Sports Injuries - Prevention, Diagnosis, Treatment and Rehabilitation (PDFDrive) [PDF]

Zitiervorschau

Mahmut Nedim Doral (Editor) Reha N. Tandoğan s Gideon Mann René Verdonk (Co-Editors)

Sports Injuries Prevention, Diagnosis, Treatment, and Rehabilitation

Editor Prof. Mahmut Nedim Doral M.D. Faculty of Medicine Department of Orthopaedics and Traumatology Chairman of Department of Sports Medicine Hacettepe University Hasırcılar Caddesi 06110 Ankara Sihhiye Turkey [email protected] Editorial Assistants Gürhan Dönmez M.D., Ankara, Turkey Egemen Turhan M.D., Zonguldak, Turkey

Co-Editors Prof. Reha N. TandoÜan M.D. Çankaya Orthopaedic Group and Ortoklinik, Cinnah caddesi 51/4 Çankaya 06680 Ankara Turkey [email protected] Prof. Gideon Mann M.D. Meir General Hospital Orthopedic Department Tsharnichovski St. 59 44281 Kfar Saba Israel [email protected] Prof. René Verdonk M.D., Ph.D. Department of Orthopaedic Surgery and Traumatology Ghent University Hospital De Pintelaan 185 B 9000 Ghent Belgium [email protected]

Advisory Board José Huylebroek M.D., Brussels, Belgium; Gian Luigi Canata M.D., Torino, Italy; Andreas Imhoff M.D., Muenchen, Germany; Ö. Ahmet Atay M.D., Ankara, Turkey; Gürsel LeblebicioÜlu M.D., Ankara, Turkey; Akın Üzümcügil M.D., Ankara, Turkey; Onur Bilge M.D., Konya, Turkey; Gazi Huri M.D., NiÜde, Turkey; Mehmet Ayvaz M.D., Ankara, Turkey; Ömür ÇaÜlar M.D., Ankara, Turkey; Gökhan Demirkıran M.D., Ankara, Turkey; Salih Marangoz M.D., Ankara, Turkey; Özgür Dede M.D., San Francisco, CA, USA; Onur Tetik M.D., ístanbul, Turkey; Defne Kaya PT, Ankara, Turkey; Volkan KaynaroÜlu M.D., Ankara, Turkey, Kivanc Atesok M.D., Toronoto, Canada

ISBN 978-3-642-15629-8 e-ISBN 978-3-642-15630-4 DOI 10.1007/978-3-642-15630-4 Springer Heidelberg Dordrecht London New York Library of Congress Control Number: 2011923421 © Springer-Verlag Berlin Heidelberg 2012 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 German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer. Violations are liable to prosecution under the German 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. Cover design: eStudioCalamar, Figueres/Berlin Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com)

Loyalty, confidence, and friendship should never be forgotten Mahmut Nedim Doral

To my Dearest Mother, Father, Esra, Ceyla and CoĜku… Mahmut Nedim Doral

Foreword I

Sports for life or to live for sports? This is probably a common question in the present day. Exercise and sports bring tremendous health benefits. However, medical problems do occur during sporting activities, and these are the focus of a particular discipline of medical science. Thus, the various medical aspects of sports have to be rigorously and comprehensively studied so as to minimize the possibility of harm to those taking part. People of all ages, but especially the young, need to lead an active life, taking advantage of the outcome of such scientific studies. This is something I see as a priority. As president of Hacettepe University, I would like to note that the teams we have assembled in many fields reflect our commitment to sports and sportsmen. In particular, the progress and success achieved by our basketball team in the last two years encourages us greatly for the future. Alongside this sporting commitment, we have endeavored to provide support to the science of sports. In this regard the, scientific support provided by the School of Sport Sciences and Technology, the Department of Orthopedics and Traumatology, and the Department of Sports Medicine has been significant. As president of the International Archery Federation for five years and as a member of the International Olympic Committee, I have always emphasized that sports need to be examined scientifically and that the best treatment of any injuries is prevention. I feel greatly honored that the present book has been prepared under the organization and leadership of the scientists of the university of which I am rector and incorporates the contributions of many eminent international scientists. I would like to thank and congratulate firstly my dear colleague Prof. Dr. Mahmut Nedim Doral and then all the distinguished authors and others who, through their efforts, have helped bring about this valuable work, which will make a lasting contribution to the global literature of sport injuries. Ankara, Turkey

Prof. UÜur Erdener M.D. President of Hacettepe University President of Archery International Federation (FITA) President of Turkish National Olympic Committee

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Foreword II

As the president of the European Federation of National Associations of Orthopaedic Sports Traumatology (EFOST), it is a great honour for me to be invited by my good friend Prof. M.N. Doral to write a foreword for this magnificent book about sports injuries. I believe that the words of the nineteenth-century American political leader Robert G. Ingersoll are more than ever true for this masterwork, realized by so many experts in the field of a special branch of medicine: prevention, diagnosis, and treatment of injuries in mostly young women and men, engaged in sports, most of whom had the desire and determination to return to their athletic activity: “Reason, observation and experience: The holy trinity of science.” This manual is not a be-all and endall of diagnostic techniques, surgical interventions and rehabilitation programs for athletes who sustain injuries.

As the great sports orthopedist Jack C. Hughston taught us so many years ago, “None of us live and work in a vacuum: I have constantly rubbed my brain against those of others to clarify and solidify my knowledge.” EFOST has played a major role in the realization of the present masterpiece And the continued rapid expansion of knowledge in sports medicine is being driven by basic scientists. Information on tissue biomechanics, coverage of extreme sports and sport-specific injuries, the important role of physiotherapy have often been covered, discussed, and illustrated during the biannual congresses of EFOST, where the condition, injury, and follow-up of the individual athletes and members of a team were the major concern of the speakers on these international meetings. Not only are the most common injuries discussed in the different chapters of this volume, but attention is conspicuously given to more specific sports-related fields as “sports after prosthesis surgery, cartilage solutions in the young athlete, and the clinical relevance of gene therapy, tissue engineering, navigation and growth factors in surgery on amateur and professional athletes.” Creating a textbook about problems in a rapid evaluating field as sports medicine is a challenge. Editing a book with enduring appeal is even more difficult. The chief-editor, Prof. M.N. Doral, should be congratulated with the result of the immense task EFOST asked of him: create a textbook about sports medicine that can serve as a solid foundation for the physician with a sports-oriented practice, a reference for the experienced surgeon, and a basic starting point for the interested scientist and researcher. As president of EFOST, reading this book I had some good feelings. The authors have very well understood the message our federation wants to spread throughout Europe and elsewhere: sports medicine is a very important part of medicine: new information has been included, future pathways are mentioned but left open.

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Foreword II

I would like to end this foreword with the wise words of Ralph Waldo Emerson, who, without knowing the result of the ambitious efforts of the editor in updating the information about sports medicine, wrote many years ago: “Progress is the activity of today and the assurance of tomorrow” Congratulations to the whole team and all the contributors. José F. Huylebroek M.D. EFOST President 2007–2010

Foreword III

Over the past several years, we have seen an international explosion in sports traumatology and knee ligament research. Tremendous efforts have been made to improve the surgical and nonsurgical outcomes of ligamentous knee injuries in both the professional and amateur athlete, with the introduction of minimally invasive arthroscopic techniques, complex graft fixation, and advanced rehabilitation protocols. Members of my research team are currently focusing on the comparative anatomy of the knee and anatomical double-bundle anterior cruciate ligament reconstruction. The members of the international sports medicine community, including the 4,000 members of the International Society of Arthroscopy, Knee Surgery. and Orthopaedic Sports Medicine from 87 countries around the world, are focusing on the need to improve reconstructive techniques, anatomical reconstructions, biological aids, imaging, and outcome measures as well as providing sports traumatologists with comprehensive data and data analysis on the future direction of knee ligament surgery. We extend our appreciation to Prof. Mahmut Nedim Doral for undertaking this tremendous effort in assembling this comprehensive text with contributions from over 100 international authors to serve as a source of sports traumatology. Prof. Freddie H. Fu M.D., D.Sc. (Hon.), D.Ps. (Hon.) President of ISAKOS 2009–2011

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For eword III

Preface

After the 5th European Federation of National Associations of Orthopaedic Sports Traumatology (EFOST) Meeting, held in November 2008 in Antalya, I never imagined that such a comprehensive volume as this would result. This book is the product of sleepless nights and the valuable efforts of more than 300 scientists from around the world: from Japan to the US, Nepal to Israel, Hungary to Spain. It gives me great honor to have integrated Eastern and Western science in my home land, which as well as being the geographical junction has since ancient times been the cultural intersection of East and West. Firstly, I would like to express my gratitude to all authors who provided their valuable experience for this work. I would also like to thank the co-editors — Dr. Mann, Dr. TandoÜan, and Dr. Verdonk — in addition to the Advisory Board. With its increasing importance, sports surgery has now reached an exciting level. Every time the sports physician turns on the television he or she sees how priceless it is to be able to bring their patient back into the sporting arena a day earlier — and thus make an impact on so many lives. As a result, scientific developments in sports traumatology have impacts on the world at large. Although we have come a long way since Masaki Watanabe undertook the first arthroscopy, the human body has so many unexplored mysteries that it invites ever-increasing scientific endeavors. Thus, in this book, we have attempted to gather together current concepts, treatment modalities, surgical techniques, and rehabilitation protocols as much as possible. We have attempted to include not only standard methods but also novel techniques and different ideas. We preferred to start our book with prevention strategies, knowing that the most important part of an athlete’s treatment is prevention. Similarly, in light of the viewpoint that diseases do not exist, only patients, we created the Sports Specific Injuries” section so that surgeons could have a better knowledge about such injuries. Some other sections in this book are Upper and Lower Extremity Injuries, Pediatric Sports Injuries, and Sports After Arthroplasty. The “Future in Sports Traumatology” section of this book covers topics that we considered particularly worthwhile, and we hope that the papers in this section will encourage readers to develop new, original ideas. Our present knowledge has to be updated every five years or so, and maybe five years from now genetically enhanced athletes and robots will be ongoing issues. At this point, with the experience of 30 years in my professional career, having treated thousands of patients, and with the help of such an experienced publisher as Springer-Verlag, it is an amazing feeling for me to produce the present book — just like the first time I picked up my lovely daughter and held her in my arms 28 years ago. I cannot express the special place I have in my heart for my precious parents NeĜ’e Füsun and Seyfi Doral, for their lifelong support.

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Preface

I would like to thank my dear wife Esra, who always supports me and considers me a “still” studying student, my daughter ěölen Ceyla from whom I always get advice, my son in law CoĜku, my wonderful teacher Dr. T. GöÜüĜ who has a special place for me, Dr. R. Ege who introduced Turkish orthopedics to the world, my colleagues, the other authors, and people who have had trust in me for this book. I would like to thank Dr. Ö.A. Atay, Dr. G. LeblebicioÜlu, Dr. A. Üzümcügil, Dr. E. Turhan who have worked with me and supported me for years, and, further, Dr. J. Huylebroek, Dr. A. Imhoff, Dr. S. Woo, Dr. M. Yazıcı, and Dr. N. Maffulli. Special thanks go to my young assistant Dr. G. Dönmez. His incredible energy and attention should be an example for all young assistants. He too has made much effort on this book. I would like to thank Springer-Verlag family and Gabriele Schröeder who have supported me. It would be the greatest present and best source of motivation for me to know that this work is in your hands to help you expand your vision in treating athletes. Please do not forget that the science has no religion, no language, no race, no color, no flag! Having the experience of years, my message to my young fellow colleagues is to share science. Please keep in mind that to progress to higher points in medicine, it is essential to educate growing new generation in a perfect way, with the best opportunities. Ankara, Turkey

Prof. Mahmut Nedim Doral M.D. President of Turkish Society of Orthopaedics and Traumatology

Contents

Part I

Introduction and History of Sports Traumatology

The History of EFOST. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mahmut Nedim Doral

3

The Past and the Future of Arthroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hans H. Pässler and Yuping Yang

5

Treatment of Athletic Injuries: What We Have Learned in 50 Years. . . . . . . . . . . . Giuliano Cerulli

15

Part II

Prevention of Sports Injuries

Biomechanical Measurement Methods to Analyze the Mechanisms of Sport Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Serdar Arıtan

19

Prevention of Ligament Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Emin Ergen

27

Prevention in ACL Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Henrique Jones and Pedro Costa Rocha

33

Neuromuscular Strategies in ACL Injury Prevention . . . . . . . . . . . . . . . . . . . . . . . . Mario Lamontagne, Mélanie L. Beaulieu, and Giuliano Cerulli

43

Anterior Cruciate Ligament Injured Copers and Noncopers: A Differential Response to Injury. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Yonatan Kaplan

53

Prevention of Soccer Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Haluk H. Öztekin

61

Sports Injuries and Proprioception: Current Trends and New Horizons . . . . . . . . Devrim Akseki, Mehmet Erduran, and Defne Kaya

67

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Part III

Contents

Sports Injuries of the Upper Extremity: Shoulder Injuries

Rotator Interval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mehmet Hakan Özsoy and Alp BayramoÜlu

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Pathology of Rotator Cuff Tears. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Achilleas Boutsiadis, Dimitrios Karataglis, and Pericles Papadopoulos

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Neurovascular Risks Associated with Shoulder Arthroscopic Portals . . . . . . . . . . . Daniel Daubresse

87

Rotator Cuff Disorders: Arthroscopic Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kevin D. Plancher and Alberto R. Rivera

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Current Concept: Arthroscopic Transosseous Equivalent Suture Bridge Rotator Cuff Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mehmet Demirhan, Ata Can Atalar, and Aksel Seyahi

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Posterosuperior and Anterosuperior Impingement in Overhead Athletes . . . . . . . Chlodwig Kirchhoff, Knut Beitzel, and Andreas B. Imhoff

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Internal Impingement and SLAP Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . íbrahim Yanmış and Mehmet Türker

127

Anterior Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mustafa Karahan, Umut Akgün, and RüĜtü Nuran

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Arthroscopic Treatment of Anterior Glenohumeral Instability . . . . . . . . . . . . . . . . Özgür Ahmet Atay, Musa UÜur Mermerkaya, ěenol Bekmez, and Mahmut Nedim Doral

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Acute Posterior Dislocations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . George M. Kontakis, Neil Pennington, and Roger G. Hackney

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Management of Recurrent Dislocation of the Hypermobile Shoulder . . . . . . . . . . . Roger G. Hackney

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Current Trends on Shoulder Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Seung-Ho Kim

165

Management of the Acromioclavicular Joint Problems . . . . . . . . . . . . . . . . . . . . . . . Onur Tetik

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Arthroscopic Double Band AC Joint Reconstruction with Two TightRope™: Anatomical, Biomechanical Background and 2 Years Follow up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hosam El-Azab and Andreas B. Imhoff Proximal Biceps Tendon Pathologies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mehmet DemirtaĜ, BarıĜ KocaoÜlu, and Mustafa Karahan

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Contents

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Rehabilitation and Return to Sports After Conservative and Surgical Treatment of Upper Extremity Injuries . . . . . . . . . . . . . . . . . . . . . . . . Kumaraswami R. Dussa Part IV

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Sports Injuries of the Upper Extremity: Elbow and Wrist Injuries

Sports-Related Elbow Problems . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Luigi Adriano Pederzini, Massimo Tosi, Mauro Prandini, Fabio Nicoletta, and Vitaliano Isacco Barberio

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Chronic Elbow Instabilities: Medial and Lateral Instability. . . . . . . . . . . . . . . . . . . Gazi Huri, Gürsel LeblebicioÜlu, Akın Üzümcügil, Özgür Ahmet Atay, Mahmut Nedim Doral, Tüzün Fırat, ÇiÜdem Ayhan, Deran Oskay, and Nuray Kırdı

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Acute Distal Biceps Tendon Ruptures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Massimo Ceruso and Giuseppe Checcucci

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Common Fractures in Sports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mahmut Kömürcü and Gökhan Çakmak

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Triangular Fibrocartilage Complex Tears in the Athlete. . . . . . . . . . . . . . . . . . . . . . Akın Üzümcügil, Gürsel LeblebicioÜlu, and Mahmut Nedim Doral

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Carpal Instability in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Emin Bal, Murat Kayalar, and Sait Ada

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Part V

Groin Injuries in Sports

Epidemiology and Common Reasons of Groin Pain in Sport . . . . . . . . . . . . . . . . . . Robert Smigielski and Urszula Zdanowicz

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Differential Diagnosis in Groin Pain: Perspective from the General Surgeon. . . . . Volkan KaynaroÜlu and Ali Konan

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Groin Pain in Pediatric Athletes: Perspectives From an Urologist . . . . . . . . . . . . . . Berk Burgu and Serdar Tekgül

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Groin Pain: Neuropathies and Compression Syndromes. . . . . . . . . . . . . . . . . . . . . . Urszula Zdanowicz and Robert Smigielski

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Bone and Joint Problems Related to Groin Pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michal Drwiega

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Part VI

Knee Injuries in Sports: A New Perspective on Meniscal Repair and Replacement

Lateral Meniscal Variations and Treatment Strategies . . . . . . . . . . . . . . . . . . . . . . . Özgür Ahmet Atay, ílyas ÇaÜlar Yılgör, and Mahmut Nedim Doral

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Contents

Mucoid Degeneration and Cysts of the Meniscus . . . . . . . . . . . . . . . . . . . . . . . . . . . . Halit Pınar and Hakan Boya

297

Mechanical Properties of Meniscal Suture Techniques . . . . . . . . . . . . . . . . . . . . . . . Yavuz Kocabey

301

New Technique of Arthroscopic Meniscus Repair in Radial Tears. . . . . . . . . . . . . . Ken Nakata, Konsei Shino, Takashi Kanamoto, Tatsuo Mae, Yuzo Yamada, Hiroshi Amano, Norimasa Nakamura, Shuji Horibe, and Hideki Yoshikawa

305

Meniscus Allograft Transplantation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Christos D. Papageorgiou, Marios G. Lykissas, and Dimosthenis A. Alaseirlis

313

Meniscal Allografts: Indications and Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . René Verdonk, Peter Verdonk, and Karl Fredrik Almqvist

321

Meniscal Substitutes: Polyurethane Meniscus Implant – Technique and Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . René Verdonk

329

New on the Horizon: Meniscus Reconstruction Using MenaflexTM, a Novel Collagen Meniscus Implant . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . William G. Rodkey

335

Collagen Meniscus Implantation in Athletically Active Patients . . . . . . . . . . . . . . . David N.M. Caborn, W. Kendall Bache, and John Nyland

341

Gait Pattern After Meniscectomy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . GüneĜ Yavuzer, Ali Öçgüder, and Murat Bozkurt

349

Part VII

Knee Injuries in Sports: Current Perspectives on Ligament Surgery

Biomechanical Variation of Double-Bundle Anterior Cruciate Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Savio L.-Y. Woo, Ho-Joong Jung, and Matthew B. Fisher

355

Ground Force 360 Device Efficacy: Perception of Healthy Subjects. . . . . . . . . . . . . John Nyland and Ryan Krupp

363

ACL Reconstruction: Timing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carlos Esteve De Miguel

369

Arthroscopic Anterior Cruciate Ligament Repair . . . . . . . . . . . . . . . . . . . . . . . . . . . Gian Luigi Canata

373

Arthroscopic Primary Repair of Fresh Partial ACL Tears . . . . . . . . . . . . . . . . . . . . Erhan Basad, Leo Spor, Henning Stürz, and Bernd Ishaque

379

Contents

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The Evolution and Principles of Anatomic Double-Bundle Anterior Cruciate Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pascal Christel and Michael Hantes ACL Reconstruction: Alternative Technique for Double-Bundle Reconstruction. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Stefano Zaffagnini, Danilo Bruni, Giovanni Giordano, Francesco Iacono, Giulio Maria Marcheggiani Muccioli, Tommaso Bonanzinga, and Maurilio Marcacci

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Double Bundle ACL Reconstruction: “My” Viewpoint . . . . . . . . . . . . . . . . . . . . . . . John A. Bergfeld and Michael A. Rauh

401

All Inside Technique of ACL Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Giuliano Cerulli, Giovanni Zamarra, Fabio Vercillo, Gabriele Potalivo, Alessandro Amanti, and Filippo Pelosi

409

Allografts: General Informations and Graft Sources. . . . . . . . . . . . . . . . . . . . . . . . . Antonios Kouzelis

415

Allografts in Anterior Cruciate Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . Michael I. Iosifidis and Alexandros Tsarouhas

421

Costs and Safety of Allografts. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Athanasios N. Ververidis

431

Role of Allografts in Knee Ligament Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mahmut Nedim Doral, Gazi Huri, Özgür Ahmet Atay, Gürhan Dönmez, Ahmet Güray Batmaz, UÜur Diliçıkık, Gürsel LeblebicioÜlu, and Defne Kaya

439

The Role of Growth Factors in ACL Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Matjaz Vogrin

443

Dealing with Complications in ACL Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . Reha N. TandoÜan, Asım Kayaalp, and Kaan Irgıt

449

Revision ACL Reconstruction: Treatment Options . . . . . . . . . . . . . . . . . . . . . . . . . . Philippe Colombet, Philippe Neyret, and Patrick Dijan and the French Society of Arthroscopy

457

Revision of Failures After Reconstruction of the Anterior Cruciate Ligament. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nuno Sevivas, Hélder Pereira, Pedro Varanda, Alberto Monteiro, and João Espregueira-Mendes Key Points in Revision ACL Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Hamza Özer, Hakan Selek, and Sacit Turanlı

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Contents

Clinical Outcomes and Rehabilitation Program After ACL Primary Repair and Bone Marrow Stimulation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alberto Gobbi, Lorenzo Boldrini, Georgios Karnatzikos, and Vivek Mahajan

475

Return-to-Play Decision Making Following Anterior Cruciate Ligament Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . John Nyland and Emily Brand

485

Evaluation and Treatment of Isolated and Combined PCL Injuries . . . . . . . . . . . . William M. Wind and John A. Bergfeld Posterior Cruciate Ligament Reconstruction, New Concepts and My Point of View . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Lutul D. Farrow and John A. Bergfeld

495

505

PCL Reconstruction: How to Improve Our Treatment and Results. . . . . . . . . . . . . Pier Paolo Mariani and Mohamed Aboelnour Elmorsy Badran

517

Allografts in PCL Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Dimosthenis A. Alaseirlis, Konstantinos Michail, Eleftherios Stefas, and Christos D. Papageorgiou

525

Combined Anterior and Posterior Cruciate Ligament Injuries . . . . . . . . . . . . . . . . Asım Kayaalp, Reha N. TandoÜan, UÜur Gönç, and Kaan S. Irgıt

529

Combined Knee Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Daniel Fritschy

537

How to Manage Anteromedial Knee Instabilities . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gian Luigi Canata

543

Reconstruction of the Posterolateral Corner of the Knee . . . . . . . . . . . . . . . . . . . . . Reha N. TandoÜan and Asım Kayaalp

547

Future Perspectives on Knee Ligament Surgery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kenneth D. Illingworth, Motoko Miyawaki, Volker Musahl, and Freddie H. Fu

555

Part VIII

Knee Injuries in Sports: Update on Patellar Injuries

Patellofemoral Pain Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sinan KaraoÜlu, Volkan Aygül, and Zafer Karagöz Will Sub-classification of Patellofemoral Pain Improve Physiotherapy Treatment?. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michael James Callaghan Conservative Treatment of Patellofemoral Joint Instability . . . . . . . . . . . . . . . . . . . John Nyland, Brent Fisher, and Brian Curtin

565

571

579

Contents

xxiii

Overview of Patellar Dislocations in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . UÜur Haklar and Tekin Kerem Ülkü

585

Arthroscopic Patellar Instability Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mahmut Nedim Doral, Egemen Turhan, Gürhan Dönmez, Özgür Ahmet Atay, Akın Üzümcügil, Mehmet Ayvaz, Nurzat Elmalı, and Defne Kaya

597

MPFL Reconstruction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Masataka Deie and Mitsuo Ochi

605

Part IX

Sports Injuries of Ankle Joint

Tendinopathies Around the Foot and Ankle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Michel Maestro, Yves Tourne, Julien Cazal, Bruno Ferré, Bernard Schlaterer, Jean Marc Parisaux, and Philippe Ballerio

613

Ankle Sprains: Optimizing Return to Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bruce Hamilton, Cristiano Eirale, and Hakim Chalabi

621

Chronic Ankle Instability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bas Pijnenburg and Rover Krips

627

Anterior Ankle Impingement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Matjaz Vogrin and Matevz Kuhta

635

Syndesmosis Injuries in the Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Jason E. Lake and Brian G. Donley

639

Osteochondral Injuries of the Talus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nurettin Heybeli and Önder KılıçoÜlu

649

Treatment of Osteochondral Talus Defects by Synthetic Resorbable Scaffolds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fabio Valerio Sciarretta Hindfoot Endoscopy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . P.A.J. de Leeuw, M.N. van Sterkenburg, and C.N. van Dijk Part X

665

673

Current Trends in Cartilage Repair

Articular Cartilage Biology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . James A. Martin and Joseph A. Buckwalter

685

The Joint Cartilage – The Synovium: “The Biological Tropism” . . . . . . . . . . . . . . . Onur Bilge, Mahmut Nedim Doral, Özgür Ahmet Atay, Gürhan Dönmez, Ahmet Güray Batmaz, Defne Kaya, Hasan Bilgili, and Mustafa Sargon

693

Surgical Treatment of Osteochondral Defect with Mosaicplasty Technique . . . . . . Gilbert Versier, Olivier Barbier, Didier Ollat, and Pascal Christel

701

xxiv

Contents

Arthroscopic Autologous Chondrocyte Implantation for the Treatment of Chondral Defect in the Knee and Ankle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Antonio Gigante, Davide Enea, Stefano Cecconi, and Francesco Greco

711

Second-Generation Autologous Chondrocyte Implantation: What to Expect… . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Johan Vanlauwe and ElizaVeta Kon

721

Second and Third Generation Cartilage Transplantation . . . . . . . . . . . . . . . . . . . . . Alberto Gobbi, Georgios Karnatzikos, and Vivek Mahajan

731

Next Generation Cartilage Solutions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Alberto Gobbi, Georgios Karnatzikos, Norimasa Nakamura, and Vivek Mahajan

739

Scaffold-Free Tissue Engineered Construct (TEC) Derived from Synovial Mesenchymal Stem Cells: Characterization and Demonstration of Efficacy to Cartilage Repair in a Large Animal Model . . . . . . . . . . . . . . . . . . . . . Norimasa Nakamura, Wataru Ando, Kosuke Tateishi, Hiromichi Fujie, David A. Hart, Kazunori Shinomura, Takashi Kanamoto, Hideyuki Kohda, Ken Nakata, Hideki Yoshikawa, and Konsei Shino PRGF in the Cartilage Defects in the Knee Joint . . . . . . . . . . . . . . . . . . . . . . . . . . . . Matteo Ghiara, Mario Mosconi, and Francesco Benazzo Part XI

751

763

Stress Fractures

Epidemiology and Anatomy of Stress Fractures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . Aharon S. Finestone and Charles Milgrom

769

Diagnosis and Treatment of Stress Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Aharon S. Finestone and Charles Milgrom

775

Stress Fractures: Overview . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gideon Mann, Naama Constantini, Meir Nyska, Eran Dolev, Vidal Barchilon, Shay Shabat, Alex Finsterbush, Omer Mei-Dan, and Iftach Hetsroni

787

Jones Fracture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gideon Mann, Iftach Hetsroni, Naama Constantini, Eran Dolev, Shay Shabat, Alex Finsterbush, Vidal Barchilon, Omer Mei-Dan, and Meir Nyska

815

Tarsal Navicular Stress Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gideon Mann, Iftach Hetsroni, Naama Constantini, Eran Dolev, Shay Shabat, Alex Finsterbush, Vidal Barchilon, Omer Mei-Dan, and Meir Nyska

821

Sesamoid Stress Fractures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gideon Mann, Iftach Hetsroni, Naama Constantini, Eran Dolev, Shay Shabat, Alex Finsterbush, Vidal Barchilon, Omer Mei-Dan, and Meir Nyska

829

Foot and Ankle Stress Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Sakari Orava and Janne Sarimo

833

Contents

xxv

Stress Fractures in Military Population. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Gilbert Versier, Didier Ollat, Dominique Lechevalier, and François Eulry

843

Stress Fractures in Military Personnel of Turkish Army. . . . . . . . . . . . . . . . . . . . . . Mustafa BaĜbozkurt, Bahtiyar Demiralp, and H. Atıl Atilla

853

Various Modalities to Hasten Stress Fracture Healing. . . . . . . . . . . . . . . . . . . . . . . . Iftach Hetsroni and Gideon Mann

859

Part XII

Muscle and Tendon Injuries

Tendinopathies in Sports: From Basic Research to the Field . . . . . . . . . . . . . . . . . . Kai-Ming Chan and Sai-Chuen Fu Thigh Muscle Injuries in Professional Football Players: A Seven Year Follow-Up of the UEFA Injury Study . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Jan Ekstrand

865

871

Chronic Muscle Injuries of the Lower Extremities in Sports . . . . . . . . . . . . . . . . . . Marc Rozenblat

877

Tennis Leg. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Kristof Sas

883

New Protocol for Muscle Injury Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Tomás F. Fernandez Jaén and Pedro Guillén García

887

Shockwave Therapy in Sports Medicine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Marc Rozenblat

895

Growth Factors: Application in Orthopaedic Surgery and Trauma. . . . . . . . . . . . . M. Garcia Balletbo and Ramon Cugat

901

Minimally Invasive Surgery for Achilles Tendon Pathologies . . . . . . . . . . . . . . . . . . Nicola Maffulli, Umile Giuseppe Longo, and Vincenzo Denaro

909

Endoscopy and Percutaneous Suturing in the Achilles Tendon Ruptures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mahmut Nedim Doral, Egemen Turhan, Gürhan Dönmez, Akın Üzümcügil, Burak Kaymaz, Mehmet Ayvaz, Özgür Ahmet Atay, M. Cemalettin Aksoy, Defne Kaya, and Mustafa Sargon Part XIII

917

Sports and Arthroplasty

Osteoporosis and Sports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . O. ěahap Atik

927

Sports After Total Knee Prosthesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Nurettin Heybeli and Cem ÇopuroÜlu

931

xxvi

Contents

Treatment of Pain in TKA: Favoring Post-op Physical Activity . . . . . . . . . . . . . . . . Maria Assunta Servadei, Danilo Bruni, Francesco Iacono, Stefano Zaffagnini, Giulio Maria Marcheggiani Muccioli, Alice Bondi, Tommaso Bonanzinga, Stefano Della Villa, and Maurilio Marcacci

937

Pain Management in Total Knee Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Paolo Adravanti, Francesco Benazzo, Mario Mosconi, Mattia Mocchi, and F. Bonezzi

941

Lateral Unicompartmental Knee Replacement and Return to Sports . . . . . . . . . . . Kevin D. Plancher and Alberto R. Rivera

945

The Arthroscopic Treatment of Knee Osteoarthritis in Sport Patients . . . . . . . . . . Carlos Esteve de Miguel

955

Sports Injuries of the Hip Region. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Ömür Çag˘lar and Mümtaz Alpaslan

957

Total Hip Arthroplasty and Sport Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Roberto Binazzi

963

Sports After Total Hip Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Bülent Atilla and Ömür Çag˘lar

967

Musculoskeletal Tumors and Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mehmet Ayvaz and Nicola Fabbri

973

Anesthesia Managements for Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Fatma SarıcaoÜlu and Ülkü Aypar

981

Part XIV

Pediatric Sports Injuries

Pediatric Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Özgür Dede and Muharrem Yazıcı

989

Prevention of Sports Injuries in Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Mario Mosconi, Stefano Marco Paolo Rossi, and Franco Benazzo

995

Physeal Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Salih Marangoz and M. Cemalettin Aksoy

999

Pediatric Spine Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1007 Deniz Olgun and Ahmet Alanay Lumbar Injuries in Pediatric Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1013 Emre AcaroÜlu and íbrahim Akel Management of Patellofemoral Problems in Adolescents . . . . . . . . . . . . . . . . . . . . . 1017 Semih AydoÜdu

Contents

xxvii

ACL Injuries in Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1023 Romain Seil, Philippe Wilmes, and Dietrich Pape ACL Reconstruction in Children and Adolescents . . . . . . . . . . . . . . . . . . . . . . . . . . . 1033 José F. Huylebroek Part XV

Extreme Sports and Sport Specific Injuries

Abdominal Injuries: Decision Making on the Field . . . . . . . . . . . . . . . . . . . . . . . . . . 1043 Cristiano Eirale, Bruce Hamilton, and Hakim Chalabi Spine Injuries in Sports . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1049 Feza Korkusuz Vascular Problems in Athletes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1055 Piotr Szopiāski and Eliza Pleban Deep Vein Thrombosis in Athletes: Prevention and Treatment . . . . . . . . . . . . . . . . 1065 Faik AltıntaĜ and ÇaÜatay Uluçay Does Injury Rate Affect a Football Team’s Level of Play? Injury Report from Turkey. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1073 Mehmet Serdar Binnet, Onur Polat, and Mehmet Armangil Archery-Related Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1081 Volkan Kaynarog˘lu and Yusuf Alper Kılıç Cricket-Associated Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1087 Chakra Raj Pandey Adventure Sports Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1093 Omer Mei-Dan, Erik Monasterio, and Michael R. Carmont Nutrition Practice of the Race Across America Winner: A Case Report. . . . . . . . . 1103 Bojan Knap Ultra-Marathon Lower Limb Injuries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1109 Iftach Hetsroni and Gideon Mann Motorsport Injuries, Current Trends and Concepts . . . . . . . . . . . . . . . . . . . . . . . . . 1113 Laszlo Gorove Driver as a High Level Athlete . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1121 Fatih Küçükdurmaz Part XVI

Role of Physiotherapy in Orthopaedic Sports Medicine

Early Rehabilitation After Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1127 ínci Yüksel and Gizem írem Kinikli

xxviii

Contents

Late-Term Rehabilitation After Surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1131 Filiz Can Return to Sport Activities . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1145 Volga Bayrakcı Tunay How Can We Strengthen the Quadriceps Femoris in Patients with Patellofemoral Pain Syndrome? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1157 Defne Kaya, Hande Güney, Devrim Akseki, and Mahmut Nedim Doral Patellofemoral Taping and Bracing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1163 ínci Yüksel Part XVII

Future of Sports Trauma

Clinical Relevance of Gene Therapy and Growth Factors in Sports Injuries . . . . . 1171 ílhan Özkan Future Trends in Sports Traumatology: The Puzzling Human Joint . . . . . . . . . . . . 1177 Gabriel Nierenberg, Michael Soudry, and Gila Maor A Tissue-Engineered Approach to Tendon and Ligament Reconstruction . . . . . . . 1185 Patrick W. Whitlock, Thorsten M. Seyler, Sandeep Mannava, and Gary G. Poehling Bioactive Radiofrequency Effects on Ligament and Tendon Injuries . . . . . . . . . . . 1193 Terry L. Whipple and Diana Villegas Wireless Arthroscopy: The Wireless Arthroendoscopy Device (Dr. Guillen’s WAD Invention) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1201 Pedro Guillén García, Antonio López Hidalgo, Marta Guillén Vicente, Jesús López Hidalgo, Isabel Guillén Vicente, Miguel López Hidalgo, and Tomás Fernandez Jaén Orthopaedic Research in the Year 2020. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1209 Savio L.-Y. Woo and Kwang E. Kim Part XVIII

Miscellaneous

Scintigraphic Applications in Sports Traumatology. . . . . . . . . . . . . . . . . . . . . . . . . . 1219 Meltem ÇaÜlar Analytical Methods for Studying Sports Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1229 Turhan Mentes¸ and Mutlu Hayran Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1237

Part Introduction and History of Sports Traumatology

I

The History of EFOST Mahmut Nedim Doral

After the First World Congress of Sports Traumatology which was held in Palma de Mallorca in May 1992, Dr. Hans Paessler from Germany and Dr. Jean-Claude Imbert from France suggested the idea of founding a new organization in Europe dealing with Sports Traumatology, based on the association of different nations through north, east, south, west, or middle of Europe. This was a formation of an amalgam in sports trauma consisting of national sports trauma societies from the different European countries. This new group was planned to be a “Federation,” not an individual society with the purpose of coordinating and improving knowledge on sports-related injuries. So, the creation of EFOST (European Federation of Orthopaedic National Association for Sport Traumatology) was completed in Munich by the initiatives of French and German National Societies (SFPTS and GOTS) (Figs. 1 and 2). With the aim of promoting a “Federation” on sports traumatology as an independent specialty within Europe, the founders contacted the National Sport Trauma Associations, and the first General Assembly of EFOST was held in Santa Margareta di Liguria, Genova (Italy) at Hotel Miramare in September 1993 with the participation of Jean-Marie Baillon (Belgium), Jean-Claude Imbert (France), Wolfgang Pförringer, Hans H. Paessler (Germany), Pantelis Nikolaou, Georgis Priftis, Nikolaos Piscopakis (Greece), Filippo Rettagliata (Italy), Arthur Dziak (Poland), Jose M. Vilarrubias (Spain), and me as delegates. A constitution for the European Federation of National Associations of Orthopaedic Sports Traumatology (EFOST) was accepted as a conclusion of this inaugural general assembly. The mission of EFOST was determined as bringing the Sport Traumatology chapter under the name of “Federation” together, spreading its concept throughout Europe and creating new ones in the countries with no such organizations. Jean-Claude Imbert was

M.N. Doral Faculty of Medicine, Department of Orthopaedics and Traumatology, Chairman of Department of Sports Medicine, Hacettepe University, Hasırcılar Caddesi, 06110 Ankara, Sihhiye, Turkey e-mail: [email protected]

elected as the first president of EFOST. The second general assembly was held at the second congress of the European Federation of National Association of Orthopaedics and Traumatology (EFORT) in 1995 in Munich and Giuliano Cerulli (1995–1997) was elected as the new president of EFOST by a unanimous vote. Dr. Huylebroek, Dr. Benazzo, and Dr. Biosca were the pioneers of EFOST. The first Specialty Day Meeting at EFORT Congress in Munich was followed by the other EFORT meetings in 1997 Barcelona, in 1999 Brussels and in 2001 Rhodes. Hans H. Paessler (1997–1999), Mahmut Nedim Doral (1999–2002), Paco Biosca (2002–2004), Franco Benazzo (2004–2007), and José Huylebroek (2007–2010) served EFOST as presidents. EFOST has organized six Congresses until now: Munich 2001, with GOTS, Congress President Dr. Hans H. Paessler, Monaco 2003, Congress President Dr. Jean-Claude Imbert

Fig. 1 EFOST logo was created by Dr. Hans Paessler

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_1, © Springer-Verlag Berlin Heidelberg 2012

3

4

Fig. 2 Official medallion of EFOST

(Fig. 3), Madrid 2004, Congress Presidents Dr. Pedro Guillen and Dr. Paco Biosca, Pavia 2006, Congress President Dr. Franco Benazzo, Antalya 2008, Congress President Dr. Mahmut Nedim Doral and the 6th organization is was

Fig. 3 Board of Trustees at Monaco 2003: (from left to right) J Borrel (Spain), R Smigielski (Poland), F Benazzo (Italy), JC Imbert (France), E Brunet (France), P Lobenhoffer (Germany), MN Doral (Turkey), P Biosca (Spain), J Huylebroek (Belgium), F Kelberine (France)

M.N. Doral

held in Brussels in 2010 with Dr. Jose Huylebroek as President. With the outstanding energy of Dr. Huylebroek, Brussels Meeting of EFOST was one of the best scientific exchange and social activities in the heart of Europe on sports traumatology. The current President of EFOST is now Dr. François Kélbérine from France and the EFOST 2012 Meeting will be combined with the World Trauma Sports Meeting by the organization of Dr. Roger Hackney and Dr. Nicola Maffulli from the UK. A lot of things have been carried out since 1993 which we still study for the development of EFOST. E-journal, Fellowship programs that are organized by Dr. Kélbérine, improving relationships with national sports traumatology societies, having more comprehensive website, E-journal and preparing continuous E-Newsletter are other current activities of EFOST. Dr. William Wind and Dr. Michael Rauh from the USA were the first two scholars of the EFOST fellowship program in 2008 and they took interest in presenting their experiences in Belgium, Italy, France, and Turkey with senior orthopedic surgeons in the fifth EFOST Meeting. We are quite sure that the new elected candidates, Dr. Omer Mei-Dan (Israel) and Dr. Mike Carmont (UK), will be great representatives of the European Sports Medicine Surgeons! I believe that EFOST family will grow more and more and they will provide a very good concept for Sports Traumatology by working in cooperation with the international associations or societies like ISAKOS, ESSKA, AOSSM, SLARD. With the help of these kinds of societies, we will be able to get into the internationally standardized concepts for the treatment of the athletes and improve that concept in Europe and the entire world.

The Past and the Future of Arthroscopy Hans H. Pässler and Yuping Yang

Content A Main Timeline of Arthroscopic Development During the Twentieth Century ................................................................

13

H.H. Pässler ( ) Center of Knee and Foot Surgery, Sports Traumatology, Atos-Klinik, Bismarckstrasse 9-15, D-69115, Heidelberg, Germany e-mail: [email protected], [email protected] Y. Yang Institute of Sports Medicine, The Third Hospital of Peking University, North Garden Road 49, 100083 Beijing, China e-mail: [email protected]

In addition to joint replacement and internal fixation of fractures, arthroscopic surgery is regarded as one of the three greatest improvements in the diagnosis and treatment of patients with conditions affecting the musculoskeletal system during the twentieth century. Unlike the other two, arthroscopy is the most minimally invasive surgical approach. Arthro means joint and scope to view from the Greek root. Arthroscopic surgery always uses tiny incisions that allow the introduction of an arthroscope or other instruments into a joint, and it has origins in the early nineteenth century. Curiosity and the desire to examine the body cavities can be traced back to ancient times with evidence of the use of the vaginal speculum and proctoscope in the ruins of Pompeii. In 1806 Philipp Bozzini, a German doctor from Frankfurt, presented his Lichtleiter, the first cystoscope developed to study the inside of the urinary bladder (Fig. 1). The Lichtleiter used two tubes with a candle to observe the inside of the bladder. In 1853, the French physician Desormeaux further refined the cystoscope, using a mixture of turpentine and gasoline, which when ignited in a small chamber produced light that was reflected through a system of mirrors into the bladder to provide visualization. The cystoscope utilized by Desormeaux is considered by medical historians to be the earliest endoscopic instrumentation (Fig. 2). J. Bruck, who was reportedly a dentist, transilluminated the bladder from the rectum, using a “diaphanoscope” in 1860, which essentially was a red hot or glowing wire encased in a quill. Dentists were involved because bladder stones were often thought to be similar to teeth and only dentists were trained to handle these hard tissues. In 1876, the German Max Nitze introduced a cystoscope that used a heated platinum loop to look inside the bladder. His first demonstration in public took place in October 1877 in the Institute of Pathology of the University Clinic in Dresden, where Michael Burman also performed his arthroscopic studies 54 years later (see below). These primitive endoscopes were made safer in 1879 with Edison’s invention of the light bulb, replacing Desormeaux’s turpentine/gasoline mixture and Nitze’s heated loop, with incandescent light as a source for cystoscopic illumination of the bladder (Fig. 3). The introduction of these early endoscopes

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_2, © Springer-Verlag Berlin Heidelberg 2012

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Fig. 1 Dr. Philipp Bozzini and his Lichtleiter

1806

BOZZINI 1779-1809

Lichtleiter im Schnitt (von oben gesehen) Section du “guide de lumiere” (vue d’en haut) Sectional view of “light transmitter”

1853

DESORMEAUX 1815-1894

Fig. 2 Dr. Desormeaux and his endoscope

provided medical science with a method of visualization using light and mirrors to examine anatomical structures in a new way. Furthermore, Nitze took the very first photograph of the interior of a bladder in 1890. The development of this groundbreaking technique to inspect the human body would have far-reaching applications in the twentieth century. The first recorded application of an endoscope to the inside of a knee joint occurred in 1912, when the Danish

Im Schnitt (von oben gesehen) Section (vue d’en haut) Sectional view

physician Dr. Severin Nordentoft from Aarhus (Fig. 4), used a laparoscope developed by the Swedish professor of internal medicine, Hans Christian Jacobeus together with the company, Georg Wolf, Berlin, Germany (Fig. 5) to examine the interior of knees and presented his work at the 41st Congress of the German Surgical Society in Berlin. It is he who first called this procedure “arthroscopy.” There is no question, from the written description in the published

The Past and the Future of Arthroscopy

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Fig. 3 Dr. Max Nitze and his heated loop endoscopes

1879

NITZE 1848-1906

1877 Dresden

1879 Wien

Optik herausgezogen Optique retirée Telescope removed

abstract, about the fact that he was really the first to look inside a knee joint. However, there was no indication in his presentation that he used the instrument clinically. The Japanese professor Kenji Takagi was credited in 1918 with using a cystoscope to view the inside of a cadaver knee (Fig. 6). His early attempts to develop an arthroscope resulted in an instrument that was 7.3 mm in diameter and much too large to be practical in the knee. Takagi continued to refine the cystoscope, so that by 1931 he had developed the No. 1 arthroscope, a 3.5-mm instrument that was to become the model for present-day arthroscopes (Fig. 7). Takagi created 12 different arthroscopes, No. 1 to No. 12, with varying angles of view, along with operative instruments small enough to perform rudimentary surgery, such as biopsy within the knee joint. In the Western world, a Swiss physician, Eugen Bircher, performed an arthroscopy in 1921, using an abdominal laparoscope like Nordentoft. Bircher published the first articles regarding arthroscopy of the knee, referring to this technique as arthroendoscopy (Fig. 8). It is interesting that Bircher never referred to Nordentoft, although they both presented their technique at the annual congress of surgery in Berlin. Bircher used this technique as a prelude to arthrotomy. Comparable to laparoscopy, he filled the joint with nitrogen or oxygen primarily to visualize and diagnose such conditions as internal derangement. His articles published between 1921 and 1926 were based on approximately 60 arthroendoscopic procedures. However, by 1930, Bircher abandoned

arthroendoscopy in favor of air arthrography, citing better visualization using contrast media with radiographic images. With their earliest contribution to arthroscopy, Takagi and Bircher are regarded as the “fathers of arthroscopy” by many historians. In 1931, Michael Burman, a young resident at the Hospital for Joint Diseases in New York began to use an arthroscope in the anatomy laboratory of New York University, having had a special instrument designed for him by a Mr. R. Wappler. But later, he had to go to Europe on a traveling scholarship in the spring of 1931 to continue his studies because there was no chance for further studies in the New York University for him. He studied under Professor George Schmorl, the renowned pathologist and director of the Institute of Pathology in Dresden, Germany (Figs. 9 and 10). A study of the effect of dyes injected into the joint cavity on degenerative joint cartilage was initiated in Dresden and was a research venture that Burman continued later in clinical trials of arthroscopy on live patients. In the autumn of 1931, Burman returned to New York and published the results of his investigation in the historical paper “Arthroscopy or the Direct Visualization of Joints” (Fig. 11). He also printed 20 colored aquarelles of endoscopy findings in different joints. These were painted by the medical artist of the Dresden Institute, Mrs. Frieda Erfurt, and were actually the first pictures of arthroscopic findings ever published. Michael Burman went on to become an

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Fig. 4 Dr. Severin Nordentoft from Aarhus Denmark

Fig. 5 Jacobaeus Laparoscope (Georg Wolf Company, Berlin, Germany)

H.H. Pässler and Y. Yang

Fig. 6 Japanese professor Kenji Takagi, “father of arthroscopy,” who was the first to view the inside of cadaver knee in 1918, using the cystoscope

The Past and the Future of Arthroscopy

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Fig. 7 Takagi’s No. 1 arthroscope

Fig. 8 Dr. Eugen Bircher performing a knee surgery with his arthroscopy in 1917. Gas was used to fill up the joint

Fig. 9 Dr. Michael Burmann 1901–1975

orthopedic surgeon and worked at the Hospital for Joint Diseases in New York throughout his professional life. During the 1950s he collected material for an Atlas of Arthroscopy, but this was never published, as he could not find an editor who appreciated his work. However, World War II delayed advancements in medical science, and it took 16 years after the end of the war to resume publication of articles reporting the progress in arthroscopic surgery.

By now in Japan, a protégé of Takagi’s, Masaki Watanabe, established himself as the “father of modern arthroscopy” by developing sophisticated endoscopic instruments, using electronics and optics, which became popular in Japan in the postWorld War II era (Fig. 12). Watanabe’s No. 21 arthroscope developed in 1959 was superior in quality and became a model for production (Fig. 13). Watanabe’s No. 21 was the instrument by which North American surgeons developed their skills in surgical arthroscopy. Yet, in spite of increasing improvements,

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Fig. 10 Burmann’s laboratory, Institute of Pathology in Dresden, Germany

VOL. XIII, NO. 4 OCTOBER, 1931

Old Series Vol. XXIX. NO. 4

The Journal of Bone and Joint Surgery

ARTHROSCOPY OR THE DIRECT VISUALIZATION OF JOINTS AN EXPERIMENTAL CADAVER STUDY* BY MICHAEL S. BURMAN, M.D., NEW YORK, N. Y. Scholar of the Henry W. Frauenthal Travel Scholarship, Hospital for joint Diseases

Fig. 11 Dr. Burmann published the results of his investigation in the historical paper “Arthroscopy or the Direct Visualization of Joints” in 1931

the No. 21 arthroscope had its disadvantages. Since the light carrier would short-circuit and the bulb would occasionally shatter in the knee, it would not be until the 1970s and the introduction of cold light fiberoptics that arthroscopes would become safe and dependable. The transition from simply a diagnostic tool to therapeutic modality can also be credited to Watanabe, who arthroscopically removed a xanthomatous tumor from the superior recess of the knee on March 9, 1955. He subsequently performed the first arthroscopic partial meniscectomy on May 4, 1962 (Fig. 14a–c). Watanabe was a true scientist and a great teacher. He freely gave his knowledge to whoever was interested. He wrote the first Atlas of Arthroscopy, which was published in English in 1957, and which was beautifully illustrated by Fujihashi (Fig. 15) His second Atlas of Arthroscopy was published in 1969 with illustrated color photographs of the interior of the joint. Dr. Ikeuchi has continued his great work to this day. In 1969, Dr. Richard O’Connor visited and studied with Watanabe. With the help of Richard Wolf Instrument

Fig. 12 Masaki Watanabe, the “father of modern arthroscopy”

Company in 1974, O’Connor developed instruments and arthroscopes that enabled him to do the first partial meniscectomies in North America. O’Connor introduced the first rod lens type operating arthroscope, thereby solidifying arthroscopy as a surgical treatment of joint pathology. O’Connor and Hiroshi Ikeuchi, a Watanabe colleague from Japan, popularized arthroscopy to include not only meniscectomy but meniscal repair as well. Another significant contribution to arthroscopic surgery can be attributed to Dr. Lanny Johnson, who with the assistance of Dyonics Corporation developed the first motorized shaver instruments in 1976. Dr. Johnson is also regarded as a pioneer in arthroscopic shoulder surgery and rotator cuff repair. Dr. John Joyce III, organized the first arthroscopy course in 1972 at the University of Pennsylvania. By 1974, the course was repeated and the International Arthroscopy Association was founded. By 1982, the Arthroscopy Association of North America was established promoting education and practice in arthroscopic surgery and has become one of the largest subspecialty organizations in orthopedics today. A boom to surgical arthroscopy in the 1970s came with the development of fiber optics and the use of television technology. Visibility improved with fiber optic light cables, and the television monitor allowed surgeons to view the image on a screen rather than rely on direct visualization with the eye

The Past and the Future of Arthroscopy

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Fig. 13 Watanabe’s No. 21 arthroscope

a

c

b

Fig. 14 (a) First surgery of arthroscopic partial meniscectomy was finished by Masaki Watanabe in 1962. (b) The tearing medial meniscus in the joint. (c) The abscised specimen of tearing meniscus

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Fig. 15 First Atlas of Arthroscopy 1957, the first edition by Watanabe

Fig. 16 3-D-arthroscopy Knittlingen, Germany)

(Richard

Wolf

Company,

through the arthroscope, freeing their hands. Television-guided imaging has helped facilitate such procedures as ligament reconstruction with minimally invasive techniques. As arthroscopic technology has advanced, the scope of treatable conditions has expanded. Today, virtually every joint in the human body can be accessed via arthroscopy. The 1980s and 1990s heralded advances in arthroscopic procedures and instrumentation that allowed orthopedists to treat disease and injury with minimally invasive incisions, further decreasing complications, downtime, and medical costs for patients with musculoskeletal disorders. Surgical arthroscopy evolved into a major therapeutic modality, rather than merely a diagnostic tool. By the mid-1980s, data showed that surgical techniques using arthroscopy were actually superior to open operative surgery. No longer would patients have to undergo debilitating and painful surgery with extensive incisions. When indicated, arthroscopy would become the preferred method of surgical treatment over conventional, old-fashioned procedures. What will be the future of arthroscopy? What are the desires of the surgeons? A three dimensional vision would be great, especially in cruciate ligament reconstructive surgery (Fig. 16). Furthermore, a manual movable optic, which can be turned from 0° to 90°, would help the surgeon significantly. For 20 years, the industry has been trying to develop these scopes, but till now it has not been of any practical use. VRATS – Virtual-Reality-Arthroscopy-Trainings simulator are coming up, but are not yet used for most of the current training workshops.

The Past and the Future of Arthroscopy

A Main Timeline of Arthroscopic Development During the Twentieth Century 1912 – Danish surgeon Severin Nordentoft presented a paper on endoscopic findings within the knee using a technique, which he named “arthroscopy”. 1918 – Japanese professor Kenji Takagi examined a cadaver knee with a cystoscope. 1921 – Swiss physician Eugen Bircher performed an arthroscopy, using an abdominal laparoscope. 1931 – Takagi developed the No. 1 arthroscope, a 3.5-mm instrument that would become the model for present-day instruments. Dr. Burmann published the results of his investigation in the historical paper “Arthroscopy or the Direct Visualization of Joints”.

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1959 – Watanabe developed sophisticated instruments using electronics and optics, and his No. 21 arthroscope became a model for production. 1962 – Watanabe performed the first partial meniscectomy in Japan. 1972 – Dr. Joyce taught the first arthroscopy course in the USA at the University of Pennsylvania. 1974 – Dr. Richard O’Connor performed the first partial meniscectomy in North America. The International Arthroscopy Association was founded. 1982 – The Arthroscopy Association of North America was established.

Treatment of Athletic Injuries: What We Have Learned in 50 Years Giuliano Cerulli

Over the past 50 years orthopedic surgery and traumatology have been divided into different sectors. Scientific societies, specific journals, books, sub-speciality research groups, congresses and courses, as well as teaching centers have been organized. Sport traumatology must be supported by a complex set of knowledge obtained by applying scientific methodology in order to gain a precise description of reality; we call this “Science.” As Galileo Galilei said “Science separates what we know from what we do not know.” However, sometimes human activity based on technical solutions, natural skills, or behavior deriving from experience, which is called “Art,” hides Science. Today, in sport traumatology, we must be scientific in our approach. The study of the biomechanics of the human body has led us to the functional biomechanical evaluations of athletes, allowing us to observe different parameters such as the proprioceptive system, joint stability, and muscle strength during sport-specific movements; the biological and tissue mechanics applied to sport as well as the morphofunctional study of athletes. These methods allow us to quantify important parameters before, during, and at the end of the sports

season. On the basis of these parameters we can implement prevention programs and personalize rehabilitation to restore the normal condition of each athlete in case of injury. In anterior cruciate ligament reconstruction (ACL-R), we do not know exactly the advantages of the different techniques (i.e., single bundle and double bundle) since, as Savio Woo has shown in his studies, so many variables affect the ACL-R as well as the role of associated lesions that significantly influence the outcome of the ACL-R. Concerning cartilage treatment – I would say that most of the novelties on this topic are pure Art, and few are Science. Hence, we must be very careful when we promise a rapid return to sport or excellent results in tissue repair, we must respect the laws of tissue biology and the healing process, the athlete’s individual characteristics, as well as the biomechanics of the sport being practiced. Today, after 50 years of sport traumatology, some aspects are Art and some are Science. Our goal must be to make sport traumatology 100% Science. In order to do this, we must use precise scientific methods in planning research projects under the guidance of true scientific commitment.

G. Cerulli Department of Orthopedics and Traumatology, School of Medicine University of Perugia and Let People Move, Via GB Pontani 9, 06128 Perugia, Italy e-mail: [email protected], [email protected] M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_3, © Springer-Verlag Berlin Heidelberg 2012

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Part Prevention of Sports Injuries

II

Biomechanical Measurement Methods to Analyze the Mechanisms of Sport Injuries Serdar Arıtan

Introduction

Contents Introduction .................................................................................

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Video Analysis Software .............................................................

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Motion Analysis Software ..........................................................

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Biomechanical Modeling ............................................................

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Classical Mechanics ....................................................................

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Choosing a Method for Deriving the Equations of Motion .............................................................

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Methodology of Biomechanical Modeling ................................

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How to Calculate .........................................................................

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Examples for Biomechanical Modeling.....................................

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Finite Element Modeling ............................................................

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Conclusion ...................................................................................

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References ....................................................................................

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The performance of an athlete is affected by numerous factors. These can be roughly grouped into three categories which are physiological, biomechanical, and psychological factors. Biomechanical factors have a profound effect on how an athlete controls and compensates movement patterns during the performance of a movement or series of movements. From a biomechanical point of view, these compensations often lead to faulty movement patterns, which decrease the sports performance. For example, if a javelin thrower had an overactive infraspinatus muscle in the shoulder, it would significantly affect the thrower’s ability to deliver a consistent high velocity throw. This is due to the shoulder’s inability to control the arm at high speed before and after the throw. The same concept applies to all arm-related events, such as golf and tennis.

Video Analysis Software

S. Arıtan Biomechanics Research Group, School of Sports Science & Technology, Hacettepe University, 06800 Ankara, Turkey e-mail: [email protected]

In order to overcome such a problem, a video analysis system can be a simple solution for athletes and their medical and training team. It helps them come to a common place in an effort to collaborate in accomplishing an athlete’s biomechanical needs. The main purpose of such an analysis is to identify an athlete’s biomechanical or movement dysfunction by using video analyses of his/her sport as well as breaking down the fundamental parts of the movement to expose the problem part that is contributing to injury and/or decreased performance. Video analysis software is one of the common tools that is used to capture, edit, and analyze various sport motions to find the weak parts in the movement which may cause injury, pain, or a drop in the performance. By using stroboscopic image extraction method in the video analysis, an athletic movement can be unfolded in time and space by compounding video images into a frame-by-frame of static images along the athlete’s trajectory. A typical output of video analysis software can be seen in Fig. 1. From this information, athletes can develop the strength and conditioning specific to

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_4, © Springer-Verlag Berlin Heidelberg 2012

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Fig. 1 Stroboscopic image extraction of triple jump movement from video recording

their movements and their sport. They can also receive suggestions and corrective exercises from the medical team to decrease the risk of injury. There are, however, shortcomings of the video analyses that cannot be ignored in some cases. Video analysis software happens to be an ineffective tool if exact position, velocity, or acceleration of an athlete’s body or his/her equipment is required for a biomechanical analysis.

Motion Analysis Software A motion analysis system enables one to record movement and then to measure positions, angles of joints, speed and distance of movement, and to compare the same movements performed at different times. Such an analysis gives the athlete or the physician clear information on the reasons of injury, muscle weakness, and degree of improvement. In general, this methodology is called Human Motion Analysis (HMA). Nowadays, the methods can be brought together as whole under the definition of marker-based methods, which are the main methods in the laboratory and clinical environments. Marker-based methods are defined as methods that rely on anatomically positioned markers recorded by camera systems. These systems work by measuring the location of markers attached to the subject. Then, in the case of a three-dimensional (3D) system, using a mathematical procedure the views from several cameras are integrated to form a 3D representation of those markers in space. Camera systems can also be classified into two main streams, which are near-infrared spectrum (it is commonly called as infrared – IR) and visible spectrum cameras. Depending on the camera type, tracing of the markers can be done manually or automatically. Because of the ease in using threshold processing in the IR cameras, infrared reflective markers are used to collect spatial–temporal and kinematic data in the most modern commercial IR camera-based motion capture systems. Whether these modern systems use automatic tracking or manual, their output is the 3D positions of the markers (e.g., ProReflex from Qualisys, Sweden; Motion Analysis from Motion Analysis

Corporation, USA; Simi Motion from SIMI Reality Motion Systems, Germany; HUBAG from Hacettepe University, Turkey). This allows the calculation of marker displacement, angles, velocities, and accelerations, etc. A movement of the rendered 3D stick figure or skeleton representation of human body can be the typical output of HMA. As an example of HMA, a trajectory of selected anthropometric point during back somersault movement can be seen in Fig. 2. The main disadvantage of the automatic tracking systems with IR cameras is that these systems can only work on controlled artificial lighting environment. The system does not work on direct or indirect sunlight, even though in the controlled environment reflective shiny spots in the camera view can be mistaken by the system as markers. Additionally, these systems are usually fixed in the laboratory environment and cannot be easily moved if an experiment requires a different location. Therefore, these systems are limited to some movements that can only be performed in the laboratory environment.

Biomechanical Modeling It is, however, viable to obtain all kinematics variables in a movement by utilizing HMA; it is not possible to measure forces that caused the movement. In order to measure the force inside a human body, a surgical operation is required to implement a force transducer. In addition to technical complications and calibration problems of force transducer, the subject would also be at risk of surgical infections. Therefore, modeling in biomechanics works as an interface between the body and measurement settings. In recent years, biomechanical modeling has become very popular in the area of sports biomechanics. Recent developments in software and hardware in the computer technology could potentially explain this popularity. Developing a biomechanical model itself improves the understanding of the mechanical system’s dynamics and the structure. On the other hand, most of the biomechanical systems are so complicated that a satisfying modeling seems extremely difficult.

Biomechanical Measurement Methods to Analyze the Mechanisms of Sport Injuries

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Fig. 2 Stick figure output of back somersault movement

One standard solution is that the complexity can be reduced by cutting down some part of the system to be modeled. A well-prepared model must be simple but yet adequately detailed to precisely represent the system. Considering the system components (i.e., limbs of the human body) as a rigid body, rather than a deformable body also helps to reduce the complexity of the model. Although, in reality, no material is absolutely rigid, deformation of limbs in sports movement can be ignored, when compared to the gross motion of the system. Basically, there are two types of approaches in biomechanical modeling. The first one is inverse dynamics and the second one is forward dynamics or direct dynamics. Inverse dynamics calculation is used to determine joint forces and torques based on the physical properties of the system being modeled and a time history of displacements from experimental kinematic data, including velocities and accelerations. Ground reaction forces, mass and inertial characteristics of segments are also required in this method. In a forward dynamical analysis, the joint torques are the inputs and the body motion is the output. It is critical to understand what generates this joint torques. Joint torques are the addition of internal body forces such as ligaments, joint constraints, and of course, muscle forces. Muscles are the actuators in this method. Therefore, the correct input into the model is definitely neural input, which drives the muscles.

particle that can be treated by Newton’s equations, which was published in 1686 in his “Philosophiae Naturalis Principia Mathematica” [15]. The rigid body that is a key element in the modeling was introduced in 1775 by Euler in his contribution entitled “Nova methodus motum corporum rigidarum determinandi” [10]. Euler already used the free body principle for the modeling of joints and constraints, which resulted in reaction forces. Thus the equations obtained are known in human body dynamics as Newton–Euler equations. In 1743, D’Alembert distinguished between applied and reaction forces in a system of constrained rigid bodies in his book entitled “Traité de Dynamique” [7]. He called the reaction forces “lost forces” having the principle of virtual work in mind. A systematic analysis of constrained mechanical systems was also established in 1788 by Lagrange [13]. The variational method applied to the total kinetic and potential energy of the system considering its kinematical constraints and the corresponding generalized coordinates result in the Lagrangian equations of the first and the second kind. Lagrange’s equations of the first kind represent a set of differential algebraical equations in Cartesian coordinates with undetermined Lagrange multipliers, while the second kind leads to a minimal set of ordinary differential equations in generalized Lagrange coordinates.

Choosing a Method for Deriving the Equations of Motion Classical Mechanics Whichever approach is used for modeling, first of all, the equation of motion has to be derived. The dynamics of biomechanical systems is based on classical mechanics. The simplest element of a multi-body biomechanical system is a free

s Lagrangian Dynamics Lagrange’s equations of motion are specified in terms of the total energy of the body in the kinematic chain. With this formulation, forces between bodies (equal and opposite) do not need to be considered because these forces do not add

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energy to the system. Although the equations of motion are generally easy to formulate, this method is relatively inefficient for inverse dynamics calculations. s Newton–Euler Dynamics In this method, the Newton–Euler equations are applied to each body in the model. All forces affecting each body must be considered, which makes this method difficult and tedious for complex systems. The overall equations of motion can be written in any suitable inertial reference frame. Recursive and non-recursive formulations are exist, which makes this method is effective for inverse dynamics. s D’Alembert’s Principle Equations of motion are derived by identifying all forces on each body go through an acceleration and writing equilibrium equations. These equilibrium equations are simultaneously solved to obtain the dynamic system response. The restriction of this method is that it can only be used for the systems which work at low speeds. s Kane’s Dynamics This method is a subset of the group of methods known as “Lagrange’s form of D’Alembert’s Principle.” The Newton– Euler equations are multiplied by “special vectors” to develop scalar representations of the forces acting on each body. In this method, there is no need to take interbody forces into consideration. Closed kinematic chains can be directly calculated, but extensive symbol manipulations are required in the formulation of the equations of motion [12].

Methodology of Biomechanical Modeling

S. Arıtan

Developing a computer program, which calculates dynamics joint software, demands a good knowledge in dynamics. Solving the equations of motion requires a great deal of time to perform the pencil-and-paper analysis of the system to put the equations into a form that can be solved numerically by computer. To use the generalized simulation toolboxes, the biomechanist must have access to the general-purpose simulation software with a powerful computer to run the software. Extensive experience in dynamics and experience with the simulation software are also essential. Even with the required software, hardware, experience, and knowledge, running the generalized simulation codes may require too much computer time for some analyses. The symbolic analysis software serves to aid the biomechanist in the development of simulation codes that may be done manually. However, a large amount of the work must still be done by the researcher, particularly in identifying forces and torques acting on bodies in the model, and in specifying constraints. Also, the symbolic programs produce only a portion of the complete simulation code.

Examples for Biomechanical Modeling Forces and torques acting on the joints during takeoff phase in the long jump were investigated by Alptekin and Arıtan [1]. They modeled the jumper as a system of seven rigid bodies. Free body diagram of the takeoff phase in the long jump is shown in Fig. 3. Kinematics and force platform (kinetics)

Bresler and Frankel established the method of determination of forces and torques at each joint by simple repetition of the free body model of each body segment [6]. This was a followup study of Elftman [9]. They measured ground reaction forces and torques using a force plate. Kinematical values of anthropometric points were determined by using photogrammetric techniques. The human body was modeled as a system of rigid body links. Kinematic and force platform data were combined to calculate the dynamics of each body segment by applying inverse dynamics with the Newton–Euler procedure. The method started at the foot and continued up the limb. Fourteen thousand calculations and 72 graphs were all manually produced. There were no computers which were used in the study. The work required a sum of almost 500 man-hours.

How to Calculate Nowadays, all necessary calculations in modeling have been done automatically on computers. This can be achieved by writing a computer program or just using commercial software. Any approach is much faster than the manual calculation without a comparison.

Fig. 3 Free body diagram of the take-off phase in long jump

Biomechanical Measurement Methods to Analyze the Mechanisms of Sport Injuries

data were collected to analyze the dynamics of each body segment by applying inverse dynamics. In their study, the Newton-Euler equations were applied to each body in the model to calculate the joint forces and torques. Modeling of pull phase in Olympic snatch (weight lifting) was accomplished by using physical modeling tools [2]. The term “physical modeling” is somewhat confusing. A physical model can be interpreted as a real wood, clay, or metal copy of a real object. In the context of biomechanics, it refers to modeling techniques that better represent the physics and the mathematics of a system. Amca and Arıtan [2] captured a successful snatch attempt of an elite weightlifter by using high speed cameras. To determine the angular kinematics of the joints and to create the model, selected points on the weightlifter and barbell were digitized. A 2D multi-body model was created on the sagittal plane of the weightlifters. Instead of deriving and programming equations, they used a multibody simulation tool to build a physical model of the weightlifter by using SimMechanics, which is a physical modeling tool that works on top of Simulink [16]. SimMechanics model of weightlifter can be seen in Fig. 4. The joint torques was calculated during the pull phase of the Olympic Snatch by utilizing inverse dynamics solvers. In addition to developing multibody models straightforwardly in SimMechanics, it also works in both forward and inverse dynamics approaches. Herrmann and Delp created a model by using OpenSim (Open-Source Software to Create and Analyze Dynamic Simulations of Movement) to analyze how the surgery will affect wrist extension strength [11]. They investigated the effects of the surgery of the transfer on wrist extensor strength by creating plots of the maximum isometric wrist moments before and after the simulated surgery. Screen shot of the wrist model in OpenSim software can be seen in Fig. 5.

Fig. 4 SimMechanics model of weightlifter

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OpenSim is a software system that enables you to create and analyze graphics-based models of the musculoskeletal system [8]. In OpenSim, a musculoskeletal model consists of a set of bones that are connected by joints. Muscle-tendon actuators and ligaments span the joints. The muscles and ligaments develop force, thus generating moments about the joints. OpenSim allows analyzing and testing a musculoskeletal model by calculating the moment arms and lengths of the muscles and ligaments. Given muscle activations, the forces and joint moments (muscle force multiplied by moment arm) that each muscle generates can be computed for anybody position. As it can be noticed from the text, the classical mechanics modeling approach is based on the assumption that the body is rigid. This assumption can be acceptable when a body exposed to a set of forces, it mainly moves rather than deforms. As an example, bones can be assumed to act as rigid bodies during gait or other activities. Alternatively, when a body responds to force by not only moving but also deforming, it must be considered as deformable body. Soft tissues such as muscle, ligament, or cartilage cannot be considered as rigid bodies, they have to be regarded as deformable bodies.

Finite Element Modeling The fundamental concept in deformable body analysis is that all structures may be considered a collection of springs. Together, this collection of springs imparts a characteristic elastic stiffness or resistance to deformation. Most biomechanists would accept that Finite Element Method (FEM) is the most appropriate method to analyze deformable biological

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S. Arıtan

Fig. 5 Screen shot of wrist model in OpenSim software

systems. The FEM is generally referred to as finite element analysis (FEA). Although FEA is preferred in soft tissue biomechanics, it can be also used in the skeletal system (joint loads, bone stress analyses, artificial joints), modeling blood flow, and heat transfer in biological tissues [14]. FEA is simply explained by algebraic equations which are given as follows: {F} [K]{u} where; {F} is the vector of nodal forces, [K] is the element stiffness matrix, {u} is the vector of nodal displacement. FEA can be divided into three sections, which can be described as model creation, solution, result validation, and interpretation. The aim of the model creation phase is the mathematical formulation of the finite element model in terms of nodes and elements, material properties, boundary and interface conditions, and applied loads. Model creation is also called as discretization, the structure is divided into a finite number of discrete subregions, called elements that are interconnected at nodal points, or nodes. This interconnected network of elements and nodes constitutes the finite element mesh. The mesh acts like a spider web in that, from each node, there extends a mesh element to each of the adjacent nodes. Mesh generation is the most tedious and timeconsuming step in FEA. Using magnetic resonance imaging (MRI) or computer tomography (CT) data can be the best way of generating 3D meshes of heterogeneous objects with complex geometry like the human body [4]. Visual procedure of generating 3D mesh of upper arm from MRI data can be seen in Fig. 6. Elements are then assigned specific material properties that represent the elasticity of the real structure. Mechanical

properties of the material must be known to establish the element stiffness matrix [3]. The time-dependent behavior of soft tissues has made it very difficult to obtain mechanical properties. In order to obtain viscoelastic material properties of soft tissue specific instrumentation and experimental setup [5] are required. This is why FEM in biomechanics has been dominated by bone and cartilage-based studies. FEM of bone enables researchers to use standard engineering testing machines to obtain the mechanical properties of bone, and bone has a comparatively simple geometrical shape. Finally, virtual loads are added to the model, typically to nodal points (Fig. 7). Constraining anchors are also determined at this step and mobility may be restricted to particular degrees of freedom. These applied loads and constraints are collectively termed the boundary conditions. On running the analysis step, nodal displacements are calculated in response to the applied boundary conditions, taking into account structural geometry and the predefined elasticity of the structure. The solution phase consists of executing a finite element computer program using the previously generated model as the input data. Finally, a crucial part of FEA is the validation and interpretation of the results. Model validation and accuracy must be checked. In other words, does the FEM represent the geometry, loads, material properties, boundary, and interface condition of the real structure?

Conclusion There are many causes of injury ranging from poor technique, not enough preparation, inadequate strength, insufficient range of movement in the relevant structures, and many others. Correct biomechanical function is a critical factor, but is generally less understood. Biomechanical measurement

Biomechanical Measurement Methods to Analyze the Mechanisms of Sport Injuries

25

Fig. 6 3D mesh of upper arm from MRI data

methods and modeling play an important role in understanding the kinematics and kinetics part of the movement. In fact, advanced biomechanical modeling simulation tools can help model the physical world at sufficient speed with a desired accuracy. Finally, biomechanical screening can be used as an integral part of sports injury prevention and management program for optimal performance.

References

Fig. 7 Image of virtual loads that are added to the nodal points of 3D mesh of upper arm

1. Alptekin, A., Arıtan S.: Biomechanical analysis of the takeoff phase in the long jump. In IV National Biomechanics Congress, Erzurum, Turkey, 16–17 October 2008 2. Amca, A.M., Arıtan, S.: Dynamic modelling of pull phase in snatch and biomechanical analysis. In IV National Biomechanics Congress, Erzurum, Turkey, 16–17 October 2008 3. Arıtan, S.: Bulk modulus. In: Akay, M. (ed.) Wiley Encyclopedia of Biomedical Engineering. Wiley, Hoboken (2006) 4. Arıtan, S., Dabnichki, P., Bartlett, R.M.: Program for generation of three-dimensional finite element mesh from magnetic imaging scans. Med. Eng. Phys. 19(8), 681–689 (1997)

26 5. Arıtan, S., Oyadiji, S.O., Bartlett, R.M.: A mechanical model representation of the in vivo creep behaviour of muscular bulk tissue. J. Biomech. 41(12), 2760–2765 (2008) 6. Bresler, B., Frankel, J.P.: The forces and moments in the leg during level walking. Trans. ASME 72, 27–36 (1950) 7. D’ Alembert, J.: Traité de Dynamique. David l’Aîné, Paris (1743) 8. Delp, S.L., Anderson, F.C., Arnold, A.S., Loan, P., Habib, A., John, C.T., Guendelman, E., Thelen, D.G.: OpenSim: open-source software to create and analyze dynamic simulations of movement. IEEE Trans. BioMed. Eng. 55, 1940–1950 (2007) 9. Elftman, H.: Forces and energy changes in the leg during walking. Am. J. Physiol. 25, 339–356 (1939) 10. Euler, L.: Nova methods motum corporum rigidarum determinandi. Novi Commentarii Acad. Sci. Petropolitanae 20, 208–238 (1776)

S. Arıtan 11. Herrmann, A., Delp, S.L.: Moment arms and force-generating capacity of the extensor carpiulnaris after transfer to the extensor carpi radialis brevis. J. Hand Surg. 24A, 1083–1090 (1999) 12. Kane, T.R., Levinson, D.A.: Dynamics: Theory and Applications. McGraw-Hill, New York (1985) 13. Lagrange, J.-L.: Mécanique Analytique. L’Académie Royal des Sciences, Paris (1788) 14. Mackerle, J.: A finite element bibliography for biomechanics (1987–1997). Appl. Mech. Rev. 51(10), 587–634 (1998) 15. Newton, I.: Philosophiae Naturalis Principia Mathematica. Royal Society, London (1687) 16. SimMechanics, Software developed by The Mathworks Inc. Natick, MA, USA

Prevention of Ligament Injuries Emin Ergen

Introduction

Contents Introduction .................................................................................

27

Ankle Injuries, Clinical Importance, and Prevention Through Proprioceptive Training..............................................

28

Knee Injuries, Clinical Importance, and Prevention Through Proprioception .............................................................

28

Effect of Fatigue on Reflex Inhibition .......................................

28

Effect of Taping ...........................................................................

28

Effect of Orthotics and Braces ...................................................

29

Proprioceptive Training for Prevention ....................................

29

Proprioceptive Training for the Knee Joint ..............................

29

Proprioceptive Training for the Ankle Joint ............................

30

Proprioceptive Exercises ............................................................ Balance Training .......................................................................... Plyometric Exercises .................................................................... Isokinetic Exercises...................................................................... Kinetic Chain Exercises ............................................................... Reaction Time .............................................................................. Sport-Specific Maneuvers ............................................................

30 30 30 30 30 31 31

References ....................................................................................

31

E. Ergen Department of Sports Medicine, Ankara University School of Medicine, Cebeci, 06590 Ankara, Turkey e-mail: [email protected]

Sometimes the proper management of sports injuries can be complex and challenging to the sports medicine clinician. It is even more demanding to prevent athletic injuries and programming the rehabilitation after a joint lesion. Structural and neuromuscular mechanisms are disrupted in case of an injury and the continuation of information processing is ceased, which would lead to performance deteriorations and re-injury. From the point of view of sports medicine, the coordination of a movement is mainly the internal organization of the optimal control of the motor system and its parts, thus ligaments play an important role. Coordination has been defined as a cooperative interaction between nervous system and skeletal muscles [33]. This is particularly important for the prevention of injuries in risky situations. During any voluntary movements or perturbations occurring in gait, running, or jumping, due to rapid responses of lower, and to some extent, upper extremities, musculature of these parts play an important role in keeping desirable posture. Afferent information for necessary fine tuning of motor control is provided by proprioceptive, visual, vestibular, and somatosensorial receptors. Somatosensorial receptors are located in muscles, tendons, joints, and other tissues. Proprioception relates primarily to the position sense of mechanoreceptive sensation, which includes tactile and position sense. Biomechanically, there is a considerable load on musculotendinous and capsular structures, together with joint contact forces. Trauma to tissues may result in partial deafferentation by causing mechanoreceptor damage, which can lead to proprioceptive deficits. Consequently, susceptibility to re-injury may become a possibility because of this decrease in proprioceptive feedback. The effect of ligamentous trauma resulting in mechanical instability and proprioceptive deficits contributes to functional instability, which could eventually lead to further microtrauma and reinjury.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_5, © Springer-Verlag Berlin Heidelberg 2012

27

28

Ankle Injuries, Clinical Importance, and Prevention Through Proprioceptive Training Ankle sprains are defined as the most common musculoskeletal injuries that occur in athletes [1, 2]. Several studies have noted that sports requiring sudden stops and cutting movements like soccer cause the highest percentage of these injuries [3]. Ankle sprains not only result in significant time loss from sports participation, they can also cause long-term disability and have a major impact on health care costs [2]. Functional instability of the ankle is one of the most common residual disabilities after an acute ankle sprain. Ankle joint instability can be defined as either mechanical or functional instability. Mechanical instability refers to objective measurement of ligament laxity, whereas functional instability is defined as recent sprains and/or the feeling of giving way. Casual factors include a proprioceptive deficit, muscular weakness, and/or absent coordination [12]. Ankle instability, as a result of partial deafferentation of articular mechanoreceptors, with joint injury was first postulated by Freeman [15]. They observed that a decrease in the ability to maintain a one-legged stance occurred in the sprained ankle versus the contralateral uninjured ankle. Konradsen and Ravn [22] attributed the cause of functional instability to both mechanical and functional causes in stating that functional instability results from “damage to mechanical receptors in the lateral ligaments or muscle/tendon with subsequent partial deafferentiation of the proprioceptive reflex”. According to the results of studies, the most frequent injuries of adolescent [4, 6] and female [7] soccer players are ankle sprains. Some of the intrinsic risk factors involved in ankle injuries have been identified as previous sprains, foot type and size, ankle instability, joint laxity, reduced lower extremity strength, and anatomic malalignment [5, 8]. Dvorak et al. [11] also supported the observation by Inklaar [18] who stated that the high rate of reinjury suggests that inadequate rehabilitation or incomplete healing is an important risk factor. Soccer, like most sports, is associated with a certain risk of injury for the players. However, scientific studies have shown that the incidence of football injuries can be reduced by prevention programs [26, 31, 36].

Knee Injuries, Clinical Importance, and Prevention Through Proprioception The presence of neuroreceptors in the human knee joint had been described by Rauber over a 100 years ago, whereas the presence of numerous mechanoreceptors in the human anterior cruciate ligament (ACL) was well documented in the 1980s [5]. Proprioception may play a protective role in acute knee injury through reflex muscular splinting. Kennedy et al. [21]

E. Ergen

hypothesized that loss of mechanoreceptor feedback from torn knee ligaments contributed to a vicious cycle of loss of reflex muscular splinting, repetitive major and minor injury, and progressive laxity. The protective reflex arc initiated by mechanoreceptors and muscle spindle receptors occurs much more quickly than the reflex arc initiated by nociceptors (70–100 m/s vs 1 m/s). Thus, proprioception may play a more significant role than pain sensation in preventing injury in the acute setting [23]. In addition to mechanical disruption of articular structures following injury, the loss of proprioception may have a profound effect on neuromuscular control and the activities of daily living. It appears that neurological feedback mechanisms originating in articular and musculotendinous structures provide an important component for the maintenance of functional joint stability [24]. Articular deafferentation results following the injury to capsuloligamentous structures. This contributes to alterations in kinesthesia and joint position sense and further degenerative changes in the joint, as the spinal reflex pathway may be impaired [24].

Effect of Fatigue on Reflex Inhibition Endurance training is known to result in neuromuscular adaptations that would alter the production and/or clearance of metabolic substrates. Soccer is considered as an endurance event, mainly. It can be speculated that fatigue may well result in lower muscular response to inversion. Walton et al. [38] have studied to determine the extent of reflex inhibition during and after fatigue in endurance-trained individuals compared to sedentary controls. Subjects have been found to produce isometric ankle plantar-flexion contractions at 30% of maximal voluntary contraction (MVC) until their MVC torque declined by 30%. H-reflexes have been measured during a brief rest period every 3 min as well as superimposed upon the contraction every minute. These experiments have demonstrated that the neuromuscular processes associated with fatigue-related reflex inhibition must be multifaceted and cannot be explained solely by small diameter afferents responding to the byproducts of muscle contraction [38]. Muscular fatigue may be associated with reflex inhibition of the motoneuron pool. However, no literature is available to reveal the possible mechanism explaining the relationship between fatigued peroneal muscle and ankle injury.

Effect of Taping It has been postulated that prophylactic effect of ankle taping is associated with sensory feedback. By uniting the skin of the leg with the plantar surface of the foot, Robbins et al. [29]

Prevention of Ligament Injuries

suggested that the sensory cues to plantar surface of the foot are increased, thereby allowing a more accurate foot placement and reducing the changes of excessive ligamentous strain. Karlsson and Andreasson [20] concluded that taping may help patients with unstable ankles by facilitating proprioceptive and skin sensory input to the central nervous system. Therefore, taping or using lace-up brace may contribute proprioception with sensory stimulation. There are some studies emphasizing that ankle taping rapidly loses its initial level of resistance; nevertheless, restraining effect on extreme ankle motion is not eliminated by prolonged activity [25, 27].

29

functional performance. The authors maintain that the effects of ankle support on joint kinematics during static joint assessment and on traditional functional performance measures (i.e., agility, sprint speed, vertical jump height) are well understood. However, they argue that the potential effects of ankle support on joint kinetics, joint kinematics during dynamic activity (e.g., a cutting maneuver), and various sensorimotor measures are not well known and future research investigating the role of external ankle bracing needs to focus on these areas.

Proprioceptive Training for Prevention Effect of Orthotics and Braces The various forms of ankle support orthotics and braces available are generally considered effective in providing mechanical stability while restricting joint range of motion. Improvement in proprioception and sensorimotor function has been shown to occur, through stimulation of cutaneous mechanoreceptors near and around the ankle through the application of ankle support [14] and tape [30]. In Sweden, 25 teams with 439 adult male soccer players have been randomized into three groups: those offered a semirigid ankle orthotics (7 teams with 124 players), those offered an ankle disk training program (8 teams with 144 players), and 10 control teams with 171 players. None of the 439 players have been allowed to use taping. Sixty of the 124 players who had been offered the orthosis elected to use it. The rate of sprains had been found to be higher among those with previous history of sprains (25% vs. 11%, p < 0.001) and among those players without interventions. Both the players who used the orthosis and those in the ankle disk training program had shown significantly lower rates of injury than had done the controls (3%, 5%, and 17%, respectively). This difference had been accounted for entirely by prevention of injury among those with previous sprains [36]. Cordova and Ingersoll [10] have investigated the immediate and chronic effects of ankle brace application on the amplitude of peroneus longus stretch reflex on 20 physically active college students. The results have revealed that the initial application of a lace-up style ankle brace and chronic use of a semirigid brace facilitates the amplitude of the peroneus longus stretch reflex. They also found that initial and longterm ankle brace use does not diminish the magnitude of this stretch reflex in the healthy ankle. This may provide more evidence that the external ankle support offered may enhance cutaneous feedback in addition to the mechanical properties of the devices. Because the lace-up brace covers more area than the semirigid brace, more receptors may be stimulated. Cordova et al. [9] have provided a comprehensive review of the literature regarding the role of external ankle support on joint kinematics, joint kinetics, sensorimotor function, and

There are several discussions about the possibilities for prevention of a soccer injury such as; warm-up with more emphasis on stretching, regular cool-down, adequate rehabilitation with sufficient recovery time, proprioceptive training, protective equipment, good playing field conditions, and adherence to the existing rules [19]. Among these, proprioceptive or neuromuscular training is strongly emphasized in the latest reviews and researches [26, 31, 32, 36]. Assessing the best injury prevention strategies for soccer requires a complete understanding of the factors that contribute to both the occurrence of these injuries and the uptake of, or compliance with, potential prevention strategies [28]. The concept of doing proprioceptive exercises to regain neuromuscular control initially was introduced in rehabilitation programs. It was considered that because mechanoreceptors are located in ligaments, an injury to a ligament would alter afferent input. Training after an injury would be needed to restore this altered neurologic function. Neuromuscular conditioning techniques have also been advocated for injury prevention. Increased postural and movement accuracy increases the consistency with which activities can be performed safely [35]. An intervention program consisting of injury awareness information, specific technical training and a program of proprioceptive training for players with a history of ankle sprains, demonstrated a 47% reduction in the incidence of ankle sprains in the course of single season. Studies have also shown that proprioceptive training not only reduces the risk of reinjury, but also the incidence of acute lateral ankle sprain if used prophylactically [3].

Proprioceptive Training for the Knee Joint Reconstructing the ACL seems to improve afferent input needed for functional joint stability, and histological studies have shown a repopulation of mechanoreceptors in ACL graft tissue [16]. Exercises to enhance motor control

30

therefore are essential after an anterior cruciate ligament reconstruction. In the past several years, there also has been a heightened awareness of the need for preseason sport conditioning to focus on lower extremity balance and conditioning to attempt to diminish the incidence of knee ligament injuries. Neuromuscular training incorporating plyometrics and agility drills and stressing the need for proper technique for pivoting, shifting, and landing has been advocated to decrease the incidence of ACL injuries. Griffis (quad–cruciate interaction), Henning Sportsmetrics (a three-part prevention consisting of stretching, plyometrics, and strengthening drills), Caraffa (a five-phase progressive skill acquisition program), and Santa Monica by Mandelbaum (a five-part program designed to improve strength, flexibility, injury awareness, plyometrics, and agility skills) are some of the program examples successfully implemented in rehabilitation [16].

Proprioceptive Training for the Ankle Joint Tropp [34] found that wobble board training during a 10-week period could improve pronator muscle strength in patients with functional instability. Further training has not been found to give any added effect. Wester et al. [39] have conducted a similar study on 48 patients (24 training and 24 no training group) with residual functional instability due to Grade II ankle sprain. Compared to no training group, 12-week training group showed significantly fewer recurrent sprains in a 230 days follow-up period. Eils and Rosenbaum [12] have carried out a research on 30 subjects to find the effects of a 6-week multi-station proprioceptive exercise program. Joint position sense, postural sway, and muscle reaction times showed significant improvements following to this multi-station training program consisting of 12 different exercises (on mat, swinging platform, air squab, eversioninversion boards, ankle disc, mini trampoline, step, uneven walkway, hanging and swinging platforms, and with exercise bands). The program has been conducted in a way that each exercise was performed for 45-s followed by a 30-s break where subjects move over to the next station.

E. Ergen

used in proprioceptive trainings and rehabilitation programs. Exercises should include repetitive, consciously mediated movement sequences performed slowly and deliberately as well as sudden, externally applied perturbations of joint position to initiate reflex, “subconscious” muscle contraction [17].

Balance Training One major category of proprioceptive exercise is balance training. These exercises help to train the proprioceptive system in a mostly static activity. In the lower extremities, activities can include one-legged standing balance exercises, progressive use of wobble board exercises, and tandem exercises in which a postural challenge (e.g., perturbations) can be applied to the individual by the therapist.

Plyometric Exercises Plyometric exercises incorporate an eccentric preload (a quick eccentric stretch) followed by a forceful concentric contraction. This exercise technique is thought to enhance reflex joint stabilization and may increase muscle stiffness. It has become increasingly popular as an example of neuromuscular control exercise that integrates spinal and brain stem levels and has been an effective addition to upper and lower extremity conditioning and rehabilitation programs [35]. As with the ankle and knee, plyometric exercises are added after near-normal strength in all targeted muscles has been achieved.

Isokinetic Exercises Isokinetic exercises can be performed to enhance joint position sense using isokinetic devices. The athlete places his/her extremity in a predetermined position and is asked to reproduce this position, initially with the eyes open and then with eyes shut to block visual cues that might aid in neuromuscular control. This exercise can be performed with and without eccentric and/or concentric loads.

Proprioceptive Exercises Although many companies sell fairly complex computerized equipment to help improve proprioceptive input and balance, such training can also be accomplished through various simple drills done on various surfaces with eyes open and eyes shut, progressing from a double to a single limb stance. However, if available, such technologically advanced devices can also be

Kinetic Chain Exercises Closed-kinetic-chain exercises challenge the dynamic and reflexive aspects of proprioception in the legs and feet. During a closed-chain movement at onejoint, a predictable movement at other joints is produced, usually involving axial forces.

Prevention of Ligament Injuries

The lower extremities function in a closed-chain manner during sports and daily life activities, so these exercises will facilitate in regaining the proper neuromuscular patterns. Leg press, squat, circle running, figure eights, single-leg hops, vertical jumps, lateral bounds, one-legged long jumps, and carioca (crossover walking) are some examples. In the upper extremities, application of graded, multidirectional manual resistance by a physiotherapist can provide proprioceptive feedback in a closed-chain fashion. Open-chain manual resistance exercises with rhythmic stabilization (rapid change in direction of applied pressure) are also considered proprioceptively useful. In either case, resistance can be modified, depending on pain tolerance, as the patient progresses.

31 Table 1 Progression of proprioception exercises EASY DIFFICULT Double leg Single leg Standing position (on the floor)

Moving platforms and different surfaces, for example, pneumatic or foam pads

Single direction (e.g., rocker board, ankle inversion-eversion boards, ankle flexionextension boards)

Multidirection (e.g., ankle disk, mini trampoline)

Eyes open

Eyes shut

Free hands

Fixed arms (crossed over the chest)

Straight leg

Flexed knee

Fewer repetitions and sets

More repetitions and sets

Simple drills (e.g., walking, stepping down and up)

Complicated drills (e.g., hops, jumps, perturbations, and plyometrics)

Reaction Time The length of reaction time indicates that motor activity cannot be regarded solely in response to environmental stimuli. In order to prevent injuries, a stored set of muscle commands is necessary. This motor programming allows the initiation of activity on exposure to unfolding event. The repetition of such exercises also enables the cerebral cortex to determine the most effective motor pattern for that task and potentially decrease the response time [35].

Table 2 General principles of a proprioceptive training program Number of exercises:

2–5

Number of repetitions of exercises:

10–15

Number of sets:

1–3

Duration of total proprioceptive training:

5–15 min (shorter for prevention, longer for rehabilitative purposes), Preferably every training day (at least 3–5 days a week)

Sport-Specific Maneuvers References A very good example for sport-specific maneuvers for prevention programs, “The 11” was developed by FIFA’s medical research center (F-MARC) in cooperation with a group of international experts [19]. The exercises focus on core stabilization, eccentric training of thigh muscles, proprioceptive training, dynamic stabilization, and plyometrics with straight leg alignment. The benefits of the program include improved performance and also injury prevention. In summary, for constructing programs with the aim of prevention, one should incorporate exercises that improve joint motion sense, increase awareness of joint motion, enhance dynamic joint stability, and improve reactive neuromuscular control. Progression of a program should be designed to proceed from easy to more difficult movements as the pain during the exercises tolerated in time [37] (Tables 1 and 2). It is generally recommended to continue such a program for at least 6–10 weeks in order to improve proprioceptive abilities, especially during preseason. It should also be remembered that proprioceptive exercises should incorporate with other specific training items such as strength, flexibility, agility, etc. during workouts [13].

1. Arnold, B.L., Schmitz, R.J.: Examination of balance measures produced by the Biodex Stability System. J. Athl. Train. 33, 323–327 (1998) 2. Aydin, T., Yildiz, Y., Yanmis, I., et al.: Shoulder proprioception: a comparison between the shoulder joint in healthy and surgically repaired shoulders. Arch. Orthop. Trauma Surg. 121(7), 422–425 (2001) 3. Bahr, R.: Injury prevention. In: Reeser, J.C., Bahr, R. (eds.) Volleyball: Handbook of Sports Medicine and Science, pp. 94–106. Blackwell, Malden (2003) 4. Barden, J.M., Balyk, R., Raso, J.V., et al.: Dynamic upper limb proprioception in multidirectional shoulder instability. Clin. Orthop. 420, 181–189 (2004) 5. Barrack, R.L., Lund, P.J., Skinner, H.B.: Knee joint proprioception revisited. J. Sport Rehabil. 3, 18–42 (1994) 6. Barrack, R.L., Skinner, H.B., Brunet, M.E., et al.: Joint kinesthesia in the highly trained knee. J. Sports Med. Phys. Fit. 24, 18–20 (1983) 7. Barrack, R.L., Skinner, H.B., Buckley, S.L.: Proprioception in the anterior cruciate deficient knee. Am. J. Sports Med. 17, 1–6 (1989) 8. Barrett, D.J.: Proprioception and function after anterior cruciate ligament reconstruction. J. Bone Joint Surg. Br. 73, 833–837 (1991) 9. Cordova, M.L., Christopher, D., Ingersoll, C.D., et al.: Efficacy of prophylactic ankle support: an experimental perspective. J. Athl. Train. 37(4), 446–457 (2002)

32 10. Cordova, M.L., Ingersoll, C.D.: Peroneus longus stretch reflex amplitude increases after ankle brace application. Br. J. Sports Med. 37, 258–262 (2003) 11. Dvorak, J., Junge, A., Chomiak, J., et al.: Risk factor analysis for injuries in football players possibilities for a prevention program. Am. J. Sports Med. 28, S69–S74 (2000) 12. Eils, E., Rosenbaum, D.: A multi-station proprioceptive exercise program in patients with ankle instability. Med. Sci. Sports Exerc. 33, 1991–1998 (2001) 13. Ergen, E., Ulkar, B.: Proprioception and ankle injuries in soccer. Clin. Sports Med. 27(1), 195–217 (2008) 14. Feuerbach, J.W., Grabiner, M.D., Koh, T.J., et al.: Effect of an ankle orthosis and ankle ligament anesthesia on ankle joint proprioception. Am. J. Sports Med. 22, 223–229 (1994) 15. Freeman, M.A.: Instabilities of the foot after lateral ligament injuries of the ankle. J. Bone Joint Surg. 47, 669–677 (1965) 16. Griffin, L.Y.E.: Neuromuscular training and injury prevention in sports. Clin. Orthop. Relat. Res. 409, 53–60 (2003) 17. Hoffman, M., Payne, V.G.: The effects of proprioceptive ankle disk training on healthy subjects. J. Orthop. Sports Phys. Ther. 21, 90–93 (1995) 18. Inklaar, H.: Soccer injuries. II. Aetiology and prevention. Sports Med. 18, 81–93 (1994) 19. Junge, A., Dvorak, J.: Soccer injuries: a review on incidence and prevention. Sports Med. 34(13), 929–938 (2004) 20. Karlsson, J., Andreasson, G.O.: The effect of external ankle support in chronic lateral ankle joint instability: an electromyographic study. Am. J. Sports Med. 20, 257–261 (1992) 21. Kennedy, J.C., Alexander, I.J., Hayes, K.C.: Nerve supply of the human knee and its functional importance. Am. J. Sports Med. 10, 329–335 (1982) 22. Konradsen, L., Ravn, J.B.: Ankle instability caused by prolonged peroneal reaction time. Acta Orthop. Scand. 61, 388–390 (1990) 23. Lephart, S.: Reestablishing proprioception, kinesthesia, joint position sense and neuromuscular control in rehabilitation. In: Prentice, W.E. (ed.) Rehabilitation Techniques in Sports Medicine, pp. 118– 137. Mosby, St. Louis (1994) 24. Lephart, S.M.: Proprioception of the ankle and knee. Sports Med. 25, 149–155 (1998) 25. Manfroy, P.P., Ashton-Miller, J.A., Wojtys, E.M.: The effect of exercise, prewrap, and athletic tape on the maximal active and passive ankle resistance of ankle inversion. Am. J. Sports Med. 25, 156–163 (1997) 26. McGuine, T.A., Keene, J.S.: The effect of a balance training program on the risk of ankle sprains in high school athletes. Am. J. Sports Med. 34, 1103–1111 (2006)

E. Ergen 27. Myburgh, K.H., Vaughan, C.L., Isaacs, S.K.: The effects of ankle guards and taping on joint motion before, during, and after a squash match. Am. J. Sports Med. 12, 441–446 (1984) 28. Olsen, L., Scanlan, A., MacKay, M., et al.: Strategies for prevention of soccer related injuries: a systematic review. Br. J. Sports Med. 38, 89–94 (2004) 29. Robbins, S., Waked, E., Rappel, R.: Ankle taping improves proprioception before and after exercise in young men. Br. J. Sports Med. 29, 242–247 (1995) 30. Simoneau, G.G., Degner, R.M., Kramper, C.A., et al.: Changes in ankle joint proprioception resulting from strips of athletic tape applied over the skin. J. Athl. Train. 32, 141–147 (1997) 31. Söderman, K., Werner, S., Pietila, T., et al.: Balance board training: prevention of traumatic injuries of the lower extremities in female soccer players? A prospective randomized intervention study. Knee Surg. Sports Traumatol. Arthrosc. 8(6), 356–363 (2000) 32. Surve, I., Schwellnus, M.P., Noakes, T., et al.: A fivefold reduction in the incidence of recurrent ankle sprains in soccer players using the Sport-Stirrup orthosis. Am. J. Sports Med. 22(5), 601–606 (1994) 33. Tittel, K.: Coordination and balance. In: Dirix, A., Knuttgen, H.G., Tittel, K. (eds.) Encyclopedia of Sports Medicine, vol. 1, pp. 194– 211. Blackwell, London (1988) 34. Tropp, H.: Pronator muscle weakness in functional instability of the ankle joint. Int. J. Sports Med. 7, 291–294 (1986) 35. Tropp, H., Alaranta, H., Renström, A.: Proprioception and coordination training in injury prevention. In: Renström, P.A.F.H. (ed.) Sports Injuries Basic Principles of Prevention and Care, pp. 277– 288. Blackwell, London (1992) 36. Tropp, H., Askling, C., Gillquist, J.: Prevention of ankle sprains. Am. J. Sports Med. 13(4), 259–262 (1985) 37. Unver, F.: The effects of proprioceptive training on ankles with inversion injuries. Doctoral thesis. Hacettepe University Institute of Health Sciences. Ankara (2004) 38. Walton, D.M., Kuchinad, R.A., Ivanova, T.D., et al.: Reflex inhibition during muscle fatigue in endurance-trained and sedentary individuals. Eur. J. Appl. Physiol. 87(4-5), 462–468 (2002) 39. Wester, J.U., Jespersen, S.M., Nielsen, K.D., et al.: Wobble board training after partial sprains of the lateral ligaments of the ankle: a prospective randomized study. J. Orthop. Sports Phys. Ther. 23, 332–336 (1996)

Prevention in ACL Injuries Henrique Jones and Pedro Costa Rocha

Introduction

Contents Introduction ..................................................................................

33

Epidemiology of Anterior Cruciate Ligament Injuries ..........................................................................................

33

ACL Injury: The Economic Costs ..............................................

34

ACL Injuries and Soccer .............................................................

34

Are Women Really at Risk? ........................................................

34

Injury Factors............................................................................... External Risk Factors ..................................................................... Internal Risk Factors ......................................................................

35 35 35

Experimental Studies About ACL Injury Mechanism .............

36

Mechanisms of Non-contact ACL Injury...................................

37

Fatigue: Understanding to Prevent Injury ................................ Temporal Effects of Neuromuscular Fatigue on ACL Injury Risk in Athletes .....................................................

38

Can We Really Prevent ACL Injuries? ......................................

38

Conclusions ...................................................................................

41

References .....................................................................................

41

H. Jones ( ) Orthopedic Surgery, Knee and Sports Traumatology, Portuguese Air Force Hospital, Lisbon, Portugal e-mail: [email protected] P.C. Rocha Orthopedic Surgery, Portuguese Air Force Hospital, Lisbon, Portugal e-mail: [email protected]

38

Anterior Cruciate Ligament (ACL) injury increases at the same time that the sports practice increases. This has influenced a strong research focused on determining the risk factors for injury and trying to establish prevention programs that can decrease the incidence of this sports correlated medical entity. Our purpose is to report potential mechanisms and risk factors for non-contact ACL injury in sports, mostly in soccer and focus on the special incidence in women that practice competitive sports. Prevention is our final goal.

Epidemiology of Anterior Cruciate Ligament Injuries Recent studies estimate that between 75,000 and 250,000 new ACL injuries occur each year in the United States alone, with approximately 175,000 resulting in reconstructions; and that approximately 1 in every 3,000 persons who practice sports sustain a ruptured or torn ACL. In the Swedish Registry Study (2005–2006) 1 in every 1,500 and in the Norwegian data (2004) 1 in 2,900 sports people, sustained an ACL injury. These injuries occur more often in the young and healthy individuals, as a result of sudden changes of speed and direction in the course of sports, without direct trauma. These are referred to as non-contact ACL injuries. The ACL is one of four primary ligaments holding the knee, important both for stabilizing and mobilizing this articulation and ruptures when it is stretched beyond its normal range of elasticity, and once the ligament tears, it does not heal, but remains loose. It has become increasingly apparent, as more women practice some sports such as soccer and basketball that females are at higher risk for non-contact ACL injuries than males. Even though the exact reason for this is not yet clear, several studies through the last decade point to some factors such as differences in anatomy, hormones, strength, or conditioning.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_6, © Springer-Verlag Berlin Heidelberg 2012

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ACL Injury: The Economic Costs Driven, among others, by the perspective of obtaining benefits from athletic participation, such as scholarships, sports practice in the female gender rose considerably in the last 30 years. In the USA, in 1972, only 1 out of 27 girls participated in high school sports, being less than 300,000 nationwide. By 2002 this proportion rose to 1 out of 2.5, with nearly 3 million girls practicing high school sports nationwide. The same happened in college sports, with the proportion of female versus male college athletes increasing from 2% to 43% in the same time frame. This dramatic increase in participation in jumping and cutting sports coupled with the higher risk of ACL injury in females, has led to a concomitant rise in ACL injuries. Many of these injuries require surgical and/or rehabilitative intervention, with the financial burden of ACL injuries in females approaching $650 million annually for the secondary and collegiate levels (Myer, Ford and Hewet 2004). However, it is estimated that less than $10 million of federal funds were awarded for research and prevention of ACL injury, in the same period. In a European study, with data derived from 2003 Sports Insurance Statistics, with the objective of determining the injury rate (%) and the associated direct and indirect medical costs of sports injuries in Flanders, ACL injuries had the highest direct medical cost – 1,358 € per injury [8].

ACL Injuries and Soccer In soccer, ACL injuries have an important role. They are one of the top five injuries, the other four being ankle and hamstring sprains, knee cartilage tears, and hernias of the abdominal wall. In a recent prospective study it was found that in one soccer season, the incidence of acute injuries in Norwegian elite female soccer players was 23.6 per 1,000 game hours and 3.1 per 1,000 training hours. The type and location of the injuries were similar to other reports both in female and men soccer, but there were more serious knee injuries compared to men [8]. It is a fact that female soccer has become increasingly popular during the last three decades. According to the International Football Association (FIFA), in 2009, there are approximately 40 million registered female soccer players in the world (in a total estimated 265 million active soccer players) [8]. Three studies in elite soccer have shown an injury incidence during games ranging from 1.26 to 2.33 injuries per 1,000 h.

H. Jones and P.C. Rocha

ACL average injuries on a soccer team, in percentage of all injuries, are 1.3% for males, and 3.7% for females [8].

Are Women Really at Risk? Scotland seems to be the first country in the world to encourage women to play football. In the eighteenth century football was linked to local marriage customs in the Highlands (Fig. 1). Single women would play football games against married women. Single men would watch these games and use the evidence of their “footballing” ability in selecting their prospective brides. Later on, already on the second half of the twentieth century, prevention warm-up began between sports women (Fig. 2). The incidence of ACL injuries in the sporting population has been estimated from a variety of sources, including data on surgical reconstructions, such as the three national Scandinavian ACL surgical registries (Norway 2004, Denmark 2005 and Sweden 2006). When looking at a possible difference between sexes, in 2005/2006, the Swedish Registry found a higher proportion of both primary and revision of ACL surgical reconstructions in men than in women. In all the studies we have come upon, women have higher rates of ACL injury than men. As early as the 1990s, higher rates of injuries to the ACL in women versus men have been observed. For the age group of 14–18 years the rates are approximately 4:1 in basketball and 2:1 in soccer. The ratio of male to female injuries decreases slightly at the college level and approximates one at the professional level. This suggests that the rate of ACL injuries decreases as female athletes mature and the level of play increases.

Fig. 1 In the eighteenth century women football seems to be born in Scotland

Prevention in ACL Injuries

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Fig. 2 Prevention warm-up begins in the middle of twentieth century

Injury Factors Understanding the underlying causes of one of the most severe sports related knee injury (ACL rupture), is important for identifying those at increased risk of injury and, once that is achieved, for the development of intervention strategies. Thinking of athletes profile, nature of practice and injury incidence, there has been much research trying to document the possible causes of this increased incidence of ACL ruptures. The risk factors for ACL injury have been considered as either internal or external.

External Risk Factors It has been suggested that athletes are at a higher risk of suffering an ACL injury during a game than during practice [15]. As for footwear and playing surfaces, the increase of traction by the increase of the friction coefficient between the sports shoe and the playing surface may improve performance, but it may also increase the risk for ACL injury. Authors associate the higher number of cleats in boots with an associated higher torsion resistance at the foot-turf interface [12]; and the artificial floors with a higher torsion resistance at the foot-floor interface [15], both associated with a higher risk for ACL injury in the female, without a parallel in the male athletes.

In a more recent study about playing surfaces the authors came to the conclusion that the number of ACL injuries suffered by football players on natural grass or on AstroTurf® (an international brand of synthetic grass) is nearly the same [9]. As for protective equipment, functional bracing appears to protect the ACL-deficient knee of alpine skiers from repeated injury [11]. However the effect of braces on an ACL graft is inconclusive given the current information [13]. Meteorological conditions have been recently implicated by Orchard et al., in their report that non-contact ACL injuries sustained during Australian football were more common during periods of low rainfall and high evaporation. This introduces the hypothesis that meteorological conditions may have a direct effect on the mechanical interface, or traction, between the shoe and playing surface, which could have a direct effect on the likelihood of an athlete suffering an ACL injury [14].

Internal Risk Factors Internal risk factors can be subdivided into hormonal and anatomical factors, the latter including several aspects: lower extremity alignment, posture, notch size, ACL properties, and posterior tibial slope. It has been considered that the lower extremity alignment, considering all the segments, hip, knee, and ankle, may

36

predispose to an increased ACL strain value and therefore contribute to a higher ACL injury risk. One of the factors pointed by the researchers is the greater angle at the knees due to the wider female pelvis compared to men. The importance of the posterior tibial slopes has recently been introduced, but for the time being, there is not a causal relationship established between a variation of the lateral and/or medial tibial slopes and ACL injury risk. The dimensions of the intercondylar notch in relation to acute ACL injuries have been the most discussed anatomical feature in the published literature (Figs. 3 and 4). Despite a lack of standardization in the measuring methods, it has been verified in a recent study that the notch width of knees with

Fig. 3 ACL reconstruction with notch plasty in a small notch injured sports women

H. Jones and P.C. Rocha

bilateral ACL injury is smaller than that of knees with unilateral ACL injury, and notch width of bilateral and unilateral knees with injury to the ACL is smaller than notch widths of normal controls. This implies a strong association between ACL injury and notch width [10]. Trying to understand the relationship between a smaller notch size and a higher risk of ACL injury, the researchers realized that the ACL is geometrically smaller in women than in men, when normalized by body mass index. It has also come to evidence that women’s ACL has lower tensile linear stiffness, characterized by a minor elongation and lower energy absorption at failure than men [4, 5]. The identification of sex hormone receptors, as estrogen and testosterone, on the human ACL has encouraged studies trying to characterize the influence of the hormonal balance in the structure, metabolism, and mechanical properties of the ligament. However, it has not been identified which or how hormones influence ACL’s biomechanics. As for the variation of the ACL injury risk during the menstrual cycle in women, there seems to be a growing consensus in the literature that it varies according to the phase of the cycle; being significantly higher during the pre-ovulatory phase [2, 18, 21]. As for the influence of oral contraceptives in ACL injury risk, to date, there is no conclusive data about a protective effect against ACL injury. Other theories put special attention in muscular imbalances, jump mechanics, and conditioning. The most promising explanation for the more common ACL tears in females seems to involve differences in neuromuscular control, namely the athlete’s ability to feel (proprioception) and control the knee with one’s muscles. Because of anatomical and strength differences between the average man and woman, females have less stability and upper body control which can lead to an awkward fall and hence an ACL injury.

Experimental Studies About ACL Injury Mechanism

Fig. 4 The importance of notch width in ACL injury

Although the primary function of the ACL is to restrain the anterior translation of the tibia, during single limb landing (when many ACL injuries occur), the tibia has been shown to actually translate posteriorly because of the inertial forces of the upper body coupled with the ground reaction force from the deceleration (Fig. 5). Recent data suggests that the combination of knee valgus with internal tibial rotation during landing causes the ACL to rupture (Fig. 6), not excessive quadriceps contraction. In addition, upper body positioning has been shown to influence the forces at the knee. Studies at the BioMotion Lab (Stanford University, Palo Alto, California) have shown that when the arms are constrained by holding a ball or stick, the peak knee abduction moment increases (Fig. 7) [6, 17].

Prevention in ACL Injuries

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Mechanisms of Non-contact ACL Injury

Fig. 5 Combined forces in ACL injury during landing

The deleterious impact of non-contact ACL injuries on the athlete’s health and performance has precipitated extensive efforts toward their prevention. In particular, recent research has focused on identifying underlying neuromuscular control predictors of ACL injury risk, as such factors are readily amenable to training, and in essence, preventable. Neuromuscular training programs continue to evolve out of this research, which attempt to modify what are considered abnormal and potentially hazardous movement strategies. The objective is to facilitate more effective prevention methods that promote successful neuromuscular adaptation within individual non-modifiable constraints [16]. Trying to develop specific methods for the prevention of sports injuries, various approaches have been used: analysis of video recordings of injuries, interviews with injured patients, in vivo and cadaver studies and mathematical models, among others. As a result, researchers have found that approximately 80% of ACL injuries are non-contact, occurring while landing from a jump, cutting or decelerating. If these movements are made awkwardly, for example with the force being applied on a single leg with the foot displaced away from the body’s mass center, an ACL injury is more likely to occur. Some biomechanical aspects like tibial translation,

Fig. 6 Valgus and internal rotation during landing, as a major cause of ACL rupture

38

H. Jones and P.C. Rocha p2 w

>4 w

At least 4 w

Soccer injuries can happen during training (pre-seasonal and seasonal) and during competitions; and predominantly affect the ankle and knee as well as the muscles of the thigh and calf [17]. The main risk factors are: 1. Player factors (joint instability, muscle tightness, insufficient warm-up and stretching, irregular cool down, inadequate rehabilitation, lack of proprioceptive training) 2. Equipment (shoes and shin guards) 3. Playing surface (grass vs. artificial turf) 4. Game rules [6] 5. Previous injury 6. Other [27] (e.g., Score celebrations) The four dominating injury types in soccer are: 1. 2. 3. 4.

Sprains to the ankle Sprains to the knee Strains to the hamstrings Strains to the groin

These account for more than 50% of all injuries, and prevention programs for soccer should therefore target these [11].

Prevention Strategies In the scientific literature on prevention of sports injury, there seems to be good evidence for the effectiveness of prevention interventions [6, 25]. Because one of the most important risk factors for a sports injury is a previous injury, prevention should begin as soon as players train or play on an organized level. Prevention strategies should be targeted: 1. Sports participant (host) 2. Potential hazard (agent of injury) 3. Surrounding environment The prevention program includes general interventions such as improvement of: 1. 2. 3. 4.

Warm-up and regular cool down Taping of unstable ankles, shin guards Adequate rehabilitation, Promotion of the spirit of fair play

Preventive ankle, knee, groin, and hamstring exercises are essential measures for injury prevention.

Prevention of ankle injuries training [24]: Weeks 1–2 Balance board

Both legs on the board, with arms crossed. Attempt to stand still and maintain the balance Simlar exercise, but now performed on one leg Both legs on the board, bouncing a ball alternately with both hands, standing as still as possible during the exercise Both legs on the board, throwing the ball, and catching it

Balance pad

One leg on the pad, maintaining balance for 30 s on alternating legs Jumping exercise-from outside the pad, landing on alternating legs

Weeks 3–5 Balance board

Ball juggling performed while standing on one leg

Balance pad

Bouncing the ball around the pad while standing on one leg Calf raise while standing on both legs on the pad

Weeks 6–10 Balance board

Soccer-specific exercises, juggling the ball while standing on one leg, also combining both the balance board and balance pad, placing the pad on top of the board

Balance pad

Closing the eyes while standing on one leg, and other exercises including landing on one or two legs while jumping from a box/stairs

Prevention of knee injuries training [7, 20]: Weeks 1–2 Balance board

Both legs on the board, with arms crossed, always keeping the knee-over toe position Similar exercise, but now performed on one leg Both legs on the board, bouncing a ball alternately with both hands, standing as still as possible during the exercise Both legs on the board, throwing the ball, and catching it

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H.H. Öztekin

Balance pad

One leg on the pad, maintaining balance for 30 s on alternating legs. Walk onto the pad, stopping and keeping the balance Jumping exercise-from outside the pad, landing on alternating legs

Weeks 3–5 Balance board

Ball juggling performed while standing on one leg Two-legged squats, with knee-over-toe position

Balance pad

Bouncing the ball around the pad while standing on one leg

Weeks 6–10 Balance board

Soccer-specific exercises, juggling the ball while standing on one leg, also combining both the balance board and balance pad, placing the pad on top of the board

Balance pad

Closing the eyes while standing on one leg, and other exercises including landing on one or two legs while jumping from a box/stairs One-legged squats, and balance exercises while closing the eyes

Floor exercise

One-legged jumping on one foot in an imaginary zigzag course

Prevention of groin injuries training [15]: Warm-up

Keeping a ball between the extended legs, pushing the legs together for 15 s, while lying on the ground. Repeated 10X. Similar exercise, only difference having the knees flexed and the ball between the knees

Transverse abdominal muscles

Lie facing the ground, only resting on the forearms and toes in a straight position, contracting the abdominal muscles, “forcing the umbilicus inwards.” Performed in 20 s, repeated 5X

Sideways jumping

Knee-over-toe position while jumping sideways with arms resting on the hips

Sliding

Wearing only socks, slide a leg alternately away and towards the other that is bearing the weight. The exercise can be performed both sideways and diagonally for 30–60 s before switching legs

Diagonal walking

Exercise described by Holmich [26] performed 5 × 15 s on each leg

Prevention of Hamstring injuries training (Nordic exercises) [19]: Weeks

No. of training sessions per week

No. of repetitions

1

1

5+5

2

2

6+6

3

3

3×6−8

4

3

3 × 8 − 10

5–10

3

12 + 10 + 8

The Nordic hamstring exercise is performed standing on the knees on a soft foundation, slowly lowering the body toward the ground using the hamstrings while the feet are held by a partner (Figs. 1 and 2). Progression is achieved by increasing the initial speed, and eventually having a partner push forward. In the web page of Fédération Internationale de Football Association (FIFA) (www.fifa.com), ten sets of exercises designed to improve the stability of ankle and knee joints, the flexibility and strength of the trunk, hip, and leg muscles, as well as to improve coordination, reaction time, and endurance. This is called as “F-MARC 11.” The eleventh set is “fair play.” Regarding dangerous collisions that might happen during a soccer game, more specific preventive instruments are defined in the literature like facial masks [12]. Special helmets are still being used by some famous goalkeepers. Being

elbowed by a rival player is another interesting and underappreciated soccer injury (Zeren B. Personal communication, Karsiyaka, Izmir, Turkey, June 2009) which is preventable by “olecranon pads” simply. Important aspects in the prevention of soccer injury concern also the laws of the game, their observance, and, especially, the spirit of fair play; a broader view and the involvement of other target groups (such as referees, official representatives) would be desirable to make soccer a healthier game. Although soccer injuries cannot be prevented completely, it is possible to avoid some types and minimize the overall number and severity. Prevention of soccer injuries should focus primarily on conditioning of the lower extremity in sport-specific activities. To summarize, prevention should begin as soon as players train or play in an organized level.

Prevention of Soccer Injuries

Fig. 1 Picture shows the athlete’s and the partner’s preparation for a Nordic exercise

Fig. 2 Picture shows the athlete’s balancing of his body with the contraction of hamstring muscles

References 1. Andersen, T.E., Floerenes, T.W., Arnason, A., et al.: Video analysis of the mechanisms for ankle injuries in football. Am. J. Sports Med. 32, 69–79 (2004)

65 2. Andersen, T.E., Tenga, A., Engebretsen, L., et al.: Video analysis of injuries and incidents in Norwegian professional football. Br. J. Sports Med. 38, 626–631 (2004) 3. Arnason, A., Andersen, T.E., Holme, I., et al.: Prevention of hamstring strains in elite soccer: an intervention study. Scand. J. Med. Sci. Sports 18, 4048 (2007) 4. Arnason, A., Tenga, A., Engebretsen, L., et al.: A prospective videobased analysis of injury situations in elite male football. Am. J. Sports Med. 32, 1459–1465 (2004) 5. Askling, C., Karlsson, J., Thorstensson, A.: Hamstring injury occurrence in elite soccer players after preseason strength training with eccentric overload. Scand. J. Med. Sci. Sports 13, 244–250 (2003) 6. Berkes, I., Kynsburg, A., Panics, G.: Prevention of football injuries. In: Volpi, P. (ed.) Football Traumatology. Current Concepts: From Prevention to Treatment. Springer, Italy (2006) 7. Caraffa, A., Cerulli, G., Projetti, M., et al.: Prevention of anterior cruciate ligament injuries in soccer. A prospective controlled study of proprioceptive training. Knee Surg. Sports Traumatol. Arthrosc. 4, 19–21 (1996) 8. Dvorak, J., Junge, A.: Football injuries and physical symptoms. A review of the literature. Am. J. Sports Med. 28, S3–S9 (2000) 9. Ekstrand, J., Gillquist, J.: Soccer injuries and their mechanisms: a prospective study. Med. Sci. Sports Exerc. 15, 267–270 (1983) 10. Ekstrand, J., Karlsson, J.: The risk for injury in football. There is a need for a consensus about definition of injury and the design of studies. Scand. J. Med. Sci. Sports 13, 147–149 (2003) 11. Engebretsen, A.H., Myklebust, G., Holme, I., et al.: Prevention of injuries among male soccer players: a prospective, randomized intervention study targeting players with previous injuries or reduced function. Am. J. Sports Med. 36, 1052–1060 (2008) 12. Eufinger, H., Heise, M., Rarreck, T.: Management of simple midfacial fractures, particularly in professional soccer players. Sportverletz. Sportschaden 14, 35–40 (2000) 13. Giza, E., Fuller, C., Junge, A., et al.: Mechanisms of foot and ankle injuries in soccer. Am. J. Sports Med. 31, 550–554 (2003) 14. Hagglund, M., Walden, M., Bahr, R., et al.: Methods for epidemiological study of injuries to professional football players: developing the UEFA model. Br. J. Sports Med. 39, 340–346 (2005) 15. Holmich, P., Uhrskou, P., Ulnits, L.: Effectiveness of active physical training as treatment for long-standing adductor-related groin pain in athletes: randomised trial. Lancet 353, 439–443 (1999) 16. Hoy, K., Lindblad, B.E., Terkelsen, C.J., et al.: European soccer injuries. A prospective epidemiologic and socioeconomic study. Am. J. Sports Med. 20, 318–322 (1992) 17. Junge, A., Dvorak, J., Graf-Baumann, T.: Football injuries during the World Cup 2002. Am. J. Sports Med. 32, 23S–27S (2004) 18. Larson, M., Pearl, A.J., Jaffet, R.: Soccer. In: Caine, D.J., Caine, C.G., Lindner, K.J. (eds.) Epidemiology of Sports Injuries. Human Kinetics, Champaign (1996) 19. Mjolsnes, R., Arnason, A., Osthagen, T., et al.: A 10-week randomized trial comparing eccentric vs. concentric hamstring strength training in well-trained soccer players. Scand. J. Med. Sci. Sports 14, 311–317 (2004) 20. Myklebust, G., Engebretsen, L., Braekken, I.H., et al.: Prevention of anterior cruciate ligament injuries in female team handball players: a prospective intervention study over three seasons. Clin. J. Sport Med. 13, 71–78 (2003) 21. Olsen, L., Scanlan, A., MacKay, M., et al.: Strategies for prevention of soccer related injuries: a systematic review. Br. J. Sports Med. 38, 89–94 (2004) 22. Orchard, J.: Orchard Sports Injury Classification System (OSICS). Sports Health 11, 39–41 (1993) 23. Rae, K., Orchard, J.: The Orchard Sports Injury Classification System (OSICS) Version 10. Clin. J. Sport Med. 17, 201–204 (2007) 24. Tropp, H., Askling, C., Gillquist, J.: Prevention of ankle sprains. Am. J. Sports Med. 13, 259–262 (1985)

66 25. Volpi, P.: Epidemiology and risk factor. In: Volpi, P. (ed.) Football Traumatology. Current Concepts: From Prevention to Treatment. Springer, Italy (2006) 26. Woods, C., Hawkins, R.D., Hulse, M., et al.: The Football Association Medical Research Programme: an audit of injuries in professional football: an analysis of ankle sprains. Br. J. Sports Med. 37, 233–238 (2003)

H.H. Öztekin 27. Zeren, B., Oztekin, H.H.: Score celebration injuries among soccer players. Am. J. Sports Med. 33, 1237–1240 (2005) 28. Elias, S.R.: 10-year trend in USA Cup soccer injuries: 1988–1997. Med. Sci. Sports Exerc. 33, 359–367 (2001)

Sports Injuries and Proprioception: Current Trends and New Horizons Devrim Akseki, Mehmet Erduran, and Defne Kaya

Introduction

Contents Introduction .................................................................................

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Unknown Issues of Proprioceptive Process .............................. Measurements of Proprioception ..................................................

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How Proprioception Can Be Improved?...................................

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Other Areas for Proprioceptive Researches .............................

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References ....................................................................................

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The role of proprioception has become increasingly clear in the etiology, prevention, and treatment of sports injuries. It has been generally believed that proprioceptive loss increases the incidence of injury but proprioceptive rehabilitation decreases that and improves the results of treatment [22, 40, 41]. Furthermore, it was also shown that sportive performance could be improved by proprioceptive rehabilitation in uninjured and injured athletes [23, 35]. Recently, there has been significant amount of investigation about the importance of proprioception (Fig. 1). Proprioception has been investigated in different types of joint injuries [11, 12, 20, 24, 32]. Most of these studies showed that the proprioceptive quality deteriorated following sports injuries [23, 32]. Not only acute injuries but also chronic sequels of acute injuries and overuse syndromes have been shown to lead to diminished proprioception [2, 21, 29]. Although decreased level of proprioception has been observed following different types of sports injuries, it is not clearly known whether injured patients have normal level of proprioception before the injury. Muaidi et al. [28] compared the proprioception of the Olympic level soccer players with non-athletes and observed that highly trained athletes possess enhanced proprioceptive

10000 9000 8000 7000 6000 5000 4000

D. Akseki ( ) and M. Erduran Faculty of Medicine, Department of Orthopaedics and Traumatology, Balıkesir University, ÇaÜıĜ Kampüsü, Balıkesir, Turkey e-mail: [email protected], [email protected] D. Kaya Faculty of Medicine, Department of Sports Medicine, Hacettepe University, Sıhhiye, 06100 Ankara, Turkey e-mail: [email protected]

3000 2000 1000 0 1930 1960

1960 1970

1970 1980

1980 1990

1990 2000

2000 2011

Fig. 1 Numbers of published studies including the word proprioception in their text as per years

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ability. Similar observations were also made by other authors in various types of sports [25, 38]. On the other hand, Schmitt et al. [37] found no improvement in ankle joint position sense after 5 months of ballet training. In our opinion, the design of the above-mentioned studies does not permit to clarify whether the enhanced proprioceptive ability is due to the training or whether it is congenital. This is still an unanswered question and prospective studies are needed to answer it. To our knowledge, no study exists in the literature evaluating the proprioceptive level before the injury. Fort his purpose, the proprioceptive level should be tested first, and then the subjects should be monitorized for having an injury by years; when an injury occured, the proprioception should be measured again to compare it with the preinjury proprioceptive level. However, the normal level of proprioception is not known. We discuss below the controversies about the proprioceptive measurements, and inexistence of a standard proprioceptive screening method that is accurate, sensitive, and reproducible. Because of difficulty in planning such a study and existing problems of proprioceptive measurements, it does not seem to be possible to compare preinjury level of proprioception to post injury level.

Unknown Issues of Proprioceptive Process Although there are plenty of studies, a lot of unknown matters exist about the proprioception issue. First of all, the mechanism of proprioception is still unknown completely. There are a lot of studies investigating the proprioceptive process, pathways, underlying mechanisms, and the data about the details of the proprioceptive process are increasing. But it is still unknown, how many mechanoreceptors are activated by the external or internal impulses, which pathway(s) are activated during the perception and reaction processes. Exact roles and effects of visual and vestibular systems, amount and physiology of their contribution to a specific condition are also unknown. Also the effect of contralateral extremity or different portions of the body are still unclear.

Measurements of Proprioception A lot of measurement methods of proprioception have been defined in the literature. Based on these measurements, scientists comment on the proprioceptive status in some specific conditions. Is the proprioception influenced by braces, elastic bandages, surgical or conservative treatments; has the increased proprioception decreased the incidence of injury and enhanced the sportive performance; the aim is to answer these and other questions about proprioception by measuring the proprioception with different methods. However, to

D. Akseki et al.

measure the proprioception is difficult and cannot be done directly. Thus, the testing conditions are not the same as that of the instant of injury. Patients are usually in supine position, and their extremity is positioned in a computerized system for proprioceptive measurements. Non weight-bearing and static positions are not relevant to the injury position in the real life. Hence, it is doubtful that the existing measurement techniques and their results can reflect the real status of proprioceptive level in injured or uninjured persons. Another important issue on testing methods of proprioception is that they are not specific to a tissue, a ligament, capsule, or a joint. For example, during a knee joint evaluation, the test results may be influenced by the pathologies of hip joint and/or ankle in almost all measurement techniques. Thus no test method can evaluate the proprioception separately when accompanying lesions are found in the same joint. According to the above mentioned problems, there are a lot of reports having the controversial results in the same injury patterns. In our opinion, because of the doubtful validity of the current measurement techniques some authors found unchanged [27] and some increased [19] proprioceptive levels in the similar conditions. Thus, incompatibility of the measurement methods of proprioception has been stressed previously [14], and investigations to find an ideal testing method are continuing [3–5, 30]. Because of these above mentioned deficiencies of proprioceptive measurements, we designed some studies investigating the effectiveness of new testing methods [3, 4]. While constituting the hypothesis of the first study, we emphasized the fact that patients are usually kept in a supine position or seated in equipment like dynamometer in most of the proprioceptive measurement techniques. However this position does not reflect the symptomatic or traumatic instant in real life. Furthermore, awareness of the patient from the amount of pressure in the weight-bearing position should be directly related to his proprioceptive ability. Thus we tested the weight bearing sense in patients with patellofemoral pain syndrome [3]. Patients were instructed to weight bear on a scale until reaching the target weight. We selected three different target weights: 10, 20, and 30 kg. Errors from the target weight were noted and compared to healthy controls. Patients with (PFPS) PatelloFemoral Pain Syndrome showed significantly increased errors than healthy controls [3]. To our knowledge it was the first study testing the availability of weight bearing sense for proprioceptive measurement, and we concluded that the new technique presented here may be used for proprioception testing [3]. In other two studies, we evaluated the vibration sense as a proprioceptive measurement method [4, 9]. Vibration sense and related neural pathways seem to be important as well as other deep senses for the perception of a motion or position of a joint. The trigger point of our study was that the current proprioception measurement methods were not specific to a tissue such as anterior cruciate ligament or menisci. We aimed to

Sports Injuries and Proprioception: Current Trends and New Horizons

evaluate the availability of vibration sense as a proprioceptive test in patients with a clinical diagnosis of patellofemoral pain syndrome and in patients with a medial meniscal tear, in two different studies [4, 9]. In the first one, 19 patients with a clinical diagnosis of patellofemoral pain syndrome (PFPS) and ten healthy controls were included in the study [4]. Symptomatic and non symptomatic knees of the patients and both knees of the volunteers were evaluated by the joint position sense (JPS) test and perception times of vibration sense (VS) were measured. A digital goniometer and 128 Hz frequency tuning fork were used for the measurements. Perception time of vibration was 7.23 ± 1.27 sc for the symptomatic knee of the patients, whereas it was 9.08 ± 1.53 sc for contralateral knees (p < 0,05). JPS testing also showed deterioration of proprioception in accordance with the vibration testing. Similar differences were obtained between the pathologic knee and the normal knees of healthy controls (p < 0.05). Results of the study showed that the perception time of vibration is diminished on symptomatic knees of the patients as compared to healthy. We believe that these results, may give rise to the thought that vibration sense may be used for tissue specific proprioceptive measurement [4]. In the second one, the study group consisted of 20 patients with isolated medial meniscal lesion and 20 healthy controls who had no experience of knee injury or disorder [9]. Perception time of vibration (PTV) was measured using a tuning fork with a frequency of 128 Hz (RIESTER®). Medial and lateral joint lines were drawn and divided into three parts (front, middle, and posterior). Midpoint of each part was marked for embedding of the tuning fork. Patients were instructed to indicate the time when they no longer percept the vibration and the chronometer was stopped at this moment. Thus, perception time of vibration (PTV) was obtained. Preoperative measurements of patient group showed longer PTV in posterior part of medial joint line in the pathologic knee (MP), which are also concordant with the arthroscopically proved location of the meniscal tear [9]. Mean perception time of vibration was 13.25 ± 3.46 sc in group I at MP, but it was 9.92 ± 2.0, 9.82 ± 2.8, and 9.93 ± 3.0 sc at the same target point in normal knee of the patients and left and right knees of external control group, respectively (p < 0.01) [9]. This study demonstrated that presented technique for measurement of perception of vibration was accurate and reliable [9].

How Proprioception Can Be Improved? This is one of the most commonly asked questions among investigators. Many internal and external factors which are believed to have a positive effect on proprioception are tested in healthy controls and patients with different clinical scenarios. The effect of proprioceptive rehabilitation techniques on the performance of an athlete in a specific sport is believed

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to be an attractive research area for scientists [7, 9, 18, 33]. Effects of elastic bandages, taping, braces, surgeries, and other factors were extensively investigated during last decades. Although some promising results were obtained, no clearly useful, standard and reproducible technique was developed for proprioceptive improvement. The investigations to improve the proprioceptive quality still continue, and this is the main reason for current efforts. Correlation between proprioception and other performance criteria such as muscle strength, balance, and laxity might be studied more in the coming years [23]. In a most recent study, Casadio et al. [8] have investigated the effect of robotic training for proprioception enhancement in stroke patients. They tested some selected tasks with a robotic system, by adding the assistive force component [8]. According to the obtained results, they suggested that robots may be useful in neuromotor rehabilitation by combining the repeatable sensorymotor exercises, continuously monitoring the actual motor performance and allowing to create new and controlled haptic environments in which patients can learn to move by only using proprioceptive information [8]. Cameron et al. [6] investigated the effect of neoprene shorts on leg proprioception in football players. They found improvement in some parameters of neuromuscular control ability by wearing close-fitting neoprene shorts. Their results can be concluded that incidence of sports injuries may be reduced by wearing some specially designed shorts, sneakers etc. We investigated the effect of hot application on knee proprioception in healthy controls and in patients with patellofemoral pain syndrome, in two different studies [1, 31]. In the first study the effect of single dose of hot application on the knee joints of the healthy controls was evaluated [31]. The study was conducted on the students of the College of Physical Education and Sports. The study group consisted of 14 male and 13 female students with a mean age of 22.2 ± 2.5 years (range: from 19 to 28 years). Proprioceptive level was measured before hot application on both knees with the technique of active joint position sense using a digital goniometer. Then, with 1 week interval, following 10 min of hot application same measurements were repeated. Proprioceptive capability significantly improved after hot application especially in further flexion angles of the knee. Results of the study showed that hot application increases the proprioceptive capability of the knee. We concluded that these findings should be considered in planning preventive and therapeutic strategies for sports injuries [31]. In a complementary fashion, we planned the second study that the proprioceptive status was monitored in patients with patellofemoral pain syndrome with or without hot application during their standard treatment protocol [1]. First group patients underwent home exercises only; second group ones same exercises plus hot application. Hot was applied three times a day, and 20 min for each session. Proven proprioceptive deficiency improved better in exercise plus hot application than exercise treatment only [1].

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Other Areas for Proprioceptive Researches

References

Proprioception seems not to be related to only sports injuries. It is gradually understood that a lot of body functions are directly related to proprioceptive capability. In a recent study, it is suggested that proprioception has an important role in handwriting [15]. Writing characteristics were quantified by using a digital writing tablet with and without visual control [15]. According to the results obtained they believed that morphological aspects of handwriting need intact proprioception. Kessiby et al. [13] reported the results of proprioceptive education for hand orientation in blind subjects. Their findings provided the first evidence of an automatic online correction mechanism for hand orientation guided only by proprioceptive inputs reaching in blind subjects [13]. In another study, Horlings et al. [16] investigated the vestibular and proprioceptive contributions to human balance corrections. They believed that proprioception is important for movement strategies and synergies, whereas vestibular functions are more active in modulation depth [16]. They also stressed that proprioceptive loss leads to changes in both movement strategies and synergies [16]. In another interesting study reported by London et al. [26], authors tried to instruct a behaving monkey by electrical stimulation of proprioceptive cortex. They demonstrated that a monkey can learn to detect such stimuli and recognize the frequency of a given stimulus, based on memory of previous stimuli [26]. Effect of whole body vibration on muscle strength and proprioception was investigated by Trans et al. [39]. They suggested that exposure of vibration exercises on a stable platform yielded increased muscle strength and proprioception [39]. Riva et al. [34] designed a study for the prevention of muscle atrophy and osteoporosis for astronauts by using high frequency proprioception. They pointed out the difficulty in applying active exercises during space flights and accordingly occurrence of muscle atrophy and osteoporosis [34]. They verified the whether an electrical system creating high frequency proprioceptive inputs reachable on the earth in microgravity conditions [34]. They postulated that high frequency proprioceptive flows could be useful for the prevention and recovery of muscle atrophy and osteoporosis [34]. Effects of proprioceptive training were also investigated in musician’s dystonia and writer’s cramp [36]. Another interesting report came from University of Pittsburg in April 2008. Researchers of this university created a human performance research laboratory for naval special warfare [17]. Researchers aimed to reduce the incidence of preventable musculoskeletal injuries during training, combat, and recreation; to enhance force readiness, reduce fatigue, and optimize performance; and to prolong the operational life [17]. All above mentioned fields of interest show that proprioception is not related only to sports injuries. Enhancement of knowledge about proprioception seems to be useful for many aspects of daily life.

1. Akkaya, G.: The effect of hot application on knee proprioception in patients with patellofemoral pain syndrome. Celal Bayar University Thesis, Counsellor: Assoc. Prof. Devrim Akseki, Manisa (2009) 2. Akseki, D., Akkaya, G., Erduran, M., Pınar, H.: Proprioception of the knee joint in patellofemoral pain syndrome. Acta Orthop. Traumatol. Turc. 42, 316–321 (2008) 3. Akseki, D., Çetinkaya, O., Vatansever, A., Turan, M., Öziç, U.: Joint weight-bearing sens: a new evaluation method of knee proprioception. 18th National Turkish Orthopaedics and Traumatology Congress, ístanbul, Turkey, 18–23 Oct 2003 4. Akseki, D., Öziç, U., Vatansever, A.: Proprioception in patients with anterior knee pain: description of a new measurement method. 5th ISAKOS Congress, Auckland, New Zealand, 10–14 Mar 2003 5. Boerboom, A.L., Huizinga, M.R., Kaan, W.A., Stewart, R.E., Hof, A.L., Bulstra, S.K., Diercks, R.L.: Validation of a method to measure the proprioception of the knee. Gait Posture 28, 610–614 (2008) 6. Cameron, M.L., Adams, R.D., Maher, C.G.: The effect of neoprene shorts on leg proprioception in Australian football players. J. Sci. Med. Sport 11, 345–352 (2008) 7. Caplan, N., Rogers, R., Parr, M.K., Hayes, P.R.: The effect of proprioceptive neuromuscular facilitation and static stretch training on running mechanics. J. Strength Cond. Res. 23, 1175–1180 (2009) 8. Casadio, M., Morasso, P., Sanguineti, V., Giannoni, P.: Minimally assistive robot training for proprioception enhancement. Exp. Brain Res. 194, 219–231 (2009) 9. Çetinkaya, O.: Proprioception in medial meniscal tears. Celal Bayar University Thesis, Counsellor: Assoc. Prof. Devrim Akseki, Manisa (2005) 10. Christensen, B.K., Nordstrom, B.J.: The effects of proprioceptive neuromuscular facilitation and dynamic stretching techniques on vertical jump performance. J. Strength Cond. Res. 22, 1826–1831 (2008) 11. Dover, G., Powers, M.E.: Cryotherapy does not impair shoulder joint position sense. Arch. Phys. Med. Rehabil. 85, 1241–1246 (2004) 12. Feuerbach, J.W., Grabiner, M.D., Koh, T.J., Weiker, G.G.: Effect of ankle orthosis and ankle ligament anesthesia on ankle joint proprioception. Am. J. Sports Med. 22, 223–229 (1994) 13. Gosselin-Kessiby, N., Kalaska, J.F., Messier, J.: Evidence for a proprioception-based rapid on-line error correction mechanism for hand orientation during reaching movements in blind subjects. J. Neurosci. 29(11), 3485–3496 (2009) 14. Grob, K.R., Kuster, M.S., Higgins, S.A., Lloyd, D.G., Yata, H.: Lack of correlation between different measurements of proprioception in the knee. J. Bone Joint Surg. Br. 84, 614–618 (2002) 15. Hepp-Reymond, M.C., Chakarov, V., Schulte-Mönting, J., Huethe, F., Kristeva, R.: Role of proprioception and vision in handwriting. Brain Res. Bull. 79(6), 365–370 (2009). doi:10.1016/j.brainstembull.2009.05.13 16. Horlings, C.G., Küng, U.M., Honegger, F., Van Engelen, B.G., Van Alfen, N., Bloem, B.R., Allum, J.H.: Vestibular and proprioceptive influences on trunk movements during quiet standing. Ann. NY Acad. Sci. 1164, 1–12 (2009) 17. http://www.medicalnewstoday.com/articles/104347.php 18. Ingle, A.: The effectiveness of strength and proprioceptive training following anterior cruciate ligament injury with or without reconstruction: a systematic review. Thesis, UMI-Mgh Institute of Health Professions, Boston (2009) 19. Iwasa, J., Ochi, M., Adachi, N., Tobita, M., Katsube, K., Uchio, Y.: Proprioceptive improvement in knees with anterior cruciate ligament reconstruction. Clin. Orthop. Relat. Res. 381, 168–176 (2000) 20. Jerosch, J., Prymka, M.: Proprioception and joint stability. Knee Surg. Sports Traumatol. Arthroscopy 4, 171–179 (1996)

Sports Injuries and Proprioception: Current Trends and New Horizons 21. Juul-Kristensen, B., Lund, H., Hansen, K., Christensen, H., Danneskiold-Samsøe, B., Bliddal, H.: Poorer elbow proprioception in patients with lateral epicondylitis than in healthy controls: a cross-sectional study. J. Shoulder Elbow Surg. 17(Suppl), 72–81 (2008) 22. Kaminski, T.W., Buckley, B.D., Powers, M.E., Hubbard, T.J., Ortiz, C.: Effect of strength and proprioception training on eversion to inversion strength ratios in subjects with unilateral functional ankle instability. Br. J. Sports Med. 37, 410–411 (2003) 23. Lee, H.M., Cheng, C.K., Liau, J.J.: Correlation between proprioception, muscle strength, knee laxity, and dynamic standing balance in patients with chronic anterior cruciate ligament deficiency. Knee. 16(5), 387–391 (2009) 24. Lephart, S.M., Pincivero, D.M., Giraldo, J.L., Fu, F.H.: The role of proprioception in the management and rehabilitation of athletic injuries. Am. J. Sports Med. 25, 130–137 (1997) 25. Lin, C.H., Lien, Y.H., Wang, S.F., Tsauo, J.Y.: Hip and knee proprioception in elite, amateur, and novice tennis players. Am. J. Phys. Med. Rehabil. 85, 216–221 (2006) 26. London, B.M., Jordan, L.R., Jackson, C.R., Miller, L.E.: Electrical stimulation of the proprioceptive cortex (area 3a) used to instruct a behaving monkey. IEEE Trans. Neural Syst. Rehabil. Eng. 16, 32–36 (2008) 27. MacDonald, P.B., Hedden, D., Pacin, O.: Proprioception in anterior cruciate ligament-deficient and reconstructed knees. Am. J. Sports Med. 24, 774–778 (1996) 28. Muaidi, Q.I., Nicholson, L.L., Refshauge, K.M.: Do elite athletes exhibit enhanced proprioceptive acuity, range and strength of knee rotation compared with non-athletes? Scand. J. Med. Sci. Sports 19, 103–112 (2009) 29. Nakasa, T., Fukuhara, K., Adachi, N., Ochi, M.: The deficit of joint position sense in the chronic unstable ankle as measured by inversion angle replication error. Arch. Orthop. Trauma. Surg. 128, 445– 449 (2008) 30. Noël, M., Cantin, B., Lambert, S., Gosselin, C.M., Bouyer, L.J.: An electrohydraulic actuated ankle foot orthosis to generate force fields and to test proprioceptive reflexes during human walking. IEEE Trans. Neural Syst. Rehabil. Eng. 16, 390–399 (2008)

71 31. Özer, M.: The effects of hot and cold application on knee joint proprioception. Celal Bayar University Thesis, Counsellor: Assoc. Prof. Devrim Akseki, Manisa (2007) 32. Pap, G., Machner, A., Nebelung, W., Awiszus, F.: Detailed analysis of proprioception in normal and ACL-deficient knees. J. Bone Joint Surg. Br. 81, 764–768 (1999) 33. Rees, S.S., Murphy, A.J., Watsford, M.L., McLachlan, K.A., Coutts, A.J.: Effects of proprioceptive neuromuscular facilitation stretching on stiffness and force-producing characteristics of the ankle in active women. J. Strength Cond. Res. 21, 572–577 (2007) 34. Riva, D., Rossittob, F., Battocchioa, L.: Postural muscle atrophy prevention and recovery and bone remodelling through high frequency proprioception for astronauts. Acta Astronaut. 65, 813–819 (2009) 35. Robbins, S., Waked, E., Rappel, R.: Ankle taping improves proprioception before and after exercise in young men. Br. J. Sports Med. 29, 242–247 (1995) 36. Rosenkranz, K., Butler, K., Williamon, A., Cordivari, C., Lees, A.J., Rothwell, J.C.: Sensorimotor reorganization by proprioceptive training in musician’s dystonia and writer’s cramp. Neurology 70, 304–315 (2008) 37. Schmitt, H., Kuni, B., Sabo, D.: Influence of professional dance training on peak torque and proprioception at the ankle. Clin. J. Sport Med. 15, 331–339 (2005) 38. Sekir, U., Yildiz, Y., Hazneci, B., Ors, F., Aydin, T.: Effect of isokinetic training on strength, functionality and proprioception in athletes with functional ankle instability. Knee Surg. Sports Traumatol. Arthrosc. 15, 654–664 (2007) 39. Trans, T., Aaboe, J., Henriksen, M., Christensen, R., Bliddal, H., Lund, H.: Effect of whole body vibration exercise on muscle strength and proprioception in females with knee osteoarthritis. Knee 16, 256–261 (2009) 40. Verhagen, E., Beek, A., Twisk, J., Bouter, L., Bahr, R., Mechelen, W.: The effect of a proprioceptive balance board training program for the prevention of ankle sprains: a prospective controlled trial. Am. J. Sports Med. 32, 1385–1393 (2004) 41. Xu, D., Hong, Y., Li, J., Chan, K.: Effect of tai chi exercise on proprioception of ankle and knee joints in old people. Br. J. Sports Med. 38, 50–54 (2004)

Part Sports Injuries of the Upper Extremity: Shoulder Injuries

III

Rotator Interval Mehmet Hakan Özsoy and Alp BayramoÜlu

Introduction

Contents Introduction ..................................................................................

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Functional Anatomy ....................................................................

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Clinical Importance .....................................................................

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References .....................................................................................

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Neer in 1970 used the term “rotator interval” to describe the space between the supraspinatus and subscapularis tendons [10]. Later studies indicated that the rotator interval (RI) is an important anatomical entity with a significant role in shoulder stability [4, 7, 10, 18, 20]. Furthermore, Rowe and Zarins showed the variability in RI size in patients with anteroinferior shoulder instability. They reported that failure in the anterior stabilization procedures were associated with enlarged RI area [17]. Moreover, another function of the rotator interval in stabilizing the long head of biceps tendon has been described [5]. Recent studies pointed out that RI is a dynamic structure of which dimensions vary with the movements of the shoulder joint [13, 14].

Functional Anatomy

M.H. Özsoy ( ) First Clinic of Orthopaedics and Traumatology, Ankara Training and Research Hospital, Ulucanlar Street, 06340, Ankara, Turkey e-mail: [email protected] A. BayramoÜlu Department of Anatomy, Hacettepe University, Sıhhiye, 06100 Ankara, Turkey e-mail: [email protected]

The RI of the shoulder refers to the interspace between the supraspinatus and subscapularis tendons through which courses the long head of biceps tendon [5, 12, 16] (Fig. 1). The base of this triangle is at the coracoid process medially and the transverse humeral ligament forms the apex laterally at the intertubercular groove (Fig. 2). The RI contains coracohumeral ligament (CHL) on the bursal side and the Superior glenohumeral ligament (SGHL) on the articular side. The floor of the RI region is variably bridged by the capsule, CHL, SGHL, and occasionally the middle glenohumeral ligament (MGHL) (Fig. 3). The CHL originates on the proximal third of the dorsal aspect of the coracoid to extend and insert in the greater tuberosity and to a smaller amount passing over the biceps tendon to insert in the proximal aspect of the lesser tuberosity. Distinct bands of the CHL span the bicipital groove (Fig. 4). Laterally, it contains two discrete bands. One of these bands blends into the greater tuberosity and the supraspinatus tendon; the other merges into the lesser tuberosity, the subscapularis tendon, and the transverse humeral ligament on the bicipital

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_11, © Springer-Verlag Berlin Heidelberg 2012

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Fig. 1 Cadaveric dissection. Left shoulder, anterior view. Coracoid removed. Long head of the biceps tendon is visualized after removal of the rotator interval area

groove. Because of this blending the insertion of the CHL often cannot be clearly distinguished from other structures [7]. The SGHL originates from the labrum adjacent to the supraglenoid tubercle and crosses the inferior surface of the RI deep to the CHL and inserts on the superior aspect of the lesser tuberosity known as fovea capitis humeri. The remaining structure of the RI is the long head of the biceps tendon, which originates from the superior glenoid labrum and supraglenoid tubercle. It traverses along the RI and exits the glenohumeral joint capsule through the apex of the RI from an anatomical structure known as the biceps pulley. The SGHL,

Fig. 2 Diagram of the left shoulder showing the borders of the rotator interval area

Fig. 3 Cadaveric dissection. Left shoulder, anterior view. Coracoid removed. Superior glenohumeral ligament (SGHL), long head of the biceps tendon and occasionally middle glenohumeral ligament (MGHL) are found in the rotator interval area

CHL, and subscapularis tendon are the essential components of the biceps pulley system (Fig. 5). They maintain the anatomic position of the biceps tendon within the bicipital groove [5]. The medial sheath of the bicipital groove (medial reflection of the CHL) consists of SGHL/CHL complex and the

Fig. 4 Cadaveric dissection. Left shoulder, anterior wiev. Coracohumeral ligament (CHL) and its anatomic relations with supraspinatus and subscapularis muscles are seen

Rotator Interval

77 Coracoid

CHL

SGHL

B

Glenoid

Subscap

Humeral head

In conclusion, both CHL and SGHL are important structures in shoulder biomechanics since most surgical interventions consider both ligaments. Rotator interval area, which does not have rotator cuff support, is also important in keeping negative pressure within the joint, and a defect significantly increases humeral head translation. Studies demonstrated that perforations in the joint capsule or the rotator interval creates a 52% increase in the humeral head translation anterior and posteriorly, simply by loss of the negative intra-articular pressure [12].

Clinical Importance Fig. 5 Diagram showing the components of the biceps pulley. Superior glenohumeral ligament (SGHL), subscapularis tendon and the medial band of the coracohumeral ligament (CHL) forms the medial part of the biceps pulley system which is the most important structure maintaining the anatomic position of the biceps tendon within the bicipital groove

insertion of the subscapularis tendon. Together, these structures contribute to the medial wall of the bicipital sheath. The SGHL together with the medial reflection of the CHL make up of more robust medial-superior pulley system. Lateral wall is formed by the CHL. The most important structure for prevention of medial biceps tendon subluxation is the pulley system or SGHL/ medial CHL complex, not the transverse humeral ligament. Cutting the transverse humeral ligament alone does not allow for biceps tendon subluxation. Clinical and biomechanical studies indicated that the rotator interval has importance in the stability and biomechanics of shoulder functions by controlling the anteroinferior and posterior translation and also the external rotation of the adducted shoulder [1, 4, 6, 7, 9]. The dominance of CHL or SGHL in this controlling function still remains controversial [1, 6, 18]. Boardman et al. claimed that CHL had greater stiffness and ultimate loads to failure compared to SGHL [1]. Similarly Itoi and coworkers suggested that the CHL was the primary structure responsible for restricting the inferior translation of the shoulder in external rotation [6]. Contrary to this, Warner et al. stated that the primary restraint to inferior translation of the adducted shoulder was the SGHL. The CHL appeared to have no significant suspensory role [18]. In a recent cadaveric study, Jost et al. distinguished two functional components of the rotator interval, a medial part consisting of two layers and a lateral part composed of four layers. The medial component, the coracohumeral ligament, was reported to mainly control inferior translation of the adducted arm and to a lesser extent the external rotation. However, the lateral component mainly controlled the external rotation of the adducted arm [7].

There is renewed interest in the function of the interval region especially the RI defects since a defect in this area has been associated with recurrent anteroinferior and multidirectional instability. Clinically, in glenohumeral instability cases, when the sulcus sign does not disappear with external rotation of the shoulder, a defect in the RI area should be suspected. In general, studies address that a complete RI capsular defect should be closed as a part of a stabilization procedure especially when inferior translation predominates [2, 4, 11, 17, 19, 20]. Pathology of the RI can be classified based on different issues. Nobuhara and Ikeda reported the RI lesions in two types according to its mechanical strength. In type I, the RI is contracted and the superficial tissues are affected primarily. When the rotator interval and the CHL are contracted the motion of the glenohumeral joint is evidently restricted [11]. In type II, the RI is lax accompanying with glenohumeral instability. Type II lesions are thought to involve basically the deeper structures of the RI. RI laxity, in contributing to shoulder instability, was shown with magnetic resonance imaging (MRI) correlation in a study by Kim et al. [8]. Clinical studies reported that suture plication or imbrication in superoinferior direction resulted in better functional outcomes in glenohumeral instability operations [3, 15]. Nobuhara and Ikeda reported 76 of 106 shoulders (101 patients) treated with open RI repair for instability. Of those cases 40% had complete pain relief, 56% had pain only with overuse of the shoulder. Seventy percent of them were able to return to normal activities of daily life whereas three patients had persistent and clinically significant shoulder instability [11]. Wolf et al. reported that, RI closure decreased anterior (17%), posterior (15%), and inferior (25%) translations [19]. Similarly the study of Yamamato et al. revealed that, RI closure between SGHL/MGHL and SGHL/SSC reduced anterior translation in the adducted shoulder. Furthermore, SGHL/ MGHL closure reduced anterior translation in abductionexternal rotation and posterior translation in adduction [20].

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However, Plausinis et al. reported that, although RI closure reduced the anteroinferior translation of the adducted shoulder it had no effect on posterior translation [15]. Similarly, Molonge claimed that interval closure had no effect on posterior stability. In conclusion, although the effects of the RI closure remain controversial, there is agreement that it decreases translation of the shoulder in anterior and inferior directions [9]. However, its effect on the posterior translation is questionable. Although RI closure decreased the instability it might result in postoperative loss in external rotation of the operated shoulder. Molonge reported that there is 14.3° loss in external rotation in adduction [9]. Similarly Plausinis et al. and Field et al. reported 10°–15° loss in external rotation postoperatively [2, 15]. The rotator interval was reported to be a dynamic structure, the dimensions of which change with shoulder rotation, with the interval opening up (tightens) with external and closing down (loosens) with internal rotation [13, 14]. Harryman et al. also mentioned that abduction and IR relaxed the interval capsule [4]. In cadaveric studies, Plancher et al. and Ozsoy et al. reported that the RI closes down (loosens) with internal rotation and opens up (tightens) with external rotation in the adducted shoulder [13, 14] (Fig. 6a, b). Furthermore, Ozsoy et al. reported that, abduction relaxed the interval capsule and concluded that, repairing the RI in internal rotation or in abduction may cause overtightening and might limit postoperative external rotation of the patient [13] (Fig. 6c). In order not to have postoperative ER restriction, plication should be made in external rotation in adducted shoulder (beach chair position) or one should be cautious to decrease the degree of shoulder abduction in addition to holding it in external rotation when performing the operation in lateral decubitus position [13, 16]. RI lesions of the shoulder remain a controversial issue in shoulder instability. Surgical treatment of the RI may be indicated in a selected group of instability procedures; however, the evidence for routine treatment is indefinite.

References 1. Boardman, N.D., Debski, R.E., Warner, J.P., et al.: Tensile properties of the superior glenohumeral and coracohumeral ligaments. J. Shoulder Elbow Surg. 5, 249–254 (1996) 2. Field, L.D., Warren, R.F., O’Brien, S.J., Altchek, D.W., Wickiewicz, T.L.: Isolated closure of rotator interval defects for shoulder instability. Am. J. Sports Med. 23, 557–563 (1995) 3. Gartsman, G.M., Roddey, T.S., Hammerman, S.M.: Arthroscopic treatment of anterior-inferior glenohumeral instability. Two to fiveyear follow-up. J. Bone Joint Surg. Am. 82, 991–1003 (2000)

Fig. 6 (a) Cadaveric dissection. Left shoulder, anterior view. Coracoid removed. The dimensions of the rotator interval in beach chair position, neutral rotation. (b) Beach chair position, 45° internal rotation. Lengthening at the coracoid base and shortening at the subscapularis border in comparison to neutral rotation (Fig. 6a) can be seen. (c) Beach chair position, 45° abduction, neutral rotation. Lengthening at the coracoid base and shortening at both the supraspinatus and subscapularis borders can be seen

Rotator Interval 4. Harryman II, D.T., Sidles, J.A., Harris, S.L., Matsen III, F.A.: The role of the rotator interval capsule in passive motion and stability of the shoulder. J. Bone Joint Surg. Am. 74, 53–66 (1992) 5. Hunt, S.A., Kwon, Y.W., Zuckerman, J.D.: The rotator interval: anatomy, pathology, and strategies for treatment. J. Am. Acad. Orthop. Surg. 15, 218–227 (2007) 6. Itoi, E., Berglund, L.J., Grabowski, J.J., et al.: Superior-inferior stability of the shoulder: role of the coracohumeral ligament and the rotator interval capsule. Mayo Clin. Proc. 73, 508–515 (1998) 7. Jost, B., Koch, P.P., Gerber, C.: Anatomy and functional aspects of the rotator interval. J. Shoulder Elbow Surg. 9, 336–341 (2000) 8. Kim, K.C., Rhee, K.J., Shin, H.D., Kim, Y.M.: Estimating the dimensions of the rotator interval with use of magnetic resonance arthrography. J. Bone Joint Surg. Am. 89, 2450–2455 (2007) 9. Mologne, T.S., Zhao, K., Hongo, M., Romeo, A.A., An, K.N., Provencher, M.T.: The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability: effect on glenohumeral translation and range of motion. Am. J. Sports Med. 36, 1123–1131 (2008) 10. Neer II, C.S.: Displaced proximal humerus fractures: I. Classification and evaluation. J. Bone Joint Surg. Am. 52, 1077–1089 (1970) 11. Nobuhara, K., Ikeda, H.: Rotator interval lesion. Clin. Orthop. Relat. Res. 223, 44–50 (1987) 12. Nottage, W.: Rotator interval lesions: physical exam, imaging, arthroscopic findings, and repair. Tech. Shoulder Elbow Surg. 4, 175–184 (2003)

79 13. Ozsoy, M.H., Bayramoglu, A., Demiryurek, D., et al.: Rotator interval dimensions in different shoulder arthroscopy positions: a cadaveric study. J. Shoulder Elbow Surg. 17, 624–630 (2008) 14. Plancher, K.D., Johnston, J.C., Peterson, R.K., Hawkins, R.J.: The dimensions of the rotator interval. J. Shoulder Elbow Surg. 14, 620– 625 (2005) 15. Plausinis, D., Bravman, J.T., Heywood, C., et al.: Arthroscopic rotator interval closure: effect of sutures on glenohumeral motion and anterior-posterior translation. Am. J. Sports Med. 34, 1656–1661 (2006) 16. Provencher, M.T., Saldua, N.S.: The rotator interval of the shoulder: anatomy, biomechanics, and repair techniques. Oper. Tech. Orthop. 18, 9–22 (2008) 17. Rowe, C.R., Zarins, B.: Recurrent transient subluxation of the shoulder. J. Bone Joint Surg. Am. 63, 863–872 (1981) 18. Warner, J.J., Deng, X.H., Warren, R.F., Torzilli, P.A.: Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am. J. Sports Med. 20, 675–685 (1992) 19. Wolf, R.S., Zheng, N., Iero, J., Weichel, D.: The effects of thermal capsulorrhaphy and rotator interval closure on multidirectional laxity in the glenohumeral joint: a cadaveric biomechanical study. Arthroscopy 20, 1044–1049 (2004) 20. Yamamoto, N., Itoi, E., Tuoheti, Y., et al.: Effect of rotator interval closure on glenohumeral stability and motion: a cadaveric study. J. Shoulder Elbow Surg. 15, 750–758 (2006)

Pathology of Rotator Cuff Tears Achilleas Boutsiadis, Dimitrios Karataglis, and Pericles Papadopoulos

Introduction

Contents Introduction .................................................................................

81

Pathology of Rotator Cuff Tearing ............................................ Extrinsic Factors ........................................................................... Intrinsic Factors ............................................................................ Rotator Cuff Vascularity ............................................................... Neural Theory of Tendinopathy .................................................... Genetic Influences in Rotator Cuff Tears ......................................

81 81 82 83 84 85

Summary......................................................................................

85

References ....................................................................................

85

Rotator cuff injuries are common, especially above the age of 60 and have an effect not only on shoulder function but also on the overall health status and quality of life of the patients [28]. Codman first attempted to describe rotator cuff tear pathology in 1934 [8]. Since then many theories have been proposed in order to explain the underlying pathology and efforts have been made to define the predicting factors leading to rotator cuff tears. During the last decades the factors contributing to this complicated disease have been teamed into two major categories: the extrinsic and the intrinsic factors. Extrinsic factors actually involve anatomic and demographic variables that predispose to supraspinatus tears, while intrinsic factors include pathologic and degenerative changes into the substance of the tendon and the muscle itself. Nowadays, it is thought that in most cases both extrinsic and intrinsic factors play a significant role in rotator cuff pathology. Despite the progress of molecular biology, many issues concerning the pathogenesis of this disease remain unknown and have not been fully understood to date.

Pathology of Rotator Cuff Tearing Extrinsic Factors Impingement and Acromial Shape

A. Boutsiadis ( ), D. Karataglis, and P. Papadopoulos 1st Orthopaedic Department “G Papanikolaou” General Hospital, Aristotelian University of Thessaloniki, Exohi Thessaloniki, 57010 Chortiatis, Greece e-mail: [email protected]; [email protected]; [email protected]

In 1987, Neer et al. [31], after intraoperative observation of 400 patients, suggested that the impingement of the tendon to the anterior third of the acromion is responsible for 95% of tears. This hypothesis was emphasized by observations from Bigliani et al. [4] that the degree of impingement was dependent on the acromial shape. They demonstrated that the shape of the acromion varied in the sagittal plane and proposed three types for it: Type I (flat), Type II (curved), and Type III (hooked acromion). Additionally, a positive correlation was found between the type of the acromion and the presence of rotator cuff tear,

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_12, © Springer-Verlag Berlin Heidelberg 2012

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with Type III having the worst influence on unobstructed tendon movement in the subacromial space [4, 25, 42]. In the early 1990s Neer’s hypothesis gained universal acceptance and either open or arthroscopic subacromial decompression was established as a very successful means for relieving shoulder pain associated with cuff pathology. However, subsequent studies suggested that Type II and III acromions were not congenital [35, 44]. Furthermore, progression from Type I to Type III acromion was found to be related to age [42]. Traction forces applied from the coracoacromial ligament to the anterior third of the acromion appear to lead to the formation of a spur at this area [35]. Additionally, many researchers found that subacromial decompression alone did not always guarantee pain relief for the patients [10, 17]. Nowadays, it is well documented that rotator cuff tears usually start on the articular side and not from the bursal side, which renders pure impingement of the rotator cuff leading to attritional changes rather unlikely. It is still thought that impingement on the traction related acromial spur may indirectly contribute to rotator cuff pathology, but its “mechanical” role is not believed to be as important as was thought before [19].

Demographic Factors A number of demographic variables are also included in extrinsic factors. However, most demographic factors have been poorly investigated, and little quality data is available. The association between hand dominance, mechanical overuse, and rotator cuff pathology is relatively well documented. Yamaguchi et al. [43] stated that tears are often more symptomatic in the dominant than in the nondominant arm. However, 36% of those with a symptomatic full-thickness tear had a co-existing asymptomatic full-thickness tear in the contralateral nondominant side. In addition, ultrasonographic investigation revealed the likelihood of this rising to 50% in patients older than 60 years old [43]. Another demographic parameter with negative influence on rotator cuff integrity is smoking. Recently, Baumgarten et al. observed in humans a strong association between smoking and rotator cuff disease. It is very important to note that supraspinatus tears appear to have a dose and a time-dependent relationship with smoking [2]. Nicotine is also strongly correlated with poorer outcomes following rotator cuff repairs. Rat animal model studies, as well as clinical investigations revealed that nicotine can have deleterious effects on tendon healing and smokers have significantly reduced postoperative function, increased pain scores and less patient satisfaction [12, 26]. Finally, other factors such as diabetes mellitus have been associated with decreased ability of tendon healing after rotator cuff repairs [6].

A. Mpoutsiadis et al.

Intrinsic Factors The term intrinsic factors encompasses a variety of mechanisms that occur within the rotator cuff itself. Among the theories proposed, age-related degeneration and repetitive microtrauma seem to be the most reliable models explaining the mechanism of cuff disease. However, we must take into account the role of cuff vascularity as well as the neural theory for tendinopathy.

Degeneration and Microtrauma Theory Epidemiological studies with ultrasound examination revealed a positive correlation between age and supraspinatus tendon tear prevalence [39]. More specifically, the frequency of these tears increased from 13% in the youngest group (50–59 years) to 20% (60–69 years), 31% (70–79 years), and 52% in the oldest group (80–89 years) [39]. It is important to note though, that the majority of the examined patients were asymptomatic. This observation leads to the hypothesis that rotator cuff tear may be a “normal” aging process. Histological studies support the previous hypothesis of an ongoing degenerative process contributing to rotator cuff disease. Loss of cellularity and vascularity, as well as fibrocartilage mass formation are age-related changes frequently found at the site of cuff insertion [1, 27]. In a recent study Hashimoto et al. [16] found seven characteristic histological findings in torn rotator cuff: 1. 2. 3. 4. 5. 6. 7.

Thinning and disorientation of the collagen fibers Myxoid degeneration Hyaline degeneration Vascular proliferation (34%) Fatty infiltration (33%) Chondroid metaplasia (21%) Intratendinous calcification (19%)

We have to lay emphasis on the fact that vascular proliferation and fatty infiltration were seen only on the bursal side of the cuff. The remaining five histological changes were found on the articular side as primary degenerative “reducers” of tendon tensile capacity [16, 18]. Moreover, in an effort to detect molecular-biochemical mediators influencing rotator cuff pathology Premdas et al. [34] observed a high level of Smooth Muscle Actin (SMA) in the nonvascular connective tissue near the edges of the torn rotator cuff. SMA in vitro causes contraction of the collagenglycosaminoglycan compounds. In vivo, this action may lead to contraction of the torn cuff edges, increasing the distance at the repair margin and inhibiting primary healing. Great importance must be given on the role of altered collagen fiber quality [21]. Generally, the central zone of the

Pathology of Rotator Cuff Tears

healthy supraspinatus tendon is primarily composed of Type I collagen fibers with smaller amounts of Type III collagen, decorin, and biglycan. On the other hand, the primary component at the zone of tendon insertion (tendon’s footprint) is Type II collagen, which can withstand better compressive loads. Histological findings in the diseased rotator cuff reveal alteration in the type of collagen at the fibrocartilaginous zone from Type II to Type III, with a subsequent tendon ability to withstand compressive loads [24]. However, it is not well known whether this change is an age-related “physiological” degeneration or the result of repetitive overuse and microinjury. Parallel to degeneration, the microtrauma theory suggests that repetitive overload stresses lead to micro-injuries and lacerations within the tendon mass that are not given sufficient time to heal before further trauma occurs. The “roots” of this theory can be found back in 1934, when Codman demonstrated that partial tears of the tendon began in the articular side, where the load capacity is lower than in the bursal side [7]. A further question is what the role of inflammatory reaction is during these repetitive overload stresses. For this reason Soslowksy et al. [37] created an animal rat model, mirroring the repetitive motion of the supraspinatus under the acromial arch. They observed downregulation of gene expression in transforming growth factor beta-1 (TGF-E1), increase in cellularity, loss of collagen orientation, and alterations in gross cell morphologic characteristics. It is important that by the end of 13 weeks the tendon had a higher cross sectional area but could withstand lower load to failure. In another rat model study using the reverse-transcriptase polymerase chain reaction (RT-PCR), acute increase in angiogenic markers (VEGF) (400% in 3 days) and subacute increase in COX-2 (300% in 8 weeks) was observed [33]. Ex vivo studies investigated the biochemical cascade of interleukin-1 beta (IL-1E) on human tendon cells. They revealed an increase of COX-2 leading to higher levels of prostaglandin E2 (PGE2) [40]. At the same time, an elevation of the levels of matrix metalloproteases (MMP), specifically MMP-1, MMP-3, and MMP-13, was found. Numerous other studies revealed an increase of the aforementioned inflammatory mediators during tensile loading of supraspinatus tendon [20, 22]. Although the significance of IL-1E in cuff tears remains unknown in vivo, it is believed that COX-2 and PGE2 are mainly pain mediators and MMPs lead to loss of tissue architecture. Despite the fact that inflammatory mediators are present, histological studies in cadaveric and postsurgical specimens with rotator cuff tears did not show any significant chronic inflammatory reaction. Benson et al. [3] found morphological evidence of degeneration and edema within the extracellular matrix, amyloid deposition (20%), but no evidence of chronic inflammation with few B- or T-lymphocytes present

83

in patients that underwent subacromial decompression. The only indirect finding of a chronic inflammatory process is the revascularization noted either intraoperatively [16] or with Doppler ultrasound [32]. In vivo studies of rotator cuff tear pathology did not prove a significant role in the inflammatory reaction in the degenerative process [3].

Oxidative Stress and Apoptosis In 2002, Yuan et al. demonstrated the presence of increased concentration of apoptotic cells at the edge of the torn rotator cuff tear (34%) compared with normal tendons (13%) [45]. Further studies demonstrated that exposure of cultured human rotator cuff tendon cells to oxidative stress via administration of H2O2 resulted in increased concentrations of key apoptotic mediators such as cytochrome–C and caspase-3 within the cells [46]. Finally, in vivo studies in human torn rotator cuff revealed decreased levels of a novel antioxidant peroxidase, peroxiredoxin 5 (PRDX5). Induced overexpression of PRDX5 results in reduction of apoptosis by 46% [47]. All the previous studies suggest that oxidative stress has an important role in supraspinatus tendinopathy and tear. Murrel and his team made a great effort to explore the mediators of this oxidative reaction and to propose a possible model pathway [41]. According to their findings in torn supraspinatus specimens in vivo, two key mediators were found to play an important role: Matrix metalloproteinase (MMP-1) within the extracellular matrix and c-Jun N-terminal protein kinase (JNK) within the intracellural matrix. MMP-1 levels are elevated within damaged tendons, leading to loss of tissue architecture, decreased collagen synthesis, and abnormal tendon biomechanics. Moreover, JNK is a mitogen-induced protein kinase that is induced in tendons by IL-1 and by cyclic mechanical stretch [36] (Fig. 1). JNK, when phosphorylated, activates a number of transcription factors linked to the apoptotic pathway [9]. When JNKspecific inhibitors were used, there was a reduction in MMP levels and tendon disruption. A possible model pathway is illustrated in Fig. 2.

Rotator Cuff Vascularity In 1990, Lohr and Uhthoff [23] reported that there is a critical hypovascular zone 10–15 mm proximal to the insertion of the supraspinatus tendon. Since then, this area and its exact role became a matter of debate. Other studies [5, 30] examining capillary distributions, vessel number, and diameter found that no significant hypovascular areas exist.

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A. Mpoutsiadis et al. MMP-1

pJNK

Normal supraspinatus tendon

Torn supraspinatus tendon

Fig. 1 Immunohistochemical detection of phosphorylated JNK and MMP1 in the longitudinal sections of rotator cuff tendons [41]

Oxidative stress

Apoptosis

JNK activation

Collagen synthesis

Moreover, recent histological and immunohistochemical studies in torn tendons revealed relative hyperperfusion at this “critical” area [11]. Additionally, intraoperative laser Doppler flowmetry showed again hyperperfusion at the tear edge [38] casting considerable doubt on the importance of the supraspinatus critical zone. Questions have been raised if arterial perfusion can be reduced during full arm adduction or during compression at the humeral head.

MMP1

Neural Theory of Tendinopathy Cellular function

Extracellular matrix degradation

Tendon degeneration

Fig. 2 Possible pathway of tendon degeneration under oxidative stress [41]

In 2006, Molloy et al. [29] observed in a rat model increased expression of a range of glutamate-signaling proteins after overuse. Culture of tendon cells in glutamate led to increase of their apoptotic frequency. It is important to note that glutamate is a peptide associated with the central nervous system and is already involved in the pathogenesis of tendon degeneration. Additionally, high concentrations of substance P have been related with the diseased rotator cuff [13]. It is

Pathology of Rotator Cuff Tears

possible that the neural overstimulation observed, leads to painful symptoms, disorganization of cuff architecture, and structural weakness that subsequently results in a tear. Previous observations constitute the cornerstone of the neural theory, which remains controversial but constitutes an exciting source for future research.

Genetic Influences in Rotator Cuff Tears Besides the presented theories, lately, questions have been raised on the importance of the underlying genetic susceptibility to the pathology of rotator cuff. Recent studies [14, 15] have shown that genetic influences may exist. An increased incidence of supraspinatus tears in siblings of patients with known tears was recently observed. It has also been suggested that genetic factors may influence the progression and the size of the tear, as well as the presence of pain in the medium term [14, 15]. Genetic factors may play their role not only in the development but also in the progression of full thickness tears. However, further studies are needed to provide more solid data on this issue.

Summary The overall incidence of full-thickness tears in the general population ranges between 7% and 27%, and that of partialthickness tears between 13% and 37%. Not all of them are symptomatic. Theories on the cause of these tears range from purely mechanical or attritional damage to intrinsic agerelated degeneration. Whether intrinsic or extrinsic factors contribute to the occurrence of tears and to what extent is still not clear. However, alteration of the cellular and extracellular matrix, with evidence of an apoptotic process within the tendon, has been noted in a number of studies, but the exact pathway for this is still unclear.

References 1. Barr, K.P.: Rotator cuff disease. Phys. Med. Rehabil. Clin. N. Am. 15(2), 475–491 (2004) 2. Baumgarten, K.M., Gerlach, D., Galatz, L.M., et al.: Cigarette smoking increases the risk for rotator cuff tears. Clin. Orthop. Relat. Res. 468(6), 1534–41 (2010). [Epub 13 Mar 2009] 3. Benson, R.T., McDonnell, S.M., Rees, J.L., et al.: The morphological and immunocytochemical features of impingement syndrome and partial-thickness rotator-cuff tear in relation to outcome after subacromial decompression. J. Bone Joint Surg. Br. 91(1), 119–123 (2009)

85 4. Bigliani, L., Morrison, D., April, E.: The morphology of the acromion and rotator cuff impingement. Orthop. Trans. 10, 228 (1986) 5. Brooks, C.H., Revell, W.J., Heatley, F.W.: A quantitative histological study of the vascularity of the rotator cuff tendon. J. Bone Joint Surg. Br. 74, 151–153 (1992) 6. Chen, A.L., Shapiro, J.A., Ahn, A.K., et al.: Rotator cuff repair in patients with type I diabetes mellitus. J. Shoulder Elbow Surg. 12(5), 416–421 (2003) 7. Codman, E.A.: The Shoulder: Rupture of the Supraspinatus Tendon and Other Lesions in or About the Subacromial Bursa. Thomas Todd, Boston (1934) 8. Codman, E.A., Ackerson, I.B.: The pathology associated with rupture of the supraspinatus tendon. Ann. Surg. 93(1), 348–359 (1931) 9. Filomeni, G., Aquilano, K., Civitareale, P., et al.: Activation of c-Jun-N terminal kinase is required for apoptosis triggered by glutathione disulfide in neuroblastoma cells. Free Radic. Biol. Med. 39(3), 345–354 (2005) 10. Flatow, E.L., Weinstein, D.M., Duralde, X.A., et al.: Coracoacromial ligament preservation in rotator cuff surgery. J. Shoulder Elbow Surg. 3(Suppl), S73 (1994) 11. Fukuda, H., Hamada, K., Yamanaka, K.: Pathology and pathogenesis of bursal-side rotator cuff tears viewed from en bloc histologic sections. Clin. Orthop. Relat. Res. 254, 75–80 (1990) 12. Galatz, L.M., Silva, M.J., Rothermich, S.Y., et al.: Nicotine delays tendon-to-bone healing in a rat shoulder model. J. Bone Joint Surg. Am. 88(9), 2027–2034 (2006) 13. Gotoh, M., Hamada, K., Yamakawa, H., et al.: Increased substance P in subacromial bursa and shoulder pain in rotator cuff diseases. J. Orthop. Res. 16(5), 618–621 (1998) 14. Gwilym, S.E., Watkins, B., Cooper, C.D., et al.: Genetic influences in the progression of tears of the rotator cuff. J. Bone Joint Surg. Br. 91(7), 915–917 (2009) 15. Harvie, P., Ostlere, S.J., Teh, J., et al.: Genetic influences in the aetiology of tears of the rotator cuff: sibling risk of a full-thickness tear. J. Bone Joint Surg. Br. 86-B, 696–700 (2004) 16. Hashimoto, T., Nobuhara, K., Hamada, T.: Pathologic evidence of degeneration as a primary cause of rotator cuff tear. Clin. Orthop. Relat. Res. 415, 111–120 (2003) 17. Hyvonen, P., Lohi, S., Jalovaara, P.: 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(5), 813–816 (1998) 18. Kannus, P., Jozsa, L.: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J. Bone Joint Surg. Am. 73(10), 1507–1525 (1991) 19. Ko, J.Y., Huang, C.C., Chen, W.J., et al.: Pathogenesis of partial tear of the rotator cuff: a clinical and pathologic study. J. Shoulder Elbow Surg. 15(3), 271–278 (2006) 20. Koshima, H., Kondo, S., Mishima, S., et al.: Expression of interleukin-1E, cyclo-oxygenase-2, and prostaglandin E2 in a rotator cuff tear in rabbits. J. Orthop. Res. 25(1), 92–97 (2007) 21. Kumagai, J., Sarkar, K., Uhthoff, H.K.: The collagen types in the attachment zone of rotator cuff tendons in the elderly: an immunohistochemical study. J. Rheumatol. 21(11), 2096–2100 (1994) 22. Li, Z., Yang, G., Khan, M., et al.: Inflammatory response of human tendon fibroblasts to cyclic mechanical stretching. Am. J. Sports Med. 32(2), 435–440 (2004) 23. Lohr, J.F., Uhthoff, H.K.: The microvascular pattern of the supraspinatus tendon. Clin. Orthop. Relat. Res. 254, 35–38 (1990) 24. Longo, U.G., Franceschi, F., Ruzzini, L., et al.: Histopathology of the supraspinatus tendon in rotator cuff tears. Am. J. Sports Med. 36(3), 533–538 (2008) 25. MacGillivray, J.D., Fealy, S., Potter, H.G., et al.: Multiplanar analysis of acromion morphology. Am. J. Sports Med. 26(6), 836–840 (1998)

86 26. Mallon, W.J., Misamore, G., Snead, D.S., et al.: The impact of preoperative smoking habits on the results of rotator cuff repair. J. Shoulder Elbow Surg. 13(2), 129–132 (2004) 27. Matthews, T.J., Hand, G.C., Rees, J.L., et al.: Pathology of the torn rotator cuff tendon. Reduction in potential for repair as tear size increases. J. Bone Joint Surg. Br. 88(4), 489–495 (2006) 28. McKee, M.D., Yoo, D.J.: The effect of surgery for rotator cuff disease on general health status. Results of a prospective trial. J. Bone Joint Surg. Am. 82(7), 970–979 (2000) 29. Molloy, T.J., Kemp, M.W., Wang, Y., et al.: Microarray analysis of the tendinopathic rat supraspinatus tendon: glutamate signaling and its potential role in tendon degeneration. J. Appl. Physiol. 101(6), 1702–1709 (2006) 30. Moseley, H.F., Goldie, I.: The arterial pattern of the rotator cuff of the shoulder. J. Bone Joint Surg. Br. 45, 780–789 (1963) 31. Neer II, C.S., Poppen, N.K.: Supraspinatus outlet. Orthop. Trans. 11, 234 (1987) 32. Ohberg, L., Lorentzon, R., Alfredson, H.: Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surg. Sports Traumatol. Arthrosc. 9(4), 233–238 (2001) 33. Perry, S.M., McIlhenny, S.E., Hoffman, M.C., et al.: Inflammatory and angiogenic mRNA levels are altered in a supraspinatus tendon overuse animal model. J. Shoulder Elbow Surg. 14(1 Suppl S), 79S–83S (2005) 34. Premdas, J., Tang, J.B., Warner, J.P., et al.: The presence of smooth muscle actin in fibroblasts in the torn human rotator cuff. J. Orthop. Res. 19(2), 221–228 (2001) 35. Shah, N.N., Bayliss, N.C., Malcolm, A.: Shape of the acromion: congenital or acquired – a macroscopic, radiographic, and microscopic study of acromion. J. Shoulder Elbow Surg. 10(4), 309–316 (2001) 36. Skutek, M., van Griensven, M., Zeichen, J., et al.: Cyclic mechanical stretching of human patellar tendon fibroblasts: activation of JNK and modulation of apoptosis. Knee Surg. Sports Traumatol. Arthrosc. 11(2), 122–129 (2003)

A. Mpoutsiadis et al. 37. Soslowsky, L.J., Thomopoulos, S., Tun, S., et al.: Neer Award 1999. Overuse activity injures the supraspinatus tendon in an animal model: a histologic and biomechanical study. J. Shoulder Elbow Surg. 9(2), 79–84 (1999) 38. Swiontkowski, M.F., Iannotti, J.P., Boulas, H.J., et al.: Intraoperative assessment of rotator cuff vascularity using laser Doppler flowmetry. In: Post, M., Morrey, B.F., Hawkins, R.J. (eds.) Surgery of the Shoulder, pp. 208–212. Mosby, St. Louis (1990) 39. Tempelhof, S., Rupp, S., Seil, R.: Age-related prevalence of rotator cuff tears in asymptomatic shoulders. J. Shoulder Elbow Surg. 8(4), 296–299 (1999) 40. Tsuzaki, M., Guyton, G., Garrett, W., et al.: IL-1 beta induces COX2, MMP-1, -3, and -13, ADAMTS-4, IL-1 beta and IL-6 in human tendon cells. J. Orthop. Res. 21(2), 256–264 (2003) 41. Wang, F., Murrell, G.A., Wang, M.X.: Oxidative stress–induced c-Jun Nterminal kinase (JNK) activation in tendon cells upregulates MMP1 mRNA and protein expression. J. Orthop. Res. 25(3), 378– 389 (2007) 42. Wang, J.C., Shapiro, M.S.: Changes in acromial morphology with age. J. Shoulder Elbow Surg. 6(1), 55–59 (1997) 43. Yamaguchi, K., Ditsios, K., Middleton, W.D., et al.: The demographic and morphological features of rotator cuff disease. A comparison of asymptomatic and symptomatic shoulders. J. Bone Joint Surg. Am. 88(8), 1699–1704 (2006) 44. Yazici, M., Kopuz, C., Gülman, B.: Morphologic variants of acromion in neonatal cadavers. J. Pediatr. Orthop. 15(5), 644–647 (1995) 45. Yuan, J., Murrell, G.A., Wei, A.Q., et al.: Apoptosis in rotator cuff tendinopathy. J. Orthop. Res. 20(6), 1372–1379 (2002) 46. Yuan, J., Murrell, G.A., Trickett, A., et al.: Involvement of cytochrome-c release and caspase-3 activation in the oxidative stressinduced apoptosis in human tendon fibroblasts. Biochim. Biophys. Acta 1641(1), 35–41 (2003) 47. Yuan, J., Murrell, G.A., Trickett, A., et al.: Overexpression of antioxidant enzyme peroxiredoxin 5 protects human tendon cells against apoptosis and loss of cellular function during oxidative stress. Biochim. Biophys. Acta 1693(1), 37–45 (2004)

Neurovascular Risks Associated with Shoulder Arthroscopic Portals Daniel Daubresse

Contents Proper Portal Placement ............................................................

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Posterior Portal ...........................................................................

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Anterior Portal ............................................................................

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Lateral Portal ..............................................................................

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Superolateral Portal ....................................................................

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Inferior Portals ............................................................................

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Anterior–Inferior (5 o’clock) Portal..........................................

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Accessory Posterior Portal .........................................................

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Posteroinferior Portals................................................................

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The 7 o’clock Posteroinferior Portal ......................................... The Superior-Medial Portal ..........................................................

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Glenohumeral Arthroscopy Portals Established Using an Outside-in Technique .............................

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Trans-Rotator Cuff Portal..........................................................

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The Axillary Nerve ......................................................................

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The Brachial Plexus and Axillary Artery .................................

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The Coracoids’ Process ..............................................................

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References ....................................................................................

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D. Daubresse Clinique du Parc Léopold, 1040 Bruxelles, Belgium e-mail: [email protected]

Arthroscopy has been established as a valuable technique in diagnosis and treatment of the injured and diseased shoulder. Arthroscopy is not a diagnostic tool but offers approaches to the surgical treatment of shoulder pathology. The patient is positioned in opposite lateral decubitus position or in beach chair position. Diagnostic arthroscopy is initiated with insertion of the arthroscope from the posterior portal into the gleno-humeral joint. Inspection should be an organized systematic visualization of the entire joint (articular surfaces of the glenoid and humeral head, glenoid labrum, long head of the biceps tendon, subscapularis tendon, axillary pouch, capsular ligaments, synovial membrane). Then, endoscopic visualization of the subacromail space is a valuable and essential adjunct to the glenohumeral arthroscopy (impingement syndrome, rotator cuff tears, calcific tendinitis, acromioclavicular joint disorders) [3].

Proper Portal Placement Meyer et al. [13] have performed an anatomic cadaveric study to determine with trocars in situ the relationships of 12 shoulder arthroscopic portals frequently used with the adjacent musculotendinous and neurovascular structures. Twelve shoulders of embalmed cadavers installed in a beach-chair position were dissected. Twelve different portals were established by using their authors’ description: posterior “soft point,” central posterior, anterior central, anterior inferior, anterior superior, 5 o’clock portal, Neviaser, superolateral, transrotator cuff approach, Port of Wilmington, anterolateral, and posterolateral. Six of these portals were placed on each shoulder so that each portal was studied six times. Dissections were conducted with trocars in situ to take their volume into account. The distance to the adjacent relevant neurovascular structures at risk (axillar and suprascapular nerves, axillar and suprascapular arteries, and cephalic vein) were measured, arm at side, by using a calliper. Musculotendinous structures crossed by portals were noticed. The cephalic vein was injured twice by anterior portals. The 5 o’clock portal is at most risk of neurovascular injury. It is located at mean distances to the axillar artery and

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_13, © Springer-Verlag Berlin Heidelberg 2012

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nerve of 13 and 15 mm, respectively. Other anterior, posterior, superior, and lateral portals are safe with mean distances higher than 20 mm. Neither musculotendinous rupture nor large injury occurred. The study shows that the trocars placement of the studied portals did not create, except for the cephalic vein, any lesion of the neurovascular adjacent structures. The general types of neurological injury that may occur secondary to arthroscopy are direct injury to a nerve, compression secondary to compartment syndrome, and reflex sympathetic dystrophy. Because direct injury to a nerve can be caused by incorrect placement of the portals, correct placement is the major way to decrease the rate of neurological injury. When the surgeon is making the portal the scalpel should penetrate only skin; a blunt trocar should then be used to enter the joint. A posterior portal site has become the accepted standard for introduction of the arthroscope for routine diagnostic procedures of the shoulder.

Posterior Portal The posterior portals allow the best visualization of the shoulder joint. The posterior portal is located 2 cm inferior and 1–2 cm medial to the posterior lateral angle of the acromion. The proper location of the posterior portal is determined by finding the soft spot formed by the interval between the infraspinatus and the teres minor, using deep palpation of the thumb along with internal and external rotation of the joint; One should avoid placing the this portal too far laterally, since this will make joint visualization more difficult. A 18 or 20 gauge spinal needle is then passed into the shoulder joint by aiming just lateral to or at the coracoid process, which is usually well palpated anteriorly; inflating the joint will push the humeral head away from the glenoid, which lessens the chance of iatrogenic chondral injury during trochar insertion. Injury to the suprascapular nerve may occur from passing instruments along the lateral border of the scapular spine. This portal is located approximately 3–4 cm superior to the quadrangular space, which contains the axillary nerve. As the indications for shoulder arthroscopy continue to expand, so too does the need for complete access to the glenohumeral joint. Specific regions of the joint, including the axillary recess, are often difficult to access using traditionally described posterior and anterior portals. Difelice et al. [6] have described a technique for the placement of an accessory posterior portal into the inferior hemisphere of the glenohumeral joint effectively in the 8 o’clock or 4 o’clock position. To demonstrate the safety and effectiveness of this portal, six cadaveric specimens were dissected after the placement

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of a standard and accessory posterior portal. The proximity of the posterior portals to the axillary and suprascapular nerves was analyzed. Measurements were made in simulated beach-chair and lateral decubitus positions. The authors show that the accessory posterior portal is safe to use and may prove useful to the surgeon who wishes to gain access to the inferior recesses of the glenohumeral joint.

Anterior Portal The anterior portal should be above and lateral to the tip of the coracoid process. It should, in no circumstances be placed inferior or medial to the coracoid process because it will jeopardize the brachial plexus. The anterior portal is usually used for introduction of instruments; and this portal is placed under arthroscopic visualization from the posterior portal; a needle is placed halfway between the AC joint and the lateral aspect of the coracoid. This portal pierces the anterior fibers of the deltoid and enters the joint in the interval between the subscapularis and the supraspinatus. The needle should be directed into the anterior triangle formed by the labrum (medial border), biceps tendon (superior border), and subscapularis (inferior border). Some surgeons, place the needle more laterally, between the AC joint and the lateral acromial border. Due to the thickness of the anterior soft tissues, consider use of a disposable sheath to facilitate passage of instruments. When this portal is switched into the subacromial space, it often passes directly thru the CA ligament. At the site of the anterior portal, the musculocutaneous nerve may be injured by medial portal placement. The “intraarticular triangle” bounded by the humeral head, the glenoid rim, and the biceps tendon has been found to be an excellent intraarticular landmark for placement of an accessory anterior portal for shoulder arthroscopy. Anatomical dissections on 20 cadaver shoulders have confirmed that instruments passed through this location are at little risk to injure adjacent neurovascular structures about the shoulder. Clinical data in 30 shoulder arthroscopies performed utilizing this landmark for placement of an anterior portal have confirmed this position to be a safe and useful location for portal placement if proper precautions are followed.

Lateral Portal The lateral portal is used for visualization of, or for insertion of instruments into, subacromial space, usually for acromioplasty or for calcific tendinitis.

Neurovascular Risks Associated with Shoulder Arthroscopic Portals

The key to lateral portal placement is that it must allow triangulation over the entire undersurface of the anterior acromion. If the portal is placed too posteriorly in a large muscular patient, it will be difficult for instruments to “turn the corner” in order to reach the anterior acromion. The lateral portal should be placed laterally, in line with the mid-clavicle, and 2–3 cm lateral to its lateral edge or alternatively inserted at a point that bisects the lateral acromion into anterior and posterior halves. When passing instruments thru the lateral portal into the subacromial space, it is often helpful to direct the instruments directly medial before triangulating toward the AC joint. It is also helpful to apply distraction to the arm, in order to avoid rotator cuff injury. Care should be taken, during placement of this portal, to avoid injury to axillary nerve, which enters deep surface of deltoid approximately 5 cm lateral to the acromion. It must be noted that smaller branches of the axillary nerve may enter deltoid as close as one centimeter lateral to acromion.

Superolateral Portal With the advent of arthroscopic procedures has come the need for better techniques for visualization of structural pathology and better techniques for visualization of intracapsular structures during operative procedures for the treatment of a variety of clinical conditions affecting the shoulder. Laurencin et al. [9] have presented a new portal for shoulder arthroscopy that is safe to insert, providing a panoramic view of the glenohumeral joint (especially anteriorly), and allowing unobstructed observation of large instruments passed through more traditional anterior portals nearby. The superolateral portal is particularly suited for use in anterior stabilization procedures of the shoulder, where it can be used for direct visualization of the anterior glenoid neck, thus permitting the surgeon to perform such tasks as debridement or mobilization of tissues, and placement of tacks or sutures.

Inferior Portals Bhatia et al. [5] have described the musculotendinous relations and neurologic structures at risk during establishment of posterior portals for access to the inferior glenohumeral recess (IGHR). Three 18-gauge spinal needles were used to establish two posteroinferior portals and one axillary pouch portal in 14 embalmed cadaveric shoulders, without joint distension

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and arthroscopic visualization. At dissection, musculotendinous structures traversed by the needles were recorded, and distances from the axillary nerve (at the deltoid undersurface, quadrangular space, and capsule), nerve to teres minor (at the inferior border of the teres minor muscle and at the capsule), and suprascapular nerve were measured. Additional parameters studied included the vertical distances between the acromion and inferior gleno humeral recess and between the acromion and axillary nerve. Statistical analysis (multiple comparisons procedure) was performed to compare relative portal safety. The mean distance of the axillary pouch portal to the three nerves, at each level, was greater than that of the posteroinferior portals. In one specimen (7.1%), the posteroinferior portal tracts were in close proximity (within 2 mm) to the axillary nerve and its branch to the teres minor. The distance of the axillary pouch portal to the nerves was significantly greater (P < .05) at every level, except at the deltoid undersurface. This study suggests that posterior portal techniques described for access to the IGHR are safe; the risk of axillary nerve injury with posteroinferior portals is low, though possible. The axillary pouch portal is relatively farther away from the neurologic structures and provides safer access to the same region. Arthroscopic procedures that require access to the IGHR can be safely performed with posteroinferior and axillary pouch portals. The axillary pouch portal may be used preferentially for this access because it is placed farthest from the neurologic structures.

Anterior–Inferior (5 o’clock) Portal Davidson and Tibone [5] describe an anterior–inferior portal for arthroscopic shoulder instrumentation at the 5 o’clock position along the glenoid rim. An anterior–inferior portal was established in 14 cadaver shoulders. The portal was created in an inside-to-outside fashion, with the humerus maximally adducted, directing the guide rod as far lateral as possible. Using the described technique, a 5 o’clock portal travels through the subscapularis to the lateral of the conjoined tendon. Distance between the portal and the musculocutaneous nerve was 22.9 ± 4.9 mm, and 24.4 ± 5.7 mm between the portal and the axillary nerve. Through a combination of proper arm positioning and rod insertion technique, the 5 o’clock portal can be created safely and is of great potential utility for arthroscopic shoulder stabilization procedures. Another study performed by Gelber et al. [7] was to assess, using a technique that minimally distorts the normal anatomy, the risk of injury when establishing a 5 o’clock shoulder portal in the lateral decubitus versus beach-chair position.

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The anteroinferior portal was simulated with Kirschner wires (K-w) drilled orthogonally at the 5 o’clock position in 13 fresh frozen human cadaveric shoulders. The neighboring neurovascular structures were identified through an anteroinferior window made in the inferior glenohumeral ligament. Their relations to the K-w and surrounding structures were recorded in both positions. The median distance from the musculocutaneous nerve to the K-w was shorter in the lateral decubitus position than in the beach chair position (13.16 vs. 20.49 mm, P = .011). The cephalic vein was closer to the portal in the beach-chair position than in the lateral decubitus position (median 8.48 vs. 9.93 mm, P = .039). The axillary nerve was closer to the K-w in the lateral decubitus position than in the beach-chair position (median 21.15 vs. 25.54 mm, P = .03). No differences in the distances from the K-w to the subscapular and anterior circumflex arteries were found when comparing both positions. The mean percentage of subscapular muscle height from its superior border to the K-w was 53.03%. This study showed the risk of injury establishing a transubscapular portal in either position. The musculocutaneous nerve and the cephalic vein are the most prone to injury. In general, the beach-chair position proved to be safer. Inserting anchor devices orthogonally would permit stronger fixation but presents the risk of damaging neurovascular structures. This study focused on showing the neurovascular risk of performing full orthogonal insertion. Considering the good results reported with the usual superior–anterior portals, they do not recommend performing a transubscapular portal in routine shoulder arthroscopy. Pearsall et al. [16] have evaluated the difficulty, accuracy, and safety of establishing a low anterior 5 o’clock portal for anterior capsulolabral repair in patients positioned in the beach-chair position during shoulder arthroscopy. An initial 5 o’clock portal was created using an inside-out technique as described by Davidson and Tibone [5]. During establishment of the portal, significant force was required to lever the humeral head laterally, and chondral indentations were noted in several specimens. Because of the difficulty noted in establishing the 5 o’clock portal using an inside-out technique, they attempted to establish a 5 o’clock anterior portal using an outside-in technique. Seven fresh-frozen cadaveric shoulders underwent shoulder arthroscopy in the beach-chair position. After the establishment of a 3 o’clock portal, a specially constructed guide was used to place a pin at the 5 o’clock position. The distances of the pins from the cephalic vein and the musculocutaneous and axillary nerves were recorded. The bottom (5 o’clock position) and top (3 o’clock position) pins varied from 12 mm to 20 mm from the musculocutaneous and axillary nerves. The bottom pin was located within 2 mm of the cephalic vein and varied from medial to lateral in different specimens. They do not recommend the use of a 5 o’clock portal using an inside-out or outside-in technique for patients positioned in the beach-chair

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position during shoulder arthroscopy because of the potential for cephalic vein or articular cartilage injury.

Accessory Posterior Portal As the indications for shoulder arthroscopy continue to expand, so too does the need for complete access to the glenohumeral joint. Specific regions of the joint, including the axillary recess, are often difficult to access using traditionally described posterior and anterior portals. Difelice et al. [6] describe a technique for the placement of an accessory posterior portal into the inferior hemisphere of the glenohumeral joint, effectively in the 8 o’clock or 4 o’clock position. To demonstrate the safety and effectiveness of this portal, six cadaveric specimens were dissected after the placement of a standard and accessory posterior portal. The proximity of the posterior portals to the axillary and suprascapular nerves was analyzed. Measurements were made in simulated beach-chair and lateral decubitus positions. The authors show that the accessory posterior portal is safe to use and may prove useful to the surgeon who wishes to gain access to the inferior recesses of the glenohumeral joint.

Posteroinferior Portals Arthroscopic access to the inferior glenohumeral recess is necessary in several surgical procedures on the shoulder. Posteroinferior portals described for access to this region may pose a theoretic risk to the posterior neurovascular structures (outside-in technique) and to the articular cartilage (inside-out technique). Bhatia [2] has devised a new posterior portal that permits direct linear access to the entire inferior glenohumeral recess. The portal is placed higher and more lateral compared with the previously described portals; this places it further away from the posterior neurovascular structures and facilitates linear access to the axillary pouch. The portal is created via an outside-inside technique, with a spinal needle to ascertain the correct portal site and angulation. The portal is placed at a mean distance of 20.45 ± 4.9 mm (range, 15–35 mm) directly inferior to the lower border of the posterolateral acromial angle and 21.3 ± 2 mm (range, 20–25 mm) lateral to the posterior viewing portal. The spinal needle or cannula is angulated medially at a mean of 30.6° ± 4.7° (range, 25–40°) in the axial plane and slightly inferiorly (mean, 2°; range, 20° superiorly to 20° inferiorly). Use of 30° and 70° arthroscopes through the axillary pouch portal facilitates visualization of the entire recess and of the humeral attachment of the inferior glenohumeral ligament complex for evaluation of humeral avulsion of the glenohumeral

Neurovascular Risks Associated with Shoulder Arthroscopic Portals

ligament lesions. The portal also permits instrumentation in combination with the standard posterior or anterosuperior viewing portal for removal of loose bodies, synovectomy, capsular shrinkage, capsulotomy, and anchor placement in the posteroinferior glenoid rim.

The 7 o’clock Posteroinferior Portal Access to the inferior glenohumeral joint of the shoulder is very limited through the traditional 2 o’clock or 3 o’clock anterior portals. The 7 o’clock posteroinferior portal offers an excellent alternative approach [4]. Six paired cadaveric shoulders were used to arthroscopically develop and test a 7 o’clock posteroinferior portal. The distances between the portal and the subscapular and axillary nerves were measured with the arm in six different positions, combining flexion, extension, abduction, and adduction. The distance from the 7 o’clock posteroinferior portal to the axillary nerve was 39 ± 4 mm and to the suprascapular nerve were 28 ± 2 mm. There was no statistically significant nerve-to-portal differential distance when the arm was placed in flexion, extension, abduction, or adduction. The inside-tooutside technique produced a 7 o’clock posteroinferior portal, approximately 5 mm further from both the axillary and suprascapular nerves than did the outside-to-inside method. The angle of divergence from the 7 o’clock posterior portal skin incision to the axillary nerve was 47° and to the suprascapular nerve was 33°. The 7 o’clock portal affords safe, direct working access to the inferior capsular recess of the glenohumeral joint.

The Superior-Medial Portal The superior-medial (SM) shoulder arthroscopic portal (Neviaser portal) is the portal anatomically closest to the suprascapular nerve, and any potential benefits of this portal would be mitigated if risk of suprascapular nerve injury were significant. The supero-medial portal is useful for arthroscopic rotator cuff repair, arthroscopic superior labrum repair, and arthroscopic distal clavicle excision. Woolf et al. [19] hypothesize that this portal is safe. Twelve fresh cadaveric shoulders were securely positioned to simulate shoulder arthroscopy in the beach-chair position with the arm at the patient’s side in neutral rotation. An SM portal was established 1 cm medial to the acromion and 1 cm posterior to the clavicle, and a 5.5-mm burr sheath was oriented toward the acromioclavicular joint. The skin and trapezius were resected, the supraspinatus was retracted,

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and the suprascapular nerve was identified. The distance between the sheath and the nerve was measured with callipers. The measured distances between the nerve and burr ranged from 18.5 mm to 35.7 mm, with a mean of 24.2 ± 5 mm. This study shows that the SM portal is safe. The distance between an instrument oriented toward the acromioclavicular joint via the SM portal and the suprascapular nerve was 18.5 mm or greater in all specimens. Shoulder arthroscopy and the introduction of suture anchors have provided the surgeon with the ability to repair rotator cuff tears through minimal incisions. Rotator cuff repair involves the use of several portals, such as the posterior portal, the anterior portal, the anterior superior portal, the anterior inferior portal, and the Neviaser portal. Nord and Mauck [14] have developed two additional portals, the new subclavian portal and the modified Neviaser portal, to improve the safety and efficacy of rotator cuff repair and solve a number of problems associated with traditional repair techniques. The subclavian portal is located directly below the clavicle, 1–2 cm from the acromioclavicular joint, and instruments are aimed medial to lateral. The modified Neviaser portal changes the angle of insertion of the Neviaser portal. Instruments are aimed 20° from the horizontal plane and 45° anterior, directly at the suture anchor. Repair techniques using each portal were reviewed. Twenty cadaveric shoulders were dissected for each portal and the anatomy from each portal was documented. The cadaveric dissections showed that this portal passes greater than 6 cm from the brachial plexus, musculocutaneous nerve, and subclavian artery and vein, and 4.7 cm from the cephalic vein. The modified Neviaser portal was shown to be safer than the Neviaser portal because it passes on top of the supraspinatus muscle, thereby protecting the suprascapular nerve. These portals provide an optimal angle of approach to the rotator cuff tendon and suture anchor as well as improved safety.

Glenohumeral Arthroscopy Portals Established Using an Outside-in Technique Lo et al. [11] examine the neurovascular structures at risk during placement of glenohumeral arthroscopy portals using an outside-in technique. Five fresh-frozen cadaveric specimens were used in this study. Each shoulder was mounted on a custom-designed apparatus allowing shoulder arthroscopy in a lateral decubitus position. The following portals were established using an outside-in technique and marked using an 18-gauge spinal needle: posterior, posterolateral, anterior, 5 o’clock, anterosuperolateral, and Port of Wilmington. Each specimen

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was carefully dissected after the procedure, and the distance from each portal site to the adjacent relevant neurovascular structures (axillary nerve, musculocutaneous nerve, lateral cord of the brachial plexus, cephalic vein, and axillary artery) was measured using a precision caliper. Except for the cephalic vein, all of the neurovascular structures were more than 20 mm away from all the portals evaluated. When creating either an anterior portal or a 5 o’clock position portal, the mean distance from the portal to the cephalic vein was 18.8 and 9.8 mm, respectively. In one anterior portal, a direct injury to the cephalic vein occurred. This study suggests that shoulder arthroscopy portals placed in an outside-in fashion are unlikely to produce neurologic injury. However, the cephalic vein is at risk during placement of an anterior or 5 o’clock position portal, although probably with minimal subsequent patient morbidity. Placing portals in an outside-in fashion guarantees the correct angle of approach, with minimal risk to adjacent neurologic structures. This study shows the safety of standard and accessory glenohumeral arthroscopy portals.

Trans-Rotator Cuff Portal There are numerous accessory portals for the arthroscopic repair of superior labral anterior and posterior lesions. Many surgeons are reluctant to make a portal through the cuff because of concern about iatrogenic injury to the cuff. Oh et al. [15] performed an analysis of 58 SLAP lesions. Fifty-eight consecutive patients undergoing superior labral anterior and posterior lesion repair using the transrotator cuff portal, who had both functional and radiological outcomes after 1 year of the operation, were enrolled. They evaluated the structural outcomes for the labrum and cuff using computed tomographic arthrography and measured various clinical outcomes (the supraspinatus power, visual analog scale for pain and satisfaction, American Shoulder and Elbow Surgeons shoulder evaluation form, University of California-Los Angeles shoulder score, Constant score, and Simple Shoulder Test) at the final visit. All functional outcomes were improved significantly (P < .001). On computed tomographic arthrography, labral healing to the bony glenoid was achieved in all patients. Subacromial leakage of contrast media was observed in three patients (5.2%) through the muscular portion without any retraction or gap of the tendon. Two of three had preoperative cuff pathologic changes, and they were older than 45 years of age. Partial articular cuff tears were observed in six patients (10.3%) and four had the lesion preoperatively. There were no statistical differences in functional scores according to the presence of preoperative lesion, postoperative leakage, or partial cuff tear.

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The data demonstrate favorable outcomes for arthroscopic superior labral anterior and posterior lesion repair using the trans-rotator cuff portal. They suggest that the trans-rotator cuff portal is an efficient and safe portal for superior labral anterior and posterior lesion repair, although there are some valid concerns of damaging the cuff in patients with a superior labral anterior and posterior lesion with concurrent cuff disorders, as well as in older patients.

The Axillary Nerve Yoo et al. [20] were to examine the morphologic features of the axillary nerve and its relation to the glenoid under an arthroscopic setup, and to determine the changes in nerve position according to different arm positions. Twenty-three fresh-frozen cadaveric shoulder specimens were used for evaluations in an arthroscopic setup with the lateral decubitus position. The main trunk of the axillary nerve with or without some of its branches was exposed after careful arthroscopic dissection. Morphologic features and the course of the axillary nerve from the anterior and posterior portals were documented. The closest distances from the glenoid rim were measured with a probe by use of a distance range system. The changes in nerve position were determined in four different arm positions. At the end of arthroscopic examination, the nerves were marked and verified by open dissections. The axillary nerve appeared in the joint near the inferior edge of the subscapularis muscle. With reference to the inferior glenoid rim horizontally, the nerve had a mean running angle of 23° (range, 14°–41°; SD, 8°). The closest points from the glenoid were between the 5:30 and 6 o’clock position (right) or 6 o’clock and 6:30 position (left). The closest distance range varied from 10 mm to 25 mm in the neutral arm position. The abduction-neutral position resulted in the greatest distance between the inferior glenoid and the nerve. The abduction-neutral rotation position was the optimal position for minimizing axillary nerve injuries, because it resulted in the greatest distance between the inferior glenoid and the nerve. Knowledge of the anatomy of the axillary nerve aids the shoulder surgeon in avoiding nerve injury during arthroscopic procedures. Abduction-neutral rotation may be more helpful for arthroscopic surgeons performing procedures in the anteroinferior glenoid with the nerve being farther away from the working field. Apaydin et al. [1] emphasize that the relationship of the axillary nerve to the shoulder capsule and the subscapularis muscle has not been well defined in orthopedic literature. Their descriptive anatomical study presents the course and the relations of the axillary nerve with neighboring neurovascular structures and the shoulder capsule and defines

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anatomical landmarks and regions that can be used practically in anterior surgical approaches to the shoulder region. To investigate the course of the axillary nerve and its relationship with neighboring structures, 30 shoulders of 15 fixed adult cadavers were dissected under the microscope through an anterior approach. A triangle-shaped anatomic area containing the axillary neurovascular bundle was defined. The closest distance between the axillary nerve and the anteromedial aspect of the coracoids’ tip and the glenoid labrum was measured as 3.7 and 1.1 cm on average, respectively. The distance between the anteromedial aspect of the coracoids’ tip and the point where the nerve passes through the medial edge of the subscapularis was measured as 2.5 cm on average. The results of this study demonstrate the anatomic pattern and the course of the axillary nerve and its relations with the shoulder capsule. They conclude that knowing the exact localization of the axillary nerve under the guidance of the defined anatomic triangle may provide a safer surgery. Following Jerosh et al. [8] the success of arthroscopic capsular release of the glenohumeral joint depends on complete incision of the inferior capsule. They determined the distance between capsule and the axillary nerve in different joint positions. In 14 human shoulder specimens the anterior joint capsule and axillary nerve were dissected, and the anterior joint capsule was incised between the 1 o’clock and 5 o’clock positions. The shortest distance between the insertion of the inferior capsule and the axillary nerve was measured at the glenoid and humeral insertions in abduction, adduction, internal, and external rotation. The axillary nerve is surrounded by soft connective tissue and is closer to the humeral than to the glenoid attachment of the joint capsule. During abduction and external rotation the nerve stays in its position while the glenohumeral capsule tightens, which increases the distance between the two structures. This result in the following distances: to the glenoid/humeral capsule insertion: in adduction and neutral rotation, 21.2 ± 4.2/14.2 ± 2.6 mm; in abduction and neutral rotation, 24 ± 4.9/15 ± 5 mm; in abduction and internal rotation, 21.1 ± 6.6/14.6 ± 3.7 mm; and in abduction and external rotation, 24.9 ± 3.8/16.4 ± 4.4 mm. Thus, when performing arthroscopic capsular release the incision of the glenohumeral joint capsule should be undertaken at the glenoid insertion in the abducted and externally rotated shoulder. Following Price et al. [17], the axillary nerve is out of the field of view during shoulder arthroscopy, but certain procedures require manipulation of capsular tissue that can threaten the function or integrity of the nerve. They studied fresh cadavers to identify the course of the axillary nerve in relation to the glenoid rim from an intra-articular perspective and to determine how close the nerve travels in relation to the glenoid rim and the inferior glenohumeral ligament. All specimens were studied with the joint secured in the lateral decubitus position used for shoulder arthroscopy.

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Microsurgical dissection through the inferior glenohumeral ligament from within the joint capsule revealed the axillary nerve as it traversed the quadrangular space. In each dissection, the teres minor branch was the closest to the glenoid rim. The coronal sectioning of the unembalmed shoulder specimens demonstrated that the closest point between the axillary nerve and the glenoid rim was at the 6 o’clock position on the inferior glenoid rim. At this position, the average distance between the axillary nerve and the glenoid rim was 12.4 mm. The axillary nerve lay, throughout its course, at an average of 2.5 mm from the inferior glenohumeral ligament. Uno et al. [18] have studied the arthroscopic relationship of the axillary nerve to the shoulder joint capsule. Twelve right shoulders in fresh cadavers were dissected to determine the relation of the axillary nerve to the shoulder capsule and glenoid. Needles transfixed the nerve to the capsule and into the shoulder joint. Arthroscopy was performed to determine the location of the needles on the glenoid clock. The needles were then removed and the position of the shoulder changed to determine the effect on the position of the axillary nerve. The axillary nerve was held to the shoulder capsule with loose areolar tissue in the zone between 5 o’clock and 7 o’clock and was close to the glenoid in the neutral position, in extension, and in internal rotation. With shoulder abduction, external rotation, and perpendicular traction, the capsule became taut and the axillary nerve moved away from the glenoid. Abduction, external rotation, and perpendicular traction increase the zone of safety during arthroscopic anteroinferior capsulotomy adjacent to the glenoid between the 5 o’clock and 7 o’clock positions.

The Brachial Plexus and Axillary Artery Following McFarland [12], iatrogenic brachial plexus injury is an uncommon but potentially severe complication of open shoulder reconstruction for instability that involves dissection near the subscapularis muscle and potentially near the brachial plexus. They examined the relationship of the brachial plexus to the glenoid and the subscapularis muscle and evaluated the proximity of retractors used in anterior shoulder surgical procedures to the brachial plexus. Eight freshfrozen cadaveric shoulders were exposed by a deltopectoral approach. The subscapularis muscle was split in the middle and dissected to reveal the capsule beneath it. The capsule was split at midline, and a Steinmann pin was placed in the equator of the glenoid rim under direct visualization. The distance from the glenoid rim to the brachial plexus was measured with callipers with the arm in 0°, 60°, and 90° of abduction. The brachial plexus and axillary artery were within 2 cm of the glenoid rim, with the brachial plexus as

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close as 5 mm in some cases. There was no statistically significant change in the distance from the glenoid rim to the musculocutaneous nerve, axillary artery, medial cord, or posterior cord with the arm in various degrees of abduction.

The Coracoids’ Process Five fresh-frozen cadaveric shoulders were dissected by Lo et al. [10] to determine the dimensions of the coracoid and the distance from the coracoid to adjacent neurologic and vascular structures. The minimal distance from the coracoid tip to the axillary nerve, musculocutaneous nerve, the lateral cord of the brachial plexus, and the axillary artery was measured using a precision calliper. Similarly, the minimal distance from the base of the coracoid to the axillary nerve, musculocutaneous nerve, the lateral cord of the brachial plexus, and the axillary artery was measured. The coracoids’ tip was defined as that portion of the bone that was distal to the “elbow” of the coracoid. Results showed that the mean width (medial-to-lateral dimension in the plane of the subscapularis tendon) of the coracoids’ tip was 15.9 ± 2.2 mm, and the mean length of the coracoids’ tip was 22.7 ± 4.5 mm. The mean thickness of the coracoids’ tip at its midportion was 10.4 ± 1.5 mm. The portion of the coracoids’ tip which was closest to the neurovascular structures was the anteromedial portion of the coracoids’ tip. The distance from the anteromedial portion of the coracoids’ tip to the axillary nerve, the musculocutaneous nerve, the lateral cord, and the axillary artery was 30.3 ± 3.9, 33 ± 6.2, 28.5 ± 4.4, and 36.8 ± 6.1 mm, respectively. Similarly, the portion of the base of the coracoid that was closest to the neurovascular structures was its anteromedial portion. The shortest distance from the anteromedial aspect of the base of the coracoid to the axillary nerve, the musculocutaneous nerve, the lateral cord, and the axillary artery was 29.3 ± 5.6, 36.5 ± 6.1, 36.6 ± 6.2, and 42.7 ± 7.3 mm, respectively. Procedures about the coracoid are relatively safe procedures. The lateral cord of the brachial plexus is at greatest risk during dissection about the tip of the coracoid, and the axillary nerve is at greatest risk during dissection about the base of the coracoid. The safety of arthroscopic coracoplasty or interval releases is further increased by the fact that most of the work is performed on the lateral aspect of the coracoid, which is even further away from the neurovascular structures.

References 1. Apaydin, N., Uz, A., Bozkurt, M., Elhan, A.: The anatomic relationships of the axillary nerve and surgical landmarks for its localization from the anterior aspect of the shoulder. Clin. Anat. 20(3), 273–277 (2007)

D. Daubresse 2. Bhatia, D.N., de Beer, J.F., Dutoit, D.F.: The axillary pouch portal: a new posterior portal for visualization and instrumentation in the inferior glenohumeral recess. Arthroscopy 23(11), 1241.e1–1241. e5 (2007) 3. Coudane, H., Hardy, P.: Shoulder arthroscopy: setting, portals and normal exploration. Chir. Main 25(Suppl 1), S8–S21 (2006) 4. Davidson, P.A., Rivenburgh, D.W.: The 7-o’clock posteroinferior portal for shoulder arthroscopy. Am. J. Sports Med. 30, 693–696 (2002) 5. Davidson, P.A., Tibone, J.E.: Anterior-inferior (5 o’clock) portal for shoulder arthroscopy. Arthroscopy 11(5), 519–525 (1995) 6. Difelice, G.S., Williams III, R.J., Cohen, M.S., Warren, R.F.: The accessory posterior portal for shoulder arthroscopy: description of technique and cadaveric study. Arthroscopy 17(8), 888–891 (2001) 7. Gelber, P.E., Reina, F., Caceres, E., Monllau, J.C.: A comparison of risk between the lateral decubitus and the beach-chair position when establishing an anteroinferior shoulder portal: a cadaveric study. Arthroscopy 23(5), 522–528 (2007) 8. Jerosch, J., Filler, T.J., Peuker, E.T.: Which joint position puts the axillary nerve at lowest risk when performing arthroscopic capsular release in patients with adhesive capsulitis of the shoulder? Knee Surg. Sports Traumatol. Arthrosc. 10(2), 126–129 (2002) 9. Laurencin, C.T., Deutsch, A., O’Brien, S.J., Altchek, D.W.: The superolateral portal for arthroscopy of the shoulder. Arthroscopy 22(10), 1133.e1–1133.e5 (2006) 10. Lo, I.K., Burkhart, S.S., Parten, P.M.: Surgery about the coracoid: neurovascular structures at risk. Arthroscopy 20(6), 591–595 (2004) 11. Lo, I.K., Lind, C.C., Burkhart, S.S.: Glenohumeral arthroscopy portals established using an outside-in technique: neurovascular anatomy at risk. Arthroscopy 20(6), 596–602 (2004) 12. McFarland, E.G., Caicedo, J.C., Guitterez, M.I., Sherbondy, P.S., Kim, T.K.: The anatomic relationship of the brachial plexus and axillary artery to the glenoid. Implications for anterior shoulder surgery. Am. J. Sports Med. 29(6), 729–733 (2001) 13. Meyer, M., Graveleau, N., Hardy, P., Landreau, P.: Anatomic risks of shoulder arthroscopy portals: anatomic cadaveric study of 12 portals. Arthroscopy 23(5), 529–536 (2007) 14. Nord, K.D., Mauck, B.M.: The new subclavian portal and modified Neviaser portal for arthroscopic rotator cuff repair. Arthroscopy 22(10), 1133.e1–1133.e5 (2006) 15. Oh, J.H., Kim, S.H., Lee, H.K., Jo, K.H., Bae, K.J.: Trans-rotator cuff portal is safe for arthroscopic superior labral anterior and posterior lesion repair: clinical and radiological analysis of 58 SLAP lesions. Am. J. Sports Med. 36(10), 1913–1921 (2008) 16. Pearsall IV, A.W., Holovacs, T.F., Speer, K.P.: The low anterior fiveo’clock portal during arthroscopic shoulder surgery performed in the beach-chair position. Am. J. Sports Med. 27, 571–574 (1999) 17. Price, M.R., Tillett, E.D., Acland, R.D., Nettleton, G.S.: Determining the relationship of the axillary nerve to the shoulder joint capsule from an arthroscopic perspective. J. Bone Joint Surg. Am. 86, 2135–2142 (2004) 18. Uno, A., Bain, G.I., Mehta, J.A.: Arthroscopic relationship of the axillary nerve to the shoulder joint capsule: an anatomic study. J. Shoulder Elbow Surg. 8(3), 226–230 (1999) 19. Woolf, S.K., Guttmann, D., Karch, M.M., Graham II, R.D., Reid III, J.B., Lubowitz, J.H.: The superior-medial shoulder arthroscopy portal is safe. Neviaser Portal. Arthroscopy 23(3), 247–250 (2007) 20. Yoo, J.C., Kim, J.H., Ahn, J.H., Lee, S.H.: Arthroscopic perspective of the axillary nerve in relation to the glenoid and arm position: a cadaveric study. Arthroscopy 23(6), e2–e3 (2007)

Rotator Cuff Disorders: Arthroscopic Repair Kevin D. Plancher and Alberto R. Rivera

Introduction

Contents Introduction .................................................................................

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Clinical Anatomy ........................................................................

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Etiology and Pathogenesis ..........................................................

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Natural History ...........................................................................

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Imaging ........................................................................................ Nonoperative Management ...........................................................

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Partial Rotator Cuff Tears ......................................................... 100 Full Thickness Rotator Cuff Tears ............................................ 101 Full Thickness Tears: Massive Rotator Cuff ............................ 101 Operative Management: Full Thickness Rotator Cuff Arthroscopic Repair, A Stepwise Approach ............................. 101

Rotator cuff disorders have been common as longevity and activity has increased. It is expected that 50% of the population over 66 years of age will have bilateral rotator cuff tears [1]. Most patients with rotator cuff disease will be asymptomatic and will arrive in the physician’s office without severe symptoms. Understanding the natural history and basic science studies have given us information to improve our understanding of this condition. These studies have also allowed us to intervene earlier and return patients back to all activities [46]. This chapter we will provide a review of rotator cuff disorders, their anatomy, basic science, nonoperative and operative arthroscopic repair techniques.

Configuration Type ..................................................................... 103 Equipment ................................................................................... 104 Full Thickness Tears: Subscapularis Tendon Tears................. 105 Operative Management: Arthroscopic Subscapularis Repair Stepwise Approach ......................................................... 105 Future Trends in Rotator Cuff Surgery .................................... 106 Summary...................................................................................... 107 References .................................................................................... 107

K.D. Plancher ( ) Albert Einstein College of Medicine, New York, NY, USA and Plancher Orthopaedics & Sports Medicine/Orthopaedic Foundation for Active Lifestyles, OFALS, 31 River Road, Cos Cob, CT 06807, USA e-mail: [email protected] A.R. Rivera Plancher Orthopaedics & Sports Medicine/Orthopaedic Foundation for Active Lifestyles, OFALS, 31 River Road, Cos Cob, CT 06807, USA e-mail: [email protected]

Clinical Anatomy An increase in understanding the footprint anatomy of the rotator cuff on the humeral head has helped achieve successful surgical management [2]. The insertion has four zones: tendon, fibrocartilage, mineralized fibrocartilage, and bone. The supraspinatus and infraspinatus are attached at the greater tuberosity while subscapularis attaches at the lesser tuberosity (Fig. 1a–c). Average maximum insertional lengths and widths are as follows: subscapularis (SC): 40 × 20 mm; infraspinatus (IS): 29 × 19 mm; supraspinatus (SS): 23 × 16 mm; and teres minor (TM): 29 × 21 mm [5]. Open surgery has always relied on an understanding of the previously described rotator interval by Codman [4]. This interval is between the subscapularis and the anterior border of the supraspinatus tendon. Arthroscopists identify a different interval between the superior glenohumeral ligament and the coracohumeral ligament [28] (Fig. 2a, b). This interval helps biceps tendon stabilization and plays a role in glenohumeral stability [7, 34]. Anterior Shoulder Pain due to biceps tendon instability because of injury to the anterior part of the supraspinatus or the subscapularis may require either a tenodesis or tenotomy to avoid further anterior

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_14, © Springer-Verlag Berlin Heidelberg 2012

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Fig. 1 (a) Arthroscopic view of normal supraspinatus muscle insertion in a right shoulder in a 32-year old professional athlete. (b) Arthroscopic view of normal infraspinatus muscle insertion in the right shoulder of

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same patient. (c) Arthroscopic view of normal subscapularis muscle insertion in a right shoulder of same patient

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Fig. 2 (a) Anatomy of the anterior rotator interval in a schematic right shoulder. (b) Anatomy of the anterior rotator interval in a cadaveric model

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97 Table 1 Intrinsic and extrinsic factors that may contribute to rotator cuff disease Intrinsic factors Muscle imbalance leading to dynamic instability Normal aging degeneration Extrinsic factors Subacromial spurs Coracoacromial enthesophyte formation Subcoracoid impingement Os acromiale Subacromial bursitis

Fig. 3 Suprascapular nerve (arrow) released at the transverse scapular notch in a right shoulder

Cumulative microtrauma may lead to symptomatic tears, pain, and eventual dysfunction in the shoulder. Painless rotator cuff tears are very common and are often associated with advancing age [46]. The source of pain in a rotator cuff tear has not been completely elucidated but it is clear that pain contributes to a cycle of kinematic abnormality that will eventually result in progression of the tear. Recent discoveries have shown that the subacromial bursa has an increased density of nociceptive nerve fibers in patients with rotator cuff disease [12, 43].

Natural History

Fig. 4 Suprascapular nerve (arrow) released at the spinoglenoid notch in a right shoulder

shoulder pain at the time of a rotator cuff repair. More recently the posterior rotator interval has been described and may need to be released at the time of surgery to mobilize the fibers between the supraspinatus and infraspinatus [36]. This interval must be closed to orient the sling of the rotator cuff in the repair of a massive tear [36]. Understanding the role of the suprascapular nerve as a pain generator will improve results for the orthopedic surgeon that undertakes a repair of a large or massive supraspinatus or infraspinatus tendon tear [8]. Recent studies have shown that large retracted tears stretch the suprascapular nerve leading to denervation atrophy [1]. The surgeon should consider nerve studies in these patients because failure to release the nerve in these patients can have a negative impact on the surgical outcome (Figs. 3 and 4).

Etiology and Pathogenesis Atraumatic rotator cuff disease is thought to be multifactorial with intrinsic and extrinsic factors playing a role in its pathogenesis. Injury can be elicited by many factors (Table 1).

Spontaneous healing of the rotator cuff does not occur in humans. There is strong evidence that all rotator cuff tears progress over time and that muscle atrophy with fatty infiltration is an irreversible process (Fig. 5a, b). Following a rotator cuff over a period of 5 years has shown that 22–50% of rotator cuff tears will enlarge even in asymptomatic patients [47]. Animal studies have shown that all tears degenerate and progress with time. These changes can occur as early as 6 weeks after detachment from the footprint with fat infiltration occurring as early as 16 weeks [44, 47]. Success in rotator cuff surgery is measured in terms of pain relief and return of function. Although tear size contributes to retraction, the configuration of a tear may be more important [27]. Different configuration patterns may need different repair techniques. Retraction results in fatty infiltration and marked strength loss [11, 15]. Progression of the rotator can cause pain and loss of function but may also lead to glenohumeral arthrosis and coracoacromial arch degeneration [48] (Fig. 6). When this progression is carried out over a long period of time, more often than not rotator cuff arthropathy will develop. The timing for repair of rotator cuff tears of all sizes has also been studied with delayed repair having poorer outcomes [10]. We strongly believe that although the percentage of patients with asymptomatic rotator cuff tears is high early intervention in the treatment of patients with a rotator cuff tear will improve results. We do not recommend that a patient wait to allow a small or medium sized tear to develop into a disabling large rotator cuff tear before it is repaired (Fig. 7).

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Fig. 5 (a) MRI demonstrating a partial thickness rotator cuff tear in a right shoulder. (b) MRI demonstrating progressions of a partial thickness to a full thickness rotator cuff tear in a right shoulder in a period of 2 years

Fig. 6 Anteroposterior radiograph demonstrating rotator cuff arthropathy changes in a right shoulder of a 75-year old female patient with massive rotator cuff tear and failed rotator cuff repair

Imaging We routinely obtain a true anteroposterior view (Grashey View) and avoid an internal and external rotation, and unless trauma has occurred, an axillary view, outlet view. The zanca view is obtained when acromioclavicular pathology is expected. Ultrasound has been successful for identifying rotator cuff tears in large academic centers (Fig. 8). Ultrasound has been found to have similar or better sensitivity for identifying rotator cuff tears than an MRI [38]. Ultrasound success is

Fig. 7 Demonstrate a positive horn-blower sign in a 50 year old female with massive rotator cuff tear on her left shoulder

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retraction, fatty infiltration, as well as the state of the biceps and subscapularis tendon most easily seen on the axial views. MRI will also reveal the presence of a spinoglenoid cyst that can complicate and or mimic rotator cuff disease [16]. Assessment of the acromioclavicular and glenohumeral joints as well as the configuration of the acromion must also be performed. This information as well as a well-documented history and physical exam will allow a roadmap to success. In our practice, we routinely convert a type III acromion to a flat type I acromion (Fig. 9a, b).

Nonoperative Management Fig. 8 Ultrasound of a left shoulder in a 59 year old male with a fullthickness rotator cuff tear. White squares indicate borders of the tendon defect. SS supraspinatus tendon, HH humeral head

dependent on the technologist performing the exam. We have begun the use of ultrasound and have found it extremely helpful in patients who return to the office in the early postoperative period with increasing pain and weakness to determine the status of the rotator cuff. MRI without contrast has been the gold standard to detect and evaluate the size and configuration of rotator cuff tears. The use of MRI also enables us to identify any associated intrarticular pathology. The MRI can assess the tear configuration, a1

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Fig. 9 (a) (1) A right shoulder radiograph (outlet view) demonstrating a type III acromion. (2) MRI showing a type III acromion. (b) A right shoulder radiograph (outlet view) after arthroscopic acromioplasty. Note a flat type I acromion

Differences in study methodology may have influenced the lack of clear consensus regarding the care of rotator cuff disease. Nonoperative management has been attempted in the past, although the risk of progression and degeneration should be considered and convened strongly to the patient at the time of any office visit. The presence of tendinopathy and a small rotator cuff tear has a minimal risk of progression over a short period of time and nonsurgical care may be attempted. Larger tears or symptomatic tears in young active individuals and acute tears (less than 3 months) have a significant risk of progression and surgical management in our opinion and others is warranted [25]. The group of b

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older patients with large or massive symptomatic tears that have progressed to include fatty infiltration may benefit from a trial of nonsurgical treatment with a special focus of reestablishing the periscapular musculature through strengthening [48]. Anti-inflammatory medications have been shown to decrease mediators in the subacromial bursa [21]. A recent study showed that COX-1 receptors may be more efficacious than COX-2 inhibitors in treating pain emanating from the subacromial bursa [22]. Subacromial injections have been shown to be more efficacious than placebo but the use of these injections should be used judiciously as there is increasing evidence that rotator cuff collagen can be altered permanently and often an injection may be inadvertently placed in the tendon or muscle with a frequency as high as 25% [24]. Physical therapy and exercise has been found to be somewhat beneficial in short- and long-term studies in patients with small rotator cuff tears [3]. Patients with larger tears on the other hand have had inconsistent results with nonoperative treatment. Many patients with rotator cuff disease develop posterior capsular tightness; therefore stretching should be incorporated in all rehabilitation protocols and especially in the overhead athlete. Strengthening of periscapular musculature is vital and the addition of proprioceptive training along with plyometrics at the later stages of rehabilitation has also been found to be helpful. Modalities such as ultrasound, acupuncture, and extracorporeal shock wave therapy have not been found to be beneficial [13]. As subacromial pressures may be decreased by external rotation it is important to emphasize external rotators strengthening [17].

Partial Rotator Cuff Tears Although debate exits as to the etiology and pathogenesis of partial-thickness rotator cuff tears, it is clear that arthroscopy has helped better define the patterns of partial tears and has

a

Fig. 10 (a) Arthroscopic views of a partial thickness bursal side rotator cuff tear in a right shoulder. (b) Arthroscopic view through the posterior portal of a small partial-thickness tear of the articular side of the rotator cuff and arthroscopic view through the posterior portal of a deep partial-thickness tear of the articular side of the rotator cuff

improved outcomes for patients. The incidence of partial tears has been found in cadavers to occur in up to 32% [19, 39]. Age and activity correlate strongly with the presence of partial rotator cuff tears. The peak incidence of tears can be noted in patients in their fifth and sixth decades. Partial tears can either be articular or bursal (Fig. 10a, b). The incidence of bursal sided partial tears in asymptomatic individuals can be as high as 26% in patients older than 60 years of age although the tensile strength of the bursal side is stronger than the articular side [6, 41]. Articular side tears are more common in younger patients participating in overhead sports [26]. The origin of partial tears is no different than full thickness tears and is related to intrinsic and extrinsic factors. Age in the bursal sided tear, as already mentioned, is one of the strongest risk factors for its creation. External Impingement syndrome has been proposed to contribute to the pathogenesis of rotator cuff tears, although its exact role has not been clearly defined. Other extrinsic factors include instability and trauma and have been proposed as contributors to bursal side rotator cuff tears. Histologic evidence supporting tears propagate with articular degeneration as the most common mechanism. This often occurs with greater involvement on the bursal side [23]. The natural history of partial tears has revealed that 50% progress at 1 year with 34% progressing to full thickness at 5 years [20]. A subacromial decompression with or without debridement of a partial tear does not halt progression. Ultrasound and MRI can both be used to detect these tears. Definition of a partial thickness tear can be improved with the use of intrarticular contrast, fat suppression, proton density and external-internal rotation views. Magnetic Resonance Arthrography (MRA) has improved our ability to diagnose these tears with a sensitivity of 91%, specificity of 85%, positive predictive value 84%, and a false negative rate of 9% [18]. The Ellman classification system has been most commonly used and its description of the tear size and pattern after arthroscopic debridement is quite helpful (Table 2) [8].

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Table 2 Ellman classification of partial-thickness rotator cuff tears Grade Description I II III

50% of tendon thickness )

Location A B C

Articular sided Bursal sided Intratendinous

Snyder has also classified partial rotator cuff tears [42]. Most recent attempts to classify partial rotator cuff tears have demonstrated that neither the classification of Snyder nor that of Ellman reproduced the extension of the partialthickness rotator cuff tear in the transverse and coronal planes related to its etiologic pathomorphology [14]. The treatment and repair of these tears is beyond the scope of this chapter.

Full Thickness Rotator Cuff Tears Full thickness rotator cuff tear was originally treated nonoperatively with poor outcome in most patients [29]. Debridement has failed to achieve good results [30]. Open techniques were developed and fair to good results were noted depending on the size of the tear. Arthroscopy evolved to yield results better or comparable to open or mini-open techniques [31]. This chapter will discuss those new techniques.

Full Thickness Tears: Massive Rotator Cuff Massive rotator cuff tears are defined as being larger than 5 cm, and or involving two or more tendons of the rotator cuff. A massive rotator cuff tear will lead to eventual loss of the force coupling action. This is required to keep the humeral head centered and that in turn leads, in a majority of patients, to a pseudoparalysis. Migration of the humeral head superiorly and the eventual formation of what is known as acetabularization of the acromial arch will ensue if the rotator cuff is not repaired. Massive rotator cuff tears, a type of full thickness tear can occur in young patients after a sporting event or trauma but may occur in older patients from chronic attrition. Patients can rarely have a well-balanced force couple even with a massive tear allowing them to have excellent function.

Fig. 11 Muscular atrophy of a right shoulder in a patient with massive rotator cuff tear and electrodiagnostic evidence of entrapment of the suprascapular nerve at the transverse scapular ligament

The physical exam of most of these patients will show atrophy of the shoulder musculature (Fig. 11). External rotation lag signs and horn blower’s sign are often positive in this patient population. Suprascapular neuropathy is present in all patients with massive rotator cuff tears and should be checked with an EMG/NCS [37]. Up to 30% of patients have nerve damage in the presence of any rotator cuff disease [9]. We have recently advocated a more aggressive approach for this reason to this nerve [34, 35].

Operative Management: Full Thickness Rotator Cuff Arthroscopic Repair, A Stepwise Approach Surgical management may be recommended after an appropriate program of nonoperative treatment. Understanding the natural history of a rotator cuff tear encourages early surgical intervention when appropriate. Arthroscopic repair of the rotator cuff has a steep learning curve and the surgeon needs to have the skills to comfortably

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perform the surgery. The goal of a tension-free repair in a reasonable amount of time should be attempted otherwise converting to a mini-open or open technique to complete the task should be performed. Tissue mobilization techniques and the principle of margin convergence allow us to treat all tears arthroscopically. When a tear is associated with biceps tendon pathology we perform a subpectoral biceps tenodesis with a 3 cm incision. Any patient that is not willing to comply with rehabilitation protocol or is medically debilitated with a very low functional demand should not have a rotator cuff repair. While fatty degeneration and atrophy can affect the outcome they are not absolute contraindications to repair in our practice. All patients with massive rotator cuff disease must have an Electromyography-Nerve Conduction study (EMG-NCS) preoperatively to verify any entrapment of the suprascapular nerve. A History and Physical exam along with all ancillary tests including an MRI help in the preoperative planning. All cuff repairs are performed with an interscalene block and position the patient in the beach chair position. Tendon

a

debridement for partial rotator cuff tears may be done with or without an acromioplasty depending on the presence of a bursal sided rotator cuff disease greater than 50% for the very low demand patient or 30% for the higher demand patient. If a tear is on the bursal side and fraying of the coracoacromial ligament is seen, we recommend a subacromial decompression with acromioplasty. A radiofrequency device or shaver may be used with a posterior cutting block technique or the procedure is performed from the lateral portal with removal of the inferior osteophyte at the acromioclavicular joint (ACJ) along with the subacromial decompression. In the throwing athlete a bursectomy is performed and a subacromial decompression is rarely necessary. This group of patient’s problem is more of internal impingement with posterior capsule tightness and anterior laxity not external impingement. They have an articular sided tear rather than a bursal sided tear. Tendon repair decisions are determined by the size and depth of the tear. Debridement of the devitalized or delaminated tissue is done followed by repair using suture anchors. If there is a partial articular sided supraspinatus avulsion with at least 25%

b

Fig. 12 (a–d) Full thickness rotator cuff tear configurations and repair with some demonstrating margin convergence techniques. SS supraspinatus, IS infraspinatus, RI rotator interval, Sub subscapularis, CHL

coracohumeral ligament. (a) Crescent-shaped rotator cuff tear. (b) U-shaped rotator cuff tear. (c) L-shaped rotator cuff tear. (d) Massive rotator cuff tear

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healthy remaining tissue on the bursal side, transtendinous repair can be done with good recreation of the anatomic footprint and tension of the rotator cuff tissue. The fixation anchors are inserted at a 45° angle to the bone. Ideally, the anchors should be 5 mm from the articular margin of the humeral head to ensure placement of a repaired tendon to the footprint.

Configuration Type Arthroscopy can evaluate rotator cuff tears from various angles. Four types of tears have been described: Crescentshaped, U-shaped, L-shaped, and the massive rotator cuff

tear (Fig. 12). Crescent-shaped tears may become massive but are often not retracted [44]. Attempts to mobilize these tears are usually successful from a medial to lateral position with placement easily on the humeral head footprint. Tears that have a U-shaped pattern are more extensive and a principle of margin convergence must be followed. Another type of rotator cuff tear is the L-shaped tear. The best way to address this tear is to use the principle of margin convergence and repair for the longitudinal split and then place the repair back down to the footprint. The fourth type of tear is seen in massive rotator cuff tears. This tear comprises 5–10% of the tears and requires, in very retracted or immobile tears, special techniques to achieve a successful repair [47].

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Equipment Thirty degree and 70° arthroscopic lens, with appropriate sized cannula, are necessary for a successful repair of the rotator cuff. Studies have shown that anchor fixation is less prone to cyclic failure than fixation through bone tunnels. Single-row fixation has been used by many surgeons (Fig. 13). In vitro has shown a mode of failure with the suture pulling out of the tendon. A configuration for single-row fixation with two double-loaded anchors placed laterally at the footprint will allow the passing of sutures through the tendon. Knots are tied in a horizontal mattress simple configuration. This description is known as the double-row technique. Recent research has pointed out that results from single- and double-row repairs are similar [40]. Double-Row Rotator Cuff repair was described originally to better reestablish the anatomic footprint [33] (Fig. 14). Opponents to this technique argue that the tissue is tightly tied at the footprint and may hinder rotator cuff revascularization and eventual healing (Snyder S, personal communication, 2009). Triple Row arthroscopic rotator cuff repair has been recently described (Fig. 15) [32]. This technique has been described as a way to better place the lateral portion of the cuff in its anatomic footprint and avoid the so called “dog

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ears.” The surgeons that champion this procedure place the patient in the lateral decubitus position with 50° arm abduction and 10–15 lbs of traction in an axial manner. Systolic blood pressure should be maintained no greater than 100 mmHg to help hemostasis as long as there are no medical contraindications. We also advocate this maintenance of blood pressure in the beach chair position. The remaining description is valid for any position that the patient is placed in. The posterior portal is established, glenohumeral arthroscopy is done and all intrarticular pathology is addressed with a working anterior portal. The lateral portal is established and the subacromial space inspected through. A subacromial bursectomy is performed in addition to acromioplasty when appropriate. The coracoacromial ligament is released with a radiofrequency device. The rotator cuff tear is defined and a grasper utilized through a lateral portal to asses tear mobility. Attention is directed to the foot print and a shaver or burr is used to decorticate lightly the surface to allow good anchor purchase and healing to bone. A bleeding surface should allow better tendon to bone healing. Anchors are inserted at 1 cm intervals, 5 mm from the articular surface at a 45° angle. Several suture passing techniques can be used. A piercing device or lasso can be used in a retrograde fashion to pass suture. An alternative way to

Fig. 13 Demonstrate single-row arthroscopic rotator cuff repair

Fig. 14 Double-row rotator cuff repair

Fig. 15 Triple row schematic rotator cuff repair construct

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pass sutures through the tendon is to use a “Bird beak” type instrument and directly grasp the desired suture after piercing the tendon. A third way of passing sutures through the tendon is to use a “Viper suture” or front loading biting instrument. The importance of secure knot tying cannot be underemphasized. In our practice we use a modified Weston Knot (Sliding Locking Knot) followed by four to five alternating half stitches.

Full Thickness Tears: Subscapularis Tendon Tears Subscapularis tendon tears can be particularly disabling. There is a bimodal distribution of the populations of these patients. The mechanism of action of this injury is a forced external rotation against a contracted subscapularis muscle. Others can tear the tendon after a repair is performed during open shoulder surgery as it is needed to gain access to the glenohumeral joint during an instability procedure. Physical exam reveals internal rotation weakness with a positive belly press and lift-off tests [2]. The belly press is more specific test for an upper subscapularis injury and the latter for lower subscapularis tendon injury. Magnetic resonance imaging is the modality of choice to define these tears and, more often than not, will reveal an associated subluxation or a dislocation of the biceps tendon. The indications to repair the subscapularis have increased but include pain Goutallier 3 fatty degeneration and or positive physical exam findings [45]. Repair is contraindicated in a patient who is pain-free, with the presence of pseudoparalysis, with fatty degeneration rotator cuff arthropathy.

Operative Management: Arthroscopic Subscapularis Repair Stepwise Approach The arthroscopic repair of the subscapularis by a surgeon should not be undertaken until a supraspinatus and infraspinatus repair can be performed routinely (Fig. 16). A 70° suture shuttle can be helpful. The beach chair position is utilized. Upon completion of a diagnostic scope with the 30° scope a spinal needle is placed in the rotator interval more medial than a standard anterior portal but still lateral to the coracoid to prevent damage to the musculocutaneous nerve. A cannula is placed. A lateral portal is established 2–3 cm from the lateral border of the acromion in line with a bisector of the anteroposterior length of the acromion. This portal will be used to perform a coracoplasty and also aid in suture management. A fourth portal, the anterolateral portal is also placed in the rotator interval with the help of a spinal needle.

Fig. 16 Arthroscopic view of a subscapularis full-thickness tear in a right shoulder beach chair position, 70° arthroscope from the posterior portal with the lesser tuberosity on the right

This portal is more lateral and anterior to the previously placed portal, typically 1–2 cm superior and 2 cm lateral to the standard anterior portal. The most medial anterior portal will be used for anchor placement as localization with spinal needle will ensure correct direct placement. The lateral portal is placed 2–3 cm inferior to the lateral border of the acromion on the anterior one-third line. A complete diagnostic exam is completed. The 30° arthroscope is kept anteriorly in place and the arm is held in place with internal rotation and with some abduction. The tendon is identified, and the rotator interval is excised through anterior portal. The periosteum of the lateral side of the coracoid is cleared with an electrothermal device. A 4 mm burr is used to remove bone from the periosteum and to remove bone from the posterolateral aspect of the coracoid to enlarge an area for the subscapularis tendon (5–6 mm space should be available between the coracoid and the subscapularis). A biceps tenodesis in now performed if the biceps is still attached as it is usually subluxed. A 30° or 70° scope is used to define subscapularis footprint. A 5 mm shaver thru the anterolateral portal or anterior portal is used to prepare the lesser tuberosity. An anchor is placed through the most medial anterior portal. The sutures are retrieved outside the cannula after placing a switching stick, taking the anterior cannula out and reinserting the cannula having all the sutures on the outside it on the medial side. A second anchor is placed more superior to the last anchor into the lesser tuberosity at least 5–8 mm from the most inferior anchor. The 70° lasso is used to pierce the subscapularis tendon. Steps are repeated and a mattress suture configuration is performed. A grasper is used from the anterolateral portal to retrieve the lasso and an unpaired suture is shuttled out the anterolateral portal using a grasper or a crochet hook. A second lasso is used to pierce the tissue inferior and 5 mm lateral to create a mattress configuration repair. All knots are tied. Portals are closed. A sling with a strap to avoid external rotation is placed on the patient (Figs. 17a, b).

106 Fig. 17 (a) Arthroscopic view of a subscapularis full-thickness tear; lesser tuberosity decortication from anteromedial portal. (b) Anchor placement at the lesser tuberosity in same patient as Fig. 17a

K.D. Plancher and A.R. Rivera

a

Future Trends in Rotator Cuff Surgery Despite all of the technological advances discussed above, there is still a high number of failed arthroscopic rotator cuff repairs. People are living longer and remain active well into the golden year which increases the likelihood of symptomatic rotator cuff tears. There are biologic and technical factors that the surgeon can and cannot control when dealing with this problem. These factors include age and general health of the patient (diabetes), operative technique, age of the tear, muscle atrophy, and environmental factors such as smoking, activity level, and rehabilitation potential and compliance. Some of the future techniques and trends that might help solve this problem are evolving today. Future suture passing devices will allow for complex suture configuration on the tendon to maximize the tendon– suture interface strength. One technique is a method that brings more blood flow and mesenchymal cells into the subacromial space. It involves a microfracture technique medially in the tendon footprint and then a single-row repair with triple-loaded anchors. Other surgeons have developed a revolutionary punch-in anchor that allows the surgeon to control the amount of tension that each individual suture places on the cuff after the anchor has been deployed in the bone as we are aware that overtensioning the repair can lead to catastrophic consequences including decreased blood supply, failure of the repair, and irreparable myotendinous junction tears. Some surgeons use a technique and instrumentation for a transosseous anchorless arthroscopic cuff repair (Fig. 18). The benefits include use of proven and gold-standard bone tunnels technique, better blood supply from the bone with marrow cells available, endless suture configurations that best

Fig. 18 “Arthrotunneler” (Courtesy Pedro Piza, M.D. With permission Tornier, Inc.)

b

suit the surgeon, cost-saving (no anchors), avoiding potential problems with anchors, no MRI/CT artifact post-op, and technically an easier revision surgery if needed. Other instruments will allow knotless repair to be performed in a reliable manner (Fig. 19a–c). Research is being performed on a high-tensile strength suture coated with growth differentiation factor-5 that has had good results with animal models. rhGDF-5 induced significant tendon hypertrophy and tendons repaired with

a

b

Fig. 19 (a–c) Schematic of the “Piton Anchor” system used to perform knotless rotator cuff repair (Courtesy Pedro Piza, M.D. With permission Tornier, Inc.)

Rotator Cuff Disorders: Arthroscopic Repair

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The care of patient with failed rotator cuff surgery is beyond the scope of this chapter. We believe that an arthroscopic rotator cuff repair has a steep learning curve and it should be done only by a surgeon with knowledge and those who practice the techniques repeatedly to perfection to help our patients return to all their activities.

References

Fig. 19 (continued)

rhGDF-5 showed an increased rate of healing versus control repairs. This group is also working on blockage of matrix metalloproteinase at the cellular level to enhance tendon healing. Finally, platelet-rich fibrin and other growth factors to promote tendon healing have been advocated. This PRP along with better biological patches to augment tenuous repairs with almost no side effects are in use. Future trends in rotator cuff tendon healing will focus on enhancing the biological environment with growth factors, pharmacologic agents, and tissue engineering to return our patients to the playing field.

Summary Arthroscopic treatment of rotator cuff surgery has improved. Although the etiology of rotator cuff disease is not completely understood, the intrinsic and extrinsic factors that may play a vital role on the pathogenesis are understood as contributing factors. Understanding of the anatomy of the rotator cuff is necessary for successful arthroscopic care. It is vital in this surgery to inspect both the bursal and articular sides of the cuff, and with this information and taking into account patient desires and their health, make an appropriate decision because the likelihood of progression for partial rotator cuff tears recommends early repair, especially in the active patient. Patients with larger tears may also benefit from a more aggressive treatment approach and a complete preoperative assessment that should include nerve conduction studies looking for suprascapular nerve dysfunction, and then performing release athroscopically as needed. We believe that surgeons should be more aggressive in repairing a tear that is smaller than 50% in a young high demand patient.

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108 18. Jung, J.Y., Jee, W.H., Chun, H.J., Ahn, M.I., Kim, Y.S.: Magnetic resonance arthrography including ABER view in diagnosing partial thickness tears of the rotator cuff: accuracy and inter and intra observer agreements. Acta Radiol. 51(2), 194–201 (2010) 19. Kane, S.M., Dave, A., Haque, A., Langston, K.: The incidence of rotator cuff disease in smoking and non-smoking patients: a cadaveric study. Orthopedics 29(4), 363–366 (2006) 20. Kartus, J., Kartus, C., Rostgard-Christensen, L., Sernert, N., Read, J., Perko, M.: Long-term clinical and ultrasound evaluation after arthroscopic acromioplasty with partial rotator cuff tears. Arthroscopy 22, 44–49 (2006) 21. Kim, Y.S., Bigliani, L.U., Fujisawa, M., et al.: Stromal cell-derived factor 1 (SDF-1, CXCL12) in increased in subacromial bursitis and downregulated by steroid and nonsteroidal anti-inflammatory agents. J. Orthop. Res. 24, 1756–1764 (2006) 22. Knorth, H., Wittenberg, R.H., Dorfmuller, P., et al.: In vitro effects of diclofenac and selective cyclooxygenase-2 inhibitors on prostaglandin release from inflamed bursa subacromialis tissue in patients with subacromial syndrome. Orthopade 34, 241–249 (2005) 23. Ko, J.Y., Huang, C.C., Chen, W.J., Chen, C.E., Chen, S.H., Wang, C.J.: Pathogenesis of partial tears of the rotator cuff: a clinical and pathologic study. J. Shoulder Elbow Surg. 15, 271–278 (2006) 24. Koester, M.C., Dunn, W.R., Kuhl, J.E., Spindler, K.P.: The efficacy of subacromial corticosteroid injection in the treatment of rotator cuff disease: a systemic review. J. Am. Acad. Orthop. Surg. 15, 3–11 (2007) 25. Krishnan, S.G., Harkins, D.C., Schiffern, S.C., Pennington, S.D., Burkhart, W.Z.: Arthroscopic repair of full-thickness tears of the rotator cuff in patients younger than 40 years. Arthroscopy (J. Arthrosc. Repair Relat. Surg.) 24(3), 324–328 (2008) 26. Lohr, J.F., Uhthoff, H.K.: The microvascular pattern of the supraspinatus tendon. Clin. Orthop. Relat. Res. 254, 35–38 (1990) 27. Meyer, D.C., Pirkl, C., Pfirrmann, C.W., Zanetti, M., Gerber, C.: Asymmetric atrophy of the supraspinatus muscle following a tendon tear. J. Orthop. Res. 23, 254–258 (2005) 28. Mologne, T.S., Zhao, K., Hongo, M., Romeo, A.A., An, K.N., Provencher, M.T.: The addition of rotator interval closure after arthroscopic repair of either anterior or posterior shoulder instability: effect on genohumeral translation and range of motion. Am. J. Sports Med. 36(6), 1123–1131 (2008) 29. Neer II, C.S.: Anterior acromioplasty for the chronic impingement syndrome in the shoulder: a preliminary report. J. Bone Joint Surg. Am. 54, 41–50 (1972) 30. Neri, B.R., Chan, K.W., Kwon, Y.W.: Management of massive and irreparable rotator cuff tears. J. Shoulder Elbow Surg. 18(5), 808– 818 (2009) 31. Osti, L., Papalia, R., Paganelli, M., Denaro, E., Maffulli, N.: Arthroscopic vs. mini-open rotator cuff repair a quality of life impairment study. Int. Orthop. 34(3), 389–394 (2010) 32. Ostrander, R.V., Andrews, J.: Arthroscopic triple-row rotator cuff repair: a modified suture-bridge technique. Orthopedics 32(8), 566– 570 (2009) 33. Park, M.C., Elattrache, N.S., Ahmad, C.S., Tibone, J.E.: Transosseous – equivalent rotator cuff repair technique. Arthroscopy 22(12), 1360 (2006)

K.D. Plancher and A.R. Rivera 34. Plancher, K.D., Johnston, J.C., Peterson, R.K., Hawkins, R.J.: The dimensions of the rotator interval. J. Shoulder Elbow Surg. 14(6), 620–625 (2005) 35. Plancher, K.D., Peterson, R.K., Johnston, J.C., Luke, T.A.: The spinoglenoid ligament anatomy, morphology, and histological findings. J. Bone Joint Surg. 87A, 361–365 (2005) 36. Richards, D.P., Burkhart, S.S.: Margin convergence of the posterior rotator cuff to the biceps tendon. Arthroscopy (J. Arthrosc. Relat. Surg.) 20(7), 771–775 (2004) 37. Rokito, A.S., Cuomo, F., Gallagher, M.A., Zuckerman, J.: Longterm functional outcome of repair of large and massive chronic tears of the rotator cuff. J. Bone Joint Surg. Am. 81, 991–997 (1999) 38. Rutten, M.J., Spaargaren, G.J., van Loon, T., de Waal Malefijt, M.C., Kiemeney, L.A., Jager, G.J.: Detection of rotator cuff tears: the value of MRI following ultrasound. Eur. Radiol. 20(2), 450–457 (2010) 39. Sano, H., Ishii, H., Trudel, G., Uhthoff, H.K.: Histologic evidence of degeneration at the insertion of 3 rotator cuff tendons: a comparative study with human cadaveric shoulders. J. Shoulder Elbow Surg. 8, 574–579 (1999) 40. Shah, A.A., Milos, S., Deutsch, A.: The strength and effects of humeral rotation on single-versus double-row repair techniques in small rotator cuff tears. Orthopedics 33(1), 22 (2010) 41. Sher, J.S., Uribe, J.W., Posada, A., Murphy, B.J., Zlatskin, M.B.: Abnormal findings on magnetic resonance images of asymptomatic and symptomatic shoulders. J. Bone Joint Surg. Am. 88, 1699–1704 (2006) 42. Snyder, S.J., Pachelli, A.F., Del Pizzo, W., Friedman, M.J., Ferkel, R.D., Patel, G.: Partial thickness rotator cuff tears: results of arthroscopic treatment. Arthroscopy (J. Arthrosc. Relat. Surg.) 7(1), 1–7 (1991) 43. Tamai, M., Okajima, S., Fushiki, S., Hirasawa, Y.: Quantitative analysis of neural distribution in human coracoacromial ligaments. Clin. Orthop. Relat. Res. 373, 125–134 (2000) 44. Van Dyck, P., Gielen, J.L., Veryser, J., Weyler, J., Vanhoenacker, F.M., Van Glabbeek, F., De Weerdt, W., Maas, M., van der Woude, H.J., Parizel, P.M.: Tears of the supraspinatus tendon: assessment with indirect magnetic resonance arthrography in 67 patients with arthroscopic correlation. Acta Radiol. 50(9), 1057–1063 (2009) 45. Williams, M.D., Ladermann, A., Melis, B., Barthelemy, R., Walch, G.: Fatty infiltration of the supraspinatus: a reliability study. J. Shoulder Elbow Surg. 18(4), 581–587 (2009) 46. Yamaguchi, K., Konstantinos, D., Middleton, W.D., Hildebotlt, C.F., Galatz, L.M., Teefey, S.A.: The demographics and morphological features of rotator cuff disease: a comparison of asymptomatic and symptomatic shoulders. J. Bone Joint Surg. Am. 88, 1699–1704 (2006) 47. Yoo, J.C., Ahn, J.H., Koh, K.H., Lim, K.S.: Rotator cuff integrity after arthroscopic repair for large tears with less-than-optimal footprint coverage. Arthroscopy 25(10), 1093–1100 (2009) 48. Zingg, P.O., Jost, B., Sukthankar, A., Buhler, M., Pfirrmann, C.W., Gerber, C.: Clinical and structural outcomes of nonoperative management of massive rotator cuff tears. J. Bone Joint Surg. Am. 89(9), 1928–1934 (2007)

Current Concept: Arthroscopic Transosseous Equivalent Suture Bridge Rotator Cuff Repair Mehmet Demirhan, Ata Can Atalar, and Aksel Seyahi

Contents Introduction ................................................................................. 109 Evolution of Arthroscopic Rotator Cuff Repair ...................... 109 Biomechanical Improvements .................................................... 110 Anatomic “Footprint” of the Rotator Cuff and “Double Row” Philosophy .................................................. 110 Author’s Preferred Technique ................................................... 111 Clinical and Anatomic Outcomes of Series .............................. 113 Future Aspects ............................................................................. 113 Summary and Conclusion .......................................................... 114 References .................................................................................... 114

Introduction Surgical repair is recognized as the standard treatment for patients with symptomatic rotator cuff tear. Physiologically young and active patients need early repair of rotator cuff tear to achieve prompt return to daily and sports activities. More evidences are now available that nonoperative treatment of the rotator cuff tears leads to irreversible changes in the tendon, and to irreparable massive tears [63] Today, even fatty degeneration of muscle belly is no longer regarded as a strict contraindication for rotator cuff repair [16]. On the other hand, in a prospective study, early repair of symptomatic supraspinatus tears has been shown to provide better clinical results and to prevent tear propagation [42]. In the light of these scientific proofs, rotator cuff repair is the preferred treatment in most cases. Arthroscopic rotator cuff repair has several advantages over open surgical repair. Arthroscopy enables the evaluation and treatment of accompanying glenohumeral joint problems [40]. It also allows better visualization and more comprehensive assessment of rotator cuff. Tendon mobilization may be facilitated precisely to allow tension-free repair. Furthermore, preserving deltoid origin results in less soft tissue damage and less postoperative pain [10].

Evolution of Arthroscopic Rotator Cuff Repair

M. Demirhan ( ) and A.C. Atalar Department of Orthopaedics and Traumatology, Istanbul University, Istanbul Medical Faculty, Çapa, Istanbul 34093, Turkey e-mail: [email protected]; [email protected] A. Seyahi Department of Orthopaedics and Traumatology, American Hospital, Guzelbahce Sokak, No. 20, Nisantasi, Istanbul 34365, Turkey e-mail: [email protected]

After 1990, with improvement of arthroscopic techniques and suture anchors, first series of all arthroscopic rotator cuff repairs were published. In the early 2000s Burkhart et al. described principles of rotator cuff repair, such as tear type recognition, correct anchor placement, multiple suture anchor design, and loop and knot security [12]. Despite the use of principle-based repair methods, failure rates in arthroscopic rotator cuff repair series remained high for nearly 10 years [8, 28, 30, 32, 34, 45]. The main problem was retear of repaired cuff. Today, rotator cuff repair

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_15, © Springer-Verlag Berlin Heidelberg 2012

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researches focuses on: (1) biomechanically strong and durable fixation methods and (2) on improving tendon-bone healing by reconstruction of anatomic footprint of rotator cuff. We will summarize improvements in these fields, evolution of double-row philosophy and our preferred arthroscopic double-row suture bridge transosseous equivalent rotator cuff repair technique.

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concept with using medial and lateral row anchor placement to strengthen the initial strength of repair complex [25, 36]. Biomechanical studies revealed that adding lateral row or a transosseous suture to the medial row anchor fixation significantly improves the initial and ongoing strength of repair [6, 21].

Biomechanical Improvements

Anatomic “Footprint” of the Rotator Cuff and “Double Row” Philosophy

“Transosseous sutures” were the preferred fixation technique in traditional rotator cuff repair. In the beginning of arthroscopic repair procedures, suture anchors played a great role [50]. Several authors showed rotator cuff repair with arthroscopy to be a feasible method [20, 32, 57]. Anchors provided secure fixation on sutures to the bone with minimal invasive methods, without transosseous tunnels. Due to high failure rates in arthroscopic repair series of larger rotator cuff tears, biomechanical properties of suture anchor repair was questioned. Weakest links in the repair chain were determined as interfaces between anchor–bone, suture–anchor, and suture–tissue [41]. Newer anchor designs had overcome the problem of cutting off from bone. Screw type, 5–6 mm diameter metallic and bioabsorbable anchors are nearly standard devices now. Placing the anchor parallel to the bisector of lines tendon pulling vector and perpendicular to bone (dead man’s angle) helped to achieve more stable bony purchase [11]. Older anchor designs might cause suture failure due to friction at the anchor eyelet [5]. But suture fixation in the anchor also was changed and this type of failure also does not occur anymore. Bioabsorbable anchors are being more preferred than metallic ones because they have high failure loads, less complication rates, and build no artifact in postoperative magnetic resonance imaging studies [44]. Tendon grasping and obtaining durable reconstruction with sound knots is technically the most demanding part in arthroscopic repair. Mason Allen type suture was known as the strongest soft tissue grasping method in classic open repair [31]. Due to retrograde and antegrade suture passing devices, arthroscopic methods replicating Mason Allen suture were introduced, by combining one mattress and one simple suture [52]. However, their holding strength did not overcome mattress or simple sutures alone [53]. Secure knots with braided sutures may also be achieved either with locking or non-locking techniques. Knot security problem was solved with well-described methods in the past years [15]. Despite these big steps in arthroscopic repair techniques, high failure rates were still reported especially in large to massive tears series [8, 28, 30, 32, 34, 45]. Ultrasound and MRI evaluations revealed retear rates up to 40–90% [28, 30, 34]. At this point, researchers introduced double-row

Anatomic studies on rotator cuff insertion had described an area called “footprint.” Footprint area of the supraspinatus tendon consists of a mean medial-to-lateral 15 mm width and 21–25 mm anterior–posterior length [19, 23] This area begins immediately at lateral end of the articular cartilage and covers the top of greater tubercle. Cadaveric and computer model studies revealed that with single-row anchor repair, only 46–67% of original anatomic footprint may be covered [3, 39]. Furthermore, with transosseous repair larger area of contact was obtained [3]. To achieve less failure rates, more anatomic repairs were aimed. Double-row anchor rotator cuff repair was introduced for enlarging the tendon bone contact area and for reducing tension over each suture [25, 36]. Biomechanical evaluations confirmed the hypothesis about contact area. Mazzocca et al. observed that double-row repair consistently restored larger footprint area than single row construct, but they did not find any significant difference between two types of repairs regarding biomechanical properties, such as load to failure and gap formation under cyclic loading [38]. In contrast, other studies reported that double-row constructs achieved superior resistance to gap formation and higher ultimate failure load than single-row repair [6, 37, 56]. Transosseous repair has a long clinical history and have been shown in multiple studies to have superior biomechanical properties when combined with suture anchors. Adding a transosseous suture to the single row suture anchor repair nearly doubled ultimate failure strength [21, 61, 62]. Contact area and pressures were also studied to compare single-row and transosseous repair techniques. Transosseous repair revealed significantly higher contact pressure in a larger area [47]. Some authors placed second-row anchors at the lateral side of the greater tubercle, outside of the foot print area, to mimic a transosseous suture, and they have reported lower failure rates than single-row repair [2, 35]. The studies also showed that repair site integrity was durable during biological healing period. In another study with animal models double-row repair resulted in better biological healing with superior biomechanical properties than the singlerow repair [46].

Current Concept: Arthroscopic Transosseous Equivalent Suture Bridge Rotator Cuff Repair

At the same time period, knotless anchors with suture locking with pressure between bone tunnel and anchor were introduced [13]. These types of anchors were used in “transosseous equivalent suture bridge technique.” Suture bridge technique was first introduced by Park et al. in 2006 and has become a widely accepted method in the treatment of medium to large tears [48]. Suture bridge is a kind of double-row repair, however, it stands one step ahead of it, due to being less difficult and reproducing larger contact area with higher pressure at the tendon – bone interface [49]. This type of repair allowed less tissue extravasation than simple suture repair in a cadaveric model. Authors concluded that double-row repair may potentially enhance rotator cuff healing [1].

Author’s Preferred Technique We prefer beach chair position in all arthroscopic rotator cuff procedures. Thorough examination of glenohumeral joint and release of intra-articular adhesions in necessary cases is the first step of arthroscopic rotator cuff repair. Medial part of footprint area is debrided from fibrous tissue while the camera is still in the glenohumeral joint (Fig. 1). This step helps to understand the shape and the size of the tear from the articular side (Fig. 2a). Afterward, the camera is moved to the subacromial space. Meticulous debridement of bursal tissue and extra-articular adhesions is essential for mobilization of torn tendon, good visualization, and easier suture passage. Acromioplasty is performed as determined in the preoperative planning. Distal clavicle resection is also added, if necessary. Before the repair, debridement of floppy fibrous tissue at the tendon-end should be done and bleeding surface on the whole footprint area should be ensured.

Fig. 1 Debridement of the footprint area. Note the greater tubercle and footprint area (black bar)

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We usually place one anchor per 1 cm of tear. If the tear size is between 1.5 and 2.5 cm in anterior to posterior dimension we prefer to use two anchors (Fig. 2b) and if the tear size is 2.5–3 cm we prefer to use three bioabsorbable screw-type anchors at the medial row. Anchors are placed more than 6 mm apart from each other (Fig. 3). Entry hole is immediately at the articular cartilage and to achieve dead man’s angle, the arm is adducted during their insertion. Every anchor is loaded with two sutures with different colors. Initially, posterior sutures are passed in U- or V-shaped tears. In L-shaped tears, where the corner of the tear has to be fixed to the anterior part of the foot print, anterior sutures might be passed first. Good tendon grasping is achieved by rotating the arm for finding the best place to pass the suture. Free bird-beak-type suture graspers (Arthrex, Naples, Florida, USA), clever hook (Depuy Mitek, Raynham, Massachusets, USA), Suture Lasso (Arthrex, Naples, Florida, USA) (Fig. 4), or Scorpion (Arthrex, Naples, Florida, USA) (Fig. 5)-type suture passing devices with different shape and angles can be used. Medial row sutures are passed at least 1 cm medial than the lateral end of tendon tissue. Arthroscopic knots are tied in sliding or nonsliding fashion by respecting the row of suture passing (Fig. 2c). First passed sutures are tied first. For each anchor one knot is left with suture ends, while the suture ends of the other knot is cut with arthroscopic scissors (Fig. 6). Remaining four suture ends from two sutures, with different colors, are used to build suture bridge (Fig. 2d). One end from the anterior and the other from the posterior anchor are fixed to the lateral cortex, approximately 1 cm lower than lateral end of the footprint, using Pushlock (Arthrex, Naples, Florida, USA) suture locking-type anchor (Figs. 2e and 7). Same step is repeated at a more posterior (7–10 mm) point on the lateral cortex. Step is repeated if three anchors were used, at a more posterior point. At the end of procedure, repair construct should look like letter “M” (Figs. 2f and 8). More recently, in cases with large to massive tears, we prefer to use tape-like suture material, Fibertape (Arthrex, Naples, Florida, USA), fixed in a tunnel with bioabsorbable screw (Bio Swivel Lock (Arthrex, Naples, Florida, USA) to build medial row (Fig. 9). Sutures are passed through the tendon and knotting is not performed. Lateral row is established using the tape-like sutures from the medial row again with knotless anchors as described before. This completely knotless repair helps to accelerate the procedure with passing fewer sutures and surpassing knotting step. Since the material is much broader than braided conventional sutures, contact area at the repair site increases. Knotless repair with tape-like suture was biomechanically tested earlier and the study showed that this type of repair complex had presented no disadvantage against double-row repair with classical suture anchors with knots [58].

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Fig. 2 (a) Footprint area and tendon ends are debrided before the repair. (b) Insertion of the medial row anchors. (c) The knots are tied and medial row repair is completed. (d) Four suture ends from two sutures are used to build suture bridge. (e) The suture ends of the medial row anchors are fixed with a pushlock to the lateral cortex for the lateral row repair. (f) At the end of procedure repair construct should look like letter “M”

Fig. 3 Medial row anchors (black arrows) are placed more than 6 mm apart from each other

Fig. 4 Use of a suture lasso (white arrow) to pass the sutures of the medial row anchors (black arrows). IS infraspinatus, SS supraspinatus

Fig. 5 Use of Scorpio (black arrow) for suture passing. A grasper (white arrow) catches the tip of the passed suture

Fig. 6 For each anchor one knot has been left with suture ends (black arrows), while the suture ends of the other knot has been cut. P posterior, M medial, A anterior, L lateral

Current Concept: Arthroscopic Transosseous Equivalent Suture Bridge Rotator Cuff Repair

Fig. 7 One end from anterior and the other from posterior anchor are fixed to the lateral cortex with a Pushlock (white arrow). P posterior, A anterior

Fig. 8 The final “M”-like view of the double-row suture bridge rotator cuff repair. Black arrows point medial anchors, and white arrows lateral pushlocks. P posterior, M medial, A anterior, L lateral

Fig. 9 Fiber tape (black arrow) is a tape-like suture materal suitable for the large and massive rotator cuff tears. A Bio Swivel Lock (white arrow) can be used for the fixation of the fiber tape in the medial row repair

Clinical and Anatomic Outcomes of Series Results of clinical series with double-row repair usually revealed good results [35, 48, 59]. However, series with control group of single-row repair reported contradicting results. A systematic review of five comparative studies revealed no

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difference between single- and double-row repair groups in terms of clinical outcome and failure rates [43]. Some series advocated better healing and less failure rate [18, 24, 59], others concluded that there was no difference between doublerow and single-row repair groups [4, 27]. Another recent systematic analysis studied six prospective randomized trials with a total number of 388 patients revealing that there appears to be a benefit in structural healing when an arthroscopic rotator cuff repair is performed with double-row fixation as opposed to single-row fixation. However, they found little evidence to support any functional differences between the two techniques, except, possibly, for patients with large or massive rotator cuff tears. They have concluded that doublerow fixation may result in improved structural healing at the site of rotator cuff repair in some patients, depending on the size of the tear [51] Burkhart and Cole [14] criticized some of these studies because of small patient numbers [27, 60] and comparing single-row repair and not the standard double-row technique [17, 38]. Authors concluded that the only prospective randomized trial with proper power analysis revealed retear rate in transosseous equivalent suture bridge group which is significantly lower than single row repair group [29]. It has been emphasized that great advantage of cuff repair is gaining strength, and the only way to assess tendon healing clinically is improved muscle forces. Therefore, they suggest that there is a need for developing new outcome tool that addresses quantifying postoperative gains in strength [14]. Despite all efforts, failures, even though their percentage declines, still do occur following arthroscopic rotator cuff repair. Patient series with long follow-up have investigated prognostic factors that might affect clinical results. Larger defects, interstitial delamination of cuff tissue, fatty degeneration, older patients, and late admittance for surgery were determined to be the main poor prognostic factors [9, 26, 45, 55]. Surgeons should consider these factors before consulting their patients about rotator cuff repair and its results.

Future Aspects While attempts are made to improve mechanical strength and enlarge contact area in the repair site, investigations are also continuing to get better and more rapid biological healing. Therefore, derivates like bone morphogenetic protein (rh BMP) [54], insulin-like growth factor (IGF-1) [22], and matrix metalloproteinase inhibitors (Alpha-2 macroglobuline) [7] were studied in animal models. All studies obtained encouraging results regarding mechanical and histological evaluations. However, mesenchymal stem cell application at the rotator cuff repair site brought no advantage yet in another animal study [33].

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Summary and Conclusion Clinical outcome of arthroscopic rotator cuff repair is proven to be successful as traditional open or mini-open techniques in long-term follow-up. For patients, early recovery and less postoperative pain, for surgeons, better visualization and tendon mobilization, are the main advantages of the arthroscopic method. Today more anatomic and stronger repair is possible with transosseous equivalent suture bridge technique. The technique had been nearly a standard operative procedure in arthroscopic repair of medium to large sized rotator cuff tears in our hands. With longer follow-up, importance of transosseous equivalent suture bridge repair will be better understood. In future, rotator cuff investigation will focus on the methods to achieve better tendon-to-bone biological healing and recover fatty infiltration at the muscle unit.

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Posterosuperior and Anterosuperior Impingement in Overhead Athletes Chlodwig Kirchhoff, Knut Beitzel, and Andreas B. Imhoff

Contents Introduction ................................................................................. 117 Kinematics of Throwing ............................................................. 118 Internal Impingement ................................................................. 118 Posterosuperior Impingement (PSI).............................................. 119 Anterosuperior Impingement (ASI) .............................................. 119 Clinical Evaluation...................................................................... 120 Imaging Modalities ..................................................................... 121 Radiographic Findings .................................................................. 121 MRI Findings ................................................................................ 121 Therapy ........................................................................................ 122 Nonoperative Treatment................................................................ 122 Surgical Treatment ........................................................................ 124 Return to Sports .......................................................................... 124 Conclusions .................................................................................. 124 References .................................................................................... 125

C. Kirchhoff ( ) Department of Orthopaedic Surgery and Traumatology, Klinikum Rechts der Isar, Technische Universitaet Muenchen, Ismaninger Strasse 22, 81675 Muenchen, Germany e-mail: [email protected] K. Beitzel and A.B. Imhoff Department of Orthopaedic Sports Medicine, Klinikum Rechts der Isar, Technische Universitaet Muenchen, Connollystrasse 32, 80809 Muenchen, Germany e-mail: [email protected], [email protected]

Introduction In overhead athletes, the shoulder is significantly stressed, especially during distinct phases of throwing motions [33]. These patients typically present with complaints of posterior shoulder pain when the arm is abducted and maximally externally rotated (late cocking and acceleration phases of throwing) [4]. Symptoms may be vague and the athlete may only report about a gradual onset of loss of velocity or control during competition often known as dead arm syndrome [11]. Other common complaints are a tight and uncomfortable feeling in the shoulder during throwing along with a difficulty in warming up the upper extremity [35]. The majority of athletes do not recall a single acute event, but report about an acute exacerbation of previous lower symptoms as the impetus for seeking medical advice [13]. Several authors described shoulder pathologies leading to a disability of powerful throws, subsuming them as internal impingement [5, 30, 49, 60]. Baseball pitchers are most commonly afflicted, although athletes of other sports requiring repetitive shoulder abduction and external rotation such as tennis, volleyball, javelin throwing, and swimming are at risk as well [1, 4, 25, 40, 46]. It has been suggested that internal impingement is most likely caused by fatigue of the muscles of the shoulder girdle resulting from a lack of conditioning or from overthrowing [13]. These reports indicate that the humerus should be aligned in the plane of the scapula during the acceleration phase of throwing. As the shoulder girdle muscles become fatigued, the humerus drifts out of the scapular plane [55]. This has been termed hyperangulation or opening up, which can lead to tensile stressing of the anterior aspect of the shoulder capsule. Loss of the anterior capsular integrity compromises the obligatory posterior roll-back of the humeral head, leading to an anterior translation and therefore causing the undersurface of the rotator cuff to abut the margin of the glenoid and labrum. Athletes occasionally acknowledge a recent episode of overuse and should specifically be asked about changes in throwing habits and training of mechanics prior to the onset of the symptoms [7]. However, internal impingement has been described in nonathletes as well [12, 33]. Careful

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analysis of athletes suffering from internal impingement revealed two distinct clinical entities, characterized by significant pathologies and clinical features. In order to achieve a maximum recovery of the athlete, an accurate understanding as well as a sophisticated diagnostic and therapeutic algorithm is necessary. Knowing the duration of symptoms, the precise anatomic location of the pain, and any previous treatment, including periods of rest, is essential. Besides the clinical assessment, especially magnetic resonance (MR) imaging is needed. In the recent past, sensitivity of imaging modalities have been significantly improved using direct MR arthrography in functional, “abduction external rotation” (ABER)position. However, arthroscopy still represents the diagnostic gold standard allowing for dynamic assessment and simultaneous therapy.

Kinematics of Throwing Meister et al. divided the throwing motion into six phases [50] with delineation by purpose and muscle activity (see Table 1). The total time of the six phases of throwing motion takes less than 2 s to occur. During phase I (wind-up) the center of gravity is raised. This is a point when minimal stress is put on the shoulder. In phase II (early cocking) the arm is prepared for maximum external rotation. The arm is abducted to 90° and external rotation [9]. Phase III (late cocking) is the point of maximal external rotation of the shoulder in elite athletes reaching close to 170°. This position of the abducted, externally rotated shoulder leads to a posterior translation of the humeral head being the point of maximum stress to the anterior capsule. These first three phases take approximately 1.5 s in total [14]. Phase IV is the acceleration phase. Although the duration of the fourth phase is only 0.05 s, the greatest angular velocities and the largest change in rotation occur during this phase. The shoulder rotates to bring the ball to the release point of 90° rotation.

Table 1 The six phases of the throwing motion: Phase I is the wind-up, phase II the early cocking, ending with planting of the striding foot. Phase III is the late cocking, in which the arm reaches maximum external rotation, in phase IV, the ball is accelerated until phase V with release of the ball and deceleration of the arm. Phase VI, the followthrough, rebalances the body til motion stop Kinematics of throwing [50] Phase I

Wind-up

Phase II

Early cocking

Phase III

Late cocking

Phase IV

Acceleration

Phase V

Deceleration

Phase VI

Follow through

Peak rotational velocity can near 7.000°/s [25]. Phase V is the deceleration phase and represents the most violent phase of the throwing motion. Deceleration occurs from the point of ball release to the point of 0° of rotation. It is a point of marked eccentric contraction of the rotator cuff to slow down the arm motion being a point of maximal posterior capsule stress. Joint loads approach posterior shear of 400 N, inferior shear of 300 N, and compressive forces of nearly 1,000 N [41]. Phase VI is the follow through. This is the rebalancing phase in which the muscles return to resting levels, but still certain stress is put onto the posterior capsule. The final two phases last approximately 0.35 s. The velocity of the ball depends on a variety of biomechanical factors but is most directly related to the amount of external rotation that the shoulder achieves. Elite pitchers can generate ball velocities that exceed 144.8 km/h. At ball release, the shoulder of a professional pitcher can be exposed to distractive forces of up to 950 N. In the deceleration phase, the compressive forces created by the rotator cuff and the deltoid muscle is in the range of 1,090 N with posterior shear forces of up to 400 N. These forces approach the ultimate tensile strengths of the soft tissues that support the shoulder. In addition to the glenohumeral motion, scapular function has to be seen as a major contributor to transfer the kinetic energy from the lower limbs and trunk to the upper extremity. In this context Kibler et al. presented an excellent characterization of the scapular dynamics [42]. Only half of the kinetic energy imparted to the ball results from the arm and shoulder action. The remaining half is generated by lower-limb and trunk rotation and is transferred to the upper limb through the scapulothoracic joint, making that articulation an important, but frequently overlooked, part of the kinetic chain [9].

Internal Impingement Unlike “external” or “subacromial” impingement, often simply called “impingement syndrome,” there is not a single pathophysiologic process at work in the painful thrower’s shoulder. Internal impingement syndrome is thought to be of fundamentally more complex character and multifactorially conditioned [35, 57, 65]. In 1993, Walch et al. published a landmark article in which 30 athletes were assessed for shoulder pain [69]. Seventeen (16 of whom were throwing athletes) of the originally enrolled 30 athletes underwent an arthroscopic shoulder examination; typical findings included the presence of posterior labral lesions and articular surfacesided rotator cuff tears, in the absence of a Bankart or SLAP tear. The authors differentiated the labral lesions from SLAP lesions, which extended anteriorly to the biceps anchor at the supraglenoid tubercle, concluding that internal impingement may be responsible for a subset of patients with isolated

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posterior SLAP tears. In each case, the impingement of the posterior aspect of the humeral head was directly observed via arthroscopy on the posterosuperior rim of the glenoid. This area of impingement corresponded precisely with the location of the lesions of the rotator cuff and the labrum, respectively, when the arm was brought into the abducted, externally rotated throwing position.

Posterosuperior Impingement (PSI) Bennett et al. first described posterior shoulder pain in throwers in 1959. Lombardo et al. identified the late cocking phase of the thrower’s motion as a possible cause of posterior shoulder pain in this group of athletes [46]. This phenomenon, which is distinct from subacromial impingement syndrome, is known as posterosuperior impingement (PSI) [23]. A posterior capsular thickening and contracture have been reported as common findings [39]. The biomechanical etiology for injury to these structures is controversial. Two possible causes for PSI have been reported, although neither is generally accepted. We favor the theory of rotational instability, which describes the ability of the throwing shoulder to overrotate into a position of hyperexternal rotation during the late cocking and acceleration phase of the throwing motion. Thereby, the anterior capsule is stressed during the late cocking phase whereas the posterior capsule is widened and traumatized during the deceleration phase. In the consequence, microinstability with corresponding posterior capsular hypertrophy develops, leading to an increased external and a reduced internal rotation. In this context Burkhart et al. formed the term glenohumeral internal rotation deficit (GIRD) [28]. They described the first step in this cascade as the development of a contracture of the posterior band of the inferior glenohumeral ligament (PIGHL) and the posteroinferior capsule. Thereby, the central contact point of the glenohumeral articulation is shifted in a posterosuperior direction possibly leading to a greater arc of external rotation to occur before the normal contact of internal impingement. These changes lead to an increase in the pathologic peel-back mechanism with an increased vector of the biceps in the cocking position transmitting heightened shearing of the biceps anchor, leading to SLAP tears [68]. This notion is supported by several authors, which report an increased incidence of SLAP-lesions (superior labrum from anterior to posterior) [45, 47, 52]. Following the undersurface of the rotator cuff the supraspinatus tendon is significantly entrapped between the humeral head and the posterior superior labrum; so that findings typical for PSI include articular-sided partial thickness rotator cuff tears and concomitant posterosuperior or posterior labral injuries.

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However, Burkhart et al. suggest a second theory claiming the posterosuperior contact to be physiological [14]. They suppose that rotator cuff tears rather originate from repetitive injury to the supraspinatus tendon during the deceleration phase. This theory is supported by the fact that a nonpathologic interposition of the rotator cuff and the posterosuperior labrum between the glenoid rim and the greater tuberosity occurs in throwers and non-throwers as well. Cadaveric, MRI, and arthroscopic studies have consistently shown that contact of the rotator cuff to the posterosuperior labrum is of physiologic nature [54, 66].

Anterosuperior Impingement (ASI) In contrast to PSI, the anterosuperior impingement (ASI) presents with a significant lower prevalence. It involves an impingement of the subscapularis tendon between the anterior humeral head and the anterosuperior glenoid and labrum during forward flexion of the arm. In a position of horizontal adduction and internal rotation of the arm, the undersurface of the reflection pulley and the subscapularis tendon impinges against the anterosuperior glenoid rim. In this context, lesions of the long head of the biceps (LHB), the pulley, and the rotator cuff have been associated with an ASI of the shoulder. Habermeyer et al. stated that a forcefully stopped overhead throwing motion might terminate in a pulley lesion [29]. During active contraction of the biceps muscle in internal rotation, the strain increases while the elbow extension is decelerated. By this deceleration, a maximal contraction of the LHB is provoked and can cause tears in the rotator interval capsule. Gerber and Sebesta described the pulley lesions resulting from repetitive forceful internal rotation above the horizontal plane [26]. This leads to frictional damage between the pulley system and the subscapularis tendon on the one hand and the anterior superior glenoid rim on the other. As a result of intrinsic degenerative changes, the rotator interval shows partial tears involving the superior glenohumeral ligament (SGHL) and the articular side of the supraspinatus tendon. In 1996, Habermeyer and Walch showed that 50% of cases of biceps tendon subluxation were associated with degenerative changes in the anterosuperior aspect of the labrum, suggestive for a correlation between these intrinsic structural changes. In a previous work we reported on another possible etiology of ASI [44]. In a large series of young patients with paraplegia of the lower extremity (wheel chairs) we observed a significant number of lesions of the anterior superior complex. This might, most likely, originate from repetitive active contractions of the biceps muscle in internal rotation during wheel turning. Similar to the theory of Habermeyer et al., this deceleration may lead to tears in the rotator interval capsule [29].

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Clinical Evaluation Internal impingement typically affects young to middle-aged adults; in most major case series of internal impingement, patients are under 40 years of age and participate in activities involving repetitive abducting and externally rotating arm motions or positions [9, 62, 67]. The majority of patients who have been identified with internal impingement are overhead athletes [61, 70]. For example, the first major series by Walch et al. primarily consisted of volleyball and tennis players [69]. The largest athletic group with internal impingement studied has been the throwing athletes, in particular baseball players [49, 58, 69]. Medial evaluation of a thrower begins with a good thorough history of the problem. In eliciting the history of the injury, a determination if the resulting symptoms are of vague character and of gradual onset, or occurred as the result of an acute incident is important [16–18, 68]. Most patients present with a progressive decrease in throwing velocity or a loss of control and performance [20–22]. Chronic diffuse posterior shoulder girdle pain is common in terms of the presenting complaint, but the pain may be localized onto the joint line. Despite posterior shoulder pain being the most common complaint among patients with internal impingement, patients may also present with symptoms similar to those associated with classic rotator cuff disease [25, 26]. Alternatively, patients may also have instability symptoms, such as apprehension or the sensation of subluxation with the arm in an abduction and external rotation position. Notably, Burkhart et al., reported in their series of 96 athletes with a disabled throwing shoulder an 80% rate of anterior corocoid pain, rather than isolated posterior shoulder pain, described as the most common presenting symptom [15]. Posterior glenohumeral joint line tenderness, increased external rotation, and decreased internal rotation are the most common physical examination findings in throwing athletes (see Fig. 1). However, all patients suspected of internal impingement should be evaluated with a complete shoulder examination due to the high rate of other pathologic shoulder conditions associated with internal impingement. During physical examination, sometimes the relative hypertrophy of the dominant arm versus areas of atrophy, especially in the infraspinatus fossa, can be palpated. In addition, for the documentation of bilateral active and passive motion of the shoulders, testing for SLAP lesions, “classic” impingement signs such as the Neer and Hawkins tests, cross-body adduction tests, and instability testing should be performed [31, 32]. Regarding assessment of laxity, which does not automatically correspond to instability, the “sulcus sign” should be determined. Additionally, other parameters of the Beighton score should be analyzed too. For evaluation of anteroposterior translation of the humeral head the “anterior-and-posteriordrawer-test” as well as the “load-and-shift-test” should be used. Despite significant controversy regarding the validity of

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a

b

Fig. 1 The typical clinical finding of a patient with GIRD is demonstrated

various physical examination maneuvers for detecting SLAP tears, because superoposterior labral tears represent a cardinal feature of pathologic internal impingement, the performance of a combination of these tests is generally indicated [37, 38]. We favor the O’Brien test, which was reported by the author with 100% sensitivity and 98.5% specificity for the active compression test. It is performed with the arm positioned in 90° forward flexion, 20° adduction, and in maximal internal rotation. Resistance creates pain in the anterior superior shoulder that is relieved by resistance with maximal external rotation or supination of the forearm. Meister et al. investigated the ability of a single maneuver, referred to as the “posterior impingement sign,” to detect the presence of articular-sided rotator cuff tears and posterior labrum lesions [51]. The subjects were tested for the presence of deep posterior shoulder pain when the arm was brought into a position similar to that noted during the late cocking phase of throwing. The sensitivity and specificity of the posterior impingement sign were 75.5% and 85%, respectively. Notably, all patients with noncontact injuries with a positive test had arthroscopic findings amenable to surgical treatment. Regarding conventional impingement tests, Mithöfer et al. reported that subacromial impingement tests are usually negative in patients with known internal impingement [53]. In contrast, one study reported that

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over 25% of the 41 professional throwing athletes arthroscopically evaluated, demonstrated a positive Neer or Hawkins sign. According to our opinion one of the absolute typical findings is GIRD, defined by a loss of greater than 30–40° of internal rotation relative to the expected gain in external rotation, compared to the contralateral side. This is supported by several studies, for example, Burkhart et al. reported the presence of GIRD in 100% of a series of 124 symptomatic baseball pitchers [15]. Regarding concomitant increased external rotation Myers et al. recently emphasized that throwers with pathologic internal impingement exhibiting significantly increased posterior shoulder tightness and glenohumeral internal rotation deficits do not necessarily gain significantly increased external rotation [55]. In addition, scapular dyskinesis is a commonly reported finding. Characteristic features include a prominent inferior medial border of the scapula and the appearance that the throwing shoulder is dropped inferior compared with the non-throwing side [43].

Imaging Modalities Radiographic Findings Radiographic evaluation of patients with signs and symptoms of internal impingement should include true AP, axillary and thoracic outlet (Y-view) radiographic views of the shoulder [10]. Usually, only minimal findings are present in patients with internal impingement. Regarding typical signs associated with internal impingement, Bennett et al. first described an exostosis of the posteroinferior glenoid rim (Bennett lesion) in baseball players [4]. He hypothesized that this might occur secondary to traction of the triceps muscle tendon on its bony origin. However, there is much controversy surrounding the cause and significance of the Bennett lesion [33, 51]. Ferrari et al. reported on baseball pitchers with posteroinferior ossifying lesions, none of which was located in the region of the triceps tendon [24]. Changes of the greater tuberosity are also commonly found on the radiographs of internal impingement patients. Mithöfer et al. stressed the importance of radiographically assessing the greater tuberosity for sclerotic and cystic changes; these findings are present in approximately half of the patients with internal impingement [53]. Interestingly, a recent radiographic study analyzing 57 asymptomatic professional baseball pitchers demonstrated that cystic changes in the humeral head were present in 39% of the examined shoulders [73]. Walch et al. noted a further pathology, the so-called posterior humeral head geodes, corresponding to osteochondral defects located superiorly close to the insertion of the supraspinatus tendon [69]. Another finding that may be seen on radiographs of internal impingement patients is rounding

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or remodeling of the posterior glenoid rim, although MRI is the optimal modality to appreciate this phenomenon [53].

MRI Findings MRI is considered the gold standard regarding the workup of any young patient presenting with shoulder pain [33]. When labral lesions are suspected, we recommend the use of direct MR-arthrography with using either gadolinium contrast material or saline [34, 56, 59]. MR-findings in internal impingement include articular-sided partial-thickness rotator cuff tears of the supraspinatus, infraspinatus, or both tendons, and posterior or superior labral lesions [72]. The tears of the rotator cuff tendons are usually small and involve the articular surface. Internal impingement tears are better diagnosed on MR arthrography as a small undersurface linear contrast extension into the tendon (see Fig. 2). Abduction and external rotation (ABER) positioning may be useful for tear detection in these patients, since a relaxation of the posterior superior rotator cuff may allow for gadolinium to seep into an otherwise occult or subtle tear [6]. Interestingly, Halbrecht et al. performed noncontrast MRI of the shoulder in an ABER-position in the throwing and non-throwing arm of asymptomatic college baseball players and observed a contact between the rotator cuff and the posterosuperior glenolabral complex in all shoulders [30]. In addition, these athletes often present with associated posterosuperior labral abnormalities. Repetitive stress encountered in pitchers also speeds up the normal aging process of the rotator cuff, leading to an early tendinosis. Rim-rent tears from tensile overload can be seen at the articular surface at the humeral tendinous insertion [27]. These tears show high signal intensity extending between the greater tuberosity tendon insertion (supraspinatus foot print) and the tendon itself on fluid-sensitive sequences. In most cases, they are located in the anterior half of the supraspinatus tendon and can be mistaken for intratendinous signal. Other tensile overload injuries usually present as tiny tears at the articular surface of the supraspinatus and infraspinatus tendon. These tears are often small and best recognized on MR arthrography in the ABER position as fluid intensity or extension of intra-articular contrast medium into the hypointense line on the articular surface of the rotator cuff tendons. The glenoid labrum is often torn, without perceptible underlying shoulder instability in pitchers [3]. SLAP tears with significant posterior extension can be disabling for pitchers, because of arising posterior superior laxity [19]. The appearance of SLAP tears on MRI includes intermediate hyperintense labral degeneration and linear fluid or gadolinium undercutting the superior labrum extending posterior to the biceps tendon origin. Cysts and impaction deformity are also seen at the posterior greater tuberosity and can increase diagnostic confidence in the diagnosis of internal impingement.

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Fig. 2 Posterior superior glenohumeral impingement. T1-weighted fat-saturated ABER image of shoulder MR arthrogram shows an articular surface tear at the posterior supraspinatus. There is also a superior labral tear and a small cysts at the greater tuberosity

Therapy The vast majority of shoulder injuries in throwers should initially be treated with conservative, nonoperative methods. Only significant structural injury such as an acute rotator cuff tear, dislocation, or SLAP lesion deserve early surgical intervention.

Nonoperative Treatment Every overhead athlete requires a training program that strengthens all elements of the kinetic chain of the throwing motion. Patients with mild symptoms and early phases

of the disorder need an active rest, including a complete break from throwing along with physical therapy. Axe et al. proposes a 2 days off-period for every day that symptoms have been present (maximum break of 12 weeks) [2]. Anti-inflammatory measures to “cool down” the irritated shoulder can be beneficial in accelerating the rehabilitative process. This includes nonsteroidal anti-inflammatory drugs (NSAIDs), occasionally a corticosteroid injection, and physical therapy modalities like iontophoresis. For patients with longer lasting problems Wilk et al. suggested a phased progression of the rehabilitation program, emphasizing dynamic stability, rotator cuff strengthening, and a scapular stabilization program [71]. Phase I – Acute Phase: The primary focus

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of the initial stage is set on the injured tissue being allowed to heal, modification of activity, decrease of pain and inflammation, and on the reestablishment of a baseline dynamic stability, a normalization of the muscle balance, and the restoration of the proprioception. A diminishment of the athlete’s pain and inflammation is accomplished through the use of local therapeutic modalities such as ice, ultrasound, and electrical stimulation. In addition, the athlete’s activities (such as throwing and exercises) must be modified up to a pain-free level. Active-assisted motion exercises may be used to normalize shoulder motion, particularly shoulder internal rotation and horizontal adduction. The thrower should perform specific stretches and flexibility exercises for the benefit of the posterior rotator cuff muscles (Fig. 3). Phase II – Intermediate Phase: When pain and inflammation have been decreased, the athlete may proceed to Phase II. The primary goals are to improve the strengthening program, continue to improve flexibility, and facilitate neuromuscular control. During this phase, the rehabilitation program is progressed to more aggressive isotonic strengthening activities with emphasis on the restoration of the muscle balance. Selective muscle activation is also used to restore muscle balance and symmetry. Contractures of the posterior structures, the pectoralis minor muscle, and the short head of the biceps muscle also contribute to a glenohumeral internal rotation deficit and increase the anterior tilting of the scapula. McClure et al. showed the use of the cross-body stretch for the treatment of patients with posterior shoulder tightness leading to a significantly greater increase of the internal rotation, compared to a control group with normal shoulder motion not performing exercises [48]. Borstad et al. found the unilateral corner stretch and the supine manual stretch to be effective for a lengthening of the pectoralis minor muscle [8]. In the overhead thrower, the shoulder external rotator muscles, scapular retractor muscles, and protractor and depressor muscles are frequently isolated due to structural weakness. Several authors have emphasized the importance of scapular muscle strength and neuromuscular control as contribution to a normal shoulder function [43]. Isotonic exercise techniques are used to strengthen the scapular muscles. Overhead throwing athletes often exhibit external rotator muscle weakness. Also, during this second rehabilitation phase, the overhead throwing athlete is instructed to perform core strengthening exercises for the abdominal and lower back musculature. In addition, the athlete should perform lower extremity strengthening and participate in a running program, including jogging and sprints. Upper extremity stretching exercises are continued as needed to maintain soft tissue flexibility. Phase III – Advanced Strengthening Phase: The goals are to initiate aggressive strengthening drills, enhance power and endurance, perform functional drills, and gradually initiate throwing activities. During this phase, the athlete performs the Thrower’s Ten exercise program, continues manual resistance stabilization drills, and initiates

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c Fig. 3 The sleeper stretch: The patient on the involved side with the shoulder in 90° of forward elevation. The contralateral arm internally rotates the involved shoulder until a stretch on the posterior aspect of the shoulder

plyometric drills. Dynamic stabilization drills are also performed to enhance proprioception and neuromuscular control. These drills include rhythmic stabilization exercise drills. Plyometric training may be used to enhance dynamic stability and proprioception, as well as gradually increase the functional stresses put on the shoulder joint. Plyometric exercises entail a rapid transfer of eccentric to concentric contraction to allow for a stimulation of muscle spindles, which facilitates a recruitment of muscle fibers. An interval throwing program

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may be initiated in this phase of rehabilitation. This program begins with short, flatground throwing at variable distances. When the throwing program is initiated, intensive strengthening should be replaced by a less intensive, high repetition, and low weight program to avoid an overtraining. Phase IV – Return-to-Throwing Phase: This phase, usually involves the progression of the interval throwing program as well as a neuromuscular maintenance. While the athlete is performing the interval throwing program, the clinician should carefully monitor the thrower’s mechanics and throwing intensity. The athlete is advanced to position-specific throwing provided that he or she remains asymptomatic. The goal is to return to the full throwing velocity over the course of 3 months. To prevent the effects of overtraining or throwing in case of poor condition, it is critical to instruct the athlete specifically on what to do through specific exercises throughout the year. A lack of improvement after 3 months, or an inability to return to competition within 6 months, constitutes failure of the nonoperative conservative management, this should result in an additional diagnostic testing and, if necessary, operative intervention should be considered.

Surgical Treatment Indications for surgery include the failure of conservative treatment with an inability to return to competition despite a prolonged rehabilitation protocol geared toward correction or resolution of the pathology diagnosed by physical examination and imaging [9, 36]. The operative approach to patients with signs and symptoms of internal impingement should be pursued in a deliberate, methodical fashion. The final therapeutic plan in symptomatic throwing shoulders depends on the specific examination findings under anesthesia because physical findings may be confusing in a patient who is awake The following arthroscopic examination is performed in terms of a systematic review of the entire shoulder. In addition, injury to many other structures in the shoulder, besides the posterosuperior labrum and the rotator cuff, have been associated with pathologic internal impingement. Jobe has suggested that as many as five anatomic structures are at risk: the posterior superior labrum, the rotator cuff tendon (articular surface), the greater tuberosity, the inferior glenohumeral ligament (IGHL) complex, and the posterior superior glenoid [39]. He noted that the majority of patients with internal impingement present with an injury of more than one of the five structures at the time of arthroscopic assessment, underscoring the importance of a thorough diagnostic arthroscopic assessment of the shoulder joint in the setting of suspected internal impingement or in cases in which a typical internal impingement lesion is unexpectedly detected. The surgeon should evaluate the entire shoulder carefully and look for evidence of instability in the

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biceps tendon, biceps anchor, labrum, and capsule. Presence of a drive-through sign should be elicited by sweeping the scope from superior to inferior to assess laxity. Consecutively, the surgeon should evaluate the rotator interval and the rotator cuff insertion. The examined arm should then be removed from traction and an ABER examination should be performed with the arm in abduction and external rotation. During this maneuver, the arthroscope is located in the posterior portal, just off the posterior superior labrum, and then the arm is carefully abducted and externally rotated. The surgeon evaluates evidence of kissing lesions between the undersurface of the rotator cuff and the posterior superior labrum as seen in pathologic internal impingement. Repetitive microtrauma to the bony greater tuberosity or the posterosuperior rim of the glenoid may represent extremes of the spectrum of injury caused by the abducted, externally rotated position associated with internal impingement, but even cases of fracture of these structures have been reported in the literature. Although osteochondral lesions of the humeral head have also been described, it is likely that these originate from a similar mechanism to greater tuberosity changes, with subtle variations in the anatomy or the throwing motion accounting for a different site of humeral head contact with the glenoid rim. Surgical intervention should be directed toward specific pathologic lesions believed to correspond to the patient’s symptoms or play a role in the complex pathophysiology of internal impingement. Subacromial bursectomy may be warranted in cases when substantial degrees of subacromial inflammation and bursitis are noted at the time of surgery [63, 64]. Mithöfer et al. also suggested that internal impingement represents a relative contraindication to acromioplasty [53].

Return to Sports A formal throwing mechanics evaluation may be helpful, particularly in the younger athlete with less specialized training. The mature athlete with altered or poor throwing mechanics may also benefit from biomechanical and professional evaluation. Once an appropriate rest period has passed and symptoms are relieved, throwing is resumed with an interval throwing program; however, the shoulder should be completely pain-free prior to resuming any throwing activities. Intensity is advanced based on symptoms, or the lack, thereof, with the goal of returning to effective throwing.

Conclusions The throwing athlete puts enormous stress on both the dynamic and the static stabilizers of the shoulder during the throwing motion. These repetitive forces cause adaptive soft

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tissue and bone changes that initially improve the performance but ultimately may lead to shoulder pathologies especially during the motion of throwing. Although a range of theories have been suggested for the pathophysiologic development of internal impingement, the causes are obviously of multifactorial nature. The cardinal lesions of internal impingement, articular-sided rotator cuff tears and posterosuperior labral lesions, have been shown to occur in association with a number of other findings, most importantly GIRD and SICK scapula syndrome, but also with posterior humeral head lesions, posterior glenoid bony injury, and rather rarely with Bankart and IGHL lesions. Extensive biomechanical and clinical research is necessary before a complete understanding and reconciliation of the varying theories of the pathomechanics of injury can be developed [74].

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C. Kirchhoff et al. 57. Rossi, F.: Shoulder impingement syndromes. Eur. J. Radiol. 27(Suppl 1), S42–S48 (1998) 58. Rossi, F., Ternamian, P.J., Cerciello, G., Walch, G.: Posterosuperior glenoid rim impingement in athletes: the diagnostic value of traditional radiology and magnetic resonance. Radiol. Med. 87(1–2), 22–27 (1994) 59. Sasaki, T., Saito, Y., Yodono, H., Prado, G.L., Miura, H., Itabashi, Y., Ishibashi, Y.: Labral-ligamentous complex of the shoulder. Evaluation with double oblique axial MR arthrography. Acta Radiol. 44(4), 435–439 (2003) 60. Schickendantz, M.S., Ho, C.P., Keppler, L., Shaw, B.D.: MR imaging of the thrower’s shoulder. Internal impingement, latissimus dorsi/subscapularis strains, and related injuries. Magn. Reson. Imaging Clin. N. Am. 7(1), 39–49 (1999) 61. Sonnery-Cottet, B., Edwards, T.B., Noel, E., Walch, G.: Results of arthroscopic treatment of posterosuperior glenoid impingement in tennis players. Am. J. Sports Med. 30(2), 227–232 (2002) 62. Struhl, S.: Anterior internal impingement: an arthroscopic observation. Arthroscopy 18(1), 2–7 (2002) 63. Tibone, J.E., Jobe, F.W., Kerlan, R.K., Carter, V.S., Shields, C.L., Lombardo, S.J., Yocum, L.A.: Shoulder impingement syndrome in athletes treated by an anterior acromioplasty. Clin. Orthop. Relat. Res. 198, 134–140 (1985) 64. Tibone, J.E., Elrod, B., Jobe, F.W., Kerlan, R.K., Carter, V.S., Shields Jr., C.L., Lombardo, S.J., Yocum, L.: Surgical treatment of tears of the rotator cuff in athletes. J. Bone Joint Surg. Am. 68(6), 887–891 (1986) 65. Ticker, J.B., Beim, G.M., Warner, J.J.: Recognition and treatment of refractory posterior capsular contracture of the shoulder. Arthroscopy 16(1), 27–34 (2000) 66. Tirman, P.F., Bost, F.W., Garvin, G.J., Peterfy, C.G., Mall, J.C., Steinbach, L.S., Feller, J.F., Crues III, J.V.: Posterosuperior glenoid impingement of the shoulder: findings at MR imaging and MR arthrography with arthroscopic correlation. Radiology 193(2), 431– 436 (1994) 67. Tirman, P.F., Smith, E.D., Stoller, D.W., Fritz, R.C.: Shoulder imaging in athletes. Semin. Musculoskelet. Radiol. 8(1), 29–40 (2004) 68. Tischer, T., Salzmann, G.M., Imhoff, A.B.: Rotator cuff tears and internal impingement in athletes. Orthopade 36(10), 950, 952–956 (2007) 69. Walch, G., Liotard, J.P., Boileau, P., Noel, E.: Postero-superior glenoid impingement. Another impingement of the shoulder. J. Radiol. 74(1), 47–50 (1993) 70. Werner, S.L., Guido Jr., J.A., Stewart, G.W., McNeice, R.P., VanDyke, T., Jones, D.G.: Relationships between throwing mechanics and shoulder distraction in collegiate baseball pitchers. J. Shoulder Elbow Surg. 16(1), 37–42 (2007) 71. Wilk, K.E., Meister, K., Andrews, J.R.: Current concepts in the rehabilitation of the overhead throwing athlete. Am. J. Sports Med. 30(1), 136–151 (2002) 72. Wörtler, K., Link, T.M., Rummeny, E.J.: Radiologische Diagnostik und Differenzialdiagnostik der Osteonekrose. Arthroskopie 16, 15–22 (2003) 73. Wright, R.W., Steger-May, K., Klein, S.E.: Radiographic findings in the shoulder and elbow of Major League Baseball pitchers. Am. J. Sports Med. 35(11), 1839–1843 (2007) 74. Kirchhoff, C., Imhoff, A.B.: Posterosuperior and anterosuperior impingement of the shoulder in overhead athletes-evolving concepts. Int Orthop. 34(7), 1049–1058 (2010)

Internal Impingement and SLAP Lesions

íbrahim Yanmış and Mehmet Türker

Contents History.......................................................................................... 127 Clinical Presentation ................................................................... 127 Etiology ........................................................................................ 128 Radiological Findings ................................................................. 128 Clinical Findings ......................................................................... 129 Physical Findings ........................................................................ 129 Treatment ..................................................................................... 130 Conservative Treatment ................................................................ 130 Surgical Treatment ........................................................................ 130 Conclusion ................................................................................... 132 References .................................................................................... 132

History Internal glenoid impingement is the most common cause of posterior shoulder pain in overhead throwing athletes. It is generally misdiagnosed as rotator cuff pathology. Bennett was the first to define symptoms of the internal impingement in 1959. He observed that the presence of a bony exostosis on the postero-inferior border of the glenoid fossa and thought that this was a symptomatic lesion that caused irritation of the capsule and the synovial membrane [2]. In 1979, Lombardo emphasized pain over the posterior shoulder area during late cocking phase in throwing athletes [14]. In the 1970s, the clinical problem named “dead arm” was a threat to the active career of throwing athletes. This clinical presentation can be briefly defined as restricted arm function and inability to throw due to shoulder pain. Before the documentation of the pathomechanics and intraarticular lesions of disease it has been suggested to be a psychological problem by some authors. In 1981 Rowe and Zarins defined minimal recurrent anterior shoulder instability in dead arm syndrome [20]. In 1985, Andrews was the first to explore the intraarticular pathology of internal impingement [1]. Andrews reported a high incidence of posterior superior labral laceration in cases operated for rotator cuff (RC) repair for partial tears. Walch and Jobe reported intraarticular pathology and anatomic location of the lesions encountered in this syndrome in their extensive study [11, 22].

Clinical Presentation

í. YanmıĜ ( ) Orthopaedic and Trauma Clinic, GATA Military Medical Academy, Gn. Tevfik Saglam Cad, 06018 Etlik Ankara, Turkey e-mail: [email protected] M. Türker Orthopaedic and Trauma Clinic, Kırıkkale University Medical Faculty, SaÜlık cad No. 1, 71100 Kirikkale, Turkey e-mail: [email protected]

Internal impingement defines three clinical presentations of the shoulder: (a) Posterior superior impingement: Posterosuperior glenoid injury is caused by impingement of the articular surface of the rotator cuff against the posterior superior part of the glenoid labrum. Anterior part of the infraspinatus, posterior part of the supraspinatus and posterosuperior part of the humeral head are common affected

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_17, © Springer-Verlag Berlin Heidelberg 2012

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areas. It is mainly seen in throwing athletes but occurs at an increasing rate in bodybuilders and weight lifters. The other main group is patients involved in occupational overhead activities such as mechanics and electricians. The mechanism of injury is extensive shoulder extension-abduction and external rotation (ABER). This is the exact mechanism of throwing action. This injury occurs in maximum late cocking or early acceleration phase of throwing. The main pathologies are tear of the RTC and degeneration of the posterior superior labrum. (b) Superior impingement: As a result of impingement between superior labrum and articular surface of supraspinatus, laceration of this musculature and degeneration of labrum occurs. Clinical signs are confined to the mid-acceleration phase of throwing. (c) Anterior impingement: This clinical picture occurs as a result of impingement between coracoid and anterior portion of humeral head. Pathomechanics of this clinical picture were sought to be Roller-Wringer effect defined by Lo et al. [13]. During internal rotation movement of shoulder, coracoid impinges on upper superficial layer of subscapularis. The clinical picture was related to the coracoidal pathologies.

I. Yanmış and M. Türker

Another mechanism was proposed by Burkhart et al. [3]. They believe that posterior capsular tightening is primary pathologic entity that is responsible for SLAP lesion and other intraarticular pathology of internal impingement. They said “When the arm is removed from traction and brought into abduction and external rotation, the biceps tendon assumes a more vertical and posteriorly directed orientation.” They called this phenomenon the “Peel-Back Sign.” In another theory, humeral retro-version may be present as an underlying etiology. Humeral retro-version is developed to rotate back into external rotation as an adaptation to repetitive forceful throwing during the growing period. Crockett et al. found that humeral retro-version is increased 17° at the dominant shoulder when compared with the contralateral side. He proposed that increased humeral retroversion may reduce internal rotation and result in posterosuperior impingement [6]. Although there are mechanical explanations it must not be over viewed that these lesions can occur without overuse activity in bodybuilders and weightlifters with same lesions.

Radiological Findings

Etiology There is still considerable debate over the etiology and pathophysiology of internal impingement. It must not be forgotten that the causative mechanisms are different in these three different clinical presentations. A common finding in these three different clinical conditions is occurrence of lesions due to microtrauma at static and dynamic intraarticular structures of shoulder during repetitive forceful throwing activity. Signs of overuse and micro/macro instability are more profound than signs of impingement. Although discussion goes on whether instability is the causative factor or the end-result of this syndrome, both theories can be case-specifically valid. One of the accepted theories suggests that anterior instability occurs as a consequence of laxity of anterior capsule and GH ligaments due to humeral head hyperangulation during throwing activity [15, 16]. Anterior instability results in excessive contact between inferior surface of rotator cuff and posterosuperior labrum during late cocking phase of throwing (Fig. 1). In many studies it was shown that this contact is solely physiologic in nature. But the problem here is that this physiologic contact, when occurred in excessive and forceful repetitive numbers may result in articular pathologies. Lacerations of the posterosuperior labrum and RC tears mirror imaging to these lacerations observed during shoulder arthroscopy supports this theory (Fig. 2).

X-ray examination of the shoulder joint does not reveal specific signs in internal impingement. In some studies, magnetic resonance (MR) and magnetic resonance arthrography (MRA) imaging of the shoulder revealed nonspecific findings [5, 8, 10, 21]. Radiological findings of MRA are more valuable in diagnosis. Three lesions are defined in MRA at neutral shoulder position: (a) Cystic degeneration at the posterolateral aspect of the humeral head where rotator cuff inserts (b) Partial rotator cuff tears at articular surface of posterior of supraspinatus and infraspinatus (Fig. 2) (c) Degeneration of posterosuperior labrum or superior labrum anterior and posterior (SLAP) lesion (Figs. 1 and 3) MR images taken at abduction-external rotation position of the shoulder facilitates visualization of RC tears at inferior articular area [12]. SLAP is an important component of internal impingement (Fig. 3). Recently MR imaging of the shoulder made valuable aids in SLAP diagnosis. Another clinical presentation of internal impingement is subcoracoid impingement that can be diagnosed by MR image findings [7, 9, 19]. In axial MR images, the distance between lateral cortex of coracoid and medial cortex of humerus is calculated. Coracohumeral distance below 6 mm is in favor of subcoracoid impingement. Other findings of anterior impingement syndrome are tears of subscapularis and degeneration of lesser tubercle.

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Clinical Findings History of the patient is the most important step in diagnosis. Age, occupation and sports activity of the patient and characteristics of pain such as initiation, distribution, duration and type give important clues to diagnosis. In some cases, diagnosis depends solely on careful history taking and physical examination. Answers to the following questions can be explored by the physician:

Fig. 1 Arthroscopic visualization of the typical appearance of a posterosuperior labral fraying in throwers (left)

(a) How did the pain begin? Generally pain in internal impingement has insidious onset. Pain progressively increases overtime. In differential diagnosis, posttraumatic instabilities and rotator cuff tears must be excluded. Initially pain and weakness occurs after strenuous training or activity. In this period there is no pain at resting state and daily activities (as disease progresses resting pain and pain provoked by overlying on the affected side occur). (b) What is the type of pain? Generally pain begins as discomfort at the posterior shoulder region and eventually progresses to pain. Pain can be localized to the posterior shoulder area and described as a burning sensation. (c) Is there functional loss in shoulder activities? Initially there is pain provoked by throwing without functional loss. As disease progresses throwing capacity decreases or diminishes. Commonly during this phase range of motion and daily activities are normal.

Fig. 2 On the right, photography shows mechanism of injury during the throwing in ABER. Repetitive contact can cause intraarticular tear of RC and fraying

(d) Has the patient received prior treatment? Did it succeed? Three different stages described for internal impingement: Stage 1: Pain due to hard overhead activity. No loss of function Stage 2: Posterior shoulder pain, Positive Jobe’s test Stage 3: Same findings as a stage 2 but, failure of an appropriate rehabilitation program

Physical Findings

Fig. 3 Arthroscopic visualization of a type 2 SLAP lesion in internal impingement

Physical examination begins with inspection. Patient must be dressed free. Inspection can be repeated statically and dynamically. During shoulder examination relevant joints also can be evaluated. Motion of the scapulothoracic joint is of paramount importance. Atrophy and asymmetry of rotator musculature may pertain to a specific disease. In internal impingement inspection is always normal. Anomalies in inspection must a need for excluding other diseases. Generally pain can be provoked by palpation at posterior shoulder area. This finding is helpful in excluding rotator cuff pathologies which cause pain over greater tubercle.

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prone to repetitive microtrauma during throwing to achieve maximum force production, motion ranges are violated. Maximum range of motion and enough stability are prerequisites of successful throwing. Initial treatment of internal impingement in athletes always begins with rest and rehabilitation. Limitation of overhead throwing activities is a rule. Physical rehabilitation must be ensued immediately. The philosophy of rehabilitation is to restore coordinated movements of the shoulder girdle with preservation of dynamic stability. It must be kept in mind that muscles of shoulder girdle include muscles of the scapula. Stretching of posterior capsule and external rotator muscles of shoulder decreases anterior displacement of humeral head and thereby clinical symptoms. Proprioceptive education also aids in relieving pain. Wilk et al. offered ten principles for conservative treatment of internal impingement [24]: Fig. 4 Increased external rotation is an important finding of physical examination in throwing shoulder

Commonly there is no pain anterior to the shoulder and at bicipital sulcus. Acromioclavicular (AC) joint and other bony prominences are painless. Adduction-internal rotation can elucidate pain in subcoracoid impingement. The most important physical examination findings in internal impingement are tests of shoulder movement and stability. In the shoulder of throwing athlete abductionexternal rotation of dominant side is 10–15° more than the contralateral side (Fig. 4). Abduction-internal rotation is limited to the same extent. Range of other shoulder movements is generally comparable with the contralateral side. Anterior instability is noted during stability testing. In conducted studies 2+ anterior and 1+ posterior instability were reported. In many of the patients, inferior instability findings can be encountered. In athletes with bulky muscles performing these tests under general anesthesia may aid in diagnosis. Internal impingement test is always positive among the provocative tests (Jobe’s test). In this test, symptoms of pain and impingement are generated in abduction and maximum external rotation and eliminated with a posteriorly directed force on the humeral head. Although there is SLAP lesion, O’ Brien test is negative. Positive results obtained at other provocative tests must recall diseases in differential diagnosis. Muscle power is generally within normal limits. Another common finding is popping and crepitation during humeral head movements in the glenoid fossa.

Treatment Conservative Treatment The aim in treatment of internal impingement is restoration of normal shoulder kinematics and range of motion while preserving glenohumeral stability. Throwing athletes are

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Never overstress healing tissue Prevent negative effects of immobilization Emphasize external rotation muscular strength Establish muscular balance Emphasize scapular muscle strength Improve posterior shoulder flexibility (internal rotation range of motion) Enhance proprioception and neuromuscular control Establish biomechanically efficient throwing Gradually return to throwing activities Use established criteria to progress

Anti-inflammatory medication at early treatment helps to reduce pain. Studies showing beneficial effects of topical and systemic steroids are lacking.

Surgical Treatment There is no consensus for surgical intervention of internal impingement. The main indications for surgery are persistent pain, decrease in performance despite conservative treatment and inability to return active sportive activity. Athletes who are at the end of their career and having pain only after strenuous activity but not due to daily activities must decide for themselves whether to proceed to surgical intervention or not. Regardless of the surgical technique to be used, arthroscopic examination must preclude this. Shoulder arthroscopy reveals important knowledge about diagnosis and treatment of coexistent pathologies. Displacement of humeral head relative to the glenoid can be evaluated and its degree can be noted. Biceps tendon, external rotators, glenoid labrum, chondral structures, subscapularis tendon, and capsule should be evaluated during shoulder arthroscopy. We prefer beach chair positioning for arthroscopic treatment of internal impingement of shoulder joint. It is relatively easy to simulate the injury mechanism in this position.

Internal Impingement and SLAP Lesions

Detachments at biceps attachment should be differentiated from normal physiological appearance. The degree of capsular laxity is a surgeon-dependent subjective issue. When there is capsular laxity, inserted scope through posterior portal readily reaches antero-inferior pouch (drivethrough sign). In our experience more than normal distance between long head of biceps tendon and superior capsule also points to capsular laxity. The articular surface of the rotator cuff should be carefully inspected. At the posterior articular surface of the rotator cuff, injuries may extend from partial lacerations to complete tears. These rotator cuff injuries at the posterior articular surface generally can be seen at the cuff attachment site of posterior part of the supraspinatus. For treatment of lacerations and partial tears, debridement should suffice. In cases where there is no doubt about coexistent pathologies, intraarticular arthroscopic management should be sufficient and subacromial arthroscopy should not generally be needed. One of the important components of internal impingement, the anterior humeral head translation may cause degeneration of glenoid chondrum. Chondral injury is generally seen at the middle and inferior parts of the glenoid and can be classified as grade 2–3 chondral injury (Fig. 5). Simple debridement is suitable treatment for small sized chondral lesion in glenoid surface and humeral head. Labral injury is generally seen at the posterosuperior portion that is typical for internal impingement. Labral injury can be seen as a fraying or detachment from glenoid. Fraying and degeneration can be debrided with shaver or electrothermal devices. SLAP lesions should be carefully evaluated. It is hard to make a decision of repair for type 1 SLAP lesions. In active athletes, choosing surgical repair would be consistent with a more favourable outcome. The repair of SLAP lesion alone is not enough for treatment of internal impingement. Other intraarticular lesions are anterior capsule and anterosuperior of subscapularis tendon degenerations resulting from anterior impingement between humeral head and coracoid.

Fig. 5 Chondral lesions generally can be seen central part of the glenoid

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Arthroscopic Debridement Initially, treatment of internal impingement with debridement of degenerated labrum and partial intraarticular rotator cuff tears was carried on but the results were dissatisfying. Arthroscopic debridement can only be a part of surgical treatment. Debridement of rotator cuff increases healing response in case of a small and partial lesion. If depth of rotator cuff tear is less than half of the cuff thickness, debridement should be satisfying. Tears exceeding this limit or full thickness tears should be repaired. Treatment of internal impingement can be achieved when accompanied by SLAP lesion repairs, debridement and capsular reconstruction.

SLAP Lesion Repair In majority of internal impingement patients, SLAP lesions are observed. SLAP lesions that are seen arthroscopically in symptomatic shoulders with appropriate clinic findings on physical examination should be repaired [4, 18, 23]. There is no consensus on the treatment of type 1 SLAP lesions. It has been suggested that type 1 SLAP lesions are anatomic variations actually. Generally, type 1 and 3 SLAP lesions should be debrided, whereas type 2 and 4 should be repaired. The repair can usually be accomplished through two portals. Many authors reported good results with arthroscopic SLAP repair in throwing athletes [17, 18, 23]. In spite of this, some authors believe that SLAP lesion repair alone is not enough for treatment of internal impingement.

Capsular Reconstruction Anterior capsular laxity observed in internal impingement can be the cause or end-result of the problem. Although discussion continues about cause or end-result mechanism, capsular shrinkage or plication remain the main stage of treatment of this pathology. Capsular reconstruction can be either done by plication via arthroscopic and open surgery or electrothermally. Open capsulorrhaphy has been offered by some author but has been able to return only 68–81% of players to their pre-injury levels. Arthroscopic treatment has been shown better results (93%). In spite of good preliminary results, it is generally believed that long term results of electrothermal capsular shrinkage would be less favourable. The middle and long term results of electrothermal capsular shrinkage in multidirectional instabilities raised suspicion on the longevity of this procedure. The balance between preserving range of motion while decreasing capsular laxity should be well maintained. The arm is positioned in 20–25°of external rotation and abduction during the capsular reconstruction. Many authors

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reported good results in arthroscopic capsular reconstruction for internal impingement.

Derotation Osteotomy As it is reported in some studies, humeral anteversion is increased in throwing athletes, humeral derotation osteotomies are proposed to correct malrotation. High complication rates and dissatisfying results have halted popularization of this treatment technique.

Conclusion Experience of the surgeon and high compliance of the patient are two important factors for successful results in treatment of internal impingement. Isolation and prevention of precipitating or triggering factors are of paramount importance for the best outcome. Whatever the surgical technique used, physical rehabilitation remains the sine qua non of a good result. Team-mates and trainers of athlete should be counselled for an earlier return to sporting activity. Technically, true muscle coordination, changing the faulty technique of throwing and strengthening exercises improves functional outcome and allows earlier return to active sports.

References 1. Andrews, J.R., Carson Jr., W., Mc Leod, W.: Glenoid labrum tears related to the long head of biceps. Am. J. Sports Med. 13, 337–341 (1985) 2. Bennet, G.E.: Shoulder and elbow lesions in the professional baseball pitcher. JAMA 119, 510–514 (1959) 3. Burkhart, S.S., Morgan, C.D.: 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 (1998) 4. Burkhart, S.S., Parten, P.M.: Dead arm syndrome: torsional SLAP lesions versus internal impingement. Tech. Shoulder Elbow Surg 2(2), 74–84 (2001) 5. Connell, D.A., Potter, H.G., Wickiewicz, T.L., et al.: Noncontact magnetic resonance imaging of superior labral lesions. 102 cases confirmed at arthroscopic surgery. Am. J. Sports Med. 27, 133–136 (1999)

I. Yanmış and M. Türker 6. Crockett, H.C., Gross, L.B., Wilk, K.E., et al.: Osseos adaptation and range of motion at the glenohumeral joint in professional baseball pitcher. Am. J. Sports Med. 30(1), 20–26 (2002) 7. Friedman, R.J., Bonutti, P.M., Genez, B.: Cine magnetic rosenance imaging of the subcoracoid region. Orthopaedics 21, 545–548 (1998) 8. Giaroli, E.L., Major, N.M., Higgins, L.D.: MRI of internal impingement of the shoulder. AJR Am. J. Roentgenol. 18(185), 925–929 (2005) 9. Giaroli, E.L., Major, N.M., Lemley, D.E., et al.: Coracohumeral interval imaging in subcoracoid impingement syndrome on MRI. AJR Am. J. Roentgenol. 186, 242–246 (2006) 10. Halbrecht, J.L., Tirman, P., Atkin, D.: Internal impingement of the shoulder: comparison of findings between the throwing and nonthrowing shoulders of college baseball players. Arthroscopy 15, 253–258 (1999) 11. Jobe, C.M.: Posterior superior glenoid impingement: expanded spectrum. Arthroscopy 11, 530–537 (1995) 12. Lee, S.Y., Lee, J.K.: Horizontal component of the partial thickness tears of rotator cuff: imaging characteristics and comparison of ABER view with oblique coronal view at MR arthrography initial results. Radiology 224, 470–476 (2002) 13. Lo, I.K., Burkhart, S.S.: The etiology and assessment of subscapularis tendon tears: a case for subcoracoid impingement, the rollerwringer effect and TUFF lesions of the subscapularis. Arthroscopy 19, 1142–1150 (2003) 14. Lombardo, S., Jobe, F., Kerlan, R., et al.: Posterior shoulder lesions in throwing athletes. Am. J. Sports Med. 5, 106–110 (1997) 15. Lui, S.H., Boynton, E.: Posterior superior impingement of the rotator cuff on the glenoid rim as a cause of shoulder pain in the overhead athlete. Arthroscopy 9, 697–699 (1993) 16. Mc Farland, E.G., Hsu, C.Y., Neira, C., et al.: Internal impingement of the shoulder: a clinic and arthroscopic analysis. J. Shoulder Elbow Surg. 8, 458–460 (1998) 17. Morgan, C.D., Burkhart, S.S., Palmeri, M., et al.: Type II lesions: three subtypes and their relationships to superior instability and rotator cuff tears. Arthroscopy 14, 553–565 (1998) 18. Pagnani, M.J., Speer, K.P., Altchek, D.W., et al.: Arthroscopic fixation of superior labral tears using a biodegradable implant: a preliminary report. Arthroscopy 11, 194–198 (1995) 19. Richards, D.P., Burkhart, S.S., Campbel, S.E.: Relation between narrowed coracohumeral distance and subscapularis tears. Arthroscopy 21, 1223–1228 (2005) 20. Rowe, C.R., Zarins, B.: Recurrent transient subluxation of the shoulder. J. Bone Joint Surg. Am. 63, 863–872 (1981) 21. Tirman, P.F., Bost, F.W., Garvin, G.J., et al.: Posterosuperior glenoid impingement of the shoulder: findings at MR imaging and MR arthrography with arthroscopic correlation. Radiology 193, 431– 436 (1994) 22. Walch, G., Boileau, J., Noel, E., et al.: Impingement of deep surface of the supraspinatus tendon on the posterior superior glenoid rim: an arthroscopic study. J. Shoulder Elbow Surg. 1, 238–243 (1992) 23. Warner, J.J.P., Kann, S., Marks, P.: Arthroscopic repair of combined bankart and superior labral detachment anterior and posterior lesions: technique and preliminary results. Arthroscopy 10, 383–391 (1994) 24. Wilk, K.E., Meister, Keith, Andrews, J.R.: Current concepts in the rehabilitation of the overhead throwing athlete. Am. J. Sports Med. 30, 1 (2002)

Anterior Shoulder Instability Mustafa Karahan, Umut Akgün, and RüĜtü Nuran

Contents Anatomy and Biomechanics ....................................................... 133 Static Factors ................................................................................. 133 Dynamic Factors ........................................................................... 135 Pathophysiology .......................................................................... 136 Diagnosis ...................................................................................... History .......................................................................................... Physical Examination.................................................................... Radiology ......................................................................................

136 136 136 137

Treatment ..................................................................................... 137 Acute Anterior Shoulder Luxation (First Episode)....................... 137 Recurrent Anterior Shoulder Instability........................................ 138

Studies in the last years prove that anterior instability occurs with the combination of many factors. Almost in every shoulder instability case; the main pathology does not involve only one anatomic lesion, but mostly it is the combination of pathologies in the joint. So all the pathologies should be treated to achieve a good stability in the diagnosis of anterior instability which is the most common type; in addition to the knowledge of anatomy and biomechanics, proper physical examination and radiological evaluation is needed. Every case should be evaluated by its own and proper treatment options should be planned according to this.

References .................................................................................... 139

Anatomy and Biomechanics

M. Karahan ( ) Orthopedics and Traumatology, Marmara University School of Medicine, Opr. Cemil Topuzlu Cd. 37/2, Fenerbahçe, 34726 ístanbul, Turkey e-mail: [email protected], [email protected] U. Akgün Orthopedics and Traumatology, Acıbadem University School of Medicine, ínönü Cd, Okur Sk, 20, KozyataÜı, 34742 ístanbul, Turkey e-mail: [email protected] R. Nuran Orthopedics and Traumatology, Acıbadem KozyataÜı Hospital, ínönü Cd, Okur Sk, 20, KozyataÜı, 34742 ístanbul, Turkey e-mail: [email protected]

While evaluating the shoulder joint, which is a ball-socket type, the main point is a large humeral head surface articulating with a small glenoid surface. Humeral head should be central to be in a stable position through its range of motion [38]. There is only 1 mm translation of the humeral head from the glenoid surface during its motion in anatomic planes [24, 50]. To gain this centralization, many factors should function together. Factors important in stabilization are studied in two main groups (Table 1). Generally, static factors play a role in the end limits of the shoulder joint motion and they are tight in the limits of motion arc, whereas generally loose during the motion. On the other hand dynamic factors work through the motion arc.

Static Factors Static factors activate during the end stages of the motion and while the arm is in a resting position next to the body. Generally, they have no function during the mid-range of motions. Basically; humeral head and glenoid cavity need version to fit properly. Different anatomic studies show that glenoid cavity has a retroversion in 75% (average retroversion

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Table 1 Static and dynamic factors in shoulder joint stability Static factors Dynamic factors Glenoid – humeral head version

Rotator cuff

Glenoid – humeral head configuration

Biceps tendon

Glenoid labrum

Scapular rotators

Glenohumeral ligaments and capsul Adhesion and cohesion (−) Intra-articular pressure Rotator cuff

Propriocepsion

has tight attachment to glenoid, superior labrum is in the attachment site of long head of biceps tendon so that it has a rather mobile structure. Anterior labrum is rich in anatomic variations, pathological lesions, and these variations should be assessed carefully [64] (Fig. 3). Glenohumeral ligaments and the capsule; are the most active tissues in shoulder joint stability. Glenohumeral ligaments are composed of; superior glenohumeral ligament (SGHL), middle glenohumeral ligament (MGHL), and inferior glenohumeral ligament (IGHL). SGHL is the smallest in all these, so it has little effect on stability. It has a close relation with superior glenoid rim, biceps tendon, and MGHL. It joins with coracohumeral ligament and runs over the bicipital groove then attaches to lesser tubercle so that it has a function in biceps pulley system. SGHL; mainly functions in inferior stability in adduction and also limits external rotation [2, 46] (Fig. 4). The coracohumeral ligament, which is an extra-articular ligament, also contributes to inferior stability during adduction [2]. MGHL has many variations, originates from the upper one-third of the glenoid labrum, and runs obliquely crossing the subscapularis tendon and attaches lesser tubercle (Fig. 4). MGHL plays major role in anterior stability in 45° of abduction and also limits external rotation [46, 60]. IGHL, has a hammock shape and forms by the combination of anterior and posterior bands and the axilla lies in between. It has its origin in the inferior glenoid labrum and attaches to humeral neck. It plays a major role in anterior stability during abduction and external rotation of the shoulder [60] (Fig. 5). Shoulder joint capsule, in addition to its ligaments, has also contributed to stability with its volume. The increase in joint volume is expected to be a reason of global instability whereas the decrease in that volume can cause limitation of joint motion [13, 36]. There is a natural negative pressure in the joint, forming a vacuum affect which resists translations and

angle is 7°), and it also has an anteversion in 25% (the angle of anteversion varies between 2° and 10°), which means that this anteversion angle may affect instability; humeral head has retroverted alignment comparing to both condyles and this version differs from 17° to 30° in different studies [57, 61]. In addition, glenoid surface has 5° of inclination vertically and according to many authors this affects inferior stability [65]. The bony structures of glenoid cavity and humeral head has little affect on stability because humeral head chondral surface is 21–22 cm2 and glenoid chondral surface is 8–9 cm2; so that only 25% of the humeral head surface can be counterbalanced by the glenoid cavity during shoulder motion [58]. Glenoid labrum is a meniscoid structure rich in collagen fibers surrounding the glenoid cavity and has the main contribution to stability. With the help of labral tissue, glenoid fossa, which has a rather shallow surface, increases its depth and contact surface [23] (Fig. 1). With the excision of labrum, which has a buffering affect with its triangular configuration, there is 20% decrease in stability [28, 35]. Labrum; surrounding the glenoid cavity attaches to glenoid medially and laterally; and it helps the attachment of the capsule and the glenohumeral ligaments. To understand the capsule and the ligaments properly glenoid is divided according to the clockwise system (Fig. 2). Although inferior labrum

Humeral head

G

le

no id

su rfa

ce

Anterior labrum

Fig. 1 Wedge effect of the glenoid labrum in the stability of the humeral head in glenoid fossa

Posterior labrum

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12

Superior

11

1

2

9

Anterior

Posterior

10

3

4

8

Fig. 4 Right shoulder arthroscopic view from posterior portal shows anterior glenohumeral ligaments. LHB long head of biceps, MGHL middle glenohumeral ligament, CHL coraco humeral ligament, SGHL superior glenohumeral ligament, ST subscapularis tendon

Inferior 7

5 6

Fig. 2 Clockwise system is useful for positioning of the labral lesions

Fig. 5 Left shoulder arthroscopic view from posterior portal, probe shows the anterior band of the inferior glenohumeral ligament at 5 o’clock position. GL glenoid labrum

Fig. 3 Left shoulder arthroscopic view from posterior portal, asteriks shows an anatomic variant “Sublabral hole.” LHB long head of biceps, MGHL middle glenohumeral ligament, GL glenoid labrum

helps stability. In addition “adhesion” between the synovial fluid and chondral tissues and “cohesion” between the synovial fluid itself contributes to stability [39]. Passive musculotendinous tension in the rotator cuff also helps in static stabilization of the joint. Subscapular muscle resists anterior translation whereas teres minor and infraspinatus resist posterior translation [47, 48].

Dynamic Factors Dynamic factors act especially during the mid-range of shoulder motions, in which the movement has the fastest torque

with many external forces acting on it. During the motion,, all dynamic factors should act together to have the humeral head centralized in the glenoid cavity [34, 35, 38, 62]. Muscles of the shoulder region, act as a stabilizer complex functioning to centralize the head in the glenoid cavity during shoulder motion; this is known as “Couple concept” [64]. For example; the action of deltoid muscle translates the humeral head superiorly while the action of rotator cuff pushes the humeral head inferiorly. [12]. In addition; the coordination between the scapular rotators during shoulder motion adjusts the inclination of the glenoid surface so that there is a stable surface underneath the humeral head [29]. Especially during overhead activities, to have the shoulder joint centralized, the amount of compressive forces are almost 90% of the body weight [25, 62]. Recent studies show that the long head of biceps also contributes to stability in different angles of the joint; in contraction, it brings the humeral head closer to the glenoid center and contributes to the superoinferior stability and helps anteroposterior stability, while the shoulder is in external rotation [30, 55].

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Pathophysiology Shoulder joint, having the widest range of motion (ROM) in the human body, is the joint with most instability episodes [10]. In addition to the knowledge of instability, which is a pathologic condition, a physiological condition known as hyperlaxity should be mastered as well. Although it is a physiological condition, hyperlaxity can predispose to instability [40]. With proper evaluation and physical examination, hyperlaxity and instability can be dissociated. Although it can be seen due to sports, hyperlaxity is genetic, mostly in women. It is a bilateral, multidirectional condition and can have other hyperlaxity criteria [3, 7]. Although shoulder instabilities are grouped as anterior, posterior, and multidirectional, anterior instability has the highest incidence. Talking about anterior shoulder instability, two clinical entity such as luxation and subluxation should be discussed. Luxation is the total disruption of the glenohumeral relation, where as subluxation is the self-limited, short-term and partial disruption of this relation. Luxations are traumatic and out of control; subluxations can be repetitive, without any trauma and can be controlled/ uncontrolled type. In addition, untreated first time luxations have the risk of becoming repetitive. Pathologies and the affected anatomic tissues are listed in Table 2. In literature, many different classifications were used for shoulder instabilities. The classical classification is TUBS (traumatic, typically unilateral, with a Bankart lesion and usually requiring surgery to stabilize the shoulder) and AMBRI (atraumatic, multidirectional, commonly bilateral, treatment by rehabilitation and inferior capsular shift in some refractory patients) [59]. As it is a general classification system, criterias like, voluntary dislocations, psychiatric conditions, and the frequency are added [45, 54]. In this part, most common anterior shoulder instabilities are going to be evaluated as follows: Table 2 Anatomic parts and pathologies in anterior shoulder instability Affected anatomic tissue Pathology

1. Acute anterior shoulder luxation 2. Recurrent anterior shoulder instability, luxation, and subluxation

Diagnosis Correct diagnosis of anterior shoulder instability and addressing of the involved pathology are two main points for the proper treatment. The steps for the correct diagnosis are; good history, physical examination, and radiology.

History Most patients have the history of acute shoulder dislocation, whereas repetitive subluxation episodes are rare to be expressed. Although the luxations can be traumatic (sudden fall or impact), minimally traumatic (swimming, throwing, etc.), or atraumatic (trying to reach backward, etc.), clinically the patient is in a noisy condition and importantly feel relaxed after relocation. Relocation, whether easy or difficult, also gives an idea about the degree of instability. During recurrent instabilities after luxation, patients will feel discomfort when the shoulder is in abduction and external rotation. In addition, symptoms of subluxation and instability are rather hard to document and complicated. For instance, patient with inferior instability can have discomfort while carrying heavy objects and paresthesia can accompany this symptom. The specific motion creating the symptoms and/or the magnitude of the trauma, if present, can help us to evaluate the patient. In some cases, the symptoms arise in the last ranges of motion during athletic activities, where as in some cases luxation or subluxation can be seen even during sleeping. In addition; evaluation of any psychiatric condition and epileptic condition should be evaluated to have a proper treatment option.

Glenoid labrum

Bankart – Perthes, ALPSA, GLAD lesions

Glenohumeral ligaments and capsul

HAGL, capsular deformity and laxity

Physical Examination

Posterolateral part of humeral head

Hill–Sachs lesion

Anterior part of glenoid cavity

Bony bankart

Glenoid cavity

Congenital or trauma-induced version insufficiency

Humeral head

Congenital or trauma-induced version insufficiency

Long head of biceps tendon

SLAP

Rotator cuff

Subscapularis tendon tears

Standard physical examination must start with inspection. Both shoulders must be examined and any asymmetry and/or atrophy should be noted. In total shoulder luxations; humeral head can be palpated just inferior and anterior to the joint with a sulcus in the deltoid area. Pain and limited motion are obvious symptoms. Superficial bony landmarks should be palpated to rule out associated injuries. Neurovascular examination of the upper extremity should be done in acute dislocations. To diagnose any axillary nerve injury, motor function

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Table 3 Brighton’s criteria of clinical hyperlaxity, 4 or more points is a sign of hyperlaxity 90° of passive dorsiflexion of fifth MCP joint

1 point (Max 2)

Touch of the thumb on the forearm

1 point (Max 2)

Hyperextension of the elbow

1 puan (Max 2)

Hyperextension of the knee

1 puan (Max 2)

Touching the ground with both palms while both knees are in full extension

1 point (Max 1)

of deltoid and superficial sensory function over the deltoid muscle should be examined. In acute conditions no further evaluation is needed. In cases of instability, physical examination continues with evaluation of passive and active ROM of the shoulder joint and should be compared with the opposite shoulder. The rotator cuff strength should be examined as well, because the risk of rotator cuff tears increase in patients with shoulder luxation more than 30 years old. After this; examination of glenohumeral joint stability should start. The patient should be in a relaxed position during this examination and the opposite shoulder should be examined as well. The most preferred tests are sulcus sign, anterior apprehension, posterior apprehension, and load-shift tests [42]. Results of these tests may differ between the patients and the physicians as well, so the most important point is to compare the opposite intact shoulder. In the suspicion of instability, hyperlaxity tests should be performed in every patient and should be ruled out clinically. Presence of any four of the hyperlaxity criterias, shown in Table 3, is positive for clinical hyperlaxity [3].

Radiology In addition to the anterior dislocation, there is also an inferior displacement, which makes the diagnosis easier with a direct AP radiography of the shoulder joint in acute dislocations. Because of pain in the acute dislocation, the patient may be unable to abduct or rotate the shoulder so that the axillary, West point or Stryker notch views are difficult to obtain. But after closed reduction, the first evaluation of the patient with direct radiographies is important to rule out any bony lesions seen in 55% of the patients [43]. Standard scapular AP and lateral views taken in internal rotation of the shoulder are important to show Hill–Sachs lesion. Stryker view is used for the Hill–Sachs lesion whereas West Point view is used for glenoid rim fractures. MRI is better to define soft tissue pathologies of the shoulder. The advantages of MRI are no exposure to ionizing radiation, good soft tissue resolution, noninvasiveness, and the advantage of multiplane evaluation.

Early MRI evaluation after reduction has 91% sensitivity in diagnosis of capsulo-labral injuries [32]. MR arthrography has the advantage of detecting variations of the capsulolabral pathologies including ALPSA (anterior labroligamentous periosteal sleeve avulsion) lesion, GLAD (glenolabral articular disruption) lesion. And also the use of arthrography for multidirectional instability provides the joint distention necessary to evaluate the capsular volume. MRI and MR arthrography has 96% sensitivity and also better than CT in diagnosis of inferior glenohumeral ligament [16].

Treatment Acute Anterior Shoulder Luxation (First Episode) Ninety-six percent of all shoulder dislocations are anterior type and mainly due to a major trauma [14]. Although the first episode of dislocation is seen in young population mostly, there are also cases seen at 45 years of age or older [15, 56]. In younger age the incidence is nine times more in men, where as the incidence in elder population is three times more in women [18]. After reduction, there are two different strategies for the treatment of acute anterior shoulder dislocation. Although conservative treatment is chosen generally after the first dislocation [21, 33, 37], the incidence of re-dislocation after the first episode is between 30% and 100% [34]. At this point, the age of the patient at the first dislocation episode and the activity level of the patient are two main concerns for the final treatment decision. The risk of re-dislocation will be higher if the first episode is at the age of 20 or below; the risk will be less after the age of 30 and even will not be after 60 years [37]. The activity level is also important; especially patients with contact sports are in great risk of re-dislocation [20]. Although there is no such criterion for choosing proper treatment after the first dislocation episode [18], it is generally well accepted to try conservative treatment in the middle age or elder population after the first episode. But in this group of patients, associated rotator cuff pathologies should be ruled out [44]. The risk of re-dislocation and the failure rate of conservative treatment in young or active patients with contact sports must be discussed with the patient in details, and the final decision should be made together. This kind of approach is well accepted. But there is a challenging group of patients who are professional athletes. In the treatment of an athlete having his/her first episode of shoulder dislocation during the season, time to return to preinjury level and concerns about missing all the season should be kept in mind

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while deciding the optional treatment. Many athletes try to return as early as possible and even postpone his/her surgery till the end of season. In a study of Buss et al., 30 athletes having their first episode during the season are taken to rehabilitation without any immobilization and permitted to return to sports when they achieve the same strength and ROM compared to opposite side. They only used braces to limit abduction. Most of these athletes are in contact sports and 27 out of 30 return to sports, and 26 of them are able to finish the season. Thirty-seven percent of the group who return to sports have at least one episode of dislocation during the game and 46% of them choose surgical treatment at the end of the season [9]. Although these results conflict with the authors who are recommending immobilization in the conservative therapy, are accepted to be a good alternative for the mid-season injuries. In the classical conservative treatment, 3–6 weeks of immobilization is recommended; the need for immobilization and the optional position are two main issues still being discussed. Generally, the conservative treatment includes 3–6 weeks of immobilization in which the arm rests on the body in internal rotation. But clinical and experimental studies are showing the opposite. Hovelius et al., in a prospective study found no difference in recurrence rates between patients with early mobilization and with prolonged immobilization [22]. There are studies showing that the position of immobilization should be opposite. In a cadaver study of Miller et al., the contact force between labrum and the glenoid rim at the Bankart lesion area during internal rotation is measured to be zero, where as the greatest contact force is achieved at 45° of external rotation [41]. Based on this data, in a study of Itoi et al., MRI studies showed that the contact area between labrum and the glenoid were higher in an externally rotated shoulder. In the followup studies, re-dislocation rates of shoulders which are immobilized in external rotation are reported to be less than the shoulders immobilized in classical position [26, 27, 31]. Besides, when all studies about this topic are evaluated, there is still no randomized controlled study about the proper conservative treatment [17]. Decision making of surgical treatment of acute anterior shoulder dislocation should be made according to the pathology in the joint. At this point, the main source of the instability should be clear. These lesions could be classical Bankart lesion, bony Bankart lesion, ALPSA, and HAGL lesions. All these lesions could be treated with open and arthroscopic techniques. Acute bony Bankart lesions can be treated successfully with open or arthroscopic techniques to avoid recurrent instability [4, 51]. Acute early surgical repair of bony Bankart lesions have better clinical outcomes than late repair [52]. Generally, the approach of the authors to acute anterior dislocation, except for the patients less than 20 yeras of age, is conservative treatment with aclose follow up. Surgical treatment is considered for those with re-dislocation or with limited activity level. Surgical treatment is recommended for acute dislocations

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in the patients less than 20 years of age and arthroscopic treatment is the first option except large bony lesions.

Recurrent Anterior Shoulder Instability Evaluation of the first episode plays a major role in the decision making of treatment in recurrent instability. If the first episode is not well known and there is no trauma history; physical treatment and rehabilitation should be considered first. In the presence of a trauma, the underlying pathology should be evaluated in details to have a proper treatment plan. According to the age and activity level of the patient, physical treatment and rehabilitation should be kept in mind. But in young and active patients, desired activity level could not be achieved with conservative treatment. In recurrent anterior instability cases, the aim of surgical treatment is to have anatomical reconstruction of the pathological lesion. Open or arthroscopic techniques could be preferred according to the underlying pathology. The goal of surgery in classical Bankart lesion is to fix capsulolabral tissue on the glenoid properly. The tension of anterior inferior glenohumeral ligament is very important at this point. But there could be some loosening due to capsular degeneration, so that south to north shifting of capsulolabral tissue is recommended. Labral tissue should be fixed at the glenoid chondral edge to achieve proper anatomical stability (Fig. 6). In recurrent instabilities, bony lesions should be evaluated carefully which might be the main reason of the failure of the treatment. Bony lesions can be missed in 60% of cases in direct graphies [8]. Recurrent instability due to bony failure can be seen at two different points, glenoid bone loss or large Hill–Sachs lesion. In lesions of glenoid anterior–inferior side, if preoperative evaluation of glenoid with CT reveals the glenoid index to be 0.75 or less, or during arthroscopic evaluation of glenoid there is a bony loss of 25% or more, bone grafting is indicated [4, 11] (Fig. 7). In early cases, bony Bankart lesions can be fixed to glenoid anatomically, but in late cases grafting is needed. Free iliac grafts, Bristow, or Laterjet procedures can be used as surgical options [1, 19]. In these lesions, authors prefer arthroscopically controlled mini-open Laterjet procedure. The presence of anterior engagement in large Hill–Sachs lesion is a condition that should be evaluated and reconstructed in addition to classical Bankart repair. During preoperative arthroscopic evaluation, engagement of defective area on the posterolateral side of humerus to glenoid anterior rim during functional ranges (abduction more than 70° and external rotation in addition) is an important criterion for additional approach. There are two different approaches in the treatment of engaged Hill–Sachs lesions. Engagement can be treated in patients with no athletic expectations with anterior capsular shifting or humeral

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a

b

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scapular periost intact, the lesion should be positioned anatomically. Because medial fixation of ALPSA lesions is the major factor of recurrence. HAGL lesion is also one of the important factors in recurrent instabilities. Especially with the use of arthroscopic techniques, diagnosis of HAGL lesions, which can be missed radiologically, become easier. The incidence of HAGL lesions in different series are reported to be 7.5–9.3% [49, 53, 66]. In the presence of HAGL lesions; according to the experience of surgeons, open or arthroscopic fixation of avulsed fragment from the humeral head should be done [5, 6, 53, 66]. Factors affecting surgical failure are failed indication and failed surgical techniques. Failure of diagnosing multidirectional instability preoperatively is the main cause of failed indication. In addition, missed HAGL lesions, glenoid bony defects, engaging Hill–Sachs lesions, and rotator interval insufficiency decreases the success of surgical treatment. Medial fixation of labral tissue on the glenoid rim is the main cause of failed surgical technique and is an important factor in postoperative recurrence. Improper placement of anchors can cause impingement and chondral damage on the articular surface.

References Fig. 6 (a) Right shoulder arthroscopic view from posterior portal, arrows show the anterior glenoid border. Anterior labrum is detached completely (Bankart lesion). (b) Repaired bankart lesion, arrows show re-attached anterior labrum with good wedge effect. LB labrum

Fig. 7 Right shoulder arthroscopic view from anterior superior portal is used for glenoid bony assessment. Dashed line shows the distance between anterior labrum and glenoid bare spot. BS bare spot

rotational osteotomy restricting external rotation. But in patients with athletic expectations osteochondral grafting of the lesion could preserve motion arc. Authors prefer anterior capsular shifting in engaged Hill–Sachs lesions. In the treatment of labral pathologies; ALPSA lesions should be evaluated carefully. Since labrum is medially displaced with the

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M. Karahan et al. immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder. Arthroscopy 15, 507–514 (1999) 34. Lee, S.B., Kim, K.J., O’Driscoll, S.W., Morrey, B.F., An, K.N.: Dynamic glenohumeral stability provided by the rotator cuff muscles in the mid-range and end-range of motion. A study in cadavera. J. Bone Joint Surg. Am. 82, 849–857 (2000) 35. Lippitt, S.B., Vanderhooft, J.E., Harris, S.L., Sidles, J.A., Harryman, D.T., Matsen, F.A.: Glenohumeral stability fromconcavity-compression: a quantitative analysis. J. Shoulder Elbow Surg. 2, 27–35 (1993) 36. Lusardi, D., Wirth, M., Wurtz, D., Rockwood, C.J.: Loss of external rotation following anterior capsulorrhaphy of the shoulder. J. Bone Joint Surg. Am. 75, 1185–1192 (1993) 37. Marans, H.J., Angel, K.R., Schemitsch, E.H., Wedge, J.H.: The fate of traumatic anterior dislocation of the shoulder in children. J. Bone Joint Surg. Am. 74, 1242–1244 (1992) 38. Matsen, F.A., Chebli, C., Lippitt, S.: Principles for the evaluation and management of shoulder instability. J. Bone Joint Surg. Am. 88, 648–659 (2006) 39. Matsen, F.A., Titelman, R.M., Lippitt, S.B., Rockwood, C.A., Wirth, M.A.: Glenohumeral instability. In: Rockwood, C.A. (eds.) The Shoulder, 3rd edn., pp. 655–794. W.B. Saunders, Philadelphia (2004); Hurov, J.: Anatomy and mechanics of the shoulder: review of current concepts. J. Hand Ther. 22, 328–343 (2009) 40. McFarland, E.G., Campbell, G., McDowell, J.: Posterior shoulder laxity in asymptomatic athletes. Am. J. Sports Med. 24, 468–471 (1996) 41. Miller, B.S., Sonnabend, D.H., Hatrick, C., O’Leary, S., Goldberg, J., Harper, W.: Should acute anterior dislocations of the shoulder be immobilized in external rotation. A cadaveric study. J. Shoulder Elbow Surg. 13, 589–592 (2004) 42. Neer II, C.S., Foster, C.R.: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J. Bone Joint Surg. Am. 62, 897–908 (1980) 43. Nelson, B.J., Arciero, R.A.: Arthroscopic management of glenohumeral instability. Am. J. Sports Med. 28(4), 602–614 (2000) 44. Neviaser, R.J., Neviaser, T.J., Neviaser, J.S.: Anterior dislocation of the shoulder and rotator cuff rupture. Clin. Orthop. 291, 103–106 (1993) 45. O’Brien, S.J., Warren, R.F., Schwartz, E.: Anterior shoulder instability. Orthop. Clin. North Am. 18(3), 395–408 (1987) 46. O’Connell, P., Nuber, G., Mileski, R., et al.: The contribution of the glenohumeral ligaments to anterior stability of the shoulder joint. Am. J. Sports Med. 18, 579–584 (1990) 47. Ovesen, J., Nielsen, S.: Stability of the shoulder joint: cadaver study of stabilizing structures. Acta Orthop. Scand. 56, 149–151 (1985) 48. Ovesen, J., Nielson, S.: Anterior and posterior instability of the shoulder: a cadaver study. Acta Orthop. Trauma Surg. 57, 324–327 (1986) 49. Page, R.S., Bhatia, D.N.: Arthroscopic repair of humeral avulsion of glenohumeral ligament lesion anterior and posterior techniques. Tech. Hand Up. Extrem. Surg. 13(2), 98–103 (2009) 50. Poppen, N.K., Walker, P.S.: Normal and abnormal motion of the shoulder. J. Bone Joint Surg. 58A, 195–201 (1976) 51. Porcellini, G., Campi, F., Paladini, P.: Arthroscopic approach to acute bony Bankart lesion. Arthroscopy 18(7), 764–769 (2002) 52. Porcellini, G., Paladini, P., Campi, F., Paganelli, M.: Long-term outcome of acute versus chronic bony bankart lesions managed arthroscopically. Am. J. Sports Med. 35, 2067 (2007); originally published online 31 Oct 2007 53. Pouliart, N., Gagey, O.: Simulated humeral avulsion of the glenohumeral ligaments: a new instability model. J. Shoulder Elbow Surg. 15, 728–735 (2006) 54. Rockwood, C.A.J.: Subluxation of the shoulder the classification, diagnosis and treatment [abstract]. Orthop. Trans. 4, 306 (1979)

Anterior Shoulder Instability 55. Rodosky, M., Harper, C., Fu, F.: The role of the long head of the biceps muscle and superior glenoid labrum in anterior stability of the shoulder. Am. J. Sports Med. 22, 121–130 (1994) 56. Rowe, C.R.: Prognosis in dislocation of the shoulder. J. Bone Joint Surg. Am. 38(5), 957–977 (1956) 57. Saha, A.: Dynamic stability of the glenohumeral joint. Acta Orthop. Scand. 42, 491 (1971) 58. Saha, A.: Theory of Shoulder Mechanism: Descriptive and Applied. Charles C Thomas, Springfield (1961); Warner, J.J.P.: The gross anatomy of the joint surfaces, ligaments, labrum, and capsule. In: Matsen, F.A. (eds.) The Shoulder: A Balance of Mobility and Stability, pp. 7–27. American Academy Orthopaedic Surgeons, Rosemont (1993) 59. Thomas, S.C., Matsen III, F.A.: An approach to the repair of avulsion of the glenohumeral ligaments in the management of traumatic anterior glenohumeral instability. J. Bone Joint Surg. Am. 71(4), 506–513 (1989) 60. Turkel, S., Panio, M., Marshall, J., Girgis, F.: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J. Bone Joint Surg. Am. 63, 1208–1217 (1981)

141 61. Walch, G., Boileau, P., Levigne, C., Mandrino, A., Neyret, P., Donell, S.: Arthroscopic stabilization for recurrent anterior shoulder dislocation: result of 59 cases. Arthroscopy 11, 173–179 (1995) 62. Walker, P.S., Poppen, N.K.: Biomechanics of the shoulder joint during abduction in the plane of the scapula. Bull. Hosp. Joint Dis. 38, 107–111 (1977) 63. Warner, J., Deng, X., Warren, R., et al.: Static capsuloligamentous restraints to superior-inferior translation of the glenohumeral joint. Am. J. Sports Med. 20, 675–685 (1992) 64. Williams, M., Lissner, H.R.: Biomechanics of Human Motion, pp. 65–68. Saunders, Philadelphia (1962) 65. Williams, M.M., Snyder, S.J., Buford, D.: The Buford complex cord-like middle glenohumeral ligament and absent anterosuperior labrum complex: a normal anatomic capsulolabral variant. Arthroscopy 10, 241–247 (1994) 66. Wolf, E.M., Cheng, J.C., Dickson, K.: Humeral avulsion of the glenohumeral ligaments as a cause of anterior shoulder instability. Arthroscopy 11, 600–607 (1995)

Arthroscopic Treatment of Anterior Glenohumeral Instability Özgür Ahmet Atay, Musa UÜur Mermerkaya, ěenol Bekmez, and Mahmut Nedim Doral

Contents Arthroscopic Treatment of Anterior Glenohumeral Instability ........................................................... 143 References .................................................................................... 148

Ö.A. Atay ( ), M.U. Mermerkaya, ě. Bekmez, and M.N. Doral Faculty of Medicine, Department of Orthopaedics and Traumatology, Chairman of Department of Sports Medicine, Hacettepe University, Hasırcılar Caddesi, 06110 Ankara, Sihhiye, Turkey e-mail: [email protected]; [email protected]; [email protected]; [email protected]

Arthroscopic Treatment of Anterior Glenohumeral Instability Among all of the joints in human body, the glenohumeral joint has the greatest range of motion. Despite glenohumeral joint geometry offers a high functional status, disruption of static or dynamic stabilizing factors can easily result in shoulder instability. Bowen and Warren [11] reported that inferior glenohumeral ligament complex (IGHL) is the major static anterior stabilizing factor of the 90° abducted shoulder. IGHL complex has anterior and posterior band. The anterior band is responsible for this anterior stabilization [51]. Subscapularis also resist anterior translation [19, 67]. The rotator cuff enhances the stability via compressing the humeral head into glenoid cavity [41]. So, the rotator cuff can be termed as a dynamic stabilizing factor of the shoulder joint. The normal passive translation of the humeral head over glenoid is termed as laxity of the joint. Excessive translation of the humeral head that alters the shoulder function is defined as instability. Anterior shoulder instability is often a sequela of an anterior glenohumeral dislocation. Anterior glenohumeral dislocation is the most common type of shoulder dislocation. The estimated incidence of anterior shoulder dislocation is 1.7% in general population [27]. It is a very common injury among young athletes especially performing contact sports. The mechanism of injury is typically a collision or a fall with an abducted and externally rotated arm. Recurrence is about 90% especially in patients less than 20 years old, and only about 10% in patients older than 40 years old [23, 44, 57, 62]. So, age is a major determinant factor of the recurrence. Recurrent instability can lead to a significant disability [72]. The most common pathology in the anterior shoulder instability is the antero-inferior capsulolabral injury and associated capsular loosening [26, 74]. Labral and capsular detachment from the glenoid rim is described by Bankart [6, 7] as the responsible lesion for anterior shoulder instability. Capsular tear and subscapularis tendon injury have also been implicated in the etiology [4, 48, 67, 71, 73]. In a systematic review of the literature, Bankart lesion is found in 400 of 472

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patients with anterior shoulder instability (85%) [1, 3, 5, 25, 37, 50, 53, 54, 60, 69]. So it cannot be recommended as an essential lesion. According to another theory, Bankart lesion alone cannot produce the anterior instability. The injuries of capsule and IGHL complex are also responsible for the pathologic anterior translation of humeral head [8, 63]. In addition, the role of glenoid bone loss is attributed to the etiology. In the 22% of initial dislocations [69] and up the 90% of recurrent instabilities [65], bony glenoid pathologies are reported. Sugaya et al. evaluated the glenoid rim morphology in 100 cases with anterior glenohumeral instability by using 3D-CT images. Only 10% of cases had normal glenoid bone anatomy. Fifty percent of cases had a “Bony Bankart” lesion (fracture of glenoid rim). Forty percent of cases had bony erosions or compression fracture pattern. Most common location is the anterior glenoid rim (between 2:30 and 4:20 o’clock) [59]. Many authors suggest that axial loading may lead to the fracture pattern. However, rotational mechanism may cause the avulsion of a small glenoid fragment by the IGHL [12]. Identifiable bone loss is frequently reported in the acute cases (6 months), fracture fragment may resorb [66]. Furthermore, the most common pattern in chronic instability is the bony erosion, and the lesion may enlarge or remodel over time [9, 47]. Instability could be intensified if there is an associated Hill–Sachs lesion [29]. It is the impression fracture of posterolateral humeral head that is resulted by the impaction of the soft base of humeral head against the relatively hard anterior glenoid rim (Fig. 1). It has been reported in the 32–51% of initial anterior dislocations [13, 28, 62] and up to 80% of cases with chronic instability [58]. More than 25% of humeral bone loss usually alters the joint stability and may cause engaging Hill–Sachs lesion which is described by Burkhart and De Beers [12]. The pathologic lesions in anterior glenohumeral instability are summarized in (Table 1). There are several clinical tests to determine the anterior instability. Apprehension/relocation test is described by

Fig. 1 Arthroscopic view of the Hill–Sachs lesion; posterolateral impaction of the humeral head

Ö.A. Atay et al. Table 1 Pathological lesions in anterior glenohumeral instability Glenoid Bony pathologies of glenoid rim Fractures of anterior glenoid rim Small (20%) Compression fractures Bony erosions Capsulolabral detachment (mostly in the anteroinferior region) IGHL lesions (anterior band) Capsular elongation/hyperlaxity Rotator cuff injury (especially supscapularis tears) Humerus Hill–Sachs lesion

Jobe [34]. The patient describes a feeling of apprehension as the humerus being subluxated anteriorly when the shoulder is abducted 90° and externally rotated. The alleviation of this feeling when a posterior force is applied to proximal humerus is the relocation component. Load and shift test is used to grade the humeral translation over glenoid [2]. Scapular protraction test provokes the involuntary movement of the patient to maintain the glenohumeral joint stable in reduced position. Conventional radiography is not useful to evaluate soft tissues around the shoulder joint, however it can be used to detect the glenohumeral dislocation, associated fractures or bony lesions of glenoid. A/P projection is efficient in evaluating most traumatic events located around the shoulder area. A/P view of shoulder with the arm is internally rotated is useful in evaluating the Hill–Sachs lesion. However, overlapping of glenoid and humeral head prevents the visualization of the joint space in A/P view. This overlapping is eliminated by internally rotating the patient towards the effected side approximately 40°. This projection is named as “Grashey Projection” and it evaluates the clear space between glenoid and humeral head. Axillary view (superoinferior projection) of shoulder is useful to determine anterior or posterior dislocation. However, the abducted position of arm is difficult to achieve in a patient who is suffering from shoulder dislocation. In this situation, West Point view is useful. This projection is a variant of the Axillary view. Furthermore, clear demonstration of the anteroinferior glenoid rim is available in the West Point view. It offers an advantage of evaluating the etiology in such patients suffering from anterior shoulder dislocation/instability. Computed tomography is useful in evaluating the exact relationship between the humeral head and glenoid fossa. Besides, CT is valuable in determining the configuration and the intraarticular extension of a fracture. Magnetic resonance imaging is the gold standard to detect the intra/extra-articular pathology associated with anterior instability. This modality is particularly effective in imaging

Arthroscopic Treatment of Anterior Glenohumeral Instability

of the soft tissues around the shoulder joint. Magnetic resonance arthrography with the intraarticular gadolinium has been found to be more efficient than MRI without gadolinium enhancement for detecting capsulolabral pathology [14–16]. In addition to, the abducted and externally rotated position of the shoulder is recommended to evaluate the glenoid labrum and capsuloligamentous complex [17]. There are many classification systems about shoulder instability. The acronyms TUBS and AMBRI are described by Thomas and Madsen [70]. TUBS: Traumatic – Unilateral – Bankart – Surgical AMBRI: Atraumatic – Multidirectional – Bilateral – Rehabilitation Rockwood described four patterns of instability [55]. Type 1: Traumatic subluxation with no previous dislocation Type 2: Traumatic subluxation with previous dislocation Type 3: (A) Voluntary subluxation with psychiatric problems (B) Voluntary subluxation without psychiatric problems Type 4: Atraumatic involuntary subluxation Gerber et al [22] have classified the instability as static (A), dynamic (B) and voluntary (C). This classification system is based on distinguishing the hyperlaxity from the instability. Hyperlaxity is confirmed as a condition that is not pathologic. Furthermore, there is an agreement that hyperlaxity is a risk factor of shoulder pathologies. Silliman and Hawkins have classified the instability by either voluntary or involuntary, direction of instability, underlying traumatic event, recurrence of the dislocation [61]. It is a commonly used algorithmic approach. Baker et al developed a classification system based on the early (11 days) arthroscopic findings of patients who had initial dislocations and were younger than 30 years old [5]. Group 1: Capsular tear with no labral lesion Group 2: Capsular tear with partial labral tear Group 3: Capsular tear with complete labral detachment The first step of management is rapid and gentle reduction of anteriorly dislocated glenohumeral joint before muscle spasm develops. Neurovascular examination should be performed before and after the attempt of reduction. Appropriate muscle relaxation is a requirement for a successful reduction procedure. There are many reduction maneuvers as listed below (Table 2). Non-operative treatment consists of immobilization, bracing and physical therapy. The duration of immobilization after traumatic anterior shoulder dislocation is controversial. Recommended duration of immobilization is 3 weeks for patients younger then 30 years old and 1 week for patients older than 30 years old [39]. The cause of longer immobilization in the younger group is the high recurrence rates

145 Table 2 Reduction maneuvers in anterior GH dislocation s (IPPOCRATESMETHOD s 4RACTIONnCOUNTERTRACTION s +OCHERSMETHOD s -ILCHMANEUVER s 3TIMSONSMETHOD s &!2%3 s 3CAPULARMANIPULATION s 3PASOTECHNIQUE

(approximately 90%) in this population [78]. In contrast, recurrence is not a frequent problem in the older population (approximately 10%) [56]. In cadaveric studies, two different pathologic lesions were shown in these different age groups. In the younger age population, there was a labral detachment from glenoid or disruption of labral fibers nears their bases. However in the older population there was no labral pathology, but there was a capsular disruption [24]. The authors suggest that labral pathology cannot heal with immobilization and it is responsible from the high incidence of recurrence in younger age group. Nevertheless, capsular pathology detected in the older age group can heal satisfactorily with conservative treatment and it is why recurrence rate is low. Immobilization in internal rotation is the traditional method. However, most recent data suggests that, immobilization in external rotation has a lower recurrence rate [30–33]. Although recent literature points out that arthroscopic treatment has a lower incidence of recurrence than conservative treatment in first-time anterior shoulder dislocations, it should be appreciated that immobilization method is internal rotation in these studies. Consequently, immobilization in external rotation is a new trend. If these early results can be reproduced in long term studies, traditional method of immobilization of first-time dislocations would be directed toward external rotation. General surgical indications for anterior shoulder instability are listed below (Table 3). Should we treat first-time anterior dislocation in young active patients surgically or conservative? It remains controversial. In a prospective study in young, active patients with initial dislocation [3], one group of patients had conservative treatment Table 3 Surgical indications for anterior glenohumeral instability s 9OUNGPATIENTAGE s &AILEDNON OPERATIVETREATMENT s &AILEDPREVIOUSSURGICALPROCEDURES s 2ECURRENTDISLOCATIONS s )RREDUCIBLEDISLOCATIONS s 3IGNIlCANTGLENOIDORHUMERALBONYDEFECTSINVOLVEMENTOFMORE than 25% of glenoid, engaged Hill–Sachs)

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with immobilization of 4 weeks and following rehabilitation program. The second group treated by arthroscopic procedures and subsequent same rehabilitation procedure. Despite the recurrence rate in the non-operative group was as high as 80%, in the operative group, recurrence rate was only 14%. The authors believe that, performing an early arthroscopic intervention before chronic changes occur (as labral degeneration, capsular loosening or Hill–Sachs lesion) has the advantage of rapid healing. Another study shows the long-term (75 months) success of immediate arthroscopic repair [38, 65]. However, the concept of immobilization in external rotation demonstrates dramatically lower recurrence rates according to the early results. For the present, it seems to be impossible to make a recommendation until long-term results or comparison with early arthroscopic interventions have been documented. There are open and arthroscopic surgical options in the management of anterior glenohumeral instability. In most cases, the pathology can either be repaired by open or arthroscopic methods. The conclusion depends on the expertise of the surgeon. Open techniques are Summarized in (Table 4). In a randomized prospective study, 72% of patients treated by open Bankart repair had good or excellent functional outcomes in 10 year follow up [32, 33]. Although arthroscopic procedures becoming the standard treatment option in anterior shoulder instability, open surgical approaches still remains the choice of treatment in the cases of major bone loss, soft tissue deficiencies and revision surgery [45]. There are several complications and pitfalls in case of open treatment. Recurrence of instability is the most common complication in the treatment of anterior shoulder instability either open or arthroscopic [76, 81]. In a study, recurrence rate was reported 17% in patients had one failed prior surgery, whereas it was 44% in patients had multiple failed prior surgical procedures [40]. Stiffness is infrequently problematic in anterior shoulder instability surgery. It is caused by the excessive tightening of the anterior capsule. Overconstraint, especially 30% loss of external rotation, causes abnormal glenohumeral Table 4 Open techniques for anterior glenohumeral instability Anatomic repairs Open Bankart repair Selective capsular shift Non-anatomic repairs Glenoid bone deficiency Coracoid process transfer Iliac crest autogreft Humeral bone deficiency Allogreft reconstruction Capsular deficiency Reconstruction with hamstrings and ITB autogrefts Subscapularis tendon tears Pectoralis major tendon transfer

Ö.A. Atay et al.

joint kinematics and increased shear forces in posterior glenoid rim. Following cartilage erosion and early osteoarthritis is called “capsulorrhaphy arthropathy” [75]. Other predisposing factors of arthrosis are iatrogenic trauma and hardware problems like impingement of malpositioned screws or anchors. Subscapularis deficiency is another complication that causes functional disability. It is very important to detect and repair immediately, because ruptured subscapularis tendon often retracts and adhere to adjacent tissues. Surrounding neurovascular structures such as brachial plexus and axillary vessels are at risk. In acute cases, direct repair of subscapularis tendon is often successful. But in chronic ruptures, Pectoralis major tendon transfer is required [77, 80]. At the present time, after advancements in arthroscopic techniques and surgical skills, arthroscopic treatment of anterior glenohumeral instability is becoming the first choice. Bottoni et al. reported that the outcomes of open and arthroscopic procedures are comparable. They also reported that postoperative ROM is greater in the arthroscopy group [10]. Otherwise using suture anchors lowered the recurrence rates compared with transglenoid suture fixation [35]. Ideally, Arthroscopic Bankart repair is indicated in a patient who had traumatic anterior glenohumeral instability with failed initial conservative treatment. After improved understanding of the pathoanatomy, with enhanced instrumentation and improved surgical technique, indications of arthroscopic treatment are becoming expanded; including initial dislocations, recurrent bidirectional instability, multidirectional instability, capsulolabral redundancy, and revision surgery after prior failed repair attempts. Also there is an advantage of detecting concomitant pathologies as SLAP lesions or rotator cuff tears. Arthroscopy is contraindicated in case of severe bony defects on glenoid or humeral head, humeral avulsion of glenohumeral ligaments (HAGL lesion), voluntary dislocation, brachial plexus lesion and scapulothoracic dysfunction. The surgical technique of arthroscopic Bankart repair is well-defined [64]. Beach chair position is recommended in most cases of isolated anterior instability. Lateral decubitus position also may be used in cases of concurrent pathology as SLAP lesion, posterior labral tears or multidirectional instability, because joint distraction is possible. But a traction injury is a known complication which is associated with lateral decubitus position. Arthroscopic procedure starts with a routine posterior portal and arthroscopic examination of glenohumeral joint is performed. Biceps tendon, glenohumeral ligaments, joint capsule, anteroinferior capsuloligamentous complex should be evaluated. Bankart lesion and other possible concurrent pathology should be determined. In the absence of anterior instability, the arthroscope is not able to pass between humeral head and glenoid at the level of inferior glenohumeral ligament. An opposite situation is called the “drive-through sign” [43] and it shows there is and excessive laxity. Anterosuperior and anteroinferior portals are then

Arthroscopic Treatment of Anterior Glenohumeral Instability Fig. 2 Insertion of the first suture anchor to the 5.30 o’clock position after the preparation of the glenoid and capsulolabral complex

a

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b

a

c

b

Fig. 3 Arthroscopic suture-passing procedure is performed by the proper instrument

formed just lateral to the coracoid process with arthroscopic guidance. At least 3 cm interval between these foregoing portals should be left. It is important to gain an adequate working space. The working cannula for inserting suture anchors and knot tying is preferably threaded and should be placed in anteroinferior portal. Anterosuperior portal has a role of assistance in the procedure. Initially, labral - ligamentous complex should be released at the antero-inferior aspect of glenoid to the level of 6 o’clock. Afterwards, glenoid bone should be decorticated to stimulate soft tissue healing. Suture anchors should be placed on the edge of articular surface [18]. The first suture anchor should be inserted at the 5.30 o’clock position in a right shoulder (Fig. 2). According to the amount of labral separation, the number of suture anchor may vary. Other available anchor positions are 3 and 4 o’clock. Finally, the capsulolabral tissue should be captured by suture-passing instrument and arthroscopic suture placement and knot tying should be performed (Figs. 3 and 4).

Fig. 4 Final arthroscopic demonstration of the Bankart repair

148

The alternative arthroscopic procedures for arthroscopic Bankart repair are thermal capsulorrhaphy and capsuleligament suture plication. The response of collagen molecule to the thermal energy is interruption of triple helical molecular structure and shortening. Foregoing thermal energy can be applied via laser or radiofrequency instruments. In cadaveric studies, it has been shown that thermal capsulorrhaphy reduces the translation of humeral head and the capsular volume up to 33% [36]. Following clinical studies investigated the efficiency of thermal capsulorrhaphy in multidirectional, unidirectional instability and rotator interval problems. Unfortunately, unacceptable failure rates and complications as nerve injury, stiffness and capsular attenuation had been reported [46, 49]. In contrast, thermal capsulorrhaphy has been reported as an effective procedure in adjunction with capsulolabral repair [21, 42]. Another alternative treatment method is arthroscopic suture plication. A 19% reduction in the capsular volume was shown in cadaveric studies [36]. There are only a few articles about the efficiency of arthroscopic capsule plication [20, 68, 79]. However, because of the high complication rates associated with thermal capsulorrhaphy, capsular plication seems to be a reasonable treatment modality for arthroscopic treatment of anterior shoulder instability (in combination with Bankart repair), or in the case of capsular laxity.

References 1. Adolfsson, L., Lysholm, J.: Arthroscopy and stability testing for anterior shoulder instability. Arthroscopy 5, 315–320 (1989) 2. Altchek, D.W., Dines, D.M.: Shoulder injuries in the throwing athlete. J. Am. Acad. Orthop. Surg. 3, 159–165 (1995) 3. Arciero, R.A., Wheeler, J.H., Ryan, J.B., McBride, J.T.: Arthroscopic Bankart repair versus nonoperative treatment for acute, initial anterior shoulder dislocations. Am. J. Sports Med. 22(5), 589–594 (1994) 4. Bach, B.R., Warren, R.F., Fronek, J.: Disruption of the lateral capsule of the shoulder: a cause of recurrent dislocation. J. Bone Joint Surg. Br. 70, 274–276 (1988) 5. Baker, C.L., Uribe, J.W., Whitman, C.: Arthroscopic evaluation of acute initial anterior shoulder dislocations. Am. J. Sports Med. 18, 25 (1990) 6. Bankart, A.S.B.: Recurrent or habitual dislocation of the shoulderjoint. BMJ 2, 1132–1133 (1923) 7. Bankart, A.S.B.: The pathology and treatment of recurrent dislocation of the shoulder-joint. Br. J. Surg. 26, 23–29 (1938) 8. Bigliani, L.U., Pollock, R.G., Soslowsky, L.J., Flatow, E.L., Pawluk, R.J., Mow, V.C.: Tensile properties of the inferior glenohumeral ligament. J. Orthop. Res. 10, 187–197 (1992) 9. Bigliani, L.U., Newton, P.M., Steinmann, S.P., Connor, P.M., McIlveen, S.J.: Glenoid rim lesions associated with recurrent anterior dislocation of the shoulder. Am. J. Sports Med. 26, 41–45 (1998) 10. Bottoni, C.R., Smith, E.L., Berkowitz, M.J., Towle, R.B., Moore, J.H.: Arthroscopic versus open shoulder stabilization for recurrent anterior instability: a prospective randomized clinical trial. Am. J. Sports Med. 34, 1730–1737 (2006) "OWEN -+ 7ARREN 2&,IGAMENTOUSCONTROLOFSHOULDERSTAbility based on selective cutting and static translation experiments. Clin. Sports Med. 10, 757–782 (1991)

Ö.A. Atay et al. 12. Burkhart, S.S., De Beer, J.F.: Traumatic glenohumeral bone defects and their relationship to failure of arthroscopic Bankart repairs: significance of the inverted-pear glenoid and the humeral engaging Hill-Sachs lesion. Arthroscopy 16, 677–694 (2000) 13. Calandra, J.J., Baker, C.L., Uribe, J.: The incidence of Hill– Sachs lesions in initial anterior shoulder dislocations. Arthroscopy 5, 254– 257 (1989) #HANDNANI 60 9EAGER 4$ $E"ERARDINO 4 ETAL'LENOIDLABRAL tears: prospective evaluation with MRI imaging, MR arthrography, and CT arthrography. Am. J. Roentgenol. 161, 1229–1235 (1993) 15. Chandnani, V.P., Gagliardi, J.A., Murnane, T.G., et al.: Glenohumeral ligaments and shoulder capsular mechanism: evaluation with MR arthro-graphy. Radiology 196, 27–32 (1995) #HOI *! 3UH 3) +IM "( ETAL#OMPARISONBETWEENCONventional MR arthrography and abduction and external rotation MR arthrography in revealing tears of the antero-inferior glenoid LABRUM+OREAN*2ADIOL2, 216–221 (2001) 17. Cvitanic, O., Tirman, P.F., Feller, J.F., et al.: Using abduction and external rotation of the shoulder to increase the sensitivity of MR arthrography in revealing tears of the anterior glenoid labrum. Am. J. Roentgenol. 169, 837–844 (1997) 18. De Beer, J.F.: Arthroscopic Bankart repair: some aspects of suture and knot management. Arthroscopy 15, 660–662 (1999) 19. DePalma, A.F., Cooke, A.J., Prabhakar, M.: The role of the subscapularis in recurrent anterior dislocations of the shoulder. Clin. Orthop. 54, 35–49 (1967) 20. Duncan, R., Savoie III, F.H.: Arthroscopic inferior capsular shift formultidirectional instability of the shoulder: a preliminary report. Arthroscopy 9(1), 24–27 (1993) 21. Gartsman, G.M., Roddey, T.S., Hammerman, S.M.: Arthroscopic treatment of anterior-inferior glenohumeral instability. Two to 5-year follow-up. J. Bone Joint Surg. Am. 82-A(7), 991–1003 (2000) 22. Gerber, C., Werner, C.M., Macy, J.C., Jacob, H.A., Nyffeler, R.W.: Effect of selective capsulorrhaphy on the passive range of motion of the glenohumeral joint. J. Bone Joint Surg. Am. 85-A(1), 48–55 (2003) 23. Henry, J.H., Genung, J.A.: Natural history of glenohumeral dislocation—revisited. Am. J. Sports Med. 10, 135–137 (1982) 24. Hertz, H.: Significance of the limbus glenoidalis for the stability of THESHOULDERJOINT7IEN+LIN7OCHENSCHR3UPPL152, 1–23 (1984) 25. Hintermann, B., Gachter, A.: Arthroscopic assessment of the unstable SHOULDER+NEE3URG3PORTS4RAUMATOL!RTHROSC2, 64–69 (1994) 26. Hintermann, B., Gächter, A.: Arthroscopic findings after shoulder dislocation. Am. J. Sports Med. 23, 545–551 (1995) (OVELIUS , %RIKSSON + &REDIN ( ETAL2ECURRENCESAFTERINItial dislocation of the shoulder: results of a prospective study of treatment. J. Bone Joint Surg. Am. 65, 343–349 (1983) 28. Hovelius, L.: Anterior dislocation of the shoulder in teenagers and young adults. J. Bone Joint Surg. 69A, 393–399 (1987) 29. Hovelius, L., Augustini, G.B.G., Fredin, O.H., et al.: Primary anterior dislocation of the shoulder in young patients. J. Bone Joint Surg. 78A, 1677–1684 (1996) )TOI % (ATAKEYAMA 9 5RAYAMA - 0RADHAN 2, +IDO 4 3ATO +0OSITIONOFIMMOBILIZATIONAFTERDISLOCATIONOFTHESHOULDER A cadaveric study. J. Bone Joint Surg. Am. 81(3), 385–390 (1999) 31. Itoi, E., Sashi, R., Minagawa, H., Shimizu, T., Wakabayashi, I., 3ATO + 0OSITION OF IMMOBILIZATION AFTER DISLOCATION OF THE GLEnohumeral joint. A study with use of magnetic resonance imaging. J. Bone Joint Surg. Am. 83-A(5), 661–667 (2001) )TOI % (ATAKEYAMA 9 +IDO 4 ETAL!NEWMETHODOFIMMOBIlization after traumatic anterior dislocation of the shoulder: a preliminary study. J. Shoulder Elbow Surg. 12(5), 413–415 (2003) 33. Jakobsen, B.W., Johannsen, H.V., Suder, P., Søjbjerg, J.O.: Primary repair versus conservative treatment of first-time traumatic anterior dislocation of the shoulder: a randomized study with 10-year follow-up arthroscopy. J. Arthrosc. Relat. Surg. 23, 118–123 (2007) *OBE &7 +VITNE 23 'IANGARRA #% 3HOULDER PAIN IN THE overhand or throwing athlete. The relationship of anterior instability and rotator cuff impingement. Orthop. Rev. 18, 963–975 (1989)

Arthroscopic Treatment of Anterior Glenohumeral Instability +ANDZIORA & *AGER ! "ISCHOF F (ERRESTHAL * 3TARKER - Mittlmeier, T.: Arthroscopic labrum refixation for post-traumatic anterior shoulder instability: suture anchor versus transglenoid fixation technique. Arthroscopy 16, 359–366 (2000) +ARAS 3' #REIGHTON 2! $E-ORAT '* 'LENOHUMERAL VOLume reduction in arthroscopic shoulder reconstruction: a cadaveric analysis of suture plication and thermal capsulorrhaphy. Arthroscopy 20(2), 179–184 (2004) +IEFT '* "LOEM *, 2OZING 0- /BERMANN 72-2IMAGING of recurrent anterior dislocation of the shoulder: comparison with CT arthrography. AJR Am. J. Roentgenol. 150, 1083–1087 (1988) +IRKLEY ! 7ERSTINE 2 2ATJEK ! 'RIFlN 30ROSPECTIVERANdomized clinical trial comparing the effectiveness of immediate arthroscopic stabilization versus immobilization and rehabilitation in first traumatic anterior dislocations of the shoulder: long-term evaluation. Arthroscopy 21(1), 55–63 (2005) +IVILUOTO / 0ASILA - *AROMA ( 3UNDHOLM !)MMOBILIZATION after primary dislocation of the shoulder. Acta Orthop. Scand. 51(6), 915–919 (1980) 40. Levine, W.N., Arroyo, J.S., Pollock, R.G., Flatow, E.L., Bigliani, L.U.: Open revision stabilization surgery for recurrent anterior glenohumeral instability. Am. J. Sports Med. 28, 156–160 (2000) 41. Matsen III, F.A., Harryman II, D.T., Sidles, J.A.: Mechanics of glenohumeral instability. Clin. Sports Med. 10, 783–788 (1991) 42. Mazzocca, A.D., Brown Jr., F.M., Carreira, D.S., Hayden, J., Romeo, A.A.: Arthroscopic anterior shoulder stabilization of collision and contact athletes. Am. J. Sports Med. 33(1), 52–60 (2005) 43. McFarland, E.G., Neira, C.A., Gutierrez, M.I., Cosgarea, A.J., Magee, M.: Clinical significance of the arthroscopic drivethrough sign in shoulder surgery. Arthroscopy 17, 38–43 (2001) 44. McLaughlin, H.L., Cavallaro, W.U.: Primary anterior dislocation of the shoulder. Am. J. Surg. 80, 615–621 (1950) 45. Millet, P.J., Clavert, P., Warner, J.J.P.: Open operative treatment for anterior shoulder instability: when and why? J. Bone Joint Surg. 87-A(2), 419–432 (2005) 46. Miniaci, A., McBirnie, J.: Thermal capsular shrinkage for treatment of multidirectional instability of the shoulder. J. Bone Joint Surg. Am. 85-A(12), 2283–2287 (2003) -OLOGNE 43 0ROVENCHER -4 -ENZEL +! 6ACHON 4! Dewing, C.B.: Arthroscopic stabilization in patients with an inverted pear glenoid: results in patients with bone loss of the anterior glenoid. Am. J. Sports Med. 35, 1276–1283 (2007) 48. Moseley, H.F., Övergaard, B.: The anterior capsular mechanism in recurrent anterior dislocation of the shoulder: morphological and clinical studies with special reference to the glenoid labrum and the gleno-humeral ligaments. J. Bone Joint Surg. Br. 44, 913–927 (1962) .OONAN 4* 4OKISH *- "RIGGS ++ (AWKINS 2* ,ASER assisted thermal capsulorrhaphy. Arthroscopy 19(8), 815–819 (2003) 50. Norlin, R.: Intraarticular pathology in acute, first-time anterior shoulder dislocation: an arthroscopic study. Arthroscopy 9, 546– 549 (1993) 51. O’Brien, S.J., Neves, M.C., Arnoczky, S.P., et al.: The anatomy and histology of the inferior glenohumeral ligament complex of the shoulder. Am. J. Sports Med. 18, 449–456 (1990) 52. Porcellini, G., Campi, F., Paladini, P.: Arthroscopic approach to acute bony Bankart lesion. Arthroscopy 18, 764–769 (2002) 53. Rafii, M., Firooznia, H., Bonamo, J.J., Minkoff, J., Golimbu, C.: Athlete shoulder injuries: CT arthrographic findings. Radiology 162, 559–564 (1987) 54. Ribbans, W.J., Mitchell, R., Taylor, G.J.: Computerised arthrotomography of primary anterior dislocation of the shoulder. J. Bone Joint Surg. Br. 72, 181–185 (1990) 55. Rockwood, C.A.J.: Subluxation of the shoulder the classification, diagnosis and treatment [abstr]. Orthop. Trans. 4, 306 (1979) 56. Rowe, C.R.: Prognosis in dislocations of the shoulder. J. Bone Joint Surg. 38A, 957–976 (1956) 57. Rowe, C.R.: Acute and recurrent anterior dislocations of the shoulder. Orthop. Clin. North Am. 11, 253–270 (1980)

149 58. Rowe, C.R., Zarins, B., Ciullo, J.V.: Recurrent anterior dislocation of the shoulder after surgical repair. J. Bone Joint Surg. 66A, 159– 168 (1984) 3AITO ( )TOI % 3UGAYA ( -INAGAWA ( 9AMAMOTO . 4UOHETI 9,OCATIONOFTHEGLENOIDDEFECTINSHOULDERSWITHRECURrent anterior dislocation. Am. J. Sports Med. 33, 889–893 (2005) 60. Seeger, L.L., Gold, R.H., Bassett, L.W.: Shoulder instability: evaluation with MR imaging. Radiology 168, 695–697 (1988) 61. Silliman, J.F., Hawkins, R.J.: Classification and physical diagnosis of instability of the shoulder. Clin. Orthop. 291, 7–19 (1993) 62. Simonet, W.T., Cofield, R.H.: Prognosis in anterior shoulder dislocation. Am. J. Sports Med. 12, 19–24 (1984) 3PEER +0 $ENG 8 "ORRERO 3 4ORZILLI 0! !LTCHEK $! Warren, R.F.: Biomechanical evaluation of a simulated Bankart lesion. J. Bone Joint Surg. Am. 76, 1819–1826 (1994) 64. Su, B., Levine, W.N.: Arthroscopic Bankart repair. J. Am. Acad. Orthop. Surg. 13, 487–490 (2005) 3UGAYA ( -ORIISHI * $OHI - +ON 9 4SUCHIYA !'LENOID rim morphology in recurrent anterior glenohumeral instability. J. Bone Joint Surg. Am. 85, 878–884 (2003) 3UGAYA ( -ORIISHI * +ANISAWA ) 4SUCHIYA ! !RTHROSCOPIC osseous Bankart repair for chronic recurrent traumatic anterior glenohumeral instability. J. Bone Joint Surg. Am. 87, 1752–1760 (2005) 67. Symeonides, P.P.: The significance of the subscapularis muscle in the pathogenesis of recurrent anterior dislocation of the shoulder. J. Bone Joint Surg. Br. 54, 476–483 (1972) 68. Tauro, J.C.: Arthroscopic inferior capsular split and advancement for anterior and inferior shoulder instability: technique and results at 2–5-year follow-up. Arthroscopy 16(5), 451–456 (2000) 69. Taylor, D.C., Arciero, R.A.: Pathologic changes associated with shoulder dislocations: arthroscopic and physical examination findings in first-time, traumatic anterior dislocations. Am. J. Sports Med. 25, 306–311 (1997) 70. Thomas, S.C., Matsen 3rd, F.A.: An approach to the repair of avulsion of the glenohumeral ligaments in the management of traumatic anterior glenohumeral instability. J. Bone Joint Surg. Am. 71(4), 506–513 (1989) 71. Townley, C.O.: The capsular mechanism in recurrent dislocation of the shoulder. J. Bone Joint Surg. Am. 32, 370–380 (1950) 4SAI , 7REDMARK 4 *OHANSSON # 'IBO + %NGSTRšM " 4šRNQVIST (3HOULDERFUNCTIONINPATIENTSWITHUNOPERATEDANTErior shoulder instability. Am. J. Sports Med. 19, 469–473 (1991) 73. Turkel, S.J., Panio, M.W., Marshall, J.L., Girgis, F.G.: Stabilizing mechanisms preventing anterior dislocation of the glenohumeral joint. J. Bone Joint Surg. Am. 63, 1208–1217 (1981) 5RAYAMA - )TOI % 3ASHI 2 -INAGAWA ( 3ATO +#APSULAR elongation in shoulders with recurrent anterior dislocation: quantitative assessment with magnetic resonance arthrography. Am. J. Sports Med. 31, 64–67 (2003) 75. Walch, G., Ascani, C., Boulahia, A., Nove-Josserand, L., Edwards, T.B.: Static posterior subluxation of the humeral head: an unrecognized entity responsible for glenohumeral osteoarthritis in the young adult. J. Shoulder Elbow Surg. 11, 309–314 (2002) 76. Wall, M.S., Warren, R.F.: Complications of shoulder instability surgery. Clin. Sports Med. 14, 973–1000 (1995) 77. Warner, J.J.: Management of massive irreparable rotator cuff tears: the role of tendon transfer. Instr. Course Lect. 50, 63–71 (2001) 78. Wheeler, J.H., Ryan, J.B., Arciero, R.A., Molinari, R.N.: Arthroscopic versus nonoperative treatment of acute shoulder dislocations in young athletes. Arthroscopy 5(3), 213–217 (1989) 79. Wichman, M.T., Snyder, S.J.: Arthroscopic capsular plication for multidirectional instability of the shoulder. Oper. Tech. Sports Med. 5, 238–243 (1997) 80. Wirth, M.A., Rockwood Jr., C.A.: Operative treatment of irreparable rupture of the subscapularis. J. Bone Joint Surg. Am. 79, 722– 731 (1997) 81. Zarins, B., Rowe, C., Stone, J.: Shoulder instability: management of failed reconstructions. Instr. Course Lect. 38, 217–230 (1989)

Acute Posterior Dislocations George M. Kontakis, Neil Pennington, and Roger G. Hackney

Contents

Introduction

Introduction ................................................................................. 151

Posterior shoulder dislocations have been characterized as easily missed injuries [9, 13]. This can be attributed to their rarity – less than 4% of all shoulder dislocations [17] – to the low index of suspicion by the clinicians and to the inappropriate evaluation of the shoulder imaging. A posterior dislocation is considered as acute if it has been diagnosed within 6 weeks from injury, whereas after 6 months, it is considered as chronic [23]. A common, unfortunate diagnostic scenario is as follows: an initial incorrect diagnosis of “shoulder contusion” changes to “post-traumatic stiffness” several weeks later and progresses to “locked posterior shoulder dislocation” some months or years after the injury [11, 13]. Missing an acute posterior shoulder dislocation has a tremendous impact on shoulder function [17]. The consequences are a permanent loss of articular surface contact, the engagement of the humeral head posteriorly on the glenoid rim, and continued pressure from the muscle forces resulting in deformity of the humeral head over time and permanent soft tissue contractures [17]. The clinician must know how to diagnose and manage a patient with this shoulder injury in a timely and appropriate manner. Posterior shoulder dislocations may be associated with a surgical or anatomical neck fracture with or without a tuberosity fracture and can be classified as two-part, three-part, or four-part fracture dislocations according to Neer [19]. However, these are injuries more easily identified and require a different therapeutic approach, either an osteosynthesis [1] or an arthroplasty [10]. In this chapter, we will focus on the traumatic acute posterior shoulder dislocation with a single dislocation and an impaction humeral head fracture (reverse Hill–Sachs lesion) of variable severity.

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Clinical Presentation ................................................................... 152 Radiological Examination .......................................................... 152 Treatment ..................................................................................... 153 Conclusions: Key Points ............................................................. 156 References .................................................................................... 157

G.M. Kontakis ( ) Department of Orthopaedics and Traumatology, University of Crete, 711 10 Heraklion, Crete, Greece e-mail: [email protected]

Mechanism of Injury – Pathologic Anatomy – Classification

N. Pennington and R.G. Hackney Department of Trauma and Orthopaedics, Leeds General Infirmary, LS1 3DL Leeds, UK e-mail: [email protected]; [email protected]

An acute posterior dislocation is the result of a force being applied to the anterior aspect of the shoulder with the arm to the side or through the long axis of flexed, adducted, and

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_20, © Springer-Verlag Berlin Heidelberg 2012

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internally rotated arm. In both situations the dislocating force is directed posteriorly. The mechanism of injury should raise the index of suspicion for a posterior dislocation. The posterior shoulder dislocation commonly occurs after a traumatic event, an electric shock (electrocution or electroconvulsive therapy) or after epileptic convulsions. A diabetic or an alcoholic patient or a drug abuser with a diagnosed posterior shoulder dislocation may obscure a seizure episode usually due to hypoglycemia or drug withdrawal [23]. The occurrence of the posterior dislocation in cases with convulsion or seizures is due to the overpowering contraction of the strong internal rotators muscles in relation to the contraction of the weak external rotators of the shoulder [5]. A reverse Hill–Sachs lesion (anterior humeral head impaction) and posterior capsular and/or labral tearing are the usual lesions of a traumatic acute posterior shoulder dislocation. However, several studies have shown that a spectrum of injury exists. Ovesen and Sojbjerg [21], in a cadaveric study, showed that an induced posterior shoulder dislocation resulted in total rupture of the posterior capsule and teres minor in all (ten) cases with a partial lesion of the infraspinatus in the majority of them. In addition, an anterior capsular lesion with a partial subscapularis muscle rupture was noticed in eight out of ten cases. In another cadaveric study, it was reported that a major injury of the anterior glenohumeral joint structures is required for the occurrence of a posterior subluxation [20]. Incision of the entire posterior shoulder capsule could result in posterior subluxation but not in a frank dislocation even if the arm is in the provocative position (flexion-adduction-internal rotation) because the anterior capsular structures become tethered and act as a checkrein [25]. Attenuation of the anterior static stabilizers of the glenohumeral joint is considered critical for the progression to a posterior dislocation [25]. MRI in 36 patients, who sustained an acute posterior shoulder dislocation, showed an incidence of 86% reverse Hill–Sachs lesions, 58% posterior capsuloligamentous complex lesions, 31% posterior glenoid rim fractures, and 42% rotator cuff tears (19% full thickness) [24]. The following types of posterior dislocation have been described [8, 22]:

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impaction (less than 20%, 20–45% and >45%), which is very important and guides the management of the patient [23].

Clinical Presentation The patient presents with shoulder pain after an injury. In individuals of slight or medium build, a deformity of the shoulder may be easily recognized because of the posterior prominence of the dislocated humeral head, the anterior prominence of the acromion and the coracoid process, and the presence of an anterior dimple (Fig. 1). This clinical picture is not easily noticed in obese patients. The patient supports the arm with the elbow 90° flexed and the palm in contact with the anterior abdominal wall (humerus internally rotated). The abduction is limited and the person is unable to externally rotate the arm either actively or passively. In the unconscious polytrauma patient, a visible deformity or indirect signs of an impact on the anterior shoulder or limitation of the passive external rotation may be clues for the suspicion of a posterior dislocation.

Radiological Examination The traditional anteroposterior shoulder view in the thoracic plane should show (Fig. 2):

s The rotational subluxation, where the humeral head is on to the posterior rim of the glenoid, in internal rotation (facing posteriorly) s The subacromial or retroglenoid type s The subspinous type (complete dislocation) s The posterior subglenoid type (rare) However, any classification scheme must include information of therapeutic and prognostic value. The above classification is of limited value because it is grossly descriptive and does not take into account the size of the humeral head

Fig. 1 This is a photograph of a 45 -year-old patient with a posterior shoulder dislocation in the operating theatre before attempting a reduction. They are obvious: the posterior prominence of the dislocated humeral head, the anterior prominence of the acromion and the coracoid process, and the presence of an anterior dimple

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for an adequate image [16]. For this reason, modifications of the axillary view have been proposed [3]. Both the Velpeaux axillary and the angle-up views are taken with the patient’s Velpeau bandage or shoulder sling in place. They are technically easy and diagnostically informative. In case of doubt, computerized tomography (CT) scan is used. It can be argued that CT scan should be performed in every case of posterior shoulder dislocation to reveal possible occult fracture lines that should be considered before attempting a reduction. CT scan is the modality that precisely depicts the size of the impression fracture of the head, which is a valuable parameter for the therapeutic decision making. MRI has no established value in acute traumatic posterior shoulder dislocation, although it could offer some additional information regarding the extent of the soft tissue damage [24]. Fig. 2 AP shoulder radiograph of a posterior shoulder dislocation (rotational subluxation – the humeral head is on to the posterior rim of the glenoid, facing posteriorly)

s Internal rotation of the humeral head s Absence of the half-moon appearance of the overlapping between humeral head and the glenoid s Flattening of the medial aspect of the humeral head due to the reverse Hill–Sachs lesion s Subluxation (superior or inferior) of the humeral head in relation to the glenoid, and s Cystic appearance of the humeral head due to the anterior position of the greater tuberosity [22]. The transthoracic shoulder view rarely is a radiograph of sufficient quality to demonstrate the interruption of the normal scapulohumeral arch which occurs with posterior dislocations. Anteroposterior radiographic views frequently present difficulties in interpretation, and the inexperienced viewer may miss the diagnosis. The evaluation of every injured shoulder necessitates “the trauma series” radiographs, which are the following [19]: s The true AP shoulder projection, which will show that the intra-articular space does not exist and an overlapping of the humeral head and the glenoid is visible. s The Y-scapular or scapular-lateral projection, which shows clearly the posterior dislocation of the head in relation to the glenoid. s The axillary view, which will reveal better the posterior dislocation. The axillary view is usually difficult to be taken with the patient awake, though only a minimal abduction is required

Treatment Closed reduction – under general anesthesia – should be performed in all patients if the articular bone defect (head impaction) is less than 20–25%. A defect greater than this, usually affects joint stability and may necessitate surgical intervention. The general condition of the patient and the size of the humeral head impaction affect the therapeutic decision making. Debilitated patients with limited demands and patients with behavioral problems and psychiatric disease should not be candidates for a surgical procedure and a “skillful neglect” strategy should be acceptable [16]. In the majority of cases a surgical approach, when indicated, may be of benefit. Any maneuvre for closed reduction should be performed carefully in order to avoid an iatrogenic humeral head fracture [12]. Gentle axial lateral traction with the arm internally rotated should unlock the humeral head from the posterior glenoid rim and permit unrestricted external rotation leading to the reduction [16]. Alternatively, a successful reduction should be achieved by traction with the arm flexed-adducted and internally rotated and gentle external rotation when the humeral head has become dis-impacted. Sometimes this maneuver can be combined with lateral traction and manual pressure applied to the humeral head in a posteroanterior direction [11, 18]. The reduction is confirmed radiographically – usually by the use of image intensifier – with the patient anesthetized. The stability of the reduction should be checked under fluoroscopy. Attention should be given to the presence of a lesser tuberosity fracture, because if this is left unaddressed a recurrence of the dislocation may occur (Fig. 3).

154

Fig. 3 AP and modified axillary views showing a posterior shoulder dislocation with an impaction of the humeral head (a and b). Fluoroscopic views showing a successful closed reduction and a lesser

The shoulder is immobilized in slight abduction and neutral or external rotation for 4–6 weeks (Fig. 4). This timespan together with an appropriate position should allow healing of the avulsed posterior capsular-labrum and reduce the incidence of recurrence [4, 7]. Isometric external rotation exercises are encouraged within the brace. The immobilization period is followed by progressive range of motion and rotator muscle strengthening exercises. Open reduction should be considered as an option if the articular head defect is between 20% and 45% of the total articular surface or in cases where propagation of an occult fracture is possible during closed maneuvers. The deltopectoral approach is usually recommended although there are reports of a direct posterior approach [15, 16]. The lesser tuberosity should be osteotomized and reflected medially (with the subscapularis muscle) to enhance visualization. The humeral head

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tuberosity fracture that was not addressed (c). Re-dislocation occurred 3 weeks after immobilization in a sling (d)

Fig. 4 Immobilization in a brace

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Fig. 5 Intraoperative photographs. (a) The lesser tuberosity has been detached (sutures), the head is reduced, and the reverse Hill–Sachs lesion is visible. (b) The lesser tuberosity has been transferred into the defect and fixed by two cannulated screws

is carefully disimpacted and reduced. The lesser tuberosity is re-attached and fixed into the humeral head depression [11] (subscapularis transfer [17]), thus eliminating the possibility of engagement of the posterior glenoid rim and the recurrence of dislocation (Fig. 5). Several alternative treatments have been described in the literature for addressing major humeral head destruction. However, the series are small and their use has not been established. These include disimpaction of the articular

a

R

surface and bone grafting [2] and reconstruction of the humeral head by the use of either an allograft or an autograft taken from the contralateral shoulder [6, 14]. Prosthetic replacement should be considered as an option in cases of humeral head destruction over 45% [16] (Fig. 6). The glenoid is not usually replaced in the acute setting. Early hemiarthroplasty can result in a successful outcome (Fig. 7).

b

L

Fig. 6 Bilateral simultaneous posterior dislocations of the shoulders in a 62-year-old male after an episode of seizures. Plain AP radiographs (a, b) and CT scan (c, d) showing the head involvement in both shoulders

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c

d

Fig. 6 (continued)

a

b

Fig. 7 (a) The patient in Fig. 6 underwent hemiarthroplasties in both shoulders. Immobilization for 4 weeks with abduction pillows. (b) Shoulder elevation 18 months postsurgery

Conclusions: Key Points s The clinician must have a high index of suspicion for a posterior shoulder dislocation in shoulder injuries. s Detailed history, clinical examination may give clues. s Trauma series radiographs should be the rule in every shoulder injury. The axillary view is highly diagnostic. s Detailed assessment of the plain radiographs for not easily seen bony injuries. s CT should be useful if available in all cases.

s Preoperative assessment of the size of the humeral impaction. s Closed reduction must always be performed under anesthesia. s Assessment of the joint stability after reduction is mandatory. s Immobilization in slight abduction and neutral or external rotation for 4–6 weeks. s Open reduction if the closed one fails or if the defect of the humeral is between 20% and 45%. Subscapularis or lesser tuberosity transfer into the defect. s Hemiarthroplasty if humeral head defect is over 45%.

Acute Posterior Dislocations

References 1. Altay, T., Ozturk, H., Us, R.M., Gunal, I.: Four-part posterior fracture–dislocations of the shoulder. Treatment by limited open reduction and percutaneous stabilization. Arch. Orthop. Trauma. Surg. 119, 35–38 (1999) 2. Assom, M., Castoldi, F., Rossi, R., Blonna, D., Rossi, P.: Humeral head impression fracture in acute posterior shoulder dislocation: new surgical technique. Knee Surg. Sports Traumatol. Arthrosc. 14, 668–672 (2006) 3. Bloom, M.H., Obata, W.G.: Diagnosis of posterior dislocation of the shoulder with use of Velpeau axillary and angle-up roentgenographic views. J. Bone Joint Surg. Am. 49, 943–949 (1967) 4. Cautilli, R.A., Joyce, M.F., Mackell Jr., J.V.: Posterior dislocations of the shoulder: a method of postreduction management. Am. J. Sports Med. 6, 397–399 (1978) 5. Cicak, N.: Posterior dislocation of the shoulder. J. Bone Joint Surg. Br. 86, 324–332 (2004) 6. Connor, P.M., Boatright, J.R., D’Alessandro, D.F.: Posterior fracture-dislocation of the shoulder: treatment with acute osteochondral grafting. J. Shoulder Elbow Surg. 6, 480–485 (1997) 7. Detenbeck, L.C.: Posterior dislocations of the shoulder. J. Trauma 12, 183–192 (1972) 8. Dorgan, J.A.: Posterior dislocation of the shoulder. Am. J. Surg. 89, 890–900 (1955) 9. Hawkins, R.J.: Unrecognized dislocations of the shoulder. Instr. Course Lect. 34, 258–263 (1985) 10. Hawkins, R.J., Switlyk, P.: Acute prosthetic replacement for severe fractures of the proximal humerus. Clin. Orthop. Relat. Res. 289, 156–160 (1993) 11. Hawkins, R.J., Neer II, C.S., Pianta, R.M., Mendoza, F.X.: Locked posterior dislocation of the shoulder. J. Bone Joint Surg. Am. 69, 9–18 (1987) 12. Hersche, O., Gerber, C.: Iatrogenic displacement of fracture-dislocations of the shoulder. A report of seven cases. J. Bone Joint Surg. Br. 76, 30–33 (1994)

157 13. Hill, N.A., Mc, L.H.: Locked posterior dislocation simulating a “frozen shoulder”. J. Trauma 3, 225–234 (1963) 14. Ivkovic, A., Boric, I., Cicak, N.: One-stage operation for locked bilateral posterior dislocation of the shoulder. J. Bone Joint Surg. Br. 89, 825–828 (2007) 15. Karachalios, T., Bargiotas, K., Papachristos, A., Malizos, K.N.: Reconstruction of a neglected posterior dislocation of the shoulder through a limited posterior deltoid-splitting approach. A case report. J. Bone Joint Surg. Am. 87, 630–634 (2005) 16. Kowalsky, M.S., Levine, W.N.: Traumatic posterior glenohumeral dislocation: classification, pathoanatomy, diagnosis, and treatment. Orthop. Clin. North Am. 39, 519–533 (2008). viii 17. Mc, L.H.: Posterior dislocation of the shoulder. J. Bone Joint Surg. Am. 24A(3), 584–590 (1952) 18. Mimura, T., Mori, K., Matsusue, Y., Tanaka, N., Nishi, Y., Kobayashi, M.: Closed reduction for traumatic posterior dislocation of the shoulder using the “lever principle”: two case reports and a review of the literature. J. Orthop. Surg. Hong Kong 14, 336–339 (2006) 19. Neer II, C.S.: Displaced proximal humeral fractures. I. Classification and evaluation. J. Bone Joint Surg. Am. 52, 1077–1089 (1970) 20. Ovesen, J., Nielsen, S.: Anterior and posterior shoulder instability. A cadaver study. Acta Orthop. Scand. 57, 324–327 (1986) 21. Ovesen, J., Sojbjerg, J.O.: Posterior shoulder dislocation. Muscle and capsular lesions in cadaver experiments. Acta Orthop. Scand. 57, 535–536 (1986) 22. Roberts, A., Wickstrom, J.: Prognosis of posterior dislocation of the shoulder. Acta Orthop. Scand. 42, 328–337 (1971) 23. Robinson, C.M., Aderinto, J.: Posterior shoulder dislocations and fracture-dislocations. J. Bone Joint Surg. Am. 87, 639–650 (2005) 24. Saupe, N., White, L.M., Bleakney, R., Schweitzer, M.E., Recht, M.P., Jost, B., Zanetti, M.: Acute traumatic posterior shoulder dislocation: MR findings. Radiology 248, 185–193 (2008) 25. Schwartz, E., Warren, R.F., O’Brien, S.J., Fronek, J.: Posterior shoulder instability. Orthop. Clin. North Am. 18, 409–419 (1987)

Management of Recurrent Dislocation of the Hypermobile Shoulder Roger G. Hackney

Contents

Introduction

Introduction ................................................................................. 159

Hypermobility is an excess of motion in a given joint. This may be restricted to a single joint but more commonly affects several joints and may be part of a systemic condition. There is a spectrum of hypermobility from normal through to benign hypermobility and on to Ehler’s Danlos disease. The incidence of generalized ligamentous joint laxity lies between 5% and 15% of the population [11]. There are several genes for hypermobility that are sited close together, but it is possible for a patient to have a hypermobile shoulder without the rest of the upper limb involved. It is important to recognize that instability is symptomatic laxity, and what may be ‘normal’ range of motion for one individual may be abnormal and symptomatic in another. Symptoms may include pain and not just a sensation of a loose or unstable shoulder. The diagnosis of hypermobility is made by the use of scoring systems. The most commonly used is the Beighton score [4]. This allows one point for each of the following, each side for 1–4, giving a total of 9. A score of greater than 5 is considered hypermobile.

Hypermobility in Sport............................................................... 160 Terminology .................................................................................. 160 Muscle Patterning and the Stanmore Triangle ........................ 161 Management of the Hypermobile, Unstable Shoulder ............ 161 Risk Factors for Recurrence ...................................................... 161 History.. ......................................................................................... 161 Redo Surgery for Recurrent Instability Post Surgery ............. 162 Conclusion ................................................................................... 163 References .................................................................................... 163

1. Passive hyperextension of the metacarpophalangeal joint of the little finger to 90° 2. Passive apposition of the thumb to the flexor aspect of the forearm 3. Passive elbow hyperextension 10° 4. Passive knee hyperextension 10° 5. Ability to place the hand flat on the floor standing with the knees straight

R.G. Hackney Department of Trauma and Orthopaedics, Leeds General Infirmary, LS1 3DL Leeds, UK e-mail: [email protected]

The disadvantage of this score when discussing glenohumeral joint laxity is that there are no references to the shoulder joint itself. There are several genes for hypermobility of different joints which are closely sited, but it is certainly possible to find patients who have hypermobility of some joints but not others. Other scoring systems have been described such as the Hospital Del Mar score [7]. This ranges from 0 to 10 and is derived by assigning one point for each of the following.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_21, © Springer-Verlag Berlin Heidelberg 2012

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160

1. Passive hyperextension of the metacarpophalangeal joint of the little finger to 90° 2. Passive apposition of the thumb to the flexor aspect of the forearm at 0.05). They concluded that arthroscopic suture anchor capsulorrhaphy showed similar results to the open Bankart procedure. Bottoni et al. [6] reported that clinical outcomes after arthroscopic and open stabilization were comparable in a randomized controlled trial. Current arthroscopic repair of anterior instability utilizes suture anchors and the outcomes are excellent [11, 20, 21, 33, 46]. Recently, bioabsorbable suture anchors are available with an excellent pullout stability. The author in the Madi Hospital uses a small suture tack-type anchors (3.0 mm BioSutureTak, Arthrex, Naples, Florida, USA). The basic principle of the repair includes a complete mobilization of the Bankart lesion from the glenoid, insertion of suture anchor as inferior as possible, and appropriate balancing the capsuloligamentous tension. Optimal visualization and approach angle are of importance for the successful arthroscopic repair. In the author’s and others’ experiences, significant number of shoulders with traumatic anterior instability has not only Bankart lesion but also HAGL, posterior HAGL, or capsular tears [25, 35, 42] (Fig. 1). Also, many of Bankart lesions are extended to the inferior and posterior labrum to make the so-called extended Bankart lesion (Fig. 2). With standard posterior portal, it is often difficult to properly repair the posterior labral tear in the extended Bankart lesion. By placing the posterior portal more anteriorly, visualization and access angle can be optimized in these situations. The author developed the triple instability portal, which initially developed for the repair of the posterior or posteroinferior multidirectional instability. The triple instability portal is also useful for the traumatic anterior instability with an extended Bankart lesion (Fig. 3).

167

Fig. 1 The posterior HAGL lesion and Hill-Sachs lesion. The posterior capsular attachment is detached from the humeral insertion

Fig. 2 Extended Bankart lesion. Anterior labral tear extends to inferior and posterior area

Anterior midglenoid portal

Transcuff superior portal

Kim posterior portal

Standard posterior portal

Fig. 3 The triple instability portal. All three portals are located highriding from the glenoid surface which allows relatively vertical access to the entire area of the glenoid rim

Bone defect in the glenoid or humeral head predisposes repair failure. The incidence of bone loss ranges from 5.4% to 78.8% of patients with anterior instability [4, 9, 16, 32, 44]. Rowe et al. [44] reported that open repair had a good result if the bone defect is less than 30% of the glenoid surface. Itoi et al. [18] found in the cadaver study that the glenoid defect

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greater than 21% of the glenoid results in a significant instability of the soft tissue repair. Burkhart et al. Burkhart and DeBeer reported a 67% recurrence rate instability repair in patients with more than 25% of glenoid defect. Inverted pear shape of the glenoid suggests the significant bone loss in the arthroscopic evaluation. Replacement of supplement of the glenoid defect has been more and more popularized. The most common bone graft comes from the coracoid process. Recently, a modified Latarjet procedure has been reported to provide excellent outcome for those with a significant glenoid defect [10]. Arthroscopic bone graft for the glenoid defect has been attempted very recently [5, 29, 36]. Future studies are needed to evaluate the efficacy of the arthroscopic bone graft in treating the glenoid defect. A large humeral head defect as a Hill-Sachs lesion may also be related to the recurrence of instability of failure of soft tissue repair. The Hill-Sachs defect often engages the glenoid rim especially when there is glenoid defect as well. Wolf et al. [48] reported arthroscopic technique of infraspinatus filling to the Hill-Sachs defect which was originally described as an open procedure by Connolly [12]. The author commonly uses posterior capsulodesis to the Hill-Sachs defect using one or two suture anchors.

Atraumatic Instability Atraumatic instability presents usually as posterior or multidirectional instability. There has been no universal agreement in the classification, terminology, and treatment options. The clinical presentation of the atraumatic instability is not as clear as traumatic anterior instability and many of patients with posterior instability are easily overlooked or treated under other diagnosis. Recent advances in the concept of the posterior instability have provided us reasonable insight to the pathology, pathogenesis, diagnostic examinations, and treatment options. The posterior instability very often presents as bidirectional posteroinferior instability, which has various degrees of inferior component of instability. Also the posterior instability is overlapping with the multidirectional instability in its diagnosis, clinical presentation, and management.

Pathogenesis Several anatomic structures have been implicated including bony and soft tissue abnormalities. Bony abnormalities include increased humeral retroversion, glenoid retroversion, and glenoid hypoplasia. Although, several studies on the glenoid version have been focused on the bony glenoid measured, the stability of glenohumeral joint is an integral function of both

S.-H. Kim

bone and soft tissue stabilizer. Lazarus et al. [30] showed a 65% decrease in mechanical stability ratio and an 80% reduction in the height of the glenoid associated with the creation of an anteroinferior chondrolabral defect. Accordingly, the measurement of the glenoid version can be more ideal when the articular cartilage and labrum are considered as a whole. Soft tissue abnormality of the atraumatic instability has been an excessive capsular laxity. However, increased capsular ligamentous laxity alone cannot entirely explain the whole pathogenesis of the atraumatic instability, which often occurs in the mid-range of motion where normally the capsular ligaments become loose. The Kim et al. [26] emphasized that loss of chondrolabral containment is a consistent finding in shoulders with atraumatic posteroinferior instability and is principally due to the loss of posterior labral height. Kim et al. [23, 26] suggest that the loss of chondrolabral containment is a result of cumulative microtrauma to the posteroinferior glenoid labrum, which initially has normal height and undergoes gradual change to retroversion by the rim-loading mechanism. With the loss of chondrolabral containment, the static restraint loses its function and the dynamic stabilizer of the shoulder becomes less effective in maintaining concavity compression of the glenohumeral joint. Bradley et al. [8] similarly measured the posterior inferior chondrolabral version and bony glenoid version for each MR at the inferior one third of the glenoid rim. In this study, there was increased bony and chondrolabral retroversion in the symptomatic group, which suggests that loss of anatomical containment predisposes to atraumatic instability (Fig. 4). The concept of chondrolabral lesion in the atraumatic instability provides further insight to the cause of symptom development. Although there are two groups of people in which one group is asymptomatic and the other is symptomatic, it is interesting to know that the amount of increased translation either in posterior, inferior, or anterior direction is the same. Also asymptomatic people often become symptomatic over the time. Although, shoulder is loose in all three directions, concurrent production of symptoms is in one or multiple directions. There are evidences that the amount of translation is not fundamentally different between healthy subject who have asymptomatic laxity and those who need surgical intervention [31, 34]. Given these facts, there may be other pathologies which are responsible for the shoulder symptom, rather than just an increased joint volume. The author found that the majority of patients with asymptomatic jerk test in the posterior instability, which was represented by painless posterior clunk, were successful with the nonoperative treatment. However, patients with symptomatic jerk test, which was represented by sharp pain with posterior clunk, were not responding with the rehabilitation and invariably had posteroinferior labral lesion in the arthroscopic finding [27]. The author concluded that the jerk test was a hallmark for predicting the failure of nonoperative treatment in the

Current Trends on Shoulder Instability Fig. 4 The capsular laxity is the initial lesion of the posteroinferior instability. Shoulders with the capsular laxity are asymptomatic or minimally symptomatic and attempted tests present painless clunk. However, rim-loading mechanism during the repetitive subluxation eventually develops posteroinferior labral lesion which is the essential lesion that is responsible for the shoulder symptom and painful clunk in the jerk or Kim test

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Capsular Laxity Initial lesion

Time Rim-Loading Mechanism

Labral Lesion Essential lesion

Pain-free subluxation

Painful subluxation

Painless jerk/Kim test

Painful jerk/Kim test

Rehabilitation

Arthroscopic Capsulolabroplasty

posteroinferior instability. Shoulders with a painful jerk test have a posteroinferior labral lesion [27]. Kim et al. [22–24] previously reported that all patients who underwent arthroscopic surgery for posterior instability had variable degree of labral lesions in the posterior and inferior portion of the glenoid. These labral lesions were classified into four types. Type I labral lesion is an incomplete detachment, in which the posteroinferior labrum is separated from the glenoid margin but not medially displaced. This type is more common in traumatic posterior instability than multidirectional instability. Type II lesion is a marginal crack, so-called Kim’s lesion, which is an incomplete and concealed avulsion of posteroinferior labrum. Type III lesion is a chondrolabral erosion, and type IV lesion is a flap tear of the labrum (Fig. 5) [22–24]. The Kim’s lesion refers to a superficial tearing between the posteroinferior labrum and the glenoid articular cartilage without a complete detachment of the labrum (marginal crack). The posteroinferior labrum lost its normal height and became a flat labrum, with subsequent retroversion of the chondrolabral glenoid. Probing the lesion demonstrates fluctuation of the posteroinferior labrum and reveals a loose attachment. These labral lesions are limited to the posteroinferior quadrant of the glenoid for shoulders with a pure posterior instability, typically present in 6–9 o’clock position for the right shoulder and 3–6 o’clock position for the left shoulder. However, the lesion is extended to entire inferior glenoid labrum from 4 or 5 to 9 o’clock in shoulders with posteroinferior multidirectional instability. When the superficial portion is incised with an arthroscopic knife, for 1 or 2 mm in depth, the lesion reveals detachment in the deep portion of the labrum from the medial surface of the glenoid [22–24]. The Kim lesion is quite similar to the intratendinous tear of the rotator cuff tendon which is often overlooked and unrecognized at the initial arthroscopic evaluation. Therefore, surgeon’s insight to this hidden lesion is of paramount importance for the diagnosis of the pathology. The four types of labral

lesions are a spectrum of severity of the instability. Perhaps, Kim’s lesion may over time be converted into type I incomplete detachment when the marginal crack is extended to the deep portion tear. It is believed that increased translation by the increased capsular laxity is initial lesion and underlying pathology of the posterior and posteroinferior multidirectional instability. This increased capsular laxity can be in-borne or developmental and asymptomatic or minimally symptomatic initially. In this stage, attempted translation does not produce symptoms. Also, jerk and Kim tests reveal posterior clunk without shoulder pain [27, 28]. However, repetitive subluxation over time overloads the posteroinferior glenoid labrum by the excessive rim-loading of the humeral head. This excessive rim-loading eventually develops posteroinferior labral lesion varying from simple retroversion to incomplete detachment. In this stage, patient’s symptom, which is shoulder pain, originates from the labral lesion when the humeral head glides over the pathologic labrum. The compressive force on the torn labrum in the jerk and Kim tests generates shoulder pain [27, 28]. The labral lesion is now the essential lesion which is responsible for the true shoulder symptom of the posterior and posteroinferior instability. Therefore, intact labrum does not produce shoulder pain no matter how lax the glenohumeral joint is. Increased translation alone produces asymptomatic posterior clunk until the repetitive rim-loading eventually develops posteroinferior labral lesion.

Physical Examination The shoulder examinations should include both laxity and instability evaluations. Laxity evaluation simply tests how much the shoulder joint is loose in anteroposterior and inferior directions. Translations in anterior and posterior direction are tested by the load and shift test. Anteroposterior

170 Fig. 5 Diagram of arthroscopic classification of the posterior and inferior labral lesion. (a) Type I: Incomplete detachment. The posteroinferior labrum is detached from the glenoid but not displaced. (b) Type II: Marginal crack or Kim’s lesion. The labrum has marginal crack and retroversion. Deep portion is loose. (c) Type III: Chondrolabral erosion. The labral surface has fraying and deep portion is loose. (d) Type IV: Flap tear. The labrum has flap tear or multiple buck handle tear

S.-H. Kim

a

b

c

d

humeral translation was rated as grade 0 (no translation), grade 1+ (translation less than the margin of glenoid), grade 2+ (translation beyond the margin of glenoid with spontaneous reduction), or grade 3+ (translation beyond the glenoid without spontaneous reduction). Inferior translation is evaluated by the sulcus sign [38]. A downward traction force is applied to the adducted shoulder and the inferior translation of the humerus is measured by estimating the distance between the inferior margin of lateral acromion and the

humeral head. 0+ is equivalent to no movement: 1+, less than 1 cm; 2+, 1–2 cm; and 3+, more than 2 cm.

Instability Tests Instability tests should involve test for symptoms related to the specific pathology, which is relevant to the posterior

Current Trends on Shoulder Instability

instability. Posterior apprehension test may reproduce the patient’s symptom but is seldom positive in the posterior instability. Two sensitive and specific physical tests are the jerk and Kim tests. Like the McMurray test for evaluation of the meniscal injury in the knee joint, the basic principle of the jerk and Kim tests is a pain provocation by compressing the labral lesion. The jerk test has been used for a long time but the significance of the test has been recently validated [27]. The jerk test is performed in a sitting position. While stabilizing the patient’s scapula with one hand and holding the affected arm at 90° abduction and neutral rotation, the examiner grasps the elbow and axially loads the humerus in a proximal direction. The arm is moved horizontally across the body. A positive result is indicated by a sudden clunk as the humeral head slides off the back of the glenoid. When the arm is returned to the original position, a second jerk may be produced by the humeral head returning to the glenoid (Fig. 6). In this test, a firm axial compression is very important. The painless jerk group includes patients with posterior clunk, but without any significant pain provocation, while the painful jerk group includes patients who show abrupt pain in accordance with posterior clunk. The author found that painful clunk in the jerk test is invariably associated with structural defect, a posteroinferior labral lesion. Kim et al. [27] reported that the painful jerk group had a higher failure rate with nonoperative treatment. In the painless jerk group, 50 shoulders (93%) responded to the rehabilitation program after a mean of 4 months. Four shoulders (7%) were unresponsive to the rehabilitation. In the painful jerk group, five shoulders (16%) were successful with the rehabilitation, whereas the other 30 shoulders (84%) failed. All 34 shoulders that were unresponsive to the rehabilitation had a variable degree of posteroinferior labral lesions. The jerk test is a hallmark for predicting the prognosis of nonoperative treatment for posteroinferior instability. Shoulders

a

Fig. 6 The jerk test. (a) Stabilizing the scapula with one hand, the other hand holds elbow with the arm in 90° abduction and internal rotation. Firm axial compression force is applied on the glenohumeral joint. (b) The arm is horizontally adducted while maintaining the firm axial load

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with symptomatic posteroinferior instability and a painful jerk test have posteroinferior labral lesions [27]. Arthroscopic finding supported that the abrupt pain during the jerk test may be elicited from a rim-loading of the humeral head over the pathologic posteroinferior labral lesion. Kim et al. [28] also developed a new test for the posteroinferior labral lesion in the posteroinferior instability. The Kim test is performed in a sitting position with the arm in 90° abduction. With examiner holding elbow and lateral aspect of the proximal arm, a simultaneous axial loading force and 45° diagonal elevation is applied on the distal arm, while downward and backward force is applied on the proximal arm. A sudden onset of posterior shoulder pain indicates positive test regardless of accompanying posterior clunk of the humeral head. During the test, it is important to apply a firm axial force compression force on the glenoid surface by the humeral head. Therefore, sitting against the back of a chair rather than a stool provides a good counter support of the axial loading in the examining arm (Fig. 7). The Kim test is more sensitive in the predominant inferior labral lesion while jerk test is more sensitive for the predominant posterior labral lesion. Correlation of the symptom with the physical examination is also mandatory in making diagnosis. Patients with mild shoulder symptom usually have asymptomatic jerk and Kim tests. The Kim and jerk tests have three components: pain, clunk, and click. Pain without clunk suggests a posterior labral lesion, whereas pain with clunk indicates posterior instability with a labral lesion. Although the Kim and jerk tests are most commonly used to diagnose posteroinferior instability, the test results are also positive for any pathologic posteroinferior labral lesions in other conditions. For instance, a positive Kim test result in a shoulder with proven traumatic anterior instability with a Bankart lesion suggests that the Bankart lesion extends all the way to the posteroinferior aspect of the glenoid. Also, it is worthwhile to note that the Kim test result can be

b

172

S.-H. Kim

Fig. 7 The Kim test was performed in sitting position with the arm in 90° abduction. (a) With examiner holding elbow and lateral aspect of the proximal arm, firm axial loading force is applied. (b) Simultaneous 45° diagonal elevation was applied on the distal arm, while downward and backward force is applied on the proximal arm

a

b

infrequently positive for a labral lesion associated with a rotator cuff tear and that such a labral lesion may be considered insignificant [28].

Radiographic Evaluation Plane radiographs includes anteroposterior, axillary lateral, and Stryker-Notch view to evaluate any bony abnormality suggesting anterior instability. Hill-Sachs lesion in the StrykerNotch view indicates traumatic anterior instability. Usually, plane radiographs do not provide any useful sign in the posterior instability. Inferior stress anteroposterior radiographs are obtained in the standing position with a 10-lb weight applied downward on both arms [37]. Asymmetric inferior translation between both shoulders may suggest superimposed traumatic instability in multidirectional instability. However, the significance of the inferior stress radiograph is unclear and is not indicated for patients with posterior instability. An MR-arthrogram using intra-articular contrast improves visualization of the labral lesion as well as capsular redundancy on the T1- and T2-weighted axial and coronal images. A high index of suspicion is needed when evaluating the labral lesion noted on an MR-arthrogram. Often the lesion is very subtle or negative. Capsular volume is increased in the posterior and axillary recess in the oblique coronal images. Posteroinferior labral lesion can be classified using the classification system of Kim et al. [22, 24] (Table 1). The MR Table 1 Kim classification of the posteroinferior labral lesion based on arthroscopic findings and MRI-arthrogram Type Finding MRI-arthrogram finding I

Incomplete stripping

Type I: Separation without displacement

II

Marginal crack

Type II: Incomplete avulsion

III

Chondrolabral erosion

Type III: Loss of contour

IV

Flap tear

Type III: Loss of contour

type I lesion is a separation without displacement, type II, incomplete avulsion (cystic lesion), and type III, loss of contour. The surgeon should be aware of the fact that the MR finding of the posteroinferior labral lesion is not always distinctive in the posterior instability compare to the anterior labral lesion in the traumatic anterior instability.

Treatment Options In patients with painless jerk or Kim test, the initial treatment is supervised rehabilitation including restoration of the scapulothoracic and glenohumeral kinematics. Although strengthening exercises do not decrease hyperlaxity of the shoulder, they improve overall control and function of the shoulder joint. Nonoperative treatment consisted of extensive rehabilitation including strengthening exercise of rotator cuff, deltoid, and scapular stabilizer muscles. In the author’s experience, a young female who has hyperlaxity and spontaneous onset of mild symptom tends to respond well with the nonoperative treatments. Despite persistent hyperlaxity, these patients show improved symptom and return to their activity. Operative treatment is indicated in patients with painful jerk or Kim test, and patients who have failed with nonoperative treatments [24, 27, 28]. Historically, open surgical treatment for the posterior instability included bony and soft tissue procedures. Bony procedures which address geometric abnormality include rotational osteotomy of the humerus, glenoid osteotomy, or bone block procedures. Soft tissue procedures are reverse Putti-Platt, reverse Bankart repair, and the Boyd-Sisk procedure. Overall the outcome of the surgical procedures has not been consistent compared to the results of the anterior instability. In 1980, Neer and Foster [37] introduced a new type of capsular procedure, a laterally based posterior capsular shift to tighten a patulous posterior inferior capsule, which they termed inferior capsular shift. Recently, Rhee et al. [41] reported the outcome of 30 shoulders with the open posterior capsulolabral reconstruction with a posterior deltoid-saving approach in

Current Trends on Shoulder Instability

posterior shoulder instability. Posterior capsular redundancy was observed in all cases, but a posteroinferior labral tear was found in only five shoulders. Posterior capsular thinning developed in six patients. The recurrence of instability was observed in four cases, including three cases of voluntary instability. The overall recurrence rate was 13.3%, but the success rate was 92.6% when cases of voluntary instability were excluded. Wolf et al. [47] recently reported the results of open posterior capsular shift procedure in 44 shoulders. The recurrence occurred in eight shoulders (19%). Of the patients, 84% were satisfied with the current status of their shoulder. No progressive radiographic signs of glenohumeral arthritis were seen up to 22 years after surgery. A limited number of studies have been reported for arthroscopic treatment of posteroinferior instability in the peer-reviewed literature. Duncan and Savoie [15] reported their preliminary results of ten patients who were treated with arthroscopic modification of the inferior capsular shift procedure. In 1–3 years of follow-up, all patients had satisfactory results according to the Neer system. Kim et al. [24] reported arthroscopic procedure for posteroinferior instability, which emphasizes the concept of restoring the loss of the chondrolabral containment and capsular laxity. Arthroscopic capsulolabroplasty was performed in 31 patients with posteroinferior multidirectional instability. All patients had a labral lesion and variable capsular stretching in the posteroinferior aspect. Thirty patients had stable shoulders, and one had recurrent instability. They concluded that symptomatic patients with posteroinferior instability had posteroinferior labral lesions, including retroversion of the posteroinferior labrum, which were previously unrecognized. Restoration of the labral buttress and capsular tension by arthroscopic capsulolabroplasty successfully stabilized shoulders with posteroinferior multidirectional instability. Provencher et al. [39] reported results of 33 patients with an arthroscopic treatment of posterior shoulder instability. The procedures include posterior arthroscopic shoulder stabilization with suture anchors or suture capsulolabral plication or both. There were seven failures: four for recurrent instability and three for symptoms of pain. Patients with voluntary instability demonstrated worse outcomes, and those with prior surgery of the shoulder also did worse. More recently, Radkowski et al. [40] reported 107 shoulders in 98 athletes with unidirectional posterior shoulder instability who underwent arthroscopic capsulolabral repair or plication. Results for 27 dominant shoulders in throwing athletes (25%) were compared with those of 80 shoulders in nonthrowing athletes (75%). Throwing athletes were less likely to return to their preinjury levels of sport (55%) compared with nonthrowing athletes (71%). There were a higher percentage of patients with atraumatic onset of injury in the thrower group. This is likely a result of microtrauma from repetitive high stresses placed on the shoulder associated with throwing. Savoie et al. [45] treated 92 shoulders with a diagnosis of primary posterior instability who failed 6 months

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of rehabilitation by operative stabilization. At an average follow-up of 28 months, 97% of the shoulders were stable. Posterior pathology varied, and a reverse Bankart lesion alone was found 51% of the time, a stretched posterior capsule 67% of the time, and a combination of a reverse Bankart lesion and capsular stretching 16% of the time. The rotator interval was obviously damaged in 61% of cases. Operative treatment should not only address the loose joint capsule but also restore the containment function of the glenoid labrum. The arthroscopic capsulolabroplasty procedure includes complete mobilization of the incomplete labral lesion from the glenoid, removal of a rim of articular cartilage, and insertion of suture anchors on the surface of glenoid, posteroinferior labroplasty, superior shift of the posteroinferior and anteroinferior capsule, and closure of the Kim posterior portal. During our extended experiences with arthroscopic treatment, we recognized that rotator interval closure is seldom indicated in most posterior instability. The basic rationale of the posteroinferior labroplasty is both restoration of the posteroinferior labral height and capsular tension. We use triple instability portal which includes Kim posterior portal, transcuff superior portal, and midglenoid anterior portal. The Kim posterior portal is placed at least 1 cm anterior from the standard posterior portal. It lies usually on about 2–3 cm distal and just anterior to the posterolateral corner of acromion. The transcuff superior portal is located just posterior to the anterolateral corner of the acromion. The transcuff superior portal trespasses musculotendinous junction of the rotator cuff when a blunt trocher is inserted, and lies far posterior from the biceps tendon when it is visualized inside. The midglenoid portal is placed just lateral to the coracoids process and lies just superior to the leading edge of the subscapularis tendon. All three portals are high-riding and vertical from the glenoid surface which allows proper access angle to the inferior aspect of glenoid.

Summary Traumatic anterior instability has higher success rate using current arthroscopic procedures except selected group of patients who has complicated pathology such as large glenoid or humeral bone loss. Glenoid defect requires bone graft procedure such as a modified Latarjet procedure while Hill-Sachs defect needs arthroscopic remplissage or posterior capsulodesis. Atraumatic instability has not only capsular laxity but also variable degree of labral lesion. Initial pathology is capsular laxity, which gradually develops labral lesion by repetitive rim-loading mechanism. Pain comes from the labral lesion. Painful jerk and Kim tests suggest labral lesion, which requires arthroscopic stabilization. Arthroscopic capsulolabroplasty addresses not only capsular laxity but also labral pathology.

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Current Trends on Shoulder Instability 36. Mochizuki, Y., Hachisuka, H., Kashiwagi, K., Oomae, H., Yokoya, S., Ochi, M.: Arthroscopic autologous bone graft with arthroscopic Bankart repair for a large bony defect lesion caused by recurrent shoulder dislocation. Arthroscopy 23(6), 677 e1–677 e4 (2007) 37. Neer 2nd, C.S., Foster, C.R.: Inferior capsular shift for involuntary inferior and multidirectional instability of the shoulder. A preliminary report. J. Bone Joint Surg. Am. 62(6), 897–908 (1980) 38. Neer 2nd, C.S., Welsh, R.P.: The shoulder in sports. Orthop. Clin. North Am. 8(3), 583–591 (1977) 39. Provencher, M.T., Bell, S.J., Menzel, K.A., Mologne, T.S.: Arthroscopic treatment of posterior shoulder instability: results in 33 patients. Am. J. Sports Med. 33(10), 1463–1471 (2005) 40. Radkowski, C.A., Chhabra, A., Baker 3rd, C.L., Tejwani, S.G., Bradley, J.P.: Arthroscopic capsulolabral repair for posterior shoulder instability in throwing athletes compared with nonthrowing athletes. Am. J. Sports Med. 36(4), 693–699 (2008) 41. Rhee, Y.G., Lee, D.H., Lim, C.T.: Posterior capsulolabral reconstruction in posterior shoulder instability: deltoid saving. J. Shoulder Elbow Surg. 14(4), 355–360 (2005) 42. Richards, D.P., Burkhart, S.S.: Arthroscopic humeral avulsion of the glenohumeral ligaments (HAGL) repair. Arthroscopy 20(Suppl 2), 134–141 (2004)

175 43. Robinson, C.M., Howes, J., Murdoch, H., Will, E., Graham, C.: Functional outcome and risk of recurrent instability after primary traumatic anterior shoulder dislocation in young patients. J. Bone Joint Surg. Am. 88(11), 2326–2336 (2006) 44. Rowe, C.R., Patel, D., Southmayd, W.W.: The Bankart procedure: a long-term end-result study. J. Bone Joint Surg. Am. 60(1), 1–16 (1978) 45. Savoie 3rd, F.H., Holt, M.S., Field, L.D., Ramsey, J.R.: Arthroscopic management of posterior instability: evolution of technique and results. Arthroscopy 24(4), 389–396 (2008) 46. Sedeek, S.M., Tey, I.K., Tan, A.H.: Arthroscopic Bankart repair for traumatic anterior shoulder instability with the use of suture anchors. Singapore Med. J. 49(9), 676–681 (2008) 47. Wolf, B.R., Strickland, S., Williams, R.J., Allen, A.A., Altchek, D.W., Warren, R.F.: Open posterior stabilization for recurrent posterior glenohumeral instability. J. Shoulder Elbow Surg. 14(2), 157–164 (2005) 48. Wolf, E.M., Pollack, M., Smalley, C.: Hill-Sach’s “remplissage”: an arthroscopic solution for the engaging Hill-Sachs lesion. Arthroscopy 23(Suppl 6), e1–e2 (2007)

Management of the Acromioclavicular Joint Problems Onur Tetik

Contents Anatomy ....................................................................................... 177 Biomechanics ............................................................................... 178 Grouping the ACJ Injury ........................................................... Trauma .......................................................................................... Acromioclavicular Derangement or Arthrosis .............................. Distal Clavicle Osteolysis .............................................................

178 178 178 178

History.......................................................................................... 179 Physical Exam ............................................................................. 180

The acromioclavicular joint (ACJ) is composed of the distal end of the clavicle and the acromion. Its function is to anchor the clavicle to the scapula and to the shoulder girdle. The subcutaneous location of this joint makes it vulnerable to injury. It is approximately 9% of all the shoulder injuries. The majority of the injuries occur in men with a male to female ratio of approximately 5:1, and patients in their 20s are the most affected age group [53]. Because of the high incidence of these injuries, orthopedists, sports medicine doctors, emergency physicians, and physical therapists should be aware of the management of these injuries [56].

Imaging ........................................................................................ 180 Nonoperative Management ........................................................ 181 Operative Management .............................................................. Conjoined Tendon Transfer........................................................... Double-Loop Repair ..................................................................... TightRope System ......................................................................... EndoButton Closed Loop.............................................................. Arthroscopic Reconstruction ........................................................ Anatomic Coracoclavicular Reconstruction .................................

182 183 183 183 183 183 184

Postoperative Management ........................................................ 184 Complications .............................................................................. 184 References .................................................................................... 184

O. Tetik Orthopedic Department, Vehbi Koç Vakfi American Hospital, Güzelbahçe Sok. No:20 NiĜantaĜı, 34365 Istanbul, Turkey e-mail: [email protected]

Anatomy The ACJ is subcutaneous and has little protection by soft tissues. It is composed of the distal end of the clavicle and the acromion and serves to anchor the clavicle to the scapula and the shoulder girdle. This is an inherently unstable articulation. ACJ capsule and the strong coracoclavicular (CC) ligaments, conoid ligament medially and trapezoid ligament laterally, support the joint and provide static stability. The dynamic stabilizers are the trapezius and deltoid muscles. The distal ends of the clavicle and the acromion are lined with hyaline cartilage, and there is a meniscal structure intraarticularly. The role of this meniscus is negligible, and generally it is thought to be degenerated during the fourth decade [56]. The clavicular origin of the conoid ligament originates an average of 46 mm medial to the ACJ, and the trapezoid ligament originates 26 mm medial to the ACJ. The conoid is more posterior compared with the trapezoid origin at the mid-portion of the inferior surface of the clavicle [52]. The superior, inferior, and posterior acromioclavicular (AC) ligaments insert an average of 16–20 mm medial to the ACJ on the clavicle. The importance of this anatomic observation is that aggressive distal clavicle excision (DCE) can destabilize the ACJ and lead to symptomatic posterior impingement against the acromion if that ranges were exceeded.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_23, © Springer-Verlag Berlin Heidelberg 2012

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Biomechanics In the intact state, joint stability is provided by static and dynamic constraints. The static constraints are the AC ligaments, CC ligaments, and coracoacromial (CA) ligament. The AC ligaments surround the ACJ and are composed of the superior (strongest), inferior, anterior, and posterior ligaments. In combination, these ligaments form the greatest restraint to displacement horizontally. They provide an estimated 90% of the constraint to horizontal motion of the ACJ [5]. The CC ligaments prevent inferior migration of the scapulohumeral complex relative to the clavicle [67]. When the AC ligaments are completely disrupted, the CC ligaments, especially conoid ligament, also become a significant restraint to anteroposterior (AP) displacement. Debski and colleagues demonstrated that in the absence of the AC ligaments, the mean in situ force in the trapezoid ligament increases 66% in response to a posterior 70 Newton (N) load in a cadaveric model [11]. The mean force in the conoid ligament increases by over 225% in response to an anterior load. The fibers from the trapezius and the deltoid muscles blend with the superior AC ligament and contribute to its strength with contraction of the muscular fibers. ACJ motion is produced with arm abduction and forward elevation. The clavicle rotates up to 40°–50°, but only 5°–8° of motion occur at the ACJ. A synchronous scapuloclavicular rotation in which the CC ligaments allow the scapula to rotate downward as the clavicle rotates upward with abduction and forward elevation of the arm was described earlier. This effectively reduces the motion at the ACJ. Also 5° of motion exist between the coracoid and clavicle, which becomes significant when a hardware fixation bridges these bony structures [53].

Grouping the ACJ Injury The ACJ pathology is generally caused by one of three processes: (A) trauma (fracture, ACJ separation, or dislocation); (B) ACJ arthrosis (posttraumatic or idiopathic); and (C) distal clavicle osteolysis (DCO).

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Acromioclavicular Separations and Dislocation The ACJ separation is one of the most common shoulder injuries. The most common mechanism of this injury is a fall with a direct force to the superior part of the shoulder and with the arm in an adducted position. These injuries have been classified according to the degree of ligamentous and other softtissue injury [32]. Cadenat originally described the process of acute ACJ disruption as a sequential injury, beginning with the AC ligaments, continuing to the CC ligaments, and ultimately violating the deltotrapezial fascia [36]. Tossy and colleagues defined distinct stages of injury, labeled as types I (AC ligament sprain), II (AC ligaments torn and CC ligaments intact), and III (AC and CC ligaments torn) [65]. Later on this was modified by Rockwood to the system most commonly used today [54]. This modification includes types IV (posterior dislocation of clavicle), V (AC and CC ligaments and deltotrapezial fascia torn), and VI (subcoracoid dislocation of clavicle) injuries in addition to a Tossy’s classification.

Acromioclavicular Derangement or Arthrosis Acute pain in the ACJ may be caused by an “internal derangement” like a tear of the intra-articular meniscus. Although being uncommon, recognition of this entity is important to distinguish it from idiopathic arthritis. Patients with internal derangement usually have abrupt onset of ACJ pain, accompanied by mechanical symptoms, such as clicking or popping. The ACJ arthrosis may be idiopathic or may be a result from an injury and/or instability. Although radiographic evidence of primary osteoarthrosis of the ACJ is common particularly in older individuals, symptoms initiated from this joint are comparatively less frequent [12, 21, 39]. Posttraumatic osteoarthrosis is more common than primary osteoarthrosis and may occur after ACJ separation, distal clavicle fracture, or postoperatively [58] Studies on the natural history of the more innocuous type I and II ACJ injuries suggest that symptoms of posttraumatic arthritis occur in 8–42% of the patients [4, 37, 63]. Mouhsine et al. concluded that the severity of the consequences after grade I and II AC separations is underestimated [37].

Distal Clavicle Osteolysis Trauma Fracture of the distal end of the clavicle may be caused by the direct trauma or falling on an arm. If it is unstable, it needs a surgical treatment (Fig. 1).

DCO is associated with heavy weight lifting [6, 57]. Scavenius and Iverson found that 28% of elite weight lifters in their series had pain of insidious onset, swelling, and ACJ tenderness consistent with distal osteolysis [57]. The pain is

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a

b

c

d

Fig. 1 Fracture of the distal end of the clavicula with joint comminution. (a) Undisplaced while lying down on the bed. (b) Displacement with standing-up and walking in an arm sling. (c) Fracture fixed with a clavicle plate (Acumed Inc., Beaverton, OR, USA), CC ligament repair

with anchor (Arthrex, Inc., Naples, FL) in the coracoid and tying sutures through the clavicular holes and primary ligament repair of the AC joint. (d) 6th week follow-up X-ray

aggravated by activity, in particular during flat bench pressing and also with dips, flies, and pushups. Slawski and Cahill reported bilateral involvement in 79% of weight lifters at the time of presentation [59].

patients are at risk for either fracture of the acromion or rotator cuff tear consequent to forceful superior humeral head displacement. Posttraumatic pain is typically localized over the anterosuperior aspect of the shoulder and is attributed to cross-innervation of this region by the suprascapular and lateral pectoral nerves. A direct injury occurs as a result of a fall onto the lateral aspect or point of the shoulder with the arm adducted. With the inherent stability of the sternoclavicular joint, energy is transferred by both the AC and CC ligaments. With inferior displacement of the upper extremity and scapula, ultimately the clavicle rests on the first rib and cannot displace inferiorly with the scapula. The force is felt across the CC ligaments, and often they will consequently be injured [19]. Patients with a more chronic or insidious onset of pain may have ACJ arthrosis or DCO. AC joint pain can be fairly specific and localize to the ACJ or refer into the trapezius or down to the arm.

History The approach to the patient with AC pathology depends on the history. Acute or chronic history helps physician to decide what to do. In the acute or posttraumatic situations, the mechanism may be either indirect or direct. An indirect injury occurs as a result of a fall onto an outstretched upper extremity, whereby the force of the fall drives the proximal humerus into its overlying acromion. This forces the scapula superiorly and medially and often injures the AC ligaments. In this case, CC ligament injury is uncommon. Instead, these

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Physical Exam There are many physical examination findings and tests to diagnose ACJ problems, but similar to other causes of shoulder pain, none of these tests has established sensitivity and specificity. There may be a various amount of deformity and tenderness after a direct trauma. There will be no deformity, mild swelling, and tenderness over the joint with palpation. In addition to tenderness and swelling, type II injuries also usually demonstrate mild prominence of the distal clavicle. With ACJ ligament disruption and injury to the conoid and trapezoid, the clavicle loses ligamentous connection with the scapulohumeral complex, and the weight of the upper extremity causes its downward displacement in type III and V injuries. To differentiate the type III and V injuries, patient should be asked to shrug both shoulders, which in a type V injury exaggerates the degree of displacement. In another technique one may try to reduce the joint and if the reduction of the deformity achieved suggests an intact deltotrapezial fascia (type III), whereas failure of the reduction indicates violation of the deltopectoral fascia in type V. Acute joint derangement presents with acute onset of painful clicking in the ACJ. There is often a history of mild trauma, and the patient will note discomfort over the superior aspect of the ACJ and mechanical catching or popping with shoulder movement. There is usually tenderness over the joint, along with palpable crepitus during circumduction of the arm or cross-body adduction. Tenderness over the ACJ is a very sensitive finding and is easy to elicit owing to its subcutaneous location [68]. A number of provocative tests are helpful in the subacute or chronic setting. Cross-arm adduction test is thought to load and reproduce pain from the ACJ. O’Brien’s active compression test helps the examiner differentiate pain attributable to a superior labral anterior to posterior (SLAP) lesion from pain owing to ACJ pathology [44]. A recent analysis of these maneuvers found cross-arm adduction to be sensitive (77%) and the active compression test of O’Brien to be 95% specific [8]. O’Brien and colleagues report a sensitivity of 100% and a specificity of 96% for ACJ pathology in patients who localized pain to the ACJ when the arm was in the internally rotated position [44]. The cross-arm adduction and O’Brien’s tests rely on compression of the ACJ to diagnose ACJ pathology; the specificity is limited by the fact that forward elevation and adduction of the arm will cause pain in patients with other shoulder disorders, such as rotator cuff tears or tendinitis, labral pathology, or biceps pathology. Pain elicited by these tests should also be localized to the ACJ rather than being nonspecifically localized to the lateral or posterior shoulder. The Paxinos test has the advantage of compressing this joint while the arm rests at the patient’s side, potentially improving the specificity of this test. Pain with active internal rotation with placement of the hand behind the back can also elicit

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discomfort directly over the ACJ. The Paxinos test examines the ACJ with the patient seated and with the arm resting along the chest [68]. The examiner places his/her thumb over the posterolateral corner of the acromion and the index and long fingers of the ipsilateral or opposite hand superior to the midportion of the ipsilateral clavicle. The test is considered positive if compression of the clavicle and acromion causes pain localized to the ACJ. This test should be performed on both shoulders to assess for subtle differences in horizontal translation to discriminate between laxity and instability. Increased translation in the horizontal plane that is associated with pain may suggest a complete tear (type II injury) rather than a sprain (type I injury) of the AC ligaments. Coronal plane instability is easier to detect. If the clavicle appears displaced superiorly, asking the patient to shrug his/ her shoulder is a useful method to determine if the deltotrapezial fascia is intact (clavicle reduces, type III injury) or if it has been violated (clavicle remains dislocated, type V injury). Local anesthetic injection intraarticularly is an important tool when evaluating the ACJ. Preinjection radiograph should be evaluated for easier injections because this joint’s obliquity varies considerably. Gentle pressure superiorly and posteriorly can elicit AC motion at the joint, an easy “pop” as the needle enters the joint could be felt, and there should be a little resistance when injecting. The joint typically will accommodate approximately 1 mL of medication, and overdistension can be painful. Such an injection with or without corticosteroid can be both diagnostic and therapeutic in patients with ACJ pathology. Relief of pain postinjection implicates the ACJ as the pain generator. Physical exam should always include the cervical evaluation.

Imaging X-ray evaluation with an AP, supraspinatus outlet, axillary, cross-arm adduction AP, and simultaneous bilateral Zanca radiograph is the first step. Stress radiographs are not used generally, because the diagnosis is usually obtained by the history, physical examination, and radiographs. AP (for type VI injury) and axillary (for type IV injury) views define the amount and direction of displacement of the clavicle relative to the scapulohumeral complex. The supraspinatus outlet permits acromial morphology classification. Zanca originally described a specialized view for the ACJ, whereby the X-ray beam is angled 10° cephalad to eliminate the overlap of the clavicle with the spine of the scapula in which the width of the ACJ is between 1 and 3 mm [73]. Petersson and RedlundJohnell reported an age-dependent decrease in ACJ width, such that a joint space of only 0.5 mm is normal in patients older than 60 years [47]. The normal CC distance is between 1.1 and 1.3 cm, on average, and Bearden and colleagues

Management of the Acromioclavicular Joint Problems

reported that complete CC ligament disruption is indicated by an increase in the CC distance of 25–50% compared with the contralateral shoulder [3, 9]. A simultaneous bilateral Zanca radiograph allows direct comparison and eliminates inaccuracy and is an effective and reliable way to assess the degree of deformity compared with the patient’s contralateral shoulder. In a cadaveric evaluation of simulated type II ACJ injuries, isolated sectioning of the conoid or trapezoid ligament permitted 4–6 mm more superior displacement on Zanca views compared with the intact state [35]. The clinical implication is the subtle differences in side-to-side CC distance may represent complete injury to one of the CC ligaments, suggesting a more severe type II injury. The role of ultrasound in imaging ACJ injuries remains unclear; a recent study using this modality identified abnormal movements of the injured ACJ with cross-arm adduction which were not identified with plain resting or stress radiographs [46].

Nonoperative Management The goals of treatment for AC injuries are achieving painless range of motion of the shoulder, obtaining full strength, and exhibiting no limitation in activity. In the atraumatic conditions, injections play an important role in the treatment of ACJ pathologies. The response to injection of local anesthetic with or without corticosteroid into the ACJ is quick and has important diagnostic and therapeutic implications. Failure to reduce a patient’s level of pain with an AC injection implicates the diagnosis of pathology and suggests that surgical intervention may be ineffective. Pain caused by AC arthrosis is not generally improved with the physical therapy. However, coexisting shoulder disorders, such as rotator cuff tendinosis, proximal biceps tendinosis, and glenohumeral instability, are common and may respond to rehabilitation. Nonoperative management of DCO is similar to the AC arthrosis; activity modification, rest, anti-inflammatory medications, and use of injections are the mainstay of the treatment. Athletes may return to the modified activity 48–72 h postinjection. By this time, the local anesthetic effect decreases and the corticosteroid takes effect. Patients should cease that activity if the activity reproduces their preinjection symptoms. If the patient received considerable relief from the first injection, second injection may be given at 3rd month. Injections are not given more than two to the same ACJ. In the traumatic conditions of the ACJ, nonoperative treatment protocols have been ranging from supportive sling to cast or strap immobilization. No evidence strongly supports one method over another and compliance to the cumbersome methods has worse results [26, 49, 61, 63, 71].

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A sling can be used for comfort initially, and rehabilitation can be initiated as soon as the symptoms resolve. The goal is early return to function. Phase 1 treatment consists of ice, immobilization, oral analgesics, and active assisted range of motion (ROM) at low levels of shoulder abduction and elevation. Once pain and tenderness have nearly resolved, phase 2 begins with restoration of full ROM and initiation of strength training. Strengthening of the rotator cuff and periscapular muscles is encouraged. Phase 3 involves further strengthening of the entire shoulder girdle, including trapezius, latissimus, and pectoralis muscles. The goal in this phase is to achieve strength comparable with the contralateral arm. Once this is achieved, patients progress to sportspecific exercises. Generally, type I and II injuries are treated nonoperatively, and most patients return to their preinjury level of function [10, 14, 20]. High-grade injuries (types IV–VI) are treated surgically [1, 9, 18, 26, 28, 41, 46, 64, 66, 69, 70]. Historically, the literature has not provided sufficient evidence to support surgical treatment of the acute type III AC separation [37]. Management of the patient with type III AC separation remains controversial, with success rates in this population ranging from 87% to 96% in both operative and nonoperative treatments. Type III separation is characterized by complete disruption of both the AC and CC ligaments, without much disruption of the deltoid or trapezial fascia. Clinically, the patient presents with a “high-riding” clavicle, which appears elevated because of the relative depression of the scapulohumeral complex. Nissen and Chatterjee surveyed nearly 600 American Orthopaedic Society for Sports Medicine members and found that 81% treated uncomplicated type III AC separations conservatively [41]. Phillips and colleagues completed a meta-analysis of 1,172 patients with type III injuries and identified 88% and 87% satisfactory outcomes in patients treated operatively and nonoperatively, respectively [48]. Spencer completed a systematic review of journals published in the English literature and concluded that nonoperative treatment is more appropriate for grade III injuries [61]. Many of the studies on this topic are retrospective case series and lack assessment by way of validated outcome measures. Patients with an acute type III AC separation are treated nonoperatively for up to 12 weeks. If the patient has a persistent pain and dysfunction that prevents them from returning to work or sport, surgical treatment is considered. Studies of elite throwing athletes suggest that anatomic reduction of the ACJ is not necessary [20, 22]. Most surgeons treat contact athletes nonoperatively owing to the high risk for reinjury. Finally, when comparing operative and nonoperative intervention, it has been shown that there is no difference in strength with either treatment regimen 2 years postinjury.

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The management of ACJ injury during the competitions is important. Periparticipation injection of local anesthetic (without cortisone) into the ACJ is an attractive option. It may reduce pain without compromising the athlete’s performance. Some physicians support such ACJ injection during competitive play as an acceptable practice, such as Nelson, who stated “blocking an acromioclavicular joint or injecting a rib injury is reasonable at the professional level, not dangerous, and done routinely” [40]. In opposite because of inhibiting the perception of pain may exacerbate the injury [60]. Orchard has published the only case series specifically evaluating the consequences of local anesthetic injection in professional football players, although these were not only ACJ injections [45]. In this series of 268 injuries, 27 ACJ injuries were managed with injection of local anesthetic, and complications were rare. Two cases of DCO occurred in this group compared with 1 case in 25 ACJ injuries managed without local anesthetic. This difference was not significant.

Operative Management Most traumatic and atraumatic ACJ problems in athletes can be treated conservatively, but in some conditions surgical treatment is necessary to prevent failure of the nonoperative treatment. Surgical interventions include ACJ resection for arthrosis and DCO, and repair and/or reconstruction of the ligaments and/or capsule for selected AC injuries. In the ACJ arthrosis and DCO, distal clavicular excision (DCE) is the treatment of choice. DCE has been described in the treatment of a painful ACJ in athletes, and many authorities have reported success with this technique [2, 16, 17, 43, 50, 59]. Indications include idiopathic ACJ arthrosis, DCO, and low-grade (grades I and II) ACJ separations that fail conservative treatment. Rabalais and McCarty completed a systematic review on this topic and concluded that the literature generally supports DCE for atraumatic ACJ arthrosis [50]. Contraindications to DCE include chronic pain from severe (grade III or higher) ACJ separations or in grade II injuries associated with hypermobility [7, 17, 21, 34, 54, 58]. DCE may be performed either arthroscopically or as an open procedure. The advantages of the open technique include technical ease and the ability to reapproximate, imbricate, or repair the ACJ capsule, which may be of value in posttraumatic AC joint arthritis with possible occult instability. The arthroscopic technique allows examination of the rest of the shoulder and subacromial space and is less invasive, but it is technically more demanding [43]. The goal is to resect approximately 8–10 mm from the distal clavicle in open and arthroscopic technique. More aggressive resection risks sacrificing the AC ligaments and destabilizing the joint. It is important to visualize the entire distal clavicle to ensure

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that a uniform resection has been achieved. Intraoperative fluoroscopy may be needed to determine the adequacy of the resection. Arthroscopic DCE can be performed directly through the ACJ, as described by Flatow and colleagues, or indirectly via the subacromial space [16, 17]. The direct technique can be used in patients who have isolated ACJ pathology and in whom the ACJ space is sufficient to accommodate the smalldiameter camera and instruments. The indirect approach is performed through the subacromial space and may be performed with concomitant glenohumeral or subacromial procedures (such as subacromial decompression). In a recent randomized trial comparing the direct and indirect arthroscopic DCE for osteolysis or posttraumatic arthritis in athletes, Charron and colleagues identified clinical improvement in both groups at a minimum 2-year followup [7]. Of greater interest, the group treated with direct arthroscopic DCE had reported a faster return to sport (21 days vs. 42 days) and had earlier improvements in their American Shoulder and Elbow Society and American Shoulder Scoring System scores than the group treated with indirect DCE. Zawadsky and colleagues reported a high success rate following arthroscopic DCE for posttraumatic or stress-induced DCO [74]. Sometimes the ACJ traumas may require surgical intervention following trauma, either acutely (within 4 weeks of presentation) or chronically. Earlier surgical management of ACJ dislocations was open joint reduction and repair of the AC capsule ligaments under direct visualization, supported with temporary internal fixation [9, 23, 55]. Sage and Salvatore reported 62–69% excellent results with this technique. Rigid internal fixation techniques do not allow the physiologic motion of the AC complex, that’s why hardware failure and migration in some patients are seen. Most of the failures of these early surgical techniques were because of hardware complications, rather than a diseased distal clavicle. Failure to remove the distal clavicle might lead to persistent symptoms in some patients and distal clavicle resection as described by Mumford became very popular [38]. There are numerous surgical techniques in which reduction and fixation of the ACJ were achieved with biological and synthetic materials for the treatment of the acute Type III and V AC Separations. These have been performed as isolated techniques or as augmentations to ligament or tendon transfers. They may be performed arthroscopically or arthroscopically assisted. The advantages of these more recent techniques include less soft tissue dissection, ability to treat concomitant intra-articular pathology, and preservation of normal joint motion. The latter feature is thought to potentially reduce the complications that can occur after more rigid stabilization with screws or wires [31, 42].

Management of the Acromioclavicular Joint Problems

Surgical principles: 1. Accurate reduction; no inferior sag of the scapula and no AP translation 2. Repair or reconstruction of the ligaments and capsules after reduction with primary repair and/or reconstruction with auto or allografts 3. Temporary protection of the surgery internally or externally 4. Removal of the rigid implants after the repair consolidated On the basis of these rules, timing of the surgery, choice of surgical approach, type of ligament reconstruction, and temporary stabilization should be decided before the surgery. Accurate joint reduction is easier and primary repair is possible in the first 2 weeks of the injury. Primary repairs are harder because of the shaving-brush quality of the torn ligaments and should be done in 2 weeks. Techniques are classified as: (A) Techniques using the native ligaments (B) Ligament substitution with local ligaments and tendons (C) Other kinds of ligament substitution Many techniques have been described to repair or reconstruct the more severely injured chronic ACJ injuries; mostly types III and V. Weaver and Dunn described an open technique to treat acute and chronic ACJ dislocations. It consists of distal clavicular resection followed by transfer of the CA ligament into the medullary cavity of the clavicle. In their original report, recurrence or incomplete reduction rate was as many as 24% of their patients [69]. The original procedure has only 30% strength and 10% stiffness of the original ligaments, and failure occurs mainly at the suture side. The mean AP laxity is 42 mm, and vertical laxity is 14 mm, whereas in the intact state they are 8 mm and 3 mm, respectively [13]. In addition, the vector of attachment from the tip of the coracoid to the distal clavicle does not anatomically recreate the normal line of pull of the CC ligaments. More recent modifications of the Weaver–Dunn procedure have been described, in which the CA ligament transfer is augmented with a loop of Mersilene tape.

Conjoined Tendon Transfer Jiang and colleagues recently reported their results in a group of patients with grade III–V AC dislocations treated with conjoined tendon transfer [25]. Distal clavicle (5–8 mm) is excised, and the lateral half of the conjoined tendon is isolated and fixed within the medullary cavity of the clavicle to augment this reconstruction; the authors placed suture anchors in the base of the coracoid, passed the sutures through bone tunnels in the clavicle, and tied them over a bone bridge.

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These authors reported 89% good or excellent results, with 92% returning to their preinjury level of function.

Double-Loop Repair Dimakopoulos and colleagues proposed another technique for acute ACJ injuries which does not require hardware and may better control AP translation of the ACJ [15]. In their series, reduction of the ACJ was maintained in 32 of 34 patients at a mean follow-up period of 33 months. The other two patients had only mild loss of reduction, and the mean Constant–Murley score was 93.5.

TightRope System Perhaps the newest technique to achieve anatomic reduction and secure fixation is an arthroscopically assisted approach using the TightRope system (Arthrex, Naples, FL). The TightRope system was designed originally to maintain the reduction of injuries to the ankle syndesmosis. Its application has been expanded to stabilization of an acute AC separation, thus permitting immediate return to sport or work because this method does not rely on biologic incorporation of autograft or allograft into clavicular bone tunnels. The presumed advantage of this technique is that it maintains reduction of the CC distance and allows normal movement of the ACJ [30]. Richards and Tennent reported their results in ten patients treated with the TightRope system [51]. At a mean of 15 months, the mean Constant score was 93, and seven of ten ACJs had no change in reduction. The remaining three had a slight loss of reduction, and this was attributed to a larger cannulated drill, which was used in this initial group.

EndoButton Closed Loop Struhl recently described the EndoButton Closed Loop (CL) (Smith & Nephew, Memphis, TN), which is similar to the TightRope in that it is a nonrigid fixation and reduces the ACJ while also permitting slight motion through the joint [62].

Arthroscopic Reconstruction Wolf and Pennington described an arthroscopically assisted method of stabilizing the ACJ with suture between the

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clavicle and coracoid [72]. The coracoid is visualized with the arthroscope in the glenohumeral joint and the distal clavicle from the subacromial space. Suture or semitendinosus allograft is looped beneath the coracoid and secured through a single small bone tunnel in the clavicle. In this technique, resection of the distal clavicle facilitated reduction of the joint. A similar arthroscopically assisted technique uses a suture anchor in the coracoid with two limbs of suture which are passed through bone tunnels in the clavicle to reconstruct the conoid and trapezoid ligaments [72].

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12 to 24 weeks, isometric exercises are begun. Contact sports, throwing, and swimming are allowed at 6 months postoperatively.

Complications

Anatomic reconstruction is the preferred method, in which the ligaments of the ACJ and CC ligaments are reestablished [33]. In fact, failure to surgically reproduce the conoid, trapezoid, and AC ligament function with current techniques may explain the observed incidence of recurrent instability and pain [24, 27]. The distal clavicle is not excised as part of this reconstruction because the congruous bony surfaces impart stability to the reduced ACJ. Semitendinosus, anterior tibialis, allograft, or autograft are suitable grafts for this procedure [29]. Lee and colleagues found no difference in peak load-to-failure between semitendinosus, toe extensors, and gracilis tendons for reconstruction of the ACJ [29]. In this technique, there are two options for handling the fixation to the coracoid process: the graft may either be looped around the base of the coracoid, or it can be secured within a bone tunnel with interference screwtype fixation. It is important to place the clavicular bone tunnels in an anatomic position to recreate the CC ligaments. Some part of the tendon graft are laid longitudinally in the direction of the ACJ and sewn to the acromion to reconstruct the superior and posterior AC ligaments.

There may be several intra- and postoperative complications with the repair or reconstruction of the dislocated ACJ. The complication rate is decreased as the anatomy and biomechanics of the ACJ are understood and the techniques are improved. Complications include wound problems and infection, hardware migration and failure, clavicle and coracoid fracture, loss of reduction, and neurovascular injury. Owing to the normal motion of the ACJ, stabilizing AC relationship with pins or screws has been associated with high rates of complications. These include screws missing the coracoid, late screw failure, wound drainage, and subluxation after screw removal [42]. Smooth Kirschner wires, threaded pins, and Steinmann pins have all been reported to migrate [31]. Hardware removal is necessary, and loss of reduction following removal has been described frequently. Complications with anatomic CC reconstruction, such as superficial wound problems, can be minimized with gentle, meticulous soft tissue handling and layered wound closure. The possibility of clavicle fracture exists owing to placement of two fairly large bone tunnels, failure to support the arm postoperatively, and premature return to activity or contact. Extreme care must be taken when preparing the conoid bone tunnel so that posterior wall “blow out” is avoided. The tendon graft can be looped around the coracoid, rather than securing it within a bone tunnel in the coracoid to prevent blowout fracture of the coronoid process. Heterotopic ossification and tunnel widening are rare findings, and their clinical significance is unclear.

Postoperative Management

References

Anatomic Coracoclavicular Reconstruction

Zanca and axillary view are obtained postoperatively and repeated for comparison at 6 weeks. Pendulum exercises three times a day are started immediately. The arm put in an arm sling with a support for 6 weeks. Patient can take the sling out only during supervised therapy, which involves active assisted ROM in all planes. With the supported sling (like platform brace), the weight of the shoulder is supported on the hip, rather than through the reconstructed ACJ. The sling is generally discontinued between 6 and 12 weeks; however, no strengthening or lifting can be done, as the graft is still maturing. Light jogging is allowed at 12 weeks. From

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Arthroscopic Double Band AC Joint Reconstruction with Two TightRope™: Anatomical, Biomechanical Background and 2 Years Follow up Hosam El-Azab and Andreas B. Imhoff

Contents Introduction ................................................................................. 187 Treatment of Acute Acromioclavicular Joint Dislocation .......................................................................... 187 Surgical Technique ........................................................................ 188 Postoperative Rehabilitation ......................................................... 190 Discussion..................................................................................... 190 Our Own Results ......................................................................... 190 References .................................................................................... 191

Introduction Acromioclavicular (AC) joint separation is a typical sports injury following blunt trauma to the shoulder and considered as a common reason that athletes seek a medical advice following an acute shoulder injury [16]; it comprises approximately 9% of all injuries to the shoulder girdle [25]. Males in their second through fourth decades of life have the greatest frequency of AC joint injuries than females in a ratio of 5:1 [25]. The complex articulation of the distal clavicle with the acromion process is secured by a variety of static and dynamic stabilizers. The static stability of the AC joint is maintained mostly by the integrated functions of the AC joint capsule and the coracoclavicular (CC) ligaments [15] (Fig. 1). The CC ligaments are considered the prime suspensory ligaments of the AC joint [16]. Each CC ligament has a different role in providing the AC joint stability in response to various loading conditions [7]. Debski et al. reported that the conoid ligament being the major restraint against superior while the trapezoid ligament against posterior loading [6]. Several studies suggest that surgery should aim to reconstruct these two ligaments as separate anatomic structures to restore the stability [1, 2, 11, 22]. Several treatment methods of AC joint separation are available. With the advance in the instrumentation and surgical techniques, the treatment becomes more precise to address the pathology of AC joint injury and more efficient to provide satisfactory clinical and structural results.

Treatment of Acute Acromioclavicular Joint Dislocation

H. El-Azab ( ) and A.B. Imhoff Department of Orthopaedic Sports Medicine, Rechts der Isar, Technische Universitaet Muenchen, Connollystrasse 32, 80809 Muenchen, Germany e-mail: [email protected], [email protected]; [email protected], [email protected]

The treatment of AC joint injuries depends on the severity of separation, which is classified according to Rockwood into six types [16]. In types I and II, a conservative treatment is sufficient for ligament healing, whereas in type IV through VI, an operative treatment is found to be mandatory to restore the AC joint stability. Although type III AC joint injury was controversly discussed in the literature regarding the choice

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landmarks (Fig. 2) representing the footprints of trapezoid and conoid ligament insertions on the clavicle, are measured 2.5 (17%) and 4.5 (30%) cm from the lateral edge of the clavicle, for optimal tunnel placement [15]. Glenohumeral joint arthroscopy is performed through the standard posterior portal. Two anterolateral portals are located through the rotator interval in order to provide working access to the coracoid undersurface (Fig. 2). In the subacromial space, AC joint is visualized and the disc is removed if damaged. The arthroscope is reinserted into the glenohumeral joint via portal two. By an ablation device through portal three, the coracoid undersurface is prepared circumferentially to visualize the medial and lateral edge as well as the base to tip (Figs. 2 and 3). Following coracoid preparation, 3-cm vertical skin incision is placed directly over and perpendicular to the clavicle,

Fig. 1 Anatomy of the AC-J showing the coracoacromial ligament; conoid and trapezoid ligaments

of treatment, it is generally accepted as an indication for surgical stabilization with heavy laborer or active athletes [14]. Traditional techniques, such as plate, wire, suture and screw fixation, as well as CC ligament transfer do not create an anatomic repair or restore the damaged anatomic structures [19], and therefore mostly do not provide the initial stability of the joint complex required to withstand common loads until biologic healing occurs [8] and lead to the different reported inferior results [14]. Osteoarthritis, redislocation, pain, malfunction, or deformity are frequently reported problems associated with traditional AC joint surgery [5]. Recently, AC joint reconstruction techniques have focused on anatomic restoration of the CC ligaments separately. Such techniques involve creating bone tunnels in the distal clavicle and coracoid process [12, 14]. Anatomical positioning is crucial when optimal joint function and stability are concerned [14].

Fig. 2 Arthroscopy portals (1,2,3), anatomical landmarks, position of the conoid and trapezoid ligament, and a vertical incision in-between on the clavicle

Surgical Technique [17] The injured shoulder is prepared and draped in sterile fashion, and the arm is fixed to a pneumatic arm holder. According to Rios et al., the total clavicle length is measured. Two independent points, in addition to the standard anatomic

Fig. 3 The coracoid undersurface prepared circumferentially with Opes™ (Electrocautery, Arthrex)

Arthroscopic Double Band AC Joint Reconstruction with Two TightRope™

between the previously marked orientation points (at 3.5 cm). The exposed clavicle is then reduced to an anatomic position. A drill guide with a marking hook (Acromioclavicular TightRope™ – ACTR – Drill Guide, Arthrex, FL, USA) (Fig. 4) is introduced through portal three with its tip positioned at the coracoid undersurface under arthroscopic control. In respect to the clavicular orientation for conoidal and trapezoidal tunnel placement, the drill sleeve is placed on top of the clavicle. Optimal tunnel placement of the conoid coracoidal tunnel should be at the posterior aspect of the coracoid close to the base and medial edge. The trapezoid coracoidal tunnel should be anterolateral to the conoidal tunnel leaving a bony bridge between tunnels of at least 10 mm. K-wires are drilled through the clavicle and the coracoid under arthroscopic visualization until each wire can be seen at the caudal coracoid in an anatomic position. K-wires are overdrilled with two 3.5-mm drill bits. Through the cannulated drill bits, two Suturelasso SD wire loops™ (Arthrex, FL, USA) are inserted and the drill bits are removed. Each loop is connected to one flip button (TightRope™, Arthrex, FL, USA) over the superior surface of the clavicle. The TightRope™ device consists of one round clavicular titanium button and one oblong coracoidal button connected by nonabsorbable sutures (FiberWire™ No. 5, Arthrex, FL, USA) (Fig. 5), which has been initially described for repair of acute syndesmosis disruptions. Each device is pulled through the tunnel via portal three until the caudal buttons can be completely visualized at the coracoid undersurface. Then, each FiberWire™ loop is pulled cranially so that the buttons flip and lock in horizontal position at the coracoid undersurface (Fig. 6). Through subacromial arthroscopic control, the clavicle is held in reduction and the clavicular buttons are tightened via its pulley system and secured by alternating knots (Fig. 7), so that a reduced secure AC joint is finally achieved.

Fig. 4 ACTR-Drill guide (Arthrex). Notice the pointed caudal end and the positioning sleeve

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Fig. 5 TightRope™ device consists of round titanium clavicular button and long coradoidal button connected by one No. 5 FiberWire™ suture

Fig. 6 The two long coracoid buttons are placed in the anatomical positions on the coracoid undersurface

Fig. 7 Through a minimally invasive approach (3 cm long incision), the AC-J held in reduction while the clavicular buttons are tightened and secured with alternating knots

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Postoperative Rehabilitation The arm is placed in a sling in an adducted and internally rotated position for 6 weeks. Limited range of motion is allowed out of the sling under physiotherapeutic instruction. Exercises to regain strength are initiated once the patient has full, pain-free passive and active range of motion, not before the 7th postoperative week. Return to contact sports activities is allowed after 6 months postoperatively.

Discussion The presented technique is a minimally invasive, arthroscopically assisted approach, leads to an anatomical AC joint reduction, that respects the two individual CC bundles and potentially allows for efficient ligament healing or biologic ligament replacement. This TightRope™ construct is designed to allow anatomic healing of the CC ligaments. It may provide a scaffold to guide this process while maintaining a stable reduction of the AC joint and restore the initial function [17]. This concept is considered the primary goal in ligament reconstruction [10]. A single TightRope™ device might not provide adequate initial stability within the AC joint, though Wellmann et al. described superior early clinical results with utilizing one flib-button device similar to the TightRope™ system [24]. However, the clinical application of a single device might be justified for augmentation in cases where only one of the CC ligaments is ruptured. Walz and Imhoff found in a biomechanical study that the application of two TightRope™ devices for fixation of a complete AC separation results in a significantly higher stability in the supero-inferior as well as the anteroposterior plane when compared to the native CC ligaments [23]. Advantages of this surgical technique, in addition to the immediate two-plane stability, include an arthroscopically assisted approach, which allows for a gold standard diagnostic evaluation of the injured shoulder while avoiding the potential complications associated with traditional open procedures. Tischer and Imhoff found concomitant injuries during AC joint dislocation occur up to 20% of cases [21]. To ensure the local CC ligament healing, this procedure is strictly recommended in fresh injured cases, within 3–4 weeks following the injury, as sufficient healing potential still exists in the surrounding soft tissues. However, in case of chronic AC joint separation, the use of a graft material is justified [9, 20]. It can be coupled with a flip-button device as described by Scheibel et al. to provide an initial mechanical stability [18].

H. El-Azab and A.B. Imhoff

We assume that anatomic healing of the CC ligaments and the corresponding soft tissues is sufficient to restore lasting stability to the AC joint, although the ligaments are not repaired with this technique. Disadvantage of this technique is technically demanding and may be performed only by advanced arthroscopists. Additionally, it does not allow concomitant repair of the deltotrapezoid fascia in types IV through VI AC joint separations, which might be mandatory to restore the horizontal stability.

Our Own Results The outcome of 23 consecutive patients (21 male, 2 female; mean age: 37.5 ± 10.2 years; range, 21–59), who underwent anatomic reduction for an acute AC joint dislocation using two TightRope™ devices, was evaluated clinically and radiographically (Fig. 8), preoperatively as well as 6, 12, and at least 24 months postoperatively. The evaluation included visual analog scale for pain, Constant score [4], simple shoulder test [13], Short Form-36 [3], and the satisfaction scale. There were three Rockwood type III, three type IV, and 17 type V separations. The mean follow-up was 30.6 ± 5.4 months (range, 24–40). The visual analog scale showed significant improvements preoperatively from 4.5 ± 1.9 to 0.25 ± 0.4 and Constant score from 34.3 ± 6.9 to 94.3 ± 3.2 at least 24 months postoperatively. The Short Form-36 was representative of similar significant improvements. In one patient, no redislocation or subluxation has occurred after device removal 6 months postoperatively

Fig. 8 Postoperative radiograph showing the reduced AC-J with the two TightRope™ devices extending between the lateral clavicle and coracoid process

Arthroscopic Double Band AC Joint Reconstruction with Two TightRope™

because of development of infection, and subsequent radiographs displayed continued reduction of the AC joint when compared to pre-removal imaging, which clues an evidence for tissue regeneration and healing surrounding the repair devices. Another disadvantage was observed in our series is the postoperative posterior clavicular displacement, which occurred in 30% of cases. It may be explained through either deficient reconstruction of the deltotrapezoidal fascia, which is ruptured in Rockwood IV and V separations, or inadequate healing of the AC ligaments or both. Our results demonstrate that anatomic placement of suture material within the CC-space provides a satisfactory clinical outcome up to 2 years postoperatively. Long-term follow-up is required to determine if this procedure results in lasting stability.

References 1. Arthrex Inc. (2006) Arthroscopic stabilization of acute acromioclavicular joint dislocation using the TightRope system: Surgical technique. Arthrex, Naples. 2. Baumgarten, K.M., Altchek, D.W., Cordasco, F.A.: Arthroscopically assisted acromioclavicular joint reconstruction. Arthroscopy 22(2), 228 e221–228 e226 (2006) 3. Bullinger, M.: German translation and psychometric testing of the SF-36 Health Survey: preliminary results from the IQOLA Project. International Quality of Life Assessment. Soc. Sci. Med. 41(10), 1359–1366 (1995) 4. Constant, C.R., Murley, A.H.: A clinical method of functional assessment of the shoulder. Clin. Orthop. Relat. Res. 214, 160–164 (1987) 5. Costic, R.S., Labriola, J.E., Rodosky, M.W., et al.: Biomechanical rationale for development of anatomical reconstructions of coracoclavicular ligaments after complete acromioclavicular joint dislocations. Am. J. Sports Med. 32(8), 1929–1936 (2004) 6. Debski, R.E., Parsons, IMt, Fu, F.H., et al.: Effect of capsular injury on acromioclavicular joint mechanics. J. Bone Joint Surg. Am. 83-A(9), 1344–1351 (2001) 7. Deshmukh, A.V., Wilson, D.R., Zilberfarb, J.L., et al.: Stability of acromioclavicular joint reconstruction: biomechanical testing of various surgical techniques in a cadaveric model. Am. J. Sports Med. 32(6), 1492–1498 (2004) 8. Dimakopoulos, P., Panagopoulos, A., Syggelos, S.A., et al.: Doubleloop suture repair for acute acromioclavicular joint disruption. Am. J. Sports Med. 34(7), 1112–1119 (2006) 9. Erak, S., Pelletier, M.H., Woods, K.R., et al.: Acromioclavicular reconstructions with hamstring tendon grafts: a comparative biomechanical study. J. Shoulder Elbow Surg. 17(5), 772–8 (2008)

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10. Fu, F.H., Shen, W., Starman, J.S., et al.: Primary anatomic doublebundle anterior cruciate ligament reconstruction: a preliminary 2-year prospective study. Am. J. Sports Med. 36(7), 1263–1274 (2008). 36 11. Fukuda, K., Craig, E.V., An, K.N., et al.: Biomechanical study of the ligamentous system of the acromioclavicular joint. J. Bone Joint Surg. Am. 68(3), 434–440 (1986) 12. Grutter, P.W., Petersen, S.A.: Anatomical acromioclavicular ligament reconstruction: a biomechanical comparison of reconstructive techniques of the acromioclavicular joint. Am. J. Sports Med. 33(11), 1723–1728 (2005) 13. Lippitt, S.B., Harryman, D.T., Matsen, F.A.: A practical tool for evaluating function: the Simple Shoulder Test. In: Matsen, F.A., Fu, F.H. (eds.) The Shoulder: A Balance of Mobility and Stability, pp. 501–18. The American Academy of Orthopaedic Surgeons, Rosemont (1993) 14. Mazzocca, A.D., Arciero, R.A., Bicos, J.: Evaluation and treatment of acromioclavicular joint injuries. Am. J. Sports Med. 35(2), 316– 329 (2007) 15. Rios, C.G., Arciero, R.A., Mazzocca, A.D.: Anatomy of the clavicle and coracoid process for reconstruction of the coracoclavicular ligaments. Am. J. Sports Med. 35(5), 811–817 (2007) 16. Rockwood, C.A.: Injuries to the acomioclaviculary joint. In: Rockwood, C.A., Green, D.P. (eds.) Fractures in Adults, pp. 860– 910. Lippincott, Philadelphia (1984). 23 17. Salzmann, G.M., Walz, L., Imhoff, A.B., et al.: Arthroscopic anatomical reconstruction of the acromioclavicular joint. Acta Orthop. Belg. 74(3), 397–400 (2008) 18. Scheibel, M., Ifesanya, A., Pauly, S., et al.: Arthroscopically assisted coracoclavicular ligament reconstruction for chronic acromioclavicular joint instability. Arch. Orthop. Trauma. Surg. 128(11), 1327–1333 (2007) 19. Shin, S.J., Yun, Y.H., Yoo, J.D.: Coracoclavicular ligament reconstruction for acromioclavicular dislocation using 2 suture anchors and coracoacromial ligament transfer. Am. J. Sports Med. 37(2), 346–351 (2009) 20. Tauber, M., Gordon, K., Koller, H., et al.: Semitendinosus tendon graft versus a modified Weaver-Dunn procedure for acromioclavicular joint reconstruction in chronic cases: a prospective comparative study. Am. J. Sports Med. 37(1), 181–190 (2009) 21. Tischer, T., El-Azab, H., Imhoff, A.B., et al.: Incidence of associated pathologies with acute acromioclavicular joint dislocations type III-V. Am. J. Sports Med. 37(1), 136–9 (2008) 22. Tomlinson, D.P., Altchek, D.W., Davila, J., et al.: A modified technique of arthroscopically assisted AC joint reconstruction and preliminary results. Clin. Orthop. Relat. Res. 466(3), 639–645 (2008) 23. Walz, L.S.G., Eichhorn, S., Imhoff, A.B., et al.: The anatomic reconstruction of AC joint dislocations using two TightRope devices – a biomechanical study. Am. J. Sports Med. 36(12), 2398–406 (2008) 24. Wellmann, M., Zantop, T., Petersen, W.: Minimally invasive coracoclavicular ligament augmentation with a flip button/polydioxanone repair for treatment of total acromioclavicular joint dislocation. Arthroscopy 23(10), 1132 e1131–1132 e1135 (2007) 25. White, B., Epstein, D., Sanders, S., et al.: Acute acromioclavicular injuries in adults. Orthopedics 31(12), 1219–1226 (2008)

Proximal Biceps Tendon Pathologies Mehmet Demirtaş, Barîş Kocaoğlu, and Mustafa Karahan

Contents

Anatomy

Anatomy ....................................................................................... 193

The long head of the biceps brachii (LHB) originates from the superior glenoid labrum and the supraglenoid tubercle of the scapula. The primary blood supply to the proximal aspect of the tendon is the anterior humeral circumflex artery [3]. The biceps tendon is widest at its origin and progressively narrows as it exits the glenohumeral joint. As the tendon exits the joint, it passes deep to the coracohumeral ligament through the rotator interval, entering the bicipital groove. The capsuloligamentous structures of the rotator interval are responsible for maintaining the biceps tendon within its proper anatomic location as it passes through the groove [9]. Fibers from the supraspinatus and subscapularis fuse to form a sheath that surrounds the tendon at the proximal extent of the groove [27]. The superior glenohumeral ligament arises from the labrum adjacent to the supraglenoid tubercle, inserts onto the superior lateral portion of the lesser tuberosity, and contributes to an anterior sling about the biceps while crossing the floor of the bicipital groove [2, 28, 29]. The coracohumeral ligament has a broad thin origin at the base of the coracoid and blends into the lesser and greater tuberosities about the bicipital groove by two discrete bands [1]. Walsh et al. demonstrated a pulley system about the bicipital groove composed of the coracohumeral ligament and fibers from the subscapularis tendon [32]. This pulley system contributes to biceps stability. Within the groove, the tendon travels beneath the transverse humeral ligament. The distal transverse humeral ligament is not believed to play a primary role in securing the biceps tendon [10]. The biceps tendon makes a 30°–45° turn into the bicipital groove as it exits the glenohumeral joint with the shoulder in neutral rotation. The bicipital groove is formed between the lesser and greater tuberosities with the medial wall made up of the lesser tuberosity [10]. Several anatomical variations of the intra-articular portion of the LHB have been described, including congenital absence, a synovial “mesentery”, fusion with the rotator cuff, and bifid tendons. These are all rare and of unknown clinical relevance [1, 10]. Equally, the origin from the supraglenoid

Function ....................................................................................... 194 Pathology ..................................................................................... 194 Biceps Tendon Degeneration and Inflammation ........................... 194 Instability and Lesions .................................................................. 195 Diagnosis and Imaging ............................................................... 195 Treatment ..................................................................................... 196 Nonoperative Treatment................................................................ 196 Operative Treatment...................................................................... 197 Postoperative Care ...................................................................... 198 Conclusion ................................................................................... 198 References .................................................................................... 198

M. DemirtaĜ ( ) Orthopaedics and Traumatology, Ankara University Faculty of Medicine, Ibni Sina Hastanesi, Cebeci, Ankara, Turkey e-mail: [email protected] B. KocaoÜlu Orthopaedics and Traumatology, Acibadem University Faculty of Medicine, Soyak Evreka. A1 blok D:43. Soganlik, Kartal, 34880 Istanbul, Turkey e-mail: [email protected], [email protected] M. Karahan Orthopaedics and Traumatology, Marmara University Faculty of Medicine, Ciftehavuzlar, cemil topuzlu cad. No:37, daire:2, Kadikoy, Istanbul, Turkey e-mail: [email protected], [email protected]

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tubercle and glenoid labrum is variable, but again is of unknown clinical relevance, apart from as a cause of diagnostic confusion at arthroscopy [1, 10].

Function The primary function of the biceps muscle is flexion of the elbow and supination of the forearm. At the shoulder, it has been shown to be a weak abductor only with the arm in external rotation [15]. The tendon’s role as a humeral head depressor and in glenohumeral stability is also highly debated. Several authors theorize that the tendon is a depressor of the humeral head [20]. Superior migration of the humeral head has been shown to occur when the proximal attachment of the tendon is released [1, 33]. It has also been postulated that the lesions in the pulley system lead to instability of the long head of the biceps tendon, allowing for anterior translation and upward migration of the humeral head [14]. Hypertrophy of the tendon is more likely to be a result of tendinosis than of functional hypertrophy. The primary function of the biceps is at the elbow, where it acts as a flexor and a supinator. There has been recent interest in its role in glenohumeral stability, especially following the description of SLAP lesions [7]. This has been studied mostly in the context of the throwing athlete [13, 15]. Anterior instability leads to increased activity in the muscle on electromyography, indicating the possible role of the biceps as a secondary glenohumeral stabilizer. However, the magnitude of this function is likely to be small. Disorders of the biceps tendon can be classified into degenerative, inflammatory, mechanical, and traumatic or sports related, but such a classification is arbitrary, and different pathologies may coexist. Although isolated pathology of the biceps does exist, it is commonly associated with abnormalities of the cuff and labrum.

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been thought to account for only 5% of biceps tendonitis [25]. Inflammation may occur with abnormalities of the bicipital groove, often from trauma, causing a severe synovitis leading to attrition of the tendon and stenosis of the groove [23]. A shallow or narrow groove may predispose an athlete to tendinitis, as do osteophytes along the supratubercular ridge. Shallow or oblique groove walls can increase the propensity for tendon subluxation and inflammation [15, 23]. As tendonitis progresses, tendon fraying may occur with rupture possible in long-standing cases (Fig. 1). This secondary deterioration of the biceps tendon lacks a true inflammatory component, hence the term “tendinosis” is more appropriate. Microscopic changes including atrophy of collagen fibers, fissuring, fibrinoid necrosis, and fibrocyte proliferation are commonly seen [15, 23]. Owing to the location of the biceps tendon in the rotator interval, one of the major causes of biceps degeneration is mechanical irritation of the tendon against the coracoacromial arch. As a result of repetitive wear, the soft tissue restraints surrounding the biceps tendon might lose their stabilizing function and subluxation or dislocation may occur [16]. Secondary biceps tendinitis occurs with associated pathologic changes in the adjacent structures of the shoulder. This is often a result of impingement syndromes. The high incidence of chronic degenerative changes found in the biceps tendon may be seen concomitantly with rotator cuff pathology [16]. In a study of 122 complete rotator cuff tears, Chen and colleagues also found that 76% of the tears were associated with pathology of the long head of the biceps, including all chronic tears. Tears greater than 5 cm were associated with more advanced biceps lesions [6]. Toshiaki studied 14 cadaver shoulders showing that hypertrophy of the tendon near the bicipital groove was associated with rotator cuff tears [27]. Conversely, Carpenter studied 14 cadaver shoulders and found no change in the cross-sectional biceps tendon area or material properties with a rotator cuff tear [5]. Boileau et al. have described an hourglass-shaped biceps tendon that may cause mechanical symptoms and anterior-based

Pathology Biceps Tendon Degeneration and Inflammation Biceps tendonitis is inflammation of the long head of the biceps tendon in or about the intertubercular groove. Tendon irritation commonly occurs in conjunction with other pathologic changes in the glenohumeral joint. Primary, or isolated, biceps tendinitis is due to inflammation of the long head of the biceps within the intertubercular groove or changes in the groove without any associated pathologic changes in the shoulder. It can be considered as a tenosynovitis, with inflammation of the sheath rather than the tendon itself. This entity has

Fig. 1 Arthroscopic view shows tendon fraying of biceps tendon, which may lead to rupture in long-standing cases

Proximal Biceps Tendon Pathologies

shoulder pain [4]. The configuration results from an irritated inflamed and thickened intra-articular segment of tendon. This thickened aspect may block tendon excursion during shoulder motion, as it cannot slide through the bicipital groove [10]. Mechanical locking may occur with loss of forward elevation. A static loss of terminal forward flexion may be seen even under anesthesia. The thickened tendon may disrupt the stabilizing structures of the rotator interval and lead to biceps instability over time [10].

Instability and Lesions Lesions of the biceps pulley system lead to instability of the long head of the biceps [23]. They may occur in isolation or in association with other pathology. Rotator cuff lesions, along with lesions of the biceps pulley, are thought to be associated with an internal anterosuperior impingement of the shoulder. Habermeyer found that almost 90% of patients with arthroscopically diagnosed pulley lesions (superior glenohumeral ligament, supraspinatus, and subscapularis) also had pathology of the long head of the biceps tendon, including synovitis, subluxation, dislocation, and partial or complete tears [4]. Internal anterosuperior impingement was seen in 44% of the patients with pulley tears and involvement of the long head of the biceps and more often in patients with acromioclavicular arthritis [4]. In a study of 200 rotator cuff tears, Lafosse reported a 45% incidence of biceps stability, with 16% anterior instability, 19% posterior instability, and 10% both anteroposterior instability [17]. He found that anterior instability was associated with subscapularis tears, whereas posterior instability was found in conjunction with supraspinatus tears. Rotator cuff tear size also correlated with the extent of long head biceps instability and lesions. Most ruptures of the long head of the biceps tendon are due to a degenerative process. In the case of a spontaneous rupture, the “Popeye” sign may be present, although autotenodesis can occur as fibrous bands fix a dislocated or hypertrophic tendon to the subscapularis or within the groove. Isolated pathology of the LHB is most commonly found in the younger, sporting population, especially in throwing athletes, gymnasts, swimmers, and participants in contact sports and martial arts. The LHB is subject to large forces of acceleration and deceleration in the throwing movement, as well as torsion and shearing, especially when coupled with forced flexion of the elbow or forearm supination. Type 2 SLAP lesions affect the biceps anchor, and type 4 lesions extend into the body of the tendon of LHB [21]. Equally, anterosuperior internal impingement as described by Gerber and Sebesta could lead to bicipital tendonitis and pulley lesions [12].

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Diagnosis and Imaging Pain related to pathology of the biceps tendon is located mainly at the anterior part of the shoulder, often at the bicipital groove. Pain at rest, night pain, and pain on rotation are common. The pain may also radiate down the arm and muscle belly, sometimes reaching the radial aspect of the hand, but lacks a precise distribution. Patients may also describe paresthesia in this distribution. This referred pain should not be confused with brachalgia, but may require investigation to exclude a cervical cause. Comparative palpation of the bicipital groove is often useful and is felt most easily in 10° of internal rotation [5]. In dislocations of the LHB, the tenderness is more medial on the lesser tuberosity, and the tendon can sometimes be rolled under the fingers. Several provocative tests have been described for isolating pathology of the LHB, including Yergason’s test, Speed’s test, and the biceps instability test (Fig. 2). For the diagnosis of SLAP lesions, the most common clinical tests are the O’Brien test and the abduction external rotation supination test. However, recent literature has shown that none of these tests is specific enough in isolation to confirm the diagnosis of biceps or superior labral pathology [1, 18, 26]. Patients with a dislocation of the LHB may present with a very typical clinical picture. Dislocation is often traumatic and almost always associated with a tear of the upper subscapularis. The patient presents with a loss of active

Fig. 2 Yergason’s test is one of the provocative tests that have been described for isolating pathology of the long head of biceps tendon

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elevation above 90°, and it is common to find a limitation of active and passive external rotation because the dislocated biceps tendon restrains the inferior part of the subscapularis. The clinical sign of a hypertrophied and entrapped “hourglass biceps” is a limitation of the terminal 10°–20° of active and passive elevation. This corresponds to a true mechanical locking of the shoulder [4]. Plain radiography is of limited benefit in the diagnosing of abnormality of the LHB. The exceptions to this are the presence of calcification in the bicipital groove and bony deformity caused by fracture or osteophytes. Cystic change in the lesser tuberosity is also a sign of tendinosis, or a tear of the upper subscapularis tendon, and may be associated with lesions of the pulley system. Arthrography and CT arthrography were probably the first imaging techniques to identify pathology reliably; rupture and dislocation are readily identified. Static subluxations and SLAP tears are well visualized by CT in conjunction with arthrography [1]. MRI is the most widely used method of imaging the rotator cuff. However, the agreement between MRI and arthroscopic findings has been shown to be poor, at only 60%, with a concordance of only 37% in diagnosing pathology in the biceps tendon [19]. The use of MR arthrography is preferable for detecting lesions of the biceps and the pulley system and is the best choice for SLAP lesions (Fig. 3). Ultrasound has shown an overall sensitivity of 49% and a specificity of 97%. However, it was poor at diagnosing intraarticular partial tears of the tendon. Currently, the definitive diagnosis of pathology of the LHB is still made at arthroscopy. It is an essential part of a diagnostic routine to draw the LHB into the joint to examine the portion within the bicipital groove. A dynamic

Fig. 3 T2 weighted MRI arthrography section shows SLAP lesion of shoulder, which is preferable for detecting lesions of the biceps and the pulley system and is the investigation of choice for SLAP lesions

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Fig. 4 Dry shoulder arthroscopy picture shows SLAP lesion, which is sometimes helpful to explore the hidden pathologies

examination of the tendon should be performed, which involves visualization of the tendon arthroscopically, while the shoulder is elevated and rotated with the elbow extended, to demonstrate an hourglass tendon or subtle instability, as well as demonstrating “hidden lesions” of the subscapularis more accurately. This dynamic visualization is an advantage of the “beach chair” position for shoulder arthroscopy. Dry arthroscopy could be sometimes helpful to explore the hidden pathologies. Sometimes pressure of the arthropump and irrigation solution can cover up lesions (Fig. 4).

Treatment Nonoperative Treatment The initial treatment of primary bicipital tendonitis is nonoperative. Rest, activity modification, ice, nonsteroidal antiinflammatory drugs, and sometimes immobilization are known as treatment methods. Physical therapy, working on strengthening the rotator cuff, deltoid, and parascapular muscles, may be started as pain subsides. Range of motion exercises concentrating on rotation should be an important part of the therapy protocol. A combination of corticosteroid and local anesthetic injection may be of value for diagnosis, injected into the subacromial space if rotator cuff pathology is suspected. A 2 mL of this may be injected anteriorly along the bicipital groove at the point of maximal tenderness, taking care to avoid intrasubstance injection into the actual tendon [24]. Ultrasound may improve the accuracy of injection, but adhesions or synovitis within the groove may prevent effectiveness of the injection [5]. Postinjection examination and symptom relief can direct diagnosis. The risk of biceps tendon rupture should be advised. Following injection, activity restriction for the next 1–2 weeks is advised before a course of physical therapy.

Proximal Biceps Tendon Pathologies

Operative Treatment If nonoperative treatment is unsuccessful, surgical intervention may be warranted. Surgical management is usually withheld for at least a 3–6-month trial of conservative treatment. Surgical alternatives in treating biceps pathology include debridement, resection of diseased tendon, tenotomy, or tenodesis. Patient age, activity level, athletic participation, goals, arm dominance, and willingness to tolerate nonoperative management must be taken into consideration when deciding on surgical treatment.

Debridement Grade I fraying is minor and involves less than 25% of the fibers. Grade II involves less than 50% of the tendon. Arthroscopic debridement is a successful treatment option for grades I to II fraying of the long head of the biceps tendon when it is isolated or combined with minimal associated pathology in the shoulder (Fig. 5). Grade III is greater than 50% of the tendon, whereas grade IV is a complete tendon rupture. Grades III and IV may be treated with subacromial decompression and biceps tenodesis. Debridement may be used, for example, on a young athlete with less than 50% fraying of the tendon fibers and minimal involvement of the rotator cuff [15].

Biceps Tenotomy and Tenodesis Open tenodesis has been the preferred surgical treatment for biceps pathology, and a variety of techniques have been described. The most reliable and mechanically sound procedure has been the keystone or the keyhold technique and simple suture fixation to the transverse humeral ligament or the tendon of pectoralis major [11]. Tenotomy may produce the classic “Popeye” sign, although reports show little

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clinical difference between the two techniques and as few as 40% of patients will notice the cosmetic deformity [22]. In some cases, hypertrophy, adhesions, and stenosis in the groove produce an “autotenodesis”, preventing retraction of the tendon. Prolonged ache in the belly of the biceps muscle is an uncommon long-term complication of tenotomy and has been described in association with tenodesis [4]. The loss of strength at the elbow resulting from rupture has been put at 20% of forearm supination and 8–20% of elbow flexion [4]. Elderly patients with low functional demand are candidates for tenotomy, whereas younger patients, manual workers, and patients who may object to a cosmetic deformity are more suitable for tenodesis. Acromioplasty has been carried out in association with a biceps tenotomy or tenodesis. Recent studies have found that associated acromioplasty has little or no additional value. In the series of 307 patients followed between 2 and 14 years, concomitant acromioplasty was beneficial only in patients who had a normal acromiohumeral interval (>7 mm) and an isolated supraspinatus tear [4]. Other patients did not benefit from acromioplasty, and indeed it may be detrimental in patients with preoperative proximal migration of the head of the humerus [31].

Arthroscopic Tenotomy of the Biceps This was described in the French literature in 1990. The clinical observation showed that spontaneous rupture of the LHB could alleviate pain in rotator cuff disease. Arthroscopic tenotomy was preferred as a simple and reproducible technique in patients with massive, irreparable tears of the rotator cuff [31]. This has now become an accepted and common arthroscopic intervention. In the study, tenotomy led to an average decrease of only 1.3 mm in the acromiohumeral space. Fatty infiltration and atrophy of the remaining rotator cuff do compromise the results of arthroscopic biceps tenotomy [31]. The results confirmed the efficacy of this simple procedure, with or without treatment of concomitant pathology [31].

Arthroscopic Tenodesis of the Biceps

Fig. 5 Arthroscopic debridement of grade II fraying of the biceps tendon

This is becoming more popular with increasing operative experience. Fixation methods have advanced with new techniques and implants and can be performed using the soft tissue or bone. The authors prefer to use an arthroscopic technique of soft tissue tenodesis to the subscapularis or rotator cuff for most patients if these structures are intact. Otherwise, tenodesis is performed with a mini-open subpectoral approach and a bio-tenodesis screw, especially in younger, high athletic, or occupational demand patients.

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The site of tenodesis should be the intertubercular groove of the humerus. Other locations are nonanatomical and nonphysiological and can potentially cause dysfunction of the shoulder and pain. When a soft-tissue biceps tenodesis is performed in the rotator interval, it is frequently associated with subluxation and will thicken and scar the rotator interval [8]. Attachment of the LHB to the coracoid process or the conjoint tendon as proposed in the past with open surgery, and more recently with arthroscopy, also changes the course of the tendon and may produce pain caused by traction or adhesions under the insertion of pectoralis major [30]. In addition, the increased proximal force on the humerus may contribute to subacromial impingement. Attaching the tendon to the greater tuberosity has also been proposed, but this can produce a prominence which will impinge on the acromial arch. The biceps tendon should never be tenodesed in the groove and left attached to the scapula, as this leads to an iatrogenic entrapment of the LHB [1]. The intra-articular portion of the biceps lying above the transverse ligament must always be resected. Finally, fixation to the pectoralis major tendon is simple but may produce pain by a cross-pull on that tendon [15]. Arthroscopic tenodesis to bone has also been shown to be successful. The technique again marks the biceps tendon with a suture, but release is more distal, near the supraspinatus. The proximal portion of the tendon is exteriorized and sutured to be placed back into a predrilled bone tunnel within the bicipital groove for both the tendon and biotenodesis screw.

Postoperative Care The postoperative protocol following treatment of biceps tendon pathology is dependent on an isolated or concomitant surgical procedure. Rest, ice, and anti-inflammatory drugs may be used in all protocols as needed for symptomatic relief [15]. If an isolated simple tenotomy is performed, patients may have unrestricted range of motion and activities limited by their symptoms. If a biceps tenodesis is performed alone, the patient is placed in a sling for 4 weeks postoperatively with exception for moderate activities of daily living and range of motion to prevent stiffness [15]. They must strictly abstain from active elbow flexion and forearm supination to avoid overloading the repair. Strengthening may begin at approximately 6–8 weeks postoperatively. Return to athletics should be appropriately started at 3–6 months postoperatively [15]. If a concomitant procedure is performed, such as rotator cuff repair or supraspinatus repair, then postoperative protocol takes precedence. Full range of motion should be included if tenotomized, or elbow flexion and forearm supination should be avoided if tenodesis is performed.

M. Demirtaş et al.

Conclusion Pathology of the LHB is increasingly recognized as an important cause of shoulder pain and dysfunction. However, it is still not completely understood, and the diagnosis is both clinically and radiologically indefinite. Dynamic arthroscopic examination of the shoulder has transformed our understanding of and approach to treatment for conditions of the LHB. Biceps tenotomy and tenodesis are options for the surgical treatment of a pathologic biceps condition. Factors that need to be taken into account when choosing between tenotomy and tenodesis are the activity expectations of the patient, the importance of the cosmetic result, and patient compliance. As it now recognized that the functional role of the LHB tendon at the shoulder is limited, surgeons should be aware that retaining a pathological tendon has a more negative functional consequence than the loss of the tendon itself.

References 1. Ahrens, P.M., Boileau, P.: The long head of biceps and associated tendinopathy. J. Bone Joint Surg. Br. 89(8), 1001–1009 (2007) 2. Barber, F.A., Field, L.D., Ryu, R.K.: Biceps tendon and superior labrum injuries: decision making. Instr. Course Lect. 57, 527–538 (2008) 3. Burkhead, W.Z., Arcand, M.A., Zeman, C., et al.: The biceps tendon. In: Rockwood, C.A., Matsen, F.A., Wirth, M.A., et al. (eds.) The Shoulder, vol. 2, 3rd edn, pp. 1059–1119. WB Saunders, Philadelphia (2004) 4. Boileau, P., Ahrens, P.M., Hatzidakis, A.M.: Entrapment of the long head of the biceps tendon: the hourglass biceps a cause of pain and locking of the shoulder. J. Shoulder Elbow Surg. 13, 249–257 (2004) 5. Carpenter, J.E., Wening, J.D., Mell, A.G., et al.: Changes in the long head of the biceps tendon in rotator cuff tear shoulders. Clin. Biomech. 20, 162–165 (2005) 6. Chen, C.H., Hsu, K.Y., Chen, W.J., et al.: Incidence and severity of biceps long head tendon lesion in patients with complete rotator cuff tears. J. Trauma 58, 1189–1193 (2005) 7. Curtis, A.S., Snyder, S.J.: Evaluation and treatment of biceps tendon pathology. Orthop. Clin. North Am. 24(1), 33–43 (1993) 8. Elkousy, H.A., Fluhme, D.J., O’Connor, D.P., Rodosky, M.W.: Arthroscopic biceps tenodesis using the percutaneous, intra-articular trans-tendon technique: preliminary results. Orthopaedics 28, 1316–1319 (2005) 9. Favorito, P.J., Harding, W.G., Heidt, R.S.: Complete arthroscopic examination of the long head of the biceps tendon. Arthroscopy 17, 430–432 (2001) 10. Friedman, D.J., Dunn, J.C., Higgins, L.D., Warner, J.J.: Proximal biceps tendon: injuries and management. Sports Med. Arthrosc. 16(3), 162–169 (2008) 11. Froimson, A.I., Oh, I.: Keyhole tenodesis of biceps origin at the shoulder. Clin. Orthop. 112, 245–249 (1975) 12. Gerber, C., Sebesta, A.: Impingement of the deep surface of the subscapularis tendon and reflection pulley on the antero-superior glenoid rim: a preliminary report. J. Shoulder Elbow Surg. 9, 483– 490 (2000) 13. Glueck, D.A., Mair, S.D., Johnson, D.L.: Shoulder instability with absence of the long head of the biceps tendon. Arthroscopy 19, 787–789 (2003)

Proximal Biceps Tendon Pathologies 14. Habermeyer, P., Magosch, P., Pritsch, M., et al.: Anterosuperior impingement of the shoulder as a result of pullet lesions: a prospective arthroscopic study. J. Shoulder Elbow Surg. 13, 5–12 (2004) 15. Hsu, S.H., Miller, S.L., Curtis, A.S.: Long head of biceps tendon pathology: management alternatives. Clin. Sports Med. 27(4), 747– 762 (2008) 16. Kuhn, J.E., Lindholm, S.R., Huston, L.J., et al.: Failure of the biceps superior labral complex: a cadaveric biomechanical investigation comparing the late cocking and early deceleration positions of throwing. Arthroscopy 19, 373–379 (2003) 17. Lafosse, L., Reiland, Y., Baier, G.P., et al.: Anterior and posterior instability of the long head of the biceps tendon in rotator cuff tears: a new classification based on arthroscopic observations. Arthroscopy 23, 73–80 (2007) 18. McFarland, E.G., Kim, T.K., Savino, R.M.: Clinical assessment of three common tests for superior labral antero-posterior lesions. Am. J. Sports Med. 30, 810–815 (2002) 19. Mohtadi, N.G., Vellet, A.D., Clark, M.L., et al.: A prospective, double-blind comparison of magnetic resonance imaging and arthroscopy in the evaluation of patients presenting with shoulder pain. J. Shoulder Elbow Surg. 13, 258–265 (2004) 20. Neer II, C.S.: Anterior acromioplasty for the chronic impingement syndrome in the shoulder. J. Bone Joint Surg. Am. 87, 1399 (2005) 21. Nam, E.K., Snyder, S.J.: The diagnosis and treatment of superior labrum, anterior and posterior (SLAP) lesions. Am. J. Sports Med. 31(5), 798–810 (2003) 22. Osbahr, D.C., Diamond, A.B., Speer, K.P.: The cosmetic appearance of the biceps muscle after long-head tenotomy versus tenodesis. Arthroscopy 18, 483–487 (2002) 23. Patton, W.C., McCluskey III, G.M.: Biceps tendinitis and subluxation. Clin. Sports Med. 20(3), 505–529 (2001) 24. Ryu, J.H., Pedowitz, R.A.: Rehabilitation of biceps tendon disorders in athletes. Clin. Sports Med. 29(2), 229–246 (2010)

199 25. Sethi, N., Wright, R., Yamaguchi, K.: Disorders of the long head of the biceps tendon. J. Shoulder Elbow Surg. 8(6), 644–654 (1999) 26. Tennent, T.D., Beach, W.R., Meyers, J.F.: A review of the special tests associated with shoulder examination: part II: laxity, instability, and superior labral anterior and posterior (SLAP) lesions. Am. J. Sports Med. 31, 301–307 (2003) 27. Tuoheti, Y., Itoi, E., Minagawa, H., et al.: Attachment types of the long head of the biceps tendon to the glenoid labrum and their relationships with the glenohumeral ligaments. Arthroscopy 21, 1242– 1249 (2005) 28. Toshiaki, A., Itoi, E., Minagawa, H., et al.: Cross-sectional area of the tendon and the muscle of the biceps brachii in shoulders with rotator cuff tears: a study of 14 cadaveric shoulders. Acta Orthop. 76, 509–512 (2005) 29. Vangsness Jr., C.T., Jorgenson, S.S., Watson, T., Johnson, D.L.: The origin of the long head of the biceps from the scapula and glenoid labrum: an anatomical study of 100 shoulders. J. Bone Joint Surg. Br. 76-B, 951–954 (1994) 30. Verma, N.N., Drakos, M., O’Brien, S.J.: Arthroscopic transfer of the long head biceps to the conjoint tendon. Arthroscopy 21, 764 (2005) 31. Walsh, G., Edwards, B.E., Boulahia, A., et al.: Arthroscopic tenotomy of the long head of the biceps in the treatment of rotator cuff tears: clinical and radiographic results of 307 cases. J. Shoulder Elbow Surg. 14, 238–246 (2005) 32. Walsh, G., Nove-Josserand, L., Levigne, C., et al.: Tears of the supraspinatus tendon associated with “hidden” lesions of the rotator interval. J. Shoulder Elbow Surg. 3, 353–360 (1994) 33. Warner, J.J.P., McMahon, P.J.: The role of the long head of the biceps brachii in superior stability of the glenohumeral joint. J. Bone Joint Surg. Am. 77, 336–372 (1995)

Rehabilitation and Return to Sports After Conservative and Surgical Treatment of Upper Extremity Injuries Kumaraswami R. Dussa

Introduction

Contents Introduction ................................................................................. 201 The Body’s Healing Process ....................................................... 201 Two Stages to the Healing Process ............................................... 202 During the Acute Phase ................................................................ 202 What Are Sports Injuries? ......................................................... 202 Common Types of Sports Injuries ................................................ 202 What Does Return to Play Mean? ............................................. Injury-Recovery Risk .................................................................... Before Making a Return to Your Sport ......................................... Unique and Different Concept ......................................................

202 202 202 202

What Should I Do If I Suffer an Injury? .................................. 202

No matter what sport you participate in, there will come a time when you pick up an injury. Knowing how to treat the injury, ensuring. that the right therapy is employed, and having the injury properly assessed, will all help in making the recovery process a lot quicker [1]. What may seem like a slight muscle twinge can sometimes develop into something a bit nastier if you decide to play on with the injury. As the body gets tired and fatigue sets in, more strain is placed on the muscles and the slight pain you felt earlier could develop into a tear or strain.

Return to Play: Making the Tough Decisions ........................... 202 It Is a Multidisciplinary Problem .............................................. So Whom Should You Listen To? ................................................. Who Has the Answers? ................................................................. Clearance Decisions ......................................................................

203 203 203 203

Understand the Patient and Sports ........................................... 203 What We Can Learn from the Pros........................................... 203 Tips from the Pros to Speed Up Your Recovery....................... 203 Components of Training ............................................................... 204 Proper Conditioning Aids Injury Recover Time ........................... 204 Sports Injuries Depend on the Type of Sports ......................... 204 Factors .......................................................................................... 204 Guidelines for Safe Return to Sports ........................................ 204 How to Speed Up Injury Recovery Time .................................. 205 Some Examples of Upper Limb Postsurgery Rehabilitation Protocol .................................................. 205 Arthroscopic Anterior Stabilization .............................................. 205 Milestones .................................................................................... 205 Shoulder SLAP Repair.................................................................. 205 References .................................................................................... 206

K.R. Dussa Department of Orthopaedics, B Y L Nair Charitable Hospital and T N Medical College, 1/31, Ganesh Co-operative Society, Shivaji Nagar, Dr. Annie Besant Road, 400030 Worli, Mumbai, Maharashtra, India e-mail: [email protected], [email protected]

The Body’s Healing Process From the moment a bone breaks or a ligament tears, your body goes to work to repair the damage. At the moment of injury: Chemicals are released from damaged cells, triggering a process called inflammation. Blood vessels at the injury site become dilated; Blood flow increases to carry nutrients to the site of tissue damage. Within hours of injury: White blood cells (leukocytes) travel down the bloodstream to the injury site where they begin to tear down and remove damaged tissue, allowing other specialized cells to start developing scar tissue. Within days of injury: Scar tissue is formed on the skin or inside the body. The amount of scarring may be proportional to the amount of swelling, inflammation, or bleeding within. In the next few weeks, the damaged area will regain a great deal of strength as scar tissue continues to form. Within a month of injury: Scar tissue may start to shrink, bringing damaged, torn, or separated tissues back together. However, it may be several months or more before the injury is completely healed. As a result, the injury site becomes tight or stiff, and damaged tissues are at risk of reinjury. That is why stretching and strengthening exercises are so important. You should continue to stretch the muscles daily as the first part of your warm-up before exercising.

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Two Stages to the Healing Process

Injury-Recovery Risk

Physical and the Psychological

When an individual returns before adequate healing and recovery, he or she can risk a reinjury and possibly a longer rehabilitation. When dealing with sports injuries, employment of the right game plan from

Even if your physical injuries may have healed, you have to make sure you are mentally ready to start playing again. Mental confidence and toughness of the patient plays a vital role for return to sports.

s Early diagnosis s Prompt treatment s Full functional rehabilitation

During the Acute Phase

can often safely accelerate an athlete’s return to play [2]

The emphasis should be on minimizing swelling and decreasing inflammation. This involves the RICE formula (R = Rest, I = Ice, C = Compression, E = Elevation), together with restricting activities. Depending on your injury, treatment may also involve surgery, bracing, or casting. Do not wait until your injury is healed to get back into shape. In the second phase of recovery, the athlete should work on regaining full motion and strength of the injured limb or joint. A specific plan should be outlined by a physician, physical therapist, or a certified athletic trainer.

Before Making a Return to Your Sport

What Are Sports Injuries? The term sports injury, in the broadest sense, refers to the kinds of injuries that most commonly occur during sports or exercise. Some sports injuries result from accidents, others are due to poor training practices, improper equipment, lack of conditioning, or insufficient warm-up and stretching.

s At least be at a minimum level of fitness s Have the confidence to perform s Be sure that you can compete without the risk of causing further injury, or damage to the injured area.

Unique and Different Concept s s s s

Every individual is unique and different Every injury is unique and different Every sport is unique and different In a team event, every sportsman’s role is unique and different

When are you willing to go back to the same sport that caused the injury? You can prevent REINJURY by holding yourself back in the early stages of a comeback. Prepare a schedule based on the following rules of thumb; then add nonimpact cross-training for extra conditioning.

Common Types of Sports Injuries

What Should I Do If I Suffer an Injury?

s Muscle sprains and strains s Tears of the ligaments that hold joints together s Tears of the tendons that support joints and allow them to move s Dislocated joints s Fractured bones, including vertebrae

Whether an injury is acute or chronic, there is never a good reason to try to “work through” the pain of an injury. When you have pain from a particular movement or activity, STOP! Continuing the activity only causes further harm.

What Does Return to Play Mean? Return to play refers to the point in recovery after an injury or surgery when an athlete is able to participate in their sport or activity at a level similar to that before the injury or the surgery took place.

Return to Play: Making the Tough Decisions s “When can I play again?” is a question sports medicine physicians are familiar with. s Those who ask this question are often seeking a definitive answer and usually hoping for a quick return to boot. s Unfortunately, medicine is not always a craft practiced in black and white but is often an art with a palette in several shades of gray [4].

Rehabilitation and Return to Sports After Conservative and Surgical Treatment of Upper Extremity Injuries

s These shades of gray appear not only in the diagnosis and treatment of medical conditions, but also in the return-toplay decisions that physicians make

It Is a Multidisciplinary Problem

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s Though our active patients’ return-to-play issues are difficult, they correctly remain in the domain of primary care physicians in conjunction with appropriate consultants s If your patient is seen by a consultant who is not familiar with his or her exercise regimen, consider asking the consultant specific questions for the patient or explaining what the patient’s athletic endeavors require.

And all these factors play a pivotal role: s Professional life span of the athlete is very short s Parents do not always put health risks in perspective s The image of highly paid professional athletes, combined with more professional sports opportunities for men and women and the growing number of organized sports for children, can create pressure on young athletes to excel and “specialize” s Concept of “the big game”, if doing so might help his or her athletic prospects s Fear of losing the place s In addition, “playing through pain” is an image many athletes, even junior high athletes, strive to emulate s Media: playing despite injury, sending wrong unfortunate message

So Whom Should You Listen To? s s s s s s

Coach Physiotherapist Sports Physician Orthopedic Surgeon Colleagues Yourself: your body

Who Has the Answers? It is important to recognize that often the answers are based on popular opinion and personal experience, because longterm clinical outcome data are scarce or nonexistent. Returning too soon can increase the risk of reinjury or lead to a chronic problem that will involve a longer recovery. Waiting too long, however, can lead to unnecessary de-conditioning [5].

Understand the Patient and Sports Each patient has his or her specific concerns. Treat each patient as an individual. Do not assume that an athlete wants to play. You may be surprised to hear the answer, but you will not know unless you ask. Consider the sport, level, and goals, as well as the disease or condition. Evaluate the risks of return to play and, if any of them is significant, rethink the decision to allow an athlete to play. We are not in a competition to see who can return an athlete to competition fastest. Our responsibility is to help patients resume activities safely. To do so, we must understand how exercise will affect the injury or illness and how the condition will affect participation. No one likes to be sidelined with an injury. One of the goals of sports medicine is to enable an athlete to participate in his or her sport as soon as possible.

What We Can Learn from the Pros Why does it seem that professional athletes return to play so much faster than recreational athletes? Professional athletes are usually in tremendous physical condition at the time of their injury. This fitness level helps them in many ways. Studies have shown that good conditioning can not only prevent injuries, but also lessen the severity of an injury and help speed up recovery. Professional athletes usually get prompt treatment after an injury. This lessens the acute phase of the injury. Early treatment often means less swelling and stiffness and loss of muscle tone. In addition, the pros work extremely hard with a physical therapist and/or a certified athletic trainer during their recovery.

Clearance Decisions

Tips from the Pros to Speed Up Your Recovery

s Always put the patient first s Understand the medical or musculoskeletal problem s If the issue is unclear or more information is needed, seek consultation

s Maintain year-round balanced physical conditioning s Make sure that injuries are recognized early and treated promptly s Participate in a full functional rehabilitation program

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s Stay fit while injured s Keep a positive, upbeat attitude

Components of Training s Duration s Frequency s Intensity Each step should be outlined and monitored by your physician and your physical therapist. Once your range of motion is fairly good, you can start doing gentle stretching and strengthening exercises. When you are ready, weights may be added to your exercise routine to further strengthen the injured area. The key is to avoid movement that causes pain. No matter what type of injury you have there are normally alternative exercises that can be done while still resting the injured area [6].

Proper Conditioning Aids Injury Recover Time One thing that can improve your recovery from an injury is a high level of conditioning prior to injury. Not only will being in great shape reduce your risk of injury and lessen the severity of an injury, but it also has been shown to reduce recovery time. Rest: Although it is important to get moving as soon as possible, you must also take time to rest following an injury. All injuries need time to heal; proper rest will help the process. Proper balance between rest and rehabilitation is essential Cold/cryotherapy: Ice packs reduce inflammation by constricting blood vessels and limiting blood flow to the injured tissues. Cryotherapy eases pain by numbing the injured area. It is generally used for only the first 48 h after injury. Heat/thermotherapy: Heat, in the form of hot compresses, heat lamps, or heating pads, causes the blood vessels to dilate and increases blood flow to the injury site. Increased blood flow aids the healing process by removing cell debris from damaged tissues and carrying healing nutrients to the injury site. Heat also helps to reduce pain. It should not be applied within the first 48 h after an injury. Electro stimulation: Mild electrical current provides pain relief by preventing nerve cells from sending pain impulses to the brain used to decrease swelling, and to make muscles in immobilized limbs contract, thus preventing muscle atrophy and maintaining or increasing muscle strength. Ultrasound: High-frequency sound waves produce deep heat that is applied directly to an injured area. Ultrasound stimulates blood flow to promote healing.

K.R. Dussa

Massage: Manual pressing, rubbing, and manipulation soothe tense muscles and increase blood flow to the injury site. Targeted pain relief: Medicated patches can be applied directly to the injury site.

Sports Injuries Depend on the Type of Sports s The shoulder is the second most frequently injured joint after the knee s Of all the sports, rugby has the highest risk per player/ hour of injury s The shoulder comprises 20% of all rugby injuries s Thirty-five percent of all injuries of the shoulder are recurrent injuries, and if a player has sustained an injury of one shoulder, there is a higher likelihood of the player sustaining an injury of the other shoulder [3] s The maneuver most strongly associated with shoulder injuries is the tackle, accounting for 49% of injury episodes in rugby matches s Other sports involving throwing and sudden movement (cricket, baseball, volley ball, tennis)

Factors s s s s s s

Types of injuries Mechanisms of injury Conservative Treatment Surgical treatment (Different methods) Rehabilitation Preinjury patient conditioning

Patient’s physical and psychological status

Guidelines for Safe Return to Sports s You are pain free s You have no swelling s You have full range of motion (compare the injured part with the uninjured opposite side) s You have full or close to full (90%) strength (compare with the uninjured side) s For upper body injuries – you can perform throwing movements with proper form and no pain s Keep in mind that even when you feel 100% fit, you may have deficits in strength, joint stability, flexibility, or skill. Take extra care with the injured part for several months.

Rehabilitation and Return to Sports After Conservative and Surgical Treatment of Upper Extremity Injuries

How to Speed Up Injury Recovery Time s s s s s s s

Stay in shape year-round. Pay attention to injury warning signs Treat injuries immediately Participate in a full injury rehabilitation program Know when it is safe to return to sports Stay fit while injured Keep a positive, upbeat attitude [7]

Some Examples of Upper Limb Postsurgery Rehabilitation Protocol Arthroscopic Anterior Stabilization s Preoperative rehabilitation is advisable (Prehabilitation) s Postoperative schedule

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Milestones Week 6: Active elevation to preoperative level Week 12: At least 80% range of external rotation compared to asymptomatic side Normal movement patterns throughout range Activity

Return to activity/sports

Sedentary job

As tolerated

Manual job

3 months

Driving

6–8 weeks

Swimming breaststroke

6 weeks

Swimming freestyle

12 weeks

Golf

3 Months

Lifting

Light lifting can begin at 3 weeks. Avoid lifting heavy items for 3 months

Contact sport

E.g., Horse riding, football, martial arts, racket sports, and rock climbing: 3 months

Level 1 Exercises: Day 1–3 Weeks Mastersling with body belt for 3 weeks Finger, wrist, and radioulnar movements Elbow flexion and extension when standing Teach axillary hygiene Teach postural awareness and scapular setting Passive flexion as comfortable to 90° Passive external rotation to neutral (as comfortable) Core stability exercises with sling (as appropriate) No combined abduction and external rotation Level 2 Exercises: 3–6 Weeks Body belt removed and wean off sling Commence active assisted flexion as comfortable Active assisted abduction to 60° Active assisted external rotation as comfortable Commence proprioceptive exercises (minimal weight bearing below 90°) No combined abduction and external rotation Level 3 Exercises: 6–12 Weeks Remove the sling by 6 weeks Regain scapula and glenohumeral stability, working for shoulder joint control rather than range Gradually increase ROM (range of motion) Strengthen rotator cuff muscles Increase proprioception through open and closed chain exercise Progress core stability exercises Ensure and treat posterior tightness, if required

Shoulder SLAP Repair Level 1 Exercises: 15%). More than 99% of them are closed injuries[6].

Radial Head and Neck Fractures The radial head is an important structure, which provides the stability of the elbow and forearm. It has a buttress effect to prevent the axial migration of the radius and resists posterior migration of the elbow. Haemarthrosis visible on a lateral x-ray of the elbow is the only evidence of the radial head or neck fracture (Fig. 1). Minimally displaced fractures can be diagnosed by radiocapitellar views (Fig. 2). Computed tomography (CT) can be used at communited and complex fractures for diagnosis and preoperative planning (Fig. 3) [6]. The first classification of radial head fractures was made by Mason in 1954. The classification is as follows [6]: s Type 1: undisplaced s Type 2: displaced s Type 3: comminuted fractures involving the whole head

M. Kömürcü ( ) Department of Orthopaedics and Traumatology, Fatih University, Ankara, Turkey e-mail: [email protected] G. Çakmak Department of Orthopaedics and Traumatology, BaĜkent University Faculty of Medicine, Ankara, Turkey e-mail: [email protected]

In 1987 Broberg and Morrey modified Mason’s classification [6]. There are four types of radial head fractures: s Type 1: 2 mm of displacement and >30% involvement of the head s Type 3: comminution involving the whole head s Type 4: radial head fracture associated with an elbow dislocation

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Fig. 1 Lateral radiographic view of the radius head fracture Fig. 3 Coronal CT scan of the fracture line

Radiographic surgical indications of radial head fractures are [3]: 1. Neck fracture with greater than 15° of angulation or greater than 25% displacement 2. Intra-articular fractures greater than 25% of the radial head with more than 2 mm of articular step-off or that create a mechanical block to motion 3. Essex-Lopressti injury with longitudinal radial instability or elbow varus-valgus laxity that may be caused by concomitant collateral ligament injury Surgical strategy of radial head fractures can be summarized according to Mason’s classification as follows [3]:

Fig. 2 Radiocapitellar radiographic view of the radius head fracture

Hotchkiss further modified this classification according to the elbow’s range of motion. There are three types [6]: s Type 1: has no mechanical block to movement and any restriction is due to pain and/or haemarthrosis s Type 2: has a mechanical block despite aspiration of haemarthrosis s Type 3: has a mechanical block necessitating excision of the radial head to restore movement (the radial head is not reconstructable and must be replaced)

s Tip I: early active mobilization s Tip II: early active mobilization/ORIF (Open reduction and internal fixation) (Fig. 4) s Tip III: ORIF/excised (radial head replacement may be considered) s Tip IV: ORIF/excised (radial head replacement) The authors describe arthroscopic radial head resection in patients with post-traumatic arthritis after fractures of the radial head. Arthroscopic radial head resection allows the surgeon to evaluate the intrinsic joint pathology such as synovitis, capsular contracture, or loose bodies. Arthroscopic treatment allows the patient to begin and maintain an early aggressive postoperative physical therapy program. This will decrease the risk of anterior scarring and joint contracture of the elbow [10, 11].

Common Fractures in Sports Fig. 4 (a) Anteroposterior view of the radius head fracture; (b, c) the exposure and fixation of the fracture with anatomic plate and screws; (d) postoperative anteroposterior view of the radius head fracture

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Olecranon Fractures Olecranon fractures are common injuries of the proximal ulna (10% of all upper extremity fractures). Olecranon fractures may be caused by direct injury to the elbow joint or avulsion by the indirect forces of triceps muscle during a fall on a partially flexed elbow. Olecranon stress fractures in throwing athletes may occur as a result of repetitive microtrauma caused by olecranon impingement or excessive triceps tensile stress. Early radiographs may be normal, and MRI (Magnetic resonance imaging), CT, or bone scan are often diagnostic [1, 13, 16]. Chalidis et al., observed that the incidence of olecranon fractures showed a higher prevalence among men until the 5th decade of life and among women in older ages [4]. Rommens et al. reported that almost 50% of males with olecranon fractures were between 21 and 40 years of age and 40% of females were between 61 and 80 years old [15].

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The olecranon fractures can be classified according to AO classification in three types: Type A – extra-articular, type B – partial articular, type C – intra articular [12]. Colton’s classification of olecranon fractures are as follows [5]: s Type A: fractures are typically avulsion fractures. s Type B: are oblique fractures which may also be comminuted. s Type C: are those where there is a fracture dislocation. s Type D: are unclassifiable. Morrey classification system takes into account the amount of displacement and comminution. Type 1 – undisplaced and stable, Type 2 – displaced but the elbow stable, Type 3 – displaced and the forearm is unstable with respect to the distal humerus. This classification has sub-classifications; Type A un-comminuted, and type B comminuted [2]. According to the intra-articular extension of fractures, anatomic reduction and early mobilization should be achieved. The only absolute indication for olecranon fixation

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Fig. 5 (a–c) Preoperative radiographic lateral view and exposure of the olecranon fracture; (d–f) radiographs and photographs of the olecranon fracture after ORIF (g, h); postoperative elbow range of motion after surgery

is associated instability. Therefore 95% of fractures which are displaced should be treated with operatively (Fig. 5) [2].

Coronoid Fractures The coronoid process of the ulna is crucial for posterior stability of the elbow. The coronoid fractures are usually associated with other fractures or ligamentous injuries. Regan and Morrey classified these fractures in three types according to the size of the coronoid fragment. They subdivided each type into A and B, with or without elbow dislocation. s Type 1: involves only the tip s Type 2: < 50% of the total height s Type 3: > 50% of the total height

Type III fractures involve greater than 50% of the coronoid process and they usually require open reduction and internal fixation to avoid recurrent instability. On the other hand, nonoperative treatment was recommended for Type I fractures. O’Driscoll et al. made a classification and told that instability may also occur with small fragments. The classification is as follows; Type I involves only the tip (A < 2 mm, B > 2 mm), type II involves the anteromedial (A, B, C) and type III involves more than 50% of the height (A, B) [14]. Conventional treatment of coronoid fractures is open reduction and internal fixation, but it requires extensive exposure and detachment of the anterior capsule may threaten the vascularity of the fragment (Fig. 6). Arthroscopic techniques can provide excellent visualization of the joint and minimal surgical dissection. Arthroscopy also preserves soft

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Fig. 6 (a, b) Fracture and dislocation of the elbow (radius head-ulna coronoid fracture) – radiographic and CT view; (c–f) exposure and ORIF of the coronoid fracture; (g, h); postoperative radiographs

tissue attachments [9]. Hausman et al., applied arthroscopic assisted repair of the coronoid fractures successfully with less soft tissue dissection [9].

Distal Part of the Humerus These fractures are more common in elderly females with osteoporotic bone. Although routine plain radiographs may be helpful for diagnosis of the fractures, CT scan may be needed to understand the configuration of the fracture and preoperative planning. The fractures can be classified as being extra-articular, intra-articular or exclusively articular where the fracture lines do not extend into the metaphyseal bone.

The AO alphanumerical system describes these fractures as group 13 with type A being extra-articular, type B partial articular and type C intra-articular. Riseborough and Radin classified “T” shaped fractures into four subtypes: s s s s

Type 1: undisplaced Type 2: displaced without rotation Type 3: displaced and rotated Type 4: comminuted and grossly displaced

Jupiter and Mehne classify distal humeral fractures according to the configuration of the fracture. They are described as high and low “T” shaped, “Y” shaped, “H” shaped and lateral and medial “lambda” configurations [6].

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The complications of surgery are severe comminution, bone loss, and osteopenia. Anatomic locking plates have improved the treatment of these injuries. Sanchez-Sotelo et al. evaluated a group of patients whose complex distal humeral fractures were fixed with parallel plates (Fig. 7). This fixation technique maximizes fixation in the distal fragments and gain stability at the supracondylar level through screw fixation in the distal segment. Hardy et al. treated a type I Hahn–Steinthal capitellum fracture by screw fixation under arthroscopic control. The arthroscopic approach allows a better evaluation of associated lesions compared with the open surgery with less damage to periarticular soft tissues and has a lower morbidity compared with open surgery (Fig. 8) [7]. Hausman et al. performed arthroscopy assisted percutaneous pinning of pediatric lateral humeral condyle fractures and had satisfactory results. This procedure decreases the risk of a vascular necrosis and malunion [8].

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Complications of Elbow Fractures Elbow stiffness can be treated with physiotherapy and contracture correction splints. If the patients do not respond to these therapies, serial casting under general anesthesia can be performed. Open or arthroscopic arthrolysis can be performed at resistant cases. The risk of neurovascular complications at arthroscopic arthrolysis is decreased by the improvement of the technique. Constrained elbow arthroplasty may be an treatment option at geriatric patients whose contractures could not be resolved by conventional treatment methods [6]. The incidence of ulnar nerve dysfunction is approximately 12% with 5% being permanent. The incidence of acute ulnar nerve injury either due to trauma or surgical injury is probably around 1%. The ulnar nerve palsy may be related to acute injury or compression of fibrous and bony tissue [6]. Heterotopic ossification is the most difficult problem after traumatic injury of the elbow. The incidence of heterotopic

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Fig. 7 (a–c) AO type C distal humerus fracture (intraoperative photographs); (d, e) postoperative radiographs

Common Fractures in Sports Fig. 8 (a) Preoperative radiographic view of the distal humerus capitellum fracture; (b, c) preoperative CT scan; (d) postoperative lateral view

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ossification is below 3% at the cases without head injury. The incidence is same at the cases which are treated operatively or nonoperatively similar whether the fracture is treated operatively or non-operatively. Aggressive stretching exercises after surgery may increase the risk of this complication [6]. Non-union is reported at 2–10% of patients and usually occurs in the supracondylar region. Further fixation with or without bone graft and conversion to elbow arthroplasty may be chosen for treatment options. Instability, posttraumatic arthritis (84%), and infections (25° (30°–40°)

Acetabular index

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28 days from training and match play

Traumatic injury

Injury with sudden onset and known cause of event

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Injury with insidious onset and without any known trauma

Foul play injury

Match injury resulting from foul play according to the decision of the referee

Most Hamstring Strains Sustained When Running or Sprinting

Injury incidence

Number of injuries per 1,000 player hours [(6 injuries/6 exposure hours) × 1,000]

The majority of hamstring strains (52%) were due to running or sprinting while 17% were due to overuse. Almost all

Thigh Muscle Injuries in Professional Football Players: A Seven Year Follow-Up of the UEFA Injury Study

(81/587) injuries were severe, causing absence more than 4 weeks. Injuries sustained during matches caused significantly longer absence compared to injuries sustained during trainings (18.3 vs 11.9 days, p < 0.001).

Injuries/1,000 h of match play

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Quadriceps Injuries 2

Most Quadriceps Strains Occur in the First Half of a Match

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Quadriceps strains Hamstring strains

Fig. 1 The risk of sustaining a thigh muscle injury in different age groups

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The majority of the quadriceps strains occurred at training (143 vs 104), the risk of sustaining a quadriceps strain during a match being four times higher than during training (1.13 vs 0.3/1,000 h). The majority (62%) of quadriceps strains occurred in the first half of the matches, the peak of risk was noted between the 16 and 45 minutes in the first half when 40% of all quadriceps strains occurred. As seen in Fig. 1, there was no difference in injury risk at matches between different age groups.

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Many Quadriceps Injuries Sustained at Shooting

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Fig. 2 Distribution of match play injuries over the football season

hamstring strains were noncontact injuries, 97% being sustained without contact with other players. According to the referees, only 1.5% (6/391) of the match play injuries was due to foul play. 13% (74/587) of the injuries were recurrent injuries. Figure 2 shows the distribution of injuries over the season. Hamstring strains were more common during the competitive season (September to May).

Consequences of a Hamstring Strain In total, there were 9,554 days lost because of hamstring strains for the teams (a mean 109 days per team and season). As a mean, a hamstring strain caused 16 (range 1–128) days of absence, with a mean of 10 (range 0–90) missed trainings and 3 (range 0–27) missed matches. Fourteen percent

As many as 28% of all quadriceps strains occurred at shooting, in contrast to hamstring strains, which were only 1.5% of injuries occurred at that action (p < 0.001). As with hamstring strains, the majority of quadriceps strains were noncontact injuries, 96% being sustained without contact with other players. None of the match play injuries were due to foul play. Similar to hamstring strains, 13% of the injuries were recurrent injuries. Figure 2 shows the distribution of injuries over the season. The highest risk of sustaining a quadriceps strain was seen in August, during the end of the preseason preparation period. In contrast to hamstring strains, no increase of risk was seen during the competitive season. Consequences of a Quadriceps Strain In total, there were 4,482 days lost because of quadriceps strains for the teams (a mean 51 days per team and season). As a mean, a quadriceps strain caused 18 (range 1–147) days of absence, with a mean of 12 (range 0–79) missed trainings and 3 (range 0–31) missed matches. Nineteen percent (46/247) injuries was severe, causing absence of more than 4 weeks. In contrast to hamstring injuries, there was no significant difference in absence days between injuries sustained at matches compared to injuries sustained at training (20 vs 17 days, ns). Examination Procedures The diagnostic procedures for thigh muscle injuries were investigated during the season 2007/2008. From the 159

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thigh muscle injuries, 72 (45%) were examined with MRI (some with ultrasonography as well). Seventy (44%) were examined with ultrasonography and 11% were diagnosed only clinically. Of the 14 clubs that participated during that season, 2 clubs examined almost all (>90%) thigh muscle injuries with MRI, while two clubs did not perform any MRI examinations at all during the period. Seven clubs used mainly MRI for diagnosis and seven used mainly ultrasonography.

Muscles Involved According to the MRI findings, the majority of hamstring strains occur to the biceps femoris muscle (86%) while rectus femoris is the most commonly affected quadriceps muscle (88%).

Discussion The strength of this study is the large homogenous material of male professional players and the fact that 861 thigh muscle injuries were included in the study. In addition, the collecting of data followed the international consensus agreements on procedures for epidemiological studies of football injuries recommended by FIFA and UEFA [9, 10]. Hamstring strain is the single most common injury subtype in male professional football [12, 17, 18] and a team of 25 players can expect a mean of seven hamstring strains each season, causing a mean absence of 109 days each season. Hamstring and quadriceps strains differ in several ways. The risk of a hamstring strain is 11 times more common in matches compared to training, and further, the majority of hamstring strains occur in sprinting and running situations. These findings probably reflect the speed and high intensity of modern elite football since hamstrings strains are commonly found in sprinters and other athletes in high intensity sports [5]. Quadriceps injuries, on the other hand, were significantly more common at shooting compared to hamstring injuries. The finding that the risk of quadriceps strains had a peak at the end of the preseason preparation period might be explained by more intensive practice of shooting at trainings during that period. It seems reasonable to assume that the finding of a higher risk of hamstring strain during the competitive season is due to the fact that more and intensive matches are played during that period. Another difference between hamstring and quadriceps strains is the distribution of injuries during a match. The peak of hamstring injuries during the 61–75 minutes in the second half might reflect fatigue of muscles [6, 15]. Further, one might speculate whether more intensive shooting could be the reason behind

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the finding that quadriceps strains occur in the first half of matches. Inadequate warming up or recurrence of previous injuries might be the alternative explanations to the finding. At top professional level, most teams use radiological examinations for diagnosis of muscle injuries. MRI and ultrasonography seem to be equally frequently used for diagnosis among the clubs in this study. A limitation in the present study is that the muscle injuries included form a heterogenous group. According to the consensus statement definition used in this study, strains include all types of total as well as partial muscle ruptures as well as cramp and muscle soreness. The wide range of absence for hamstrings (1–128 days) as well as quadriceps injuries (1–147) is a reflection of this heterogenocity. Future studies using MRI examinations to separate injuries into different groups, might be more adequate in prognosticating absence and return to play information [4, 14]. Acknowledgements We gratefully acknowledge the clubs involved in the study. The help from the medical personnel and the contact persons are greatly appreciated: Rodolfo Tavana and Bill Tillson (AC Milan), Piet Bon and Edwin Goedhart (AFC Ajax), Leo Groenweghe and Jose Huylebroek (RSC Anderlecht), Joao-Paolo Almeida and Paulo Rebelo (SL Benfica), Egid Kiesouw (BV Borussia Dortmund), Gary Lewin (Arsenal FC), Bryan English and Alex Nieper (Chelsea FC), Dimitri Dobbenie, Jan de Neve and Michel D’Hooghe (ClubBrugge KV), Jordi Ardevol, Lluis Til, Gil Rodas, Ricard Pruna and Ramon Canal (FC Barcelona), Dieter Gudel, Oliver Dierk and Nikolaj Linewitsch (Hamburger SV), Francesco Benazzo, Franco Combi, Giorgio Panico, Cristiano Eirale and Pier-Luigi Parnofiello (FC Internazionale Milano), Fabrizio Tencone and Antonio Giordano (Juventus FC), Mark Waller (Liverpool FC), Roddy McDonald (Newcastle United FC), Mike Stone and Steve McNally (Manchester United FC), Hakim Chalabi (Paris St Germain FC), Nelson Puga (FC Porto), Cees-Rein van den Hoogenband and Luc van Agt (PSV Eindhoven), Ian McGuiness (Rangers FC), Denis Bucher (RC de Lens), Luis Serratosa (Real Madrid CF), Paco Biosca and Viktor Kirilenko (Shakhtar Donetsk) and Pierre Rochcongar (Stade Rennais FC).

References 1. Andersen, T.E., Tenga, A., Engebretsen, L., Bahr, R.: Video analysis of injuries and incidents in Norwegian professional football. Br. J. Sports Med. 38, 626–631 (2004) 2. Arnason, A., Andersen, T.E., Holme, I., Engebretsen, L., Bahr, R.: Prevention of hamstring strains in elite soccer: an intervention study. Scand. J. Med. Sci. Sports 18, 40–48 (2008) 3. Askling, C., Karlsson, J., Thorstensson, A.: Hamstring injury occurrence in elite soccer players after preseason strength training with eccentric overload. Scand. J. Med. Sci. Sports 13, 244–250 (2003) 4. Askling, C., Saartok, T., Thorstensson, A.: Type of acute hamstring strain affects flexibility, strength, and time to return to pre-injury level. Br. J. Sports Med. 40, 40–44 (2006) 5. Askling, C., Tengvar, M., Saartok, T., Thorstensson, A.: Acute firsttime hamstring strains during high-speed running: a longitudinal study including clinical and magnetic resonance imaging findings. Am. J. Sports Med. 35, 197–206 (2007)

Thigh Muscle Injuries in Professional Football Players: A Seven Year Follow-Up of the UEFA Injury Study 6. Bangsbo, J., Iaia, F.M., Krustrup, P.: Metabolic response and fatigue in soccer. Int. J. Sports Physiol. Perform. 2, 111–127 (2007) 7. Ekstrand, J., Gillquist, J.: Soccer injuries and their mechanisms: a prospective study. Med. Sci. Sports Exerc. 15, 267–270 (1983) 8. Ekstrand, J., Timpka, T., Hägglund, M.: Risk of injury in elite football played on artificial turf versus natural grass: a prospective twocohort study. Br. J. Sports Med. 40, 975–980 (2006) 9. Fuller, C.W., Ekstrand, J., Junge, A., Andersen, T.E., Bahr, R., Dvorak, J., Hägglund, M., McCrory, P., Meeuwisse, W.: Consensus statement on injury definitions and data collection procedures in studies of football (soccer) injuries. Br. J. Sports Med. 40, 193–201 (2006) 10. Hägglund, M., Waldén, M., Bahr, R., Ekstrand, J.: Methods for epidemiological study of injuries to professional football players: developing the UEFA model. Br. J. Sports Med. 39, 340–346 (2005) 11. Hägglund, M., Walden, M., Ekstrand, J.: Injury incidence and distribution in elite football – a prospective study of the Danish and the Swedish top divisions. Scand. J. Med. Sci. Sports 15, 21–28 (2005) 12. Hägglund, M., Waldén, M., Ekstrand, J.: Injury incidence and distribution in elite football – a prospective study of the Danish and the

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Swedish top divisions. Scand. J. Med. Sci. Sports 15, 21–28 (2005) 13. Hawkins, R.D., Hulse, M., Wilkinson, C., Hodson, A., Gibson, M.: The association football medical research programme: an audit of injuries in professional football. Br. J. Sports Med. 35, 43–47 (2001) 14. Koulouris, G., Connell, D.: Imaging of hamstring injuries: therapeutic implications. Eur. Radiol. 16, 1478–1487 (2006) 15. Mohr, M., Krustrup, P., Bangsbo, J.: Match performance of highstandard soccer players with special reference to development of fatigue. J. Sports Sci. 21, 519–528 (2003) 16. Waldén, M., Hägglund, M., Ekstrand, J.: Injuries in Swedish elite football-a prospective study on injury definitions, risk for injury and injury pattern during 2001. Scand. J. Med. Sci. Sports 15, 118–125 (2001) 17. Waldén, M., Hägglund, M., Ekstrand, J.: UEFA Champions League study: a prospective study of injuries in professional football during the 2001–2002 season. Br. J. Sports Med. 39, 542–546 (2005) 18. Waldén, M., Hägglund, M., Ekstrand, J.: Injuries in Swedish elite football – a prospective study on injury definitions, risk for injury and injury pattern during 2001. Scand. J. Med. Sci. Sports 15, 118– 125 (2005)

Chronic Muscle Injuries of the Lower Extremities in Sports Marc Rozenblat

Introduction

Contents Introduction ................................................................................. Level 0: Reversible Lesion Without Conjunctive Lesion ............. Level 1: Irreversible Lesion of Some Muscular Fibers Without Conjunctive Lesion – SPASM........................... Level 2: Irreversible Lesion of Some Muscular Fibers with Conjunctive Lesion – PULLED MUSCLE............. Level 3: Irreversible Lesion of Some Muscular Fibers with Conjunctive Lesion and Hematoma – SPRAINED MUSCLE .................................................... Level 4: Partial or Complete Muscular Rupture ...........................

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Compartment Syndrome ............................................................ 880 DOMS (Delayed Onset Muscle Soreness) ................................. 881 Prevention .................................................................................... 881 References .................................................................................... 881

Chronic muscle injuries of the lower extremities in sports can begin with an inappropriate treatment of an acute lesion. In France, Rodineau’s classification is used: Level 0: Reversible lesion without conjunctive lesion (Fig. 1) Level 1: Irreversible lesion of some muscular fibers, without conjunctive lesion (Fig. 2) Level 2: Irreversible lesion of some muscular fibers, with conjunctive lesion (Fig.3) Level 3: Irreversible lesion of some muscular fibers, with conjunctive lesion and hematoma (Fig. 4a, b) Level 4: Partial or complete muscle rupture (Fig. 5a, b) Each level has a specific treatment [5, 6, 8, 9, 11, 13, 14, 17, 18].

Level 0: Reversible Lesion Without Conjunctive Lesion Only some muscular fibers or/and sarcolemma lesions are observed. There is moderate pain with muscular spasm.

M. Rozenblat Coralis Sport Center, 32ter avenue du Général Leclerc, 77330 Ozoir La Ferrière, France e-mail: [email protected]

Fig. 1 Level 0: Reversible lesion without conjunctive lesion

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_112, © Springer-Verlag Berlin Heidelberg 2012

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Muscular strength is recovered within hours and it is a reversible lesion. No treatment is necessary.

Level 1: Irreversible Lesion of Some Muscular Fibers Without Conjunctive Lesion – SPASM Irreversible muscular fiber lesions are observed but there is an integrity of connective tissue. Clinically, the pain and spasm are more important than in level 0. Recovery is a matter of days. Treatment is “no treatment” thanks to spontaneous recovery. For 7 days, mild sporting activity, aerobic work and no acceleration are recommended. Stretching and soft massage could be of help. Fig. 2 Level 1: Irreversible lesion of some muscular fibers without conjunctive lesion – spasm

Level 2: Irreversible Lesion of Some Muscular Fibers with Conjunctive Lesion – PULLED MUSCLE Irreversible muscular fiber lesions with moderate lesion of connective tissue are observed. The pain is acute. Recovery is within 10–15 days. Treatment is with analgesics but without NSAI for the initial 5 days. Painless, isometric, concentric and eccentric tensing is necessary before restarting sport. Generally aerobic sport could be restarted on Day 7 and sprint sport on Day 21.

Level 3: Irreversible Lesion of Some Muscular Fibers with Conjunctive Lesion and Hematoma – SPRAINED MUSCLE Fig. 3 Level 2: Irreversible lesion of some muscular fibers with conjunctive lesion – pulled muscle

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Irreversible muscular fiber lesions and important lesion of connective tissue is observed. Hematoma confirms the diagnosis. Acute pain leads to interruption of physical activities.

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Fig. 4 (a) Level 3: Irreversible lesion of some muscular fibers with conjunctive lesion and hematoma. (b) Level 3: Irreversible lesion of some muscular fibers with conjunctive lesion and hematoma – sprained muscle

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Fig. 6 US, fibrosis nodule

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Fig. 5 (a) Level 4: Partial or complete muscular rupture (b) Level 4: Partial or complete muscular rupture

Recovery is within 30–90 days. Ultrasound scan is of capital importance for diagnosis and supervision. Treatment is analgesics, no NSAI during the initial 5 days and compression during 8 days. Evacuation on Day 5 or Shock wave on Day 1 could be used to clear the hematoma. Static then dynamic tensing could be useful afterwards. Massage near Day 10, stretching near Day 21, aerobic sport near Day 45 are recommended. Sprint sport is restarted in absence of pain in tension in eccentric external movements.

Level 4: Partial or Complete Muscular Rupture Irreversible muscular fiber lesions with an important lesion in connective tissue is observed together with an hematoma.

Acute pain interrupts physical activities. Recovery is within 45–90 days. Ultrasound scan is of a capital importance for diagnosis and supervision. Surgery is required because of the voluminous compressive hematoma with large disinsertion (hamstring). In all these cases there is generally no problem if the biological time of recovery is respected. But recurrence may be the problem in the event of incomplete recovery or a weakness in muscle. Four possible muscular adverse effects with bad healing could be observed. They are named Chronic Muscle lesions considered aftereffects. 1. Fibrotic nodule (Fig. 6) With ultrasound scan or RMI, anarchic fibrotic tissue proliferation and no muscular fiber organization are observed. Treatment is transversal deep massage, shock wave therapy, physiotherapy, ionophoresis and/or ultrasound. With these treatments all aftereffects usually disappear. 2. Cyst or pseudo cyst (Fig. 7a, b) It is a cap on a residual hematoma. Treatment is infiltration or puncture, or sometimes surgery. 3. Intramuscular calcification (Fig. 8a, b) It is residual pain after reiterated muscular accidents. Treatment is sometimes corticosteroids infiltration but controversy exists. Absolute rest, indomethacine drug treatment, shock wave therapy and surgery could be proposed. The management of the treatment is case by case.

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Fig. 7 (a) US, cyst or pseudo cys. (b) RMI, cyst or pseudo cyst

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Fig. 9 Muscular ossification, negative scintigraphy for surgery

4. Muscular ossification (Fig. 9) Clinical test is like for intramuscular calcification but the lesion is an ossification extended from the bone. X-Ray and scintigraphy are of capital importance for diagnosis and supervision. Absolute rest, Indometacine drug treatment, shock wave therapy and surgery (with negative scintigraphy) could be proposed. Management of the treatment is case by case. Other muscle lesions could be regarded as chronic lesions but they have their own identities: compartment syndrome and DOMS.

Compartment Syndrome

Fig. 8 (a) Intramuscular calcification. (b) US, intramuscular calcification

It is a source of controversy: three different features are required for positive diagnosis (Fig. 10):

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during and after exercise. Extra caution is required for patients on statine and quinolone and people over 30 years. In the beginning cycling and swimming are necessary prior to restarting sport.

References

Fig. 10 Compartment syndrome, pressure measurement

s Pressure at rest >15 mmHg s Post exercises pressure >75 mmHg s Time needed to return to normal pressure >6 min But other data could be present: s Pressure after 1 min rest >35 mmHg s Pressure after 5 min rest >25 mmHg s Pressure after 15 min rest >15 mmHg Treatment is physiotherapy with or without vasculary drugs but the most effective is surgery by aponeurectomy.

DOMS (Delayed Onset Muscle Soreness) They are frequent in sport and observed within 12–48 h after intensive and/or unusual eccentric muscle action. What’s more, decreased proprioception is frequent. Generally they disappear within 2–10 days before complete functional recovery. The explanation is not certain and it is perhaps inflammation in the muscle. But there is a consensus that DOMS are not an indicator of muscle damage but a sign of the regenerative process. Treatment alleviates but by no means accelerates structural or functional recovery.

Prevention Prevention [1–5, 7, 10, 12–18] is capital to avoid chronic muscle lesions: warm-up exercises, arguable stretching, muscular limberness and suppleness, hydration before,

1. Bahr, R., Maehlum, S., (eds.): Clinical Guide to Sports Injuries, 451 p. Human Kinetics, Champaign. ISBN: 0-7360-4117-6 (2004) 2. Brooks, J., Fuller, C., Kemp, S., Reddin, D.: Incidence, risk, and prévention of hamstring muscle injuries in professional rugby union. Am. J. Sports Med. 36, 1297–1306 (2006) 3. Croisier, J.L.: Factors associated with recurrent hamstring injuries. Sports Med. 34, 681–695 (2004) 4. Croisier, J.L., Crielaard, M.J.: Hamstring muscle tear with recurrent complaints: an isokinetic profile. Isokinet. Exerc. Sci. 8, 175–180 (2000) 5. Croisier, J., Forthomme, L., Namurois, B.: Hamstring muscle strain recurrence and strength performance disorders. Am. J. Sports Med. 30, 199–203 (2002) 6. Garret, W.E.: Muscle strain injuries. Am. J. Sports Med. 24, S2–S8 (1996) 7. Hawkins, R.D., Hulse, M.A., Wilkinson, C.: The association football médical research program: an audit of injuries in professional football. Br. J. Sports Med. 35, 43–47 (2001) 8. Jarvinen, T., Jarvinen, T.L.N., Kaariainen, M., Kalino, H., Jarvinen, M.: Muscel injuries biology in treatment. Am. J. Sports Med. 33, 745–764 (2005) 9. Jonhagen, S., Nemeth, G., Erikson, E.: Hamstring injuries in sprinters. The role of concentric and eccentric hamstring muscle strength and flexibility. Am. J. Sports Med. 22, 262–266 (1994) 10. Junge, A., Rösch, D., Peterson, L.: Prevention of soccer injuries: a prospective intervention study in youth amateurs players. Am. J. Sports Med. 30, 652–659 (2002) 11. Kaariainen, M., Kaariainen, J., Jarvinen, M.: Correlation between biochemical and structural changes during the regeneration of skeletal muscle after laceration injury. J. Orthop. Res. 16, 198–206 (1998) 12. Mc Hugh, M.P.: The role of passive muscle stiffness in symptoms of exercise induced muscle damage. Am. J. Sports Med. 27, 594– 599 (1999) 13. Orchard, J.W.: Intrinsic and extrinsic risk factor for muscle strains in Australian footballers. Am. J. Sports Med. 28, 300–303 (2001) 14. Orchard, J., Best, T.M.: The management of muscle strain injuries and early return versus the risk of recurrence. Clin. J. Sport Med. 12, 3–5 (2002) 15. Puranen, J., Orava, S.: The hamstring syndrome, a new diagnostic of gluteal sciatic pain. Am. J. Sports Med. 16, 17–21 (1988) 16. Safran, M., Garrett, W., Searber, A.: The role of warm-up in muscular injury prevention. Am. J. Sports Med. 16, 123–128 (1988) 17. Scott, D., Mair, A., Seaber, R., Glisson, W., Garrett, W.E.: The role of fatigue in susceptibility to acute muscle strain injury. Am. J. Sports Med. 24, 137–143 (1996) 18. Witvrouw, E.: Muscle flexibility as a risk factor for developing muscle injuries in male professional soccer players: a prospective study. Am. J. Sports Med. 31, 41–46 (2003)

Tennis Leg Kristof Sas

Contents Tennis Leg .................................................................................... 883 Sequence of Injuries of Player A ............................................... 884 References .................................................................................... 885

Tennis Leg Delgado [1] came in 2002 to the following definition of the tennis leg: s A partial or complete rupture of the medial head of the

gastrocnemius s A fluid collection between the aponeurosis of the medial

gastrocnemius and the soleus without a muscle rupture s A rupture of the plantaris tendon s A partial rupture of the soleus muscle

In our team, we saw during the last 2 years two players with a tennis leg. Player A is a center forward, 26 years old, and he had initially no pain, but just stiffness and swelling. On ultrasonography (US) we found a fluid collection of 10 × 2 cm with a thickness of 6 mm. Player B is a midfielder, 34 years old; he had a sudden onset of pain. On US we found a fluid collection of 10 × 4 cm with a thickness of 5 mm. The initial treatment was the same for both players. They both underwent an aspiration of the fluid collection, with a compressive bandage afterward. They both got the same relative rest and physiotherapy. After the first aspiration, neither of them got crutches and neither of them got an immobilization plaster. But after the second aspiration we gave player A crutches, but not an immobilization plaster. For both players we followed the evolution on US (Table 1). Both players underwent the same sequence of rehabilitation with first bike and crosstrainer and later on running, individual soccer training, and finally collective soccer training (Table 2). We saw that player B was always 2 weeks earlier to the same step as player A. There are a few causes to explain this:

K. Sas RSC Anderlecht, Rovorst 19, 9660 Brakel, Belgium e-mail: [email protected]

1. First of all: player A was much more afraid to do something with an US that was not that good. 2. Secondly, we were more careful with player A because he was a more important player for the squad. So we can draw the following conclusions:

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Table 1 Sequence of US and therapy Player A Player B 19/01

12/04

s 10 cm × 2 cm × 6 mm

s 10 cm × 3.9 cm × 5 mm

s Aspiration: all 5 mL

s 17/04

s Compression

s 5.5 cm × 5 cm × 5 mm

s Relative rest

s 23/04

23/01

s 5 × 5 cm

s Aspiration: all 3 mL

s Aspiration 35 mL

s Compression

s Compression

s Crutches

28/04

04/02

s 3.3 cm × 3 cm × 3 mm

s 3.2 cm × 6.8 mm 2.2 mm

s Aspiration: 10 mL

11/02

s Compression

s 2.3 cm × 5.7 mm × 1.2 mm

03/05

14/02

s 4.5 cm × 4.7 cm × 6 mm

s 2.7 cm × 4.1 mm × 1.6 mm

s But: start of a better cicatrization

s Aspiration

07/05

s Injection of betamethasone

s 3 cm × 2.9 cm × 3 mm

21/02

s 10/05

s US –

s 3 cm × 2.5 cm × 3 mm

After 8 months

15/05

s US –

s 3 cm × 3 cm × 3 mm s 21/05 s 4.4 cm × 3.7 cm × 2.2 mm 02/07 s Scar: 6 × 2 cm

Table 2 Sequence of rehabilitation program Player A Player B Bike

Bike

Crosstrainer

Crosstrainer

Running (5 weeks)

Running (3 weeks)

Individual soccer training (6.5 weeks)

Individual soccer training (4.5 weeks)

Collective soccer training (8 weeks)

Collective soccer training (5.5 weeks)

They had the same kind of injury. They underwent the same starting strategy: aspiration and compression. After relapse on US: the rehabilitation of player A was much slower. But in the end player A had no scar, while player B had a definitive scar of 6 by 2 cm. Thus, we can ask ourselves the following questions: Do we have to do an aspiration? Yes Do we have to apply a compressive bandage? Yes

Do we need immobilization and non-weight bearing/ crutches? Here we see advantages and disadvantages: Immobilization and non-weight bearing could prevent, more easily, a new fluid collection. As disadvantage we have to consider a loss of muscle strength. Do we need a strengthening program? Yes When do we have to start the rehabilitation? It depends on the US, the intentions of the player, and may be even the coach. I did not mention aqua training, but it is certainly very useful in the beginning of the rehabilitation program.

Sequence of Injuries of Player A Now I would like to discuss a little bit about the sequence of injuries of player A: In the last 2 years he suffered from Achilles tendinopathy, Haglund exostosis and a peroneal tendon problem for which we didn’t find the exact diagnosis, but which got better after 3 weeks with conservative therapy, and at last a Achilles tendinopathy of the middle third of the tendon. When we take a look at the etiology: We see important biomechanical factors: In the running analysis we see that he is an extreme “heel runner” and a supinator. In an attempt to resolve this problem we gave him inlay soles and we adapted them already a couple of times. We also made an adaptation of the heel cap of his shoe; we made it soft because he couldn’t support his soccer shoes, even after his Haglund surgery. He suffered too much. Of course this caused a loss of stability of the shoe, which was not ideal either. But at that time it was the only solution. But we also took a look to find a relationship between the different pathologies and we came to the following astonishing conclusions: The Haglund surgery caused a calf muscle weakness This weakness was responsible for the tennis leg In the whole process of the tennis leg the player lost some more muscle strength, which could lead to the peroneal tendon problem and the new Achilles tendinopathy. In the literature we found this evidence: Ohberg [3] wrote in 2001 that in Achilles tendinopathy not only preoperatively, but also postoperatively calf muscle weakness was found. Miller [2] found that muscle strains in the calf are frequently related to overuse of the gastrocnemius, and that a loss of muscle strength means a greater risk of overuse. And as we know, a loss of calf muscle strength is a risk factor for Achilles tendinopathy.

Tennis Leg

Then we come to the most important questions: Could we prevent these injuries? Was the primary surgery for the Haglund exostosis necessary? If we know that only 10% recovers after a Haglund excision. What about the tennis leg? Did we do a sufficient strength rehabilitation program after surgery, knowing that the player was not training too much and when he joined practice the intensity was low? Could we prevent the Achilles tendinopathy? Again, did we do a sufficient strength rehabilitation program after the tennis leg? Did we have to clean/open the tendon in the former surgery? Because we still see that the tendon is weaker at that spot. So, we can draw the following conclusions: About the tennis leg (in the form as we mentioned above): 1. We have to perform an aspiration and apply a compressive bandage. 2. Secondly, we must follow the evolution on US, and adapt the rehabilitation in function of the US. 3. Maybe we should consider using crutches, more frequently, in the beginning; and maybe we can avoid easier relapse of the collection by applying more frequently an immobilization plaster.

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Concerning the sequence of injuries of player A, 1. Is there a necessity to operate a Haglund? 2. We absolutely need a strengthening program after s Surgery for Achilles tendinopathy s Tennis leg s Achilles tendinopathy

N.B.: I didn’t mention growth factors as a possible treatment because this method was not yet approved by WADA; but now I would certainly mention it as a valuable treatment.

References 1. Delgado, G.J., Chung, C.B., Lektakul, N., Azocar, P., Botte, M.J., Coria, D., Bosch, E., Resnick, D.: Tennis leg: clinical US study of 141 patients and anatomic investigation of four cadavers with MR imaging and US. Radiology 224(1), 112–119 (2002) 2. Miller, W.A.: Rupture of the musculotendinous juncture of the medial head of the gastrocnemius muscle. Am. J. Sports Med. 5(5), 191–193 (1997) 3. Ohberg, L., Lorentzon, R., Alfredson, H.: Good clinical results but persisting side-to-side differences in calf muscle strength after surgical treatment of chronic Achilles tendinosis: a 5-year follow-up. Scand. J. Med. Sci. Sports 11(4), 207–212 (2001)

New Protocol for Muscle Injury Treatment Tomás F. Fernandez Jaén and Pedro Guillén García

Introduction

Contents Introduction ................................................................................. 887 Justification to Establish a New Strategy of Treatment ................................................................................ 887 Goal .............................................................................................. 888 Biological Foundation of This Protocol ..................................... Acute Injury Stage or First Stage .................................................. Regeneration Stage or Second Stage ............................................ Fibrogenesis Stage or Third Stage ................................................ Conclusions ...................................................................................

888 888 889 890 890

Concept Test ................................................................................ 890 Protocol ......................................................................................... 891 References .................................................................................... 892

T.F.F. Jaén ( ) Servicio de Medicina y Traumatología del Deporte, Clínica CEMTRO, C/ Ventisquero de la Condesa #42, 28035 Madrid, Spain and Cátedra Traumatología del Deporte, Universidad Católica, Murcia, Spain e-mail: [email protected] P.G. García Servicio de Traumatología y Cirugía Ortopédica, Clínica CEMTRO, Madrid, Spain and Catedrático de Traumatología del Deporte, Universidad Católica, Murcia, Spain e-mail: [email protected]

The most common pathology in sports is muscle injury. It amounts to 35–55% of all injuries in sports [41]. It determines mobility and disqualifies temporarily for the practice of sports [21]. Investigation of all of its causes and ongoing search for new treatments for every single injury stands as a challenge for sports medicine. The best possible treatment for muscle injuries [45] has not yet been determined mainly because of the great variety of injuries listed [15, 18], also because there is no one single method of diagnosis [17], there is a great deal of muscles that can be injured, and finally because of the very different functional repercussions of each sports discipline. Several different treatments [24] have been tried to minimize time and improve quality in the recovery of muscle regeneration. Various techniques have been applied from physiotherapeutic methods to platelet-rich plasma [20] and autologous conditioned serums [59] and proceedings to increase the number of stem cells at the muscle injury site [41]. Also fermented milk food diets rich in antioxidant substances [3] have proven to repair muscles. On the other hand, one of the main features of muscle tissue is being a dynamic soft tissue capable of interacting with extracellular matrix and reacting to foreign stimuli [2]. This allows external manipulation both through physical (massages, magnetic fields, etc.) and chemical proceedings (NSAIDs, antifibrotic agents, etc.) Nonetheless, the regenerative capacity from muscles of human beings slows down with age as the appearance of fibrosis becomes more evident [6].

Justification to Establish a New Strategy of Treatment There are several reasons to establish a new Protocol for the treatment of muscle injuries: there is no such thing as a single criterion that says how and when treatments or certain patterns of treatment need to be applied; there are several classifications

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of nonhomogeneous muscle injuries [9] with a great variety of interobserver; patterns of treatment have been based on individual medical experience rather than scientific homogeneous reproducible criteria. As a consequence, functional results have proven diverse, unpredictable, and unforeseeable.

Goal Goal is to elaborate a Protocol to reconcile and combine the therapeutical process by applying actual knowledge on biophysiology, which will eventually set up a plan of treatment based on temporary biological criteria of muscle repair. Today, we know that chronology of muscle injury repairs is not homogeneous in time. The importance of any given growth factor and its biological repercussion varies and changes with time; quantity and intensity of certain biological reactions also change. We can establish different stages during muscle injury repairs mainly based on the predominant biological features – inflammation, degeneration, regeneration, and fibrosis [22]. Also we wish to stress that the muscle healing pattern varies from one muscle to the other; it depends on whether it is the inner calf or the quadriceps and changes from one injury to the other evolving, whether it is a myotendinous junction injury or in the middle third muscle injury. As a consequence, this Protocol pretends to be a basic guideline for timelines and patterns of treatment not a specific by-the-book kind of rigid Protocol for muscle therapy. Our Protocol is close to these stages and induces measures to enhance the normal physiobiological response and inhibit, block, or try to disguise an abnormal or unwanted response.

Biological Foundation of This Protocol This Protocol [13] consists of three fundamental stages from the day the muscle injury occurs; Fig. 1. The first stage also called the Acute Injury Stage takes place between the occurrence of the injury and the first 24/48 h. The second stage also called the Regeneration Stage spans from the first 24 h after the occurrence of the injury to the next 14 days, and the third stage also called the Fibrogenesis Stage spans from the second week up to the fourth week.

Acute Injury Stage or First Stage Regardless of the mechanism that led to the muscle injury [15, 19] during the first 24/48 h the hematoma appears due to blood extravasations from broken blood vessels, cytokine liberation [52], inflammation, stimulation of macrophages [51],

T.F.F. Jaén and P.G. García Chronology of muscle repair Acute injury 0 24 hours

Regeneration 24 h - 14 days

Haematoma

Myofibrillar injury

Inflammation

Fibrogenesis 14 28 days Scar

Satellite Cells

Muscle regeneration

Muscular fibrosis

Degeneration

Fig. 1 Scheme of the chronology of muscle repair Effects of inflammation Cells and fibrillar degeneration

Inflammation

Vasodilatation and angiogenesis VEGF, PDGF, ON Cell activation Macrophages Neutrophyles Limphocytes Satellite Cells Fibroblasts

Fig. 2 Effects of inflammation

and neutrophils [54]. Recruitment of macrophages takes place and eventually leads to degenerative phenomena. Inflammation is going to cause fibrillar degeneration of myofibrillar proteins: actin and myosin – the basic goals of fibrillar [50] and cell degeneration. Vasodilatation and angiogenesis are induced by the plateletderived growth factor-D (PDGF-D) and the vascular endothelial growth factor-E (VEGF-E). Several studies prove the VEGF capacity to produce angiogenesis and vasodilatation [36, 39], stimulate the pericite layer of blood vessels to stimulate angiogenesis and increase interstitial blood pressure and blood vessel maturation [55]. The strongest vasodilator, that is, nitric oxide (NO) is produced from arginine through endothelial nitric oxide synthase [57]. This enzyme inhibition is linked to a decrease in transversal section and tendon-muscle strength. Neovascularization, improvement of the cellular metabolic condition, and increase of oxygen supply at the injury area are very important to achieve a good biological response. On the other hand, during inflammation, cytokine liberation [61] – Fig. 2 takes place and cell activation of

New Protocol for Muscle Injury Treatment

macrophages, neutrophils, and lymphocytes is produced, which will eventually lead to a strong activation of satellite cells and fibroblasts. In sum, most injuries occurring during the Acute Injury Stage need to be treated in a conservative way [1, 38]. It is very important to monitor and minimize the size and number of hematomas all through physical therapy. To that end we suggest applying local ice for 10 min several times a day, compression and elevation [26] of the affected limb during the first 24 h – RICE (Rest, Ice, Compression, Elevation). Should the hematoma be massive and encapsulated evacuation might be necessary to perform an echo-guided puncture or even through surgery [21, 25]. Monitoring inflammation through physical means is a necessity as well. We cannot use anti-inflammatory drugs because they constrain and interfere with the mechanisms that start all stages of biological repair. It has been demonstrated that blocking cyclooxygenase delays and decreases muscle regeneration and induces fibrosis [44]. Vasodilation and angiogenesis need to be induced too, the metabolic condition of the affected area needs to be secured, and satellite cell stimulation also needs to be fostered. At this stage we will only be using analgesics, which will not interfere with any of the aforesaid mechanisms; pain relieving electrotherapy can be applied too [56]. Immobilization needs to be highly restrictive and short in time because it produces muscle atrophy, increases inflammation, reduces the capacity of healing, increases the chances of something going wrong, and complicates posterior mobilization [20].

Regeneration Stage or Second Stage It spans from the first 24 h after the occurrence of the injury to the first 2 weeks. The main occurrence in this stage is activation and stimulation of muscle satellite cells, thanks to growth and other chemical substances. The fibroblast growth factor basic (bFGF or FGF-2) is great for its mediating effect. The bFGF is crucial in the machinery of muscle regeneration [14] and together with PDGF B they remain as very important components to induce arteriogenesis and myogenesis in the damaged muscle [12]. Also heparan sulfate [29] (HS) at rest until this stage is important. Satellite cells differentiate based on growth factors. They can generate three fundamental cell lineages: fibroblasts, which will later join further fibroblasts in the injury area; myofibroblasts, cells halfway through muscle fibers and fibroblasts; or myoblasts, precursors of the very muscle fibers. This is a very important stage since based on the treatment we apply we will be able to produce fibrotic repair – fibrosis or scar, or muscle regeneration. Find below all the different substances acting at the satellite cell level. At the Regenerative Stage (Fig. 3), inhibition of myostatin should be considered. Myostatin acts as an endogenous inhibitor of the muscle satellite cells. It has been demonstrated that

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Between 0 14 days after injury Myostatin SATELLITE CELLS IGF-1, bFGF, PDGF TGF-b, HSPGs MYOBLAST

TGF-B1 Cytokines NGF TGF-A

FIBROBLAST

Relaxine MYOFIBROBLASTS

Muscle fiber

TGF B 1 CTGF Sust P CTGF

Scar

Fig. 3 Scheme of differentiation of the satellite cells

its inhibition increases the number of muscle tissue in cases of muscle dystrophy and sarcopenia [33, 47, 48, 58]. Also, at the end of muscle regeneration, an increase of myostatin has been observed [60]. As a fundamental fibrogenetic factor the transforming growth factor-beta (TGF-beta) should be stressed too. TGF beta is a powerful collagen synthesis inducer, cytokine producer, and myofibroblast trans-differentiator, all involved in fibrosis [23]. Also it increases the number of fibroblasts, migration, adhesion, and formation of the extracellular matrix [32].TGF beta 1 is fundamental for the satellite cell transformation into a fibroblast [49] and to a lesser extent into a myofibroblast, and this is why blocking such a factor is paramount. As a TGF beta 1 inhibitor curcumine is a key factor to avoid fibrosis during muscle repair. The connective tissue growth factor (CTGF) is a family member of the TGF. CTGF is a molecule induced by TGF beta and plays an important role in skeletal-muscle fibrosis [42]. Also it stimulates the fibroblast differentiation into myofibroblasts. Other significant factor in the mechanics of muscle regeneration is insulin growth factor type 1 (IGF-1). Muscle type is the muscle insulin-like growth factor isomorfon type 1 (mIGF-1), which maintains tissue integrity during aging and exercise. Tissue concentration decreases in degenerative illnesses and caquexia and increases during postinjury repair [40]. IGF 1 and IGF 2 act through IGF-1 receptors and are keys to hypertrophy and muscle fiber growth [43]. They are of paramount importance for satellite cell differentiation into myoblasts. Also IGF intratissue injection increases the capacity of muscle fiber recovery [40]. To a lesser extent PDGF, TGF b, and HSPGs induce satellite cell differentiation into myoblasts. The intracellular IL-1 antagonist receptor – IL1a – has been reported at the skin level as having a possible effect on the muscle, decreasing fibrosis produced by fibroblasts [27]. Also it has been reported that the activity of the kinase inhibitor of NF-kappaB kinase 2 (IKKA2) induces regeneration through satellite cell activation and fibrosis decrease [34].

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On the other hand myoblast migration from the injury area is essential. Such migration is induced by the tumor necrosis factor-alpha (TNF) alpha through direct chemotactic or indirect ways by increasing the activity of the matrix metalloproteinases (MMPs) [53]. One hormone capable of acting at the regenerative stage level is relaxine. It induces myoblast differentiation into mature muscle fibers. Satellite cell differentiation into myofibroblasts is powered by cytokines, the nerve growth factor (NGF), and the TNG-alpha. P substance is a peptide that stimulates the expression of the TGF beta family, induces proliferation, fibroblast differentiation, and scar formation during healing [28]. In sum, when the satellite cell is at rest it remains undifferentiated yet when it is activated by the mediation of specific growth factors it expands itself and differentiates into myoblasts, myofibroblasts, or fibroblasts. On the whole, differentiation into any given cell line depends on stimulation of a specific growth factor. Studies demonstrate that implanting mother cells from the marrow into the injury area increases muscle regeneration [7]. In cases of significant muscle flaws, matrices built to act as mother cell supports have been reported [11]. It is necessary to promote and induce all growth factors that produce satellite cell differentiation into myoblasts and to a lesser extent into myofibroblasts, and inhibit all factors that condition stimulation and fibroblast production and eventually the appearance of fibrosis or scars at the bottom of the injury.

T.F.F. Jaén and P.G. García

deposits type I and III [30]; peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is another fibrogenesis inhibitor [31]; gamma interferon, human recombining protein; curcumine – a TGB beta 1 vegetal stain-inhibitor and radiotherapy protector [37]; IKK2/NF-kappaB; HGF + PPARgamma; metalloproteinases – enzymes responsible for collagen degradation. Direct injection of MMP-1 in the injury area during fibrogenesis may increase muscle regeneration following an increase in the number of myofibers, and growth-liberating factors. The MMP-1 injection decreases fiber tissue [5] too. Physiotherapy [1] followed by small frequent moves, eccentric muscle workout, and resistance workout all increase the muscle contractile capacity and decrease the chances of suffering relapses [16]; electrotherapy [56] can be applied too. From day 28, physical training needs to be increased, first stretching, then higher intensity of isometric and isokinetic muscle contractions but always in the absence of pain. Active sporting practice will only be possible once basic physical activity is absolutely painless [25]. It is very important to remind that the sportsman should not be back to active sporting practice until he is fully recovered since the rate of recurrent injury is very high [38]. In the world of sports and in particular in Sports Medicine methods to reuse or manipulate growth factors like the IGF-1 need to comply with all codes, rules, and regulations set forth by the World Anti-Doping Agency (WADA) [10].

Conclusions Fibrogenesis Stage or Third Stage Between 14 and 28 days, cell activity in all of the aforesaid cell lines increases while cell differentiation decreases. Some therapeutic agents have proven their capacity to inhibit fibrogenesis and increase muscle regeneration through the inhibition of the TGF beta 1. Here are some of these inhibitors: Angiotensine receptor blockers [4]; suramin – that blocks the TGF-beta 1 stimulator effect on muscle cells derived from fibroblasts. In vivo: decreases fibrosis, increases strength and muscle tension [8]; relaxine – that increases differentiation and proliferation of myoblasts and decreases the activity of myofibroblasts which eventually decreases fibrosis. In vivo: increases muscle regeneration, decreases fibrosis, and increases strength of the damaged muscle [35]; decorin – a small leucine surrounded by a proteoglycan matrix that plays an important role in TGF beta [46] controlled fibrogenesis which in turn has proven to have a correlation between decorin, myostatin, and TGF beta 1 in fibrosis decrease [62]; triple helix collagen containing-1 (Cthrc1) has proven to be a specific inhibitor of TGF beta that modifies collagen

This Protocol observes all the stages involved in muscle repair and the predominant biological reaction. Goals of these stages: First Stage – Control hematomas and swelling through physical means. Second Stage – Induce activation of satellite cells and its differentiation into myoblasts. Third Stage – Fibrogenesis inhibition. This regenerates the damaged muscle back into muscle and not fibrosis.

Concept Test Popliteus muscle injury pretreatment. Subject: 42 year-old male. Injury: popliteus muscle tears. Treatment; Protocol (Fig. 4a, b). Results: Images resonance magnetic (IRM) acute injury and 1 month later posttreatment (Fig. 5a, b).

New Protocol for Muscle Injury Treatment Fig. 4 (a) IRM sagittal and (b) axial images shows injury popliteus muscle

a

a

891

b

b

Fig. 5 (a) IRM sagittal and (b) axial images shows popliteus muscle posttreatment injury 1 month later

Protocol Find below the correct adequate Protocol for patients with tendon–muscle tears: 1. Evaluate the injury surgical indication. On the whole, the tendon muscle injury needs to be treated in a conservative way. Once surgical indication has been ruled out move on to the next step. 2. Check time elapsed from the occurrence of the injury until medical attention. 2.a. First Stage or Acute Injury Stage. Less than 24 h after the occurrence of the injury: 2.a.1. Intense intramuscular bleeding causing intense rising pain and growing pressure. Extract the hematoma through echographic control or whatever available technique at the medical center. Then move to step 2.a.2.

2.a.2. Nonintense intramuscular bleeding and/or hematoma post-evacuation. Apply RICE Protocol – Rest, Ice, Compression, and Elevation to stop the bleeding. Rest, Ice – local cold: Apply 10–15 min local cold in the injury area every 30 min for the first 24 h from the occurrence of the injury. Compression. Elevation of the affected limb. 2.a.3. Minimum bleeding or controlled bleeding: Start with vasoactive medication if it is not contraindicated. 2.b. Second Stage or Regenerative Stage. Twenty four hours after the occurrence of the injury and less than 14 days: Pharmacological measures to increase blood circulation. Avoid NSAIDs. When in pain provide pain relievers: Paracetamol, metamizol, etc. Avoid the RICE Protocol.

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Avoid immobilization, start with a mild mobilization from the beginning and if there is good tolerance start isometric and isotonic workout and eventually move to isokinetic workout. Avoid massaging. 2.c. Third Stage or Fibrogenetic Stage. Fourteen days after the occurrence of the injury and approximately less than 3–4 weeks: Pharmacological measures. Cut vasoactive medication and if it is not contraindicated provide fibrosis inhibitors until the fourth week from the occurrence of the injury. Initiate monitored adequate physiotherapy. 3. Back to the practice of sports. Only when stretchings, mobility, and contractions are painless. Start with basic moves, warm up and stretching to keep general physical shape going. Acknowledgments Carlos Revilla, MD. Clínica CEMTRO, Madrid, Spain. Prof. Pedro Cuevas. Hospital Ramon y Cajal, Madrid, Spain. Antonio Manquillo, MD. Clínica CEMTRO, Madrid, Spain.

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New Protocol for Muscle Injury Treatment action of peroxisome proliferator-activated receptor-gamma agonists. J. Am. Soc. Nephrol. 17, 54–65 (2006) 32. Maeda, K., Kanda, F., Okuda, S., Ishihara, H., Chihara, K.: Transforming growth factor-beta enhances connective tissue growth factor expression in L6 rat skeletal myotubes. Neuromuscul. Disord. 27, 234–240 (2005) 33. Magee, T.R., Artaza, J.N., Ferrini, M.G., Vernet, D., Zuniga, F.I., Cantini, L., Reisz-Porszasz, S., Rajfer, J., Gonzalez-Cadavid, N.F.: Myostatin short interfering hairpin RNA gene transfer increases skeletal muscle mass. J. Gene Med. 8, 1171–1178 (2006) 34. Mourkioti, F., Kratsios, P., Luedde, T., Song, Y.H., Delafontaine, P., Adami, R., Parente, V., Bottinelli, R., Pasparakis, M., Rosenthal, N.: Targeted ablation of IKK2 improves skeletal muscle strength, maintains mass, and induces regeneration. J. Clin. Invest. 116, 2866–2868 (2006) 35. Negishi, S., Li, Y., Usas, A., Fh, Fu, Huard, J.: The effect of relaxin treatment on skeletal muscle injuries. Am. J. Sports Med. 33, 1816–1824 (2005) 36. Ochoa, O., Sun, D., Reyes-Reyna, S.M., Waite, L.L., Michalek, J.E., McManus, L.M., Shireman, P.K.: Delayed angiogenesis and VEGF production in CCR2-/- mice during impaired skeletal muscle regeneration. Am. J. Physiol. Regul. Integr. Comp. Physiol. 293, 651–661 (2007) 37. Okunieff, P., Xu, J., Hu, D., Liu, W., Zhang, L., Morrow, G., Pentland, A., Ryan, J.L., Ding, I.: Curcumin protects against radiation-induced acute and chronic cutaneous toxicity in mice and decreases mRNA expression of inflammatory and fibrogenic cytokines. Int. J. Radiat. Oncol. Biol. Phys. 65, 890–898 (2006) 38. Orchard, J.: Management of muscle and tendón injuries in footballers. Aust. Fam. Physician 32, 489–493 (2003) 39. Payne, T.R., Oshima, H., Okada, M., Momoi, N., Tobita, K., Keller, B.B., Peng, H., Huard, J.: A relationship between vascular endothelial growth factor, angiogenesis, and cardiac repair after muscle stem cell transplantation into ischemic hearts. J. Am. Coll. Cardiol. 50, 1685–1687 (2007) 40. Quinn, L.S., Anderson, B.G., Plymate, S.R.: Muscle-specific overexpression of the type-1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3-K, and not calcineurin, signaling. Am. J. Physiol. Endocrinol. Metab. 293, 1538–1551 (2007) 41. Quintero, A.J., Wright, V.J., Fu, F.H., Huard, J.: Stem cells for the treatment of skeletal muscle injury. Clin. Sports Med. 28, 1–11 (2009) 42. Rönty, M.J., Leivonen, S.K., Hinz, B., Rachlin, A., Otey, C.A., Kähäri, V.M., Carpén, O.M.: Isoform-specific regulation of the actinorganizing protein palladin during TGF-beta1-induced myofibroblast differentiation. J. Invest. Dermatol. 126, 2387–2396 (2006) 43. Schertzer, J.D., Lynch, G.S.: Comparative evaluation of IGF-I gene transfer and IGF-I protein administration for enhancing skeletal muscle regeneration after injury. Gene Ther. 13, 1657–1664 (2006) 44. Shen, W., Li, Y., Tang, Y., Cummins, J., Huard, J.: NS-398, a cyclooxygenase-2-specific inhibitor, delays skeletal muscle healing by decreasing regeneration and promoting fibrosis. Am. J. Pathol. 167, 1105–1117 (2005) 45. Shi, M., Ishikawa, M., Kamei, N., Nakasa, T., Adachi, N., Deie, M., Asahara, T., Ochi, M.: Acceleration of skeletal muscle regeneration in a rat skeletal muscle injury model by local injection of human peripheral blood-derived CD133-positive cells. Stem Cells 27, 949–960 (2009) 46. Shi, Y.F., Zhang, Q., Cheung, P.Y., Shi, L., Fong, C.C., Zhang, Y., Tzang, C.H., Chan, B.P., Fong, W.F., Chun, J., Kung, H.F., Yang, M.: Effects of rhDecorin on TGF-beta1 induced human hepatic stellate cells LX-2 activation. Biochim. Biophys. Acta 1760, 1587–1595 (2006)

893 47. Shibata, M., Matsumoto, K., Aikawa, K., Muramoto, T., Fujimura, S., Kadowaki, M.: Gene expression of myostatin during development and regeneration of skeletal muscle in Japanese Black Cattle. J. Anim. Sci. 84, 2983–2989 (2006) 48. Siriett, V., Salerno, M.S., Berry, C., Nicholas, G., Bower, R., Kambadur, R., Sharma, M.: Antagonism of myostatin enhances muscle regeneration during sarcopenia. Mol. Ther. 15, 1407–1409 (2007) 49. Smith, C.A., Stauber, F., Waters, C., Alway, S.E., Stauber, W.T.: Transforming growth factor-beta following skeletal muscle strain injury in rats. J. Appl. Physiol. 102, 755–761 (2007) 50. Strasser, E.M., Wessner, B., Roth, E.: Cellular regulation of anabolism and catabolism in skeletal muscle during immobilisation, aging and critical illness. Wien. Klin. Wochenschr. 119, 337–348 (2007) 51. Summan, M., Warren, G.L., Mercer, R.R., Chapman, R., Hulderman, T., Van Rooijen, N., Simeonova, P.P.: Macrophages and skeletal muscle regeneration: a clodronate-containing liposome depletion study. Am. J. Physiol. Regul. Integr. Comp. Physiol. 290, 1488–1495 (2006) 52. Suzuki, K., Peake, J., Nosaka, K., Okutsu, M., Abbiss, C.R., Surriano, R., Bishop, D., Quod, M.J., Lee, H., Martin, D.T., Laursen, P.B.: Changes in markers of muscle damage, inflammation and HSP70 after an ironman triathlon race. Eur. J. Appl. Physiol. 98, 525–534 (2006) 53. Torrente, Y., El Fahime, E., Caron, N.J., Del Bo, R., Belicchi, M., Pisati, F., Tremblay, J.P., Bresolin, N.: Tumor necrosis factor-alpha (TNF-alpha) stimulates chemotactic response in mouse myogenic cells. Cell Transplant. 12, 91–100 (2003) 54. Toumi, H., F’guyer, S., Best, T.M.: The role of neutrophils in injury and repair following muscle stretch. J. Anat. 208, 459–470 (2006) 55. Uutela, M., Wirzenius, M., Paavonen, K., et al.: PDGF-D induces macrophage recruitment, increased interstitial pressure, and blood vessel maturation during angiogenesis. Blood 104, 3198–204 (2004) 56. Vega, A.: Tratamiento con electroterapia y masoterapia simultanea. Lesiones deportiva Ed. Mapfre Med. 269–274 (1996) 57. Viita, H., Markkanen, J., Eriksson, E., Nurminen, M., Kinnunen, K., Babu, M., Heikura, T., Turpeinen, S., Laidinen, S., Takalo, T., Ylä-Herttuala, S.: 15-Lipoxygenase-1 prevents vascular endothelial growth factor A and placental growth factor induced angiogenic effects in rabbit skeletal muscles via reduction in growth factor mRNA levels, NO bioactivity, and downregulation of VEGF receptor 2 expression. Circ. Res. 102, 177–184 (2008) 58. Wagner, K.R., Liu, X., Chang, X., Allen, R.E.: Muscle regeneration in the prolonged absence of myostatin. Proc. Natl Acad. Sci. USA 102, 2519–2524 (2005) 59. Wehling, P., Moser, C., Frisbie, D., McIlwraith, C.W., Kawcak, C.E., Krauspe, R., Reinecke, J.A.: Autologous conditioned serum in the treatment of orthopedic diseases: the orthokine therapy. BioDrugs 21, 323–332 (2007) 60. Welle, S., Bhatt, K., Pinkert, C.A., Tawil, R., Thornton, C.A.: Muscle growth after postdevelopmental myostatin gene knockout. Am. J. Physiol. Endocrinol. Metab. 292, E985–E991 (2007) 61. Willecke, K., Sáez, J.C.: Injury of skeletal muscle and specific cytokines induce the expression of gap junction channels in mouse dendritic cells. J. Cell. Physiol. 211, 649–660 (2007) 62. Zhu, J., Li, Y., Shen, W., Qiao, C., Ambrosio, F., Lavasani, M., Nozaki, M., Branca, M.F., Huard, J.: Relationships between transforming growth factor-beta1, myostatin, and decorin: implications for skeletal muscle fibrosis. J. Biol. Chem. 282, 25852–25863 (2007)

Shockwave Therapy in Sports Medicine Marc Rozenblat

Contents Introduction ................................................................................. 895 History.......................................................................................... 895 Technology ................................................................................... 895 Physiopathology .......................................................................... 896 Action Modes ............................................................................... 896 Contraindications........................................................................ 896 Technical Parameters.................................................................. 896

Introduction Shockwave is an innovation in the arsenal of therapies in sports medicine. Two types exist: Extracorporeal shockwave therapy (ESWT) and Radial (RSWT) shock wave therapy. The principle is the same in both cases: it uses ultrasonic waves. In the RSWT, there is a direct percussion on the skin and through connecting tissue, fat, and muscles without damaging them.

Adverse Effects ............................................................................ 896 Session Frequency and Valuation .............................................. 897 Blazina Levels Are Used to Help with the Assessment ............ 897 Evolution During Treatment ...................................................... 897 French Open Study ..................................................................... 897 Conclusion ................................................................................... 897 References .................................................................................... 898

History The beginning of this therapy was in the 1980s [2]. The principle of shockwave finds its origin lithotrity with the destruction of urinary calculi. ESWT is used in the bath. RSWT is used with a urethroscope to have an intracorporeal action. In the 1990s, ESWT was used on in vitro bone tissue fragmentation. In 1996, Rompe used RSWT in veterinary treatment on horse spine. Now, RSWT is used in many indications.

Technology RSWT uses an applicator on the skin (Fig. 1). The bobweight is propelled by an air pistol. The action is limited to the area directly impacted by the jet from the nozzle of the applicator. It is effective to a depth of 3.5 cm. The energy is about 0.02– 0.54 mJ/mm2. There are two different types of nozzles: s Standard source with divergent and wide treatment s Focused source with convergent and more precise treatment M. Rozenblat Coralis Center, 32ter avenue du Général Leclerc, Ozoir La Ferriere, France e-mail: [email protected]

The nozzle obliqueness and the patient’s suitable settlement are adaptable. The therapist can use medial or lateral treatment, with or without back support.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_115, © Springer-Verlag Berlin Heidelberg 2012

895

896

M. Rozenblat

Fig. 1 Bobweight propelled by air pistol

PRESSION

AIR-IN

AIR-OUT

FREQUENCE NBE DE COUPS APPAREIL A MAIN UNITE DE CONTRÔLE

s Gate-control: RSWT interrupts the perception of pain by stimulating the high-caliber sensitive nerve fibers. s Mechanical: it is the essential effect with a defibrotic action similar to that in deep transversal massage (CyriaxTroisier)

Pressure (p)

p+

tw

p

ta

Contraindications Time (t)

Fig. 2 Transitory phenomenon with two phases: positive (compression), negative (relaxation)

Some situations are not recommended: use near the abdomen in pregnancy, child epiphyseal plate, cutaneous neurologic pathologies, vascular pathologies, infection, proximity of pulmonary tissue, coagulation perturbation or usage of anticoagulant drugs treatment, and also tumors. Consequently, X-rays are needed before RSWT.

Generally, anesthesia is not required but contact gel is used for better comfort during the therapy.

Physiopathology RSWT uses sound wave and acoustic resonance (Fig. 2). The pressure is a transitory phenomenon with two phases. The first has a positive pressure. It last 10 ns. It is the compression phase. The second is the continuation of the first. It is a negative pressure with cavitation phenomenon. Relaxation and decompression of the tissue are observed.

Technical Parameters The number of strokes is generally always 2,000 by session. The frequency of the strokes is a function of the depth of the lesion. When the lesion is superficial the frequency is high (near 15 Hz). When the lesion is deep, the frequency is low around 3 Hz. The pressure is dependent on each patient’s tolerance and can be changed every session. The most important thing is to remember that shockwave therapy must not be painful (“primum non nocere”).

Action Modes There are three different action modes: s Chemical: with liberation of pain-inhibiting endorphines. Sometimes there is an immediate anesthetic effect.

Adverse Effects They are unusual but possible and described in medical literature: increased pain, ecchymosis, swelling, and edema.

Shockwave Therapy in Sports Medicine

Session Frequency and Valuation In the beginning (the 1990s), German practitioners used 6–12 sessions with 15 days between 2 sessions [3]. Now, 1 or 2 sessions weekly, for a total of 3–6 sessions with 7 days between 2 sessions is recommended. So the treatment lasts 15–45 days and the number of sessions is determined depending on individual result.

Blazina Levels Are Used to Help with the Assessment s Level 0: asymptomatic s Level 1: pain at the beginning of exercise and/or during sporting activity s Level 2: pain at the beginning of exercise, decreasing during sporting activity and restarting after exercise s Level 3: continuous pain

Evolution During Treatment There are three cases: s Excellent cases (Blazina 1 or 2): the asymptomatology is covered with 3 sessions in 15 days. Intensive sport could be resumed 6 weeks after the first session. s Less favorable cases. Pain disappears after 4–6 weeks. Intensive sport is authorized after less than 15 days in the absence of pain. s Bad cases (Blazina 3). Pain persists after 5 or 6 sessions. No intensive sport is admitted. Other treatments must be proposed.

French Open Study Seven thousand associated cases of shockwave therapy in sport over a period of 5 years in three French medical centers are reported. Here is a tabular distribution of these 7,000 cases (Table 1). A lot of chronic locomotor pathologies are cited in the literature and treated [4, 5, 9, 12, 15, 18, 32, 36, 37, 39–41]. s Tendinitis with or without calcification [7, 8, 10, 11, 13, 14, 19, 23, 25, 28–30, 34] s Periosteum lesions [33, 35]

897 Table 1 Properties of seven thousand patients involved in French open study Distribution of 7,000 cases

s s s s

Men

4,643

66%

Women

2,357

34%

Average age

35

18%–75%

Competitive sport

1,820

24%

Regular leisure exercise

2,100

30%

Occasional exercise

2,170

31%

No physical training

910

13%

Chronic muscle lesions [24, 27] Bone lesions: non-union and pseudarthrosis [6, 26, 31] Chronic ligamentous lesions [16, 17, 20–22] Trigger points [1, 38]

In different localizations [5, 32] and principal indications: Shoulder: supraspinatus tendinosis, supraspinatus calcification, bursitis ± calcification, tenosynovitis Elbow: Lateral corporeal epicondylitis, lateral enthesis epicondylitis, medial epicondylitis, medial enthesis epicondylitis Wrist: De Quervain tenosynovitis, bursitis, radial styloïditis Hand: rhizarthrosis, digital pulley bursitis, Dupuytren’s contracture Pelvis: gluteus medius bursitis, hamstrings lesions, pubalgia, pubic arthropathy, adductor tendinosis Knee – extensor apparatus: quadriceps femoris enthesopathy, patellar ligamentosis Knee – others: iliotibial bursitis, Pellegrini Stieda syndrome, Pes anserinus tendinosis Leg: peroneus tenosynovitis, tibial periostosis, periosteum lesions Calcaneal tendinosis: corporeal, calcification, insertion Fasciitis plantaris: insertion, fibrosis lesion Foot end ankle: Morton’s neuralgia, tibial tendinosis, talo crural conflict Muscles: hamstrings lesion, quadriceps lesion, calf lesion, lumbago Some results are given (Table 2).

Conclusion Shockwave therapy in sports medicine is a brand-new innovation. With harmlessness, swiftness, and effectiveness, 70% of patients have satisfaction and relief within the initial 15 days

898 Table 2 Results of French open study Examples

M. Rozenblat

Cases

Average sessions extremes

Satisfied patients (%)

Retrospect months extremes

Calcific tendinitis of rotator cuff

760

3.4 (1–6)

78

43 (1–60)

Shoulder impingement syndrome

677

2.8 (1–4)

86

36 (1–60)

Corporeal epicondylitis humeri lateralis

945

3.8 (1–6)

78

36 (1–60)

Corporeal epicondylitis humeri medial

175

4.3 (3–6)

66

18 (1–54)

De Quervain tenosynovitis

350

4.3 (3–6)

66

25 (1–54)

Patellar tendinosis

560

4.6 (1–6)

73

32 (1–60)

Intramuscular fibrosis

362

5.1 (3–8)

85

36 (1–60)

Fasciitis plantaris

1,000

2.3 (1–60)

89

36 (1–60)

Achilles insertion

16

5.3 (3–6)

20

8 (3–54)

Corporeal Achilles tendinosis

1,213

3.4 (1–6)

82

36 (1–60)

of treatment with 3 sessions; 75–80% return to intensive sport after 6 weeks. RSWT is a workable alternative to conventional treatment in sports medicine traumatology.

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13. Haupt, G., Haupt, A., Gerety, B., Chvapil, M.: Enhancement of fracture healing with extra-corporeal shock waves. J. Urol. 143, 230 (1990) 14. Haupt, G., Dieschr, R., Straub, T., et al.: A new cost-effective treatment for calcaneal spur and tennis elbow; ballistic extracorporeal shock-wave therapy. In: 2è Congrès de la société européenne des traitements par ondes de choc radiales sur l’appareil locomoteur, Londres, 27–29 May 1999 15. Haupt, G., Dieschr, R., Straub, T., et al.: Comparison of conventional extracorporeal shock-wave therapy and the new method of radial shock therapy in the treatment of calcaneal spurs. In: 8è Congrès mondial de la société internationale de recherche orthopédique et traumatologie, Sydney, Avr 1999 16. Krischek, O., et al.: Symptomatic low energy shockwave therapy in heel pain and radiologically detected plantar heel spur. Z. Orthop. Ihre Grenzgeb. 136(2), 169–174 (1998) 17. Krischek, O., Pompe, J.D., Hopf, C., Vogel, J., Herbsthofer, B., Nafe, B., Bürger, R.: Extracorporeal shock wave therapy in epicondylitis humeri ulnaris or radialis-a-prospective, controlled, comparative study. Z. Orthop. Ihre Grenzgeb. 136(1), 3–7 (1998) 18. Labareyre, H. (de), Saillant G.: Evaluation de l’efficacité des traitements par ondes de choc radiales sur les tendinopathies du membre inférieur chez le sportif (à propos de 52 patients): le spécialiste de Médecine du. Sport au Service des Praticiens, 28, 34–40 (2000) 19. Loew, M., et al.: Shock-wave therapy is effective for calcifying tendinitis of the shoulder. J. Bone Joint Surg. Br. 81(5), 863–867 (1999) 20. Lohrer, H., Schöll, J., Hirschmann, M.: Mechanical versus electromagnetic energy generation in extracorporeal shock-wave therapy (ESWT) of plantar fasciitis. In: 4è congrès de l’EFORT, Bruxelles, Juin 1999 21. Lohrer, H., Schöll, J., Haupt, G.: Prospekive, multizentrische und placebokontrollierte studie zur beh dlung der fasciitis plantaris/fersensporn mit ballistisch generierten stobwellen 22. Lohrer, H., Schöll, J., et al.: Mechanically versus electromagnetically energy generation in extracorporeal shock-wave therpy (ESWT) of plantar fasciitis. In: 4th congress of the European federation of national associations of orthopaedics and traumatology (EFFORT). Brussels, 3–8 June 1999 23. Maier, M., et al.: Analgesic effect of low energy extracorporeal shock waves in tendinosis calcarea, epicondylitis humeri radialis and plantar fasciitis. Z. Orthop. Ihre Grenzgeb. 138(1), 34–38 (2000) 24. Merskey, H., Bogduk, N. (eds.): Classification of Chronic Pain, p. 182. IASP, Seattle (1994) 25. Perlick, L., et al.: High energy shock wave therapy treatment of the painful heel spur. Unfallchirurg 101(12), 914–918 (1998)

Shockwave Therapy in Sports Medicine 26. Rompe, J.D., Rumler, F., Hopf, C., Nafe, B., Heine, J.: Extracorporeal shock wave therapy for the calcifying tendinitis of the shoulder. Clin. Orthop. 321, 196–201 (1995) 27. Rompe, J.D., Rumler, F., Hopf, C., Nafe, B., Heine, J.: Extracorporeal shock wave therapy in the treatment of near to bone soft tissue pain in sportsmen. Int. J. Sports Med. 17, 79 (1996) 28. Rompe, J.D., et al.: Extracorporeal shock wave therapy for calcifying tendinosis of the shoulder. Clin. Orthop. 321, 196–201 (1995) 29. Rompe, J.D., et al.: Low energy extracorporeal shock wave therapy for persistent tennis elbow. Ins. Orthop. 20(1), 23–27 (1996) 30. Rompe, J.D., et al.: Extracorporeal shock wave therapy of radiohumeral epicondylopathy – an alternative treatment concept. Z. Orthop. Ihre Grenzgeb. 134(1), 63–66 (1996) 31. Rompe, J.D., et al.: Shoulder function after extracorporeal shock wave therapy for calcifying tendinitis. Shoulder Elbow Surg. 7, 505–509 (1998) 32. Rozenblat, M.: Utilisation simultanée des ondes de chocs radiales et de la cryothérapie gazeuse hyperbare en cabinet de traumatologie sportive. A propos de 333 cas. J. Traumatol. Sport 20, 211–218 (2003) 33. Schöll, J., Lohrer, H.: Radial stobwellentherapie bei insertionstendinopathien. Dtsch. Z. Sportmed. 50(D-067), 115 (1999) 34. Schöll, J., Lohrer, H.: Radial extracorporeal shock-wave therapy for insertion tendinopathies. Int. J. Sports Med. 20(D-067), S106 (1999)

899 35. Schöll, J., Lohrer, H.: Successful therapy of insertional tendinopathies of the elbow and heel by a new, unfocused shock-wave devicea-prospective, randomized, blind study. In: 4è congrès de l’EFORT, Bruxelles, Juin 1999 36. Simons, D.G., Stolov, W.C.: Microscopic features and transient contraction of palpable bands in canine muscle? Am. J. Phys. Med. 55, 65–88 (1976) 37. Straub, T., Penninger, E., Froelich, T., et al.: Therapieerfolgder stobwellenbehandlung beim fersensporn – eine prospektive, multizentrische, placebokontrollierte studie. Dtsch. Z. Sportmed. 50(D-068), 115 (1999) 38. Travell, J.G., Simons, D.G.: Myofascial Pain and Dysfunction: The Trigger Point Manual, pp. 5–164. Williams and Wilkins, Baltimore (1993) 39. USTA, Roetert, E.P., Ellenbecker, T.S.: Complete Conditioning for Tennis, p. 184. Human Kinetics, Champaign (1998) 40. Valchanov, V.D., Michailov, P.: High energy shock waves in the treatment of delayed and nonunion fractures. Int. Orthop. 15, 181–184 (1991) 41. Wang, C.J., et al.: Treatment of painful heel using extracorporeal shock wave. J. Formos. Med. Assoc. 99(7), 580–583 (2000)

Growth Factors: Application in Orthopaedic Surgery and Trauma M. Garcia Balletbo and Ramon Cugat

History

Contents History.......................................................................................... 901 Physiological Processes ............................................................... 902 Regenerative Biology .................................................................. 902 Growth Factors: GFs .................................................................. 902 Functions ....................................................................................... 902 Classification ................................................................................. 903 PRP .............................................................................................. 903 PRGF® Definition ........................................................................ 903 Obtaining Technique ..................................................................... 904 GFs Therapy ................................................................................ Cartilage ........................................................................................ Menisci.......................................................................................... Ligament ....................................................................................... Bone .............................................................................................. Tendon ..........................................................................................

904 905 905 905 905 905

References .................................................................................... 905

M.G. Balletbo Regenerative Medicine Unit, Fundation Garcia Cugat, Hospital Quiron Barcelona, Plaza Alfonso Comin, 5 – 7 Planta (-1), 08023 Barcelona, Spain e-mail: [email protected] R. Cugat ( ) Orthopaedic Surgical Department, Fundation Garcia Cugat, Hospital Quiron Barcelona, Plaza Alfonso Comin, 5 – 7 Planta (-1), 08023 Barcelona, Spain e-mail: [email protected]

One of the pioneers in the study of bioactive molecules is Professor Marshall R. Urist, who in 1965 published: “The extracellular matrix of bone tissue that has the capacity of inducing bone formation, it is known as Bone Morphogenetic Protein (BMP)” [55]. Some years later studies carried out by Samuel Balk demonstrated that specific animal cells such as chicken fibroblasts, rat thymus, and bone marrow cells require appreciable extracellular concentrations of calcium ions or factors peculiar to serum but not to plasma, to initiate their division [10]. After this, papers from different authors started being published: “evidence that platelets are an enriched source of growth-promoting activity for BTB mouse fibroblasts”, published by Nancy Kohler et al. “The role of Factors Derived from blood serum in promoting cell proliferation in vitro” was studied and published by Russell Ross’ team [31, 40]. It is important to highlight a paper describing the Human Platelets, which contain a Polypeptide Growth Factor that stimulates the Proliferation of Connective Tissue Cells. The authors identified two types, PDGF I and PDGF II; both were constituted from two aminoacid chains of different molecular weight” .The paper was published by Antoniades et al. [7]. And Heldin et al. studied the chemical properties of PDGF and the utilization of these properties in a purification protocol for PDGF, which led to an electrophoretically pure product [26]. In 1987, after a scientific meeting hosted by the US National Science Foundation where the objective was to discuss an upcoming concept combining biology and engineering, Professor Fung of California University, San Diego, in La Jolla (USA), coined the term “Tissue Engineering” for treatments with cells, bioactive molecules – growth factors (GFs) and cytokines – and scaffolds to regenerate tissues such as the skeletal muscle [60]. More recently, in 1995, the multidisciplinary group led by oral surgeon Eduardo Anitua, founder of the Biotechnology Institute, and the foundation named after him increased the knowledge of platelet function and its therapeutic applications [3, 4].

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_116, © Springer-Verlag Berlin Heidelberg 2012

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Platelets are small blood cell fragments that arise from the megakaryocytes without nucleus and have two functions: that of interrupting bleeding when there has been a vascular injury (haemostatic function) and stimulating cell proliferation and tissue scarring (bio-therapeutic function) when they release GFs that have been synthesized by the megakaryocytes and stored in the D granules [3, 4, 23, 24, 37].

Physiological Processes All body tissue cells are in a process of continuous renovation. Bone tissue cells are submerged in the extracellular matrix, which is a network formed from macro-molecules. The extracellular matrix participates in cellular metabolism and behaviour regulation of the cells in contact with it. Soluble factors, which are proteins, can be found in it; these include BMP morphogenetic proteins and Growth Factors (GFs), which give volume and are involved in biological tissue function, directing cell, tissue and organ embryological development, and play an important role in postfoetal physiology [3]. There are two important concepts in regenerative biology: Regeneration and Repair. Regeneration is tissue property restoration that is indistinguishable from the original. Repair is the restoration of tissue physical and mechanical properties, such as architecture and function, where the result is inferior to the original. It is a spontaneous transformation resulting in a scar.

Regenerative Biology Bearing regeneration and repair in mind, after tissue injury the objective is to Reconstruct the Form and Restore the Function. The combination of biology and engineering, tissue engineering, using artificial or natural biosubstances can achieve regeneration. Tissue regeneration has three phases, cell migration, proliferation and differentiation, and the above mentioned biosubstances have different mechanisms in the process. The artificial biosubstances are called scaffolds. They encourage cells to proliferate rapidly and synthesize proteins vigorously. And the natural biosubstances which are GFs and cytokines regulate key events in repair and regeneration. The use of GFs has been considered a way to manipulate the host healing response at the site of injury: they identify signals that regulate cell proliferation and differentiation.

M.G. Balletbo and R. Cugat

Regeneration is brought about by activating certain cells providing adequate stimulation signals and/or neutralising certain suppressive signals. One requirement is the potential for cell division which can be classified into: labile, stable and permanent. Lost permanent cells cannot be substituted, but on the other hand they have a long life and live in protected areas: i.e. nerve cells. Most differentiated cells are not permanent and renew themselves. The new ones are produced in two ways: simple duplication of pre-existing cells: i.e. liver cells, or from nondifferentiated stem cells via a process of differentiation which involves a change in the cellular phenotype. The precursor cells: stem cells, GFs and BMPs play an important role in the post foetus physiology and are essential in embryogenesis and repair. Both processes have great similarities [4].

Growth Factors: GFs Growth Factors (GFs) are soluble and diffusible Polypeptides. In numerous types of cells they are responsible for growth regulation, differentiation and phenotype: i.e. muscularskeletal system cells. Their molecular weight range is from 5 to 35 KDa. A big variety of cells produce them. The sources of the GFs are the extracellular matrix, the platelets megakaryocytes, the plasma and others. They carry out their function by joining specific membrane receptors situated in the surface of the cell when being sent from one cell to another in order to transmit a specific signal: i.e. cellular migration, cellular differentiation etc. This signal can be sent from one cell directly to another cell when they are close or through the factor when further apart. Some are synthesized by almost all the cells, for example TGFE1, which is involved in almost all physiological processes [4].

Functions Each one has one or several specific activities in a predetermined cell, depending on the specific environmental circumstances. Therefore, GFs are multifunctional. As mentioned previously they are involved in repair and regeneration and also, regulate key processes such as Mitogenesis, Chemotaxis, Cell Differentiation and Metabolism [4].

Growth Factors: Application in Orthopaedic Surgery and Trauma

Classification They are named according to their origin or activity. GFs found in bone tissue and in those tissues involved in regeneration are: PDGF: Platelet Derived GF. Produced by the platelets, macrophages and endothelial cells, it is a protein stored in the platelets’ alpha granules and is released when the platelets group together and the coagulation cascade begins. The connective tissue cells in the area respond by initiating a replication process [4]. VEGF: Vascular Endothelial GF. Its aminoacid sequence has a 24% similarity to that of PDGF-E. It has different biological effects because it joins different receptors: a powerful selective mitogene for endothelial cells and has an angiogenic action in vivo [4]. TGF-E: Transformed GF. Is a protein super-family which includes morphogenetic bone proteins among others. It has three fundamental functions and according to the environmental circumstances of the cells, it carries out one or another. Its functions are as follows: s Modulates cell proliferation: it is a suppressor; s Increases extracellular cell matrix synthesis and inhibits its degradation; s Exerts an immunosuppressor effect [4]. AFGF and bFGF: Acidic and Basic Fibroblastic GFs are synthesized by a variety of cells: i.e. fibroblast, osteoblasts, etc. and are identified by four different types of receptors. They stimulate the proliferation of most cells involved in repair: endothelial capillaries, endothelial vessels, fibroblasts, keranocytes, chondrocytes, myoblasts, etc. [4]. IGF-I and IGF-II: Insulin like GF Type I and II. Both are abundant in bone tissue. IGF-I is produced by osteoblastic cells, stimulates bone formation by triggering cell proliferation. It increases the number of osteoclastic multinucleated cells, the differentiation and Type I Collagen biosynthesis [4]. EGF: Epidermal GF. Similar to TGF-D in structure and biological action, and it joins the same receptors. It is synthesized in the kidneys, submandibular, lachrymal, and Brunner glands. It is also synthesized by the megakaryocytes. It is found in saliva, tears, and urine. It stimulates migration and mitosis of the epithelial cells and increases protein synthesis: i.e. fibronectin. It increases the collagen because it attracts fibroblasts by chemotaxis, which synthesizes collagen [4]. HGF: Hepatocyte GF is multifunctional inducing diverse biological events [66]. The GFs related with the number of platelets are: PDGF, TGF E1 and TGF E2, VEGF, EGF and bFGF. They are produced by the megakaryocytes and stored in the alpha-granules

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of the platelets. The plasma GFs not related to the number of platelets are IGF I and HGF [3]. The TGF-E1, PDGF and IGF-I: modulate cell proliferation and migration, and extracellular matrix synthesis. And the VEGF, HGF and bFGF are chemotactic and mitogenic for endothelial cells promoting angiogenesis and vascularization a key step in healing [3].

PRP It is a plasma preparation containing platelets and fibrin. Its properties are: anti-inflammatory, anti-bacterial, analgesic, it is involved in healing process and biological glue [3]. The platelets which come from megakaryocytes, don’t have nucleus but alpha granules which contain GFs. They play a role in coagulation, haemostasis and the healing process. Their presence in PRGF® gives the properties, antiinflammatory, anti-bacterial, analgesic and regenerative-repair while the fibrin gives the biological glue property [3]. Currently there are several commercial products available for obtaining PRP, all of which have some steps in common: 1. Patient’s peripheral blood is required. 2. Then it is centrifuged. 3. The result is divided into three layers: the base, red, contains erythrocytes; the middle, white thin ring, contains leukocytes and inflammatory cytokines; and the top, yellow, is plasma with platelets and GFs. And the differences are: 1. The speed and number of centrifugations resulting in different platelet concentrations. 2. The use of anticoagulant in the blood sample container. 3. The presence of leukocytes in the final preparation. 4. The use of an activator. Obviously the final product obtained performing one method or another is different and therefore the results obtained with their application could be different [35].

PRGF® Definition PRGF® is Plasma Rich in Platelets with all the Proteins and Plasmatic Coagulation Factors. The GFs which compose the PRGF® are PDGF Platelet Derived Growth Factors, TGF E1 & TGF E2 Transformed Growth Factor E1 & Transformed Growth Factor E2, IGF I Insulin Growth Factor Type I, VEGF Vascular Endothelial Growth Factor A & C, FGF

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Fig. 1 Laboratory equipped with specific technology for carrying out PRGF® technique described by Anitua

M.G. Balletbo and R. Cugat

Fig. 3 The “red tube” shows haemolysis. Anitua’s technique rejects this sample

Fig. 4 Anitua’s technique also rejects inclusion of leukocytes in the final product

Fig. 2 Blood aspect in anticoagulant sterile tubes after centrifugation. Red layer, thin white ring, yellow layer can be observed

Basic Fibroblastic Growth Factor, EGF Epidermic Growth Factor and HGF Hepatic Growth Factor [3].

Obtaining Technique It is obtained following the technique described and patented by Anitua (Fig. 1). The main characteristics are: s It is carried out using small quantities of blood: from 9 to 72 ml (Fig. 2).

s The plasma fraction is obtained from a single slow spin at 460 g for 8 min. s The clot is obtained by adding Calcium (Calcium Chloride) without having to use bovine thrombin. s The final product contains no leukocytes and the platelet concentration is from ×2 to ×3. PRGF® does not contain leukocytes because leukocytes make fibrin unstable by accelerating fibrinolysis and also contain MMPs that contribute to the extracellular matrix degradation (Figs. 3 and 4) [3, 4].

GF Therapy The aim is to use platelets mimicking the physiological process when a tissue is damaged [37]. Many studies in different fields of medicine have recently been published on the study and clinical use of the BMP

Growth Factors: Application in Orthopaedic Surgery and Trauma

morphogenetic proteins and on GFs. The goal of each of these is to identify: the optimum combinations of these proteins, with higher power, the most effective exposure time, the most effective therapeutic dosages and as well as how to define the right ways to release them [2, 11, 12, 14, 20, 21, 27, 35, 39, 53, 59, 65]. The current applications in orthopaedic surgery and sports medicine are:

Cartilage The aim of treating chondral injuries with PRGF® is to re-fill defects with new chondral tissue [1, 5, 15, 17, 22, 32, 33, 42, 46, 49, 50]. Technique: In osteoarthritic joints the advised protocol is 3–5 intraarticular PRGF® injections of 7–9 cc, one injection every 7–10 days [16, 56].

Menisci The objective of applying PRGF® in meniscal injuries is to start the repair process. It is currently being applied in meniscus suture and transplantation [13]. Technique: PRGF® 7–9 cc injected intraarticular at the end of the surgery [13].

Ligament The aim of treating ligament injuries with PRGF® is increased collagen synthesis, increased fibroblast synthesis, improved scarring speed, increased tension strength resistance, increased maturing speed [9, 28–30, 34, 41, 47, 48, 51, 52, 54, 58, 61–64]. Currently it can be used as conservative treatment for MCL and ankle lateral ligament injuries [13] as well as surgical treatment of ACL ruptures [13, 38, 45]. Technique: Conservative treatment: PRGF® 5 cc local injection. Then the joint is braced avoiding stress ligament injury and permitting full range of motion [13]. The use of PRGF® in ACL surgery has two goals: to prevent anterior knee pain and to achieve a quicker fixation and maturity of the graft [38, 45]. Technique: Some orthopaedic surgeons keep the graft submerged in PRGF® throughout the surgery [45]. Others inject 5 cc of PRGF® in the graft in the last phase of surgery and another 5 cc PRGF® in the donor part of the patella and patella tendon [13, 38].

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In partial ACL tears 5 cc of PRGF® is injected in the remaining fibres of the ACL under arthroscopic control. Then the knee is kept in extension with a brace for 4 weeks [13].

Bone The objective of applying PRGF® in bone fractures is: improve bone healing, stimulate the proliferation of trabecular bone cells and osteoblast-like cells, and by doing so avoid pain and disability [18, 44, 57]. Technique: Local PRGF® injection, amount administered according to the fracture site and its surrounding areas [44].

Tendon The goal is to obtain a new healthy tendon tissue [6, 8, 19, 25, 36, 43]. Technique: PRGF® can be applied by local injection or as a gel during a surgical procedure when the tendon is sutured [13, 43]. The local injection is carried out in and around the injured area of the tendon, after which healing progress is evaluated by ultrasonography to confirm whether or not a repeat injection is required. For target area accuracy, the injection can be carried out under ultrasonography control [13, 43].

References 1. Aito, M., Takahashi, K.A., Arai, Y., et al.: Intra-articular administration of platelet-rich plasma with biodegradable gelatin hydrogel microspheres prevents osteoarthritis progression in the rabbit knee. Clin. Exp. Rheumatol. 27, 201–207 (2009) 2. Alsousou, J., Thompson, M., Hulley, P., Noble, A., Willett, K.: The biology of platelet-rich plasma and its application in trauma and orthopaedic surgery. A review of the literature. J. Bone. Joint. Surg. 91B, 987–996 (2009) 3. Anitua Aldecoa, E.: Un enfoque biológico de la implantología. Team Work Media España, Vitoria, pp. 43–53 (2008) 4. Anitua, E., Andía, I., Ardanza-Trevijavo, B., Bozzi, L., Fombellida, F., Nurden, P., Nurden, A., Saracibar, N., Vicinay, S.: Un nuevo enfoque en la regeneración ósea. Plasma Rico en Factores de Crecimiento (PRGF®) (2000) 5. Anitua, E., Sanchez, M., Nurden, A.T., Zalduendo, M.M., De La Fuente, M., Azofra, J., et al.: Platelet-released growth factors enhance the secretion of hyaluronic acid and induce hepatocyte growth factor production by synovial fibroblasts from arthritic patients. Rheumatol 46, 1769–1772 (2007) 6. Anitua, E., Sanchez, M., Nurden, A.T., et al.: Autologous fibrin matrices: a potential source of biological mediators that modulate tendon cell activities. J. Biomed. Mater. Res. A 77, 285–293 (2006)

906 7. Antoniades, H., Scher, Ch, Stiles, Ch: Purification of Human plateletderived growth factor. Proc. Natl. Acad. Sci. 76, 1809–1813 (1979) 8. Arnoczky, S.P., Anderson, L., Fanelli, G., HO, S., Mishra, A., Sgaglione, N.: The role of platelet-rich plasma in connective tissue repair. Orthop. Today 26, 29 (2009) 9. Azuma, H., Yasuda, K., Tohyama, H., et al.: Timing of administration of transforming growth factor-beta and epidermal growth factor influences the effect on material properties of the in situ frozenthawed anterior cruciate ligament. J. Biomech. 36, 373–381 (2003) 10. Balk, S.: Calcium as a regulator of the proliferation of normal, but not of transformed, chicken fibroblasts in a plasma-containing medium. Proc. Natl. Acad. Sci. 68-A, 271–275 (1971) 11. Bramono, D.S., et al.: Matrix metalloproteases and their clinical applications in orthopaedics. Clin. Orthop. Rel. Res. 4, 434–439 (2005) 12. Cugat, R.: PRGF: application in orthopaedic surgery and trauma. Orthopaedics Today Europe. SLACK (11): editorial (2008) 13. Cugat, R.: Platelet derived growth factors: experience in soft tissue injuries and in joint trauma. Presented at the 7th Biennial International Society of Arthroscopy, Knee Surgery & Orthopaedic Sports Medicine (ISAKOS) Congress, Osaka, Japan, April 5–9 2009 14. Cugat, R., Garcia-Balletbo M.: Growth factors. Brief review. J. Eur. Musculoskelet. Rev. 5(2):32–35 (2010) 15. Cugat, R., Carrillo, J.M., Serra, C.I., Soler, C.: Articular cartilage defects reconstruction by plasma rich growth factors. In: Timeo, (ed.), Basic Science, Clinical Repair and Reconstruction of Articular Cartilage Defects: Current Status and Prospects, Chapter 88. pp. 801–807 (2006) 16. Cugat, R., Garcia-Balletbó, M.: Treatment of chondral lesions with plasma-rich growth factors. Oral presentation at the Japan knee society 29th annual meeting. Hiroshima, Japan, 2004 17. Cugat, R., Carrillo, J.M., Sopena, J., et al.: Treatment results of chondral lesions using plasma rich in growth factors and other substances. Electronical Poster at ISAKOS Bi-annual Congress. Hollywood, FL, US (2005) 18. Einhorn, T.A.: Clinical applications of recombinant human BMPs: early experience and future development. J. Bone. Joint. Surg. 85-A(Suppl 3), 82–88 (2003) 19. Filardo, G., Kon, E., Della Villa, S., Vincentelli, F., Fornasari, P.M., Marcacci, M.: Use of platelet-rich plasma for the treatment of refractory jumper’s knee. Int. Orthop. 34(6), 909–915 (2009) 20. Folkman, J., Browder, T., Palmblad, J.: Angiogenesis research: guidelines for translation to clinical application. Thromb. Haemost. 86, 23–33 (2001) 21. Foster, T.E., Puskas, B.L., Mandelbaum, B.R., Gerhardt, M.B., Rodeo, S.A.: Platelet-rich plasma. From basic science to clinical applications. Am. J. Sports. Med. 37, 2259–2272 (2009) 22. Fu, F.H., Musahl, V.: The treatment of focal articular cartilage lesions of the knee future trends and technologies. Sports. Med. Arthro. 11, 202–212 (2003) 23. George, J.N.: Platelets. Lancet 29, 1531–1539 (2000) 24. George, J.N., Nurden, A.T., Phillips, D.R.: Molecular defects in interactions of platelets with the vessel wall. New. Engl. J. Med. 311, 1084–1098 (1984) 25. Gosen, T., Sluimer, J. et al.: Prospective randomized study on the effect of autologous platelets injection in lateral epicondylitis compared with corticosteroid injection. Poster P25–444 Presented at: 13th Congress of the European Society of Sports Traumatology, Knee Surgery and Arthroscopy (ESSKA), Porto, Portugal, May 21–24 2008 26. Heldin, C.-H., Westermark, B., Wasteson, A.: Platelet-derived growth factor: purification and partial characterization. Proc. Natl. Acad. Sci. 76, 3722–3726 (1979) 27. Howell, H.T., Fiorellini, J.P., Paqutte, D.W., Offenbacher, S., Giannobile, W.V., Lynch, S.E.: A phase I/II clinical trial to evaluate a combination of recombinant human platelet-derived growth

M.G. Balletbo and R. Cugat factor-BB and recombinant human insulin-like growth factor-I in patients with periodontal disease. J. Periodontol. 68, 1186–1193 (1997) 28. Howell, S.M., Knox, K.E., Farley, T.E., et al.: Revascularization of a human anterior cruciate ligament graft during the first 2 years of implantation. Am. J. Sports. Med. 23, 42–49 (1995) 29. Ju, Y.J., Tohyama, H., Kondo, E., et al.: Effects of local administration of vascular endothelial growth factor on properties of the in situ frozen thawed anterior cruciate ligament in rabbits. Am. J. Sports. Med. 34, 84–91 (2006) 30. Kawamura, S., Ying, L., Kim, H.J., Dynbil, C., Rodeo, S.A.: Macrophages accumulate in the early phase of tendon-bone healing. J. Orthop. Res. 23, 1425–1432 (2005) 31. Kohler, N., Lipton, A.: Platelets as a source of fibroblast growthpromoting activity. Exp. Cell. Res. 87, 297–301 (1974) 32. Kon, E., Buda, R., Filardo, G., DI Martino, A., Timoncini, A., Cenacchi, A., et al.: Platelet-rich plasma: intra-articular knee injections produced favorable results on degenerative cartilage lesions. Knee. Surg. Sports. Traumatol. Arthrosc. 18, 472–479 (2009) 33. Kon, E., Buda, R., Filardo, G., Timocini, A., Marcacci, M., Giannini, S.: The treatment of severe Chondropaties of the knee: platelet rich plasma vs hyaluronic acid. Presented at: 8th World Congress of the International Cartilage Repair Society (ICRS), Miami, May 23–26 2009 34. Kuroda, R., Kurosaka, M., Yoshiya, S., Mizuno, K.: Localization of growth factors in the reconstructed anterior cruciate ligament: immunohistological study in dogs. Knee. Surg. Sports. Traumatol. Arthrosc. 8, 120–126 (2000) 35. Lopez-Vidriero, E., Goulding, K.A., Simon, D.A., Sanchez, M., Johnson, D.H.: The use of platelet-rich plasma in arthroscopy and sports medicine: optimizing the healing environment. Arthroscopy 26, 269–278 (2010) 36. Maniscalco, P., Gambera, D., Lunati, A., et al.: The “cascade” membrane: a new PRP device for tendon ruptures. Description and case report on rotator cuff tendon. Acta. Biomed. 79, 223–226 (2008) 37. Nurden, A.T., Nurden, P., Sanchez, M., Andia, I., Anitua, E.: Platelets and wound healing. Front. Biosci. 13, 3525–3548 (2008) 38. Radice, F., Yánez, R., Gutiérrez, V., Pinedo, M., Rosales, J., Coda, S.: Uso de Concentrado Autólogo Rico en Factores de Crecimiento en la Reconstrucción del LCA. Rev. Argent. Artroscopia. 15, 31–40 (2008) 39. Reddi, A.H.: Bone morphogenetic proteins: from basic science to clinical application. J. Bone. Joint. Surg. 83A, 1–6 (2001) 40. Ross, R., Glomset, J., Kariya, B., Harker, L.: A platelet dependent serum factor that stimulates the proliferation of arterial smooth muscle cells in vitro. Proc. Natl. Acad. Sci. 71, 1207–1210 (1974) 41. Sakai, T., Yasuda, K., Tohyama, H., et al.: Effects of combined administration of transforming growth factor-beta 1 and epidermal growth factor on properties of the in situ frozen anterior cruciate ligament in rabbits. J. Orthop. Res. 20, 1345–1351 (2002) 42. Sanchez, M., Anitua, E., Azofra, J., Aguirre, J.J., Andia, I.: Intraarticular injection o fan autologous preparation rich in growth factors for the treatment of knee OA: a retrospective cohort study. Clin. Exp. Rheumatol. 26, 910–913 (2008) 43. Sanchez, M., Anitua, E., Azofra, J., Andia, I., Padilla, S., Mujika, I.: Comparison of surgically repaired achilles tendon tears using plateletrich fibrin matrices. Am. J. Sports. Med. 35, 245–251 (2007) 44. Sánchez, M., Anitua, E., Cugat, R., et al.: Nonunions treated with autologous preparation rich in growth factors. J. Orthop. Trauma. 23, 52–59 (2009) 45. Sanchez, M., Azofra, J., Aizpurua, B., Elorriaga, R., Anitua, E., Andia, I.: Aplicación de Plasma Autólogo Rico en Factores de Crecimiento en Cirugía Artroscópica. Cuad. Artroscopia. 10, 12–19 (2003)

Growth Factors: Application in Orthopaedic Surgery and Trauma 46. Sánchez, M., Azofra, J., Anitua, A., et al.: Plasma rich in growth factors to treat an articular cartilage avulsion: a case report. Med. Sci. Sports. Exerc. 35(10), 1648–1652 (2003) 47. Scheffler, S.U., Unterhauser, F.N., Weiler, A.: Graft remodeling and ligamentization after CL reconstruction. Knee. Surg. Sports. Traumatol. Arthrosc. 16, 834–842 (2008) 48. Schmidt, C.C., Georgescu, H.I., Kwoh, C.K., Blomstrom, G.L., Engle, C.P., Larkin, L.A., Evans, C.H., Woo, S.L.: Effect of growth factors on the proliferation of fibroblasts from the medial collateral and anterior cruciate ligaments. J. Orthop. Res. 3, 184–190 (1995) 49. Serra, C.I.: Análisis Biomecánico e Histológico del Tejido de Reparación en Defectos Condrales de Espesor Completo tras la Aplicación de Plasma Rico en Plaquetas Autólogo. Estudio Experimental. Doctoral Thesis. Universidad Cardenal Herrera CEU. Valencia, Spain, 2006 50. Soler, M.C.: Análisis Macroscópico, Histólógico e Inmunohistoquímico del Efecto del Plasma Rico en Plaquetas Autólogo en la Reparación de Defectos Condrales en Conejo. Estudio Experimental. Doctoral Thesis. Universidad Cardenal Herrera CEU. Valencia, Spain, 2006 51. Steiner, M.E., Murray, M.M., Rodeo, S.A.: Strategies to improve anterior cruciate ligament healing and graft placement. Am. J. Sports. Med. 36, 176–189 (2008) 52. Tohyama, H., Yasuda, K.: Extrinsic cell infiltration and revascularization accelerate mechanical deterioration of the patellar tendon after fibroblast necrosis. J. Biomech. Eng. 122, 594–599 (2000) 53. Uludag, F.L., Gao, T., Porter, T.J., Friess, W., Wozney, J.M.: Delivery systems for BMPs: factors contributing to protein retention at an application site. J. Bone. Joint. Surg. 83-A, 128–135 (2001) 54. Unterhauser, F.N., Weiler, A., et al.: Endoligamentous revascularization of an anterior cruciate ligament graft. Clin. Orthop. Relat. Res. 414, 276–288 (2003) 55. Urist, M.R.: Bone: formation by autoinduction. Science 150, 893–899 (1965) 56. Wang-Saegusa, A.: Infiltración de PRGF (PRP) en OA de Rodilla. Efecto-Repercusión en la Calidad de Vida y Función Física. Tesina para Máster en Medicina Cosmética y Antienvejecimiento. UAB Barcelona, Spain, 2008

907 57. Weibrich, G., Hansen, T., Kleis, W., Buch, R., Hitzler, W.E.: Effect of platelet concentration in platelet-rich plasma on peri-implant bone regeneration. Bone 34, 665–671 (2004) 58. Weiler, A., et al.: The influence of locally applied Platelet-Derived Growth Factor–BB on free tendon graft remodelling after anterior cruciate ligament reconstruction. Am. J. Sports. Med. 32, 881–891 (2004) 59. Wikesjö, U.M., Sorensen, R.G., Wozney, J.M.: Augmentation of alveolar bone and dental implant osseo integration: clinical implications of studies with rhBMP-2. J. Bone. Joint. Surg. 83-A, 136–145 (2001) 60. Woo, S.L.Y.: Tissue engineering: use of scaffolds for ligament and tendon healing and regeneration. Knee. Surg. Sports. Traumatol. Arthrosc. 17, 559–560 (2009) 61. Yamazaki, S., Yasuda, K., et al.: The effect of Transforming Growth Factor- 1 on intraosseous healing of flexor tendon autograft replacement of anterior cruciate ligament in dogs. Arthroscopy 21, 1034–1041 (2005) 62. Yasuda, K., Tomita, F., Yamazaki, S., Minami, A., Tohyama, H.: The effect of growth factors on biomechanical properties of the bone– patellar tendon–bone graft after anterior cruciate ligament reconstruction. A canine model study. Am. J. Sports. Med. 32, 870–880 (2004) 63. Yoshikawa, T., Tohyama, H., Enomoto, H., et al.: Temporal changes in relationships between fibroblast repopulation, VEGF expression, and angiogenesis in the patellar tendon graft after anterior cruciate ligament reconstruction. Trans. Orthop. Relat. Res. Soc. 29, 236 (2003) 64. Yoshikawa, T., Tohyama, H., Katsura, T., Kondo, E., Yasuda, K., et al.: Effects of local administration of Vascular Endothelial Growth Factor on mechanical characteristics of the semitendinosus tendon graft after anterior cruciate ligament reconstruction in sheep. Am. J. Sports. Med. 36, 1918–1925 (2006) 65. Zarins, B., Cugat, R., Garcia-Balletbó, M.: Platelet-Rich Plasma (PRP)-potential orthopaedic applications of autologous preparations rich in growth factors (PRGF). Hvd. Ortho. J. 11, 125–127 (2009) 66. Zhang, Y.W., Vande Woude, G.F.: HGF/SF-met signaling in the control of branching morphogenesis and invasion. J. Cell. Biochem. 88, 408–417 (2002)

Minimally Invasive Surgery for Achilles Tendon Pathologies Nicola Maffulli, Umile Giuseppe Longo, and Vincenzo Denaro

Introduction

Contents Introduction .................................................................................

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Achilles Tendinopathy Management .........................................

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Multiple Percutaneous Longitudinal Tenotomies ....................

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Ultrasound-Guided Percutaneous Tenotomy ...........................

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Minimally Invasive Stripping.....................................................

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Postoperative Care ......................................................................

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Acute AT Rupture .......................................................................

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Percutaneous Repair of Acute Achilles Tendon Rupture .......................................................................... 912 Chronic AT Ruptures..................................................................

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Peroneus Brevis Transfer ...........................................................

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Ipsilateral Free Semitendinosus Tendon Graft Transfer for Chronic Tears of the Achilles Tendon ................................. 913 Conclusions ..................................................................................

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References ....................................................................................

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Achilles tendon (AT) pathology is one of the more common conditions encountered by the foot and ankle surgeon. While it most frequently affects the athletic population, it can also lead to significant morbidity in older and sedentary patients. In the last few years, new minimally invasive surgical approaches have been developed [4, 5, 14, 32, 42] to reduce the risk of infection and morbidity [40]. Minimally invasive AT surgery seems to obtain faster recovery times, shorter hospital stays, and improved functional outcomes when compared to traditional open techniques [4, 5, 8, 9, 14, 32]. Open procedures on the AT have been associated with increased risk of wound healing because of the tenuous blood supply and increased chance of wound breakdown and infection [40]. Moreover, the broad exposure given by open procedures may cause extensive iatrogenic disruption of the subcutaneous tissues and paratenon, increasing the potential for peritendinous adhesions. We present the recent advances in the field of minimally invasive surgery for the most common pathologies of the AT, including management of tendinopathy of the main body of the AT (multiple percutaneous longitudinal tenotomies [32, 42] and our minimally invasive technique of stripping of the AT [14]), acute ruptures (our percutaneous technique to operate on acute AT ruptures [5]), and chronic tears (our minimally invasive reconstruction of chronic tears of the AT using the peroneus brevis [4] and the semitendinosus autologous tendon graft [25]).

Achilles Tendinopathy Management N. Maffulli ( ) Centre for Sports and Exercise Medicine, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Mile End Hospital, 275 Bancroft Road, London E1 4DG, UK e-mail: [email protected] U.G. Longo and V. Denaro Department of Orthopaedic and Trauma Surgery, Campus Biomedico University, Via Alvaro del Portillo, 200, 00128 Rome, Italy e-mail: [email protected]; [email protected]

Achilles tendinopathy is characterised by pain, impaired performance, and swelling in and around the tendon [18]. The aetiology of pain in Achilles tendinopathy is still unknown, with recent evidence suggesting that neo-vascularisation and neo-innervation play an important role [1, 13, 15, 29, 33, 35, 37]. Neo-vascularisation is a feature of tendinopathy, and the area where most neo-vascularisation occurs on power or colour

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Doppler ultrasound scan seems to correlate with the area in which patients perceive most pain [37]. Classically, the aim of surgery was to remove degenerated nodules and to excise fibrotic adhesions. Other options included performance of multiple longitudinal tenotomies along the long axis of the tendon to (1) detect intratendinous lesions, (2) restore vascularity, and (3) possibly stimulate the remaining viable cells to initiate cell matrix response and healing [39]. To this aim, we describe a technique of percutaneous longitudinal tenotomies [32], eventually ultrasound scan guided to accurately determine the precise area of tendinopathy [42]. New surgical management options aim to address the area of neovascularisation outside the tendon [14]. To this aim, we have developed a new minimally invasive stripping of the AT.

Multiple Percutaneous Longitudinal Tenotomies The patient lies prone on the operating table with the feet protruding beyond the edge, and the ankles resting on a padded sandbag [32]. The tendon is accurately palpated, and the area of maximum swelling and/or tenderness is marked and checked again by US scanning. The skin and the subcutaneous tissues over the Achilles tendon are infiltrated with 10–15 mL of plain 1% lignocaine (Lignocaine Hydrochloride, Evans Medical Ltd., Leatherhead, England). A number 11 surgical scalpel blade is inserted parallel to the long axis of the tendon fibres in the marked area(s), with the cutting edge pointing cranially (Fig. 1). This initial stab incision is made in the central portion of the diseased tendon. With the blade held still, a full passive ankle dorsiflexion movement is produced. After the position of the blade is reversed, a full passive ankle plantarflexion movement is

Fig. 1 A Number 11 surgical scalpel blade is inserted parallel to the long axis of the tendon fibres in the marked area with the cutting edge pointing cranially

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produced. A tenotomy is thereby produced over a length of up to approximately 3 cm using only a stab incision. The procedure is repeated 2 cm medial and proximally, medial and distally, lateral and proximally, and lateral and distally to the site of the first stab wound. The pattern of the 5 stab incisions is similar to the number 5 on a dice. The 5 wounds are closed with steristrips, dressed with cotton swabs, and several layers of cotton wool and a crepe bandage are applied.

Ultrasound-Guided Percutaneous Tenotomy The patient is positioned as described for the previous technique. A bloodless field is not necessary. The tendon is accurately palpated, and the area of maximum swelling and/or tenderness is marked and checked by US scanning [42]. The skin is prepped with an antiseptic solution, and a sterile longitudinal 7.5 MHz US probe is used to confirm the area of tendinopathy. Before infiltration of the skin and subcutaneous tissues over the Achilles tendon with 10 mL of 1% Carbocaina (Pierrel, Milan, Italy), 7 mL of 0.5% Carbocaina is used to infiltrate the space between the tendon and the paratenon. This brisement procedure attempts to free the paratenon from the tendon by disrupting adhesions between the two structures. Under US guidance, a number 11 surgical scalpel blade (Swann-Morton, England) is inserted parallel to the long axis of the tendon fibres in the centre of the area of tendinopathy, as assessed by high-resolution US imaging. The cutting edge of the blade points caudally and penetrates the whole thickness of the tendon. With the blade held still, a full passive ankle flexion is produced. All subsequent tenotomies are performed through this same stab incision unless there is an extensive area of tendinopathy or an additional area of tendon disease. The scalpel blade is then retracted to the surface of the tendon inclined 45° on the sagittal axis, and the blade is inserted medially through the original tenotomy. With the blade held still, a full passive ankle flexion is produced. The whole procedure is then repeated with the blade inclined 45° laterally to the original tenotomy and inserted laterally through the original tenotomy. Again with the blade kept still, a full passive ankle flexion is produced. The blade is then partially retracted to the posterior surface of the Achilles tendon, reversed 180° so that its cutting edge now points cranially, and the procedure is repeated, with care taken to dorsiflex the ankle passively. Preliminary cadaveric studies have demonstrated that on average a 2.8 cm tenotomy is obtained using this technique. A steristrip (3 M United Kingdom PLC, Bracknell, Berkshire, England) can be applied on the stab wound, or the stab wound can be

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left open [23, 28]. The wound is dressed with cotton swabs, and several layers of cotton wool and a crepe bandage are applied.

Minimally Invasive Stripping The patient is positioned prone. A calf tourniquet is not necessary. Four skin incisions are made. The first two incisions are 0.5 cm longitudinal incisions at the proximal origin of the Achilles tendon, just medial and lateral to the origin of the tendon. The other two incisions are also 0.5 cm long and longitudinal, but 1 cm distal to the distal end of the tendon insertion on the calcaneus. A mosquito is inserted in the proximal incisions, and the Achilles tendon is freed of the peritendinous adhesions. A Number 1 unmounted Ethibond (Ethicon, Somerville, NJ) suture thread is inserted proximally, passing through the two proximal incisions (Fig. 2). The Ethibond is retrieved from the distal incisions, over the anterior aspect of the Achilles tendon. Using a gentle see-saw motion, similar to using a Gigli saw (Fig. 3), the Ethibond suture thread is made to slide anterior to the tendon, which is stripped and freed from the fat of Kager’s triangle. If necessary, using an 11 blade, longitudinal percutaneous tenotomies parallel to the tendon fibres are made [32, 41, 42]. The subcutaneous and subcuticular tissues are closed in a routine fashion, and Mepore (Molnlycke Health Care, Gothenburg, Sweden) dressings are applied to the skin. A removable scotch cast support with Velcro straps can be applied if deemed necessary.

Fig. 2 A Number 1 unmounted Ethibond (Ethicon, Somerville, NJ) suture thread is inserted proximally, passing through the two proximal incisions

Fig. 3 Using a gentle see-saw motion, similar to using a Gigli saw, the Ethibond suture thread is made to slide posterior to the tendon, which is stripped and freed from the fat of Kager’s triangle

Postoperative Care Post-operatively, patients are allowed to mobilise fully weight bearing. After 2 weeks, the cast, if used is removed, and physiotherapy is commenced, focusing on proprioception, plantar-flexion of the ankle, inversion and eversion.

Acute AT Rupture Despite the AT is the strongest and largest tendon in the human body, it is also the most frequently ruptured [2, 19, 34]. The highest incidence of acute AT ruptures occurs in men in their third and fourth decades of life who participate in sports intermittently [12, 25]. Options include non-operative (cast immobilization or functional bracing) or operative (open or percutaneous) management [10]. Recent evidences suggest a beneficial effect of early weight bearing and early mobilization [21, 30, 31]. Systematic reviews showed that open surgical management of acute AT ruptures significantly reduces the risk of rerupture compared with nonoperative treatment. although it is associated with a significantly higher risk of wound healing problems [40]. Operative risks may be reduced by percutaneous surgery [10, 12, 26]. Aims of management of AT ruptures are to reduce the morbidity of the injury, optimize rapid return to full function, and prevent complications. A recent study found that the Achillon repair had comparable tensile strength to the Kessler repair [11].

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Preliminary biomechanical studies on our suture technique [5] seem to show that our technique allows a stronger repair when compared to the Achillon repair, as it allows use of a greater number of suture strands (eight) for the repair of the AT. Moreover, in comparison with the Achillon repair, is cheaper and faster.

Percutaneous Repair of Acute Achilles Tendon Rupture The patient is positioned prone. Areas 4–6 cm proximal and distal to the palpable tendon defect and the skin over the defect are infiltrated with 20 ml of 1% Lignocaine. Ten millilitre of Chirocaine 0.5% are infiltrated deep to the tendon defect. A calf tourniquet, skin preparation and steridrapes are applied. A 1 cm transverse incision is made over the defect using a size 11 blade. Four longitudinal stab incisions are made lateral and medial to the tendon 6 cm proximal to the palpable defect. Two further longitudinal incisions on either side of the tendon are made 4–6 cm distal to the palpable defect. Forceps are then used to mobilise the tendon from beneath the subcutaneous tissues. A 9 cm Mayo needle (BL059N, #B00 round point spring eye, B Braun, Aesculap, Tuttlingen, Germany) is threaded with two double loops of Number 1 Maxon (Tyco Healthcare, Norwalk, CT), and this is passed transversely between the proximal stab incisions through the bulk of the tendon. The bulk of the tendon is surprisingly superficial. The loose ends of the sutures are held with a clip. In turn, each of the ends is then passed distally from just proximal to the transverse Maxon passage through the bulk of the tendon to pass out of the diagonally opposing stab incision. A subsequent diagonal pass is then made to the transverse incision over the ruptured tendon. To prevent entanglement, both ends of the Maxon are held in separate clips. This suture is tested for security by pulling with both ends of the Maxon distally. Another double loop of Maxon is then passed between the distal stabs incisions through the tendon, in a half Kessler configuration and in turn through the tendon and out of the transverse incision starting distal to the transverse passage. The ankle is held in full plantar flexion, and in turn opposing ends of the Maxon thread are tied together with a double throw knot, and then three further throws before being buried using forceps. A clip is used to hold the first throw of the lateral side to maintain the tension of the suture. A subcuticular Biosyn suture 3.0 (Tyco Healthcare) is used to close the transverse incision, and Steri-strips (3 M Health Care, St Paul, MN) are applied to the stab incisions. Finally, a Mepore dressing (Molnlycke Health Care, Gothenburg, Sweden) is applied, and a bivalved removable scotch cast in full plantar flexion is applied being held in place with Velcro straps.

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The patient is allowed home on the day of surgery, and fully weight bears as able in the cast in full plantar flexion. At 2 weeks, the wounds are inspected, and the back shell is removed allowing proprioception, plantar flexion, inversion and eversion exercises. The front shell remains in place for 6 weeks to prevent forced dorsiflexion of the ankle. We recently showed that percutaneous repair of the AT is a suitable option for patients older than 65, producing similar outcomes when compared to percutaneous repair in younger patients of previous reports [27].

Chronic AT Ruptures Chronic ruptures of AT can be difficult to manage, as the tendon ends normally are retracted [4, 20, 22], and the tendon ends must be freshened to allow healing. Primary repair is not generally possible, because of the increased gap between the two tendon ends [20]. Traditional open surgical options include flap tissue turn down using one [6, 17] and two flaps [3], local tendon transfer [7, 36, 43, 45], and autologous hamstring tendon harvesting [24]. Main concerns of these techniques, include complications, especially wound breakdown and infections [38]. They, are probably related to the scanty soft tissue vascularity, and may require plastic surgical procedures to cover significant soft tissue defects [16]. We have described a less invasive technique of peroneus brevis transfer for reconstruction of chronic tears of the AT [4]. When the gap produced is greater than 6 cm despite maximal plantar flexion of the ankle and traction on the AT stumps [4], less invasive ipsilateral hamstring tendon augmentation can be an option [36].

Peroneus Brevis Transfer The patient is positioned prone. Three skin incisions are made, and accurate haemostasis by ligation of the larger veins and diathermy of the smaller ones is performed [4]. The first incision is a 5 cm longitudinal incision, made 2 cm proximal and just medial to the palpable end of the residual tendon. The second incision is 3 cm long and is also longitudinal but is 2 cm distal and lateral to the distal end of the tendon rupture. Care is taken to prevent damage to the sural nerve by making this incision as close as possible to the anterior aspect of the lateral border of the Achilles tendon to avoid the nerve. At the level of the Achilles tendon insertion, the sural nerve is 18.8 mm lateral to the tendon but, as it progresses proximally, the nerve gradually traverses medially crossing the lateral border of the tendon 9.8 cm proximal to the calcaneum [42]. Thus, the second incision avoids the sural nerve by being placed on the lateral side of the Achilles

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tendon but medial to the nerve. The third incision is a 2 cm longitudinal incision at the base of the fifth metatarsal. The distal Achilles tendon stump is mobilised, freeing it of all the peritendinous adhesions, particularly on the lateral aspect. This allows access to the base of the lateral aspect of the distal tendon close to it insertion. The ruptured tendon end is then resected back to healthy tendon, and a Number 1 Vicryl (Ethicon, Edinburgh) locking suture is run along the free tendon edge to prevent separation of the bundles. The proximal tendon is then mobilised from the proximal wound, any adhesions are divided, and further soft tissue release anterior to the soleus and gastrocnemius allows maximal excursion, minimising the gap between the two tendon stumps. A Vicryl locking suture is run along the free tendon edge to allow adequate exposure and to prevent separation of the bundles. The tendon of peroneus brevis is harvested. The tendon is identified through the incision on the lateral border of the foot at its insertion at the base of the fifth metatarsal. The tendon is exposed, and a No.1 Vicryl locking suture is applied to the tendon end before release from the metatarsal base. The tendon of peroneus brevis is identified at the base of the distal incision of the Achilles tendon following incision of the deep fascia overlying the peroneal muscles compartment. The tendon of peroneus brevis is then withdrawn through the distal wound. This may take significant force, as there may be tendinous strands between the two peroneal tendons distally. The muscular portion of peroneus brevis is then mobilised proximally to allow increased excursion of its tendon. A longitudinal tenotomy parallel to the tendon fibres is made through both stumps of the tendon. A clip is used to develop the plane, from lateral to medial, in the distal stump of the Achilles tendon, and the peroneus brevis graft is passed through the tenotomy. With the ankle in maximal plantar flexion, a No. 1 Vicryl suture is used to suture the peroneus brevis to both sides of the distal stump. The tendon of peroneus brevis is then passed beneath the intact skin bridge into the proximal incision, and passed from medial to lateral through a transverse tenotomy in the proximal stump, and further secured with No. 1 Vicryl. Finally, the tendon of peroneus brevis is sutured back onto itself on the lateral side of the proximal incision. The reconstruction may be further augmented using a Maxon (Tyco Health Care, Norwalk, CT) suture. The wounds are closed with 2.0 Vicryl, 3.0 Biosyn (Tyco Health Care, Norwalk, CT) and Steri-strips (3 M Health Care, St Paul, MN), taking care to avoid the risk of post operative haematoma and minimise wound breakdown. A previously prepared removable scotch cast support with Velcro straps is applied. Postoperatively, patients are allowed to weight bear as comfort allows with the use of elbow crutches. It would be unusual for a patient to weight bear fully at this stage. After 2 weeks, the back shell is removed, and physiotherapy is

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commenced with the front shell in situ preventing dorsiflexion of the ankle, focusing on proprioception, plantar-flexion of the ankle, inversion and eversion. During this period of rehabilitation the patient is permitted to weight bear as comfort allows with the front shell in situ although full weight bearing rarely occurs on account of balance difficulties and patients usually still require the assistance of a single elbow crutch as this stage. The front shell may be finally removed after 6 weeks. We do not use a heel raise after removal of the cast, and patients normally regain a plantigrade ankle over a couple of weeks.

Ipsilateral Free Semitendinosus Tendon Graft Transfer for Chronic Tears of the Achilles Tendon The patient is positioned prone with a calf tourniquet. Skin preparation is performed in the usual fashion, and sterile drapes are applied. Pre-operative anatomical markings include the palpable tendon defect and both malleoli [25]. Two skin incisions are made, and accurate haemostasis by ligation of the larger veins and diathermy of the smaller ones is performed. The first incision is a 5 cm longitudinal incision, made 2 cm proximal and just medial to the palpable end of the residual tendon. The second incision is 3 cm long and is also longitudinal but is 2 cm distal and in the midline over the distal end of the tendon rupture. Care is taken to prevent damage to the sural nerve [44]. Thus, the second incision avoids the sural nerve by being placed medial to the nerve. The ruptured tendon end is then resected back to healthy tendon, and a Number 1 Vicryl (Ethicon, Edinburgh) locking suture is run along the free tendon edge to prevent separation of the bundles. The proximal tendon is then mobilised from the proximal wound, any adhesions are divided, and further soft tissue release anterior to the soleus and gastrocnemius allows maximal excursion, minimising the gap between the two tendon stumps. A Vicryl locking suture is run along the free tendon edge to allow adequate exposure and to prevent separation of the bundles. After trying to reduce the gap of the ruptured AT, if the gap produced is greater than 6 cm despite maximal plantar flexion of the ankle and traction on the AT stumps, the ipsilateral semitendinosus tendon is harvested through a vertical, 2.5–3 cm longitudinal incision over the pes anserinus. The semitendinosus tendon is passed through a small incision in the substance of the proximal stump of the AT, and it is sutured to the AT at the entry and exit point using 3–0 Vicryl (Polyglactin 910 braided absorbable suture; Johnson & Johnson, Brussels, Belgium). The semitendinosus tendon is then passed beneath the intact skin bridge into the distal

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incision, and passed from medial to lateral through a transverse tenotomy in the distal stump. With the ankle in maximal plantar flexion, the semitendinosus tendon is sutured to the AT at each entry and exit point using 3–0 Vicryl (Polyglactin 910 braided absorbable suture; Johnson & Johnson, Brussels, Belgium). The repair is tensioned to maximal equines. One extremity of the semitendinosus tendon is then passed again beneath the intact skin bridge into the proximal incision, and passed from medial to lateral through a transverse tenotomy in the proximal stump. The other extremity of the semitendinosus tendon is then passed again from medial to lateral through a transverse tenotomy in the distal stump. The reconstruction may be further augmented using a Maxon (Tyco Health Care, Norwalk, CT) suture. The wounds are closed with 2.0 Vicryl, 3,0 Biosyn (Tyco Health Care, Norwalk, CT) and Steri-strips (3 M Health Care, St Paul, MN). A previously prepared removable scotch cast support with Velcro straps is applied. Post-operatively, patients are allowed to weight bear as comfort allows with the use of elbow crutches [30, 31]. It would be unusual for a patient to weight bear fully at this stage. After 2 weeks, the back shell is removed, and physiotherapy is commenced with the front shell in situ preventing dorsiflexion of the ankle, focusing on proprioception, plantarflexion of the ankle, inversion and eversion [30, 31]. During this period of rehabilitation, the patient is permitted to weight bear as comfort allows with the front shell in situ although full weight bearing rarely occurs on account of balance difficulties and patients usually still require the assistance of a single elbow crutch as this stage. The front shell may be finally removed after 6 weeks. We do not use a heel raise after removal of the cast, and patients normally regain a plantigrade ankle over 2 or 3 weeks [30, 31].

Conclusions In our hands, minimally invasive surgery for the management of AT pathologies provided results similar to those obtained with open surgery, with the advantages of providing decreased perioperative morbidity, decreased duration of hospital stay, and reduced costs. The evidence for using these techniques is inadequate at present. Given the limitations of the case series on the topic, especially the extensive clinical heterogeneity, it is not possible to determine clear recommendations regarding the systematic use of minimally invasive surgery for AT pathologies, even though preliminary results are encouraging. Clearly, studies of higher levels of evidence, including large randomised trials, should be conducted to help answer these questions. Future trials should use validated functional and clinical outcomes, adequate methodology, and be sufficiently powered.

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References 1. Alfredson, H., Ohberg, L., Forsgren, S.: Is vasculo-neural ingrowth the cause of pain in chronic Achilles tendinosis? An investigation using ultrasonography and colour Doppler, immunohistochemistry, and diagnostic injections. Knee. Surg. Sports. Traumatol. Arthrosc. 11, 334–338 (2003) 2. Ames, P.R., Longo, U.G., Denaro, V., Maffulli, N.: Achilles tendon problems: not just an orthopaedic issue. Disabil. Rehabil. 30(20–22), 1646–1650 (2008) 3. Arner, O., Lindholm, A.: Subcutaneous rupture of the Achilles tendon: a study of 92 cases. Acta. Chir. Scand. Suppl. 116, 1–51 (1959) 4. Carmont, M.R., Maffulli, N.: Less invasive Achilles tendon reconstruction. BMC. Musculoskelet. Disord. 8, 100 (2007) 5. Carmont, M.R., Maffulli, N.: Modified percutaneous repair of ruptured Achilles tendon. Knee. Surg. Sports. Traumatol. Arthrosc. 16, 199–203 (2008) 6. Christensen, I.: Rupture of the Achilles tendon: analysis of 57 cases. Acta. Chir. Scand. 106, 50–60 (1953) 7. Dekker, M., Bender, J.: Results of surgical treatment of rupture of the Achilles tendon with use of the plantaris tendon. Arch. Chir. Neerl. 29, 39–46 (1977) 8. Doral, M.N., Bozkurt, M., Turhan, E., Ayvaz, M., Atay, O.A., Uzumcugil, A., Leblebicioglu, G., Kaya, D., Aydog, T.: Percutaneous suturing of the ruptured Achilles tendon with endoscopic control. Arch. Orthop. Trauma Surg. 129, 1093–1101 (2009) 9. Doral, M.N., Tetik, O., Atay, O.A., Leblebicioglu, G., Oznur, A.: Achilles tendon diseases and its management. Acta. Orthop. Traumatol. Turc. 36(Suppl 1), 42–46 (2002) 10. Ebinesan, A.D., Sarai, B.S., Walley, G.D., Maffulli, N.: Conservative, open or percutaneous repair for acute rupture of the Achilles tendon. Disabil. Rehabil. 30(20–22), 1721–1725 (2008) 11. Ismail, M., Karim, A., Shulman, R., Amis, A., Calder, J.: The Achillon Achilles tendon repair: is it strong enough? Foot Ankle Int. 29, 808–813 (2008) 12. Khan, R.J., Fick, D., Keogh, A., Crawford, J., Brammar, T., Parker, M.: Treatment of acute Achilles tendon ruptures. A meta-analysis of randomized, controlled trials. J. Bone. Joint. Surg. Am. 87, 2202– 2210 (2005) 13. Knobloch, K., Schreibmueller, L., Longo, U.G., Vogt, P.M.: Eccentric exercises for the management of tendinopathy of the main body of the Achilles tendon with or without the AirHeel Brace. A randomized controlled trial. A: effects on pain and microcirculation. Disabil Rehabil. 30, (20–22), 1685–91 (2008) 14. Knobloch, K., Schreibmueller, L., Longo, U.G., Vogt, P.M.: Eccentric exercises for the management of tendinopathy of the main body of the Achilles tendon with or without an AirHeel Brace. A randomized controlled trial. B: effects of compliance. Disabil. Rehabil. 30, 1692–1696 (2008) 15. Kristoffersen, M., Ohberg, L., Johnston, C., Alfredson, H.: Neovascularisation in chronic tendon injuries detected with colour Doppler ultrasound in horse and man: implications for research and treatment. Knee. Surg. Sports. Traumatol. Arthrosc. 13, 505–508 (2005) 16. Kumta, S.M., Maffulli, N.: Local flap coverage for soft tissue defects following open repair of Achilles tendon rupture. Acta. Orthop. Belg. 69, 59–66 (2003) 17. Longo, U.G., Lamberti, A., Maffulli, N., Denaro, V.: Tendon augmentation grafts: a systematic review. Br Med Bull. 94, 165–88 (2010) 18. Longo, U.G., Ronga, M., Maffulli, N.: Achilles tendinopathy. Sports. Med. Arthrosc. 17, 112–126 (2009) 19. Longo, U.G., Ronga, M., Maffulli, N.: Acute ruptures of the Achilles tendon. Sports. Med. Arthrosc. 17, 127–138 (2009) 20. Maffulli, N.: Rupture of the Achilles tendon. J. Bone. Joint. Surg. Am. 81, 1019–1036 (1999)

Minimally Invasive Surgery for Achilles Tendon Pathologies 21. Maffulli, N.: Immediate weight-bearing is not detrimental to operatively or conservatively managed rupture of the Achilles tendon. Aust. J. Physiother. 52(3), 225 (2006) 22. Maffulli, N., Ajis, A., Longo, U.G., Denaro, V.: Chronic rupture of tendo Achillis. Foot Ankle Clin. 12(4), 583–596 (2007). vi 23. Maffulli, N., Dymond, N.P., Regine, R.: Surgical repair of ruptured Achilles tendon in sportsmen and sedentary patients: a longitudinal ultrasound assessment. Int. J. Sports. Med. 11, 78–84 (1990) 24. Maffulli, N., Leadbetter, W.B.: Free gracilis tendon graft in neglected tears of the Achilles tendon. Clin. J. Sport. Med. 15, 56–61 (2005) 25. Maffulli, N., Longo, U.G., Gougoulias, N., Denaro, V.: Ipsilateral free semitendinosus tendon graft transfer for reconstruction of chronic tears of the Achilles tendon. BMC. Musculoskelet. Disord. 9, 100 (2008) 26. Maffulli, N., Longo, U.G., Maffulli, G.D., Khanna, A., Denaro V.: Achilles tendon ruptures in diabetic patients. Arch. Orthop. Trauma. Surg. Apr 6, 131(1), 33–38 (2011) 27. Maffulli, N., Longo, U.G., Ronga, M., Khanna, A., Denaro, V.: Favorable outcome of percutaneous repair of Achilles tendon ruptures in the elderly. Clin. Orthop. Relat. Res. 468(4), 1039–1046 (2009) 28. Maffulli, N., Pintore, E., Petricciuolo, F.: Arthroscopy wounds: to suture or not to suture. Acta. Orthop. Belg. 57, 154–156 (1991) 29. Maffulli, N., Sharma, P., Luscombe, K.L.: Achilles tendinopathy: aetiology and management. J. R. Soc. Med. 97, 472–476 (2004) 30. Maffulli, N., Tallon, C., Wong, J., Lim, K.P., Bleakney, R.: Early weightbearing and ankle mobilization after open repair of acute midsubstance tears of the Achilles tendon. Am. J. Sports. Med. 31, 692–700 (2003) 31. Maffulli, N., Tallon, C., Wong, J., Peng Lim, K., Bleakney, R.: No adverse effect of early weight bearing following open repair of acute tears of the Achilles tendon. J. Sports. Med. Phys. Fit. 43, 367–379 (2003) 32. Maffulli, N., Testa, V., Capasso, G., Bifulco, G., Binfield, P.M.: Results of percutaneous longitudinal tenotomy for Achilles tendinopathy in middle- and long-distance runners. Am. J. Sports. Med. 25, 835–840 (1997)

915 33. Maffulli, N., Testa, V., Capasso, G., Ewen, S.W., Sullo, A., Benazzo, F., King, J.B.: Similar histopathological picture in males with Achilles and patellar tendinopathy. Med. Sci. Sports. Exerc. 36, 1470–1475 (2004) 34. Maffulli, N., Waterston, S.W., Squair, J., Reaper, J., Douglas, A.S.: Changing incidence of Achilles tendon rupture in Scotland: a 15-year study. Clin. J. Sport. Med. 9, 157–160 (1999) 35. Maffulli, N., Wong, J., Almekinders, L.C.: Types and epidemiology of tendinopathy. Clin. Sports. Med. 22, 675–692 (2003) 36. McClelland, D., Maffulli, N.: Neglected rupture of the Achilles tendon: reconstruction with peroneus brevis tendon transfer. Surgeon 2, 209–213 (2004) 37. Ohberg, L., Lorentzon, R., Alfredson, H.: Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surg. Sports Traumatol. Arthrosc. 9, 233–238 (2001) 38. Pintore, E., Barra, V., Pintore, R., Maffulli, N.: Peroneus brevis tendon transfer in neglected tears of the Achilles tendon. J. Trauma. 50, 71–78 (2001) 39. Rolf, C., Movin, T.: Etiology, histopathology, and outcome of surgery in achillodynia. Foot Ankle Int. 18, 565–569 (1997) 40. Saxena, A., Maffulli, N., Nguyen, A., Li, A.: Wound complications from surgeries pertaining to the Achilles tendon: an analysis of 219 surgeries. J. Am. Podiatr. Med. Assoc. 98, 95–101 (2008) 41. Sayana, M.K., Maffulli, N.: Eccentric calf muscle training in nonathletic patients with Achilles tendinopathy. J. Sci. Med. Sport. 10, 52–58 (2007) 42. Testa, V., Capasso, G., Benazzo, F., Maffulli, N.: Management of Achilles tendinopathy by ultrasound-guided percutaneous tenotomy. Med. Sci. Sports. Exerc. 34, 573–580 (2002) 43. Wapner, K.L., Pavlock, G.S., Hecht, P.J., Naselli, F., Walther, R.: Repair of chronic Achilles tendon rupture with flexor hallucis longus tendon transfer. Foot Ankle 14, 443–449 (1993) 44. Webb, J., Moorjani, N., Radford, M.: Anatomy of the sural nerve and its relation to the Achilles tendon. Foot Ankle Int. 21, 475–477 (2000) 45. Wilcox, D.K., Bohay, D.R., Anderson, J.G.: Treatment of chronic Achilles tendon disorders with flexor hallucis longus tendon transfer/augmentation. Foot Ankle Int. 21, 1004–1010 (2000)

Endoscopy and Percutaneous Suturing in the Achilles Tendon Ruptures Mahmut Nedim Doral, Egemen Turhan, Gürhan Dönmez, Akın Üzümcügil, Burak Kaymaz, Mehmet Ayvaz, Özgür Ahmet Atay, M. Cemalettin Aksoy, Defne Kaya, and Mustafa Sargon

Contents Historical Perspective ................................................................. 917 Anatomy ....................................................................................... 917 Introduction ................................................................................. 918 Indications ................................................................................... 918 Contraindications........................................................................ 918 Procedure ..................................................................................... 918 The Technique of Endoscopy-Assisted Percutaneous Repair ................................................................... 918 Rehabilitation .............................................................................. 920 Evaluation .................................................................................... 920 Authors Experience..................................................................... 920 Discussion..................................................................................... 920 References .................................................................................... 921

Historical Perspective The Achilles is the strongest tendon which takes its name from Achilles, from Homer’s Iliad [39]. Achilles, the ancient Greek hero of the Trojan War, gives his name to the Achilles tendon (AT). Achilles was the son of the nymph, Thetis, who tried to make him immortal by dipping him in the river Styx. However, he was left vulnerable at the part of the body she held him by – his heel. Achilles was killed by a poisoned arrow fired by the Trojan prince Paris which embedded in his only vulnerable point, his heel. This has given rise to the description of a person’s weakest point being called their “Achilles heel.” Hippocrates said “this tendon, if bruised or cut, causes the most acute fevers, induces shocking, deranges the mind and at length brings death” [8]. Since Ambroise Paré initially described in 1575 and reported in the literature in 1633, Achilles tendon breakage has received a lot of attention [9].

Anatomy

M.N. Doral ( ), A. Üzümcügil, B. Kaymaz, M. Ayvaz, Ö.A. Atay, M.C. Aksoy, and M. Sargon Faculty of Medicine, Department of Orthopaedics and Traumatology, Chairman of Department of Sports Medicine, Hacettepe University, Hasırcılar Caddesi, 06110 Ankara, Sihhiye, Turkey e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected] E. Turhan Department of Orthopaedics and Traumatology, Zonguldak Karaelmas University, Zonguldak, Turkey e-mail: [email protected] G. Dönmez and D. Kaya Faculty of Medicine, Department of Sports Medicine, Hacettepe University, 06100 Ankara, Turkey e-mail: [email protected]; [email protected]

The Achilles tendon begins near the middle of the calf and is the conjoint tendon of the gastrocnemius and soleus muscles. The relative contribution of the two muscles to the tendon varies. Spiralization of the fibers of the tendon produces an area of concentrated stress and confers a mechanical advantage. The calcaneal insertion is specialized and designed to aid the dissipation of stress from the tendon to the calcaneum. The insertion is crescent shaped and has significant medial and lateral projections. The blood supply of the tendon is from the musculotendinous junction, vessels in surrounding connective tissue, and the osteotendinous junction [12]. The vascular territories can be classified simply into three, with the midsection supplied by the peroneal artery, and the proximal and distal sections supplied by the posterior tibial artery. This leaves a relatively hypovascular area in the mid-portion of the tendon where most problems occur. The Achilles tendon derives its innervation from the sural nerve with a smaller supply from the tibial nerve. Tenocytes

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_118, © Springer-Verlag Berlin Heidelberg 2012

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produce type I collagen and form 90% of the normal tendon. Evidence suggests ruptured or pathological tendon produce more type III collagen, which may affect the tensile strength of the tendon. Direct measurements of forces reveal loading in the Achilles tendon as high as 9 KN during running, which is up to 12.5 times body weight.

Introduction Achilles tendon ruptures are the third most common major tendon ruptures after rotator cuff and quadriceps ruptures [21, 52]. Nevertheless, there is no consensus on the treatment method, and it is still determined by the surgeon and the patient. Cast immobilization, a conservative treatment, may lead to elongation of the tendon with reduced strength of the calf muscles and in a high rate of re-ruptures, with an incidence up to 37% [15, 23, 24, 31, 33, 47, 53, 54]. Similarly, open surgical repair of the Achilles tendon also includes potential problems like joint stiffness, muscle atrophy, tendocutaneous adhesions, deep venous thrombosis due to prolonged immobilization after surgical repair, and infection, scarification, algodystrophy, and particularly the breakdown of the wound [4, 18, 35, 43, 46, 53]. Ma and Griffith introduced the percutaneous repair technique to avoid all of these complications. However, the technique involves difficulties in achieving satisfactory contact of the tendon stumps and adequate initial fixation [38]. Also sural nerve entrapment seems to be a potential complication of this technique [29, 45]. Nevertheless percutaneous repair has become popular technique for the orthopedic surgeons [11, 16, 30, 32, 51]. The minimally invasive percutaneous repair techniques combine the advantages of the operative and conservative methods, but they do not provide direct observation. Therefore, the aim of the current concept is to evaluate the results of the percutaneous repair with endoscopic control and to discuss the pathophysiologic effects of this type of treatment. Also authors share their experiences about this issue in this chapter.

Indications Patients were selected for percutaneous repair as if the following criteria were fulfilled: 1. Closed traumatic Achilles tendon rupture 2. First time of surgery 3. Complete rupture in the tendinous portion within the last 7–10 days

Contraindications Patients have to be treated with other modalities rather than a percutaneous procedure if the following criteria were fulfilled:

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1. 2. 3. 4.

Having skin lesions Previous Achilles tendon surgery Previous ankle joint surgery Distal tendon end smaller than 2 cm

The optimal treatment period is 7–10 days after acute total rupture. According to the authors’ experience, systemic diseases like diabetes mellitus is not an absolute contraindication for percutaneous repair. Also this technique is useful for bilateral injuries.

Procedure The diagnosis was based on the following clinical criteria: 1. Palpable gap in the tendon 2. Positive Thompson test 3. Clinical signs of the rupture (patients unable to rise on their toes or heels) 4. More dorsiflexion on the ruptured side than in the healthy side In any equivocal case, ultrasonography or magnetic resonance imaging has to be performed to confirm the diagnosis.

The Technique of Endoscopy-Assisted Percutaneous Repair The operation is performed with the patient in the prone position and with the injured foot in approximately 15° plantar flexion in order to achieve a comfortable portal for the scope, under infiltrative anesthesia without a tourniquet. Full communication with the patient is ensured to instruct the active motion of the ankle. No antibiotic or antithrombotic prophylaxis is given. Before starting the procedure, the rupture and location of the diastases (gap) are determined. Then, to minimize local bleeding, proximal (about 5 cm) and distal (about 4 cm) to the palpated gap, the cutis, subcutis, and peritendon are infiltrated with saline solutions through eight puncture holes, four midmedial and four midlateral, two in the proximal and two distal from the line of the rupture from the proximal to the distal with a 3–4 cm interval between the portals, which are later enlarged and used for needle entry (Fig. 1). Special attention is paid to the lateral side, particularly proximally, where the sural nerve lies in the vicinity and crosses the Achilles tendon. Under infiltrative anesthesia (Citanest 5 cc + Marcain 5 cc), the patient is prompted to report any changes or soreness felt in the sural nerve area during the puncture or infiltration. When this is experienced, the puncture site is shifted approximately 0.5–1 cm toward the middle (internally).

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a

Fig. 1 Schematic drawing of entry points

After the level of the rupture is determined by endoscope, the continuum of the surrounding synovial tissue, its thickness, and vascularization are endoscopically evaluated. By these evaluation characteristics of tendons surrounding synovial tissues, paratenon and tendons are noted. Acquired data are used for classifying the cases: Grade I as minimal disruption at surrounding synovial tissues of tendon, linear tear at paratenon, and minimal degeneration at the ends of Achilles tendon (Fig. 2a); Grade II as marked corruption of paratenon continuity, degenerative rupture of paratenon, marked degeneration at the ruptured ends of Achilles tendon, and tendinosis signs (Fig. 2b); Grade III as defective rupture at the paratenon, marked tendinosis at the tendon, and advanced tendinosis signs at the ruptured ends (Fig. 2c). Biopsy has to be performed routinely in patients from the ruptured area. Then, the plantar tendon are observed, two medial and two midline lateral incisions of 1 cm each are inflicted on the proximal and the distal of the rupture level followed by suturing starting from the proximal through modified Bunnell technique using PDS No. 5 (Ethicon Inc, Johnson & Johnson, Somerville, NJ). The sutures are tied in a manner to end in the proximal lateral end at the ankle 90° of neutral position (Fig. 3). This procedure has to be repeated once or twice. Attention should be paid to check the 90° position on the ruptured side after prompting the patients to set the foot to neutral 90° throughout suture fastening. After fastening the sutures, the patient is instructed to activate the ankle motions while the knee is in 90° position. The final checkup is performed and if needed, the second knot is performed. After dorsiflexion performed willfully by the patient and plantar flexion, strikingly, the “gap” vanishes. Thus, the intratendinous bracing performed is evaluated for functionality. Finally, the skin incisions were closed and then a walking brace with the ankle in neutral position was applied for 3 weeks.

b

c

Fig. 2 Endoscopically evaluation of Achilles paratenon (a) intact paratenon with a minimal degeneration. (b) Corruption of paratenon continuity, degenerative rupture of paratenon. (c) Defective rupture at the paratenon

Fig. 3 The sutures were tied in a manner to end in the proximal lateral end at the ankle at neutral position

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Rehabilitation

Authors Experience

A standard rehabilitation program for percutaneous repair of Achilles tendon is developed based on literature in Hacettepe University, Departments of Orthopedics, Sports Medicine and section of Rehabilitation. At first day after surgery, early tolerated weight-bearing alternating with passive range of motion exercises are initiated. Physiotherapy approach includes electrical stimulation technique for reeducation of gastrocnemius and soleus muscles; ice and therapeutic ultrasound application around of Achilles tendon to relieve the edema: transverse friction massage to promote scar and tendon reformation. Patients are instructed to move the ankle four times a day between 20° of plantar flexion and 10° of extension. Patients complete neuromuscular exercises as flexion and extension of the toes in a supine position; plantar flexion of the ankle and dorsiflexion to neutral in a supine position; extension of the knee in a sitting position; flexion of the knee in a prone position; extension of the hip in a prone position within first 3 weeks. From sixth week to third month, rehabilitation program is included in advanced exercises as ankle extension against Thera-band®; rotation of the ankles; standing on the toes and heels; ankle stretching exercises to flexion with the help of a rubber strip; stretching of the calf muscle by standing with the leg to be stretched straight behind and the other leg bent in front and leaning the body forward, with support from a wall or physiotherapist; stretching exercises for the toes and ankle against the hand in a sitting position; balance and proprioception exercises using different surface from bilateral to unilateral; controlled squats, lunges, bilateral calf raise (progress to unilateral), toe raises, controlled slow eccentrics versus body weight. After 3 months, patients start training jogging/ running, jumping and eccentric loading exercises, noncompetitive sporting activities, sports-simulated exercises and return to physically demanding sport and/or work.

Sixty-two patients (58 males, 4 females, mean age 32) were treated by percutaneous suturing with modified Bunnel technique under endoscopic control within 10 days after acute total rupture. Physiotherapy was initiated immediately after the operation and patients were encouraged to weight-bearing ambulation with a walking brace-moon boot as tolerated. Full weight-bearing was allowed minimum after 3 weeks postoperatively without brace. The procedure was tolerated in all patients. There were no significant ROM limitation observed. Two patients experienced transient hypoesthesia in the region of sural nerve that spontaneously resolved in 6 months. Fifty-nine patients (95%) including professional athletes returned to their previous sportive activities, while 18 of them (29%) had some minor complaints. The interval from injury to return to regular work and rehabilitation training was 11.7 weeks (10–13 weeks). At the latest follow-up (mean: 46 months; range: 12–78 months), all the patients had satisfactory results with a mean American Orthopedic Foot and Ankle Society’s ankle-hindfoot score of 94.6. No reruptures, deep venous thrombosis, or wound problems occurred [13]. For the last 1 year we inject platelet-rich plasma to stimulate the biologic repair process at the end of suturing process. We believe the benefit of biological stimulation after mechanical repair. But we do not have enough evidence that support our belief yet. So it is an issue that should be further investigated and need to be evaluated with long-term results.

Evaluation At the follow-up, we recommend measuring the calf diameter of injured and uninjured side, examining the ankle range of motion with goniometry, and performing a detailed neurological examination focused on sural nerve. As suggested by Kitaoka et al., we are assessing other factors more specific to repair of an Achilles tendon rupture, namely, the strength of ankle plantar flexion with the patient standing on tiptoe, the ability to perform repeated toe raises and singlelimb hopping, and the neurological status of the foot [28]. For single-limb hopping, patients are asked to hop as many times as possible until they could not lift the heel off the floor. We note the integrity of the paratenon of Achilles tendon and subgroup.

Discussion Rupture of the Achilles tendon is a common injury encountered by the orthopedic surgeon. It is prevalent in the athletic population and much more common in the aging athlete [2]. In patients who have no history of steroid treatment or systemic disease, the etiology of spontaneous rupture of the Achilles tendon is uncertain. Some of the investigations have supported the theory of chronic degenerative changes based on histological examination of material obtained from ruptured area during the operation [3, 27]. On the other hand, Inglis and Sculo have performed histological examination of acute Achilles tendon rupture and have found evidence of acute pathological changes like hemorrhage and inflammation rather than chronic tendonitis [20]. Hypoxia due to a vascular lesion, aging, and repeated microtraumas from overuse are the factors most commonly considered [26, 27, 33, 53]. We found hypovascular areas around the ruptured tendon side by electron microscopy in Grade III patients (Fig. 4). Also Zantop at al. showed this subject via immunohistochemical methods and concluded that diminished vascularization in the middle

Endoscopy and Percutaneous Suturing in the Achilles Tendon Ruptures

Fig. 4 Electron micrograph showing the course of collagen fibers in different directions in a patient with ruptured Achilles tendon. No blood vessels were seen in the micrograph. (Original magnification ×7500)

part of the Achilles tendon may play a role in the reduced healing of microruptures, leading to degeneration and spontaneous rupture of the Achilles tendon [56]. Because of increasing incidence of the Achilles tendon rupture during the last decade it has been the subject of focus in many studies and meta-analyses and there is no consensus about the optimal management strategy of acute total Achilles tendon rupture [10, 34, 37, 41, 46]. Conservative treatment has worse functional results and higher re-rupture rates [40, 53, 55]. However Nistor found only minor differences between the results of surgical and nonsurgical treatment [44]. Numerous open surgical procedures have been proposed for repairing ruptures of the Achilles tendon, but there is no single, uniformly superior technique. Delayed wound healing necrosis, suppuration, and adhesions are potential complication of open procedures which are not rare [6, 7, 19, 29, 36, 38, 40]. Augmented open procedures have to be performed for neglected or defective Achilles tendon ruptures [1, 5, 17, 48, 49]. Percutaneous repair can avoid the risks of open procedures but results in a higher number of re-ruptures and thus considered a weaker repair compared to open suturing. Therefore, it is not recommended for patients with high demands [6, 21, 22, 23, 29, 39]. On the other hand, in endoscopy-assisted percutaneous repair, suturing of the tendon is observed, which not only eliminates some of the disadvantages of the percutaneous repair particularly difficulties about evaluating the contact status of the torn ends but is also a safer method than open surgery with minimally invasive approach [21, 23, 50]. Nonetheless, endoscopy-assisted percutaneous repair let early active ankle mobilization and weight-bearing after a short period of cast immobilization and by the way prevent complications due to the prolonged immobilization such as arthrofibrosis, joint stiffness, calf atrophy, damage of the articular cartilage and deep vein thrombosis [25, 43]. Considering these advantages, it can be said that

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endoscopy-assisted percutaneous repair of Achilles tendon seems to prevent certain problems of open, conservative, or percutaneous techniques. On the other hand, this technique could not help to prevent risk of damage to neural structures by facilitating the visual observation of the sural nerve [50]. We used midlateral portals in order to keep expanse with sural nerve. In endoscopic repair, the synovia of the tendon is protected, providing a biomechanically strong biological healing through intratendinous reinforcement. Nevertheless, Momose et al. showed that preservation of paratenon decreases the gliding resistance of the extrasynovial tendons after repetitive motion in vitro [42]. As in the example of synovial covering in the healing process of the posterior cruciate ligament, a mechanically strong Achilles tendon is achieved. Achilles tendoscopy made possible a more definitive repair. Hematoma protection, exact incision points, and controlled adaptation created better circumstances for the tendon healing without damaging paratenon of Achilles tendon [21]. Doral et al. emphasized the importance of endoscopic repair with protecting paratenon on biological healing of the Achilles tendon ruptures [14] and also the importance of biologic stimulation of healing process and advise the use of platelet-rich plasma after the repair processes. However, in ruptures associated with Achilles tendinosis, the synovia is weak. Therefore, our mechanical sutures maybe more effective in healing than biological healing. In the light of all these, it should be kept in mind that the ruptures of the Achilles tendon may be secondary to Achilles tendon disease. Such patients should also be evaluated for possible systemic diseases in the contralateral Achilles tendon and other tendons. This will ensure optimal treatment approach as well as contribute to decision making on the postoperative physiotherapy and time to return to sports activities. The percutaneous technique seems to contribute to tendon lengthening. This may have been due to a lack of close approximation of the tendon ends. Nevertheless, the direct visualization of the tendon ends through the middle incision should reduce or eliminate this phenomenon. The main disadvantage of this procedure is requirement of experience on soft tissue endoscopy. In conclusion, percutaneous repair of Achilles tendon with endoscopic control surpasses the disadvantages of open and only percutaneous repair and provides excellent results with earlier return to preinjury activities.

References 1. Abraham, E., Pankovich, A.M.: Neglected ruptures of Achilles tendon. J. Bone Joint Surg. Am. 57, 253–255 (1975) 2. Assal, M., Jung, M., Stern, R., Rippstein, P., Delmi, M., Hoffmeyer, P.: Limited open repair of Achilles tendon ruptures: a technique with a new instrument and findings of a prospective multicenter study. J. Bone Joint Surg. Am. 84-A(2), 161–170 (2002)

922 3. Barfred, T.: Experimental rupture of the Achilles tendon. Comparison of various types of experimental rupture in rats. Acta Orthop. Scand. 42(6), 528–543 (1971) 4. Bhandari, M., Guyatt, G.H., Siddique, F., et al.: Treatment of acute Achilles tendon ruptures a systematic overview and meta-analysis. Clin. Orthop. Relat. Res. 400, 190–200 (2002) 5. Bosworth, D.M.: Repair of defects in the tendo Achillis. J. Bone Joint Surg. Am. 38, 111–114 (1956) 6. Bradley, J.P., Tibone, J.E.: Percutaneous and open surgical repairs of Achilles tendon ruptures. Am. J. Sports Med. 18, 188–195 (1990) 7. Buchgrabber, A., Pässler, H.H.: Percutaneous repair of Achilles tendon rupture. Immobilization versus functional postoperative treatment. Clin. Orthop. Relat. Res. 341, 113–122 (1997) 8. Carden, D.G., Noble, J., Chalmers, J., et al.: Rupture of the calcaneal tendon. The early and late management. J. Bone Joint Surg. Br. 69, 416–420 (1987) 9. Cetti, R., Christensen, S.E., Ejsted, R., et al.: Operative versus nonoperative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am. J. Sports Med. 21, 791–799 (1993) 10. Cetti, R., Henriksen, L.O., Jacobsen, K.S.: A new treatment of ruptured Achilles tendons. A prospective randomized study. Clin. Orthop. Relat. Res. 308, 155–165 (1994) 11. Chillemi, C., Gigante, A., Verdenelli, A., Marinelli, M., Ulisse, S., Morgantini, A., De Palma, L.: Percutaneous repair of Achilles tendon ruptures: ultrasonographic and isokinetic evaluation. Foot Ankle Surg. 8, 267–276 (2002) 12. Doral, M.N., Alam, M., Bozkurt, M., Turhan, E., Atay, O.A., Donmez, G., Maffulli, N.: Functional anatomy of the Achilles tendon. Knee Surg. Sports Traumatol. Arthrosc. 18, 638–643 (2010) 13. Doral, M.N., Bozkurt, M., Turhan, E., Ayvaz, M., Atay, O.A., Uzumcugil, A., Leblebicioglu, G., Kaya, D., Aydog, T.: Percutaneous suturing of the ruptured Achilles tendon with endoscopic control. Arch. Orthop. Trauma. Surg. 129(8), 1093–1101 (2009). Epub 29 Apr 2009 14. Doral, M.N., Tetik, O., Atay, O.A., Leblebicioglu, G., Oznur, A.: Achilles tendon diseases and its management. Acta Orthop. Traumatol. Turc. 36(Suppl. 1), 42–46 (2002) 15. Fierro, N., Sallis, R.: “Achilles tendon rupture. Is casting enough? Postgrad. Med. 98, 145–151 (1995) 16. FitzGibbons, R.E., Hefferon, J., Hill, J.: Percutaneous Achilles tendon repair. Am. J. Sports Med. 21, 724–727 (1993) 17. Gerdes, M.H., Brown, T.D., Bell, A.L., et al.: A flap augmentation technique for Achilles tendon repair. Postoperative strength and functional outcome. Clin. Orthop. Relat. Res. 280, 241–246 (1992) 18. Gillespie, H.S., George, E.A.: Results of surgical repair of spontaneous rupture of the Achilles tendon. J. Trauma 9, 247–249 (1969) 19. Gorschewsky, O., Vogel, U., Schweizer, A., et al.: Percutaneous tenodesis of the Achilles tendon. A new surgical method for the treatment of acute Achillis tendon rupture through percutaneous tenodesis. Injury 30, 315–321 (1999) 20. Halasi, T., Tállay, A., Berkes, I.: Percutaneous Achilles tendon repair with and without endoscopic control. Knee Surg. Sports Traumatol. Arthrosc. 11(6), 409–414 (2003). Epub 3 Oct 2003 21. Hattrup, S.J., Johnson, K.A.: A review of ruptures of the Achilles tendon. Foot Ankle 6(1), 34–38 (1985). Review 22. Hockenbury, R.T., Johns, J.C.: A biomechanical in vitro comparison of open versus percutaneous repair of tendon Achilles. Foot Ankle 11(2), 67–72 (1990) 23. Inglis, A.E., Scott, W.N., Sculco, T.P., et al.: Ruptures of the tendo Achillis. J. Bone Joint Surg. Am. 58, 990–993 (1976) 24. Jacobs, D., Martens, M., van Audekercke, R., et al.: Comparison of conservative and operative treatment of Achilles tendon ruptures. Am. J. Sports Med. 6, 107–111 (1978)

M.N. Doral et al. 25. Kangas, J., Pajala, A., Siira, P., et al.: Early functional treatment versus early immobilization in tension of the musculotendinous unit after Achilles rupture repair: a prospective, randomized, clinical study. J. Trauma 54, 1171–1180 (2003) 26. Kannus, P.: Etiology and pathophysiology of chronic tendon disorders in sports. Scand. J. Med. Sci. Sports 7(2), 78–85 (1997) 27. Kannus, P., Józsa, L.: Histopathological changes preceding spontaneous rupture of a tendon. A controlled study of 891 patients. J. Bone Joint Surg. Am. 73((10), 1507–1525 (1991) 28. Kitaoka, H.B., Alexander, I.J., Adelaar, R.S., Nunley, J.A., Myerson, M.S., Sanders, M.: Clinical rating systems for the ankle-hindfoot, midfoot, hallux, and lesser toes. Foot Ankle Int. 15(7), 349–353 (1994) 29. Klein, W., Lang, D.M., Saleh, M.: The use of the Ma-Griffith technique for percutaneous repair of fresh ruptured tendo Achillis. Chir. Organi Mov. 76(3), 223–228 (1991). English, Italian 30. Kosanovic, M., Cretnik, A., Batista, M.: Subcutaneous suturing of the ruptured Achilles tendon under local anaesthesia. Arch. Orthop. Trauma. Surg. 113, 177–179 (1994) 31. Lea, R.B., Smith, L.: Non-surgical treatment of tendo Achillis rupture. J. Bone Joint Surg. Am. 54, 1398–1407 (1972) 32. Lecestre, P., Germanville, T., Delplace, J., The Société Orthopédique Rochelaise: Achilles tendon ruptures treated by percutaneous tenorraphy: multicentric study of 60 cases. Eur. J. Orthop. Surg. Traumatol. 7, 37–40 (1997) 33. Leppilahti, J., Puranen, J., Orave, S.: Incidence of Achilles tendon rupture. Acta Orthop. Scand. 67, 277–279 (1996) 34. Lim, J., Dalal, R., Waseem, M.: Percutaneous vs open repair of the ruptured Achilles tendon. A prospective randomized controlled study. Foot Ankle Int. 22, 559–568 (2001) 35. Lindholm, A.: A new method of operation in subcutaneous rupture of the Achilles tendon. Acta Chir. Scand. 117, 261–270 (1959) 36. Lo, I.K.Y., Kirkley, A., Nonweiler, B., et al.: Operative versus nonoperative treatment of acute Achilles tendon ruptures. A quantitive review. Clin. J. Sport Med. 7, 207–211 (1997) 37. Lynn, T.A.: Repair of the torn Achilles tendon using the plantaris tendon as a reinforcing membrane. J. Bone Joint Surg. Am. 48, 268–272 (1966) 38. Ma, G.W.C., Griffith, T.G.: Percutaneous repair of acute closed ruptured Achilles tendon. A new technique. Clin. Orthop. Relat. Res. 128, 247–255 (1977) 39. Maffulli, N.: Current concepts review: rupture of the Achilles tendon. J. Bone Joint Surg. Am. 81, 1019–1036 (1999) 40. Majewski, M., Rickert, M., Steinbrück, K.: Achilles tendon rupture. A prospective study assessing various treatment possibilities. Orthopade 29(7), 670–676 (2000) 41. Möller, M., Movin, T., Granhed, H., et al.: Acute rupture of tendo Achillis. A prospective randomized study of comparison between surgical and non-surgical treatment. J. Bone Joint Surg. Br. 83, 843–848 (2001) 42. Momose, T., Amadio, P.C., Zobitz, M.E., Zhao, C., An, K.N.: Effect of paratenon and repetitive motion on the gliding resistance of tendon of extrasynovial origin. Clin. Anat. 15(3), 199–205 (2002) 43. Mortensen, N.H.M., Skov, O., Jensen, P.E.: Early motion of the ankle after operative treatment of a rupture of the Achilles tendon: a prospective randomized clinical and radiographic study. J. Bone Joint Surg. Am. 81, 983–990 (1999) 44. Nistor, L.: Surgical and non-surgical treatment of Achilles tendon rupture. A prospective randomized study. J. Bone Joint Surg. Am. 63, 394–399 (1981) 45. Rowley, D.I., Scotland, T.R.: Rupture of the Achilles tendon treated by a simple operative procedure. Injury 14(3), 252–254 (1982) 46. Schram, A.J., Landry, J.R., Pupp, G.R.: Complete rupture of the Achilles tendon: a new modification for primary surgical repair. J. Foot Surg. 27, 453–457 (1988)

Endoscopy and Percutaneous Suturing in the Achilles Tendon Ruptures 47. Stein, S.R., Luekens, C.A.: Closed treatment of Achilles tendon ruptures. Orthop. Clin. North Am. 7, 241–246 (1976) 48. Takao, M., Ochi, M., Naito, K., et al.: Repair of neglected Achilles tendon rupture using gastrocnemius fascial flaps. Arch. Orthop. Trauma. Surg. 123, 471–474 (2003) 49. Teuffer, A.P.: Traumatic rupture of the Achilles tendon: reconstruction by transplant and graft using the lateral peroneus brevis. Orthop. Clin. North Am. 5, 89–95 (1974) 50. Turgut, A., Günal, I., Maralcan, G., Köse, N., Göktürk, E.: Endoscopy, assisted percutaneous repair of the Achilles tendon ruptures: a cadaveric and clinical study. Knee Surg. Sports Traumatol. Arthrosc. 10(2), 130–133 (2002) 51. Webb, J.M., Bannister, G.C.: Percutaneous repair of the ruptured tendo Achillis. J. Bone Joint Surg. Br. 81, 877–880 (1999)

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52. Weiner, A.D.: Lipscomb PR, rupture of muscles and tendons. Minn. Med. 39(11), 731–736 (1956) 53. Wills, C.A., Washburn, S., Caiozzo, V., et al.: Achilles tendon rupture. A review of the literature comparing surgical versus nonsurgical treatment. Clin. Orthop. Relat. Res. 207, 156–163 (1986) 54. Winter, E., Weise, K., Weller, S., et al.: Surgical repair of Achilles tendon rupture. Arch. Orthop. Trauma. Surg. 117, 364–367 (1998) 55. Wong, J., Barrass, V., Maffulli, N.: Quantitative review of operative and nonoperative management of a Achilles tendon ruptures. Am. J. Sports Med. 30(4), 565–575 (2002) 56. Zantop, T., Tillmann, B., Petersen, W.: Quantitative assessment of blood vessels of the human Achilles tendon: an immunohistochemical cadaver study. Arch. Orthop. Trauma. Surg. 123(9), 501–504 (2003). Epub 24 Apr 2003

Part Sports and Arthroplasty

XIII

Osteoporosis and Sports O. Sahap Atik

Contents Physical Activity and Osteoporosis ........................................... 927 Female Athlete Triad .................................................................. 928 Management ................................................................................ 928 Conclusion ................................................................................... 928 References .................................................................................... 929

Osteoporosis is a major health problem characterized by compromised bone strength predisposing patients to an increased risk of fracture. It has a complex etiopathogenesis, and may cause morbidity and mortality in elderly men and women [5]. Osteoporosis most commonly affects postmenopausal women. The strategies for preventing osteoporotic fractures are maximizing peak bone mass, counteracting age- and menopause-related bone loss [11]. The number of the people with osteoporosis increases as the population ages. Increasing number of patients with osteoporotic fractures may have a serious economic impact on society and on the quality of life of the patient [3]. Awareness among clinicians and health care professionals on osteoporosis should be increased to overcome the burden of the disease [2, 3]. Although most of the osteoporotic fractures are treated by orthopedic surgeons, many patients with these problems are not diagnosed appropriately and treated for underlying osteoporosis. Early diagnosis of the disease is essential to prevent osteoporotic fractures and related mortality and morbidity. Indirect costs and sociologic and psychological impact of fractures should be evaluated together with the direct costs of the disease [3].

Physical Activity and Osteoporosis

O.S. Atik Department of Orthopaedics and Traumatology, Gazi University Medical Faculty, 06500 Ankara, Turkey e-mail: [email protected]

Physical activity is one of the major non-pharmacological methods for increasing and maintaining bone mineral density (BMD) and geometry [6]. However, not all exercises are effective, so a prescription in terms of optimal type, intensity, frequency, and duration is required. Sport activity and exercise across the life span of the average female should be encouraged in the maintenance of bone health. Athletes have a greater bone mineral density compared with non-active and physically active females. Participation in high school athletics is associated with greater BMD. Impact loading sports such as gymnastics, rugby, or volleyball tend to produce a better overall osteogenic

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response than sports without impact loading such as cycling, rowing, and swimming [14]. Moderate impact exercise contributes to skeletal integrity even in older age [12]. Tai Chi Chuan is a low- to moderate-intensity exercise particularly suitable for the elderly, and has been practiced by Chinese for centuries. Runners and swimmers and divers demonstrated some deficits in site-specific BMD values when compared with athletes in other sports [13]. An elite Kenyan runner presented with a tibial fracture sustained during an international cross-country race [16]. There was no clear history of symptoms suggestive of preceding overload and no radiological features of stress fracture. He was found to have sustained an osteoporotic, insufficiency fracture. Competitive running prior to the perimenopausal period seems to be associated with improved hip BMD [9]. However, continued competitive running during the perimenopausal period is not associated with prevention of a perimenopausal hip BMD decline. In contrast, competitive running had little effect on perimenopausal lumbar spine BMD. When treating a female athlete, athletic trainers should consider her mass and sport type with regard to her bone health. The positive impact of sports participation on bone mass can be tempered by nutritional and hormonal status [5]. Zinc deficiency may lead to the increase of endogenous heparin probably causing degranulation of mast cells and release of endogenous heparin, and an increase in the bone-resorbing effect of prostaglandin E2 [1, 4]. Endogenous heparin and prostaglandin E2 are probably cofactors of parathyroid hormone and may have a role in the pathogenesis of senile osteoporosis enhancing the action of parathyroid hormone. Therefore, zinc replacement by dietary zinc supplementation might be valuable to prevent osteoporosis.

Female Athlete Triad Due to the increased energy expenditure of exercise and/or the pressure to obtain an optimal training bodyweight, some female athletes may develop low energy availability or an eating disorder and subsequently amenorrhoea and a loss of bone mineral density. The three interrelated clinical disorders are referred to as the female athlete triad (FAT). A substantial number of high school athletes (78%) and a surprising number of sedentary students (65%) have one or more components of the triad [10]. A significant proportion of female athletes suffer from the components of the FAT. In addition, the FAT is also present in normal active females [20]. Therefore, prevention of one or more of the FAT components should be geared toward all physically active girls and young women.

O.S. Atik

In a study among elite Malaysian athletes, the prevalence of the FAT was low (1.9%), but the prevalence for individual triad component was high, especially in the leanness group [17]. The prevalence of subjects who were at risk of menstrual irregularity, poor bone quality, and eating disorders were 47.6%, 13.3%, and 89.2%, respectively, in the leanness group; and 14.3%, 8.3%, and 89.2%, respectively, in the non-leanness group. In another study, the prevalence of amenorrhea/oligomenorrhea in elite Iranian female athletes was investigated [8]. It is found that 71 (9.0%) individuals had amenorrhea/oligomenorrhea, among those, 11 (15.5%) had polycystic ovary syndrome. Brazilian investigators studied the prevalence of FAT in adolescent elite women swimmers [18]. The prevalence of FAT was low. However, a significant number of athletes presented a partial status of FAT, especially of disordered eating. They concluded that this study suggests the need to monitor the causes of these disorders to create preventive actions that will reverse or avoid the development of the syndrome, thus preserving the athletes’ health.

Management For the management of disordered eating (DE) in athletes, an interdisciplinary approach representing medicine, nutrition, mental health, athletic training, and athletics administration is necessary. It is also important to establish educational initiatives for preventing DE [7]. Also physical therapists must have an important role for recognizing, treating, and preventing the female athlete triad [15]. There is still a greater need for knowledge regarding the triad to be incorporated into physical therapy curriculums, continuing education programs, and professional practice.

Conclusion In conclusion, high-impact and resistive exercise in childhood appears to be an important determinant of future peak bone mass and bone strength. However, exercise throughout adolescence and adulthood is necessary for the preservation or the bone mass and bone strength. Exercise later in life should focus on balance training and muscle strengthening to reduce fall risk [19]. Following the occurrence of osteoporotic vertebral or hip fractures, early mobilization and a multidisciplinary rehabilitation program is important for having the prefracture level of activity.

Osteoporosis and Sports

References 1. Atik, O.S.: Zinc and senile osteoporosis. J. Am. Geriatr. Soc. 31(12), 790–791 (1983) 2. Atik, O.S.: Hip arthroplasty and bone strength. Eklem Hastalik. Cerrahisi 20(1), 1 (2009) 3. Atik, O.S., Gunal, I., Korkusuz, F.: Burden of osteoporosis. Clin. Orthop. Relat. Res. 443, 19–24 (2006) 4. Atik, O.S., Surat, A., GöÜüĜ, M.T.: Prostaglandin E2 – like activity and senile osteoporosis. Prostaglandins Leukot. Med. 11(1), 105–107 (1983) 5. Atik, O.S., Uslu, M.M., Eksioglu, F., et al.: Etiology of senile osteoporosis: a hypothesis. Clin. Orthop. Relat. Res. 443, 25–27 (2006) 6. Bailey, C.A., Brooke-Wavell, K.: Exercise for optimizing peak bone mass in women. Proc. Nutr. Soc. 67(1), 9–18 (2008) 7. Bonci, C.M., Bonci, L.J., Granger, L.R., et al.: National athletic trainers’ association position statement: preventing, detecting, and managing disordered eating in athletes. J. Athl. Train. 43(1), 80–108 (2008) 8. Dadgostar, H., Razi, M., Aleyasin, A., et al.: The relation between athletic sports and prevalence of amenorrhea and oligomenorrhea in Iranian female athletes. Sports Med. Arthrosc. Rehabil. Ther. Technol. 1(1), 16 (2009) 9. Fanning, J., Larrick, L., Weinstein, L., et al.: Findings from a 10-year follow-up of bone mineral density in competitive perimenopausal runners. J. Reprod. Med. 52(10), 874–878 (2007) 10. Hoch, A.Z., Pajewski, N.M., Moraski, L., et al.: Prevalence of the female athlete triad in high school athletes and sedentary students. Clin. J. Sport Med. 19(5), 421–428 (2009)

929 11. Iwamoto, J., Sato, Y., Takeda, T., et al.: Role of sport and exercise in the maintenance of female bone health. J. Bone Miner. Metab. 27(5), 530–537 (2009) 12. Lui, P.P., Qin, L., Chan, K.M., et al.: Tai Chi Chuan exercises in enhancing bone mineral density in active seniors. Clin. Sports Med. 27(1), 75–86 (2008) 13. Mudd, L.M., Fornetti, W., Pivarnik, J.M.: Bone mineral density in collegiate female athletes: comparisons among sports. J. Athl. Train. 42(3), 403–408 (2007) 14. Nichols, D.L., Sanborn, C.F., Essery, E.V.: Bone density and young athletic women. Sports Med. 37(11), 1001–1014 (2007) 15. Pantano, K.J.: Strategies used by physical therapists in the U.S. for treatment and prevention of the female athlete triad. Phys. Ther. Sport 10(1), 3–11 (2009) 16. Pollock, N., Hamilton, B.: Osteoporotic fracture in an elite male Kenyan athlete. Br. J. Sports Med. 42(12), 1000–1001 (2008) 17. Quah, Y.V., Poh, B.K., Ng, L.O., et al.: The female athlete triad among elite Malaysian athletes: prevalence and associated factors. Asia Pac. J. Clin. Nutr. 18(2), 200–208 (2009) 18. Schtscherbyna, A., Soares, E.A., de Oliveira, F.P., et al.: Female athlete triad in elite swimmers of the city of Rio de Janeiro, Brazil. Nutrition 25(6), 634–639 (2009) 19. Schwab, P., Klein, R.F., et al.: Nonpharmacological approaches to improve bone health and reduce osteoporosis. Curr. Opin. Rheumatol. 20(2), 213–217 (2008) 20. Torstveit, M.K., Sundgot-Borgen, J.: The female athlete triad exists in both elite athletes and controls. Med. Sci. Sports Exerc. 37(9), 1449–1459 (2005)

Sports After Total Knee Prosthesis Nurettin Heybeli and Cem ÇopuroÜlu

Contents

Abbreviations

Abbreviations .............................................................................. 931

BW IS TKR

Introduction ................................................................................. 931

body weight impact score total knee replacement

Knee Prosthesis and Expectations ............................................. 932 Return to Sports .......................................................................... 932 Prosthesis Wear ........................................................................... 932 Recommendations ....................................................................... 933 Unicompartmental Knee Arthroplasty: Different Than Total Knee? ........................................................................ 934 Discussion..................................................................................... 934 References .................................................................................... 935

N. Heybeli ( ) and C. ÇopuroÜlu Department of Orthopaedics and Traumatology, Trakya University School of Medicine, Edirne, Turkey e-mail: [email protected], [email protected]; [email protected], [email protected]

Introduction Joint replacement, also known as arthroplasty, is a surgical procedure which changes the original joint surfaces with an artificial one, including a combination of metal, polyethylene, and/or ceramic implants. It is an effective and reliable treatment of end-stage arthritis of the joint [8]. Arthritic joints are associated with pain, stiffness, reduced function, and limitation of activity [9]. The usual indication for arthroplasty is to relieve pain and to improve function of the disabled arthritic joint. Correction of the deformities, increasing social mobility, preserving an independent lifestyle and contributing to psychological well-being are profits of joint replacements providing substantial improvements in quality of life as well as being cost-effective medical treatments [10]. Obvious improvement in ambulation is beneficial for patients’ mental and physical health [8]. Advances in surgical techniques and surgical implant materials made an increase in patient expectations and now there is a demand for joint replacement surgery to allow a patient to return to higher function activities, such as sports. The ability to return to sports activities is important for patients especially participating in some sports activities before surgery. Current expectations of the patients are: a successful operation with a short recovery period, little or no discomfort after the operation, pain-free movement of the joints, improved function, long-term durability of the implantation, without complications and limitations of activity. If such expectations are not met, there may be dissatisfaction even after a technically successful surgery [3]. Total knee replacement (TKR) is a reliable and effective treatment modality of arthritic knees [8]. It is predicted that TKR applications will grow by 673%, respectively, between

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2005 and 2030 [17], because of changing demographics and wider indications [5]. Joint replacement surgery allows patients with arthritic joints to increase their physical activity, and regular exercise reduces anxiety, depression, and mortality. Thus, joint replacements are associated with improved function, improved quality of life, and longer life [10]. With the increase in joint replacement surgeries and expectation profile of the patients, it is important to determine whether these surgeries meet the expectations and allow the patients return to sports activities.

Knee Prosthesis and Expectations The factors influencing the expectations from the knee replacement surgery are mostly the habitual status before surgery [33]. Patients’ personality characteristics, social class, interactions with health professionals, and information obtained through individual research are the other factors effective in framing patient expectations [25]. Patients participating in sporting activities preoperatively expect to participate in a higher rate postoperatively. Wylde et al. reported that 85% of TKR patients who returned to sports activities took part in sports in the year before operation [38]. Trying to achieve a level of skill and activity that was not achieved preoperatively subjects the patient to risk of injury [8]. Patient expectations related to recovery from surgery shows significant associations with patient characteristics such as age, gender, comorbidity, and preoperative level of physical and mental health [33]. Kennedy et al. [15] evaluated functional measures and a self-report measure of function in 1,805 total hip (761) and knee (1,044) arthroplasty candidates (1,063 women, 742 men), preoperatively. Women represented 59% of the study subjects and showed greater disability than men in the physical performance and selfreport measures [15]. With increasing life expectancy and elective surgery improving quality of life, age alone is not a factor that affects the outcome of joint arthroplasty [14]. Higher rates of sports participation in some cultures may also affect the return capacity to sports activities [4]. This may be explained by the fact that these patients are less disabled preoperatively. Young and active patients are more prone to turn back to sports activities when compared with old and inactive patients, because they are used to sporting facilities [31].

Return to Sports Current recommendation for old people is to participate in low impact and low duration activities to optimize implant longevity; however, little data exist on the participation in

N. Heybeli and C. ÇopuroÜlu

sports activities of middle-aged patients with TKR [8]. Higher rates of sports participation in some cultures may affect the preoperative disability and may be determinative in the ability to return to sports earlier [23]. The extension of the disability is another important factor influencing the postoperative success of the replacement. If the symptoms have been present for a long time before joint replacement, some patients may have had to give up sports for a long time and return to sports is a handicap for them. The involvement of the number of joints is also a determinant for the ability to return to sports. If only a single joint is involved and it is operated, then the success rate will be higher according to the multi-articular involvement [22]. In a study by Huch et al. [12], pain elsewhere in the body, and pain at the site of the replaced joint were mentioned as reasons for avoiding athletic activity following joint replacement. Additional symptoms such as back pain, feet problems, low body mass index are also determinants of the ability to return to sports activities [22]. Patients and surgeons must be realistic about the probability to return to sports before operation in order to obviate unrealistic expectations. Patient expectations can be modified with preoperative education [10]. The ability to return to sports participation after TKR is dependent on preoperative athletic activity, preoperative rehabilitation, surgical reconstruction, implant fixation, implant failure, wear of the bearing surfaces, and trauma [9].

Prosthesis Wear Activity can cause particles to form on the joint surface. These particles in prosthetic joints are associated with the development of particulate-induced osteolysis [1]. Younger patients tend to be more active, subjecting their prosthetic joint to higher loads more often and thus shortening the life of the implant [1]. Patients who participate in sports activities after joint replacement procedures have increased; force crossing the replaced joint causing wear in the bearing surfaces, increased stress at the bone-implant fixation surface, and higher incidence of traumatic injury in the operated joint when compared with low level activity patients [10]. The knee replacement is not an anatomic reproduction of the human knee, so that there is a decrease in proprioception compared with an age-matched non-arthritic knee [16]. Duration of the implantation is also important in the determination of the implant wear, as well as the activity level. All modes of failure increase with increased activity seen in younger patients. The patient involved in sports increases the level of wear subjecting the knee replacement to early failure [8]. However, it is not clearly described how much activity level is allowed or recommended for the survival of the joint replacement.

Sports After Total Knee Prosthesis

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Muscles crossing the knee joint act by many vectors with different directions and magnitudes. The dynamic effect of these combined forces is the resultant load acting on the knee of a moving person, which is several times higher than the body weight. Kuster et al. [18] evaluated the contact stress distribution and contact area of different knee joint designs for loads occurring during recreational activities. In knee prosthesis, the stresses are concentrated on smaller areas than in normal knees. Bicycling produces a peak load of 1.2× body weight (BW) that occur on the surfaces of a total knee prosthesis, while power walking produces 4× BW, hiking produces 8×BW and jogging produces 9× BW. The load of the joint surfaces of the total knee joint depends also on the position of the knee joint. Walking uphill produces tibiofemoral compressive forces of 4–5× BW, while downhill walking tibiofemoral loads as high as 8×BW at 40° knee flexion [20]. The contact area is greater during power walking, downhill walking, or jogging for the mobile bearing design compared with the flat or curved designs. According to this study, cycling and power walking are the least demanding endurance activities for the knee joint. Because these activities load the knee joint at different flexion angles, different parts of the tibial inlay is stressed and ensure a more even wear pattern. The conclusion was as follows: jogging or sports involving running should be discouraged after TKR [20]. The failure of knee prosthesis is primarily related to polyethylene wear with increased activity. Increased stresses at the bone implant interface are the reasons for early implant loosening [8]. Excessive and sudden loads during sports participation may induce periprosthetic fracture, knee dislocation, and polyethylene dissociation from modular components [19]. Trauma caused by athletic participation is the primary Table 1 Grouping of sports according to their difficulty Allowed Allowed with experience

concern among orthopedic surgeons [8]. Susceptibility to mechanical failure caused by excessive loads and fatigue makes most surgeons recommend low demand and low duration activity sports.

Recommendations According to the members of the Knee Society in 2005, stationary cycling, bowling, golf, ballroom dancing, canoeing, road cycling, normal walking, swimming, square dancing, shuffleboard, hiking, and speed walking are allowed sports. Some sports were allowed with experience. These were; horseback riding, rowing, downhill skiing, doubles tennis, cross-country skiing, stationary skiing, and ice-skating. There are some other sports with no consensus between observers. These are fencing, roller skating, weight lifting, baseball, gymnastics, handball, hockey, rock climbing, squash/rocketball, singles tennis, and weight machine. Some other sports like football, basketball, jogging, volleyball, and soccer are not recommended [10] (Table 1). According to a survey performed at the Mayo Clinic [27], golf, swimming, cycling, sailing, bowling, scuba diving, and cross country skiing are recommended sports after TKR. Handball, racquetball, hockey, waterskiing, karate, soccer, baseball, running, basketball, and football are high level sports and are discouraged. Mont et al. stated that patients playing tennis were satisfied with their knee replacements. The players noted increased court mobility and a loss of court speed following the total knee arthroplasty [30]. However, many orthopedic surgeons discourage their patients with a joint replacement from playing

No consensus

Not recommended

Bowling (IS 1)

Rowing (IS 1)

Fencing (IS 1)

Basketball (IS 3)

Stationary cycling (IS 1)

Ice skating (IS 2)

Roller skating (IS 2)

Football (IS 3)

Ballroom dancing (IS 1)

Cross-country skiing (IS 2)

Weight lifting (IS 2)

Volleyball (IS 3)

Golf (IS 1)

Stationary skiing (IS 2)

Baseball (IS 3)

Jogging (IS 3)

Shuffleboard (IS 1)

Doubles tennis (IS 1)

Gymnastics (IS 3)

Soccer (IS 3)

Swimming (IS 1)

Horseback riding (IS 1)

Handball (IS 3)

Normal walking (IS 1)

Down-hill skiing (IS 2)

Hockey (IS 3)

Canoeing (IS 1)

Rock climbing (IS 3)

Road cycling (IS 1)

Squash/rocketball (IS 3)

Square dancing (IS 1)

Singles tennis (IS 2)

Hiking (IS 1)

Weight machine (IS 2)

Speed walking (IS 1) According to Healy and Sharma [10] sports were separated into four groups: allowed, allowed with experience, no consensus, and not recommended after knee prosthesis. According to Marker and Mont [26], impact scores which correlated with the difficulty of the sports were marked. Allowed sports according to Healy were regarded as IS 1 according to Marker and Mont, not recommended sports were regarded as IS 3, and sports allowed with experience and no consensus gained a mixture of impact scores

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tennis in order to avoid high-impact loading and twisting at the hip and knee joints, which might be associated with wear of the bearing surfaces, implant loosening or trauma [35]. Mallon and Callaghan [24], reported about 83 active golfers who had TKR surgery. Eighty-seven percent used a golf cart, 60% experienced a mild ache in the operated knee while playing golf, and 36% experienced a mild ache in the operated knee after playing golf [24]. Jackson et al. [13] made a survey between 151 golfers who had undergone primary TKR and concluded that total knee arthroplasty reliably relieved pain that had been previously experienced while golfing, and increased or maintained this group’s enjoyment of playing golf.

Unicompartmental Knee Arthroplasty: Different Than Total Knee? Unicompartmental knee arthroplasty is a surgical treatment procedure for painful unicompartmental knee arthritic patients. It is a less invasive surgical procedure and one of its theoretical advantages is quick return to athletic activity [9]. Rehabilitation is much quicker and proprioception is better with unicondylar knee replacement [8]. This allows the patient to participate at a higher skill level as opposed to having a TKR [8]. Naal et al. [32] observed 83 patients for 18 months postoperatively, with a fixed bearing unicompartmental knee replacement, and 88% of the patients returned to sports activities while 93% was performing sports activities preoperatively. Fisher et al. [7] evaluated 76 patients with a mobile-bearing medial unicompartmental knee arthroplasty, for 18 months. Prior to the operation, 55% participated in sports activities, and 51% returned to the sports activities. Ninety-three percent of the patients successfully returned to their regular sports after the unicompartmental knee replacement surgery. However; a middle-aged patient with a unicondylar knee replacement who returns to high level sports may be subject to early revision to a TKR [8]. Hopper et al. [11] compared participation in sporting activities following total and unicompartmental knee arthroplasties. The patients had a significantly greater return rate to sport after unicompartmental arthroplasty than total knee arthroplasty. Patients in unicompartmental group took part in more sporting sessions preoperatively and postoperatively and for a longer period of time than patients in the total arthroplasty group [11].

Discussion Orthopedic surgeons have a duty to recommend activities that promote durability and survival of the reconstructed joint [21]. In a recent study, Mont et al. [28] compared high- and

N. Heybeli and C. ÇopuroÜlu

low-activity patients with total knee replacement. Overall satisfaction, rate of revision, and clinical and radiographic results were compared at a minimum follow-up of 4 years and mean 7 years. While long-term results have to be waited, the results suggest that low- to moderate-impact sports activities had no effect on the clinical and/or radiographic outcomes of total knee arthroplasties at midterm follow-up [28]. However, patients must be cautioned to minimize component overload [6]. Swanson [37] reported a questionnaire, which was distributed to the members of the American Association for Hip and Knee Surgeons attending the 2007 annual meeting. More than 95% of the responses placed no limitations on low-impact activities including level surface walking, stair climbing, level surface bicycling, swimming, and golf. Higher impact activities were more commonly discouraged, although there was considerable variability [37]. In making activity recommendations, peak force as well as the number of loading cycles should be considered [37]. High-impact activities are not appropriate for most patients after total knee arthroplasty. Mont et al. [29] indicate that some patients can participate in high-impact sports, such as jogging, down-hill skiing, and singles tennis, and can enjoy excellent clinical outcomes during the first 4 years after surgery [29]. Bradbury et al. [2] reported that more than 75% of patients who had a total knee arthroplasty returned to sports postoperatively, with 20% returning to highimpact activities [2]. All patients should be encouraged to remain physically active to improve general health, maintain good bone quality, and improve implant fixation [36]. Marker et al. [26] analyzed whether the increase in physical activity of patients following surgery is associated with their level of functional and objective treatment. They reported that change in activity level is more closely associated with improved function than changes in objective measures [26]. Santaguida et al. [34] searched four bibliographic databases (MEDLINE 1980–2001, CINAHL 1982–2001, EMBASE 1980–2001, HealthStar 1998–1999) for studies involving arthritic patients with one or more of the following outcomes after total joint arthroplasty: pain, physical function, postoperative complications (short and long term), and time to revision. Findings suggest that younger age and male sex are associated with increased risk of revision and older age and male sex are associated with increased risk of mortality; older age is related to worse function (particularly among women), and age and sex do not influence the outcome of pain. All subgroups derived benefit from total joint arthroplasty [34]. Orthopedic surgeons should inform their patients preoperatively that the patients participating in sports activities before surgery have more chance to participate in sports activities postoperatively. Mobility and regular exercises improve patients’ physical and mental health. High-impact

Sports After Total Knee Prosthesis

sports can be a reason for component overload and cause fatigue and implant failure. Low-impact sports should be encouraged as soon as possible after surgery.

References 1. Bauman, S., Williams, D., Petrucelli, D., et al.: Physical activity after total joint replacement: a cross-sectional survey. Clin. J. Sport Med. 17(2), 104–108 (2007) 2. Bradbury, N., Borton, D., Spoo, G., et al.: Participation in sports after total knee replacement. Am. J. Sports Med. 26(4), 530–535 (1998) 3. Chatterji, U., Ashworth, M.J., Lewis, P.L., et al.: Effect of total hip arthroplasty on recreational and sporting activity. ANZ J. Surg. 74, 446–449 (2004) 4. Chatterji, U., Ashworth, M.J., Lewis, P.L., et al.: Effect of total knee arthroplasty on recreational and sporting activity. ANZ J. Surg. 75, 405–408 (2005) 5. Crowninshield, R.D., Rosenberg, A.G., Sporer, S.M.: Changing demographics of patients with total joint replacement. Clin. Orthop. 443, 266–272 (2006) 6. Farr, J., Jiranek, W.A.: Sports after knee arthroplasty: partial versus total knee arthroplasty. Phys. Sportsmed. 37(4), 53–61 (2009) 7. Fisher, N., Agarwal, M., Reuben, S.F., et al.: Sporting and physical activity following Oxford medial unicompartmental knee arthroplasty. Knee 13, 296–300 (2006) 8. Hartford, J.M.: Sports after arthroplasty of the knee. Sports Med. Arthrosc. Rev. 11, 149–154 (2003) 9. Healy, W.L., Iorio, R., Lemos, M.J.: Athletic activity after total knee arthroplasty. Clin. Orthop. Relat. Res. 380, 65–71 (2000) 10. Healy, W.L., Sharma, S., Schwartz, B., et al.: Athletic activity after total joint arthroplasty. J. Bone Joint Surg. Am. 90, 2245–2252 (2008) 11. Hopper, G.P., Leach, W.J.: Participation in sporting activities following knee replacement: total versus unicompartmental. Knee Surg. Sports Traumatol. Arthrosc. 16, 973–979 (2008) 12. Huch, K., Müller, K.A.C., Stürmer, T., et al.: Sports activities 5 years after total knee or hip arthroplasty: the Ulm Osteoarthritis Study. Ann. Rheum. Dis. 64, 1715–1720 (2005) 13. Jackson, J.D., Smith, J., Shah, J.P., et al.: Golf after total knee arthroplasty: do patients return to walking the course? Am. J. Sports Med. 37(11), 2201–2204 (2009) 14. Jones, C.A., Voaklander, D.C., Johnston, W.C., et al.: The effect of age on pain, function, an quality of life after total hip and knee arthroplasty. Arch. Intern. Med. 161, 454–460 (2001) 15. Kennedy, D., Stratford, P.W., Pagura, S.M.C., et al.: Comparison of gender and group differences in self-report and physical performance measures in total hip and knee arthroplasty candidates. J. Arthroplasty 17(1), 70–77 (2002) 16. Koralewicz, L.M., Engh, G.A.: Comparison of proprioception in arthritic and age matched normal knees. J. Bone Joint Surg. Am. 82, 1582–1588 (2000) 17. Kurtz, S., Ong, K., Lau, E., et al.: P Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J. Bone Joint Surg. 89-A, 780–785 (2007) 18. Kuster, M.S.: Exercise recommendations after total joint replacement: a review of the current literature and proposal of scientifically based guidelines. Sports Med. 32(7), 433–445 (2002)

935 19. Kuster, M.S., Spalinger, E., Blanksby, B.A., et al.: Endurance sports after total knee replacement: a biomechanical investigation. Med. Sci. Sports Exerc. 32(4), 721–724 (2000) 20. Kuster, M.S., Wood, G.A., Stachowiak, G.W., et al.: Joint load considerations in total knee replacement. J. Bone Joint Surg. 79-B, 109–113 (1997) 21. Laupacis, A., Bourne, R., Rorabeck, C., et al.: The effect of total hip replacement on health-related quality of life. J. Bone Joint Surg. Am. 75, 1619–1626 (1993) 22. Liebs, T.R., Herzberg, W., Rüther, W., et al.: Ergometer cycling after hip or knee replacement surgery: a randomized controlled trial. J. Bone Joint Surg. Am. 92, 814–822 (2010) 23. Lingard, E.A., Sledge, C.B., Learmonth, I.D.: Patient expectations regarding total knee arthroplasty: differences among the United States, United Kingdom, and Australia. J. Bone Joint Surg. Am. 88-A, 1202–1207 (2006) 24. Mallon, W.J., Callaghan, J.J.: Total knee arthroplasty in active golfers. J. Arthroplasty 8, 299–306 (1993) 25. Mancuso, C.A., Graziano, S., Briskie, L.M., et al.: Randomized trials to modify patients’ preoperative expectations of hip and knee arthroplasties. Clin. Orthop. Relat. Res. 466, 424–431 (2008) 26. Marker, D.R., Mont, M.A., Seyler, T.M., et al.: Does functional improvement following TKA correlate to increased sports activity? Iowa Orthop. J. 29, 11–16 (2009) 27. McGrory, B.J., Stuart, M.J., Sim, F.H.: Participation in sports after hip and knee arthroplasty: review of literature and survey of surgeon preferences. Mayo Clin. Proc. 70(4), 342–348 (1995) 28. Mont, M.A., Marker, D.R., Seyler, T.M., et al.: Knee arthroplasties have similar results in high- and low-activity patients. Clin. Orthop. Relat. Res. 460, 165–173 (2007) 29. Mont, M.A., Marker, D.R., Seyler, T.M., et al.: High-impact sports after total knee arthroplasty. J. Arthroplasty 23(6 Suppl 1), 80–84 (2008) 30. Mont, M.A., Rajadhyaksha, A.D., Marxen, J.L., et al.: Tennis after total knee replacement. Am. J. Sports Med. 30, 163–166 (2002) 31. Naal, F.D., Fischer, M., Preuss, A., et al.: Return to sports and recreational activity after unicompartmental knee arthroplasty. Am. J. Sports Med. 35, 1688–1695 (2007) 32. Naal, F.D., Maffiuletti, N.A., Munzinger, U., et al.: Sports after hip resurfacing arthroplasty. Am. J. Sports Med. 35, 705–711 (2007) 33. Razmjou, H., Finkelstein, J.A., Yee, A., et al.: Relationship between preoperative patient characteristics and expectations in candidates for total knee arthroplasty. Physiother. Can. 61, 38–45 (2009) 34. Santaguida, P.L., Hawker, G.A., Hudak, P.L., et al.: Patient characteristics affecting the prognosis of total hip and knee joint arthroplasty: a systematic review. Can. J. Surg. 51(6), 428–436 (2008) 35. Schmalzried, T.P., Shepherd, E.F., Dorey, F.J., et al.: Wear is a function of use, not time. Clin. Orthop. Relat. Res. 381, 36–46 (2000) 36. Seyler, T.M., Mont, M.A., Ragland, P.S., et al.: Sports activity after total hip and knee arthroplasty: recommendations concerning tennis. Sports Med. 36(7), 571–583 (2006) 37. Swanson, E.A., Schmalzried, T.P., Dorey, F.J.: Activity recommendations after total hip and knee arthroplasty: a survey of the American Association for Hip and Knee Surgeons. J. Arthroplasty 24(6 Suppl 1), 120–126 (2009) 38. Wylde, V., Blom, A., Dieppe, P., et al.: Return to sport after joint replacement. J. Bone Joint Surg. 90-B, 920–923 (2008)

Treatment of Pain in TKA: Favoring Post-op Physical Activity Maria Assunta Servadei, Danilo Bruni, Francesco Iacono, Stefano Zaffagnini, Giulio Maria Marcheggiani Muccioli, Alice Bondi, Tommaso Bonanzinga, Stefano Della Villa, and Maurilio Marcacci

Contents Postoperative Pain Management ............................................... 938 Immediate Postoperative Period ................................................ 938 Recommendations for Home Rehabilitation ............................ 938 TKA and Sport Activity Resumption ........................................ 939 Sport-Specific Recommendations .............................................. 939 References .................................................................................... 939

M.A. Servadei ( ) and S. Della Villa Isokinetic Sports Rehabilitation Center, via di Casteldebole, 8/10, 40100 Bologna, Italy e-mail: [email protected]; [email protected] D. Bruni, F. Iacono, S. Zaffagnini, G.M. Marcheggiani Muccioli, A. Bondi, T. Bonanzinga, and M. Marcacci 9th Division of Orthopaedic and Traumatologic Surgery, Biomechanics Laboratory – Codivilla-Putti Research Center, Rizzoli Orthopaedic Institute, Bologna University, via di Barbiano, 1/10, 40136 Bologna, Italy e-mail: [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]; [email protected]

Degenerative Joint Disease (DJD) progressively produces pain and functional impairment. The increase in the longevity of the general population results in a higher and higher prevalence for DJD, so that osteoarthritis equals to more than a half of the chronic pathologic conditions involving people older than 65 years [6]. However, continuous evolution of biotechnologies and surgical techniques has made joint replacement surgery always more popular and more effective [4]. Nowadays, patients treated with joint replacement surgery for primary DJD are younger and often more functionally demanding than in the past decades. When consulting to an orthopedic surgeon who suggests a hip or knee replacement, nearly all patients ask the doctor if they will be able to resume sports activity after surgery. Positive effects of a regular sports activity in preventing disabling and chronic pathologies like obesity, high blood pressure, cardiovascular diseases, diabetes, osteoporosis, and depression have been widely underlined and promoted by the mass media. This sort of positive selection pressure has pushed middle-aged people to think about sport activity as a sort of long life elixir, so that the largest part of patients with a hip or knee replacement absolutely need some level of sport activity resumption after surgery. To satisfy the functional demands of these patients, a deep and complete collaboration between the orthopedic surgeon and the physiatrist is mandatory and a complete exchange of information and knowledge is necessary to obtain a fast and functionally complete healing process. In this holistic approach, it is important to firmly bear in mind that every patient has to be addressed as a single unit, made by a psychological component, a neuromuscular/neurosensitive component, and a musculoskeletal component. The surgical treatment of a severe DJD of the knee with a total knee arthroplasty (TKA) produces a new surgical normality and just solves the functional problems and the symptoms directly related to the pathological deformity. To develop a new functional normality starting from this new surgical normality is never an easy step, most of all when the new functional normality is expected to be at a high demand activity level.

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_121, © Springer-Verlag Berlin Heidelberg 2012

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The fundamental steps of the functional recovery process are: s s s s s

Pain resolution Range of motion (ROM) recovery Strength recovery Proprioception recovery Daily activities recovery, including work-related functions and sports-related functions.

Postoperative Pain Management Postoperative pain resolution is obviously the first and mandatory request to be satisfied in order to progress toward a new complete functional normality. A correctly administered and well-dosed postoperative physical activity is a highly effective tool to control pain and to obtain a rapid functional improvement. Unfortunately, in our experience, a specific rehabilitation protocol, after hospital discharge, is usually administered just to a small and restricted subpopulation of patients treated with a TKA (Fig. 1). Nevertheless, it is important to underline how a correct rehabilitation protocol, based on a correctly administered physical activity, is fundamental in reducing the incidence of functional complications which are incompatible with sport activity resumption, such as flexion contracture, extensor mechanism deficit, limited ROM, foot and ankle-related gait dysfunctions, incomplete proprioceptive recovery, or persistent pain.

Immediate Postoperative Period The fundamental objective for the acute postoperative phase is to avoid excessive joint swelling, reduce inflammation, and prevent wound suffering-related complications. Patients are positioned with operated leg elevated and ice on their knee, for not more than 20 consecutive minutes. TKA Patients with specific rehabilitation protocol

no rehab rehab rehab-sport

Fig. 1 A specific rehabilitation protocol is unfortunately usually administered just to a restricted subpopulation of TKA patients

We usually position a support under the heel of the operated leg to promote a complete extension recovery in the first postoperative days. Patients are not allowed to leave the bed for the first postoperative day and until the drainage removal. Continuous passive-assisted motion is usually started on the second postoperative day with flexion progressively increased as tolerated. However, if persistent pain is referred or if evident swelling is noted, we strongly recommend to stop continuous passive motion and just focus on complete extension recovery, while an additional dose of non steroidal anti-inflammatory drugs can be administered until the resolution of the symptoms, which is usually achieved in 1 or 2 days. It is fundamental to underline that no forced manual mobilization in flexion has to be performed at all. After first medication and drainage removal, patients usually start functional and assisted walking exercises.

Recommendations for Home Rehabilitation It is important to underline the usefulness of a simple program of basic exercises that the patient can execute independently at home, starting from the fourth to fifth postoperative day. The fundamental point is that the patient has to learn to correctly walk with two crutches, with the operated knee completely extended during the stance phase of the gait. Walking with a flexed knee can lead to persistent anterior knee pain and to a plastic retraction of posterior muscular and capsular structures, with an abnormal gait and an overload on prosthetic implant, which can impair osteointegration and medium- and long-term stability of the implant. During the first 2 weeks after surgery, the patient has to focus on isometric open chain exercises to recover correct extensor mechanism muscle recruitment and to prevent the danger of any extension lag. These simple routine exercises have to be executed at least twice a day. It is fundamental to underline that full weightbearing has to be allowed just when the patient has achieved full active and passive extension. Any unsolved functional deficit, particularly a persistent extension lag, can lead to long lasting problems like an algodistrophy, which can impair the osteointegration of our implant and can produce a persistent pain. To solve immediately any functional deficit is the key point to obtain an excellent functional and clinical long-term result, most of all in patients with risk factors correlating with a poor final outcome, such as female gender, older age, low socioeconomical status, a lot of comorbidities, a worse preoperative status, depression, low self-efficacy, poor pain coping strategies, somatization, low social support [7]. After suture removal and complete healing of the surgical wound, the patient can start with the water-based and land-based

Treatment of Pain in TKA: Favoring Post-op Physical Activity

phase of the rehabilitation protocol and, according to his general health status and his psychological and motivational conditions, with a sport-specific playground-based phase.

TKA and Sport Activity Resumption In literature, we have no general consensus regarding sports that can be safely practiced after a TKA. A reduced physical activity after TKA generally should not be recommended, because this can lead to a reduction of aerobic threshold, a loss of muscle mass, a reduction of coordination and a lower postural control, producing a weakening of the host bone and a higher risk of falls and fractures. However, some papers have demonstrated that a correctly implanted TKA provides in more than 90% of the cases a complete pain relief and an excellent functional improvement, finally leading to a more active lifestyle ant to a superior cardiovascular performance. After a successful TKA, it has been noted that there has been an improvement in physical activity resistance, an improvement in maximal load, a superior peak in oxygen consumption, and a higher oxygen extraction by the peripheral tissue [5]. Nevertheless, the risk of wear and loosening of the implant is logically expected to be directly related to mechanical load and so to the intensity of physical activity [2]. Younger patients, with high functional demands tend to recover a more active lifestyle and to resume sport activity after surgery, with an increased risk of aseptic loosening [8]. Seventy-five percent of the patients regularly involved in some kind of sport activity resume it after surgery, while on the contrary just 35% of the patients with a preoperative sedentary lifestyle start some kind of physical activity after surgery [1]. Timing is fundamental for sports resumption after TKA and an excellent and complete functional recovery is mandatory. Before the patient is allowed to resume his sport activity, we have to clearly assess: s s s s s s

A complete pain resolution; A complete range of motion of the implant A natural joint motion A side-to-side strength difference lower than 20% A normal stabilometric analysis A normal proprioceptive and gait pattern.

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effective and the patient can achieve a good or excellent functional result, but he has to accept a significant reduction of his physical activity level. Further research is needed to develop new surgical techniques and new implant designs to provide an optimal solution for younger patients with high functional demands, unwilling to reduce their physical activity level or to give up their recreational sport practice. Future improvements in biotechnologies and basic science knowledge will permit to perform minimally invasive surgery, sparing host bone and ligamentous structures, to better reproduce native kinematic and overcome intrinsic mechanical limits of cemented implants.

Sport-Specific Recommendations Sport activity after TKA has to be considered like a medication, with dose-dependent positive and adverse effects. Moderate running or jogging is one of the patients’ preferred physical activities and it is not generally considered a dangerous exercise. However, running or jogging is not so harmless because the stance phase takes place with the knee flexed at nearly 30° and so at every step there is a high mechanical load on the operated knee, possibly producing an overstress at the bone–cement interface and an accelerated polyethylene insert wear. Moreover, the faster the running is, the higher is the mechanical load on the knee, so that at 7 km/h, we have four times the body weight loading the knee at every step [3]. Also mountain trekking is usually considered as a harmless activity, but we have to bear in mind that downward walking produces a higher load on the knee joint more than eight times the body weight. Using trekking poles, this load can be reduced to more than 20%. Biking is surely the physical activity with the lowest impact on the knee after TKA, because compressive load is just 1.2 times the body weight and this can be further reduced increasing the highness of the seat. Tennis can be performed, but it is preferable to play double matches on red ground.

References According to recent literature, patients with a large number of comorbidities and low socioeconomical status are at risk of a poor final outcome, while on the opposite side patients with a high functional level and an excellent general health status are at risk to compromise the medium- and long-term result through overusing their TKA. For this new category of very active patients, conventional surgical technique and implant design cannot be completely

1. Bradbury, N., Borton, D., Spoo, G., et al.: Participation in sports after total knee replacement. Am. J. Sports Med. 26, 530–535 (1998) 2. Holt, G., Murnaghan, C., Reilly, J., et al.: The biology of aseptic osteolysis. Clin. Orthop. Relat. Res. 460, 240–252 (2007) 3. Kuster, M.S.: Exercise recommendations after total joint replacement: a review of the current literature and proposal of scientifically based guidelines. Sports Med. 32, 433–445 (2002)

940 4. Pandit, H., Aslam, N., Pirpiris, M., et al.: Total knee arthroplasty: the future. J. Surg. Orthop. Adv. 15, 79–85 (2006) 5. Ries, M.D., Philbin, E.F., Groff, G.D., et al.: Improvement in cardiovascular fitness after total knee arthroplasty. J. Bone Joint Surg. Am. 78, 1696–1701 (1996) 6. Servadei, M.A.: Il ritorno allo sport dopo intervento di artroprotesi. Ital. J. Rehab. Med. 22, 145–151 (2008)

M.A. Servadei et al. 7. Wilde, V., Dieppe, P., Hewlett, S., et al.: Total knee replacement: is it really an effective procedure for all? Knee 14, 417–423 (2007) 8. Zahiri, C.A., Schmalzried, T.P., Szuszczewicz, E.S., et al.: Assessing activity in joint replacement patients. J. Arthroplasty 13, 890–895 (1998)

Pain Management in Total Knee Arthroplasty Paolo Adravanti, Francesco Benazzo, Mario Mosconi, Mattia Mocchi, and F. Bonezzi

Contents

Introduction

Introduction ................................................................................. 941

Pain is perceived at the CNS level as a consequence of peripheral nociceptor activation and the cells that take part in the transmission of the signal to the somatosensitive area of the cerebral cortex. This process is called nociception. A peripheral nociceptor is activated following a mechanical, thermic or chemical stimulus. The first neuron along the pain path is situated in the ganglions of the dorsal roots of the spine nerves. This neuron has long dendrites and transmits efferent messages through an axon to the second neuron found in the posterior horn of the spinal cord. The signal is subsequently transmitted to the nuclei of the thalamus. This is home to the third neuron which projects information principally to the somatosensitive area of the cerebral cortex (SI post-central and SII at the end of the superior portion of the central sulk). It is at this level that pain awareness occurs. For nociceptor activation, a stimulus superior in strength to the activation threshold is required (the likes of which, as we will later discuss, can be influenced by various factors, first of all the inflammation). The greater the stimulus and the number of nociceptors activated, the greater is the pain perceived. There are two types of fibres involved in the transmission of this type of signal:

Diagnostic Principles of Pain ..................................................... 942 Pain Control................................................................................. 942 References .................................................................................... 943

P. Adravanti ( ) Orthopaedic Department, Clinic “Casa di Cura Città di Parma”, Piazza Maestri 5, 43100 Parma, Italy e-mail: [email protected], [email protected] F. Benazzo, M. Mosconi, and M. Mocchi Orthopaedics and Traumatology, Università degli studi di Pavia, Fondazione IRCCS Policlinico San Matteo, Piazzale Glogi 2, 27100 Pavia, Italy e-mail: [email protected]; [email protected]; [email protected] F. Bonezzi Unità di Medicina del Dolore, Fondazione Salvatore Maugeri, Via S. Maugeri 10, 27100 Pavia, Italy e-mail: [email protected]

Fibre A-delta: myelin fibres which transmit the signal at a speed of 10–30 m/s. These are activated by mechanical and thermic stimuli. Activation generally results from an acute stimulus and is responsible for the immediate sense of pain. Fibre C: amyelinated fibres which transmit at 0.5–2 m/s and are activated by chemical, mechanical, thermic and polymodal stimulus. Chronic knee pain can be caused by constant nociceptor activation. A tissue lesion (e.g., cartilaginous damage) leads to a pathological pattern (e.g., arthrosis) which can trigger an inflammatory reaction responsible for pain pathogenesis by

M.N. Doral et al. (eds.), Sports Injuries, DOI: 10.1007/978-3-642-15630-4_122, © Springer-Verlag Berlin Heidelberg 2012

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liberating substances whose main effect is to lower the stimulation threshold of nociceptors. Acute pain has been accurately conceptualised as a symptom of an underlying disease, not a disease in itself. Furthermore, it is generally accepted that treating the underlying pathology provides adequate pain relief [3]. Inflammatory pain is initiated by tissue damage inflammation and neuropathic pain caused by nervous system lesions. Both are characterised by hypersensitivity at the site of damage and in adjacent normal tissue. Pain may appear to arise spontaneously, stimuli that would never normally produce pain begin to do so (allodynia) and noxious stimuli evoke more severe and prolonged pain (hyperalgesia) [2]. Brief noxious stimuli do not result in permanent nociception alteration, but continuous nociceptive activity can eventually lead to long-term physiological changes, a phenomenon known as neuronal plasticity [3]. Neuronal plasticity is therefore responsible for allodynia, to the left of the line, (pain is generated by stimuli which would not usually induced it) and hyperalgesia, on the right (a painful stimulus which provokes excessive pain). Nociceptor sensitization occurs when certain substances such as K ions, bradykinin, serotonin, histamine, prostaglandins and leukotriens (eicosanoids) are released near nociceptors following tissue damage or an inflammatory process [1]. When cells die as a result of a mechanical stimulus, the potassium released directly depolarises the nociceptors’ membrane whilst other substances, such as bradykinin, bind themselves to membrane receptors and act by way of second messengers. Other substances, however, are released by the nociceptors themselves through an assonic reflex: substance P (SP) and calcitonin gene-related peptide (CGRP) [1]. A simulated nociceptor, in fact, also transmits antidromic impulses which can cause the release of these substances which, in turn, increases vasodilatation and capillary permeability subsequently causing also cutaneous reddening, temperature increase, and swelling. Rubor, Calor, Tumour, Dolor. A high-threshold stimulus is one which can produce a sensation of pain in physiological conditions by activating the nociceptors, and hence, the nociception path, performing the function of a defence mechanism. Bone or ligament damage stimulates pain which triggers defensive behaviour such as the decreasing of load exerted on the damaged area.

Diagnostic Principles of Pain There are four diagnostic principles of pain to define with different treatments. The first diagnostic principle of pain is based on nociceptor activation which can be brought about by the following: Mechanical stimulation Inflammation

P. Adravanti et al.

In the first case, it is necessary to remove the mechanical stimulus responsible for the pain. For knee pathologies, for example, a selective meniscectomy is carried out in order to remove the damaged area of the meniscus. In the second case, however, NSAIDs are administered with a view to lowering the stimulation threshold of the nociceptors, the likes of which respond more frequently to lowthreshold stimuli. The second diagnostic principle of pain identifies the neuron in the posterior horn of the spinal cord (II neuron in the pain path) as the element responsible for pain generation. Threshold changes in the healthy segment of the spinal lesion are caused by hypersensitization of the second neuron. Hypersensitivity of spinal neurons results in increased pain intensity, the area subject to pain increases (referred pain) and pain evoked by non-painful stimuli in undamaged areas (secondary allodynia). In this case, drugs which act on a spine synaptic level are used: Tramadol + paracetamol Min-May opioids Antidepressants and antiepileptics Drugs which act on calcium channels If the pre-existing disease is inflammatory, in addition to activating the nociceptors, the spinal neuron may be affected. This does not occur if the stimulus is purely mechanical. The third diagnostic principle of pain. Pain can be caused by lesions in the afferent pain paths. Whilst the pathological process ceases, mechanisms are generated which continue to cause pain over time. Hypersensitivity of the ectopic areas following peripheral and central nerve path lesion manifests itself as pain in the damaged nervous path area in both spontaneous and evoked form. The fourth diagnostic principle of pain. This regards deafferentiation pain which develops following nociceptive path interruption caused by nerve and meningeal damage from root avulsions. Deafferentiation hypersensitivity, which follows the complete interruption of the nociceptive paths, manifests itself as pain in an area of the body which no longer has nociception.

Pain Control Pain control is an essential aspect of surgery. It can modify the result of surgery. Good analgesic therapy can decrease morbidity, mortality and the length of stay in hospital. Negative effects of pain include physical and emotional suffering, sleep disturbance, cardiovascular implications and increased oxygen consumption. Several clinical studies have shown that moderate or severe pre-operative pain can influence post-operative pain:

Pain Management in Total Knee Arthroplasty

Patients have to be administered the right drug in the right dosage regularly, not just when they feel the need. Dosage of drugs is chosen according to the specific requirements of each patient. Tramadol, tramadol-paracetamol and oxycodone-paracetamol are suitable pre-operative drugs. It has been demonstrated that, in the case of severe chronic pain (>6 months), using drugs which act on nociception at a spinal synaptic level (gabapentin, pregabalin) can reduce post-operative pain. The chronic use of NSAIDs must be replaced with paracetamol (it does not modify coagulation) The use of acetylsalicylic acid (60 years, an intact ACL, minimal pain at rest, range of motion arc > 90°, with 32 is a good predictor for adversely affecting survivorship and early failure, we strongly believe there is a large host of patients with a BMI less than this and much greater than a weight of 90 kg that would be appropriate candidates for UKA. Other series much like our experience show high success rate >95% at 10 years [1, 18]. We believe the utilization of a metal-backed implant and improved surgical techniques as well as design modifications has allowed for improved results in a heavier population. Likewise, these changes have also afforded a larger success in younger patients. The presence of patellofemoral arthritis while previously held to be a contraindication has been shown, in studies (Fig. 2), to be successfully ignored even with grade 4 chondromalacia as long as the patient is asymptomatic in this articulation [2, 39]. The Controversy as to whether an ACL deficient knee can have an implantation of a UKA with a successful result is fought hard by both sides. It is felt by many because the lateral compartment has inherently more motion than its counterpart (the medial side) that increased translation will occur

leading to instability in the presence of a UKA [15]. This group of authors has felt that this will lead to increased failure rates due to the increased sliding motion and abnormal contact motions. Our experience has not been met with the same problems or failures and in fact, although all patients complain of a pes bursitis at some time early during the first 6 months postoperatively, this can be simply treated by corticosteroid injection with complete resolution. We do agree until the capsule contracts it is the increased sliding of the prosthesis that forces the hamstrings to function as a makeshift ACL. Patients, preoperatively, who complain of anterior– posterior instability, rather than medial lateral instability, when walking as most lateral-sided arthritic patients sense should not go forward with a UKA unless they first have an ACL reconstruction. Studies by others that caution patients to avoid a UKA procedure in the absence of an ACL were done in vitro and we believe do not allow for interpretation in vivo, and in fact in our results, good mid-term results without limitation of activities have been noted by others [2, 11, 49]. We therefore encourage our patients to consider UKA even in the absence of an ACL [22, 23].

History The preoperative clinical decision requires a detailed history and assessment of the patient’s complaints. Many patients in this cohort have had previous surgery for partial or total menisectomies which 20 or 25 years later have now led to lateral-sided pain. Patients with lateral-sided unicompartmental knee arthritis almost universally complain of pain on the outside of the knee. Patients also state that their knee hurts when ascending stairs. It is very important that patients localize their pain to one side of the knee with minimal to no

Lateral Unicompartmental Knee Replacement and Return to Sports

947

Fig. 4 Anterior drawer performed on a preoperative patient indicating anterior instability

Fig. 3 “One finger test” for evaluation of a patient with isolated symptoms to the lateral side of the left knee

pain on the opposite side. Pain should never exist in the middle of the knee behind the patella. In our practice, we ask the patient to point to the area of pain with one finger as has been described by others (Fig. 3) [6]. This “one-finger test” has proven reliable for us and in fact when a patient is unclear where the pain is located we give them a marker and divide the knee in half and ask them to go home and mark their knee where it hurts as they walk on level ground, up stairs and down stairs to be certain that their pain is localized. If the patient grabs his/or her knee with hand, failing to localize pain in a more global pain distribution, we believe this is a patient who will fail a unicompartmental knee replacement.

Physical Examination The physical exam must make note of the alignment of the extremity, knee ligament stability, and the presence of isolated compartment symptoms. Being meticulous in this assessment cannot be overemphasized. Routine physical examination focusing on stability in the medial–lateral plane as well as noting any Lachman, anterior or posterior drawer, pivot and reverse pivot shift is essential (Fig. 4). The presence of a provocative exam should elicit a wakeup call and an MRI or further testing with a KT-1000 should be performed. Most patients who require treatment for

lateral-sided arthritis will have a range of motion arc > 120° although note of any unusual extension lag or flexion contracture must be recorded. All muscle and skin integrity is noted. Any observation of significant synovitis should prompt an evaluation for an inflammatory arthropathy. The patellofemoral joint must be rigorously investigated to note any symptoms upon patellar compression, crepitus, or maltracking.

Imaging Standard radiographic views should include a long leg standing anteroposterior standardized protocol with the patient standing facing the technologist with the patella anterior (Fig. 5), a weight bearing anteroposterior, a 45° flexed-knee posteroanterior (Fig. 6), lateral, and an axial patellofemoral view to asses degeneration [38]. Any sign of tibiofemoral subluxation must be noted and we caution the use of a UKA in these patients. We also encourage the routine use of a magnetic resonance image to grade the cartilage of the opposite compartment (Fig. 7). We have used the Outerbridge classification system in the past and have trained our radiologists accordingly to assist us [34]. We believe this extensive workup avoids a decision from being made in the operating room by indirect or direct visualization of the cartilage surfaces. Patient expectations can now be met because of the preoperative assessment.

Treatment Options Nonsurgical treatment is always the first option in the treatment of lateral unicompartmental osteoarthritis. Physical therapy, nonsteroidal anti-inflammatory medications, and/or

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Fig. 7 Coronal view of MRI T1 image with lateral-sided disease only

Fig. 5 Three-foot standing anteroposterior radiographic view for leg alignment

Fig. 6 PA Rosenberg radiograph of lateral bilateral knee osteoarthritis

chondoprotective agents and activity modification are the standards of care [20]. Unfortunately there are no disease modifying drugs for osteoarthritis [44]. When nonoperative treatment fails though, surgical treatment, which can include an arthroscopic debridement, distal femoral osteotomy, or a total knee replacement can be considered [8, 12, 26, 28]. Distal femoral osteotomy, as a correction for a valgus deformity (lateral sided osteoarthrosis), has been successful in some surgeons’ hands although we have not seen longevity in our active patients as has been predicted in the literature [7, 28, 30, 35, 51]. We found a 55% survivorship rate at 5–10 years with osteotomy and a higher rate of intraoperative and postoperative complications [7]. It is also well known that osteotomy of an already severely arthritic knee is associated with an increased likelihood of revision to a TKA [51]. This revision to a TKA has been shown to be much more difficult than revision of a UKA to a TKA or the ability to perform a primary TKA [10, 24, 30, 35]. Stukenborg et al. compared the results of proximal tibial osteotomy and UKA with a 7–10 year follow-up [48]. They concluded that the results of UKA were significantly better and that a proximal tibial osteotomy was associated with a higher complication rate rather than UKA [48]. This randomized, prospective study of 62 patients had a survivorship analysis of 77% for UKA and 60% for high tibial osteotomy (HTO) [48]. UKA has also shown to have reduced morbidity and preserved bone stock, which when needed for a TKA permits a simpler prosthesis revision [2, 14].

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949

Literature Results Twelve percent of the US population between the ages of 25–75 demonstrate some sign or symptom of osteoarthritis [23]. The disability of this arthritis is only matched by that of cardiac disease [16]. Recent resurgence of interest in the UKA has created a new body of literature. Studies though directed specifically at lateral-sided arthritis are limited to short, and medium term results, economic data, and bias. This is the only chapter we know of that discusses return to sport as an outcome for the lateral UKA. In 2008, surgeons from France reported on 39 patients in 40 lateral cemented metal-backed UKA. This retrospective study with mean follow-up of 12.6 years showed a prostheses survivorship of 92% at 10 years and 84% at 16 years [2]. In a 89 months follow-up of 14 other patients only one failure was reported [26]. Pennington showed in a mid-term follow-up of 12.4 years that a mixed series of a metal-backed tibia and all poly tibia implant revealed a survivorship of 100% with no revisions [37]. These same authors showed satisfactory results in patients below 60 years of age. They also performed the UKA in their cohort even when the uninvolved compartment had up to grade 2 osteoarthritis. Engh reported likewise his series at 12 years with no revisions in the young, active patient and Argenson has reported a 84% survivorship in 16 years [2]. Short- to medium-term results reported by Volpi using the Miller-Galante prosthesis for a lateral unicompartmental replacement had good results with HSS scores that improved from a pre-op mean of 59.92 (range 48–68) to 88.04 (range 71–95) [50]. These patients all had a decrease in pain, with an increase in function and range of motion. Reported increase in range of motion following UKA has reached an average of 123° compared with 109° in the TKA although our experience in patients less than 60 years of age has shown an average range of 145° (Fig. 8) [2, 22, 31]. A recent comparative study in which patients underwent TKA on one side and UKA on the contralateral side revealed that patients felt that the UKA side was more normal and had better function [22]. That “more normal feeling” was studied with the kinematics of stair climbing in vitro and it was found that femoral rollback in the UKA more closely resembled normal knee function rather than a TKA [36]. Newman et al. in a prospective, randomized study of 102 knees showed that the UKA group had less perioperative morbidity and regainedknee motion more rapidly [31]. The authors felt that the procedure required expert surgical technique for a successful outcome. In fact, the review of the literature above confirms that surgical technique at the primary surgery can decrease the modes of failure. Component positioning and alignment and soft-tissue balancing can lead to a successful arthroplasty and avoid failures.

Fig. 8 Patient with unicondylar knee able to perform sitting lotus position

The table below summarizes the results of several UKA series (Table 1). These studies and others reveal the rapid increase in the number of UKA. While the data may reveal excellent long-term results, early failures from experienced authors have also been noted [13, 41]. The importance of training, proper patient selection, modifications in instrumentation as well as prosthesis design is hoped to eradicate these failures. In fact, some of these studies have taught us that when using an all poly tibia a revision will more often than not require augments and stem prosthesis [1]. Patient selection, as stated before, is critical to the success of a UKA and a report recently has shown an unacceptable revision rate of 10% in a worker’s compensation group with loose tibial components at 40 months [27]. Cost Analysis most recently revealed that the UKA is cost-effective in the elderly population (75–84 years of age) as long as the revision rate does not rise above 4%. In fact, these authors concluded that UKA resulted in a higher number of accumulated quality-adjusted life-years and a lower accumulated cost for this cohort of patients [45].

Our Results When our nonsurgical treatment for lateral unicompartmental disease has failed we proceed with a consideration of an arthroscopic intervention as long as the patient’s standing films and Rosenberg view do not demonstrate a bone on bone articulation [38]. When a patient arrives in our office with an x-ray that reveals bone on bone with single-sided disease in the lateral compartment, we believe a lateral UKA is the procedure of choice [8, 12, 25, 29]. Lateral UKA is preferred

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Table 1 Results of the different series of lateral UKA in the literature (Adapted with permission of Springer) Type of implant Number of Mean follow-up Authors Date of Number of surgeons (years) publication evaluated UKAs

Survivorship (number of revisions)

Marmor [9]

1984

14

Cemented all poly

1

7.4 (2.5–9.83)

NA(2)

Gunther et al. [17]

1996

53

Cemented, metal-backed, mobile bearing

2

5 (2.5–9.83)

82% at 5 years (11)

Ohdera et al. [11]

2001

18

Four different designs

NA

8.25 (5–15.75)

NA (2)

Ashraf et al. [50]

2002

83

Cemented all poly tibia

4

9 (2–21)

74% at 15 years (15)

O’Rourke et al. [33]

2005

14

Cemented all poly tibia

1

10.6 (1–22)

72% at 25 years (2)

Pennington et al. [18]

2006

29

Cemented, metal-backed (75%); all poly tibia (25%)

NA

12.4 (3.1–15.6)

100% at 12.4 years (0)

Sah and Scott [3]

2007

49

Three different designs

1

5.2 (2–14)

100% at 5.4 years (0)

Argenson et al. [13]

2008

38

Four different designs

2

12.6 (3–23)

84% at 16 years (5)

Plancher

In submission

97 (medial and lateral)

Cemented, metal-backed, nonmobile bearing

1

5.3 (3.7–12)

96% (1) at 6 years

dentist repairing a cavity with a cap but if there is destruction of all areas of the knee (tricompartmental disease) then a TKA is appropriate much like giving patient dentures when issues in the mouth are irreparable. Our results on 45 knees with UKA with minimum followup of 24 months and average follow-up of 47 months have shown a mean Lysholm score improve from 59.2 (range 32–92) to 93.2 (range 69–100) following surgery. HSS scores improved from an average of 64.1 (range 35–87) preoperatively to 93 (range 77–100) postoperatively. The average Tegner activity score increased from 3.1 (range 0–6) to 4.8 (range 1–8).We have looked critically with scoring systems that discuss return to previous activity levels, long-term radiographic findings, and survivorship data with an endpoint of revision and or conversion to a total knee arthroplasty (Fig. 9).

Postoperative Care and Rehabilitation

Fig. 9 Postoperative x-ray of left knee with successful implantation of lateral UKA

over TKA because of the preservation of the anterior and posterior cruciate ligaments as well as bone stock maintenance. Our discussion with patients uses an analogy of the

Following surgery, patients are started, in the recovery room, on a continuous passive motion (CPM) machine no different than postoperative care for a TKA for 3–4 weeks. Physical therapy with gait training, range of motion, patellar mobilization, and edema control are commenced immediately. All patients receive cryotherapy treatment and a hemovac drain is removed at day 3. Isometrics and straight leg raise exercises progress to close chain strengthening at 4 weeks.

Lateral Unicompartmental Knee Replacement and Return to Sports

Special Situations The ACL Deficient Knee in the past has been an absolute contraindication for performing unicompartmental knee replacement. In this decade, several series challenge that dogma [19]. Recent studies give greater importance to the slope on the tibial cut. The tibial slope must be 7° or less. This slope will restrict most anterior tibial translational forces. The availability of more conforming designs of UKA has also allowed success in an ACL deficient knee. Our patients are informed that a pes bursitis may exists for 6 months postoperatively as the hamstrings play an active role to restrain any early anterior translational forces. Obesity, another controversial topic, has not limited our selection process. We have followed our patients for an average of 9 years and to date have not had to revise any morbid obese patient to a TKA. Likewise, patients with arthritic changes in the contralateral compartments can be candidates for UKA as long as they are asymptomatic, as was previously discussed. We have found that grade 3–4 chondromalacia in the patellofemoral compartment is not a problem when preoperatively asymptomatic. The investigation of the contralateral compartment with the MRI and arthroscopic intervention has helped us extend our indications with a successful outcome.

Return to Sports Many authors have written that elderly patients with more sedentary lifestyles are the best candidates for lateral UKA rather than younger and more physically active patients [20, 21, 43]. With the improvement in prosthesis design this has now been shown by others and us to no longer be a strict

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contraindication [15, 37]. We have found in our practice that active younger patients with a lateral UKA achieve successful results. In fact, our patients have been as young as 47 years of age and returned to sports such as downhill skiing in 5 months, singles tennis in 4 months, and walking as well as jogging in 1–2 months.

Tips and Tricks We believe attention to detail when approaching the patellofemoral compartment is essential. All patella osteophytes are removed with a rongeur and small nasal rasp. It is important to avoid component oversizing and proper placement of the femoral component with the anterior femur in the sagittal plane to prevent impingement [5]. The true nature of wear in a UKA is unclear but correlation with the shelf life of the polyethylene tibial component may account for the difference in wear rates and ultimate survivorship of implants. If the surgical technique and alignment guidelines are followed, predictable outcomes will be seen. We recommend undercorrection of the deformity when undertaking a lateral UKA to avoid medial compartment osteoarthritis progression [46]. The femoral prosthesis, because of the normal femoral divergence of the lateral condyle, must therefore be moved medially to avoid impingement of the tibial spines when the knee is flexed and then brought into extension [9]. When performing this procedure with a lateral arthrotomy without subluxation of the patella, the component is placed as medially as possible to also avoid overload and edge loading of the lateral part of the tibial plateau when the knee is flexed 30° [37]. When completing the sagittal tibial cut, the

Too large

Too small

Fig. 10 Artwork demonstrating appropriate sizing of femoral compartment to avoid over stuffing

Proper sizing

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tibial component must be placed in internal rotation to accommodate the “screw home” mechanism during knee flexion. The sulcus terminalis or leading edge of the weight bearing portion of the femoral condyle may be used as a reference for sizing the femoral component. It is crucial not to be beyond this important landmark (Fig. 10).

Summary Lateral degenerative disease of the joint can be very disabling but with a properly performed lateral UKA successful management of this problem can be achieved. Through a minimally invasive technique, avoiding large soft tissue dissection, minimizing bone loss, and conserving natural knee kinematics this procedure produces the results that can be comparable and perhaps superior to a TKA. With careful implant selection, individualizing patient selection, and more aggressive indications such as permitting this procedure in an ACL deficient patient who does not have clinical A-P instability or patients with high BMIs within certain limits can allow many patients to continue with an active lifestyle. Our goal is to always, if possible, to not restrict a patient from any activity. This approach has been successfully tested with gait training without assistive devices, to produce a more normal gait, better range of motion, and consequently return to all sports the patient had engaged in prior to the lateral osteoarthritis that limited their physical ability [22, 25, 31, 32]. Adherence to appropriate surgical indications and patient selection with meticulous technique is important to obtain the outcomes desired.

References 1. Aleto, T., Berend, M., Ritter, M., Faris, F., Meneghini, R.: Early failure of unicompartmental knee arthroplasty leading to revision. J. Arthroplasty 23(2), 159–163 (2008) 2. Argenson, J.N., et al.: Long-term results with a lateral unicondylar replacement. Clin. Orthop. Relat. Res. 466(11), 2686–2693 (2008) 3. Ashraf, T., Newman, J.H., Evans, R.L., Ackroyd, C.E.: Lateral unicompartmental knee replacement survivorship and clinical experience over 21 years. J. Bone Joint Surg. Br. 84(8), 1126–1130 (2002) 4. Berend, K.R., George, J., Lombardi Jr., A.V.: Unicompartmental knee arthroplasty to total knee arthroplasty conversion: assuring a primary outcome. Orthopedics 32(9), 684 (2009) 5. Berger, R.A., Nedoff, D.D., Barden, R.M., et al.: Unicompartment knee arthroplasty: clinical experience at 6 to 10 year follow-up. Clin. Orthop. Relat. Res. 367, 50–60 (1999) 6. Bert, J.M.: Unicompartmental knee replacement. Orthop. Clin. North Am. 36(4), 513–522 (2005) 7. Broughton, N.S., Newman, J.H., Baily, R.A.: Unicompartmental replacement and high tibial osteotomy for osteoarthritis of the knee. J. Bone Joint Surg. 68, 447–452 (1986) 8. Cameron, H.U., Botsford, D.J., Park, Y.S.: Prognostic factors in the outcome of supracondylar femoral osteotomy for lateral compartment osteoarthritis of the knee. Can. J. Surg. 40(2), 114–118 (1997)

K.D. Plancher and A.R. Rivera 9. Cartier, P., Khefacha, A., Sanouiller, J.L., Frederick, K.: Unicondylar knee arthroplasty in middle-aged patients: a minimum 5-year follow-up. Orthopedics 30(8 Suppl), 62–65 (2007) 10. Chakrabarty, G., Newman, J.H., Ackroyd, C.E.: Revision of unicompartmental arthroplasty of the knee. Clinical and technical considerations. J. Arthroplasty 13(2), 191–196 (1998) 11. Christensen, N.O.: Unicompartmental prosthesis for gonarthrosis. A nine-year series of 575 knees from a Swedish hospital. Clin. Orthop. Relat. Res. 273, 165–169 (1991) 12. Coventry, M.B.: Proximal tibial varus osteotomy for osteoarthritis of the lateral compartment of the knee. J. Bone Joint Surg. Am. 69(1), 32–38 (1987) 13. Emerson Jr., R.H., Potter, T.: The use of the McKeever metallic hemiarthroplasty for unicompartmental arthritis. J. Bone Joint Surg. Am. 67(2), 208–212 (1985) 14. Engh, G.A.: Orthopaedic crossfire – can we justify unicondylar arthroplasty as a temporizing procedure? in the affirmative. J. Arthroplasty 17(4 Suppl 1), 54–55 (2002) 15. Engh, G., Ammeen, D.: Is an intact anterior cruciate ligament needed in order to have a well-functioning unicondylar knee replacement? Clin. Orthop. Relat. Res. 428, 170–173 (2004) 16. Guccione, A.A., et al.: The effects of specific medical conditions on the functional limitations of elders in the Framingham study. Am. J. Public Health 84(3), 351–358 (1994) 17. Gunther, T., Murray, D., Miller, R.: Lateral unicompartmental knee arthroplasty with Oxford meniscal knee. Knee 3, 33–39 (1996) 18. Hanssen, A.D., Stuart, M.J., Scott, R.D., Scuderi, G.R.: Surgical options for the middle-aged patient with osteoarthritis of the knee joint. Instr. Course Lect. 50, 499–511 (2001) 19. Hernigou, P., Deschamps, G.: Posterior slope of the tibial implant and the outcome of unicompartmental knee arthroplasty. J. Bone Joint Surg. Am. 86-A(3), 506–511 (2004) 20. Insall, J., Walker, P.: Unicondylar knee replacement. Clin. Orthop. Relat. Res. 120, 83–85 (1976) 21. Kozinn, S.C., Scott, R.: Unicondylar knee arthroplasty. J. Bone Joint Surg. Am. 71(1), 145–150 (1989) 22. Laurencin, C.T., Zelicof, S.B., Scott, R.D., Ewald, F.C.: Unicompartmental versus total knee arthroplasty in the same patient. A comparative study. Clin. Orthop. Relat. Res. 273, 151–156 (1991) 23. Lawrence, R.C., Helmick, C.G., Arnett, F.C., et al.: Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum. 41, 778–799 (1998) 24. Levine, W.N., Ozuna, R.M., Scott, R.D., Thornhill, T.S.: Conversion of failed modern unicompartmental arthroplasty to total knee arthroplasty. J. Arthroplasty 11(7), 797–801 (1996) 25. Marmor, L.: Lateral compartment arthroplasty of the knee. Clin. Orthop. Relat. Res. 186, 115–121 (1984) 26. Marmor, L.: Unicompartamental and total knee arthroplasty. Clin. Orthop. Relat. Res. 192, 75–85 (1985) 27. Masri, B.A., Bourque, J., Patil, S.: Outcome of unicompartmental knee arthroplasty in patients receiving Worker’s Compensation. J. Arthroplasty 24, 444–447 (2009) 28. McDermott, A.G., Finklestein, J.A., Farine, I., Boynton, E.L., MacIntosh, D.L., Gross, A.: Distal femoral osteotomy for valgus deformity of the knee. J. Bone Joint Surg. Am. 70(1), 110–116 (1988) 29. McDermott, J.E.: What’s new in orthopaedic surgery. J. Am. Coll. Surg. 199(6), 924–931 (2004) 30. Nelson, C.L., Saleh, K.J., Kassim, R.A., Windsor, R., Haas, S., Laskin, R., Sculco, T.: Total knee arthroplasty after varus osteotomy of the distal part of the femur. J. Bone Joint Surg. Am. 85-A(6), 1062–1065 (2003) 31. Newman, J.H., Ackroyd, C.E., Shah, N.A.: Unicompartmental or total knee replacement? Five-year results of a prospective, randomised trial of 102 osteoarthritic knees with unicompartmental arthritis. J. Bone Joint Surg. Br. 80, 862–865 (1998)

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32. Ohdera, T., Tokunaga, J., Kobayashi, A.: Unicompartmental knee arthroplasty for lateral gonarthrosis: midterm results. J. Arthroplasty 16(2), 196–200 (2001) 33. O’Rourke, M.R., Gardner, J.J., Callaghan, J.J., Liu, S.S., Goetz, D.D., Vittetoe, D.A., Sullivan, P.M., Johnston, R.C.: The John Insall Award: unicompartmental knee replacement: a minimum twenty-one-year followup, end-result study. Clin. Orthop. Relat. Res. 440, 27–37 (2005) 34. Outerbridge, R.E.: The etiology of chondromalacia patellae. J. Bone Joint Surg. Br. 43, 752 (1961) 35. Parvizi, J., Hanssen, A.D., Spangehl, M.J.: Total knee arthroplasty following proximal tibial osteotomy: risk factors for failure. J. Bone Joint Surg. Am. 86-A(3), 474–479 (2004) 36. Patil, S., Colwell, C.W., Ezzet, K.A., D’Lima, D.D.: Can normal knee kinematics be restored with unicompartmental knee replacement? J. Bone Joint Surg. Am. 87, 332–338 (2005) 37. Pennington, D.W., Swienckowski, J.J., Lutes, W.B., Drake, G.N.: Unicompartmental knee arthroplasty in patients sixty years of age or younger. J. Bone Joint Surg. Am. 85-A(10), 1968–1973 (2003) 38. Pires e Albuquerque, R., Carvalho, A.C., Giordano, V., Djahjah, M.C., do Amaral, N.P.: Comparative study between different radiographic plans in knee osteoarthritis. Acta Reumatol. Port. 34(2B), 380–387 (2009) 39. Price, A.J., Rees, J.L., Beard, D.J., Gill, R.H., Dodd, C.A., Murray, D.M.J.: Sagittal plane kinematics of a mobile-bearing unicompartmental knee arthroplasty at 10 years: a comparative in vivo fluoroscopic analysis. Arthroplasty 19(5), 590–597 (2004) 40. Riddle, D.L., Jiranek, W.A., McGlynn, F.J.: Yearly incidence of unicompartmental knee arthroplasty in the United States. J. Arthroplasty 23, 408–412 (2008) 41. Robertsson, O., Lidgren, L.: The short-term results of 3 common UKA implants during different periods in Sweden. J. Arthroplasty 23, 801–807 (2008) 42. Sah, A.P., Scott, R.D.: Lateral unicompartmental knee arthroplasty through a medial approach. Surgical technique. J. Bone Joint Surg. Am. 90(Suppl 2 (Pt 2)), 195–205 (2008)

43. Scott, R.D., Santore, R.F.: Unicondylar unicompartmental replacement for osteoarthritis of the knee. J. Bone Joint Surg. Am. 63(4), 536–544 (1981) 44. Sharma, L., Song, J., Felson, D.T., Cahue, S., Shamiyeh, E., Dunlop, D.D.: The role of knee alignment in disease progression and functional decline in knee osteoarthritis. JAMA 286(2), 188– 195 (2001) 45. Slover, J., Espehaug, B., Havelin, L.I., Engesaeter, L.B., Furnes, O., Tomek, I., Tosteson, A.: Cost-effectiveness of unicompartmental and total knee arthroplasty in elderly low-demand patients. A Markov decision analysis. J. Bone Joint Surg. Am. 88, 2348– 2355 (2006) 46. Squire, M.W., Callaghan, J.J., Goetz, D.D., Sullivan, P.M., Johnston, R.C.: Unicompartmental knee replacement: a minimum 15 year followup study. Clin. Orthop. Relat. Res. 367, 61–72 (1999) 47. Stern, S.H., Becker, M.W., Insall, J.N.: Unicondylar knee arthroplasty. An evaluation of selection criteria. Clin. Orthop. Relat. Res. 286, 143–148 (1993) 48. Stukenborg-Colsman, C., Wirth, C.J., Lazovic, D., Wefer, A.: High tibial osteotomy versus unicompartmental joint replacement in unicompartmental knee joint osteoarthritis: 7–10-year follow-up prospective randomised study. Knee 8(3), 187–194 (2001) 49. Suggs, J.F., Li, G., Park, S.E., Steffensmeier, S., Rubash, H.E., Freiberg, A.A.: Function of the anterior cruciate ligament after unicompartmental knee arthroplasty: an in vitro robotic study. J. Arthroplasty 19(2), 224–229 (2004) 50. Volpi, P., Marinoni, L., Bait, C., Galli, M., Denti, M.: Lateral unicompartmental knee arthroplasty: indications, technique and shortmedium term results. Knee Surg. Sports Traumatol. Arthrosc. 15(8), 1028–1034 (2007) [Epub 12 May 2007] 51. Weale, A.E., Newman, J.H.: Unicompartmental arthroplasty and high tibial osteotomy for osteoarthrosis of the knee. A comparative study with 12–17 year follow-up period. Clin. Orthop. Relat. Res. 302, 134–137 (1994)

The Arthroscopic Treatment of Knee Osteoarthritis in Sport Patients Carlos Esteve de Miguel

Contents Conclusions .................................................................................. 956 References .................................................................................... 956

C. Esteve de Miguel Department of Orthopaedic surgery, Centro Esteve de Miguel, Virgen de la Salud, 78, 08024 Barcelona, Spain e-mail: [email protected]

In this chapter we outline the prognostic factors when performing arthroscopic surgery. Orthopedic surgeons treat more and more patients involved in sports with knee osteoarthritis. The increase of the number of patients needing treatment is due to population aging and an increase in physical exercise at any age [5]. Arthroscopic surgery can approach knee degenerative lesions by a combination of various surgical techniques: lavage of the articulation [9, 13], synovectomy, debridement of the cartilaginous and meniscal tissue, and extirpation of loose bodies and osteophytes. In cases with serious chondral lesions, subchondral penetration techniques such as abrasion arthroplasty, microfractures, or drilling, can also be indicated, with the aim of obtaining a reparative fibrocartilaginous tissue [2, 11, 12, 14, 16]. Arthroscopy of the arthritic knee intends to restore the damaged articular surfaces. With arthroscopic procedures, the life of a knee may be prolonged by improving its function and relieving its painful symptomatology, with the purpose of avoiding or postponing an osteotomy or a prosthesis. Candidates to an arthroscopic procedure should have tried, without success, a conservative treatment modality. Patients must be informed that arthroscopy is not a cure, but a therapeutical method which may provide relief in most cases. Arthroscopic surgery is generally well accepted, since patients wish to avoid, as far as possible, major surgical operations. In cases of malalignment in varus or valgus the arthroscopic treatment may not solve the problem because of the fast degeneration of the reparative postoperative fibrocartilage [11, 17]. Patients should be informed about the possible necessity of a non-weight-bearing for 2 month period if subchondral penetration techniques are required. Treatment of full thickness chondral lesions with penetration techniques of the subchondral bone require a non-weight-bearing period of 2 months to obtain the maturity of the fibro-cartilaginous tissue covering the abraded surface. Since 1934, when Burman [6] used the arthroscope for the first time to treat osteoarthritic knees, a great number of studies analyzing the results of the arthroscopic treatment in

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degenerative knee lesions have been published. In these publications, contradictory results are found; largely due to the fact that different protocols were used in different studies, mainly because there is a great variability between the groups of patients (age, type and severity of the knee degenerative changes, articular alignment, physical activity level of the patient, or recovery expectation). Analyzing the results of the most important works about arthroscopic debridement one can find an average of 68% of good results with an average follow-up of 38 months [1, 3, 4, 8, 10, 15]. When, besides debridement, penetration techniques of the subchondral bone were practiced good results were obtained in 60–80% of the cases [10, 11, 17]. The best results have been obtained when patients have complied with the requirement of 2 months of non-weight bearing. Prognosis factors: Although long-term success is difficult to predict, analysis of those results suggest that patients with the following features have better prognosis: s s s s s s s

Short duration of symptoms Mechanical symptoms Good articular alignment Unstable meniscal lesions Loose bodies Isolated chondral lesions with flaps Minimal radiographic signs of degeneration

The following situations have a less favorable prognosis: s s s s s s s s

Pain at rest Chronic pain Malalignment in varus or valgus Decrease of radiological articular space Diffuse or more extensive chondral lesions Severe patello-femoral osteoarthritis Chondrocalcinosis Bipolar lesions

Conclusions Understanding surgical indications and clinical results, arthroscopy is useful in the treatment of degenerative arthritis of the knee [7]. It offers relief from pain and disability in two-thirds of cases during 3 years or more. It has low morbidity and does not preclude future reconstructive procedures. Many patients are pleased to find a less aggressive alternative to arthroplasty. The procedure has achieved better

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results in patients with pain of short duration, normal lower extremity alignment, and mechanical symptoms. Patients must have a realistic expectation that the goal of arthroscopy is to diminish pain and improve function and not to cure the arthritis.

References 1. Aichroth, P.M., Patel, D.V., Moyes, S.T.: A prospective review of arthroscopic debridement for degenerative joint disease of the knee. Int. Orthop. 15, 351–355 (1991) 2. Akizuki, S., Yasukawa, Y., Takizawa, T.: Does arthroscopic abrasion arthroplasty promote cartilage regeneration in osteoarthritic knees with eburnation? A prospective study of high tibial osteotomy with abrasion arthroplasty versus high tibial osteotomy alone. Arthroscopy 13, 9–17 (1997) 3. Baumgaertner, M.R., Cannon, W.D., Vittori, J.M., et al.: Arthroscopic debridement of the arthritic knee. Clin. Orthop. Relat. Res. 253, 197–202 (1990) 4. Bruce Mosely Jr., J.: Arthroscopic treatment of osteoarthritis of the knee: a prospective, randomized, placebo-controlled trial. Results of a pilot study. Am. J. Sports Med. 24(1), 28–34 (1996) 5. Buckwalter, J.A., Lane, N.E.: Does participation in sports cause osteoarthritis? Iowa Orthop. J. 17, 80–89 (1997) 6. Burman, M.S., Finkelstein, H., Mayer, L.: Arthroscopy of the knee joint. J. Bone Joint Surg. Am. 16, 255–268 (1934) 7. Esteve de Miguel, C.: Tratamiento de las lesiones degenerativas de rodilla y hombro por artroscopia. Revista de la Real Academia de Medicina de Barcelona (1999) 8. Goldman, R.T., Scuderi, G.R., Kelly, M.A.: Arthroscopic treatment of the degenerative knee in older athletes. Clin. Sports Med. 16, 51–68 (1997) 9. Ike, R.W.: Joint lavage. In: Brandt, K.D., Doherty, M., Lohmander, L.S. (eds.) Osteoarthritis, pp. 359–377. Oxford University Press, Oxford (1998) 10. Johnson, L.L.: Arthroscopic abrasion arthroplasty: historical and pathological perspective: present status. Arthroscopy 2, 54–69 (1986) 11. Johnson, L.L.: Arthroscopic abrasion arthroplasty. In: McGinty, J.B. (ed.) Operative Arthroscopy, pp. 341–360. Raven Press, New York (1991) 12. Magnuson, P.B.: Joint debridement: surgical treatment of degenerative arthritis. Surg. Gynaecol. Obstet. 73, 1–9 (1941) 13. Ogilvie-Harris, D.J., Fitsialos, D.P.: Arthroscopic management of the degenerative knee. Arthroscopy 7, 151–157 (1991) 14. Pridie, A.H.: A method of resurfacing osteoarthritic knee joints. J. Bone Joint Surg. Br. 41, 618 (1959) 15. Steadman, J., Ramappa, A., Maxwell, R., Briggs, K.: An arthroscopic treatment regimen for osteoarthritis of the knee. Arthroscopy 23(9), 948–955 (2007) 16. Steadman, J.R., Rodkey, W.G., Rodrigo, J.J.: Microfracture: surgical technique and rehabilitation to treat chondral defects. Clin. Orthop. Relat. Res. 391, 362–369 (2001) 17. Tippett, J.W.: Articular cartilage drilling and osteotomy in osteoarthritis of the knee. In: McGinty, J.B. (ed.) Operative Arthroscopy, pp. 325–339. Raven Press, New York (1991)

Sports Injuries of the Hip Region Ömür Çag˘lar and Mümtaz Alpaslan

Contents Introduction ................................................................................. 957 History.......................................................................................... 957 Physical Examination ................................................................. 958 Radiographic Examination ........................................................ 958 Common Hip and Pelvic Injuries .............................................. 958 Muscle Strains............................................................................... 958 Avulsion Fractures ...................................................................... 959 Stress Fractures of the Femoral Neck ....................................... 959 Hip Instability.............................................................................. 959 Piriformis Syndrome................................................................... 959 Snapping Hip Syndrome ............................................................ 960 Femoroacetabular Impingement ............................................... 960 References .................................................................................... 961

Introduction Sports injuries around the hip joint are less frequent than injuries of the more distal part of the lower extremities [2]. Previous studies have shown that the rate differs from 5% to 9% among high-school athletes. These injuries can be difficult to diagnose and rehabilitation programs can last longer than anticipated. Appropriate and well-organized approach to treatment is mandatory. Most of the injuries leading to hip pain are extra-articular, caused by muscular strains and sprains [7]. Intra-articular pathologies are less common, which include stress fracture of the femoral neck, labral tears and degenerations, chondral injuries, loose bodies, etc. The diagnostic tools regarding hip injuries have evolved during the past decade with the recent improvements in imaging technologies, especially magnetic resonance imaging and hip arthroscopy. Labral tears associated with femoroacetabular impingement syndrome (FAI) have become an important cause of early hip pain leading to early-onset of degenerative arthritis. Treatment of FAI is becoming more popular with the aim of restoring the normal hip anatomy.

History

Ö. Çag˘lar ( ) and M. Alpaslan Department of Orthopaedics and Traumatology, Hacettepe University, Samanpazarı, 06100 Ankara, Turkey e-mail: [email protected]; [email protected]

The differential diagnosis of the hip pain in the athletic population is very important and sometimes can be challenging. Without an appropriate workup, hip pain in an athlete should not be attributed to a simple muscle sprain. The history should begin with the starting time of the complaint. The location of the pain, any swelling or history of a traumatic event and developmental abnormality should also be questioned. Mechanical symptoms such as locking, catching should be noted, which mostly indicate an intraarticular pathology. Mechanical symptoms such as clicking may show a problem which usually can be managed with surgical interventions. Risk factors that may contribute to avascular necrosis of the hip such as systemic steroid therapy should also be

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958 Table 1 Common causes of hip pain in sports injuries Acute Hip dislocations and instability Muscle strains Avulsion fractures and apophyseal injuries Proximal femoral fractures Acetabular labral tears and loose bodies Chronic Femoroacetabular impingement Snapping hip syndrome Piriformis syndrome Stress fractures Bursitis Osteitis pubis Dysplasia of the hip

questioned. Common extra-articular causes of hip symptoms should be discussed during the evaluation of the patient. Referred pain from lumbar spine problems, sacroiliac joint, or sciatic nerve should not be undermined. Hamstring and ischial symptoms can easily be diagnosed. The sprains of hip flexors and adductors may be misdiagnosed as intra-articular pathologies unlike abductor problems or trochanteric bursitis. Deep tendinous structures such as piriformis tendon or ilio-psoas pathologies may mimic intraarticular causes and may be difficult to differentiate. The presence of popping or clicking can sometimes occur from extra-articular problems as sometimes can be totally normal. The pain is usually aggravated with activities. Activities with rotational maneuvers such as turning toward the affected side may alter the complaints. Rising from a chair or climbing up and down the stairs may produce symptoms. The common pathologies that can present with hip pain are summarized in Table 1.

Ö. Çag˘lar and M. Alpaslan

also be noted. If there is a suspicion for a specific muscle group, resisted active motion of the joint may mimic the original symptoms. There are also special tests to evaluate different pathologies of the hip. Straight leg raising test is important for examining the signs originating from the lumbar spine. The Faber Test (flexion-abduction-external rotation) has been described for the pathologies of the hip and the sacro-iliac joint. The leg rolling test which is applied in supine position with gentle movements of the thigh rolling internally and externally shows only the movement of the hip without applying any tension to the surrounding structures suggests an intra-articular involvement if it is positive [6, 24]. Patients with femoroacetabular impingement have restrictive range of motion especially with flexion, abduction, and internal rotation. The impingement sign is a provocative test showing anterior FAI is positive while pain is triggered with the hip in 90° of flexion and adduction with slightly forced internal rotation. Pain in the buttock which can be provoked with extension and external rotation is a sign for posterior impingement [27].

Radiographic Examination Plain radiograms should be a routine part of evaluation of any hip problem of an athletic population. Antero-posterior radiograph of the pelvis and lateral imaging of the involved hip should be routinely ordered. Additional radiographs such as cross-table lateral view or false profile view can be ordered for further diagnosis. One should look for any degree of dysplasia; collum-diaphyseal angle; proximal femoral abnormality or osseous bumps. Special attention should be for femoral neck including the cortical integrity and the trabecular pattern for the possibility of a non-displaced fracture of the femoral neck. MRI and MRI-arthrography can show the damage of the intra-articular cartilage, the acetabular labrum tears or degeneration; allows better determination for stress fracture or an avascular necrosis of the femoral head.

Physical Examination The examination begins with the inspection. There can be an antalgic gait typically with a shortened stance phase. In the stance phase, the patient usually slightly flexes the hip to relieve the pain. There can be some degree of limping due to abductor problems. A complete neurovascular examination should be performed, and gait, posture, muscle contractures, limb-length inequality, and scoliosis should be assessed. Range of motion of the joint should also be examined. The degree of flexion should be noted and any possible flexion contracture should be examined with Thomas test. Extension also should be recorded with the patient in prone position. Rotation of the joint can be examined with the hip in 90° of flexion. Abduction and adduction should

Common Hip and Pelvic Injuries Muscle Strains One of the most common injuries around the hip joint is muscle strain in the athletic population. Strain or tear frequently occur near the myo-tendinous junction, although they also may result from the muscle belly. The commonly injured muscles are those which cross to joints during an eccentric contraction [2, 13]. The adductor muscles are frequently involved in football players. Groin pain is the most common complaint. Strains of rectus femoris muscle may result from

Sports Injuries of the Hip Region

hip flexion moment such as kicking or sprinting. Physical examination shows weak and painful extension of the knee with an anterior swelling and or mass. MRI imaging may be used as a diagnostic tool with probability for adding a clue for recovery period. Greater than 50% of the cross-sectional area involvement, fluid collections, and deep muscle tears were the factors associated with a longer recovery [2]. Initial treatment begins with rest, ice, and a compressive bandage. After the pain is controlled, gentle range of motion exercises can begin. After full ROM has been achieved, strengthening exercises can begin. Return to full activity should be carefully planned after full recovery has been observed with a pain-free movement [14].

Avulsion Fractures Avulsion fractures are a relatively common injury in adolescent athletes. The mechanism of the injury is mostly a sudden, strong contraction of a muscle through the attachment to the apophysis [1, 28]. The apophysis is particularly prone to injury because of its biomechanically weak properties. Among 91 pelvic avulsion fractures reported in four series, 38% were ischial, 32% were ASIS, and 18% were anteroinferior iliac spine. Avulsion of the iliac spine and lesser trochanter were the remaining sites [1, 22]. Avulsion fracture of the ischial tuberosity generally is a result of maximum hamstring contraction. Activities such as sitting or walking can be painful. Treatment of these fractures is mostly conservative including rest, ice, nonsteroidal anti-inflammatory drugs. Some authors advocate surgical intervention if the displacement is more than 2 cm [1]. Avulsion of anterior superior iliac spine (ASIS) occurs after a forceful contraction of the sartorius muscle. This generally occurs with hip extension and knee flexion during running or kicking. Excessive callus formation may be painful, especially fractures of the ischial spine that can impair sport activities. The patients with persistent symptoms may need an excision of the ischial apophysis [22].

Stress Fractures of the Femoral Neck Femoral neck stress fractures were first reported in military recruits undergoing training but since then these injuries have been described in athletes, particularly runners [1, 9, 15]. Female athletes can have a susceptibility to fractures especially those suffering from eating and hormonal disorders [4]. Stress fractures of the femoral neck can be seriously complicated especially if the fracture displaces. Avascular necrosis and non-union of the fracture are reported, so accurate diagnosis should be made as soon as possible [21].

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Typically, an athlete will report a pain deep inside around the hip that worsens with weight bearing. The pain may radiate to the knee. Point tenderness is usually not present. If the radiographic findings are subtle or absent, MRI can be used to detect bone marrow edema and outlined by the high-signal intensity of adjacent bone marrow [10]. Treatment of the fracture is based on the type of the fracture with the degree of displacement. All displaced fractures requires internal fixation [1, 21]. Stress fractures of the femoral neck can be divided into two types: the fractures that are on the tensile side of the neck are more prone to complications and displacement than fractures on the compressive side. Compression-type fractures have better prognosis and can be followed closely for any chance of displacement. Usually, protective weight bearing with serial radiographic examinations is adequate. Tension-type fractures should undergo internal fixation [9, 21].

Hip Instability Hip instability is uncommon in the athletic population, having a range from subluxation to complete dislocation. Hip dislocations can be observed in American football, rugby, skiing, jogging, basketball, soccer, biking, and gymnastics [23]. Patients with posterior dislocation of the hip present with leg flexed, internal rotated, and adducted. And those with anterior dislocation present with abduction and external rotation of the extremity. Hip dislocation is an orthopedic emergency and should be reducted as soon as possible. Most hip dislocations during sports are pure dislocations and due to relative low energy injury, have no associated acetabular fractures. Surgical stabilization is often not necessary and hip joint motion can be ordered. Hip arthroscopy can have a major role for the treatment of intra-articular pathologies but usually should be planned after 6 weeks if there are no loose bodies present. Six weeks after the event, MRI can be ordered to demonstrate an early AVN [19, 23]. Traumatic posterior subluxation of the hip may be associated with posterior acetabular lip fracture, hemarthrosis, and iliofemoral ligament disruption. The hemarthrosis should be aspirated under image control to decrease the intracapsular pressure. Patients should be kept non-weight bearing for 6 weeks and can return to sports if there is no sign of osteonecrosis after a control with MRI and free and painless range of motion [2, 18].

Piriformis Syndrome Piriformis syndrome is the entrapment of the sciatic nerve by the muscle itself near the greater sciatic notch or by chronic irritation. Clinical signs of the syndrome can be pain

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or cramping in the buttock with or without an extension through the leg. Activities that involve flexion, internal rotation may alter the pain. Skiing, ice skating, and gymnastics are the most common associated sports. Straight leg raising test can be possible during the clinical examination. Pain on forced internal rotation with the extension of the thigh may be positive. Radiological studies can be used to eliminate other sources such as lumbar disc herniation. Immediate relief of the pain with an infiltration of a local anesthetic can be helpful in diagnosis. Management usually consists of physical therapy with the help of nonsteroidal anti-inflammatory drugs. Surgery should be considered only if physical therapy fails.

Snapping Hip Syndrome Coxa saltans or snapping hip syndrome is a mostly tendinous problem caused by the ilio-tibial band or iliopsoas tendon with a feeling of snapping with or without pain in the hip region. Both pathologies, either the rubbing of the ilio-tibial band over the greater trochanter or snapping of the ilio-psoas tendon over lesser trochanter, the femoral head, or iliopectineal eminence can usually be treated conservatively. Snapping occurs due to rubbing of the ilio-tibial band over the greater trochanter when the hip is brought from extension to flexion [17]. Dancers, cyclists, or runners are more prone to the pathology. Snapping is usually painless but one can have symptoms related to the bursitis of the greater trochanter. Treatment usually consists of stretching of the band with antiinflammatory medication. Surgical treatment may be indicated for chronic cases, usually consisting of Z lengthening. The snapping of the ilio-psoas tendon should be distinguished from an intra-articular hip pain and differential diagnosis is important. Running, tennis, swimming, football can be associated with the pathology. The snapping can be tested with bringing the hip from a position of flexion, external rotation, and abduction to extension. The conservative treatment consists of stretching the hip flexors with anti-inflammatory medication. Surgical treatment is the release of the tendon either arthroscopic or in an open procedure [5, 17, 29].

Femoroacetabular Impingement Femoroacetabular impingement (FAI) is a recently described mechanical abnormality with pathological contact stresses around the hip joint and may lead to early osteoarthritis of the hip and groin pain in adolescents and active adults [16]. FAI can be explained as “premature pathologic contact between the femur and acetabulum during normal range

Ö. Çag˘lar and M. Alpaslan

of hip joint motion” [27]. Pincer type of impingement which is more common in middle-aged women is because of general or local overcoverage of the acetabulum. The first structure that is damaged in the pincer type of impingement is the labrum. Consequently, with the bone apposition in time the labrum becomes thinner and labral ossification may occur [12]. In cam type FAI, an aspherical portion of the femoral head–neck junction is forced into the acetabulum especially during flexion and internal rotation [26]. The resulting pathology ends with separation of the labrum from the subchondral bone. The amount of the acetabular cartilage damaged with the cam type of acetabular impingement is larger than the pincer type. The majority of patients, however, have both types of the pathologies termed as mixed typed of pincer and cam impingement [3]. Philippon et al. have pointed out that FAI is one of the major causes of hip pain, reduced range of motion, and decreased performance in the sports population [20]. Hockey, ballet, football, and soccer are the most common sports with such an injury. The initial stage of the disease is manifested with anterior groin pain which is worse with the use of the hip during sports. On clinical examination, patients have usually positive impingement sign with hip motion. The “Drehman sign” is unavoidable passive external rotation of the hip with flexion [27]. The diagnosis of the femoroacetabular impingement depends on positive clinical findings with additional imaging studies mostly conventional AP and cross-table lateral view of the pelvis and MRI arthrography. Pincer type of impingement is evaluated by measuring the acetabular coverage and examining the relationship of the anterior and posterior walls of the acetabulum. Coxa profunda or protrusio acetabuli should be noted as global over-coverage. Relative anterior over-coverage is termed as “acetabular retroversion” and is diagnosed when the anterior acetabular wall lies more lateral than the posterior wall in the cranial aspect of the acetabulum [25]. Cam impingement can be diagnosed with an aspheric portion of the femoral head. The MRI arthrography can be more precise for showing the extent of articular cartilage damage or labral tears (Fig. 1). The treatment of FAI usually requires surgical intervention as conservative treatment does not address the morphological pathology. Surgery should be performed for correcting the abnormality and gaining hip range of motion within normal limits. Surgical dislocation, which is defined by Ganz et al. [11], can be used for both types of impingement. In case of pincer-type FAI resection, osteoplasty of the overcovering acetabulum can be performed. The labral detachment and refixation can be ordered with this procedure. Osteochondroplasty of the aspherical femoral head can be done either with open or, more recently, in an arthroscopic way. Early results of arthroscopic cam-type FAI treatment is

Sports Injuries of the Hip Region

Fig. 1 An antero-posterior view of the pelvis in a 28-year-old runner. Note the acetabular retroversion as anterior wall is more lateral than posterior with crossover sign on both hips. The aspherical femoral head can be easily recognized. Mixed type of femoroacetabular impingement is the diagnosis

showing promising results [8, 20]. Acetabular reorientation osteotomy can be performed in hips with retroverted acetabulum to antevert the acetabulum.

References 1. Amendola, A., Wolcott, M.: Bony injuries around the hip. Sports Med. Arthrosc. 10(2), 163–167 (2002) 2. Anderson, K., Strickland, S.M., Warren, R.: Hip and groin injuries in athletes. Am. J. Sports Med. 29(4), 521–533 (2001) 3. Beck, M., et al.: Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. J. Bone Joint Surg. Br. 87(7), 1012–1018 (2005) 4. Bennell, K.L., et al.: Risk factors for stress fractures in female track-and-field athletes: a retrospective analysis. Clin. J. Sport Med. 5(4), 229–235 (1995) 5. Byrd, J.W.T.: Snapping hip. Oper. Tech. Sports Med. 13, 46–54 (2005) 6. Byrd, J.W.: The role of hip arthroscopy in the athletic hip. Clin. Sports Med. 25(2), 255–78, viii (2006) 7. Byrd, J.W., Jones, K.S.: Hip arthroscopy in athletes. Clin. Sports Med. 20(4), 749–761 (2001) 8. Byrd, J.W., Jones, K.S.: Arthroscopic femoroplasty in the management of cam-type femoroacetabular impingement. Clin. Orthop. Relat. Res. 467(3), 739–746 (2009) 9. Egol, K.A., et al.: Stress fractures of the femoral neck. Clin. Orthop. Relat. Res. 348, 72–78 (1998)

961 10. Fredericson, M., et al.: Stress fractures in athletes. Top. Magn. Reson. Imaging 17(5), 309–325 (2006) 11. Ganz, R., et al.: Surgical dislocation of the adult hip a technique with full access to the femoral head and acetabulum without the risk of avascular necrosis. J. Bone Joint Surg. Br. 83(8), 1119–1124 (2001) 12. Ganz, R., et al.: The etiology of osteoarthritis of the hip: an integrated mechanical concept. Clin. Orthop. Relat. Res. 466(2), 264–272 (2008) 13. Garrett Jr., W.E.: Muscle strain injuries. Am. J. Sports Med. 24(6 Suppl), S2–S8 (1996) 14. Jarvinen, T.A., et al.: Muscle strain injuries. Curr. Opin. Rheumatol. 12(2), 155–161 (2000) 15. Johansson, C., et al.: Stress fractures of the femoral neck in athletes. The consequence of a delay in diagnosis. Am. J. Sports Med. 18(5), 524–528 (1990) 16. Leunig, M., Beaule, P.E., Ganz, R.: The concept of femoroacetabular impingement: current status and future perspectives. Clin. Orthop. Relat. Res. 467(3), 616–622 (2009) 17. Melamed, H., Hutchinson, M.R.: Soft tissue problems of the hip in athletes. Sports Med. Arthrosc. 10, 168–175 (2002) 18. Moorman III, C.T., et al.: Traumatic posterior hip subluxation in American football. J. Bone Joint Surg. Am. 85-A(7), 1190–1196 (2003) 19. Mullis, B.H., Dahners, L.E.: Hip arthroscopy to remove loose bodies after traumatic dislocation. J. Orthop. Trauma 20(1), 22–26 (2006) 20. Philippon, M.J., Schenker, M.L.: Arthroscopy for the treatment of femoroacetabular impingement in the athlete. Clin. Sports Med. 25(2), 299–308, ix (2006) 21. Pihlajamaki, H.K., et al.: Displaced femoral neck fatigue fractures in military recruits. J. Bone Joint Surg. Am. 88(9), 1989–1997 (2006) 22. Rockwood, C.A., et al.: Rockwood and Wilkins’ Fractures in Children, 5th ed., xv, 1200 p. Lippincott Williams & Wilkins, Philadelphia (2001) 23. Shindle, M.K., Domb, B.G., Kelly, B.T.: Hip and pelvic problems in athletes. Oper. Tech. Sports Med. 15, 195–203 (2007) 24. Shindle, M.K., et al.: Hip arthroscopy in the athletic patient: current techniques and spectrum of disease. J. Bone Joint Surg. Am. 89(Suppl 3), 29–43 (2007) 25. Siebenrock, K.A., Schoeniger, R., Ganz, R.: Anterior femoroacetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J. Bone Joint Surg. Am. 85-A(2), 278–286 (2003) 26. Siebenrock, K.A., et al.: Abnormal extension of the femoral head epiphysis as a cause of cam impingement. Clin. Orthop. Relat. Res. 418, 54–60 (2004) 27. Tannast, M., Siebenrock, K.A.: Femoroacetabular impingement. Eur. Instr. Course Lect. 8, 123–133 (2007) 28. Waters, P.M., Millis, M.B.: Hip and pelvic injuries in the young athlete. Clin. Sports Med. 7(3), 513–526 (1988) 29. Zoltan, D.J., Clancy Jr., W.G., Keene, J.S.: A new operative approach to snapping hip and refractory trochanteric bursitis in athletes. Am. J. Sports Med. 14(3), 201–204 (1986)

Total Hip Arthroplasty and Sport Activity Roberto Binazzi

Contents Conclusions .................................................................................. 964 References .................................................................................... 965

R. Binazzi Department of Orthopaedics and Hip Surgery, University of Bologna, Villa Erbosa Hospital, Bologna, Italy e-mail: [email protected], [email protected]

Total Hip Arthroplasty (THA) is probably the most frequently performed orthopaedic operation today and one could say that it has improved the quality of life of many people radically who otherwise would be condemned to a sedentary life. Until a few years ago, though, the excellent results of the first post-op period were followed, after a few years, by a progressive wear of the articular surfaces, leading to gradual loosening of the prosthetic components. This was mainly due to polyethylene (PE) wear producing an enormous amount of particles that were overcoming the elimination capacity of the lymphatic system, activating an inflammatory response. This phenomenon was more frequent and more intense in younger patients because of their high functional demands. The conclusion was that usually Orthopaedic Surgeons had to discourage patients below 50 years from undergoing a total hip replacement. More recently, with the introduction of bearings alternative to conventional PE, such as Metal-on-Metal, Cross-linked PE or Ceramic-on-Ceramic, this attitude has drastically changed. In fact, with Metal-on-Metal but above all with Ceramicon-Ceramic, wear of articular surfaces has been reduced to almost zero with expectancy of a very long implant duration. The big advantage of Ceramic over all other materials is that the minimal amount of debris which is generated is totally bio-inert. But, what happens when the patient is a high-level athlete? First of all, we must say that most studies on the subject are not prospective randomised but retrospective and limited to anecdotal results that are inadequate for broad application across all patient population. According to most authors [1–4], returning to competitive sports after joint replacement is extremely difficult: almost all professional athletes who tried to accomplish this goal failed. The most important negative factors of sport activity on a THA are: 1. Frequency of repetitive motions 2. Magnitude of joint loading 3. Potentials for falls and/or contacts

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Table 1 Sports participation for patients with joint replacement based upon level of impact loading Level of impact Sport Observations Low

s PROSTHETIC FIXATION and s WEAR OF ARTICULAR COMPONENTS

Cycling Golf Swimming Walking Ballroom dancing Potentially low Bowling

These activities are desirable for most patients but may increase rate of wear

Rowing Sailing Speed walking Table tennis Jazz dancing Intermediate Hiking Horseback riding Ice skating

Appropriate only for selected patients Excellent physical condition necessary

Tennis Rock climbing Downhill skiing High Baseball

To be avoided

Contact sports (soccer, football, basket) Jogging Water skiing Volley ball

Table 2 Sports allowance for patients with joint replacement Allowed Allowed with Not allowed Undecided experience Golf

Downhill skiing

Squash

Singles tennis

Swimming

Weightlifting

Jogging

Martial arts

Walking Doubles tennis

Skating Rollerblading

Contact sports (football, soccer, basket)

Dancing

Pilates

Baseball

Bowling

Snowboarding

Hiking

High impact aerobics

Road cycling Rowing Elliptical

These factors produce their negative effects through TORSIONAL LOADING and IMPACT that influence negatively

These are the key factors for long-term durability of the implant. In recent years, enormous steps have been made in order to improve the characteristics and consequently the quality of bearing surface materials. Today, metal and ceramic couples show no wear and the newest cross-linked PE shows negligible wear after 27 million cycles in hip simulators. Thus, the bearing surfaced is not the weak link any more in the total joint system. The only real problem today appears to be components fixation and how the attachment can be improved. Keeping in mind that repetitive motions, magnitude of loading and trauma are the three factors able to destabilise an implant, the question is how much is too much exercise and how much impact loading is tolerable? I have analysed and summarised the literature extracting the level of impact loading (Table 1) and the guidelines for sporting activities after THA (Table 2). Sports have been divided into four groups, Allowed, Allowed with experience, Not Allowed and Undecided. It is an interesting principle that sports potentially very dangerous like downhill skiing, ice-skating and rollerblading are allowed, provided that the athlete is technically trained. In fact, these sports performed by an expert require a minimal amount of muscular strength and torsional loading, while if the athlete is not technically skilled can become extremely dangerous. It is also important to note that jogging is included among the “not allowed” activities together with all contact sports (football, soccer, basket), snowboarding and squash. Considering the diffusion of jogging in the world, especially in Anglo-saxon countries, this is a strong point of view. The consequences of engaging in such activities can result in major complications and the need for further surgery with predictably poorer outcomes is a real risk.

Conclusions THA can give today excellent results even in young athletes with high functional demands. While the problem of components wear appears to be solved with the introduction of the new strengthened ceramic, of the second generation metal-on-metal and of the new cross-linked PE, component fixation can still be improved. The factors that influence most negatively the attachment of an implant to the bone are torsional loading and impact.

Total Hip Arthroplasty and Sport Activity

The safest sport activities are obviously those having the lowest level of impact loading, such as walking, golf, swimming, cycling, while contact sports, jogging, and baseball should be avoided for the high probability of injury to the implant.

References 1. Clifford, P.E., Mallon, W.J.: Sports after total hip replacement. Clin. Sports Med. 24, 175–186 (2005)

965 2. Klein, G.R., Levine, B.R., Hozack, W.J., Strauss, E.J., D’Antonio, J.A., Macaulay, W., Di Cesare, P.E.: Return to athletic activity after total hip arthroplasty. Consensus guidelines based on a survey of the Hip Society and American Association of Hip and Knee Surgeons. J. Arthroplasty 22(2), 171–175 (2007) 3. Naal, F.D., Maffiuletti, N., Munzinger, U., Hersche, O.: Sports after hip resurfacing arthroplasty. Am. J. Sports Med. 35, 705–711 (2007) 4. Wylde, V., Blom, A., Dieppe, P., Hewlett, S., Learmonth, I.: Return to sport after joint replacement. J. Bone Joint Surg. Br. 90B, 920–923 (2008)

Sports After Total Hip Arthroplasty Bülent Atilla and Ömür Çag˘lar

Contents Loading of the Joints .................................................................. 967 What Kind of Activities Are Allowed for Total Hip Patients?................................................................ 968 Complications due to Athletic Activity ..................................... 968 Should a Surgeon Encourage Sports After THA? ................... 968 Return to Sport After Joint Replacement................................. 969 Role of Preoperative Rehabilitation .......................................... 970 Will Sports Lead to Early Revision? ......................................... 970 Revision Rate ................................................................................ 970 Summary...................................................................................... 970 References .................................................................................... 970

THA is among the most commonly performed operations in Western countries with a remarkable success rate [9]. Every year almost 500,000 total hip arthroplasties are performed in USA. This figure is about 20–25,000/year in Turkey. The projected demand for total joint replacement will increase by 174% and 673%, respectively, between 2005 and 2030 because of population aging and wider indications [7] and seniors are demonstrating a strong desire to stay active in activities of daily living and athletics. Some of these patients are fairly young and feel that sporting activities are an integral part of their lives [3]. Historically, pain relief and compliance to a sedentary life were the only requirements for a successful total hip arthroplasty (THA). However, improved surgical technique, better prosthesis design and fixation have led to better performance and further expectations [9]. Currently, patients with total hip arthroplasty are often curious about the sports they will be able to participate in after the procedure. Despite the cultural differences among populations, it is a fact that younger individuals tend to be more demanding when compared to patients who had undergone such a surgery 20 years ago. Today’s patients have multiple expectations after total hip arthroplasty including active participation in various sports [7]. Before we prescribe sports activity that is suitable for total hip prosthesis we need to know the loading properties of the normal hip during various sports activities.

Loading of the Joints Sports impose additional mechanical loads on the hip, which theoretically may risk the survival of total hip arthroplasty [5]. Excess force loaded on human hip during activity in terms of body weight is determined as:

B. Atilla ( ) and Ö. ÇaÜlar Department of Orthopaedics and Traumatology, Hacettepe University, Samanpazarı, 06100 Ankara, Turkey e-mail: [email protected]; [email protected]

s Walking

×3 Body weight (BW)

s Jogging 5 km/h

×4.7 BW on hip

×2.8 BW on knee

s Jogging 12 km/h

×6 BW on hip

×13 BW on knee

Some deliver more stress and load to the joints. The most harmful loads are sudden repeated impacts while running,

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football, and skiing due to high sudden loading and unloading moments and possibly rotational shear during performance. Van den Bogert classified them as “High Impact Activities” and [15]: s Joggers are subjected to “sudden and repetitious impact” s Football, rugby, ski involves rotation under load s Mediolateral and anteroposterior stresses during skiing

may lead to THA dislocation Activities are classified in terms of impact level by Clifford and Mallon [2] and they recommended guidelines based on American Association of Hip and Knee Surgeons. They have classified jogging, contact sports, racquetball, high-impact aerobics, martial arts as sports inducing high impact; singles tennis, doubles tennis, hiking, downhill skiing, snowboarding, weight machines, weightlifting, ice skating, low-impact aerobics as intermediate; and bowling, road cycling, dancing, golf, pilates, swimming, walking, stationary bicycle, and treadmill as low-impact activities [4].

What Kind of Activities Are Allowed for Total Hip Patients? There is no clear-cut answer to this question and it is interesting to note that the correct answer has changed throughout the years [16]. Developing surgical techniques, better soft tissue preservation with emphasis on reconstruction of joint mechanics, development of wear-resistant material of hip arthroplasty, and better fixation have probably positively influenced the accommodative potential of THA to various high-impact sports. s During 1980s and 1990s Walking, golf, bowling, swim-

ming and cycling were allowed, when contact sports and water ski were definitely restricted by physicians’ advice. Tennis, ski (Alpine) and volleyball were considered to be controversial. In 1999, The Hip Society conducted a survey on 54 of its members regarding their recommendations for athletics and sports participation for their total hip patients. Among 42 different athletic activities they were asked to rate the activity as recommended/allowed, allowed with experience, no opinion, and not recommended. The 54 responses were analyzed to determine a consensus recommendation for each activity and 73% of agreement was required to achieve significance. If a valid percentage was not achieved for either a positive or negative recommendation, no conclusion was drawn. Most common sports are listed according to HSS recommendation level: Recommended/allowed: Stationary bicycling, ballroom dancing, golf, shooting, swimming, doubles tennis, walking Allowed with experience: Low-impact aerobics, road bicycling, bowling, hiking, horseback riding, cross-country skiing

B. Atilla and Ö. Çağlar

Not recommended: High-impact aerobics, baseball/softball, basketball, football, gymnastics, handball, jogging, squash, rock climbing, singles tennis, volleyball No conclusion: Jazz dancing, ice skating, roller/inline skating, downhill skiing, weight lifting Individual sports are subjected to interest according to their popularity and investigated as such. Michael Mont [10] surveyed the surgeons’ decision for playing tennis after total hip arthroplasty and he has received: s Single 14%

Yes

s Double 34%

Yes

s 52%

No

Of course, all total hip patients are not similar and there are significant differences related to age, level of experience, weight, and type of operation that has been performed which contribute to different risk groups. In fact, evaluation of the individual patient demographics and related risk factors are important before prescribing a sporting activity to an individual. These are: s Preoperative level of athletic activity s Successful surgery s Fixation of the implant s Rehabilitation

Complications due to Athletic Activity Complications of total hip arthroplasty related to sports are all well-known common complications of total hip arthroplasty. However, the incidence may differ: s Dislocations s Periprosthetic fractures s Implant breakage s Higher revision rate?

The association of high activity level and particle regeneration and bone destruction as a tissue response to particles is now a well-recognized problem in total joint replacements [6]. Currently, there is no evidence-based study that compares two different activity level groups to find an answer if individuals that are involved in sports activity are more prone to certain complications.

Should a Surgeon Encourage Sports After THA? Are there scientific reasons to support sport activity even after the total hip arthroplasty or is it a modern-life rumor that everyone should participate in some sort of sports for their health?

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As a general approach to that question, The American College of Sports Medicine states that 20 min aerobic activity three times per week leads to physical and physiologic well-being, so it is advisable to all individuals who may be able to participate including total joint patients. Pollock has determined that regular exercise can be beneficial for patients with anxiety, depression, obesity, high blood pressure, coronary artery disease, diabetes mellitus, osteoporosis, and low-back pain [11]. Ries searched for the effect of THA and total knee on cardiovascular fitness [12, 13]. Patients with total knee arthroplasty performed an exercise test for cardiovascular fitness preoperatively and tested again at 1 year postoperatively and at 2 years postoperatively. Another group of patients in whom osteoarthritis of the knee was being treated medically were tested at the time of enrollment in the study and 1 year later. Physical activity had increased in the arthroplasty group but not in the control group. He concluded that TKA increases workup time, maximum loading, peak oxygen consumption and oxygen intake, and resumption of routine walking activities after total knee arthroplasty improves cardiovascular fitness. His second study investigating the effect of total hip arthroplasty on cardiovascular fitness indicates that better fitness is associated with a decreased risk for the manifestations of coronary heart disease [13].

after THA, hip resurfacing, and age is the most significant determinant. This suggests that hip resurfacing confers no advantage over conventional THR (Fig. 1). a

b

Return to Sport After Joint Replacement Patients are interested in continuing sporting activities and even advancing their previous activity level with the expected relief from pain [17]. If such expectations are not met, there may be dissatisfaction with the outcome of technically successful surgery [14]. Most common reasons generated by the patients for an inability to return to sport because of the reasons attributed to joint replacement were: s Pain

27%

s Inability to do required joint movements

26%

s Medical advice by the surgeon

21%

s Fear of damaging the joint

10%

s Lack of confidence

7%

Return to sport after joint replacement was questioned on patient having THA and hip surface replacement; 34.9% of THA patients and 64.3% resurfacing patients were active in sports preoperatively. At the time of the last postoperative follow-up, 26.4% of THA and 22.7% of hip resurfacing patients were unable to return to sports because of joint replacement. The difference was insignificant [17]. There was no significant difference in rate of return to sports

Fig. 1 (a) A 62-year-old regular tennis player’s both hips were presented with severe hip destruction. (b) Five years after sequential bilateral hip resurfacing, he regularly participates in doubles tennis since 5 months after his second hip replacement

970

Chatterji et al. surveyed patients 1 and 2 years after total hip arthroplasty, to ascertain how the arthroplasty had affected their recreational and sporting ability [1]. Preoperative and postoperative activity along with the time to resume was recorded. The study demonstrated that the number of individuals participating in sport and recreational activities increased slightly after the index operation. It also demonstrated that the number of sporting events decreases after a primary THA despite good postoperative scores suggesting a well-functioning hip replacement. Studies have also shown that the sports performed most frequently before operation by patients undergoing joint replacement include cycling, walking, bowling, and swimming.

Role of Preoperative Rehabilitation Preoperative rehabilitation of scheduled total hip patients has been suggested to initiate and improve the postoperative rehabilitation eventually leading to better postoperative hip scores. Preoperative rehabilitation may decrease hospital stay, and contribute to quicker resumption of activities [8].

B. Atilla and Ö. Çağlar

common belief states that revision burden of total hip arthroplasty is not increased due to regular sports participation.

Summary s Participation in sports is beneficial for THA patients’

health. s Low-impact sports should be preferred. s Patients should refrain from competitive and sports that

cause heavy loading. s Preoperative activity level, previous experience level on

particular sport, and age are the determinants of return to sports after THA. s Revision risk probably does not increase. s Patients should consult and follow the orders of a surgeon before sports participation after total hip arthroplasty. One should discuss specific expectations in detail and individual patient characteristics during preoperative evaluation.

References Will Sports Lead to Early Revision? Patients with hip replacements can expect 90% or greater good-to-excellent results for 10–20 years after hip replacement surgery. There may be concern in a patient with total hip arthroplasty whether participation in sports activity consecutively will risk early revision. A high level of participation in sports is associated with an at least twofold increase in the polyethylene wear rate after 10 years. This suggests a higher risk of aseptic loosening due to granuloma-induced osteolysis [4]. Dubs et al. have showed in 1989 that among 110 THA patients at a mean 55 years of age after 5.8-year follow-up revealed revision rates: s w/ sports 1.6% revision s w/o sports 14.3% revision

This paradoxical result was explained by the authors with probable higher muscle mass and less bad habits of the patients’ participating in sport activities.

Revision Rate Revision rate among patients with total hip arthroplasty exercising regularly are investigated in the literature by different authors. There are some controversial results but, currently,

1. Chatterji, U., Ashworth, M.J., Lewis, P.L., Dobson, P.J.: Effect of total knee arthroplasty on recreational and sporting activity. ANZ J. Surg. 75(6), 405–408 (2005) 2. Clifford, P.E., Mallon, W.J.: Sports after total joint replacement. Clin. Sports Med. 24(1), 175–186 (2005). Review 3. Crowninshield, R.D., Rosenberg, A.G., Sporer, S.M.: Changing demographics of patients with total joint replacement. Clin. Orthop. Relat. Res. 443, 266–272 (2006) 4. Gschwend, N., Frei, T., Morscher, E., Nigg, B., Loehr, J.: Alpine and cross-country skiing after total hip replacement. Acta Orthop. Scand. 71, 243–249 (2000) 5. Kilgus, D.J., Dorey, F.J., Finerman, G.A., Amstutz, H.C.: Patient activity, sports participation, and impact loading on the durability of cemented total hip replacements. Clin. Orthop. Relat. Res. 269, 25–31 (1991) 6. Lequesne, M., Catonné, Y.: Total hip arthroplasty: how much physical activity is too much? Joint Bone Spine 73, 4–6 (2006) 7. Lieberman, J.R., Thomas, B.J., Finerman, G.A., Dorey, F.: Patients’ reasons for undergoing total hip arthroplasty can change over time. J. Arthroplasty 18, 63–68 (2003) 8. Lorig, K., Fries, J.F.: The Arthritis Helpbook, 3rd edn. AddisonWesley, Reading (1990) 9. Mancuso, C.A., Jout, J., Salvati, E.A., Sculco, T.P.: Fulfillment of patients’ expectations for total hip arthroplasty. J. Bone Joint Surg. Am. 91, 2073–2078 (2009) 10. Mont, M.A., Marker, D.R., Seyler, T.M., Jones, L.C., Kolisek, F.R., Hungerford, D.S.: High-impact sports after total knee arthroplasty. J. Arthroplasty 23(6 Suppl 1), 80–84 (2008) 11. Pollock, M.L., Wilmore, J.H.: Exercise in Health and Disease: Evaluation and Prescription for Prevention and Rehabilitation, 2nd edn, pp. 1–2. W.B. Saunders, Philadelphia (1990) 12. Ries, M.D., Philbin, E.F., Groff, G.D., et al.: Improvement in cardiovascular fitness after total knee arthroplasty. J. Bone Joint Surg. 78A, 1696–1701 (1996)

Sports After Total Hip Arthroplasty 13. Ries, M.D., Philbin, E.F., Groff, G.D., et al.: Effect of total hip arthroplasty on cardiovascular fitness. J. Arthroplasty 12, 84–90 (1997) 14. Ritter, M.A., Meding, J.B.: Total hip arthroplasty. Can the patient play sports again? Orthopedics 10(10), 1447–1452 (1987) 15. van den Bogert, A.J., Read, L., Nigg, B.M.: An analysis of hip joint loading during walking, running, and skiing. Med. Sci. Sports Exerc. 31(1), 131–142 (1999)

971 16. Wylde, V., Hewlett, S., Learmonth, I.D., Cavendish, V.J.: Personal impact of disability in osteoarthritis: patient, professional and public values. Musculoskelet. Care 4, 152–166 (2006) 17. Wylde, V., Blom, A., Dieppe, P., Hewlett, S., Learmonth, I.: Return to sport after joint replacement. J. Bone Joint Surg. 90B(7), 920–923 (2008)

Musculoskeletal Tumors and Sports Injuries Mehmet Ayvaz and Nicola Fabbri

Contents Musculoskeletal Tumors and Sports Injury ............................. 973 Caveat Arthroscopy .................................................................... 974 Soft Tissue Tumors...................................................................... 975 Bone Tumors ................................................................................ 977 How to Avoid Misdiagnosis ........................................................ 978 References .................................................................................... 979

The practice of sports medicine is an exciting field, crossing many subspecialties and age groups. However, several important diagnostic issues may be easily overlooked or even totally missed. Sports-related lesions around joints are very common in young athletes. Although musculoskeletal tumors are much less common, they frequently occur in the same age group and also around the joints – most commonly knee joint – and patients often recall some traumatic event with pain and swelling about the knee [5, 11, 12, 22, 27–32, 36]. At oncologic musculoskeletal centers, it is not too uncommon to see patients who had intra-articular procedures for bone or soft tissue knee tumors because of erroneous diagnosis of sports injury. The cause of this misdiagnosis is usually the lack, insufficiency, or misinterpretation of preoperative imaging studies [8, 20, 31, 32]. For sports medicine physician, it is crucial to have basic knowledge about bone and soft tissue tumors and tumor-like conditions that may mimic sports-related injury. Here, the key points for the correct diagnosis of these conditions are discussed.

Musculoskeletal Tumors and Sports Injury

M. Ayvaz ( ) Department of Orthopaedics and Traumatology, Hacettepe University, 06100 Ankara, Turkey e-mail: [email protected] N. Fabbri Orthopaedic Surgery, Adult Reconstruction and Musculoskeletal Oncology, Rizzoli Orthopaedic Institute, Via Pupilli, 1 - 40136 Bologna, Italy e-mail: [email protected]

The exact number of tumors compared with the number of true sports injuries occurring in the general population is not known. Widhe et al. reported 47% of the patients with osteosarcoma and 26% of those with Ewing sarcoma related the onset of symptoms to a sports trauma occurring at a similar time [43] (Fig. 1). Musculo et al. reported nearly 4% of knee tumors originally managed as sports injury [32]. In their series, 13 among 25 patients treated with intra-articular procedures. The type of definitive treatment needed was altered for 6 of the 11 patients with a final diagnosis of a benign bone or soft tissue tumor and 9 of the 14 patients with a malignant tumor also had an alteration in the final treatment required, as a result of changes in the original tumor stage or because of soft tissue contamination. According to the initial records, eight of those nine patients would have been treated with an intra-articular

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974 Fig. 1 Nineteen -year-old basketball player admitted to emergency department with a complaint of left shoulder pain after a fall during the match. (a) Radiographic examination revealed a fracture and infiltrative type of bone destruction. (b) MRI shows the extent of tumor. Core-needle biopsy confirmed the diagnosis of Ewing sarcoma. (c) Postoperative x-ray after wide-excision and prosthetic reconstruction

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resection and one would have been treated with an extraarticular resection, but three were finally treated with an extra-articular tumor resection and six had an amputation. A delay in the appropriate treatment caused by an inaccurate diagnosis seemed to be the most frequent cause for the selection of a more aggressive procedure. Also, in three patients, the type of treatment ultimately needed was substantially altered by tumor contamination of originally unaffected tissues caused by the initial procedure.

Caveat Arthroscopy Schwartz and Limbird reported on 13 patients who had had arthroscopy before they eventually were diagnosed as having a musculoskeletal tumor that is called caveat arthroscopy [37]. Caveat arthroscopy is defined as an arthroscopy done with the intention of managing intra-articular nonneoplastic disease that suddenly escalates into the surgical treatment of an extraarticular neoplasm [22, 37]. Diagnoses included five soft tissue

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sarcomas, five benign bone tumors, two skeletal sarcomas, and one benign soft tissue tumor. In each case, there were complications related to prereferral biopsy. Every subject had at least one untoward event consisting of either compartment contamination, inaccurate diagnosis, or delay in diagnosis. None of these patients had MRI prior to the arthroscopic procedure, reinforcing how adequate imaging should always be obtained before surgery. Economic considerations may also play a role in the selection of diagnostic technique. Even if MRI is the most effective imaging technique for visualizing both sports injuries and musculoskeletal tumors, it has been reported as too expensive as standard routine method, especially for district hospitals in Europe [2, 4, 6, 23, 26]. However, not performing such a study may substantially delay diagnosis and have serious consequences on treatment and prognosis, possibly leading to an unnecessary amputation and reducing the chances of patient’s survival [1]. An intentional arthroscopic biopsy of a known juxta-articular mass is never indicated. If a mass is unexpectedly encountered during an arthroscopic procedure, biopsy should be performed only if the lesion is intrasynovial, otherwise it is always contraindicated. The best way to avoid the complications of caveat arthroscopy is to obtain always adequate imaging preoperatively and avoid biopsy of extraarticular lesions. In these circumstances, the patient should be always referred to a center specialized in the management of musculoskeletal tumors. a

Soft Tissue Tumors Although 1% of all neoplasms are soft tissue sarcomas, synovial sarcoma – one of the most common soft tissue sarcomas in adolescents and young adults – is the most likely to occur in patients between 15 and 40 years of age, a time when many people are active in sports as their favorite sparetime activity [13–15]. Most sarcomas are characterized by slow growth. The clinical presentation of a musculoskeletal tumor may mimic that of a sports-related injury [8, 20, 31, 32, 35]. Subfascial soft tissue sarcomas may be clinically inapparent or may be accidentally detected as a hematoma in association with a sports injury (Fig. 2). The frequency of tumors masquerading as hematomas is approximately 6% of soft tissue sarcomas [40]. An exact history regarding the mode of injury may be helpful for the physician considering the diagnosis of a soft tissue sarcoma. Whenever the clinical findings are inadequate regarding the mode of injury, the physician should take into account the differential diagnosis of a malignancy. Sports physicians should be aware of soft tissue sarcomas because, when unrecognized, mismanagement can lead to disastrous results. Large hematomas can form within the lesions of angiogenic tumors, synovial sarcoma, epithelioid sarcoma, extraskeletal Ewing’s sarcoma, leiomyosarcoma,

b Fig. 2 Thirty -year-old football player seen with a complaint of a swelling at his left thigh for 2 months. He was previously treated as hematoma but the swelling had not disappeared. Physical examination revealed a 6 × 6 cm of solid mass. MRI examination showed a subfascial mass located at the medial thigh. Saggital (a) and axial (b). Biopsy confimed the diagnosis of synovial sarcoma

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liposarcoma, rhabdomyosarcoma or malignant fibrous histiocytoma [17, 24, 38, 40, 41]. The key to the correct diagnosis of chronic hematomas is the confirmation of a history of trauma [40]. Therefore, a history of trauma should be taken into account, as it may lead the clinician to the correct diagnosis of chronic hematoma. For sports physicians, it is important to realize that a prolonged and atypical swelling of soft tissue, even in combination with a previous traumatic lesion and the absence of subcutaneous ecchymosis carries the risk of malignancy. The presence of a slightly atypical soft tissue mass should be a cause for suspicion. Any mass that is larger than 5 cm diameter fixed in position, or deep requires further evaluation and presumed to be malignant proved otherwise. Common findings in the manifestation of soft tissue sarcomas are a slowly enlarging mass with a variable incidence of pain, tenderness, and edema [38]. These clinical findings combined with a well-defined history of trauma should induce further investigations. Malignant tumors with intralesional hemorrhage that masquerade as simple hematomas most frequently do not have associated subcutaneous ecchymosis. However, sports traumarelated hemorrhages usually do have associated subcutaneous ecchymosis. Although not diagnostic, this differentiation provides a diagnostic clue suggesting the possibility of tumorassociated hemorrhage whenever sports physicians evaluate suspected hematomas in patients lacking subcutaneous ecchymosis. In the absence of observable ecchymosis, the likelihood of tumor-associated hemorrhage is somewhat increased. Indications for magnetic resonance imaging under these circumstances remain controversial; ultrasound has been suggested as first-line diagnostic technique but echogenicity does not allow for a clear conclusion about the nature of the tumor [9, 16, 19, 34, 40]. An intramuscular organized hematoma, for example, also shows inner inhomogeneous areas as seen in soft tissue sarcomas. Synovial sarcomas presents with focal calcifications on plain radiographs in 30–50% of cases and by bony erosions in 15–20% of all case, demonstrating that radiographic and also ultrasound examination may be misleading. Infiltration of the fascia is an important finding for differentiation of aggressive soft tissue lesions. The probability that a subcutaneous lesion that crosses the superficial fascia is malignant is about seven times greater than that for lesions that do not cross the fascia [16]. Magnetic resonance imaging is considered to be the procedure of choice for preoperative staging of soft tissue sarcoma and to visualize soft tissue and bony invasion [9, 16, 19, 34]. Magnetic resonance imaging generally shows an invasive, heterogeneous, multiloculated, and particularly septated mass. If clinical symptoms are nonspecific and common diagnostic techniques such as radiography and ultrasound are not conclusive, use of the MRI technique is essential. On MRI, the margins and septae of all hematomas should be evaluated carefully

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for thickened areas with gadolinium contrast enhancement. Whenever diagnosed, hematomas should be appropriately evaluated and followed. Nevertheless, even MRI does not provide a specific histologic diagnosis. The only way to diagnose soft tissue sarcomas definitively is by histopathologic examination. In any case of suspicion of soft tissue sarcoma, the best way is to refer the patient to primary musculoskeletal oncology center. Unplanned excisions or poorly performed biopsy complicate subsequent definitive surgical management of patients with soft tissue sarcomas. In sarcomas, it is difficult to reach a solid diagnosis using fine-needle aspiration biopsy (cytology), because histologic architecture and grading are difficult to assess on cytology; difficulties are even greater in case of sarcoma associated with hematoma [33]. In these instances, either a carefully placed core-needle biopsy or an incisional biopsy should be considered for diagnosis; it is crucial to obtain an adequate tissue volume [3, 25, 39, 42]. Enough tumor material is essential for exact histopathologic diagnosis and tumor grading [3]. Biopsy procedures are therefore subject to guidelines designed to ensure that the subsequent surgical resection is optimally executed (Table 1). The sampling site should be defined on the basis of the imaging results in a conference of radiologists, pathologists, and surgeons with the aim of obtaining the most reliably representative, whenever possible nonossified or necrotic material. Tourniquet application may be performed if considered necessary. Bandaging the extremity for exsanguination could cause tumor compression leading to dissemination of tumor cells. It appears preferable not to arrest the blood supply because hemostasis occurs immediately and not until after opening the tourniquet. Hematomas are to be avoided because they lead to extensive contamination of the surrounding area. Only longitudinal incisions should be made on extremities. The most important criterion is to select the incision site such that it can be removed en bloc together with the tumor in the later tumor resection procedure, because the biopsy scar is regarded as being contaminated with tumor cells. For bone sarcomas without soft tissue infiltration, the intervention is made intentionally through one of the muscle compartments. Dissection in the fascial recess between the muscle compartments is disadvantageous because the recesses

Table 1 Principles of biopsy Incision must be in line with eventual resection incision Longitudinal incision Coincide with excision incision Direct approach through one muscle compartment Meticulous hemostasis Close fascia watertight Seal bone If needed, drain in line with the incision

Musculoskeletal Tumors and Sports Injuries

promote contamination with tumor cells. Surgical dissection is performed in direct approach to the tumor; dissection towards the side is to be avoided. In biopsies, proximity to vessels and nerves is to be avoided due to the risk of contamination. If the bony lesion has a soft tissue component, the biopsy should be taken from this tissue provided that other criteria are not violated. After collecting sufficient tissue, careful hemostasis is performed. At the time of closure, chances of bleeding should be minimized because of the potential catastrophic consequences of hematoma infiltrating soft tissue planes. If need, the use of a drainis reasonable but the drainage channel should not additionally cross or contaminate healthy tissue or compartments. This means that the drain should exit immediately from the wound angle or about 1 cm in an extension of the incision. Skin closure should be atraumatic with intracutaneous suture or a narrow transcutaneous suture. Again, definitive treatment should include principles of tumor surgery and multimodal treatment and should be performed in specialized referral centers for musculoskeletal tumors [10, 42].

Bone Tumors The most common bone tumors with similar symptoms to the sports-related injury are osteoid osteoma, chondroblastoma, giant cell tumor, osteosarcoma, and Ewing’s sarcoma [7, 18, 21]. Osteoid osteoma is a benign bone tumor mostly seen between ages 5–25 years. It produces an intense pain mostly felt at night. Pain subsides with usage of oral salicylates or nonsteroidal anti-inflamatory drugs. The most common location is the proximal femu, where the lesion may often cause referred knee pain mimicking a sport injury (Fig. 3). The characteristic radiographic features are the intense periosteal and endosteal reactive bone formation with a central radiolucent nidus. Nidus can be detected on thin-cut axial computed tomography (CT) scans. Current treatment of osteoid osteoma is CT-guided radiofrequency ablation. Chondroblastoma is a benign bone tumor that is most commonly located at epiphysis of long bones. Most of the patients are in the second decade of life. The typical symptoms are intermittent pain, decreased range of motion, and joint swelling. Radiographically lesion is a well defined, radiolucent, round, lytic, epiphyseal lesion. Axial CT scans demonstrate punctate calcifications and T2-weighted MRI studies show the presence of calcification and hemosiderin. The treatment is curettage and bone grafting with or without internal fixation. Giant cell tumor is a locally aggressive juxta-articular tumor with a peak incidence at age of 20–40 years. The most common locations are the distal femur, the proximal tibia, and the proximal humerus and distal radius. Knee joint is the most

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frequently affected joint. This can lead to confusion of this tumor with many sports-related injuries, resulting in a delay in diagnosis (Fig. 4). The tumor causes pain, mechanical symptoms, and pathological fractures. Radiographically, tumor is a purely lytic, eccentric, metaphyseal-epiphyseal subchondral lesion. Intralesional curettage and bone grafting is a limbsparing option that is associated with good functional and oncologic outcomes. However, simple curettage with or without bone graft has recurrence rates of 27–55%. The relatively high risk of local recurrence has led several surgeons to use local adjuvants such as phenol, liquid nitrogen and polymethylmethacrylate (PMMA) instead of simple bone grafting of the lesion. In addition, the use of PMMA provides immediate stability and may allow easier identification of recurrences at the interface bone-PMMA. However, whether or not the use of local adjuvants reduces the incidence of local recurrence in curettage of giant cell tumor remains controversial. Osteosarcoma is the most commonly seen malignant bone tumor [7, 18]. It most commonly occurs in the long bones of the extremities near metaphyseal growth plates of adolescent patients. Upto 60% of cases knee joint is affected. The most common presenting symptom of osteosarcoma is pain, particularly with activity. The patient often has a history of sportsrelated trauma. Physical findings are usually limited to those of the primary tumor site. A palpable mass may be present. No single feature on radiographs is diagnostic. Osteosarcomatous lesions can be purely osteolytic (about 30% of patients), purely osteoblastic (about 45% of patients), or a mixture of both. Elevation of the periosteum may appear as the characteristic Codman triangle. Extension of tumor through the periosteum may result in a so-called sunburst appearance. MRI of the primary tumor is the best imaging technique to assess the intramedullary extent of the lesion. Patients with suspected osteosarcoma should be referred to orthopedic oncology center for diagnosis and further follow-up. Ewing’s sarcoma is the second most common malignant bone tumor in young patients, and it is the most lethal bone tumor [41–43]. This tumor is most frequently observed in children and adolescents aged 4–15 years and rarely develops in adults older than 30 years. The most important and earliest symptom is pain, which is initially intermittent but becomes intense. Most patients have a large palpable mass, which grows rapidly, with a tense and tender local swelling. In the long bones, the tumor is almost always metaphyseal or diaphyseal. Most commonly, radiographs show a long, permeative lytic lesion in the metadiaphysis and diaphysis of the bone, with a prominent soft tissue mass extending from the bone. MRI is essential to demonstrate soft tissue involvement because the tumor has low signal intensity on T1-weighted images compared with the normal high signal intensity of the bone marrow. On T2-weighted images, the tumor is hyperintense compared with muscle [18, 21].

978 Fig. 3 Sixteen –year-oldmale athlete admitted to sports medicine department with the complaint of nocturnal knee pain that is resolving with analgesics. (a) Radiographic examination showed a 1 cm of sclerotic lesion located at distal femur. (b) Computed tomography sections showing the nidus of osteoid osteoma. (c) Treatment of the patient with CT-guided radiofrequency ablation

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How to Avoid Misdiagnosis Misdiagnosis of sports medicine injuries of the joints can be avoided with a careful history, focused physical examination, and understanding of the pathoanatomy of the affected joints. On examination, if bony tenderness is noted, a possible indication of fracture, tumor, or bone infection, plain films are typically indicated. Often owing to normal or abnormal plain films and a clinical picture suggestive of fracture, tumor, or infection, further clarification of an area of suspected bony pathology is sought. The continued improvement in quality and accessibility of MRI provides

invaluable information to the physician regarding the management of bone, joint, and soft tissue disease. A significant cost issue continues to dim the light of enthusiasm regarding this modality as some persist in ordering an MRI in inappropriate patients. More and more people of all ages engage in sports practice and physical activity for good health and well-being. The increasing levels of participation in organized sports and leisure or fitness activities, along with the broad range of age groups, have greatly expanded the number of sports-related injuries. The increasing incidence of athletic injuries, as a result of more people participating in sports, has been in acute injuries and, even

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Fig. 4 Seventeen -year-old female volleyball player had knee pain after a fall during match for 3 months and treated as soft tissue injury. She was admitted to our clinic with persistent pain. (a) Anteroposterior x-ray of patient showing lytic metaphysioepiphyseal lesion at distal

femur. (b) MRI sections showing the extent of lesion. (c) Biopsy confirmed the diagnosis of giant cell tumor and curettage, phenolization, cementing and prophylactic fixation is preformed

more, in overuse injuries. This area is becoming an important part of medical practice, with a growing impact on resources. Therefore, interest in early diagnosis and assessment of athletics injuries has dramatically increased. Advances in sports medicine are depending upon improvements in adequate imaging capability to allow for best diagnostic accuracy, which in turn determines specific treatment and prognosis. The overlapping clinical appearance of some sports related injuries and orthopedic oncologic conditions continues to associate with delayed diagnosis and incorrect arthroscopic management. Sports medicine physicians must be familiar with common orthopedic oncologic conditions because of this not uncommon differential dignosis in skeletally immature and young adult patients. To avoid misdiagnosis, appropriate, good quality radiographs and selective MRI studies should be obtained before any invasive procedure such as arthroscopy. Imaging studies should be carefully reviewed by the surgeon and radiologist. If any lesion is discovered, it should be carefully evaluated surgery. Thorough history and physical examination with attention to possibility of referred pain is crucial to diagnosis and proper management. Arthroscopic biopsy is only reasonable if the diagnosis of pigmented villonodular synovitis, synovitis or synovial chondromatosis is radiologically obvious.

In case of frank neoplastic condition, the patient should be referred to an orthopedic oncologist.

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980 8. Damron, T.A., Morris, C., Rougraff, B., Tamurian, R.: Diagnosis and treatment of joint-related tumors that mimic sports related injuries. Instr. Course Lect. 38, 833–847 (2009) 9. De Schepper, A.M., De Beuckeleer, L., Vandevenne, J., Somville, J.: Magnetic resonance imaging of soft tissue tumors. Eur. Radiol. 10, 213–223 (2000) 10. Eilber, F.C., Rosen, G., Nelson, S.D., Selch, M., Dorey, F., Eckardt, J., Eilber, F.R.: High-grade extremity soft tissue sarcomas: factors predictive of local. Ann. Surg. 237(2), 218 (2003) 11. Engel, C., Kelm, J., Olinger, A.: Blunt trauma in soccer. The initial manifestation of synovial sarcoma. Zentralbl. Chir. 126(1), 68–71 (2001) 12. Enneking, W.F.: Muskuloskeletal Tumor Surgery. New York, Churchill Livingstone (1983) 13. Enzinger, F.M., Weiss, S.: Soft Tissue Tumors, 3rd edn, pp. 929– 964. Mosby, St. Louis (1995) 14. Ferrari, A., Casanova, M., Massimino, M., et al.: Synovial sarcoma: report of a series of 25 consecutive children from a single institution. Med. Pediatr. Oncol. 32, 32–37 (1999) 15. Fisher, C.: Synovial sarcoma. Ann. Diagn. Pathol. 2, 401–421 (1998) 16. Galant, J., Marti-Bonmati, L., Soler, R., et al.: Grading of subcutaneous soft tissue tumors by means of their relationship with the superficial fascia on MR imaging. Skeletal Radiol. 27, 657–663 (1998) 17. Gomez, P., Morcuende, J.: High-grade sarcomas mimicking traumatic intramuscular hematomas: a report of three cases. Iowa Orthop. J. 24, 106–110 (2004) 18. Heare, T., Hensley, M.A., Dell’Orfano, S.: Bone tumors: osteosarcoma and Ewing’s sarcoma. Curr. Opin. Pediatr. 21, 365–372 (2009) 19. Hermann, G., Abdelwahab, I., Miller, T., Klein, M., Lewis, M.: Tumour and tumour-like conditions of the soft tissue: magnetic resonance imaging features differentiating benign from malignant masses. Br. J. Radiol. 65, 14–20 (1992) 20. Imaizumi, S., Morita, T., Ogose, A., Hotta, T., Kobayashi, H., Ito, T., Hirata, Y.: Soft tissue sarcoma mimicking chronic hematoma: value of magnetic resonance imaging in differential diagnosis. J. Orthop. Sci. 7(1), 33–37 (2002) 21. Iwamoto, Y.: Diagnosis and treatment of Ewing’s sarcoma. Jpn J. Clin. Oncol. 37(2), 79–89 (2007) 22. Joyce, M.J., Mankin, H.J.: Caveat arthroscopos: extra-articular lesions of bone simulating intra-articular pathology of the knee. J. Bone Joint Surg. Am. 65(3), 289–292 (1983) 23. Kelly, M.A., Flock, T.J., Kimmel, J.A., Kiernan Jr., H.A., Singson, R.S., Starron, R.B., Feldman, F.: MR imaging of the knee: clarification of its role. Arthroscopy 7, 78–85 (1991) 24. Kelm, J., Ahlhelm, F., Engel, C., Duchow, J.: Synovial sarcoma diagnosed after a sports injury. Am. J. Sports Med. 29, 367–369 (2001) 25. Kilpatrick, S.E., Cappellari, J.O., Bos, G.D., Gold, S.H., Ward, W.G.: Is fine-needle aspiration biopsy a practical alternative to open

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Anesthesia Managements for Sports Injuries Fatma SarıcaoÜlu and Ülkü Aypar

Contents Anesthesia Management and Postoperative Analgesia for Sports Injury........................................................ 981 General Anesthesia ....................................................................... 981 Regional Anesthesia...................................................................... 982 Neuraxial Blockade in the Setting of Anticoagulants and Antiplatelet Agents ............................... 983 Peripheral Nerve Blocks ............................................................. 983 Local Infiltration ......................................................................... 984 Field Block ................................................................................... 984 References .................................................................................... 985

Anesthesia Management and Postoperative Analgesia for Sports Injury Sports injuries, which are injuries that result from acute trauma or repetitive stress associated with athletic activities have to be treated with surgical procedures and anesthetic management can be necessary. There is no one anesthetic to meet the needs of a patient. Rather, an anesthetic plan should be formulated that will optimally accommodate the patient’s baseline physiological state, including any medical conditions, previous operations, the planned procedure, drug sensitivities, previous anesthetic experiences, and psychological makeup (Table 1). Preoperative physical status classification of patients according to the American Society of Anesthesiologists is useful in planning anesthetic management, particularly monitoring techniques (Table 2). Routine laboratory testing for healthy asymptomatic patients is not recommended when the history and physical examination fail to detect any abnormalities, but many physicians continue to order a hematocrit or hemoglobin concentration, urine analysis, serum electrolyte measurements, coagulation studies, an electrogram, and a chest radiograph for all patients [1, 4]. An informed consent must be taken from the patient before the operation and must always be obtained for general anesthesia in case other techniques prove inadequate. Documentation is important for both quality assurance and medico legal purpose. Preoperative notes, intraoperative anesthesia records, and postoperative notes should be written in the patient chart [13].

General Anesthesia

F. SarıcaoÜlu ( ) and Ü. Aypar Department of Anesthesiology and Reanimation, Hacettepe University, Sihhiye, 06100 Ankara, Turkey e-mail: [email protected]; [email protected]

General anesthesia is appropriate in hemodynamically unstable patients for life-threatening injuries such as head and spinal cord trauma. Any trauma victim with altered consciousness must be considered to have brain injury [10]. Common injuries requiring immediate surgical intervention include brain hematoma. The degree of physiological derangements following

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Table 1 The anesthetic plan Premedication Anesthesia General Airway management Induction Maintenance Regional Technique Agents Monitored anesthesia care Supplemental oxygen Sedation Intraoperative management Monitoring Positioning Fluid management Postoperative management Pain control Hemodynamic monitoring

Table 2 Preoperative physical status classification of patients according to the American Society of Anesthesiologists Class Definition P1

A normal healthy patients

P2

A patient with mild systemic disease (no functional limitations)

P3

A patient with severe systemic disease (some functional limitations)

P4

A patient with severe systemic disease that is a constant threat to life (functionally incapacitated)

P5

A moribund patient who is not expected to survive without the operation

P6

A brain-dead patient whose organs are being removed for donor purposes

E

If the procedure is an emergency, the physical status is followed by “E”

spinal cord injury is proportional to the level of the lesion. Great care must be taken to prevent further injury during transportation and intubation. Short-term high-dose corticosteroid therapy with methylpredisolone (30 mg/kg followed by 5.4 mg/kg/h for 23 h) improves the neurological outcome of patients with spinal cord trauma [3]. Airway management is critical because the most common cause of death with acute cervical spinal cord injury is respiratory failure. All patients with severe trauma or head injuries should be assumed to have an unstable cervical fracture until proven otherwise radiographically. Fiberoptic-assisted awake intubation may be necessary with general anesthesia induced only after voluntary upper and lower extremity movement is confirmed.

In a truly emergent situation, oral intubation of trachea with direct laryngoscopy (minimal flexion or extension of the neck) is the usual approach [6, 12].

Regional Anesthesia Neuraxial blocks: Almost all operations below the neck can be performed under neuraxial anesthesia. Some clinical studies suggest that postoperative morbidity and possibly mortality may be reduced when neuraxial blockade is used either alone or in combination with general anesthesia in some settings (Table 3). Spinal and epidural blocks are also known as neuraxial anesthesia. Each of these blocks can be performed as a single injection or with a catheter to allow intermittent boluses or continuous infusion. Neuraxial techniques have proven to be extremely safe when managed well; however, there is still risk for complications and we have to know the contraindications and avoid performing it. (Table 4). Adverse reactions and complications range from self-limited back pain to neurological deficits [8]. Table 3 Advantages of regional anesthesia versus general anesthesia for orthopedic surgical procedures Improved postoperative analgesia Decreased incidence of nausea and vomiting Less respiratory and cardiac depression Improved perfusion because of sympathetic nervous system block Decreased blood pressure Blood flow redistribution to large caliber vessels Locally decreased venous pressure

Table 4 Contraindications to neuraxial blockade Absolute Infection at the site of injection Patient refusal Coagulopathy Severe hypovolemia Increased intracranial pressure Severe aortic and mitral stenosis Relative Sepsis Uncooperative patients Preexisting neurological deficits Stenotic valvular heart lesions Severe spinal deformity Controversial Prior back surgery at the site of injection Prolonged operation Major blood loss

Anesthesia Managements for Sports Injuries

Neuraxial Blockade in the Setting of Anticoagulants and Antiplatelet Agents Oral anticoagulants: If neuraxial anesthesia is to be used in patients on long-term warfarin therapy, it must be stopped and a normal prothrombin time (PT) and international normalized ratio (INR) should be documented prior to the block [5]. Fibrinolytic and thrombolytic drugs: Patients receiving fibrinolytic and thrombolytic drugs should be cautioned against receiving spinal or epidural anesthetics except in highly unusual circumstances. Data are not available to clearly outline the length of time neuraxial puncture should be avoided after discontinuation of these drugs. Standard (unfractionated) heparin: During subcutaneous (mini-dose) prophylaxis, there is no contraindication to the use of neuraxial techniques. The risk of neuraxial bleeding maybe reduced by delay of the heparin injection until after the block, and maybe increased in debilitated patients after prolonged therapy. Since heparin-induced thrombocytopenia may occur during heparin administration, patients receiving heparin for greater than 4 days should have a platelet count assessed prior to neuraxial block and catheter removal. Low-molecular weight heparin (LMWH): Patients on preoperative LMWH thromboprophylaxis can be assumed to have altered coagulation. In these patients, needle placement should occur at least 10–12 h after the LMWH dose. Patients receiving higher (treatment) doses of LMWH, such as enoxaparin 1 mg/kg every 12 h, enoxaparin 1.5 mg/kg daily, dalteparin 120 U/kg every 12 h, dalteparin 200 U/kg daily, or tinzaparin 175 U/kg daily will require delays of at least 24 h to assure normal hemostasis at the time of needle insertion. Neuraxial techniques should be avoided in patients administered a dose of LMWH 2 h preoperatively (general surgery patients), because needle placement would occur during peak anticoagulant activity. Postoperative LMWH: Patients with postoperative initiation of LMWH thromboprophylaxis may safely undergo single injection and continuous catheter techniques. Management is based on total daily dose,