the labrum with eventual degeneration and ossification of the labrum. Chondral lesions in pincer impingement are often limited to a shallow rim that may be nearly circumferential [50-53]. Pincer impingement can result in levering of the head in the acetabulum, causing a “contre-coup” chondral injury at the posteroinferior acetabulum or posteromedial femoral head [50, 52]. Patients with FAI most commonly present with mixed cam pathology at the femoral neck and pincer pathology at the anterior-superior acetabular rim [23, 36, 51]. FAI is a major cause of hip pain, reduced ROM, and decreased performance in the athletic population. Anterior groin pain usually begins insidiously, but may be associated with minor trauma. Initially, the pain is intermittent and may be exacerbated by hip flexion, athletic activities, or prolonged walking or sitting. On examination, patients have significantly limited hip flexion and internal rotation. A positive anterior “impingement sign” results when passive hip flexion to 90°, adduction, and maximal internal rotation elicit sharp groin pain [51-53]. The posterior impingement test places the hip in extension and external rotation.


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Fig. 23.7 Femoroacetabular impingement. a Cam impingement: the aspherical portion of the femoral head impacts the anterolateral acetabulum during hip flexion. Shear-induced acetabular cartilage and chondrolabral separation may occur as a result. b Chondrolabral separation lesion associated with cam impingement. c Pincer impingement: acetabular overcoverage results in impact at the femoral neck. The superior labrum may be damaged and a contrecoup lesion of the cartilage of the femoral head and corresponding posteroinferior acetabulum may result as the femoral head subluxes posteriorly. (Used with permission from Marc R. Safran, MD)

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Pelvic radiographs (AP and lateral views) should be obtained in patients with suspected FAI. Pincer lesions can be detected on the AP pelvis radiograph by positive cross-over and posterior wall signs for acetabular retroversion (Fig. 23.5). The AP pelvic image is inspected for additional signs of acetabular overcoverage such as coxa profunda and protrusio acetabuli as well as an increased CE angle of Wiberg. Cam lesions of the proximal femur can be seen in the AP view, and femoral head-neck irregularities or a reduction in the anterior head-neck offset on the lateral radiograph. MR arthrography is performed with the addition of anesthetic to confirm the intra-articular origin of the patient’s symptoms. MRI can be used to assess the anterior femoral head-neck offset by measuring the “alpha angle” on an oblique axial imaging sequence in the plane of the femoral neck [53]. Most clinicians set 50-55° as the threshold for diagnosing cam impingement using the alpha angle. However, recent reports confirm the inter-observer variability of this measurement [54]. Anti-inflammatory medications and activity modification may improve symptoms in patients with FAI. However, because hip impingement is a mechanical problem, physical therapy has not been shown to be beneficial in its management [51]. Surgical treatment of FAI is performed to decompress the bony lesions responsible for mechanical impingement and

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to address intra-articular pathology, such as cartilage lesions and labral tears; this may be done with an open surgical dislocation or arthroscopy [23, 50, 51, 53]. Early ROM exercises are performed postoperatively for 2-4 weeks to reduce the risk of arthrofibrosis. Protected weight-bearing (20 pounds on flat-foot) is recommended, although the length of time varies depending on the approach (open vs. arthroscopic) and the procedures performed (e.g., microfracture). A recent review of the literature [55] included 11 studies on the surgical treatment of FAI, with a minimum 2-year follow-up. Reduced pain and improved hip function were reported in 68-96% of patients at a mean follow-up of 3.2 years (range: 2-5.2 years). Conversion to total hip arthroplasty was reported in 0-26% of patients with major complications occurring in 0-18% of the procedures [55]. Early experience with open and arthroscopic treatment of FAI has been encouraging, with clinical outcome likely dependent on the integrity of the labrum and the extent of cartilage damage [53]. Long-term follow-up studies are necessary to determine survivorship and impact on osteoarthritis progression and natural history [55].

23.4.5 Hip Instability Symptomatic hip instability can be traumatic or atraumatic in origin. The intrinsic stability of the hip joint is a function of its bony architecture, surrounding capsule, joint reaction forces, and associated extra-articular ligaments. Traumatic hip dislocation and subluxation are well-established causes of hip capsule laxity and instability. Recently, atraumatic hip instability has received increased attention as a source of hip pathology [23, 36, 56]. Recognized causes of atraumatic instability include acetabular dysplasia and global ligamentous laxity, associated with disorders such as Marfan’s, EhlersDanlos, or Down syndrome. Developmental dysplasia of the hip results in a shallow acetabulum and instability due to insufficient coverage of the femoral head. Atraumatic instability has also been attributed to overuse injuries in athletes due to repetitive hip rotation and axial loading, which may lead to “micro-instability” [23, 36, 56]. This repetitive, forceful rotation may cause capsular laxity, iliofemoral ligament elongation, and labral pathology. The resulting capsuloligamentous laxity and labral insufficiency may eventually lead to symptomatic hip instability [23, 36]. Furthermore, these abnormal stresses may initiate a cascade of disorders that includes coxa saltans, psoas major muscle spasm, and further anterior labral and capsular damage from increased loading of the iliopsoas tendon [23, 36]. Capsular laxity with rotational instability is seen in athletes who participate in golf, figure skating, football, baseball, ballet, martial arts, gymnastics, and hockey [36, 56]. Atraumatic instability may be difficult to diagnose given the absence of an acute inciting event and the non-specific nature of the symptoms, as well as difficult examination. Patients may complain of generalized pain with activity (e.g., getting in and out of a seated position) and mechanical symptoms of clicking, catching, or giving way. Athletes may be able to describe the motion that reproduces the pain. Most patients with capsular laxity will present with normal active but increased passive ROM [56]. Evaluation for generalized ligamentous laxity may provide a clue to atraumatic hip instability. Furthermore, increased exter-


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nal rotation of the leg with the patient lying supine may provide a clue to iliofemoral ligament insufficiency. Apprehension may be elicited by placing the hip in extension and external rotation, which engages the posterior aspect of the femoral head and stresses the anterior capsule. An axial or longitudinal distraction force applied to a symptomatic lower extremity may also elicit pain or apprehension in patients with capsular pathology. Radiography is important for assessing acetabular dysplasia. A CE angle (Fig. 23.5) measured in the AP view of the pelvis of 20-25° is considered borderline dysplastic. MR arthrography may show thickening of the joint capsule at the lateral margin of the anterior capsule in cases of hip instability. The optimal treatment of atraumatic hip instability remains somewhat controversial. Initial treatment should include NSAIDs and physical therapy to interrupt the cycle of capsule-labral irritation. Arthroscopic surgery may be considered if pain persists despite conservative management and an intra-articular anesthetic injection provides pain relief. The goals of arthroscopy include anatomic restoration of the labrum and reduction of capsular laxity. Techniques such as thermal capsulorrhaphy and capsular plication, with imbrication of the medial and lateral limbs of the iliofemoral ligament, have been attempted to enhance joint stability [56].

23.5 Conclusions The increased interest in the athlete with hip pain is in part due to the enhanced awareness of various pathologies about the hip in the athlete, and the improved ability to diagnose these problems. In addition, the advent of hip arthroscopy allows the treatment of many of these problems in a minimally invasive way, with markedly less morbidity than is the case with open approaches. Evaluation of the athlete with hip pain must include differentiating between intra-articular and extra-articular causes of the pain and rule out referred pain from sources such as the lower back, genitourinary and gastrointestinal systems, and other pelvic musculoskeletal sources. Furthermore, bony and soft-tissue sources of pain must be evaluated. This chapter has reviewed many of the common pathologies that may result in hip pain in the athletic population, as well as their evaluation and treatment.

References 1. DeAngelis NA, Busconi BD (2003) Assessment and differential diagnosis of the painful hip. Clin Orthop 406:11-18 2. Domb BG, Brooks AG, Byrd JW (2009) Clinical examination of the hip joint in athletes. J Sport Rehabil 18:3-23 3. Guanche CA (2009) Clinical update: MR imaging of the hip. Sports Med Arthrosc Rev 17: 49-55 4. Byrd JW, Jones KS (2001) Hip arthroscopy in athletes. Clin Sports Med 20:749-761 5. Feeley BT, Powell JW, Müller MS et al (2008) Hip injuries and labral tears in the National Football League. Am J Sports Med 36:2187-2195

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6. Amendola A, Wolcott M (2002) Bony injuries around the hip. Sports Med Arthrosc Rev 10:163167 7. Widmann RF (2006) Fractures of the pelvis. In: Beaty JH, Kasser JR (eds) Rockwood and Wilkins’ Fractures in children, 6th edn., Lippincott Williams & Wilkins, Philadelphia, PA, pp 838-841 8. Metzmaker JN, Pappas AM (1985) Avulsion fractures of the pelvis. Am J Sports Med 13:349358 9. Fredericson M, Jennings F, Beaulieu C et al (2006) Stress fractures in athletes. Top Magn Reson Imaging 17:309-325 10. Epstein NJ, Safran MR (2009) Stress fracture of the acetabular rim: arthroscopic reduction and internal fixation. A case report. J Bone Joint Surg Am 91:1480-1486 11. Fullerton LR, Snowdy HA (1988) Femoral neck stress fractures. Am J Sports Med 16:365-377 12. Tornetta P, Mostafavi HR (1997) Hip dislocation: current treatment regimens. J Am Acad Orthop Surg 5:27-36 13. Herrera-Soto JA, Price CT (2009) Traumatic hip dislocations in children and adolescents: pitfalls and complications. J Am Acad Orthop Surg 17:15-21 14. Anderson K, Strickland SM, Warren R (2001) Hip and groin injuries in athletes. Am J Sports Med 29:521-533 15. Melamed H, Hutchinson MR (2002) Soft tissue problems of the hip in athletes. Sports Med Arthrosc Rev 10:168-175 16. Garrett WE Jr (1996) Muscle strain injuries. Am J Sports Med 24:S2-S8 17. Orchard J, Best TM, Verrall GM (2005) Return to play following muscle strains. Clin J Sport Med 15:436-441 18. Orchard J, Best TM (2002) The management of muscle strain injuries: an early return versus the risk of recurrence. Clin J Sport Med 12:3-5 19. Levine WN, Bergfeld JA, Tessendorf W et al (2000) Intramuscular corticosteroid injection for hamstring injuries. A 13-year experience in the National Football League. Am J Sports Med 28:297-300 20. Paluska SA (2005) An overview of hip injuries in running. Sports Med 35:991-1014 21. Williams BS, Cohen SP (2009) Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment. Anesth Analg 108:1662-1670 22. Safran MR (2005) Evaluation of the hip: history, physical examination, and imaging. Oper Tech Sports Med 13:2-12 23. Tibor LM, Sekiya JK (2008) Differential diagnosis of pain around the hip joint. Arthroscopy 24:1407-1421 24. Torriani M, Souto SC, Thomas BJ et al (2009) Ischiofemoral impingement syndrome: an entity with hip pain and abnormalities of the quadratus femoris muscle. Am J Roentgenol 193:186-190 25. Byrd JWT (2005) Evaluation and management of snapping iliopsoas tendon. Tech Orthop 20:45-51 26. Ilizaliturri VM Jr, Chaidez C, Villegas P et al (2009) Prospective randomized study of 2 different techniques for endoscopic iliopsoas tendon release in the treatment of internal snapping hip syndrome. Arthroscopy 25:159-163 27. Ilizaliturri VM Jr, Martinez-Escalante FA, Chaidez PA et al (2006) Endoscopic iliotibial band release for external snapping hip syndrome. Arthroscopy 22:505-510 28. Voos JE, Rudzki JR, Shindle MK et al (2007) Arthroscopic anatomy and surgical techniques for peritrochanteric space disorders in the hip. Arthroscopy 23:1246.e1-1246.e5 29. Bunker TD, Esler CNA, Leach WJ (1997) Rotator-cuff tear of the hip. J Bone Joint Surg [Br] 79(B):618-620 30. Kirschner JS, Foye PM, Cole JL (2009) Piriformis syndrome, diagnosis and treatment. Muscle Nerve 40:10-18 31. Windisch G, Braun EM, Anderhuber F (2007) Piriformis muscle: clinical anatomy and considerations of the piriformis syndrome. Surg Radiol Anat 29:37-45 32. Diesen DL, Pappas TN (2007) Sports hernias. Adv Surg 41:177-187 33. Gilmore J (1998) Groin pain in the soccer athlete: fact, fiction, and treatment. Clin Sports Med 17:787-793


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34. Meyers WC, Yoo E, Devon ON et al (2007) Understanding “sports hernia” (athletic pubalgia): the anatomic and pathophysiologic basis for abdominal and groin pain in athletes. Oper Tech Sports Med 15:165-177 35. Meyers WC, Foley DP, Garrett WE et al and PAIN (Performing Athletes with Abdominal or Inguinal Neuromuscular Pain Study Group) (2000) Management of severe lower abdominal or inguinal pain in high-performance athletes. Am J Sports Med 28:2-8 36. Shindle MK, Domb BG, Kelly BT (2007) Hip and pelvic problems in athletes. Oper Tech Sports Med 15:195-203 37. Martin RL, Kelly BT, Leunig M et al (2010) Reliability of clinical diagnosis in intraarticular hip diseases. Knee Surg Sports Traumatol Arthrosc 18:685-690 38. Martin HD, Kelly BT, Leunig M et al (2010) The pattern and technique in the clinical evaluation of the adult hip: the common physical examination tests of hip specialists. Arthroscopy 26:161-172 39. Czerny C, Hofmann S, Neuhold A et al (1996) Lesions of the acetabular labrum: accuracy of MR imaging and MR arthrography in detection and staging. Radiology 200:225-230 40. Byrd JW, Jones KS (2004) Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip arthroscopy patients. Am J Sports Med 32:1668-1674 41. Kelly BT, Weiland DE, Schenker ML et al (2005) Arthroscopic labral repair in the hip: surgical technique and review of the literature. Arthroscopy 21:1496-1504 42. Burnett RSJ, DellaRoca GJ, Prather H et al (2006) Clinical presentation of patients with tears of the acetabular labrum. J Bone Joint Surg Am 88:1448-1457 43. Seldes RM, Tan V, Hunt J et al (2001) Anatomy, histologic features, and vascularity of the adult acetabular labrum. Clin Orthop Relat Res 382:232-240 44. Ranawat AS, Kelly BT (2005) Function of the labrum and management of labral pathology. Oper Tech Orthop 15:239-246 45. Robertson WJ, Kadrmas WR, Kelly BT (2007) Arthroscopic management of labral tears in the hip: a systematic review. Clin Orthop Relat Res 455:88-92 46. McCarthy JC, Noble PC, Schuck MR et al (2001) The role of labral lesion to development of early degenerative hip disease. Clin Orthop Relat Res 393:25-37 47. Philippon MJ, Schenker ML, Briggs KK et al (2008) Can microfracture produce repair tissue in acetabular chondral defects? Arthroscopy 24:46-50 48. Crawford K, Philippon MJ, Sekiya JK et al (2006) Microfracture of the hip in athletes. Clin Sports Med 25:327-335 49. Rao J, Zhou YX, Villar RN (2001) Injury to the ligamentum teres: mechanism, findings, and results of treatment. Clin Sports Med 20:791-799 50. Ganz R, Parvizi J, Beck M et al (2003) Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clin Orthop Relat Res 417:112-120 51. Guanche CA, Bare AA (2006) Arthroscopic treatment of femoroacetabular impingement. Arthroscopy 22:95-106 52. Philippon MJ, Schenker ML (2006) Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin Sports Med 25:299-308 53. Philippon MJ, Stubbs AJ, Schenker ML et al (2007) Arthroscopic management of femoroacetabular impingement: Osteoplasty technique and literature review. Am J Sports Med 35:15711580 54. Lohan DG, Seeger LL, Motamedi K et al (2009) Cam-type femoral-acetabular impingement: is the alpha angle the best MR arthrography has to offer? Skeletal Radiol 38:855-862 55. Clohisy JC, St John LC, Schutz AL (2010) Surgical treatment of femoroacetabular impingement: a systematic review of the literature. Clin Orthop Relat Res 468:555-564 56. Philippon MJ, Zehms CT, Briggs KK et al (2007) Hip instability in the athlete. Oper Tech Sports Med 15:189-194

Anatomy and Biomechanics of the Knee

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D.E. Bonasia, P. Rossi and R. Rossi

Abstract An understanding of the knee’s fundamental anatomy and biomechanics serves as the basis for the clinical examination, therapeutic indications, surgical approaches, and successful operative techniques. In this chapter, the clinically relevant aspects of the anatomy and biomechanics of the knee joint are presented. Particular emphasis has been placed on the bony anatomy, menisci, cruciate ligaments, medial and lateral aspects of the knee, and neurovascular structures. The basic science of the patellofemoral joint is described in a separate section.

24.1 Introduction An understanding of knee’s fundamental anatomy and biomechanics serves as the basis for the clinical examination, therapeutic indications, surgical approaches, and successful operative techniques. In this chapter, the basic science of the knee joint is presented, with an emphasis on the clinically relevant aspects. In the following, the knee joint is considered as a complex made up of the patellofemoral and tibiofemoral compartments.

24.2 Tibiofemoral Joint 24.2.1 Bony Anatomy The epiphysis of the femur comprises two rounded condyles joined anteriorly to form the articular surface of the patellofemoral joint and separated posteriorly by the intercondylar fossa (Fig. 24.1). The condyles, which are almost in line with the cortex of the femoral Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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a

b

Fig. 24.1 Bony anatomy of the (a) distal femur and (b) proximal tibia (see text). LAT, lateral; MED, medial

shaft anteriorly, project well beyond the shaft posteriorly. The medial condyle is larger, more curved, and projects backwards to a greater extent than the lateral condyle, which is longer in addition to being wider at its contact with the tibia. Along the sides of the condyles are the medial and lateral epicondyles. The intercondylar notch of the femur is occupied by the anterior and posterior cruciate ligaments (Fig. 24. 1). The tibial plateau presents two articular surfaces, with the medial facet being longer in the sagittal than in the lateral plane. Both facets are slightly concave in the coronal plane, but the lateral facet is convex in the sagittal plane. Thus, in the lateral compartment of the knee, the rounded femoral condyle rests on the convex surface of the tibia. Between the tibial plateaus lie the medial and lateral intercondylar eminences (Fig. 24.1). The relevant angles of the normal tibiofemoral joint are listed in Table 24.1. The complex arrangement of the knee’s anatomic interrelationships provides it with six degrees of freedom of motion: three translations and three rotations. The translations are anteroposterior (5-10 mm), compression-distraction (2-5 mm), and mediolateral (1-2 mm). These motions are limited by the ligaments, capsule, and the intercondylar eminences of the tibia. The rotations are flexion/extension, varus/valgus, and internal/external rotation, and in general they are much more extensive than the translations. Normal flexion and extension of the knee are variable, ranging from 0° to 15° of hyperextension to 130° to 150° of flexion. In-

Table 24.1 Relevant angles of the tibiofemoral joint (see also Fig. 24.2) [1] Angles

Mean + SD

Anatomic Posterior proximal tibial angle (aPPTA) Lateral distal femoral angle (aLDFA)

81° (SD 3°) 81° (SD 2°)

Mechanical Lateral distal femoral angle (mLDFA) Medial proximal tibial angle (mMPTA) Joint-line congruency angle (JLCA)

88° (SD 3°) 87° (SD 3°) 2° (SD 1°)

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c

d

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Fig. 24.2 Relevant angles of the tibiofemoral joint (see Table 24.1 for normal values). a Mechanical medial proximal tibial angle, b mechanical lateral distal femoral angle, c anatomic lateral distal femoral angle, d joint line congruency angle, e anatomic posterior proximal tibial angle

ternal and external rotation ranges from little or no motion in full extension to 20-30° with the knee flexed [2]. The knee’s bony, meniscal, and ligamentous anatomies have numerous biomechanical implications. First of all, because of the shape of the femoral and tibial condyles, flexion and extension of the knee joint are not simple hinge movements about a fixed transverse axis of rotation. During the arc of motion, a combination of flexion/extension, internal/external rotations, and anterior/posterior translation occurs in the joint. The center of rotation is constantly changing and, when plotted, its path describes a J-shaped curve about the femoral condyles. The motion of the femur relative to the tibial plateau during flexion is initially a pure rolling motion. Around 10-15° of flexion on the medial side and by 20° on the lateral side, sliding of the femur begins relative to the tibia and becomes progressively more important until flexion is complete. Thus, at full flexion, the posterior aspect of the femoral condyles is in contact with the posterior portion of the tibial plateau. Furthermore, because of the ligamentous restraint and the asymmetry of the contact areas of the tibia on the two femoral condyles, the tibia internally rotates relative to the femur during the first 10-20° of knee flexion. Conversely, the tibia is obligated to externally rotate significantly during the last few degrees of full extension, as the tibial plateau rolls farther forward on the medial femoral condyle than on the lateral condyle [2, 3].

24.2.2 Menisci The medial meniscus (MM) is a C-shaped fibrocartilaginous structure, with the posterior horn larger than the anterior one (Fig. 24.3). The anterior horn of the medial meniscus is variable and attaches well forward on the anterior surface of the proximal tibia. Four types of anterior horn medial meniscal attachments have been described [4]. The type IV

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Fig. 24.3 Anatomy of the menisci (see text). LAT, lateral

variant has no firm bony attachment and is connected by soft tissue to the anterior cruciate ligament (ACL) insertion. The posterior root of the MM attaches anterior to the insertion of the posterior cruciate ligament (PCL) and behind the medial tibial spine. The remainder of the MM is firmly attached to the joint capsule and the surface of the deep medial capsular ligament. The capsular attachment of the MM on the tibial side is referred to as the coronary ligament. A thickening of the capsular attachment in the mid-portion spans from the tibia to the femur and is referred to as the deep medial collateral ligament. The lateral meniscus (LM) has an almost circular shape (Fig. 24.3). It covers a larger portion of the tibial articular surface than does the MM. Discoid lateral menisci have been reported in 3.5-5% of the general population [5]. The anterior and posterior horns attach much closer to each other than do those of the MM, making this anatomic area very consistent and therefore easy to maintain during meniscal transplantation. The anterior horn of the LM and the ACL attach adjacent to each other, thus providing important landmarks during ACL reconstruction and meniscal transplantation. The posterior root is posterior to the lateral tibial eminence. In Wrisberg’s variation of discoid LM, the bony attachment of the posterior horn is absent and the posterior meniscofemoral ligament (of Wrisberg) is the only stabilizing structure. This type of insertion can result in posterior horn instability, although a hypermobile meniscus may occur with a normal bony attachment. The anterior meniscofemoral ligament (of Humphrey) runs from the posterior horn of the LM anterior to the PCL and inserts on the femur. The popliteus tendon lies posterior and lateral to the posterior root insertion of the LM. The popliteal hiatus consists of a portion of the LM, where there is no firm peripheral attachment to the femur and tibia [6]. Thompson et al. [7], using 3D magnetic resonance imaging (MRI), demonstrated the greater mobility of the LM than the MM throughout the whole range of motion of the knee. The excursion of the LM averaged 11.2 mm vs. 5.2 mm for the MM. This phenomenon can be explained by the less rigorous attachments of the LM to the articular capsule. Ultrastructurally, the meniscus is composed of two types of fibrochondrocytes: fusiform superficially and round in the deeper layers. The fibrochondrocytes maintain the extracellular matrix, which is composed of collagen (90% type I and the remainder made up of types II, III, V, and VI) and various proteoglycans. Elastin accounts for approximately


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0.6% of the dry weight of the meniscus, and non-collagenous proteins for 8-13% [8]. The collagen fibers (three layers) lie mostly along the longitudinal axis, with oblique and radial fibers enhancing the ligament’s structural integrity [9]. This orientation allows compressive loads to be dispersed by the circumferential fibers, while the radial fibers act as tie fibers to resist longitudinal tearing. The orientation of the surface fibers resembles a meshwork or random configuration and is thought to be important in the distribution of shear stress. Arnoczky and Warren [10] studied the vascularity of the menisci in the adult and demonstrated that only the outer 10-25% of the LM and 10-30% of the MM is vascular. The blood supply to the meniscus comes from the perimeniscal capillary plexus, which arises from the superior and inferior branches of the medial and lateral geniculate arteries. The menisci are historically divided into three zones: red-red, red-white, and white-white. The red-red zone consists of the outer third of the meniscus and is vascular; the red-white zone represents the middle third and receives nourishment from both the blood supply and the synovial fluid; the white-white zone is totally avascular and is nourished by the synovial fluid only [11]. The menisci are essential in many aspects of knee function, including load sharing, shock absorption, reduction of joint contact stresses, passive stabilization, increasing congruity and contact area, limitation of extremes of flexion and extension, and proprioception [6]. The medial and lateral menisci transmit, respectively, about 50% and 70% of the load with the knee extended; this increases to 85% with the knee flexed 90° [12]. Removal of the MM results in a 50-70% reduction in the contact area of the femoral condyle and in a 100% increase in contact stress [13, 14]. Total lateral meniscectomy causes a 40-50% decrease in contact area and increases contact stress in the lateral compartment to 200300% of normal [6]. Because of these biomechanical considerations and the bony anatomy of the knee (less congruent articular surfaces), the lateral compartment is more meniscus-dependent than the medial one. The improved joint congruity, which occurs through normal meniscus contact, is thought to play a role in joint lubrication and cartilage nutrition [11]. Furthermore, meniscectomy was reported to reduce the shock absorption capacity of the normal knee by 20% [15]. The menisci also have an important function in providing joint stability [6]. Medial meniscectomy in the stable knee has little effect on anteroposterior motion, but in the ACL-deficient knee it results in increased anterior tibial translation of up to 58% at 90° of flexion [16, 17]. In conclusion, although the inner two-thirds of the meniscus are important in maximizing joint contact area and increasing shock absorption, the integrity of the peripheral one-third is essential for load transmission and stability.

24.2.3 Anterior Cruciate Ligament The ACL is enveloped by the two layers of the synovium of the human knee joint and is thus defined as intra-articular and extra-synovial. From the origin at the lateral femoral condyle, the fibers of the ACL run obliquely to its tibial insertion with a distal-anterior-medial direction [18]. The ACL can be functionally divided in the anteromedial (AM) and posterolateral (PL) bundles; in full knee extension, both are arranged in parallel, while at 90° of knee flex-

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a

b

c

Fig. 24.4 Anatomy of the anterior cruciate ligament (ACL) (see text). a Intercondylar notch with anteromedial (AM) and posterolateral (PL) bundles of the ACL. b Femoral insertions of the AM and PL bundle with the knee in full extension. Note that the two bundles are parallel. c Femoral insertions of the AM and PL bundle with the knee at approximately 90° of flexion

ion they are twisted (Fig. 24.4). Both bundles resist anterior translation of the tibia relative to the femur, with the AM bundle more tensioned from 30° to 90°, and the PL bundle from 0° to 30° of knee flexion [19]. Furthermore, cadaveric studies have shown that the PL bundle plays a more important role than the AM bundle in providing rotational stability [20, 21]. The femoral attachment of the ACL is on the posterior part of the medial surface of the lateral condyle well posterior to the longitudinal axis of the femoral shaft. During knee flexion, the femoral origin of the PL bundle is anterior and inferior to the AM bundle whereas in extension the origin of the PL bundle is posterior and inferior to the AM bundle (Fig. 24.4). The quadrant method described by Bernard et al. [18, 22] defines the center of the femoral insertion site of the ACL on conventional true lateral X-rays. These authors showed that the center of the ACL attachment on the lateral femur condyle can be located at 24.8% of the distance defined by the intersection of Blumensaat’s line and the contour of the lateral femoral condyle on lateral X-rays, and at 28.5% of the height of the lateral femoral condyle from Blumensaat’s line. By dividing the intercondylar fossa into quadrants, this point can be found inferior to the most superoposterior quadrant [18, 22]. The width of the ACL reportedly ranges from 7 to 12 mm [18]. In the mid-substance of the ligament, the narrowest diameter is oval shaped and in females and males has a cross-sectional area of, respectively, 36 and 44 mm2 [23]. At both proximal and distal insertion sites, the ligament fans out, and the area increases by approximately 3.5-fold compared to the mid-substance [24]. The intra-articular length of the ACL has been reported to range from 22 to 41 mm, with a mean of 32 mm [18, 25, 26]. Little is known about the intra-articular length of the PL bundle. According to measurements by Kummer and Yamamoto [27], made in 50 cadavers, the mean length is 17.8 mm. The tibial insertion site has a broad oval shape with a diameter of approximately 11 mm in the coronal plane and 17 mm in the sagittal plane [18]. The insertion site for the


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ACL on the tibia is located in the area between the medial and the lateral tibial spines. The fibers of the AM bundle insert at the anteromedial portion of the insertional area, while the fibers of the PL bundle insert in the posterolateral part of the ACL’s tibial attachment [18]. In some cases, the fibers of the ACL’s tibial insertion appear to be confluent with the anterior and posterior roots of the lateral meniscus. The blood supply to the ACL is mainly provided by the middle geniculate artery and the fat pad. The ACL is composed of 90% type I collagen and 10% type III. The average tensile strength of a normal ACL is 2,160 (± 157) N [28]. At time zero (immediately after ACL reconstruction), the most commonly used autografts and allografts have shown comparable or superior strength compared to native ACL. Nevertheless, animal studies have shown that the structural properties of the neo-ligament decrease during the phases of healing and remodeling inside the joint [18].

24.2.4 Posterior Cruciate Ligament The PCL comprises two functional bundles, anterolateral (AL) and posteromedial (PM) (Fig. 24.5), according to their relative positions on the femur. As is the case for the ACL, they are not anatomic separations of the ligament but can be distinguished by their distinct

a

b

Fig. 24.5 Anatomy of the posterior cruciate ligament (PCL) (see text). a Intercondylar notch with anterolateral (AL) and posteromedial (PM) bundles of the PCL. b Femoral insertions of the AL and PM bundle with the knee at approximately 90° of flexion

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patterns of tension at differing angles of knee flexion [29]. The PM bundle is taut in extension and loose in flexion whereas the AL bundle tightens in flexion and loosens in extension. The PCL provides 95% of the total restraining force to straight posterior translation of the tibia relative to the femur and is also a secondary restraint to varus, valgus, and external rotations. Grood et al. [30] evaluated the effect of sectioning the PCL and the posterolateral structures (lateral collateral ligament, popliteus, and arcuate complex) on different degrees of knee flexion (from 0° to 90°). Isolated sectioning of the PCL resulted in an increase in posterior translation that increased as the knee was progressively flexed, to a maximum at 90°. These results reflect the increasing slackness in the remaining secondary restraints to posterior translation as the knee flexes. Conversely, when the posterolateral structures were sectioned together with the PCL, the knee demonstrated a similar increase in posterior translation at 30° and at 90° [30, 31]. The PCL attachment on the medial femoral condyle varies in terms of size and shape. In general, the femoral attachment can be described as “half-moon” shaped (Fig. 24.5). The AL bundle attachment reaches and crosses the 12-o’clock position of the femoral intercondylar notch and is bounded distally by the edge of the articular cartilage of the trochlear groove and medial femoral condyle. The anterior meniscofemoral ligament (Humphrey’s ligament), when present, indents into the AL bundle attachment. Its fibers, adjacent to the AL bundle, interdigitate with those of the bundle itself. Humphrey’s ligament attaches distally between the PCL and the articular cartilage. The posterior meniscofemoral ligament (Wrisberg’s ligament), when present, is consistently found to be separate from and proximal to the PM bundle attachment to the femur. The maximal anteroposterior length of the PCL attachment is 22 ± 3 mm (range: 13-27 mm). The AL bundle lies between the 09:00 and 12:30 o’clock positions (for a left knee). The PL bundle’s clock positions depend on the orientation in which they are viewed. When viewed parallel to the femoral long axis, the PL bundle is between 07:00 and 10:30 o’clock [29]. The average length of the PCL is 38 mm, and the average width is 13 mm. The ligament is enclosed within synovium and is therefore intra-articular and extra-synovial. The synovium is reflected from the posterior capsule and covers the medial, lateral, and anterior aspects of the PCL. Distally, the posterior portion of the PCL blends with the posterior capsule and periosteum [31]. The vascular supply to the PCL is provided by the middle geniculate artery. The position and shape of the tibial attachment of the PCL are more consistent than the proximal origin. The AL bundle occupies a central area covering almost the entire flat intercondylar surface of the posterior tibial plateau (“posterior intercondylar fossa”), from the posterior edge of the root of the posterior horn of the medial meniscus to within 2 mm of the posterior edge of the plateau. Its shape is trapezoidal, with the base posterior. The PM bundle occupies a central area of the posterior surface of the tibia, from the edge of the posterior tibial plateau distally to a ridge where it becomes indistinguishable from the tibial periosteum distally. Thus, the tibial attachment of the PM bundle is distal and lateral to the AL bundle attachment [29].

24 Anatomy and Biornedlmics ofthl! Knee

lO9

24.2.5

Medill Aspect of the Knee The st:ructw'es of the medial side of the knee can be divided into three different layers. Tho ".,.,n.ruJ Iayo< (boyer ~ i. fmmod by the deop (m onmo1) ra.cia (Fig. 24.6), wIll,h extends from the patella to the midline of the popliteal fossa. Anteriorly, this layer blends with layer II in a vertical line [31]. The medial patcllotibial1igament is an oblique thickening of the medial retinaculum of layer I. This ligament inserts 1.5 em inferior to the jcrint line, on the anteromedial border of the tibia, and joins the fibers of the medial patellofemoral1igament of layer II [31]. The medial patellomeni9Cal1igameut is deep to the patellotibial ligament and runs from the inferior two-thirds of the patella along the medial border of the Hoffa body to insert on the anterior portion of the medial meniscus. Posteriorly, layer I overlies the two heads of the gastrocnemius and serves to support the neurovascular structures of the popliteal fossa. The sartorius inserts into the crural fascia without a distind tendon of insertion. The gracilis and semitendinosus tendons run between layer I and II. Anteriorly and distally, layer I joins the periosteum of the bbia and posteriorly becomes the deep fascia of the leg [31]. Layer II contains the superficial MeL, which originates on the medial femoral epicondyle and runs downward, as a triangular band, approxb:nately 11 em to its tibial insertion (Fig. 24.6), which is located deep to the gracilis and semitendin09US tendons. The superfwial MCL can be further subdivided into anterior and posterior portions. The anterior margin lies free, except at its attachment sites to the tibia and femur, and is

Fig.1U Anatmny ofthc medial aspoot of tILe knee (sec text).• Layer L MR. medial retinaculum; mo, Vastus mcdialis obIiquus. b Layer II. Proximal and distal. insertions ofthc supctfu:iaJ. medial collateral :Ii.gamcnt (sMCL). OPL, obliquc poplitca1ligamcnt; 8M, Semimembranosus tmldon

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separated from the medial meniscus and deep capsular ligament by a bursa. The anterior portion is taut in extension and progressively tightens over the entire range of motion, whereas the posterior portion slackens with flexion [31]. From the region of the femoral insertion of the anterior fibers, a transverse band runs forward in the plane of layer II from the adductor tubercle toward the patella, forming the medial patellofemoral ligament. The patellofemoral ligament runs deep to the vastus medialis to insert on the superomedial patella. The posterior fibers of the superficial MCL are oblique in orientation and blend with the fibers of layer III at the posteromedial corner of the knee, to form a pouch. The pouch is augmented by contributions from the semimembranosus sheath and tendon, forming the oblique popliteal ligament. The semimembranosus sheath contributes fibrous extensions into the posteromedial and posterior capsule [31]. Layer III is formed by the joint capsule. The lines of attachment of the capsule follow the joint margins, except anteriorly, where the capsule extends proximally to form the suprapatellar pouch. Deep to the superficial MCL, the capsule thickens to form the vertically oriented, short fibers of the deep MCL. The meniscofemoral portion of the deep ligament extends from the femur to the mid-portion of the peripheral margin of the meniscus. The meniscotibial portion of the ligament anchors the meniscus and is readily separated from the overlying superficial MCL. The remainder of the capsule is thin, bulging as it extends from the femur to the meniscus. The meniscus is attached distally, along its margin, to the tibia by the coronary ligament [31]. The MCL represents the main restraint to valgus forces and a secondary restraint to external rotation and medial/lateral rotation of the tibia. The superficial portion of the MCL contributes the most to stability [32]. Sectioning only the superficial portion of the ligament results in both opening of the joint space under valgus load, over the entire range of motion, and increased external rotation (2-fold in extension and 3-fold at 90° of flexion). Sectioning the deep ligament, if the superficial fibers are intact, produces almost no change in terms of medial stability [32]. The contribution of the MCL to valgus stability increases with knee flexion (78% at 25° knee flexion), as the posterior capsular structures become slack. Conversely, with the knee extended, the posteromedial capsule structures are in tension and provide some valgus stability [33].

24.2.6 Lateral Aspect of the Knee Seebacher et al. [34] divided the lateral and posterolateral structures of the knee into three different layers (Fig. 24.7). The most superficial contains the iliotibial band (ITB) and the biceps femoris. The ITB has three distal insertions: (1) the first inserts onto Gerdy’s tubercle; (2) the second blends into the intermuscular septum and inserts onto the supracondylar tubercle; and (3) the third inserts onto the lateral patella. This last insertion is responsible for lateralization of the patella during knee flexion. The biceps consists of a long and a short head and also has numerous insertions. The major insertion runs posteriorly to the ITB and inserts on the fibular head. The common peroneal nerve lies on the deep side of layer I, just posterior to the biceps tendon [35]. Layer II is formed anteriorly by the retinaculum of the quadriceps and posteriorly by two patellofemoral ligaments: the proximal ligament joins the terminal fibers of the lat-


'"

Fig.:z4.7 Anatomy of the lateral aspect of the knee (sec text). BF,1ateral head ofdie biceps femoris; CPN, common peroneal nerve; LCL, Iataal collateml ligament;

UlG, latera1 head of 'the gastrocnemius; PT, popliteus tendon

eral intermuscular septum and the distal ligament ends posteriorly on the fabella or on the femoral condyle at the insertions of the posterolateral capsularrein:forcements and the lateral head of the gastrocnemius. Also included in layer II is the patellomeniscalligament, which travels obliquely from the patella to the margin of the lateral meniscus and inserts on Gerdy's tubercle [31, 35]. The deepest layer (Fig. 24.7), layer ill, also called the posterolateral comer (PLC), can be divided into a superficial and deep lamina. The superficial lamina is formed by the lateral collateral ligament (LCL) and the fabellofibular ligament. The LCL originates from the lateral distal femoral condyle and inserts onto the lateral aspect of the fibular head. The femoral site of origin is posterior and superior to the popliteus origin and the fibular site of insertion is distal to the insertions of the arcuate ligament and popliteofibular ligament (PFL). When a fabella is present, the fabeUofibular ligament is found coursing parallel to the LCL, from the fabella to the fibula, to insert posterior to the insertion of the biceps tendon [31,35]. The deep lamina contains the popliteofibular ligament (PFL), arcuate ligament, and popliteus muscle. It nms along the edge of the lateral meniscus, forming the coronary ligament and the hiatus for the popliteus tendon, and terminates posteriorly at the Y-shaped arcuate ligament. The latter spans the junction between the popliteus muscle and its tendon, from the fibula to the femur. The popliteus tendon passes through the hiatus in the coronary ligament to attach to the femur, anterior and distal to the attachment of the LCL. The inferior lateral geniculate artery runs in the space between the two laminae. The PFL is found deep to the lateral limb of the arcuate ligament, arising from the posterior part of the fibula, posterior to the biceps insertion, and joining the popliteus at the musculotendinous junction [31, 35]. The structures of the PLC function primarily to resist varus rotation, external tibial r0tation. and posterior tibial translation [36]. The LCL is the primary static restraint to varus opening of the knee. Direct force measurements of the LCL during an applied varus moment demonstrate loading responses at all angles of knee flexion. with the response at 300 of flexion significantly bigher than at 90 0 of flexion [36, 37].

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Isolated sectioning of the PCL has no effect on varus rotation. However, when the PLC is deficient, additional sectioning of the ligament produces a significant increase in varus instability, indicating a role for the PCL as a secondary restraint [36]. The PLC is the primarily stabilizer of external rotation of the tibia at all knee flexion angles. In in-vitro studies, isolated sectioning of the PLC produced a maximal average increase of 13° of rotation at 30° of knee flexion, which decreased to an average of 5.3° at 90°. Conversely, isolated sectioning of the PCL had no effect on external tibial rotation. Combined injury to the PCL and PLC produced significantly greater increases in external tibial rotation, especially at 90° of knee flexion (20.9°) [30, 36, 38]. For these reasons, the dial test should be performed at both 30° and 90° of flexion, in order to determine the presence of an isolated PLC or combined PLC/PCL injury [36]. LaPrade et al. [37] found that the mean load responses to external rotation in the LCL were significantly higher than those of the popliteus tendon and PFL at 0° and 30° of flexion, whereas the popliteus and PFL demonstrated higher loads at higher knee flexions, peaking at 60°. Therefore, as stabilizers to external rotation, the LCL has a primary role at lower degrees of knee flexion and the popliteus complex at higher flexion. The primary restraint to posterior tibial translation is the PCL. Isolated sectioning of the ligament produces increased posterior tibial translation at all angles of knee flexion, with a maximum at 90°. Isolated sectioning of the PLC also produces increased posterior tibial translation at all angles of knee flexion, with a maximum at early knee flexion. Therefore, the PLC, not the PCL, is the primary restraint to posterior tibial translation near full knee extension [30, 36, 38]. Biomechanical analysis of PLC deficiency in the setting of ACL or PCL reconstruction showed increased loads in the grafts, further demonstrating the interdependent relationship of the PLC and the cruciate ligament.

24.2.7 Vessels and Nerves Around the Knee The popliteal artery enters the fossa between the biceps and semimembranosus muscles, then descends beneath the tibial nerve between the heads of the gastrocnemius to divide into the anterior and posterior tibial arteries. The anterior tibial artery lies on the anterior surface of the interosseous membrane between the tibialis anterior and the extensor hallucis longus muscles. The posterior tibial artery travels in the deep posterior compartment obliquely. It gives off a main branch (peroneal artery) 2.5 cm distal to the popliteal fossa, which runs lateral to the posterior tibial artery between the tibialis posterior and the flexor hallucis longus muscles. The knee receives five geniculate branches from the popliteal artery: medial superior and inferior geniculate arteries, lateral superior and inferior geniculate arteries, and the middle geniculate artery (Fig. 24.8). These branches, together with the recurrent anterior tibial artery, create a complex anastomosis on the anterior aspect of the knee [39]. The sciatic nerve gives off the tibial and peroneal branches that supply the muscles of the lower extremities (Fig. 24.8). The tibial nerve travels deep in the thigh to the long head of the biceps before entering the popliteal fossa, where it crosses over the popliteus muscle before splitting the two heads of the gastrocnemius muscle. The muscles of the posterior leg are supplied by motor branches of the tibial nerve. The common peroneal nerve is


'"

Flg.24.I Vessels and nerves of the popliteal fossa (see text).• !GA., inferior geniculate artmiea; SGA., Superior genicu1atc arteries. b CPN, common pcroncal IlCIVej PTN, posterior tibial IlCIVej SGA., Supcrlor gcni.culatc artcrica

smaller than the bbial nerve (Fig. 24.8) and nms lateral to the popliteal fossa, between the medial border of the biceps and lateral head of the gastrocnemius. It then travels around the neck of the fibula deep to the peroneus longus muscle, where it divides into superficial and deep branches. The superficial branch runs along the border between the lateral and anterior compartments, supplying the peroneus longus and brevis. The deep peroneal branch, also called the anterior tibial nerve, runs along the anterior surface of the interosseouB membrane to supply the muscles of the anterior compartment. The saphenous nerve travels subcutaneously on the medial aspect of the knee, between the sartorius and gracilis. This branch of the femoral nerve supplies sensation to the medial aspect of the foot [39].

24.3

Patellofemoral Joint

The patella is the largest !JeSamoid bone of the human body and together with the patellar groove of the femur forms the pateUofcmoral joint. The articular surface, consisting of seven facets, is situated on the proximal two-thirds of the underlying surface of the patella. The distal pole, as the extra-articular part of the patella, attacbes to the patellar tendon. Three me 2.5 cm2) or those with associated bone loss (avascular necrosis, osteochondral fractures, and osteochondritis dissecans). This procedure is most often used as a secondary treatment option in patients who have failed previous attempt at cartilage repair, but can be a first-line treatment for high-demand patients with large lesions [16]. Most commonly, OA are used for medium-sized to large articular cartilage defects involving the femoral condyle, but may also be used for lesions of the tibial plateau, trochlea, and patella. Major concerns associated with allograft transplantation, such as tissue mismatching and immunologic response, do not play a major role in OA, as the transplanted tissue is avascular and alymphatic. In addition, before transplantation, the donor tissue is washed using pulsatile irrigation in an attempt to remove marrow elements that may contribute to suboptimal graft incorporation. However, one of the challenges faced by the operating surgeon is the availability of allograft donor tissue. Clinical studies have suggested that there is higher chondrocyte viability and subsequently improved maintenance of cartilage matrix in fresh grafts, and most surgeons currently prefer the use of fresh grafts. Once harvested, the fresh grafts are kept in physiologic medium at 4°C to preserve chondrocyte viability. The storage time has also been shown to have an effect on chondrocyte viability, with fewer viable cells observed with prolonged storage [32]. Studies have shown a significant decrease in cell viability after 14 days, from 91.2% to 80.2%, with further detrimental effects at 28 days, with a cell viability of 28.9% [33]. Therefore, the current recommendation is that a fresh OA should ideally be used between 14 and 28 days from harvest [34-36]. OA transplantation is typically performed through a small arthrotomy to expose the lesion site (Arthrex, Naples, FL). The preparation of the graft involves the use of a reamer to convert the defect into a circular recipient socket with a uniform depth of 6-8 mm. An instrumentation system is used to size and harvest a cylindrical plug from the allograft, which is then implanted into the socket after careful alignment of the four quadrants to the recipient site. If a large allograft is used, fixation may be augmented with a bioabsorbable or metal compression screw (Fig. 32.4). Post-operative rehabilitation consists of immediate CPM and weight-bearing limited to toe-touch for 6 weeks. Patients with patellofemoral grafts are allowed to weight bear as tolerated in extension, with flexion generally limited to 45° for 4 weeks. A return to the normal activities of daily living and sport activity is considered at 8-12 months. Post-surgical outcomes of OA are presented in Table 32.5.

S. Bajaj et al.

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a

b

c

d

e Fig. 32.4 Osteochondral allograft transplantation. a Focal chondral defect of the lateral femoral condyle; b reamed donor site using appropriately sized reamer; c fresh donor femoral allograft secured in a commercially available holding apparatus. Device has the ability to move with 6° of freedom to match the anatomy of the femoral condyle. d Cored donor plug, sized to match the reamed donor site; e graft inserted into donor site. Bio-absorbable screw used to augment fixation

32.6.3 Concomitant Procedures Combined pathologies are frequently encountered by the operating surgeon treating articular cartilage defects. Meniscal injury or deficiency, malalignment, and ligamentous instability are known to contribute to the development of articular lesions. Surgically addressing these concomitant pathologies assures an effective and durable cartilage repair, ensures the integrity of the primary cartilage repair, and does not negatively affect the patient’s ability to return to their day-to-day activities. It is also advantageous to treat combined pathologies at the time of primary cartilage repair, thus sparing the patient a prolonged rehabilitation.

32 Lower Extremity-Artiallar cartilage Injuries

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Table 32.4 Clinical outcomes of osteochondral autcgraft (OAl)

Authon

Study group

Lesion

characteristics

Outcomes

Comments

Good/excellent

Histological f'mdings: survival of ilie transplanted hyaline cartilage; fibmcartilage covering the donor sites

and site

Hangody et al. [29]

1097 cases

Mean age

36 years Mean follow-up 14 years

Marcacci et al. [30]

30 cases Mean age

29.3 years 2- aod 7-year follow-up

Dom etal. [31]

25 patients Mean age

798 femoral condyle 147 patellfemoral 31 tibia 120 o1hcrs 1hao knee Small aod medium foeal defects (1-4 em2)

results in 92%

offemoral eoodylar implaots, 87% of tibial resurfacements. 74% of patellar and/or trochlear mosaicplastics Graft survival in 81 of 98 cases

MFC LFC Mean lesion

76.7% report good! Redoced sporta activity from 2excellent results to 7 year follow-op according to ICRS objective evaluation IKDC subjective score improvement (34.8 to 71.8) Tegner score improvement (2.9 to 5.6 at 7 years) MRI f'mdings: good integration and survival of ilie graft in 62.5% of patients at 7 years

8% femoral condyles 32% patella

hnprovement in Lyshobn score in 88% of patients No failures

size < 2.5 cm2

27 years Mediao follow-op Mean lesion 300 days size 1.88 cm2

LFC, lateral femoral condyle; MFC, medial femoral condyle

32.7 Conclusions Articular cartilage repair is aimed at returning patients back to their pre-injury level of activities. While nutritional supplements may play a role in ilie prevention and treatment of cartilage injuries, more often than not surgical intervention is required. Several surgical techniques have been shown to alleviate patient's symptoms and improve functioo but determining which technique to apply requires a iliorougb clinical history iliat includes

the patient's age, activity level, post-operative expectations and lesion size. Each technique presented above is associated with advantages and disadvantages, however second-generation techniques are under development to improve current shortcomings.

S. Bajaj .1 al.

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1abl.32.5 Clinical outcomes of osteochondral allograft (OA)

Authon

Study group

Lesion

characteristics

Outcomes

Comments

and site GrossAE et al. [37]

60 fresh allografts Mean age 27 years

30MFC 30LFC

12 failures Survival: 95% at

5 years, 85% at 10 years, 65% at

Mean follow-up

15 years

10 years

Davidson

Fresh allografts

et al. [38]

in 8 patients

6MFC 2MFC

(10 knees), Mean age 32.6 years

2 trochlea Mean defect

Mean follow-up

(range 2.517.2 em')

40 months

size 6.2 cm2

No failures hnprovemeot in

IKDC score, SF-36, Tegner, Lyshohn

Histological fmdings: cellular density am! viability similar in host and donor

cartilage MRI: complete:

incorporation and improvement in scores

McCulloch et al. [39]

25 fresh allografts

Mean age

Femoral condyle

hnprov=tin Lyshohn, IKDC, KOOS, SF-12 scores 88% (22) of radiographs showed graft in corporation at last follow-up

Patellofemoral

5 failures

35 years (range 17-49)

Mean follow-up 35 months Jamali et al. [40]

Fresh allograft in 18 patients (20 knees) Mean age 42 years (range 19-64)

Mean follow-up 94 months

No re-alignment 60"/0 (12 of 20) procedure excellent/good performed results Improvement in

Clinical and radiographic study

clinical scores

LFC, lateral femoral condyle; MFC, medial femoral condyle

References I. Sellards RA, Nho SJ, Cole BJ (2002) Chondral injuries. Curr Opin RheumatoI14:134-141 2. Widuchowski W, Widuchowski J, Trzaska T (2007) Aricular cartilage defects: 25124 knee artbroscopies. The Koee 14:177-182 3. Outerbridge RE (1961) The etiology of chondromalacia patella. J Bone Joint Surg 43(B):752757 4. Curl ww, Krome J, Gorodon ES et al (1997) Cartilage injuries: a review of 31,516 knee artbroscopies. Arthroscopy 13:460-466 5. Huot N, Sanchez-Ballester J, Pandit R et al (2001) Chondral lesions of the knee: a new localization method and coorelation with associated pathology. Arthroscopy 17:481-490

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6. Brittberg M (2000) Evaluation of cartilage injuries and cartilage repair. Osteologie 9:17-25 7. Tomford WW (2000) Chondroprotective agents in the treatment of articular cartilage degeneration. Operative Tech Sport Med 8:120-121 8. Barclay TS, Tsourounis C, McGart GM (1998) Glucosamine. Ann Pharmacother 32:574-579 9. Da Camara CC, Dowless GV (1998) Glucosamine sulfate for osteoarthritis. Ann Pharmacother 32:580-587 10. Hepper CT, Halvorson JJ, Duncan ST et al (2009) The efficacy and duration of intra-articular corticosteroid injection for knee osteoarthritis: a systematic review of level I studies. J Am Acad Orthop Surg 17:638-646 11. Watterson JR, Esdaile JM (2000) Viscosuplementation: therapeutic mechanisms and clinical potential in osteoarthritis of the knee. J Am Acad Orthop Surg 8:277-284 12. Strauss EJ, Hart JA, Miller MD et al (2009) Hyaluronic acid viscosupplementation and osteoarthritis: current uses and future directions. Am J Sports Med 37:1636-44 13. Miller M, Cole B (2009) (eds) Text of arthroscopy: knee cartilage: diagnosis and decision making. Saunder, Philadelphia, pp 555-567 14. Fond J, Rodin D, Ahmad S, Nirschl RP (2002) Arthroscopic debridement for the treatment of osteoarthritis of the knee: 2- and 5-year results. Arthroscopy 18:829-834 15. Steadman J, Rodkey W, Singleton S et al (1997) Microfracture technique for full thickness condral defects: technique and clinical results. Oper Tech Ortho 7:300-304 16. Cole BJ, Pascual Garrido C, Grumet RC (2009) Surgical management of articular cartilage defects in the knee. J Bone Joint Surg Am 91:1778-179 17. Magnussen R, Dunn W, Carey J, Spindler K (2008) Treatment of focal articular cartilage defects in the knee: a systematic review. Clin Orthop Relat Res 466:952-962 18. William R, Harnly H (2007) Microfracture: indications, technique and results. Instr Course Lect 56:419-428 19. Knutsen G, Drogset JO, Engebretsen L et al (2007) A randomized trial comparing autologous chondrocyte implantation with microfracture. Findings at 5 years. J Bone Joint Surg Am 89:2105-2112 20. Solheim E, Oyen J, Hegna J et al (2009) Microfracture treatment of single or multiple articular cartilage defects of the knee: a 5-year median follow-up of 110 patients. Knee Surg Sports Traumatol Arthrosc 18:504-508 21. Steadman JR, Briggs KK, Rodrigo JJ et al (2003) Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy 19:477-484 22. Farr J, Schepsis A, Cole B et al (2007) Anteromedialization. J Knee Surg 20:120-128 23. Mandelbaum B, Browne JE, Fu F et al (2007) Treatment outcomes of autologous chondrocyte implantation for full thickness articular cartilage defects of the troclea. Am J Sports Med 35:915-921 24. Zaslav K, Cole B, Brewster R et al; STAR Study Principal Investigators (2009) A prospective study of autologous chondrocyte implantation in patients with failed prior treatment for articular cartilage defect of the knee: results of the Study of the Treatment of Articular Repair (STAR) clinical trial. Am J Sports Med 37:42-55 25. Rosenberger RE, Gomoll AH, Bryant T, Minas T (2008) Repair of large chondral defects of the knee with autologous chondrocyte implantation in patients 45 years or older. Am J Sports Med 36:2336-2344 26. Steinwachs M, Kreuz PC (2007) Autologous chondrocyte implantation in chondral defects of the knee with a type I/III collagen membrane: a prospective study with a 3-year followup. Arthroscopy 23:381-387 27. Kreuz PC, Steinwachs M, Erggelet C et al (2007) Importance of sports in cartilage regeneration after autologous chondrocyte implantation: a prospective study with a 3-year followup. Am J Sports Med 35:1261-1268 28. McNickle AG, L’Heureux DR, Yanke AB, Cole BJ (2009) Outcomes of autologous chondrocyte implantation in a diverse patient population. Am J Sports Med 37:1344-1350 29. Hangody L, Vasarhelyi G, Hangody LR et al (2008) Autologous osteochondral grafting – technique and long term results. Injury 39(Suppl 1):S32-S39

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30. Marcacci M, Kon E, Delcogliano M et al (2007) Arthroscopic autologous osteochondral grafting for cartilage defects of the knee: prospective study results at a minimum 7-year followup. Am J Sports Med 35:2014-2021 31. Dozin B, Malpeli M, Cancedda R et al (2005) Comparative evaluation of autologous chondrocyte implantation and mosaicplasty: a multicentered randomized clinical trial. Clin J Sport Med 15:220-226 32. Ball ST, Amiel D, Williams SK et al (2004) The effects of storage on fresh human osteochondral allografts. Clin Orthop Relat Res 418:246-252 33. Wingenfeld C, Egli RJ, Hempfing A et al (2002) Cryopreservation of osteochondral allografts: dimethyl sulfoxide promotes angiogenesis and immune tolerance in mice. J Bone Joint Surg Am 84-A(8):1420-1429 34. Wang CJ (2002) Treatment of focal articular cartilage lesions of the knee with autogenous osteochondral grafts. 2- to 4-year follow-up study. Arch Orthop Trauma Surg 122:169-172 35. Williams JM, Virdi AS, Pylawka TK et al (2005) Prolonged-fresh preservation of intact whole canine femoral condyles for the potential use as osteochondral allografts. J Orthop Res 23:831837 36. Williams SK, Amiel D, Ball ST et al (2003) Prolonged storage effects on the articular cartilage of fresh human osteochondral allografts. J Bone Joint Surg Am 85(A):2111-2120 37. Gross AE, Shasha N, Aubin P (2005) Long term follow-up of the use of fresh osteochondral allografts for post-traumatic knee defects. Clin Orthop Relat Res 435:79-87 38. Davidson PA, Rivenburgh DW, Dawson PE et al (2007) Clinical, histologic and radiographic outcomes of distal femoral resurfacing with hypotermically stored osteoarticular allografts. Am J Sports Med 35:1082-1090 39. McCulloch PC, Kang RW, Sobhy MH et al (2007) Prospective evaluation of prolonged fresh osteochondral allograft transplantation of the femoral condyle: minimum 2-year follow-up. Am J Sports Med 35:411-420 40. Jamali AA, Emmerson BC, Chung C et al (2005) Fresh osteochondral allografts: results in the patellofemoral joint. Clin Orthop Relat Res 437:176-185

Ankle Injuries

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D.E. Bonasia, A. Amendola

Abstract Ankle sprains are among the most common injuries encountered in sports, with an important financial impact on professional sports clubs. While the majority of these injuries respond well to conservative management, acute ankle sprains are frequently associated with chronic conditions that persist beyond the expected recovery period. The most common causes of disability following chronic ankle sprains, in addition to the excessive laxity, are: intra-articular pathologies (chondral lesions, loose bodies, ossicles, synovitis, and arthrosis), impingement lesions (soft-tissue and bony), and instabilities other than lateral (subtalar, syndesmotic, and medial). When dealing with athletes, it is important not to under-treat acute sprains or chronic associated symptoms and to always consider in the decision-making process whether the athlete is in active competition or in the off season.

33.1 Introduction Ankle sprains are among the most common injuries encountered in work and sport, with well over two million individuals experiencing ankle ligament trauma each year in the United States [1]. Ankle sprains also have a financial impact on professional sports clubs. For example, in England’s Football Association, ankle sprains collectively resulted in 12,138 days and 2,033 matches being missed in a 2-year period, with a 9% re-injury rate. Initial ankle sprains resulted in an average of 18 days and three matches missed, while re-injuries resulted in an average of 19 days and four matches missed [2]. While the majority respond well to conservative management [3], acute ankle sprains are frequently associated with pathology resulting in chronic symptoms, including pain and instability, that persist beyond the expected recovery period. In a survey of 84 high school varsity basketball players, Smith et al. [4] reported that over 70% had experienced an ankle sprain in their athletic lifetime. Chronic symptoms following an acute Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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sprain were reported by 50%, with 15% noting a performance deficit due to the dysfunction. The most common causes of disability following chronic ankle sprains, in addition to the excessive laxity, are: intra-articular pathologies (chondral lesions, loose bodies, ossicles, synovitis, and arthrosis), impingement lesions (anterior and anterolateral), and instabilities other than lateral (subtalar, syndesmotic, and medial) [5]. Therefore, when dealing with athletes, it is important not to under-treat acute sprains and to thoroughly evaluate chronic ankle instability, in order to precisely assess the causes of the complaints.

33.2 Anatomy and Biomechanics The lateral ligamentous complex of the ankle joint, consisting of the anterior talofibular ligament (ATFL), calcaneofibular ligament (CFL), and posterior talofibular ligament (PTFL), is the most frequently injured structure in sports. The ATFL is the primary restraint to anterior displacement, internal rotation, and inversion of the talus at all angles of flexion. The ATFL’s average width is 7 mm and its average length 25 mm: it is directed an average of 45° medially from the fibula toward the talus in the coronal plane. The CFL restrains subtalar inversion and thereby indirectly limits talar tilt within the ankle mortise. The CFL average width is 5 mm and its average length is 36 mm. With the foot in plantigrade position, the CFL forms an angle of 133° (range 113-150°) with the fibula. The CFL inserts on the anterior edge of the distal fibula, centered 9 mm from the distal tip. The PTFL has a long attachment on the posterior portion of the talus measuring 24 × 6 mm. This attachment involves nearly the entire non-articular portion of the posterior talus and extends to the groove for the flexor hallucis longus tendon. The fibular attachment is centered an average of 10 mm proximal to the distal tip in the digital fossa. The anteroposterior diameter averages 10 mm and the proximal-distal diameter 7 mm. The width of this ligament varies markedly with foot position. The deltoid ligament is composed of a superficial and a deep layer. The deep deltoid takes origin in the intercollicular groove and the posterior colliculus of the medial malleolus, and inserts into the posterior medial talus. The superficial layer takes origin from the anterior colliculus and fans out anteriorly to insert into the navicular, the spring ligament, the sustentaculum tali, and the posterior talus. The deep layer of the deltoid resists external rotation of the talus and the superficial layer resists abduction of the talus. The anterior inferior tibiofibular ligament attaches to the anterolateral distal tibia and runs distally and laterally in an oblique direction to attach to the anteromedial distal fibula. The tibial attachment is wider than the fibular attachment, giving the ligament a trapezoidal shape. The anterior inferior tibiofibular ligament has a width of approximately 18 mm and a thickness of 2-4 mm. The posterior inferior tibiofibular ligament attaches to the posterolateral distal tibia and runs horizontally to the posteromedial distal fibula. This ligament has a width of approximately 18 mm and a thickness of approximately 6 mm.

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33.3 Acute Treatment of Ankle Sprains 33.3.1 Clinical Assessment Lateral ankle sprains most commonly occur following excessive inversion and internal rotation of the hindfoot while the leg is in external rotation [6]. This places maximal strain on the lateral ankle ligaments. The ATFL is the most commonly involved, followed by the CFL in 50-75% of such injuries, and the PTFL in < 10% of sprains [2]. The history of the patient and the traumatic mechanism should be thoroughly evaluated. Recurrent sprains should be investigated to rule out chronic instability as well other causes that mimic instability. Location and amount of swelling and hematoma must be determined. Palpation of bone and soft tissues is important to rule out fractures and locate tenderness. Palpation must include the leg and the foot, in order to exclude proximal fibular fractures (i.e., Maisonneuve fracture) and 5th metatarsal base avulsions. Range of motion (ROM) is evaluated. When a fracture/dislocation is excluded, specific tests can be performed. The anterior drawer test evaluates the anterior talus displacement from the ankle mortise. It is performed with the foot in neutral position and must also always be performed for comparison purposes on the uninjured side. The ATFL is the main restraint to anterior talar subluxation. The test is positive with excessive anterior talar displacement and soft end-point, when the ATFL is deficient. The inversion test is used to assess the integrity of the CFL. This test determines the amount of talar tilt compared to the uninjured side, when the hindfoot is inverted and the talocrural joint is dorsiflexed. Specific tests for the distal tibio-fibular syndesmosis (see below) should be performed as well. Radiographs of both ankles are required, with anteroposterior, lateral, and mortise views, to assess possible associated conditions (fractures, osteochondral lesions, syndesmotic disruption, etc.). Stress radiographs do not provide information essential to the clinical assessment and therefore are not routinely obtained [7]. Magnetic resonance imaging (MRI) may be useful to assess the amount of soft-tissue damage or whether osteochondral defects are present. Acute lateral ankle sprains are graded from I to III [8] (Fig. 33.1). In grade I, no instability is present on examination and only a few fibers of the ATFL are stretched or torn. Grade II sprains involve a complete tear of the ATFL with or without a partial CFL lesion. In grade III, both ATFL and CFL are torn and, in the most severe sprains the PTFL and articular capsule may be damaged as well [8].

33.3.2 Treatment The three most common treatments for acute lateral ankle ligament injury include: cast immobilization, functional management, and surgical anatomic repair. Conservative treatment is the management of choice for grade I and II ankle sprains in all patients. Cast im-

...

D.E. BonilSia,A.Amendola

33

". """"'" latcnl iIIIkIc sprain gmding (sec text). ATFL, Anterior talofibular ligament; CFL,

"""""

Grade III

Fig.J3.1 Acute calamcofibu1a:r Iigamcn1; PIFL, posterior talofibular Iigamcnt

mobilization usually entailB a 3-week: period in a below-knee walling cast, followed by ROM, strengthening, and proprioceptive rehabilitation. Immobilization is contraindicated in the high-performance athlete but may be advantageous for low-demand, heavy, or ctderiypatients [6]. In young. active, and compliant patients with grade lorn ankle sprains. functional management is indicated. This implies early mobilization with extemaJ. support, rest, ice, compression. and elevation. and is followed by a rehabilitation program consisting of ROM exercises, strengthening. proprioception, and activity-specific training [6]. The treatment for grade m lateral ankle ligament injury is controversial. Currently, our tcndcncy is to manage conservatively low-demand patients and to surgically repair the lateral ligaments in a few selected athletes. Presently, once the decision to stabilize an ankle

has been made. our preferred method is a modified Brostr6m with a Gould modification [9. 10]. In addition. arthroscopy is pcdonned prior to the:incision, if synovial or bony impingement, loose bodies. osteochondral defects, or syndesmotic disruption are suspected [11]. Anteromedial and anterolateral portals are used, with the anterolateral portal incorporated into the Bros1:r6m incision anteriorly (Fig. 33.2). Swelling from fluid extravasation is present but usually of no impediment to identifying anatomy and carrying out the procedure [5]. The patient is positioned supine, with a bump under the hip of the affected side and a thigh tourniquet in place. The incision is performed anterior to the distal fibula and then curved posteriorly around the lateral malleolus in a hockey stick fashion. This must include the anterolateral portal, if arthroscopy is perf'ormed. The superficial peroneal nerve is identified and protected. The extensor retinaculum is identified and isolated with blunt dissection. Deep to the retinaculum. the Iateralligamcnt:ous complex of the ankle is identified, and the tom ligaments visualized and :repaired with 2-0 non-abSOIbable threaded sutures. The lateral edge of the lateral retinaculum is then sutured to the lateralligamentous complex as an augmentation (Fig. 33.3). The post-operative regimen includes nonweight bearing for 2-3 weeks and early ROM exercises. At 3 weeks, weight-bearing is allowed as tolerated and the patient proceeds to strengthening and proprioceptive protocols.

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a

b

Fig. 33.2 Arthroscopic evaluation and Broström-Gould repair incision. a Arthroscopy is performed first to assess and treat any intra-articular pathologies. b The anterolateral portal is incorporated into the Broström-Gould incision anteriorly

a

b

c

d

e

f

Fig. 33.3 Surgical technique for Broström-Gould lateral ankle repair. a The superficial peroneal nerve is identified and visualized throughout the entire procedure. b Blunt dissection of the lateral edge of the extensor retinaculum. The torn portions of the ATFL (c) and CFL (d) are identified and repaired (e). The lateral edge of the lateral retinaculum is then sutured to the lateral ligamentous complex as an augmentation (f)

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33.3.3 Results A level I meta-analysis comparing immobilization and functional management for acute lateral ankle ligament injuries found that functional management was superior in terms of: (1) percentage of patients returning to sports, (2) time before return to work, (3) persistent swelling and laxity, (4) ROM, and (5) rate of patient’s satisfaction [12]. In a systematic review of functional management, Kerkhoffs et al. concluded that lace-up supports were most effective, that tapes were associated with skin irritation and were not superior to semi-rigid supports, and that elastic bandages were the least effective form of management [13]. More recently, another systematic review of nine level I studies of the effect of immobilization vs. early functional treatment concluded that functional treatment is superior in terms of: (1) return to pre-injury activity, (2) subjective instability, and (3) re-injury rate. Patient satisfaction was not substantially different between studies evaluating this parameter. The authors concluded that the current best evidence suggested a trend favoring early functional treatment over immobilization for the treatment of acute lateral ankle sprains [3]. A meta-analysis of surgical vs. non-surgical management of acute ankle injuries found that all available trials had methodological drawbacks [12]. Therefore, the authors were unable to draw any conclusions. In a randomized controlled trial comparing surgical with functional management, however, statistically significant differences were found in favor of surgical intervention with regard to: pain, giving way, and recurrent sprains. Objective scores at follow-up were statistically better for patients who received surgery. Despite superior results in surgically managed patients, the authors cited cost, risk of surgical complications, and similar results with delayed and acute repair as reasons not to manage all acute injuries surgically. They suggested that surgery instead be reserved for the high-demand patient [14].

33.4 Lateral Ankle Instability 33.4.1 Clinical Assessment The history of patients with chronic ankle pain should be thoroughly investigated. The complaints reported by the patients may include: (1) isolated or recurrent ankle sprains, (2) pain during normal or sustained activities, (3) giving way of the ankle, and (4) locking or catching [15]. True mechanical instability, due to ligamentous laxity, must be differentiated from functional instability related to muscular weakness or pain inhibition reflexes from associated injury. If pain is not present between sprains, true mechanical instability may be the primary problem [5]. Symptoms are typically exacerbated by prolonged weight-bearing or high impact activities such as demanded in sports involving running or jumping [15].

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Physical examination should include inversion stress and anterior drawer tests for lateral instability as well as an eversion stress test for medial instability. Specific tests for syndesmotic instability (see below) must be performed. Flexion-extension ROM must be evaluated to exclude anterior or posterior impingement. Joint effusion and localized tenderness over the joint line may indicate intra-articular disorders (ossicles, loose bodies, osteochondral lesions, arthritis, etc.). Foot alignment and potential deformities (hindfoot varus, first ray plantar flexion, and midfoot cavus) must be evaluated as either may predispose to recurrent sprains [15]. A correct work-up must include plain radiographs with weight-bearing anteroposterior, lateral, and mortise views of both ankles. Stress radiographs may be useful to confirm the diagnosis but are not mandatory. MRI evaluation is essential in demonstrating ligament injury signs (ligament swelling, discontinuity, a lax or wavy ligament, and nonvisualization), but more importantly in revealing associated causes of ankle pain (chondral injury, bone bruising, radiographically occult fractures, sinus tarsi injury, peri-articular tendon tears, and impingement syndrome) [15]. Chronic subtalar instability is believed to be associated with lateral mechanical instability in 10-25% of patients [5]. The structures considered to be most important in stabilizing the subtalar joint are the extensor retinaculum, CFL, LTCL, the interosseous talocalcaneal ligament, and cervical ligament. The mechanism of injury involves supination with the ankle in dorsiflexion. Chronic repetitive stress on the ligaments due to jumping has also been proposed. MRI has recently been shown to be more accurate than stress radiographs in displaying ligamentous injury of the subtalar joint [5].

33.4.2 Treatment Initial treatment for all patients is conservative and entails a physical therapy program of peroneal muscle strengthening and proprioceptive training, combined with use of a laceup brace for high-risk activities. This regimen is effective in 90% of patients [5]. The remaining patients are candidates for operative stabilization. The most common stabilization procedures for lateral ankle instability can be divided into anatomic repair (Broström [9], Broström-Gould [10], Karlsson [16]) and non-anatomic reconstruction (Watson-Jones [17], Evans [18], Chrisman-Snook [19]). A high rate of intra-articular pathology associated with lateral instability has been described and indicated as the main factor responsible for residual complaints after ankle stabilization [5]. Thus, we always recommend ankle arthroscopy combined with lateral ankle stabilization. If pain is present between instability episodes and an associated lesion has been identified, it may be an option to treat this cause prior to considering surgical stabilization of the ankle or to treat it concurrently (Fig. 33.4). If no clear associated lesion is identified, arthroscopy is carried out immediately preceding the lateral repair. Our preferred technique to treat chronic lateral instability is the Gould modification of the Broström procedure (Figs. 33.2, 33.3), as previously described. In patients with excessive laxity, failed Broström, augmentation with an allograft semitendinosus or


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a

b

c

Fig. 33.4 a Patient with chronic lateral ankle instability and anterior bony impingement (white circle). b Arthroscopic assessment of the tibial and talar bone spurs. c Arthroscopic picture after osteoplasty

Achilles, or autograft hamstring tendon may be used [20-23]. Recalcitrant inversion injury in the presence of a varus hindfoot may warrant consideration of supramalleolar or calcaneal osteotomy [5]. Another anatomic repair option was described by Karlsson et al. [16]. The authors recommended shortening the ATFL and the CFL and reattaching them to the fibula at their anatomic origins through drill holes. In the past, non-anatomic reconstructions that sacrifice all or part of the peroneus brevis tendon to provide a tenodesis effect across the ankle and subtalar joints were frequently performed. Concerns regarding loss of the dynamic stabilizing effect of the peroneus brevis and over-tightening of the subtalar joint have contributed to their decrease in popularity. Among the non-anatomic reconstructions, Watson-Jones technique entails the use of a peroneus brevis graft distally attached, passed through the fibula and the talus (Fig. 33.5). This technique was later simplified by Evans, who passed the distally attached peroneus brevis graft through an oblique posterosuperior drill hole in the distal fibula (Fig. 33.6), with a neo-ligament lying between the ATFL and the CFL. In the Chrisman and Snook method, a split peroneus brevis is passed through the fibula and the calcaneus in order to maintain some peroneus brevis function (Fig. 33.7). When there is associated chronic subtalar instability, initial treatment is the same as the rehabilitation protocol for lateral instability. When conservative treatment fails, any anatomic or non-anatomic technique can be used [5].

33.4.3 Results The Broström technique produced good or excellent functional results in 91% of patients at 26-year follow-up [24]. Karlsson’s technique yielded 87% good to excellent results at 2- to 12-year follow-up [16]. Of the non-anatomic repair methods, the Watson-Jones procedure demonstrated 88% good to excellent clinical results at 10- to 18-year follow-up, but with a high rate of complications (18%) [25].

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a

b

Fig. 33.5 Watson-Jones’ lateral ankle reconstruction. a, b The peroneus brevis tendon, proximally detached, is passed through the fibula (from posterior to anterior), then in a talar tunnel (with a plantar to dorsal direction), and finally sutured on itself a

b

c

d

Fig. 33.6 Evans’ lateral ankle reconstruction. a The peroneus brevis tendon is proximally detached, and then (b, c) is passed through a fibular tunnel (with a distal to proximal and anterior to posterior direction). d The tendon is finally sutured on the peroneus longus tendon a

b

c

Fig. 33.7 Chrisman-Snook’s lateral ankle reconstruction. a The peroneus brevis tendon is identified and (b) split. c The half-tendon graft is passed through the fibula (from anterior to posterior) and the calcaneus (from dorsal to plantar) and then sutured on itself

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Long-term results of the Evans technique were favorable in only 33-52% of the cases, with swelling, stiffness, instability, bony impingement, and osteoarthritis as the main residual post-operative complaints [16, 26, 27]. The Chrisman-Snook procedure yielded 94% excellent or good results at 10-year follow-up [28]. Nevertheless, a randomized controlled trial comparing the outcomes of the modified Broström and Chrisman-Snook procedures showed that patients treated with modified Broström repair had markedly better Sefton scores and fewer complications (wound dehiscence, sural nerve injury, stiffness, and persistent instability) at 2.5-year follow-up [29]. A meta-analysis of seven randomized trials assessing surgical treatment for chronic lateral ankle instability was unable to draw any conclusions, due to the poor methodological quality of the studies available in the literature [30].

33.5 Syndesmotic Instability 33.5.1 Clinical Assessment Syndesmosis injuries are more common than lateral ankle sprains in collision sports and in those that involve rigid immobilization of the ankle in a boot, such as skiing and hockey [31]. In the general athlete population, the incidence of syndesmosis sprains is between 10 and 20% of all ankle sprains [32,33]. Specific tests for the evaluation of syndesmosis injuries include: (1) the squeeze test, (2) the external rotation stress test, (3) the fibula translation test, (4) the Cotton test, (5) the crossed-leg test, and (6) the stabilization test [31]. The stabilization test is performed by tightly applying several layers of 5-cm athletic tape just above the ankle joint to stabilize the distal syndesmosis. The patient is then asked to stand, walk, and perform a toe raise and jump. The test result is positive if these maneuvers are less painful after taping. This test is particularly useful to confirm the diagnosis during the subacute or chronic phase of injury, once acute swelling and pain have subsided. All of the stress tests cited must clearly demonstrate a significant difference between the affected and normal ankles before they can be considered diagnostic [31]. Imaging of syndesmosis injuries of the ankle should begin with plain radiographs to rule out fracture and to look for the presence of diastasis of the syndesmosis. Common views include weight-bearing anteroposterior, mortise, and lateral. Diastasis is identified by an increased tibiofibular clear space on an anteroposterior radiograph to a value ≥ 6 mm [34]. External rotation stress views may be obtained as well. Nevertheless, neither weight-bearing radiographs nor stress views are sensitive enough to diagnose partial syndesmotic disruption [31]. However, if widening of the mortise is seen on radiographs, it indicates a more severe injury and potentially complete disruption of the syndesmosis, which requires operative stabilization [31]. High-resolution MRI can effectively image the structures of the syndesmosis and has a sensitivity of 100% and a specificity of 93% for

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diagnosis of anterior inferior tibiofibular ligament tear, and a sensitivity and specificity of 100% for diagnosis of posterior inferior tibiofibular ligament tear [31, 35]. Gerber et al. [33] described the West Point Ankle Grading System, which classifies syndesmotic injuries into three categories (grade I, II, or III) based on evidence of syndesmosis instability [34]. Grade I refers to no instability; grade II, some evidence of instability; and grade III, definite instability.

33.5.2 Treatment In grade I syndesmotic sprains, treatment is usually conservative and based on a threephase rehabilitation protocol [31]. The first phase (acute) emphasizes protection of the joint, minimization of the inflammatory response, and pain control. In this phase, partial or non-weight-bearing are mandatory, while immobilization is controversial and the decision should mainly depend on the symptoms: cast immobilization is recommended in case of severe pain while the use of an ankle brace, stirrup, or taping is a reasonable alternative in case of moderate to mild pain. In the second phase (subacute), the goals are to restore mobility, strength, and normal gait. The remaining phase includes advanced training, neuromuscular control, and sport-specific exercises [31]. In grade III syndesmotic disruptions, a frank diastasis is evident and surgical treatment is indicated. Ankle arthroscopy is recommended to assess and treat any associated intraarticular pathologies and to debride the torn ligaments. Gravity inflow must be used in case of combined ankle fractures. Trans-syndesmotic fixation is achieved, under fluoroscopic control, with one or two cannulated screws inserted percutaneously. Three or four cortices can be achieved with each screw, according to the surgeon’s preference. The position of the foot during fixation (neutral or dorsiflexed) seems not to affect the post-fixation ROM of the ankle [36]. The patient should be placed in a non-weight-bearing cast for 6 weeks postoperatively and then start progressive weight-bearing and ROM exercises. These can begin with the screws in place, with the screws removed at 8-10 weeks [31]. Syndesmosis reconstruction techniques have been described as well [37], but are still not widely performed. In grade II sprains, if there are no radiographic signs of syndesmotic diastasis, treatment is controversial (Fig. 33.8). Surgery may be indicated if conservative treatment fails or with arthroscopic evidence of syndesmotic instability.

a

b

c

Fig. 33.8 (a, b) Arthroscopic evaluation of partial anterior inferior tibiofibular ligament lesion (grade II). c Debridement of the torn portions of the ligament

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33.5.3 Results A review of the literature regarding syndesmotic sprain treatment is inconclusive. Jones and Amendola, in their systematic review, identified six articles that evaluated treatment of syndesmosis injuries [3]. All of the studies were case series and represented the highest level of evidence available; however, the authors were unable to draw any conclusions regarding the most reliable treatment for syndesmotic sprains [3]. Ogilvie-Harris et al. [38] treated nine patients with arthroscopic diagnosis of syndesmotic instability and normal radiographs. The treatment consisted of arthroscopic debridement of torn ligaments and of the chondral damage, if present. Screw fixation was not performed. Seven patients were completely satisfied with the results and two were partially satisfied. The authors concluded that pain was caused by the intra-articular disruption, not by biomechanical laxity, and that arthroscopic debridement was sufficient in these patients. Similar results and conclusions were reported by Han et al. [39] in their 20-patient series with arthroscopic diagnosis and treatment of chronic syndesmosis injuries. Wolf and Amendola [40] treated 14 athletically active patients with arthroscopic debridement and percutaneous trans-syndesmotic fixation. Three patients required additional lateral ligament reconstruction (Broström). Of the 14 patients, two (14%) had an excellent result, 10 (71%) a good result, and 2 (14%) a fair result (according to the Edwards and DeLee scale). Schuberth et al. [41], at 24 months minimum follow-up, reported excellent results in six patients with latent syndesmotic instability treated with arthroscopic debridement and percutaneous fixation. Beumer et al. [37] evaluated the results of nine patients who underwent late reconstruction of the syndesmosis an average of 27 months after injury. At a mean follow-up of 45 months, all patients reported improvement, and none complained of instability.

33.6 Transchondral Fractures 33.6.1 Clinical Assessment Transchondral fractures may be isolated or associated with ankle sprains, instability, and fractures. The incidence of transchondral fractures is reportedly as high as 23-95% and associated with ankle instability. The talar dome, in particular its posteromedial aspect, is the most frequently involved site [42]. Patients with isolated acute or chronic transchondral fractures typically report pain, catching, snapping, grinding, swelling, and tenderness around the tibiotalar joint. When the osteochondral lesion is combined with fractures or instability, the symptoms are mainly related to the associated injury. Plain radiographs (anteroposterior, lateral, and mortise views of both ankles) are essential in the diagnosis. However, because plain radiographs may

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Fig. 33.9 Berndt and Harty classification of transchondral fractures (see text)

miss up to 50% of osteochondral lesions and are unable to assess the state of the cartilage, more-advanced imaging techniques (i.e., MRI) are indicated [42, 43]. Berndt and Harty described a four-stage classification for transchondral fractures that has been widely accepted [44] (Fig. 33.9). Type I is a small subchondral depression (Fig. 33.9a), type II is a partially detached osteochondral fragment (Fig. 33.9b), type III is a completely detached osteochondral fragment, without displacement (Fig. 33.9c), and type IV is a displaced osteochondral fragment [42] (Fig. 33.9d).

33.6.2 Treatment Osteochondral defects type I, II, or III are amenable to conservative treatment when symptomatic. Surgery is indicated only after an adequate trial (up to 3 months) of non-operative therapy fails [42]. There also seems to be agreement that patients with stage IV frac-


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a

b

c

d

Fig. 33.10 a Symptomatic transchondral fracture of the posteromedial talar dome. b Arthroscopic picture of the lesion. c, d Curettage and abrasion arthroplasty

tures should be treated surgically from the onset. Presently, an arthroscopic approach is widely accepted for patients who require curettage or drilling of a transchondral fracture < 2 cm [42]. The principal aim of these treatments is bone marrow stimulation and revascularization of the bony defect. Curettage or abrasion arthroplasty (Fig. 33.10) are sufficient when the bed of the lesion is made by bleeding cancellous bone whereas microfractures are indicated when the bed of the lesion is formed by subchondral bone [42]. Retrograde drilling with bone or bone-substitute grafting is indicated for subchondral bone lesions with intact cartilage. With larger (> 2 cm) acute osteochondral fragments, open excision or internal fixation is indicated. In large chronic transchondral fractures, open excision and osteochondral auto/allograft transplantation (OATS) or autologous chondrocytes implantation (ACI) may be needed [42]. In most patients, anterior ankle arthroscopy is sufficient to treat the transchondral fracture, with posterior arthroscopy indicated in limited cases, including: (1) posterior talar or tibial transchondral fractures of the ankle joint, (2) loose bodies, (3) posterior post-traumatic calcifications, avulsion fragments, or osteophytes, (4) chondromatosis, and (5) chronic synovitis [42].

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33.6.3 Results The literature is inconclusive about the most reliable treatment for transchondral fractures around the ankle. Good evidence seems to exist for the arthroscopic treatment of isolated osteochondral injuries of the ankle [45]. Non-surgical therapy yields successful results in 45% of the cases and is indicated in stage I, II, or III lesions [46]. In a systematic review of the literature, debridement with bone marrow stimulation was superior to other methods, with 86% good/excellent results in 21 studies [47]. However, OATS and ACI were not included in the systematic review. Recently, a randomized controlled trial comparing chondroplasty, microfracture, and OATS showed similar results for the three methods at 2-year follow-up [48]. However, in decision-making, one should consider that chondroplasty and microfractures are related to less postoperative pain than reported for other procedures [46]. Choi et al. [49] evaluated, in terms of prognostic significance, the size of 120 osteochondral lesions of the talus treated with arthroscopic bone marrow stimulation techniques. They found that lesions > 150 mm2 are more likely to fail. Recently, Lee et al. [50] reported 90% good to excellent clinical results with microfracture at 1-year follow-up, but 40% out of 20 chondral lesions were incompletely healed at second-look arthroscopy.

33.7 Ankle Impingement Syndrome 33.7.1 Anterior Bony Impingement Anterior ankle impingement syndrome is characterized by anterior ankle pain with limited/painful dorsiflexion, catching, and subjective feelings of giving way from pain. The cause can be either soft-tissue or bony impingement. The presence of osteophytes has been reported in as many as 60% of professional soccer players, and is also common in athlete of other sports that are demanding on the ankle. The exact cause of osteophyte formation is not fully understood. However, in repetitive sports, bony spur formation may be due to traction from repetitive micro-trauma (damage to the rim of the anterior ankle cartilage) or forced plantar or dorsi-flexion (i.e., traction on the joint capsule during maximal plantar flexion, as occurs during kicking a ball in soccer), and not to arthritic changes as in the general population. These ankles are not osteoarthritic and debridement is generally successful. Lateral ankle radiographs reveal these osteophytes on the anterior tibia and talar neck. These spurs have been described as “kissing osteophytes” but there is no evidence that the tibial and talar osteophytes are actually impinging. The talar spur peak lies medial to the midline, while the tibial spur peak lies lateral to the midline. Two hypotheses have been proposed and both may be correct: (1) traction is a possible mechanism for tibial


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spur formation, and (2) micro-trauma caused by ball impact may be the causative mechanism for the talar neck spur. The treatment of lesions that fail to respond to an ankle rehabilitation program is arthroscopic debridement.

33.7.2 Posterior Impingement of the Ankle Posterior tibio-talar impingement is unusual in the athlete. It more commonly results from flexor hallucis longus (FHL) irritation, due to a prominent posterior process of the talus or a symptomatic os trigonum. This has been classically described in dancers who present with a painful hyper-plantar-flexed position. These athletes are not severely disabled and are usually able to complete the season. Physical examination reveals tenderness posteromedially and posterolaterally over the talus and the FHL, most of all by applying resistance to hallux flexion, and pain reproduced by maximal plantar flexion. X-rays commonly demonstrate the bony prominence, while MRI or bone scan shows increased uptake or edema around the os trigonum (Fig. 33.11) or the prominent posterior process. Treatment includes local injection of the FHL sheath, bracing, and in unresponsive cases debridement and excision of the prominent os trigonum. The results of this procedure are good to excellent with open or arthroscopic methods. A posterior arthroscopic approach in the prone position has been described, with the advantage of improved visualization, minimal surgical exposure, and earlier recovery.

33.7.3 Soft-tissue Impingement of the Ankle Both anterolateral and posteromedial soft-tissue impingement of the ankle have been described. These conditions are causes of persistent pain following ankle sprains.

a

b

c

Fig. 33.11 Os trigonum. a Impingement in plantar flexion posteriorly. b MRI demonstrating edema and fluid around the os trigonum. c Post-resection X-ray

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Anterolateral soft tissue impingement may occur after an ankle sprain, Hemorrhage into the joint is followed by traumatic synovitis, with thickening and exudation usually removed during the repair process. In some cases, however, there is incomplete resorption of the exudates, which become thickened and hyalinized, resulting in a synovial impingement lesion. Clinically, these patients present with anterolateral ankle pain with weight-bearing, forced dorsiflexion, and palpation of the anterolateral joint line. X rays are usually normal, while MRI shows good sensitivity and specificity in diagnosing this condition. Posteromedial soft tissue impingement of the ankle is an uncommon condition, occurring with severe inversion injures, which involve the deep posterior fibers of the medial deltoid ligament. Occasionally, thick disorganized fibrotic scar tissue persists and impinges between the talus and the posterior margin of the medial malleolus. On physical examination, there is deep soft-tissue induration and localized tenderness immediately posterior to the medial malleolus and reproduction of pain on provocative testing (palpation of the tender site while moving the ankle into plantar flexion and inversion). If the symptoms of soft-tissue impingement are refractory to physical therapy, strengthening, and corticosteroid injection, arthroscopy is indicated, with thorough debridement and synovectomy resolving the symptoms in the majority of cases.

33.8 Conclusions While the goal of treatment for acute ankle sprains and syndesmotic sprains is almost the same in every patient, special considerations should be made for the athlete with chronic ankle instability and transchondral fractures. For the off-season athlete, the treatment of these two conditions is comparable to that in any other patient. For the in-season athlete with chronic ankle instability, however, the cause of the complaints must be thoroughly evaluated. In many cases it is related to associated intra-articular conditions, including: ossicles, loose bodies, soft-tissue or bony impingement, osteochondral lesions, synovitis, and initial arthrosis. In this scenario, ankle arthroscopy is indicated to remove the cause of complaints as well as to allow a quick return to the sport activity, with lateral ankle repair/reconstruction delayed until the end of the season. The same consideration should be made regarding dislocated transchondral fractures following ankle sprains. In this case, the injury in the in-season athlete is amenable to ankle arthroscopy and loose body removal. Every cartilage-resurfacing procedure can be performed at the end of the season. This strategy is valid as long as the surgeon is not “burning any bridges”. For example, it is not acceptable to remove a large osteochondral fragment amenable to fixation and then, at the end of the season, put the patient through a more complex procedure (i.e., OATS), with a lower success rate.

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References 1. Beynonn BD, Renstrom PA, Alosa DM et al (2001) Ankle ligament injury risk factors: a prospective study of college athletes. J Orthop Res 19:213-220 2. Ferran NA, Maffulli N (2006) Epidemiology of sprains of the lateral ankle ligament complex. Foot Ankle Clin 11:659-662 3. Jones MH, Amendola AS (2007) Acute treatment of inversion ankle sprains: immobilization versus functional treatment. Clin Orthop Relat Res 455:169-172 4. Smith RW, Reischl SF (1986) Treatment of ankle sprains in young athletes. Am J Sport Med 14:464-471 5. Amendola A, Bonasia DE (2010) When is ankle arthroscopy indicated in ankle instability? Oper Tech Sports Med 18:2-10 6. Maffulli N, Ferran N (2008) Management of acute and chronic ankle instability. J Am Acad Orthop Surg 16:608-615 7. Frost SC, Amendola A (1999) Is stress radiography necessary in the diagnosis of acute or chronic ankle instability? Clin J Sport Med 9:40-45 8. Chorley JN, Hergenroeder AC (1997) Management of ankle sprains. Pediatr Ann 26:56-64 9. Broström L (1966) Sprained ankles: surgical treatment of “chronic” ligament ruptures. Acta Chir Scand 132:551-565 10. Gould N, Seligson D, Gassman J (1980) Early and late repair of lateral ligament of the ankle. Foot Ankle 1:84-89 11. Amendola A, Petrik J, Webster-Bogaert S (1996) Ankle arthroscopy: outcome in 79 consecutive patients. Arthroscopy 12:565-573 12. Kerkhoffs GM, Rowe BH, Assendelft WJ et al (2002) Immobilisation and functional treatment for acute lateral ankle ligament injuries in adults. Cochrane Database Syst Rev 3:CD003762 13. Kerkhoffs GM, Struijs PA, Marti RK et al (2003) Functional treatments for acute ruptures of the lateral ankle ligament: a systematic review. Acta Orthop Scand 74:69-77 14. Pijnenburg AC, Bogaard K, Krips R et al (2003) Operative and functional treatment of rupture of the lateral ligament of the ankle: a randomised, prospective trial. J Bone Joint Surg Br 85:525-530 15. Amendola A, Bonasia DE (2010) The role of arthroscopy in the treatment of chronic ankle instability. Mc Ginty Operative Arthroscopy, 4th edition. Edited by Don Johnson et al (in press) 16. Karlsson J, Bergsten T, Lansinger O et al (1988) Reconstruction of the lateral ligaments of the ankle for chronic lateral instability. J Bone Joint Surg Am 70:581-588 17. Watson-Jones R (1952) Recurrent forward dislocation of the ankle joint. J Bone Joint Surg Br 134:519 18. Evans DL (1953) Recurrent instability of the ankle: a method of surgical treatment. Proc R Soc Med 46:343-344 19. Chrisman OD, Snook GA (1969) Reconstruction of lateral ligament tears of the ankle: An experimental study and clinical evaluation of seven patients treated by a new modification of the Elmslie procedure. J Bone Joint Surg Am 51:904-912 20. Coughlin MJ, Schenck RC Jr, Grebing BR et al (2004) Comprehensive reconstruction of the lateral ankle for chronic instability using a free gracilis graft. Foot Ankle Int 25:231-241 21. Espinosa N, Smerek J, Kadakia AR et al (2006) Operative management of ankle instability: reconstruction with open and percutaneous methods. Foot Ankle Clin 11:547-565 22. Oyer DS, Younger AS (2006) Anatomic reconstruction of the lateral ligament complex of the ankle using a gracilis autograft. Foot Ankle Clin 11:585-595 23. Paterson R, Cohen B, Taylor D et al (2000) Reconstruction of the lateral ligaments of the ankle using semi-tendinosis graft. Foot Ankle Int 21:413-419 24. Bell SJ, Mologne TS, Sitler DF et al (2006) Twenty-six-year results after Broström procedure for chronic lateral ankle instability. Am J Sports Med 34:975-978

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25. Sugimoto K, Takakura Y, Akiyama K et al (1998) Longterm results of Watson-Jones tenodesis of the ankle: Clinical and radiographic findings after ten to eighteen years of followup. J Bone Joint Surg Am 80:1587-1596 26. Kaikkonen A, Lehtonen H, Kannus P et al (1999) Long-term functional outcome after surgery of chronic ankle instability: a 5-year follow-up of the modified Evans procedure. Scand J Med Sci Sports 9:239-244 27. Krips R, Brandsson S, Swensson C et al (2002) Anatomical reconstruction and Evans tenodesis of the lateral ligaments of the ankle: clinical and radiological findings after followup for 15 to 30 years. J Bone Joint Surg Br 84:232-236 28. Snook GA, Chrisman OD, Wilson TC (1985) Long-term results of the Chrisman-Snook operation for reconstruction of the lateral ligaments of the ankle. J Bone Joint Surg Am 67:1-7 29. Hennrikus WL, Mapes RC, Lyons PM et al (1996) Outcomes of the Chrisman-Snook and modified-Broström procedures for chronic lateral ankle instability: a prospective, randomized comparison. Am J Sports Med 24:400-404 30. de Vries JS, Krips R, Sierevelt IN et al (2006) Interventions for treating chronic ankle instability. Cochrane Database Syst Rev CD004124 31. Williams GN, Jones MH, Amendola A (2007) Syndesmotic ankle sprains in athletes. Am J Sports Med 35:1197-207 32. Cedell CA (1975) Ankle lesions. Acta Orthop Scand 46:425-445 33. Gerber JP, Williams GN, Scoville CR et al (1998) Persistent disability associated with ankle sprains: a prospective examination of an athletic population. Foot Ankle Int 19:653-660 34. Harper MC, Keller TS (1989) A radiographic evaluation of the tibiofibular syndesmosis. Foot Ankle 10:156-160 35. Takao M, Ochi M, Oae K et al (2003) Diagnosis of a tear of the tibiofibular syndesmosis: the role of arthroscopy of the ankle. J Bone Joint Surg Br 85:324-329 36. Tornetta P 3rd, Spoo JE, Reynolds FA et al (2001) Overtightening of the ankle syndesmosis: is it really possible? J Bone Joint Surg Am 83:489-492 37. Beumer A, Heijboer RP, Fontijne WP et al (2000) Late reconstruction of the anterior distal tibiofibular syndesmosis: good outcome in 9 patients. Acta Orthop Scand 71:519-521 38. Ogilvie-Harris DJ, Gilbart MK, Chorney K (1997) Chronic pain following ankle sprains in athletes: the role of arthroscopic surgery. Arthroscopy 13:564-574 39. Han SH, Lee JW, Kim S et al (2007) Chronic tibiofibular syndesmosis injury: the diagnostic efficiency of magnetic resonance imaging and comparative analysis of operative treatment. Foot Ankle Int 28:336-342 40. Wolf BR, Amendola A (2002) Syndesmosis injuries in the athlete: when and how to operate. Curr Opinion Orthop 13:151-154 41. Schuberth JM, Jennings MM, Lau AC (2008) Arthroscopy-assisted repair of latent syndesmotic instability of the ankle. Arthroscopy 24:868-874 42. Bonasia DE, Rossi R, Saltzman CL et al (2010) The role of arthroscopy in the treatment of fractures around the ankle. J Am Acad Orthop Surg (in press) 43. O’Loughlin PF, Heyworth BE, Kennedy JG (2010) Current Concepts in the Diagnosis and Treatment of Osteochondral Lesions of the Ankle. Am J Sports Med 38:392-404 44. Berndt AL, Harty M (1959) Transchondral fractures (osteochondritis dissecans) of the talus. J Bone Joint Surg Am 41:988-1020 45. Glazebrook MA, Ganapathy V, Bridge MA et al (2009) Evidence-based indications for ankle arthroscopy. Arthroscopy 25:1478-1490 46. van Dijk CN, van Bergen CJ (2008) Advancements in ankle arthroscopy. J Am Acad Orthop Surg 16:635-646 47. Verhagen RAW, Struijs PAA, Bossuyt PMM et al (2003) Systematic review of treatment strategies for osteochondral defects of the talar dome. Foot Ankle Clin 8:233-242 48. Gobbi A, Francisco RA, Lubowitz JH et al (2006) Osteochondral lesions of the talus: randomized controlled trial comparing chondroplasty, microfracture, and osteochondral autograft transplantation. Arthroscopy 22:1085-1092

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49. Choi WJ, Park KK, Kim BS et al (2009) Osteochondral lesion of the talus: is there a critical defect size for poor outcome? Am J Sports Med 37:1974-1980 50. Lee KB, Bai LB, Yoon TR et al (2009) Second-look arthroscopic findings and clinical outcomes after microfracture for osteochondral lesions of the talus. Am J Sports Med 37 (Suppl 1):S63-S70

Lower Limb Rehabilitation

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J. Espregueira-Mendes, R. Barbosa Pereira and A. Monteiro

Abstract This short chapter presents the critical thinking behind the guidelines concerning rehabilitation of the lower limb, a wide but incomplete field. Rehabilitation involves the management of injuries, essentially through the use of several different physical agents and therapeutic exercises. Knowledge related to the time frame of tissue healing, inflammatory process, basic training principles, the underlying science, and biomechanics is of utmost importance to every sports medicine professional. Here, essential information is provided about four of the most prevalent injuries of the lower limb: hamstring ruptures, patellar tendinopathy, anterior cruciate ligament rupture (reconstruction), and acute ankle sprains. Rehabilitation goals, treatment strategies, new assessment devices, criteria to return to play, and promising new therapies are discussed. The discussion of injury prevention provides the most up-to-date evidence related to ACL rupture. The current focus is on strength, balance, proprioceptive, and neuromuscular training programs.

34.1 Introduction Rehabilitation is a wide but incomplete field in which knowledge, experience, and “art” come together to achieve the desired clinical and sportive goals, for both health care professionals and athletes. However, although much remains to be learned, we (sports medicine physicians, orthopedists, and physical therapists) much achieve fast and effective results, which sometimes can lead to failure, mainly when the adherence to criteria for a return to play are endangered by the need for a time-sensitive return. Marketing/commercial criteria for a return to play should not influence treatment and are not discussed or encouraged herein. Instead, we present what we believe to be the critical thinking behind the guidelines to accomplish the ultimate goal of rehabilitation following an athletic injury, that is, the return to play at the pre-injury level. Rehabilitation includes the application of several different physical agents and therapeutic exercises, always embedded in a teamwork atmosphere. The guidelines to physical Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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therapy practice published by the American Physical Therapy Association (APTA) documents the great variety of interventions in the therapeutic exercise domain, in addition to other important therapeutic considerations. The APTA guidelines are essential in the design of a professional, customized, and effective plan of care that meets the athlete patient’s rehabilitation and prevention needs. The setting of appropriate goals for the rehabilitation process follows the diagnostic evaluation, in which the nature, location, and extent of the injury as well as the accurate status of the daily-living domains of the injured athlete are determined. The rehabilitation team should address not only the psychomotor domain but also, if needed, the affective and, albeit rarely, cognitive domains, all of which provide informative material to establish rehabilitation goals. In order to reach these goals, the physiological effects of the physical agents and therapeutic exercise must be matched with the identified symptoms, signs, and functional status. Nevertheless, an adequate symptomatic and functional outcome can only be achieved by an understanding of the pathology, healing process, anatomy, physiology, kinesiology, biomechanics, and other core subjects. Establishing a plan of care is therefore demanding and also involves ethical and moral issues since our choices and decisions can interfere with the athlete’s health and general well-being. In addition, rehabilitation progress made by the athlete must be continuously reassessed. This is essential for adapting the recovery program such that it allows improvement towards adequate healing and subsequent high levels of performance. The tissues of the human body have a great aptitude to respond and adjust to the stresses placed upon them. Thus, after taking into consideration any precautions or contraindications as well as the stage of inflammation, healing, and conditioning, we should adapt and re-adapt the therapeutic exercise program to accomplish the main goals set for the athlete with respect to healing and functional parameters, without avoidable delays – an approach that is very different from the potential deleterious time-based rehabilitation programs. The basic training principles, such as specificity, overload, individuality, reality, balance, progression, recovery, variety, and regularity, are fundamental to maximize rehabilitation gains, safety, and effectiveness. Respect for these principles will result in specific anatomical and physiological adaptations that enable tissues to withstand the stresses imposed during rehabilitation. Compliance with these principles reduces the risk of re-injury and allows the athlete to reach his or her full potential. In addition, training principles should be integrated as soon as possible in the progression of rehabilitation and in a way that mimics the sport-specific demands of the injured athlete. This is also of major significance in prevention programs. The overall goal is to achieve, within a monitored environment, a structural and functional “readiness” that meets the objectives of both performance and prevention. Although expressions like “it remains a substantial challenge”, “the treatment is controversial”, and others of same semantic nature only serve to point out our incomplete knowledge, we should nonetheless be aware of the well known guidelines, make an effort to remain up to date regarding helpful new sources, and rely on the principles of basic science and biomechanics, which can provide us with a safe and effective basis for determining the ideal rehabilitation program. Primum non nocere! Rehabilitation should begin immediately after the injury and develop through the acute and subacute phases of injury. Even if there are indications for surgery, the plan of care should be initiated beforehand and carried on until the athlete returns to play.

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In the following, the reader will find a brief discussion of some of the most prevalent lower-extremity injuries associated with locomotion, stability, and sport-specific drills. The aim is not to present a detailed set of protocols but instead to highlight a few of the rehabilitation and prevention issues that we consider to be of major importance in optimizing the planning of care and prevention. We also aim to equip the reader with an awareness of what we believe to be the essential “codex” needed to implement suitable rehabilitation and prevention programs. The three overlapping stages of inflammation are a normal and necessary response to the vascular changes suffered in the injury process. The inflammatory response triggers a set of events required for the healing or repair of injured tissue. The acute stage can take 3-4 days; the subacute stage continues for 2 weeks, and the chronic stage (which does not occur in every case) may be present for months or longer. An understanding of this time frame along with the tissue-healing processes themselves is critical to appreciate that progression in the rehabilitation program to, for instance, resistive exercise cannot be forced with respect to either volume or intensity. Performing resistive exercise in the presence of active inflammation will lead to trauma and exacerbate pain and swelling, which may delay significantly the athlete’s return to play and potentially compromise his or her return to overall health. Whether the normal healing process can be overcome and accelerated is not clear; nonetheless, a customized rehabilitation program can be designed in order to maximize gains. This requires the treating physician’s or physiotherapist’s awareness of the inflammatory process, the normal phases of healing, and their time frames. This knowledge, along with a complete understanding of the sport-specific demands placed on the athlete, will allow selection of the appropriate physical agents to control the inflammatory process and maximize the goals of therapeutic exercise. It will also guide progression, in due/safe time, of the mechanical loads tolerated by the injured (and grafted) tissues. Compromises made, on an individual basis, between time frames and desirable but safe progression, will reveal the correct timing in which the different stages of rehabilitation should be enacted, thus avoiding delays in the return to play, decreasing the risk of re-injury, and allowing the athlete to maximize his or her potential. These and the abovediscussed considerations are the key to reaching the goals of rehabilitation: the absence of pain and swelling, restoration of range of movement (ROM), flexibility, strength, proprioception and neuromuscular control, and the return to sports at the pre-injury level, with only the smallest risk of re-injury. Instead of “copying and pasting” protocols into the subsequent pages, we have chosen to “think out loud” about the parameters we feel are crucial to rehabilitation, and rehabilitation only, thus avoiding overlap with information presented in other chapters of this volume.

34.2 Hamstring Ruptures Treatment of hamstring ruptures should begin at the sideline of the athletic field according to the PRICE (protection, rest, ice, compression, and elevation) principle and continue for 3 or 4 days. The primary goal of the PRICE approach is to avoid the formation of


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a large hematoma, which may affect the dimension and time frame of scar tissue formation. Anti-inflammatory medication can be prescribed, once it does not adversely affect healing in the initial phase (no more than 10 days). Light stretching and strengthening, physical agents to improve healing, and therapeutic exercise goals must start after 5 days. Special attention should be paid to exacerbating and remitting factors, as they determine the pace of progression. Clinical experience combined with knowledge of the time frame for muscle healing in important strains reminds us of the need to be especially gentle in the first 2 weeks with respect to muscle mechanical load, in order to not disrupt the healing of soft tissue. Along with strengthening (isometric, isotonic, isokinetic, and variable-resistance) and neuromuscular exercises, the athlete should start running on a level surface, gradually increasing the intensity and incorporating sports-specific exercises (cutting, jumping). Eccentric exercise is important to recovery and to the prevention of injury/re-injury; it should begin when the muscle reacts without pain to a maximal isometric contraction in a fully stretched out position. MRI scan or ultrasonography can be helpful in confirming structural integrity, in addition to serving as a criterion for the return to sports activity. Antagonist strength ratios and knee flexor strength differences between limbs have to be assessed before return, as strength imbalances may predispose athletes to injury and because restoration of the strength profile can decrease the incidence of injury [1, 2]. Stem cells are believed to be of great potential for the treatment of debilitating tendon, ligament, and muscle injuries [3]. Growth factors also are being used with promising results.

34.3 Return-to-Play Criteria • • • •

Let the tissue heal fully before encouraging a return to play. Muscle strength within 90% of the opposite side or of the pre-injury value. Standard antagonist strength ratios. Capability to perform all sport-specific demands without pain or altered kinematics.

34.4 Patellar Tendinopathy The treatment of painful tendon disorders is a difficult task and varies according to functional, structural, and symptomatic conditions. We begin our discussion here with a critical and up-to-date review of a chronic and non-inflammatory condition known as “jumper’s knee”. The origin of the pain appears to be related to a combination of mechanical and biochemical causes [4]. Both conservative and surgical management options have yielded incomplete and often unpredictable success. The efficacy of several different therapeutic modalities has not been proven but that does not necessarily mean they are ineffective. Iontophoresis, electrotherapy, ultrasound, and other techniques may be employed if they


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result in pain relief. However, the effect of low-intensity pulsed ultrasound (LIPUS) in treating tendinopathies remains to be confirmed in powered human studies [5]. Therapeutic exercise has a positive effect on tendon fibers, whose strength is related to their number, size, and orientation. Isometric, concentric, and flexibility exercises have a role in the plan of care, but it is mostly through eccentric training, which has become a popular conservative treatment model for patellar tendinopathy, that it is possible to achieve a satisfactory symptomatic and functional outcome. For flexibility exercises, particular attention should be paid to the neurophysiologic properties of contractile tissue in order to ensure that the injured athlete takes full advantage of stretching techniques. Extracorporeal shockwave therapy (ESWT) seems to be a safe and effective treatment of patellar tendinopathy and of chronic insertional Achilles tendinopathy [6, 7]. Further research is warranted, however, to better define the working mechanism, a specific treatment protocol, and the effectiveness of ESWT for patellar tendinopathy (Fig. 34.1). Eccentric loading can improve the effectiveness of treatment of patellar tendinopathy and stimulate healing. According to Jonsson and Alfredson [8], eccentric, but not concentric, quadriceps training on an inclined board reduces pain associated with patellar tendinopathy. The eccentric exercise protocol used in that study was: • Treatment period (weeks): 12 (first six without sports activity). • Exercise prescription: 3 sets of 15 repetitions twice a day after warm-up.

Fig. 34.1 Extracorporeal shockwave therapy (ESWT) for the treatment of tendinopathy. (Reprinted courtesy of Saúde Atlântica Clinic and J. Milheiro, shown in the photo)

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• Intervention: eccentric train on a 25º inclined board (exercising into tendon pain). • Progressing load: weight (backpack). • Assessment and reassessment: pain (VAS) and VISA score. Future research should aim at shedding further light on the complex processes underlying the mechanism of eccentric loading and also on new management strategies, such as growth factor treatment, stem cell therapy, and gene transfer.

34.5 Anterior Cruciate Ligament Reconstruction The message we want to stress here relates to rehabilitation goals, criteria to return to play after ACL reconstruction, and strategies to prevent ACL injuries. A detailed protocol is beyond the scope and extent of this chapter but complete protocols can be achieved by a key-word and a single “enter” on your laptop. The goals of ACL reconstruction and subsequent rehabilitation are: • Absence of pain, swelling, and instability. • Restoration of ROM and muscle strength. • Restoration of proprioception and neuromuscular control. • Restoration of normal knee kinematics and kinetics (movements and moments). • Return to play at the pre-injury level. Clearance to return to play should be a multidisciplinary decision, which must be criteria-based and not time-based. Also, progression through the rehabilitation program should be made in accordance with careful monitoring of the athlete’s functional and symptomatic status. Objective criteria for a return to play after ACL surgery are needed in order to decrease the risk of re-injury and, later, osteoarthritis, monitor the rehabilitation process (creating comparative databases and evidence for financial support by healthcare authorities), and determine clearance to return to play. In a study with high-level football players [9], ACL-injured players had a four-fold higher risk of knee re-injury than the non-ACL-injured group and 50% of the injured players who had undergone ACL surgery the season before incurred a new knee injury shortly after comeback. This may have been due to a lack of sports readiness (altered knee kinematics and proprioception) and premature sports re-integration (overloading of still not healed or remodeled tissues). Specific criteria are needed to monitor the rehabilitation process, including muscle strength assessment, hop tests, landing strategies, and knee kinematics. A muscle strength evaluation can be based on isokinetic testing, with special attention to unilateral ratios and bilateral imbalances. A test battery of hop tests well discriminates between the injured and uninjured side in ACL-deficient and reconstructed athletes [10]. Altered landing strategies after ACL reconstruction can be a risk factor in re-injury. Therefore, it is important to determine whether athletes demonstrate lower limb asymmetries in landing and takeoff force following ACL reconstruction [11]. A goal of ACL reconstruction is the restoration of normal mechanics. This can be evaluated by the Lachman test, the KT-1000 arthrometer (Med-Metric, San Diego, CA), and


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Fig. 34.2 Anteroposterior translation of the tibia evaluated using the Porto KTD arthrometer (J. Espregueira-Mendes)

the new KTD arthrometer (J. Espregueira Mendes); the latter can be used concomitantly with MRI and CT scan. Its unique feature is its ability to evaluate both sagittal and rotational laxity with MRI and CT scan (Fig. 34.2). Scores such as the IKDC, Lysholm, Noyes, and Tegner are reliable to evaluate the outcome of ACL reconstruction. However, data collection is not enough to determine when and which patient with ACL reconstruction can safely and successfully return to play. Consequently, reliable criteria are needed such as: • Muscle strength and performance: isokinetic testing and one-leg hop test showing sideto-side deficit < 10-15% • Functional and static knee stability • Social and psychological factors • Considerations related to associated injuries • No pain or effusion. In 2008, several large-scale studies reported that serious knee injuries can be decreased by neuromuscular and proprioceptive training programs. A randomized controlled study of non-contact ACL injury prevention in female collegiate soccer players showed a decrease of 41% in the overall rate of ACL injury [12]. The PEP program (prevent injury and enhance performance) consists of stretching, strengthening, plyometrics, and agility exercises to address potential deficits in strength and neuromuscular coordination of the muscles acting around the knee (Fig. 34.3). However, such measures are not sufficient. There is a need to refine the programs currently in use in order to address critical factors related to the mechanism of injury and the true groups at risk. Nevertheless, the PEP program can be carried out during normal practice time and without the need for special equipment. Prevention is the most rewarding work for the orthopedic team and for the athletes. Therefore, it is of utmost importance to and produce evidence in order to prevent injuries.

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Fig. 34.3 Part of a PEP (prevent injury and enhance performance) program. (Reprinted courtesy of the University Fernando Pessoa and A.S. Maia, shown in photo)

34.6 Acute Ankle Sprains Ligament injuries of the ankle are among the most common lower-extremity injuries in sports (numbers point to a quarter of all sports injuries). Sports such as basketball, soccer, and volleyball have a particularly high incidence of ankle injuries. According to estimates, the cost to society may reach 40 million euro per one million people. The typically ankle sprain (inversion injury) occurs when a plantar-flexed ankle is inverted. An isolated anterior talofibular ligament tear is present in most cases. The medial ankle sprain (eversion injury) is caused by eversion of the ankle with internal rotation of the tibia. This can tear the deltoid ligament but isolated rupture of this ligament is rare and is often associated with fractures of the peroneal malleolus and rupture of the syndesmosis (high ankle sprains). Up to 10% of all ankle sprains can tear the syndesmosis. It is critical to rule out this kind of injury because, if present, it will require a totally different clinical approach. Urgent evaluation is recommended for patients with a high level of pain, rapid onset of swelling, coldness or numbness in the injured foot, and inability to bear weight. A differential diagnosis should be achieved by history, comprehensive physical examination, Ottawa’s rules/radiographs to rule out fracture, evaluation of the degree of instability, imaging (CT, MRI), and other examination devices or techniques. Ankle soft-tissue injuries are divided into grades I, II, and III. The diagnosis guidelines presented above, when followed by an experienced examiner, allow accurate grading of the injury. The rehabilitation goals are basically the same as presented in the discussion of ACL reconstruction and subsequent rehabilitation. Nevertheless, it is important to stress the role


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of recurrent ankle sprain prevention and functional ankle instability (FAI) avoidance through strengthening, proprioception, neuromuscular control, and external ankle supports. The initial treatment (48-72 h) of most ankle injuries, independent of their grade, consists of the PRICE principle and NSAIDs (taking into account studies on the efficacy of different drugs in ligament healing) in order to reduce swelling, pain, and further damage. This first phase may speed healing and reduce limitations in the ROM. In the absence of syndesmosis tear and fracture, rehabilitation proceeds to the second phase, as soon as pain control has been achieved, with graded exercise regimens. This sequence involves a functional treatment instead of an immobilization approach. Nevertheless, the authors of a recent study [13] concluded that the use of a 10-day below-the-knee cast or an air cast brace is the best initial treatment for the management of severe ankle sprains. While this study may call into question the current standard of aggressive functional treatment, it did not include a comparison with functional treatment and its outcome. The second phase comprises exercises to restore motion, strength, and proprioception. Assuming that the injured ligaments have been correctly identified, safe ROM, gently stressing the ligament and thus stimulating new collagen formation along the lines of maximal stress, should be explored. This seems to be essential to attain a strong healed ligament. Early motion exercises combined with suitable physical agents are required to diminish swelling and prevent ankle stiffness but exercises that induce pain should be discontinued. The exercises should be done with selective inhibition of motion (motion that mimics the mechanism of lesion). Cardiovascular conditioning should not be neglected, and non-impact exercises, such as swimming and single-leg stationary biking, are recommended. Proprioceptive training can be done by single-leg stance (eyes open/closed). As the athlete’s rehabilitation progresses, the proprioceptive exercises can be made more challenging by changing the surfaces and other ambient factors (Fig. 34.4).

Fig. 34.4 Graded proprioceptive and neuromuscular training. (Reprinted courtesy of University Fernando Pessoa and A.S. Maia, shown in photo)

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Fig. 34.5 Isokinetic training of the ankle. (Reprinted courtesy of University Fernando Pessoa and A.S. Maia, shown in photo)

Ankle-disk training is also a highly effective proprioceptive and neuromuscular training exercise. Once the second phase is well underway and the athlete is pain-free, he or she can progress to phase 3. The time frame for this transition varies according to the severity of the injury (phase 2 can take up to 1-4 weeks or even longer). The third phase aims to restore sport-specific and locomotion skills, such as running, jumping, and cutting. In this phase, strengthening (isotonic, isokinetic) proprioceptive, and neuromuscular training should be continued. Isokinetic training of the available motions on the ankle is of great advantage due to the velocity and intensity with which it can be done. This complementary exercise brings about great gains in neuromuscular control, strength, power, and endurance (Fig. 34.5). We recommend, even during the return to play, that exercise regimens of proprioceptive and neuromuscular training be continued for at least for 10 weeks. Ankle taping or an orthotic device should be used for the first 6 months after injury. A recent study on intrinsic factors showed that a history of previous acute ankle injury was the only significant risk factor in re-injury [14]. Exercise regimens of proprioceptive and neuromuscular enhancement combined with the use of external ankle supports were reported to be very effective in preventing acute ankle injuries [15]. It is our duty to embrace current evidence and apply it on the athletic field in order to see our athletes running faster, jumping higher, and always wining.

References 1. Crosier JL, Ganteaume S, Binet J et al (2008) Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am J Sports Med 36:14691475 2. Brown LE (2000) Isokinetics in human performance. Human Kinetics, Champagne, IL 3. Johns Hopkins University (2009) Students Embed Stem Cells In Sutures To Enhance Healing. ScienceDaily. Retrieved November 30, 2009, from http://www.sciencedaily.com /releases/ 2009/07/090720191145.htm


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4. Khan KM, Cook JL, Mafulli N et al (2000) where is the pain coming from in tendinopathy? It may be biochemical, not only structural, in origin. Br J Sports Med 34:81-83 5. Khanna A, Nelmes RTC, Gougoulias N et al (2009) The effects of LIPUS on soft-tissue healing: a review of literature. Brit Med Bull 89:169-182 6. Leeuwen MTV, Zwerver J, Akker-Scheek IVD (2008) Extracorporeal shockwave therapy for patellar tendinopathy: a review of the literature. Br J Sports Med 43:163-168 7. Rompe JD, Furia J, Mafulli N (2008) Eccentric loading compared with shock wave treatment for chronic insertional Achilles tendinopathy. J Bone Joint Surg Am 90:52-61 8. Jonsson P, Alfredson H (2005) Superior results with eccentric compared to concentric quadriceps training in patients with jumper’s knee: a prospective randomised study. Br J Sports Med 39:847-850 9. Waldén M, Hagglund M, Ekstrand J (2006) High risk of new knee injury in elite footballers with previous anterior cruciate ligament injury. Br J Sports Med 40:158-162 10. Gustavsson A, Neeter C, Thomeé P et al (2006) A test battery for evaluating hop performance in patients with an ACL injury and patients who have undergone ACL reconstruction. Knee Surg Sports Traumatol Arthrosc 14:778-788 11. Paterno MV, Ford KR, Myer GD et al (2007) Limb asymmetries in landing and jumping 2 years following anterior cruciate ligament reconstruction. Clin J Sport Med 17:258-262 12. Gilchrist J, Mandelbaum BR, Melancon H et al (2008) A randomised controlled trial to prevent noncontact anterior cruciate ligament injury in female collegiate soccer players. Am J sports Med 36:1476-1483 13. Lamb SE, Marsh JL, Hutton JL et al (2009) Mechanical supports for acute severe ankle sprain: a pragmatic, multicentre, randomised controlled trial. Lancet 373:575-581 14. Engebretsen AH, Mykelebust G, Holme I et al (2010) Intrinsic risk factors for acute ankle injuries among male soccer players: a prospective cohort study. Scand J Med Sci Sports Epub 2010 Mar 11 PMID:20338006 15. Handoll HH, Rowe BH, Quinn KM et al (2001) Interventions for preventing ankle ligament injuries. Cochrane database Syst Rev (3):CD000018

Section VI Spine

Spinal Disorders in Sports Medicine

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A. Maiello, J.D. Smucker

Abstract Recent advances in research, patient assessment, and rehabilitation have changed the management of spine trauma and in general the outcome of patients with back pain. Little has been written about spinal disorders in athletes. Nevertheless, this pathology has significant effects on the athlete population. Moreover, athletes place higher demands on their spine and cannot tolerate limitations of their activities. Strong forces are exerted on the cervical and lumbar spine during various athletic maneuvers and may cause catastrophic injuries. Chronic back pain also has a significant impact on athletes and may compromise their performance. Considering these factors, prompt diagnosis and assessment of patients with spine trauma or chronic back pain are mandatory, as are rehabilitation and return to activities. This chapter discusses the main issues related to cervical and lumbar spine injuries, the return to play, after these kinds of traumas, and the management of chronic back pain in the athlete population.

35.1 Introduction The prevalence of back pain is 50-80% in the general population, although up to 95% of Americans over the course of their lifetime will be affected [1]. Back pain is not limited to sedentary individuals; it has significant effects on athletes as well. Depending on the sport, incidence rates of back pain in athletes range from 1.1% to 30% [2]. Such differences with the general population may be due to greater conditioning, greater flexibility, and higher pain thresholds. While these factors may be considered protective, athletes place high demands on the lumbar spine and typically cannot tolerate limitations on their activities [3]. The incidence rate in athletes varies according to the sport. For example, back pain has been reported in 11% of gymnasts and 50% of football linemen. Moreover, there may be sport-specific injuries: herniated lumbar disk is more common in football players and weight Orthopedic Sports Medicine. Fabrizio Margheritini, Roberto Rossi (Eds.) © Springer-Verlag Italia 2011

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lifters, degenerative disks and spondylolysis are most common in gymnast and volleyball players [4]. As in the general population, the exact source of pain in athletes may be difficult to determine. Possible causes include intervertebral disc disease, facet joints injury, paraspinal musculature strain/sprain, and ligament injury. Other causes, such as deformities (i.e., Scheuermann’s kyphosis or instability in spondylolisthesis), may interfere with correct diagnosis and treatment. A number of biomechanical, psychosocial, and demographic risk factors for sustaining an acute low back injury have been identified in the general population, but it is difficult to find similar risks in athletes. A history of prior spine injury was found to be the most significant predictor of further injury in the lumbar spine [5]. Repetitive loading [6], age, and level of competition also play important roles. Other authors advocate the importance of flexibility of the lumbar spine as a predictive factor for low back pain, but there is no agreement in the literature [7]. An appropriate differential diagnosis at presentation must be considered to avoid misdiagnosing less frequent sources of pain symptoms. These include: (1) spinal conditions (i.e., sacral stress fracture, sacralization of L5, transverse process impingement, facet stress fracture, discitis, osteomyelitis, neoplasm) and (2) non-spinal conditions (intrapelvic/gynecologic conditions, renal disease, sacroiliac joint dysfunction) [8].

35.2 Cervical Spine Injuries in Sports Injuries to the cervical spine represent uncommon but devastating conditions to those participating in athletic events. These injuries occur primarily in athletes involved in contact sports, such as football, wrestling, and ice hockey, with football injuries constituting the largest number of cases. An axial load or a significant compressive force applied to the top of the head is the major mechanism of serious cervical injuries. These mechanisms are more dangerous when the neck is flexed and without the normal lordotic alignment, because the forces are not correctly distributed over the thorax [9].

35.2.1 Syndromes of Spinal Cord Injuries Complete spinal cord injury. Anatomic disruption of the spinal cord results in transverse myelopathy, with total loss of spinal function below the level of the lesion. More commonly, the syndrome is caused by a hemorrhagic or ischemic lesion at the site of injury. Complete injury patterns are rarely reversible. Central cord syndrome. Hemorrhagic and ischemic injury to the corticospinal tracts are accompanied by an incomplete loss of motor function, with a disproportionate weakness of the upper vs. the lower extremities. This syndrome is more frequent in older adults (with

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baseline spondylotic narrowing of the cervical canal) or in those with hyperextension injuries (with infolding of the ligamentum flavum and transient compression of the spinal cord, its blood supply, or both). Anterior cord syndrome. Here, a complete motor deficit is accompanied by a loss of pain and temperature sensation below the level of the lesion, but with intact sense of deep pressure, vibration, and proprioception. The symptoms are due to ischemia in the distribution of the anterior spinal artery. Posterior cord syndrome. These patients suffer a loss of deep pressure, vibration, and proprioception following a loss of dorsal column function but with corticospinal and spinothalamic tract functions intact. Brown-Sequard syndrome. Hemisection of the spinal cord results in a loss of ipsilateral motor function and contralateral spinothalamic (pain and temperature) modalities. Burning hands syndrome. Burning dysesthesias and paresthesias in both hands may be experienced by athletes who participate in contact sports, for example, football and wrestling, in which there is repeated cervical trauma.

35.2.2 Nerve Root Injuries Acute cervical disk herniation or minor trauma in pre-existing cervical arthritis with osteophytic foraminal encroachment may cause discrete nerve root injury in athletes. For example, tennis players may develop radicular symptoms during the cervical spine hyperextension portion of their service motion. Radiculopathy may be diagnosed with a combination of specific history and physical examination findings as well as advanced neuro-imaging studies such as magnetic resonance imaging (MRI). Nerve avulsion is much rarer but can develop in contact and high-velocity sports. Diagnosis is confirmed by electromyography (EMG) and CT-myelogram (contrast around the avulsed nerve root). Treatment may require nerve-grafting or muscle-transfer procedures [10].

35.2.3 Nerve Root-brachial Plexus Neuroapraxia Neuroapraxia of the nerve roots or brachial plexus is the most frequent cervical spine injury in football. These injuries are typically referred to as “stingers” or “burners” and affect offensive and defensive linemen as well as linebackers. Traction or compression injuries to the spinal nerve root or brachial plexus may cause transient stinging and burning: shoulder depression, lateral head flexion toward the unaffected side, and simultaneous head rotation toward the affected side may compress exiting nerve roots in a narrowed neural foramen. Clinically, the athlete presents with burning dysesthesia and upper-ex-

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tremity weakness on one side only, holding the affected arm with the other hand after a tackle. Pain and weakness of the biceps and shoulder girdle muscles are present [11].Treatment is typically conservative; after the first episode, the athlete returns to play when free of symptoms and when the neurological examination is normal. If neurological symptoms persist for 3 weeks after injury or multiple episodes occur, the athlete must be fully evaluated for associated radiographic instability, cervical disk herniation, or occult fracture. In all circumstances, before returning to play, the athlete must be free of symptoms in the cervical spine, demonstrate a full painless cervical spine ROM and full motor strength, and have a normal neurological examination, along with no radiographic signs of instability [12].

35.2.4 Soft-tissue Injuries In athletes, soft-tissue injuries to the cervical spine are the most common sport-related accidents [13]. Sprains and strains. Strains are defined as injuries to the muscle-tendon unit, and sprains as ligamentous or capsular injuries. Treatment is conservative, with rest, collar immobilization, medications (NSAIDs and anti-spasm agents), massage, and physical therapy. Major ligamentous injuries. These are characterized by destruction of the posterior ligamentous complex, with segmental instability. On plain radiographs, segmental widening of the spinous process gap with variable translation and angulation of the involved interspace may be noted. Flexion-extension radiographs and MRI are useful to document dynamic instability and to assess the extent of damage. MRI may produce false-positive results in acute studies, but is helpful in assessing ligamentum flavum injury and posterior ligament and capsular disruption. Treatment is conservative in the vast majority of cases; however, in case of persistent symptoms or instability after long standing conservative management, a fusion procedure may be indicated to restore segmental stability (Fig. 35.1).

35.2.5 Cervical Disk Injuries Cervical disk injuries and herniations (Figs. 35.2, 35.3) usually affect older athletes and are less common than lumbar disc injuries. Traditionally, cervical disk injuries have been classified as soft herniations (acute process with compression and irritation of nerve roots, in which the nucleus pulposus herniates through the posterior annulus) and hard-disc disease (chronic process with degenerative changes consisting of loss of disk height and formation of marginal osteophytes). Athletes with symptomatic disk degenerative changes and acute disc herniations typically complain of neck or arm pain. Treatment modalities include rest, activity modification, NSAIDs, immobilization, cervical traction, and/or therapeutic injections. If a myelopathy or progressive neurological deficit is present, surgery


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Fig. 35.1 C5-C6 ligament tear (in isolation). a Neutral lateral, b lateral flexion, and (c) lateral extension views; d T2-weighted MRI, e MRI STIR

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Fig. 35.2 C6-C7 herniated nucleus pulposus with C7 radiculopathy and triceps weakness (a) T2weighted MRI, (b) axial T2-weighted MRI

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Fig. 35.3 Multi-level cervical degenerative disk disease with spondylosis

is indicated during the first 6-8 weeks of symptoms [13]. There is a lack of literature about a return to play after a posterior disk procedure, but it is reasonable that athletes may do so when they are asymptomatic and have regained full strength and mobility.

35.2.6 Cervical Spine Trauma Atlanto-occipital dislocation. The mechanism of this injury is hyperextension, rotation, and distraction. While typically seen in motor vehicle accidents, this injury is rare in sport. There are many radiographic signs of atlanto-occipital dislocation but the most sensitive are: (1) prevertebral soft-tissue swelling, (2) basion to dens interval < 5 mm, (3) a clivus that does not point to the tip of the dens, (4) a mastoid that does not overlie the dens, and (5) a power ratio (distance between the basion and C1 posterior arch divided by the distance between the opisthion and the anterior arch) > 1. All occipital-cervical dislocations should be treated initially with a halo vest, but because the majority of these lesions are unstable, posterior occipital fusion is the surgical treatment of choice. Return to play is not typical. C1-atlas fracture (Jefferson’s fracture). This injury results generally from axial loading, i.e., falling on the top of the head. If axial loading is associated with flexion torque, the injury may be isolated to the anterior arch. If it is associated with extension torque, then the injury may be isolated to the posterior arch. If the transverse atlas ligament is intact, the fracture is considered stable. The treatment of stable injuries is conservative, with a hard collar to allow bony healing. Unstable injuries are immobilized in a halo vest for 8 weeks, followed by a cervical collar for 4 more weeks. If the fracture is painful or there are radiographic signs of instability, a C1-C2 fusion may be considered.


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Atlanto-axial subluxation and dislocation. In the adult population, the lesion occurs most frequently following motor vehicle accidents. The clinical presentation is typical: the patient has a “cock robin” appearance, with the head tilted toward and rotated away from the side of dislocation. The “wink sign” is typical on plain radiographs (overriding of the C1-C2 joint on one side with a normally aligned joint on the contralateral side). The reduction of a dislocation in adults is achieved by skull tong traction, but if the reduction is difficult then a halo vest may be necessary. If closed reduction fails, open reduction and a posterior C1-C2 fusion is an option. Odontoid fracture (Fig. 35.4). Both extension and flexion mechanisms may cause the fracture, which is usually seen on open-mouth and lateral radiographs of the cervical spine. The Anderson and D’Alontzo classification [14] describes three patterns of fracture: type I (avulsion injuries of the tip of the dens), type II (fractures that occur through the base of the dens at the junction of the dens and central body of the axis), and type III (fractures that extend into the body of the axis). Type I fractures can be treated non-operatively with a rigid cervical collar for 3 months. Flexion-extension radiographs should then be obtained to evaluate stability. Type II fracture is the most common and the most troublesome, with a reported rate of non-union of around 32%. Risk factors for non-union are: age > 40, ini-

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Fig. 35.4 Odontoid fracture. a Neutral lateral view, b MRI, c CT scan

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tial displacement amount > 5 mm, initial displacement direction (posterior worse than anterior), angulation > 10°, delayed diagnosis and redislocation in a halo vest. However, a significant number of type II fractures heal with halo vest immobilization, if anatomic reduction is achieved and maintained and overdistraction in the halo vest avoided. Primary posterior C1-C2 fusion and anterior screw fixation are surgical alternatives for the treatment of patients in the high-risk group. Type III fractures can be treated with 12 weeks of immobilization in a halo vest, with the majority healing by bony union. Traumatic spondylolisthesis of the axis. The mechanism of this injury, which is also called “hangman fracture”, is forceful extension of an already extended neck. If a flexion component is added to the injury, disruption of the disk and ligaments may occur, causing a forward subluxation of C2 on C3. Levine and Edwards [15] classified these fractures as: type 1 (minimally displaced, amenable to conservative treatment with a Philadelphia collar for 8-12 weeks); type 2A (significant angulation and translation are present; initial traction in extension followed by immobilization in halo vest are indicated); type 2B (type 2 with widening of the posterior part of the C2-C3 disk with traction; immediate halo vest without traction is indicated); type 3 (angulation and dislocation with unilateral or bilateral facet dislocation at C2-C3; open reduction and fixation is indicated) [15].

35.2.7 Injuries to the Lower Cervical Spine These injuries, especially if associated with neurological deficits, have devastating consequences on the athlete population [16]. Avulsion injuries. Disruption of C7 spinous processes (“clay shoveler’s” fracture) has been reported in power lifters and football players. Symptomatic cases are treated conservatively (cervical orthosis). Extension teardrop fracture (avulsion of the antero-inferior corner of the vertebral body by the anterior longitudinal ligament) commonly occurs at C2 and in the lower cervical spine. Symptomatic treatment in a cervical collar is the correct choice. Compression fractures. Anterior wedge compression occurs at C4-C5 and C5-C6 and is caused by compression-flexion forces. In the presence of associated posterior longitudinal ligament involvement, there is a risk of post-traumatic kyphosis. Common treatment is rigid cervical orthosis for 8-12 weeks (if the posterior longitudinal ligament is intact). Facet joint injuries. These injuries are very common at C5-C6 and C6-C7 and may be due to a distraction-flexion mechanism. There are variable degrees of injuries, from facet joint subluxation to perched facet and from unilateral facet dislocation to facet subluxation/dislocation associated with facet fracture. There may be associated neurological complications. If the patient is awake and alert, it may be reasonable in some circumstances to attempt a closed reduction with skeletal traction before performing MRI. Debate continues regarding this treatment algorithm, with some arguing that only patients with a complete


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neurological deficit should be immediately reduced without a prior MRI, as this may be the most likely method of restoring a compromised spinal cord. If the patient is not alert before entering the operating room for reduction and stabilization, an MRI should be obtained. In the presence of a substantial disk herniation, the treatment of choice is anterior decompression and discectomy, anterior fusion, and plate stabilization. Highly unstable fracture/dislocation patterns may require anterior and posterior stabilization approaches. Vertebral body burst fractures. These lesions are due to compression-flexion forces or vertical compression forces and may be associated with canal involvement and neurological injuries. If neurological deficit is present, the treatment of choice is anterior corpectomy and strut graft reconstruction with plating to ensure immediate stability. Teardrop fractures [16]. These fractures most frequently occur at C5, C4 and C6 following axial loading with an associated flexion force vector. Typically seen in divers, football spearing injuries and motor vehicle collisions, teardrop fractures involve primary antero-inferior vertebral corner (the teardrop). Five stages have been described according to severity. Stage 1, 2, and 3 injuries have variable degrees of vertebral comminution without gross angular or translational malalignment. Stage 4 injuries have f 3 mm of retrolisthesis with probable injury to the posterior ligament complex. Stage 5 injuries have > 3 mm retrolisthesis and are associated with posterior ligament instability. Treatment varies depending on neurological status and the posterior ligament complex stability. Stages 1 and 2 are treated non-operatively, with 12 weeks in a cervical orthosis or halo vest. Treatment in stages 3, 4, and 5 is usually surgical (corpectomy and anterior instrumented arthrodesis or posterior instrumented arthrodesis).

35.2.8 Return To Play There are limited data regarding the return to play after cervical injuries in athletes. Instead, recommendations derive from biomechanical studies of cervical spine injuries in the general population. In general, absolute contraindications include: (1) radiographic evidence of segmental instability (defined as > 11° of kyphotic deformity compared with the cephalad or caudal vertebral spinal segment or 3.5 mm of translational motion), (2) radiographic evidence of C1 to C2 instability (anterior atlanto-dental interval > 3.5 mm in an adult and > 4 mm in a child), (3) radiographic evidence of a distraction/extension cervical spine injury, and (4) the presence of a healed subaxial spine fracture with sagittal plane kyphosis or coronal plane deformity [17].

35.2.8.1 Congenital Conditions Odontoid anomalies. Odontoid agenesis, odontoid hypoplasia, and os odontoideum are absolute contraindications to contact sports.

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Congenital atlanto-occipital fusion. The symptoms of partial or complete fusion of C1 to the base of the occiput are usually those of compression of posterior column. Sudden death has been reported. This anomaly is an absolute contraindication to contact sports. Klippel-Feil syndrome. Type I (congenital mass fusion of the cervical and upper thoracic vertebrae) is an absolute contraindication to contact sports. However, in type II (fusion of 1 or 2 interspaces at C3 and below), with full cervical ROM, no instability, and no herniated or degenerative disk disease, there is no contraindication to sports participation.

35.2.8.2 Developmental Conditions Neuropraxia of the spinal cord with transient quadriplegia. This condition, which is caused by forced hyperextension, hyperflexion, or axial load, is clinically characterized by bilateral burning paresthesias associated with varying degrees of bilateral extreme weakness or paralysis. There is associated developmental stenosis of the spine, congenital fusion, cervical instability, or cervical disk protrusion. In the presence of disk herniation, radiographic evidence of instability, or chronic degenerative changes, the athlete is restricted from contact sports. Stenosis of the cervical spine. A canal/vertebral body ratio v 0.8 is not a contraindication to contact sports in asymptomatic individuals. A canal/vertebral body ratio f 0.8 and an episode of cervical cord neuroapraxia is a relative contraindication. Documented episodes of cervical cord neuroapraxia associated with intervertebral disk disease and/or degenerative changes also indicate a relative contraindication. Documented episodes of cervical spine neuroapraxia and associated MRI evidence of cord compression or cord edema define a relative or absolute contraindication. Finally, a documented episode of cervical cord neuroapraxia associated with ligamentous instability and symptoms indicative of neurological findings lasting > 36 h and/or multiple episodes is an absolute contraindication.

35.2.8.3 Spear Tackler’s Spine The technique of spearing (in football players, divers, and hockey players) involves contact at the crown of the head with the neck flexed to about 30°. This causes straightening of the cervical spine and its conversion into a segmental column. In this type of injury, patients have complaints referred to the cervical spine or brachial plexus, ranging from quadriplegia, to incomplete hemiplegia, to residual long tract signs. Torg [18] identified a subset of football players with the following characteristics who are therefore at risk for this injury: (1) developmental narrowing of the cervical spine; (2) persistent straightening or reversal of the normal cervical lordosis on erect lateral radiographs obtained in the neutral position; (3) pre-existing post-traumatic radiographic changes of the cervical spine; (4) documented habit of spear tackling techniques. Athletes with these characteristics are not allowed to participate in collision activities that expose the cervical spine to axial energy inputs.


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35.2.8.4 Traumatic Conditions of the Upper Cervical Spine (C1-C2) Atlanto-axial instability. Athletes with atlanto-axial instability (at any degree) are at risk for a potentially dangerous injury. Contact sports are contraindicated. Atlanto-axial rotary fixation. Patients with atlanto-axial rotary fixation present with torticollis, often resistant to treatment. This complaint may be a manifestation of fixed rotatory subluxation of the atlanto-axial joint. The transverse ligament may or may not be disrupted. This is a potential source of neural damage or death, and is thus an absolute contraindication to contact sports. Fractures. In general, fractures involving C1-C2 are an absolute contraindication for contact sports. Healed non-displaced Jefferson fractures, healed type I and type II odontoid fractures, and healed lateral mass fractures of C2 are considered relative contraindications (if the athlete is pain free, has a full range of cervical motion, and no neurological findings). C1-C2 fusion. Arthrodesis of the upper cervical spine constitutes an absolute contraindication to contact sports, regardless of how successful the fusion appears on radiographs.

35.2.8.5 Traumatic Conditions of the Middle and Lower Cervical Spine Ligamentous injuries. The criteria for instability remain unclear because a certain level of instability with no adverse effects is present in every athlete. Nevertheless, absolute contraindications are: (1) disruption or functional deficit of anterior or posterior ligamentous structures, (2) radiographic evidence of segmental instability, (3) radiographic evidence of C1 to C2 instability, and (4) radiographic evidence of a distraction/extension cervical spine injury, as mentioned above. Fractures. Acute fracture is an absolute contraindication to play, no matter how stable it is. However, athletes may return to play in the following cases: (1) stable healed compression fractures of a vertebral body without a sagittal component on anterior/posterior radiographs and without involvement of either the ligamentous or posterior bony structures; (2) healed stable end-plate without a sagittal component on anterior/posterior radiographs or involvement of the posterior or bony ligamentous structures; (3) healed spinous process “clay shoveler” fractures (only if the athlete is pain free, with full ROM, and no neurological deficits). Intervertebral disk injuries. An athlete with a disk injury treated conservatively with full resolution of symptoms or with a single-level anterior fusion following diskectomy may return to play if there are no symptoms in the cervical spine and full cervical spine ROM with no sign of instability on radiographs. In addition, neurological findings have to be negative.

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35.3 Lumbar Spine Injuries in Sports The cumulative prevalence of low back pain is nearly 80% in the general population. In athletes, the prevalence varies between 1% and 30% among studies and represents (for sports clinicians) one of the most challenging situations to diagnose and treat. Moreover, it is not clear whether athletes are at higher risk of low back pain than the general population. According to Granhed and Morelli [19], the prevalence of back pain in wrestlers is significantly higher than in a control population, but Videman et al. [2] reported a lower prevalence of back pain in elite athletes than in non-athletes. However, low back pain is a common reason for lost playing time by competitive athletes, as demonstrated by McCarroll [20] and Hainline [21]. Moreover, there are certainly risk factors that predispose athletes to low back pain, including a history of prior low back injuries, poor conditioning, excessive or repetitive loading, improper techniques, abrupt increase in training, and inadequate equipment [3]. Low back pain also may be due to specific traumatic events or, more commonly, to repetitive trauma. Large forces are produced in the lumbar spine region during various athletic maneuvers. For example, in vivo, there are many forces acting on the intervertebral disks and posterior elements. In the former, the disk is always under load as a result of the combined effects of body weight and muscle activity. These loads, under certain conditions (as in sports), far exceed the tolerance of the disk and may cause degenerative or traumatic changes (degenerative disk disease or disk herniation). In the second case, repetitive hyperextension and repetitive axial loading overload the posterior elements and predispose the athlete to pars interarticularis fracture (spondylolysis) and consequent back pain. For these reasons, low back injuries affect in particular wrestlers, gymnasts, weight lifters, football players, and rowers. Low back injuries most frequently involve the soft tissues surrounding the spine but also the intervertebral disks and the pars interarticularis. Fractures in the lumbar region are rare.

35.3.1 Strains and Sprains Strains and sprains are the most common causes of low back pain [22]. The application of excessive forces on muscles (strains) or on ligaments (sprains) may cause tears of these structures. Moreover, fatigue from repetitive loading may reduce injury thresholds. Inflammation may be the direct consequence of these injuries and directly correlate with pain and muscle spasm. In the lumbar spine region, the symptoms produced by strains include: acute pain (more intense 24-48 h after injury) and spasm localized at a trigger point. However, recurrent strains (if a short asymptomatic period lies between episodes) and chronic strain (if the pain is continuous and correlated to muscle injury) may occur. Patients report pain radiating to the hips, which may be a sign of lumbodorsal fascia spasm extending to the tensor fasciae latae.


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In contrast to strains, sprains are less localized. In the lumbar region, it is not clear which ligament is primarily involved. According to Keene and Drummond [23], the lesion is commonly localized in the interspinous ligament. Both sprains and strains generally present with localized tenderness that worsens with particular motions. The neurological examination is normal. Negative imaging may help to exclude other diagnoses. The treatment is usually conservative. A suitable rest period from activity resolves the symptoms in the majority of cases. Other beneficial therapies include cryotherapy or heat (in particular to decrease pain). Electrical stimulation with high-voltage pulse galvanic stimulation and transcutaneous electric nerve stimulation may help to reduce the pain in the acute stage of injury, but the positive effects of these treatments have not been demonstrated yet. The use of NSAIDs may decrease pain and reduce the production of prostaglandins; by contrast, there is no evidence for the use of muscle relaxant drugs, which may cause oversedation. Rehabilitation must include strengthening of the core musculature, flexibility of the lower extremities, and ROM exercises of the lumbar spine to minimize exacerbating movements and to prevent recurrences. Following these injuries, an athlete may return to sport when free of symptoms and after correct rehabilitation.

35.3.2 Disk Herniation Disk herniations may occur when annular tears allow the nucleus pulposus to enter the surrounding epidural space. Although herniation is often thought to be the result of a mechanically induced rupture, in vitro studies [24] have demonstrated that degenerative changes to the annulus fibrosus are necessary to allow disk herniation. Moreover, in some cases the herniation-induced pressure on the nerve root is not the only cause of pain. This may explain the high rate of asymptomatic protrusions (70%), according to Boden et al. [25]. When symptoms are present, they may be due to molecules arising from the inflammatory cascade (prostaglandin E2, thromboxane, phospholipase A2, tumor necrosis factor alpha, etc.). The association between disk herniations and sporting activities is not clear. Some studies have verified a higher prevalence of disk displacement in athletes than in a non-athlete control group [26]. However, other studies did not find a higher incidence of lumbar disk herniation in athletes than in the general population [27]. Nevertheless, athletes exposed to considerable axial loading, flexion, and rotation, as occurs during weight lifting (and sports requiring heavy lifting in competition or training), collision sports, and bowling seem to have higher rates of lumbar disc herniations [27]. Clinically the patient presents with back pain associated with radicular symptoms. The pain generally worsens with flexion and Valsalva maneuvers and improves with supine position. Pain is exacerbated by paravertebral palpation at the affected disk level. The ROM of the lumbar spine is reduced due to paraspinal contracture and the pain; lumbar lordosis may be reduced and a scoliotic attitude may be present (in both the bending and the orthostatic position). Radicular symptoms include pain along the correspondent dermatome of the herniated disk. For L4-L5 herniations, weakness of ankle dorsiflexion, great toe


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dorsiflexion, and sensory changes at the lateral aspect of the lower leg and middorsum of the foot (L5 distribution). For L5-S1 herniations, patients may complain of weakness in ankle eversion and plantar flexion strength as well as sensory changes at the lateral aspect of the foot (S1 distribution). The straight leg test is generally positive. Another clinical entity that must be ruled out is cauda equina syndrome. Typically, cauda equina presents in an acute fashion, with saddle paresthesias, bowel and bladder dysfunction, and occasionally radiculopathy at the lower lumbar level – but it may present with a prevalence of back pain over the other symptoms. Imaging studies are necessary in patients with disk herniation. Plain radiographs may demonstrate the loss of disk height or segmental instability. However, MRI (Fig. 35.5) is frequently necessary to locate the herniated disk and the involved neural element. Disk herniations have a very favorable natural history (with the exception of cauda equina syndrome) and most symptoms resolve as the disks reabsorb and root irritation decreases. Treatment is conservative in the majority of the cases, consisting of rest, oral anti-inflammatory medications (to reduce irritation of nerve roots), or a corticosteroid dose pack to reduce swelling and inflammation. If the symptoms improve, physical therapy with strengthening of the lumbar trunk muscles is mandatory. If the radicular symptoms do not improve, selective nerve block injection may be considered. However, there is no significant literature dictating a standard protocol for non-surgical treatment in athletes. Athletes may return to sporting activity when they reach a full painless ROM, the ability to maintain a neutral spine position during sports-specific exercises, and normal muscle strength, endurance and control. Surgical treatment may be considered if non-surgical treatments fail, symptoms are not tolerated, in the presence of cauda equina syndrome or in the case of progressive neurological deficit. Standard microsurgical diskectomy and percutaneous microendoscopic diskectomy are the techniques of choice in the athlete population. Tissue disruption (i.e.,

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Fig. 35.5 L3-4 herniated nucleus pulposus with left L4 radiculopathy and footdrop


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bilateral laminectomies or wide annular opening) indeed has to be minimal to allow a relatively fast return to the pre-injury level of physical performance. After surgical treatment, the rehabilitation program is of paramount importance. Athletes may return to sports activities after an adequate time has been allowed for healing and recovery, when symptoms are resolved, and ROM is normal. This is often best achieved through good communication and coordination with the athlete’s trainers, team therapists, and coaching staff. With these recommendations, many authors [28, 29] have described good results after diskectomies in affected athletes.

35.3.3 Degenerative Disk Disease Currently, neither the reason for the high rates of degenerative disk disease in asymptomatic individuals nor the relationship between degenerative disk disease and back pain is known. The pathogenesis of degenerative disk disease is elusive. Some authors advocate nutritional pathways that lead to disk degeneration; for example, atherosclerosis involving the arteries that supply the vertebral body together with endplate calcification may cause loss of cellular activity and cell death in the disk [30]. Others advocate a mechanical pathway, in which abnormal mechanical loads are thought to provide a pathway to disk degeneration. Heavy forces imposed on the intervertebral disk may cause initial structural damage that leads to disk degeneration [31], annular tears, nuclear desiccation, and loss of proteoglycan content. When these changes occur, mild loss of disk space height may be observed on plain radiographs, while MRI demonstrates decreased signal intensity on T2-weighted images. In this condition, the disk fails to sustain loads and thus overloads the posterior facet joints, causing articular degeneration. Moreover, the pain generators in degenerative disk disease are not well defined: nociceptive innervation of the posterior aspect of the annulus, anterior aspect of the annulus, and facet joints have all been implicated. Many authors described compressive forces on lumbar intervertebral disks in certain sports. Gatt et al. [32] measured an average peak compressive load of 8600 N and an average peak compressive shear force of 3300 N on L4-L5 in football linemen during blocking maneuvers. Cholewicki et al. [33] measured an average compressive load of 17000 N on L4-L5 motion segment in competitive weight lifters. These studies may explain why degenerative disk disease is more frequent in certain athletes, like weight lifters and football players, but also golf players and soccer players. The patient with degenerative disk disease generally presents with persistent low back pain over the lumbosacral region, occasionally with pain radiation to the sacroiliac joints, buttocks, and posterior thighs. The sitting position and prolonged walking worsen the pain. No radicular symptoms are evident, unless disk herniation or foraminal stenosis (noted in end-stage degenerative disk disease) is present. There may be point tenderness over the lumbar spine; the ROM of the lumbar spine is usually limited, particularly in flexion so that returning to an upright position is often painful while extension may relieve pain. Radicular signs are negative (straight leg rise test negative, normal neurological findings).

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Imaging studies are mandatory. On plain radiographs, narrowing of the disk space, endplate sclerosis, osteophytes, degenerative spondylolisthesis, and degenerative scoliosis may be present. On MRI, common findings are: loss of water (dark disk), high-intensity zone lesions (common finding for annular tears), and endplate changes (well described in the Modic classification [34]). In athletes, the treatment begins always with non-surgical options. However, there is no standard protocol that may be derived from randomized clinical trials for treatment of degenerative disk disease in this population. Cook and Lutz [35] described a five stage program for the treatment of discogenic lumbar pain. Stage I consists of a brief period of rest, application of heat or ice, NSAIDs, soft-tissue mobilization, and epidural injection. In stage II, co-contraction exercises of the abdominal and lumbar extensor muscles and isometric exercises are initiated. This is followed in stage III by strengthening of the lumbar muscles and in stage IV with a return to play. Treatment is continued in stage V in the form of a maintenance program, with regular home and warm-up exercises. If conservative treatments fail or the symptoms do not improve, surgical intervention may be necessary. In the English literature, however, there are no published protocols for surgical indication(s) in athletes. Surgery may be indicated when pain is correlated with positive findings on imaging studies, the athlete’s symptoms do not improve for at least 4-6 months despite active non-operative treatment, and there is midline spinal tenderness that corresponds to the radiographic level of the disease. It is challenging to recommend a specific diagnostic modality in athletes that will correlate with a good surgical outcome, just as it remains challenging in the general population. Disc replacement technologies have not proven to be a good alternative to fusion techniques in the surgical care of athletes. The surgical treatment of discogenic back pain has traditionally been spinal fusion, the goal of which is to eliminate motion of the “affected” spinal segment. Limited data are available in the literature regarding spinal fusion in athletes, but it is known that in the general population spinal fusion techniques have reasonable results in the selective treatment of low back pain. In their randomized controlled multicenter study, Fritzell et al. [36] found a significant reduction of back pain in the spinal fusion group compared to the non-surgical group. More recently, Carreon and coworkers obtained similar results in their systematic review [37]. Several fusion techniques have been described: posterolateral, anterior interbody, posterior interbody, transforaminal interbody, and circumferential (anterior and posterior) fusion techniques, with or without instrumentation. Better clinical results and higher fusion rates are reported with interbody fusion techniques than with posterolateral techniques [38].

35.3.4 Spondylolysis and Spondylolisthesis Spondylolysis is a defect of the pars interarticularis (the isthmus of bone between the cephalad and caudal articular processes). Many patients with spondylolysis also may have spondylolisthesis, defined as the forward slipping of one vertebra on an adjacent vertebra.


515

Almost 90-95% of spondylolytic defects occur at L5, with L4 as the second most affected level. The true prevalence of spondylolysis in the general population is not known because a relevant number of patients are asymptomatic, but it is believed to be 3-6%, with a male/female ratio of 2:1 [39]. By contrast, spondylolisthesis affects females two to three times more often than males. Many classification systems are used in spondylolisthesis, but the most widely accepted is the Wiltse-Newmann classification. Spondylolysis and spondylolisthesis are subdivided in two major groups. In type I (or “dysplastic” disease), there is a congenital abnormality of the facet that allows forward displacement of L5 on S1. In type II (or “isthmic”), which is the most common in athletes and in the general population, there is a defect in the pars interarticularis. Type II deformities are subdivided into type IIA (fatigue or stress fracture of the pars interarticularis), type IIB (elongated pars interarticularis with no damage), and type IIC (acute injury of the pars interarticularis). Regarding the pathogenesis, many authors advocate the “nutcracker” theory; that is, the inferior articular process of the cranial vertebra impacts the pars interarticularis of the caudal vertebra when the lumbar spine is fully extended. Repetitive impacts may cause fatigue or stress fractures of the pars interarticularis. These findings support the observation that spondylolysis is frequent in gymnasts and football players and may explain why 40% of these athletes report prior lumbar back injury. The natural history of spondylolisthesis is well known in adolescents. Pain is rarely correlated with the development of deformity and only 15% of known spondylolyses develop spondylolisthesis. High slip rates occur during growth spurts in adolescents, but usually slow down with skeletal maturity [40]. However, low-grade isthmic spondylolysis may progress in adults, probably as a result of degenerative changes in the intervertebral disks. The incidence of progression is 5% in asymptomatic adults with bilateral defects and 20% in symptomatic patients with a degenerated disk. The slip progression is asymptomatic, as is the development of spondylolysis. Beutler and colleagues [40] found no difference in responses to SF36 questionnaires between a group affected by spondylolysis and spondylolisthesis and an age-correlated control group. Generally, patient presents with complaints of back pain correlated with certain activities and relieved with supine positioning. Leg pain may be present in correlation with slip grade. Tenderness at the midline may be elicited with palpation and a step at the slip level may be appreciated. ROM in the lumbar spine is limited in flexion by the paraspinal muscles spasm. In high-grade spondylolisthesis, trunk foreshortening and hamstring tightness may be appreciated. Compensatory hyperlordosis is often seen and a waddling gait may be present. Neurological findings (motor weakness or sensory deficits) depend on the degree of nerve compression in the lateral recess. Radiographic evaluation should consist of antero-posterior and lateral radiographs. Flexion-extension lateral projections are useful to evaluate the stability. Oblique radiographs provide additional information (Fig. 35.6). The “collar on the Scotty dog” is indeed a pathognomonic sign of a defect in pars interarticularis. Slip grade may be evaluated with Meyerding’s classification, in which the amount of slippage is measured as a percentage of anterior translation of the superior vertebral body on the inferior body: grade 0 (only spondylolysis), grade 1 (1-25%), grade 2 (26-50%), grade 3 (51-75%), grade 4 (76-100%), and grade 5 (spondyloptosis or complete


516

35

a

b

c

d

Fig. 35.6 Spondylolysis and spondylolisthesis. a AP and neutral lateral, b lateral extension, c lateral flexion, and (d) oblique views

a

b

Fig. 35.7 Spondylolysis and spondylolisthesis. a T2-weighted MRI, b T1-weighted MRI

slippage of the posterior portion of the L5 body past the anterior border of the sacrum). CT scan may be useful to evaluate bony details of the defect and MRI (Fig. 35.7) may help to evaluate soft-tissue changes (e.g., disk condition, foramen and nerve root involvement). Single-photon emission CT (SPECT) should be useful if radiographs are inconclusive or impending pars fractures are suspected.


517

The majority of athletes have a good response with non-surgical treatment. NSAIDs, pain management, rest, restriction of sports activity and physiotherapy (strengthening of abdominal and paraspinal musculature, stretching to improve flexibility, and aerobic conditioning programs) are treatments of choice with spondylolysis alone or grade I spondylolisthesis. Bracing may be useful with acute or delayed spondylolysis, grade 1 spondylolisthesis, and unilateral pars fracture. The goal of bracing is to limit hyperextension of the lumbar spine. D’Hemecourt [41] reported good clinical results in non-operative treatment with bracing and physical therapy with a focus on flexion exercises. Blanda and colleagues [42] reported a higher rate of radiographic healing (independent of clinical outcome) for unilateral defects than for bilateral defects. The athlete may return to play when asymptomatic in extension ROM of the lumbar spine, when the neurological examination is negative, and after an adequate period of physiotherapy. In selected cases, some authors do not consider radiological healing as a criterion for return to play [43]. Indications for surgery are: failure of extensive non-operative measures (6 months at least), neurological deficit(s) related to spondylolisthesis, a progressive slip, or a grade III or higher-grade slip at presentation. The goals of surgical treatment are the stabilization of affected levels and the decompression of neural elements. There are many options in the surgical treatment of isthmic spondylolisthesis, but the most often used are posterolateral fusion techniques (with or without instrumentation), circumferential fusion, and direct pars repair. Decompression of the nerve root and posterolateral fusion should be considered in all patients younger than age 30, and when disk height is normal. Instrumentation should be considered if instability is present. Clinical outcomes in athletes are lacking for this procedure, but the results are good in the general population. A recent meta-analysis found an overall 83% fusion rate and a 75% clinical success rate in patients undergoing posterior fusion for isthmic spondylolisthesis, and better results if associated with instrumentation [44]. Posterior decompression of neural elements may be combined with posterior instrumented fusion and with interbody fusion (anterior lumbar interbody fusion, posterior lumbar interbody fusion, transforaminal lumbar interbody fusion), with the theoretical advantage of large vertebral end-plates (increased likelihood of fusion) and combined release and distraction of disk space (improved deformity correction). The same meta-analysis reported better results with these techniques than achieved with posterolateral fusion alone [44]. They are also suitable in high-grade spondylolisthesis (grade III). Direct repair may be indicated in spondylolysis not responsive to non-surgical treatment for at least 6 months in patients with non-degenerated disks, inactive bone scans, or defects < 7 mm. The most common technique is excision of the nonunion site, placement of a pedicle screw, bone-grafting, and placement of a sublaminar hook with connection of each hook by means of a rod to the ipsilateral pedicle screw. With this technique many authors [45] obtained good healing rates as well as good clinical results, also in athletes [46].

518

35


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26. Ong A, Anderson J, Roche J (2003) A pilot study of prevalence of lumbar disk degeneration in elite athletes with lower back pain at Sydney 2000 Olympic Games. Br J Sport Med 37:263266 27. Munt D, Kelsey JL, Golden AL et al (1993) An epidemiologic study of sport and weight lifting as possible risk factors for herniated lumbar and cervical disk: the northeast collaborative group on low back pain. Am J Sport Med 21:854 28. Watkins RG, Williams LA (2003) Microscopic lumbar diskectomy results for 60 cases in professional and Olympic athletes. Spine J 3:100-105 29. Wang JC, Shapiro MS, Hatch JD et al (1999) The outcome of lumbar diskectomy in elite athletes. Spine 24:570-573 30. Nachemson A, Lewin T, Maroudas A (1970) In vitro diffusion of dye through the end plates and annulus fibrosus of human lumbar intervertebral disks. Acta Orthop Scand 41:589-607 31. Allan DB, Waddel G (1989) An historical perspective on low back pain and disability. Acta Orthop Scand Suppl 234:1-23 32. Gatt CJ Jr, Hosea TM, Palumbo RC et al (1997) Impact loading of the lumbar spine during football blocking. Am J Sports Med 25:317-321 33. Cholewicki J, McGill SM, Norman RW (1991) Lumbar spine loads during the lifting of extremely heavy weights. Med Sci Sports Exerc 23:1179-1186 34. Modic MT, Steinber PM, Ross JS et al (1988) Degenerative disk disease: assessment of changes in vertebral body marrow with MR imaging. Radiology 166:193-199 35. Cooke PM, Lutz GE (2000) Internal disc disruption and axial back pain in the athlete. Phys Med Rehab Clin N Am 11:837-865 36. Fritzell P, Hagg O, Wessberg P et al (2001) 2001 Volvo Award Winner in Clinical studies: lumbar fusion versus non surgical treatment for chronic low back pain: a multicenter randomized controlled trial from the Swedish Lumbar Spine Study Group. Spine 26:2521-2532 37. Carreon LY, Glassman SD, Howard J (2008) Fusion and nonsurgical treatment for symptomatic lumbar degenerative disease: a systematic review of Oswestry Disability Index and MOS Short Form-36 outcomes. Spine 5:747-755 38. DeBerard MS, Colledge AL, Masters KS et al (2002) Outcomes of posterolateral versus BAK titanium cage interbody lumbar fusion in injured workers: a retrospective cohort study. J South Orthop Assoc 11:157-166 39. Fredrickson BE, Baker D, McHolick WJ et al (1984) The natural history of spondylolysis and spondylolisthesis. J Bone Joint Surg Am 66:699-707 40. Beutler WJ, Fredrickson BE, Murtland A et al (2003) The natural history of spondylolysis and spondylolisthesis: 45-year follow-up evaluation. Spine 28:1027-1035 41. D’Hemecourt PA, Zurakowski D, Kriemler S et al (2002) Spondylolysis: returning the athlete to sports participation with brace treatment. Orthopaedics 25:653 42. Blanda J, Bethem D, Moats W et al (1993) Defects of pars interarticularis in athletes: a protocol for nonoperative treatment. J Spinal Disord 6:406-411 43. Sys J, Michielsen J, Bracke P et al (2003) Nonoperative treatment of active spondylolysis in elite athletes with normal X-ray findings: literature review and results of conservative treatment. Eur Spine J 10:498-504 44. Kwon BK, Hilibrand AS, Malloy K et al (2005) A critical analysis of the literature regarding surgical approach and outcome for adult low-grade isthmic spondylolisthesis. J Spinal Disord Tech 18(suppl):S30-S40 45. Reitman CA, Esses SI (2002) Direct repair of spondylolytic defects in young competitive athletes. Spine J 2:142-144 46. Debnath UK, Freeman BJ, Gregory P et al (2003) Clinical outcome and return to sport after surgical treatment of spondylolysis in young athletes. J Bone Joint Surg Br 85:244-249

Subject Index

A Acetabulum 266-268, 270, 275, 279-280, 290-296 Acj conditions 149 ACL – reconstruction 7, 13-14, 304, 307, 341, 349-350, 353-354, 371-372, 490-492 – rupture 333-336, 341, 349, 352, 485 Acromioclavicular – joint injury 5, 200-202, 207 Acute ankle sprains 64, 465, 481, 485, 492 Adhesive capsulitis 145, 150-151, 161, 217 Aging 12, 22, 42, 45, 59, 66-67, 86, 211, 213 Ankle – impingement 479 – instability 23, 65, 466, 470-472, 474, 476, 481, 493 – sprains 10, 64, 465-468, 470, 474, 476, 480-481, 485, 492-493 Anti-doping 39, 117 Arthroscopy 6-7, 10, 127, 129, 131, 196, 207, 246-247, 249, 251-252, 261, 276, 287, 291-294, 296-297, 397, 406, 408, 413, 427, 429, 432, 434, 437, 453, 462, 468-469, 471, 475, 478-479, 481 Articular cartilage 11, 13, 49-57, 124, 189, 265-268, 270, 272, 290-293, 308, 320, 324, 360, 383, 390, 447-449, 451, 453, 455-456, 458-461

Articular cartilage injury 11, 54, 189, 265, 272, 383, 447 Athlete 3-7, 10-12, 31-33, 35, 37-39, 45, 59-61, 63-67, 73-81, 83-86, 91-102, 105-111, 113, 117-118, 123-126, 137139, 141-142, 145, 152-153, 156-157, 160-161, 164, 166-168, 173, 175-176, 178, 180-182, 187, 193, 195-196, 199200, 202, 204, 207-208, 211, 213, 216, 218-219, 224, 227-234, 236-238, 241245, 247, 250, 252-253, 257, 259, 261, 265, 275-276, 278-280, 282-284, 286, 288-291, 293-294, 296-297, 341-344, 348-349, 352-353, 375-377, 436, 441, 465-466, 468, 474. 479-481, 485-491, 493-494, 499-502, 504, 506-515, 517 Athlete’s heart 91-92 Athletic – injuries 227 – performance 67, 97, 105, 113 – pubalgia 275-276, 289 Autologous 10-11, 29, 38-39, 117, 120, 122, 124-125, 272, 433-434, 437, 454458, 478 Avulsion 45, 171, 189, 221, 231, 244, 246, 249, 268-269, 275-279, 284, 345-347, 366-369, 388, 391, 393, 439, 441, 467, 478, 501, 505-506 Axis 42, 46, 146, 151, 154, 164, 246-247, 303, 305-306, 308, 314, 316, 322-323, 350, 400-401, 505-506 521

522

B Bankart 5, 146, 179, 187-189, 192-193, 195, 258 Biceps tendon 5, 168, 171, 176, 179, 185, 190, 206, 228, 236, 310-311, 360 Biochemistry 50, Biologics 3, 9, 12-13, 223, 412 Biomaterials 21, 26-28, 456 Biomechanical 4, 7-8, 12, 28, 41, 49, 54, 57, 59, 65, 75, 80, 84, 138, 182, 192, 206, 209, 223, 259, 265, 268, 272, 279, 281, 303, 305, 312, 342, 350, 361, 376-378, 391, 418-419, 435, 457, 476, 500, 507 Biomechanics 42, 51, 145-147, 154, 173174, 196, 199-200, 211-212, 228, 267, 272-273, 276, 301, 352, 359-360, 376, 411, 418, 424, 466, 485-486 Blood 13, 22-23, 29, 33, 35, 54, 56, 95, 98, 106, 111, 119-120, 123-125, 133, 138, 142, 149, 243, 245, 268, 293, 305, 307, 324, 403, 418, 420, 425-427, 437, 501 Blunt trauma 32, 54-55, 283, 448 Bone 10, 13-14, 22, 25, 27-28, 33, 37-38, 41-43, 47, 49-51, 53-57, 67, 73-75, 7779, 81-86, 117, 119-120, 123, 125, 141, 146, 150, 161, 175, 189-191, 193, 195, 197, 206, 227, 234, 236-237, 241-243, 245, 247-248, 259, 268, 272, 279-280, 294, 313, 347, 350, 370, 372, 378, 391393, 405, 412, 418, 421, 424-426, 431, 433, 437, 441, 447-451, 453-454, 458459, 467, 471-472, 478-480, 514, 517 Bone stress 75 Brace 59-60, 63-65, 84, 139, 141, 167, 204, 368, 371, 378, 388-389, 393-394, 426427, 440, 453, 471, 475, 493-494 Bursitis 6, 148, 167, 188, 215, 275-276, 283-285, 287, 290, 425 C Capsular laxity 177, 265, 270-271, 296-297 Cardiovascular disease 59, 67, 109, 113 Carpal tunnel syndrome 245, 248, 253 Cartilage – injury 189, 265, 272, 293

Subject Index

– lesions 49, 54, 57, 272, 296, 324, 343, 424, 431-433, 447-449, 451 – repair 13, 56, 123-124, 433, 448-450, 459-461 – restoration 451 Cervical 217, 471, 499-502, 506-509 Chondral – injury 268, 286, 293-294, 471 – lesion 49, 272, 275-276, 293-294, 319, 324-326, 341, 343, 432, 447, 450-451, 454, 456, 462, 465-467, 479 Chondrocyte 11, 22, 49-51, 54-57, 121, 123-124, 272, 433, 448-449, 451, 454459, 478 Clinical examination 34, 138, 159-160, 166, 235, 281, 284, 292, 301, 319, 328-329, 377, 397, 403-404, 406, 419-420, 435, 438 Collagen 7, 22-28, 32, 36, 42-46, 50-54, 56, 119-122, 124, 266, 304-305, 307, 399401, 407, 412, 448, 456-457, 493 Concomitant lesions 189 Concussion 3, 11 Conservative 5, 31, 38, 60, 179, 182, 196, 199, 203-205, 208, 227, 231-232, 234236, 238, 243, 248-250, 252-254, 257, 260-261, 272, 278-279, 285, 288, 297, 341, 348-349, 353, 368, 370-371, 375, 383, 409, 418, 426-427, 431, 434-437, 439, 465, 467, 471-472, 475, 477, 488489, 502, 504, 506, 511-512, 514 Contusion 31-32, 34-35, 37, 65-66, 139, 142, 275, 283 Coracoclavicular ligaments 149-150, 199 Criteria 93, 118, 132, 204, 244, 349, 353, 378, 485, 488, 490-491, 509 Cruciate ligaments 150, 301-302, 328, 331, 365, 387, 392 D Dabigatran 130 DeQuervain’s 252 Diagnostic 14, 79, 83, 94, 131, 138, 142, 160161, 179, 216, 241, 246-247, 252-254, 267, 273, 276, 285, 289, 325, 359, 403, 405-406, 417, 421, 426, 474, 486, 514

Subject Index

Disk 494, 499, 501-502, 504, 506-517 Disk herniation 501-502, 507-508, 510-513 Distal radius 80, 241-244, 249 Double bundle 7, 14, 209, 341, 350, 378 E ECG 94-99, 101-102, 138 Elbow 3-4, 6, 13, 122, 145, 154, 156-157, 159, 161-171, 174-175, 200, 203, 213, 216, 227-238, 253, 257, 260-261 Elbow instability 145, 156 Emergencies 85, 137-139 Epicondylitis 6, 122, 157, 159, 168, 171, 227-228, 230-234, 236 Ergogenic aids 105, 109 F FAI 6, 265, 268-270, 272, 276, 280-281, 290-296, 493 Fatigue fractures 73, 280 Femoral head 6, 266-272, 281, 286, 290291, 293-297, 438 Femoroacetabular impingement 6, 265, 268, 275-276, 294-295 Fondaparinux 127-129 Fracture 6, 10, 13, 55-56, 73-85, 123, 127, 129, 131-132, 139, 141-142, 150-151, 156-157, 182, 188-189, 191, 194, 202203, 205, 227, 233, 237, 241-246, 248250, 254, 275-283, 290, 345-346, 363, 366, 384, 388, 424-425, 439-441, 449, 451, 459, 467, 471, 474-479, 481, 492493, 500, 502, 504-507, 509-510, 515-517 Future of sports medicine 3 G Gene therapy 11-12, 27-28, 39, 46-47 Glenohumeral internal rotation deficit 173, 175, 216, 259 Growth factors 11, 13, 21, 27-29, 32, 38-39, 46-47, 49, 117-125, 437, 449, 488 H Hamate hook 244-245, 254 Hamstring ruptures 485, 487

523

Healing processes 117, 122, 487 Hematoma 31-33, 35-37, 39, 46, 56, 122, 128, 160, 283-284, 329, 386, 434, 467, 488 Hill Sachs 189, 191-193 Hip – arthroscopy 7, 276, 287, 291-292, 297 – dislocation 275-276, 282, 296 – fracture surgery 127, 129 – injury 265, 267 – instability 265, 270, 272, 275-276, 290, 296-297 – pain 265, 268, 270, 273, 275-276, 281, 283, 285, 288, 290, 292-294, 297 Histology 25 Hypercompression 424, 434 I Iliotibial band 271, 285, 287, 310, 315, 321, 353, 361, 419-420, 424-425, 434436, 438 Impingement 6, 10, 28, 146-148, 151-154, 157, 159, 164-167, 173, 175-177, 180, 182, 197, 211-214, 216-217, 221, 227, 229-230, 237, 252, 265, 268-269, 275276, 279, 286, 291-295, 342, 435-436, 465-466, 468, 471-472, 474, 479-481, 500 Inflammatory process 232, 325, 485, 487 Injury 3, 6-8, 10-14, 22, 29, 31-38, 41, 4547, 49, 54-57, 59-68, 73-74, 76, 83, 110, 119, 122-123, 125, 127, 132, 138-141, 150, 156, 160, 173-174, 177-178, 181182, 189, 194-195, 199-208, 211, 213214, 227-231, 233-235, 238, 241, 243248, 252, 260, 265-268, 270-273, 275276, 278-279, 281, 283-284, 286, 289, 291-294, 312, 324, 327-329, 331, 333, 339-349, 352-354, 359, 362-363, 365366, 368-372, 375-377, 380, 383-391, 393-394, 404, 406, 410, 413, 418, 436, 441, 448, 450, 453, 460-461, 465, 467468, 470-472, 474, 476, 481, 485-488, 490-492, 494, 500-502, 504, 506-511, 513, 515

524

Instability 5,7-10,23,54,64-65, 100, 145148, 150-152, 155-156, 159, 161-163, 167-170,173-175,177,179,182,185-197, 202, 206, 208, 213, 216, 227-228, 230231, 233, 237, 244-250, 257-261, 265, 270-272, 275-276, 290-291, 293-294, 296-297,304,312,319,323-325,328-330, 332, 334-340, 343, 348, 360-362, 366, 369, 371, 375, 378, 383, 390, 417, 419420, 424-425, 427, 429, 432, 447, 450, 460,465-467,470-472,474-476,481,490, 492-493,500,502,504,507-509,512,517 Internal impingement 148, 152-154, 173, 180, 182, 197,213-214,216 J Joint 5-{i, 8-10,12,14,24-25,32-33,36-39, 41-42,45,49-57,59-60,64-65,67, 124, 141, 145-146, 148, 150, 154-156, 159164, 166-170, 177-179, 185-191, 194, 196-197,199-209,211-212,224,227-231, 233, 235, 237, 241, 244-249, 254, 258260,266-267,271-272,276-277,279-280, 282-283,286,290-294,296-297,301-305, 307,309-310,313-315,319-322,324-328, 330-331, 333, 336-337, 343, 348-349, 351, 360-366, 377-378, 385, 388, 397, 399,403-404,406-407,411-413,417-419, 421, 424-425, 427, 429-435, 438, 441, 447-448, 450-453, 455, 462, 466-467, 471-472, 474-476, 478-479, 481, 500, 505-506, 509, 513 Joint capsule 162,200,266,286,297,304, 310,360-361,427,429,434,479 K

Kinetic chain 65,173-174,176,182,348, 350 Knee - arthroscopy 127, 129, 131 - collatera11igaments 345, 360, 366, 387, 390,399 - ligament evaluation and trea1ment 330, 387 KID arthrometer 491

Subject Index L Labral tear 5,179,194,213,216-217,265, 268,270,275-276,289-294,296 Labrum 5-6, 146-147, 152-154, 163, 174, 178-180, 185-186, 189, 192, 194-195, 197, 213-214, 259, 266, 268-270, 272, 283, 286, 290-292, 294-297 Laceration 31,56,387 Latsrjet procedure 5 Lateral elbow tendinopathy 261 Ligament reconstruction 8, 205-209, 247, 360,383,389,392-393,476,490 Ligaments 7,9,22,41-46,67,75,142,145, 147, 149-150, 154-155, 163, 170, 174, 185-186, 194, 199-206, 208-209, 233, 248-249, 260-261, 266-267, 296, 301302,310,327-328,331,333,338,343345, 360-366, 383-385, 387, 389-390, 392-393,399,403-404,417,451,467468,471,475-476,493,506,510 Little 1eagoe shoulder 173, 182 Low molecular weight heparin 127-129 Lower extremities fractures 127 Lower limb 51,61-62,67,73-75,77,79, 81,84, 138, 174, 314, 330, 333, 335, 344,404-405,438,485,490 Lumbar 77-78, 165, 174, 276, 283, 287, 321-322,499-500,502,510-515,517 Luxations 139, 141, 191, 199 M Management 3-6,8, 11-12, 14, 23, 28-29, 35,37-38,60,64,77-79,83-85,91,137, 139,141,149,151,156,173,179,181182, 194,204,208,211,216,219-222, 224, 243-244, 247, 250, 253-254, 258, 260-261, 265, 267-268, 271-272, 275, 278,281,285-287,295,297,348,359360, 368, 370-371, 383-385, 388-390, 418,427,430,437,439,447,451,465, 467-468, 470, 485, 488, 490, 493, 499, 502,517 Marrow stimulation techniques 433, 448, 479 McLaughlin lesion 194

Subject Index

MCL 8-9, 42, 45-46, 154-156, 169, 189, 194, 228, 230-231, 309-310, 328, 330331, 340, 359, 361-367, 371-372, 390391, 393 Medial collateral ligament 9, 42, 154, 168169, 227-228, 230, 260, 304, 309, 340, 359, 367, 384, 390, 399, 411 Medial instability 175, 231, 237, 339-340, 371, 471 Meniscal tear 13, 324-328, 343, 397, 403404, 407-408, 410 Microinstability 173, 177, 182, 196 MMPS 24 Morphology 5-6, 49-51, 92, 175, 194, 213, 217, 267-268, 313, 409, 417, 430 Muscle 12-13, 22, 25, 31-39, 41, 59-60, 65-68, 75-77, 81, 84-86, 91, 106-113, 118, 121-123, 125, 142, 145-149, 151154, 159-160, 164-165, 167-168, 171, 173-175, 180, 182, 194-195, 197, 200, 202-204, 206, 211-212, 216, 218, 228229, 236, 243, 245, 253-254, 259-260, 267, 275-279, 281, 283-285, 287-290, 296, 311-314, 316, 321-322, 330, 335, 343-344, 352, 361, 377-378, 390, 394, 417-419, 427, 434-435, 438-439, 471, 488, 490-491, 501-502, 510-512, 514515 Musculotendinous lesions 139 Myositis ossificans 37-38, 122, 284, 288 N Neuromuscular and proprioceptive training 491 Neuromuscular control 12, 63, 65, 177, 342, 352, 475, 487, 490, 493, 494 Non-anatomic reconstruction 471-472 O Osteitis Pubis 275-276, 279 Osteoarthritis 8, 11, 13, 49, 54, 57, 60, 67, 148, 150-151, 204, 206, 208, 267-268, 272, 294, 296, 341, 344, 411, 418, 420, 424-425, 427, 431-432, 438, 441, 451, 455, 474, 490

525

Osteochondral lesion 10, 49, 56, 63, 272, 427, 432, 449, 454, 467, 471, 476-477, 479, 481 Osteochondritis dissecans 6, 157, 227-228, 230, 234-235, 449, 459 Overuse 10, 25-26, 63, 65, 68, 73-74, 80, 86, 148, 176, 196, 216, 227-228, 236, 241, 250, 252, 259, 261, 271, 284, 288, 296, 417-418, 425, 436 P Palliative treatments 122, 453 Patellar tendinopathy 13, 63, 436-437, 485, 488-489 Patellofemoral – disorder 9, 417, 424-425 – joint 9, 301, 313-315, 319-322, 417419, 424, 430-433, 447, 450-451, 453, 455 Pathophysiology 22, 31-33, 35, 41, 49, 75, 147-148, 265, 267, 448 Patient history 290, 319, 324, 328, 362 Platelet-rich plasma 9, 13, 29, 38, 118-121, 223, 288 Platelets 28, 119-120, 130 Posterior Cruciate Ligament 8, 302, 304, 307, 334, 340, 345, 360-363, 365, 375, 377, 387, 392 Posterior impingement 167, 230, 294, 471, 480 Posterolateral corner 8, 311, 332, 334, 336, 338-340, 359, 364-365, 369, 380, 384, 387 Posteromedial corner 310, 328, 337, 359, 362, 372 Pre-participation screening 101 Prevention 7, 24, 37-38, 50, 59-61, 63-68, 76, 85-86, 101, 127, 130-131, 139, 173, 177, 272, 341, 352, 461, 485-488, 491, 493 Prohibited substances 113, 117-118 Prophylaxis 128-129, 131-133 Proteoglycan 22, 24-25, 42, 46, 50-55, 124, 304, 399-400, 448-449, 513

526

R Radial nerve 229, 252, 254 Rehabilitation 4-5, 12, 31, 35-36, 38, 60, 65, 85, 173, 176, 180, 182, 187, 192, 197, 243-244, 257-260, 278-279, 284285, 290, 293, 341, 344, 348-351, 389390, 393-395, 410, 413, 417, 440, 453, 457, 459-460, 468, 472, 475, 480, 485487, 490, 492-493, 499, 511, 513 Reparative treatments 453 Restorative treatments 454 Rivaroxaban 130-131 ROM evaluation 168 Rotator cuff 4, 13, 145, 147-151, 153-154, 159-160, 173-177, 179-182, 185-187, 189-190, 194, 197, 204, 211-224 Running 59, 66, 68, 76-77, 81, 84, 86, 111, 113, 276, 278, 280, 285, 289-291, 329, 336, 353, 389, 394, 435, 470, 488, 494 S Scaphoid 241-243, 246-247 Scapholunate 242, 244, 246-248 Scapular dyskinesia 145, 151-152, 160, 173, 182, 259 Shoulder 3-5, 31, 59, 65, 80, 137, 141, 145, 147-150, 152-153, 159-167, 169-170, 173-177, 179-182, 185-197, 199-200, 202-205, 207, 211-212, 215-217, 221, 229-230, 253, 257-261, 501-502 Shoulder instability 5, 145, 173-174, 177, 182, 185, 187-190, 194-196, 257-259 Skeletal muscle 13, 39, 108-109, 125 SLAP 152-154, 159, 163-164, 173, 175, 177-180, 182, 189-190, 194, 197, 259 Soft tissue injury 3, 12 Spine 3, 10, 67, 74-75, 77, 79, 161, 165, 217, 266, 275-278, 287-288, 304, 307, 314, 320, 322, 325, 346, 399, 438, 499502, 504-513, 515, 517 Spondylolisthesis 500, 506, 514-517 Sport – cardiology 101 – medicine 238 – physician 86

Subject Index

Sprain 10, 12, 62, 64, 139, 141, 199, 201, 344, 366, 465-468, 470-471, 474-476, 480-481, 485, 492-493, 500, 502, 510511 Strain 7, 12, 22, 24-26, 31-32, 34, 38, 44, 51-53, 57, 66, 157, 213, 260-261, 275276, 279, 283-284, 288, 435-436, 438439, 467, 488, 500, 502, 510-511 Stress fractures 10, 73, 75, 78, 275-276, 279-281, 290, 515 Sudden cardiac death 93-94, 99-100 Superficial lesions 54 Supplements 105, 107, 109-111, 113, 461 Syndesmotic instability 471, 474-476 Synovial plicae 227 T Tendon – histology 25 – injuries 21, 23-24, 29 – mechanobiology 25 – pathology 21-23, 28-29, 224 Tendonitis 10, 13, 182, 188, 213, 250, 285, 287, 322, 325, 327 Test 43, 80-81, 97-99, 101-102, 110, 113, 138, 159-166, 168-171, 176, 179, 188, 196-197, 216-217, 232-233, 242, 246248, 250-251, 253, 283, 285, 287-288, 290, 292, 294, 312, 316, 319, 321-323, 325-340, 344-345, 349, 363-366, 377, 386-388, 397, 405, 419-420, 435, 467, 471, 474, 490-491, 512-513 Therapeutic exercise 220, 485-489 Throwing – athlete 6, 12, 77, 80, 145, 152.153, 157, 161, 164, 167-168, 173, 176, 178, 180182, 187, 196, 199, 204, 216, 219, 230, 234, 253, 259 – shoulder 65, 259 Time frame of tissue healing 485 Tissue repair 13, 117, 119-120, 124-125 Total hip replacement 127 Total knee replacement 127, 344, 432 Traumatology 138

Subject Index

Treatment 3-8, 10-12, 14, 21, 29-31, 3539, 50, 54, 57, 64-65, 68, 73-74, 78-81, 83-86, 118, 122-126, 130, 132, 141142, 152, 159-160, 167, 176, 180-182, 185, 187-188, 191-197, 199, 203-209, 211, 215-216, 219-224, 227, 231-234, 238, 241-245, 247-253, 257-258, 261, 265, 267-268, 272, 275-276, 278-285, 287-289, 292, 295-297, 341, 348-349, 353, 359-360, 368-372, 375, 377-380, 383-384, 388, 393-395, 397, 406-409, 411, 413, 417, 426-427, 431-432, 434437, 439, 447, 451-455, 459, 461, 467468, 470-472, 474-481, 485-490, 493, 500-502, 504, 506-507, 509, 511-514, 517

527

Triangular fibrocartilage complex (TFCC) 244, 247-250, 252 U Ulnar nerve 157, 167-168, 229-230, 232, 237, 245, 253-254 Unfractionated heparin 129 V Venous thromboembolism 127, 129 Vitamin K antagonists 127-128, 130 W Warfarin 127-128 Wounds 139, 142, 385, 388 Wrist injury 241-244, 246

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