Clinical Sports Medicine (4th Edition) - Brukner, Khan [PDF]

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Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The editors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord w ith the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the editors, nor the publisher, nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete. Readers are encouraged to confirm the information contained herein with other sources. For example, and in particular, readers are advised to check the product information sheet Included in the package of each drug they plan to administer to be certain that the information contained In this book is accurate and that changes have not been made in the recommended dose or in the contra indications for adm inistration. This recommendation is of particular importance in connection with new or infrequently used drugs. First published 1993 Second edition 2001 Revised second edition 2002 Third edition 1006 Revised third edition 2009 Text 0 2011 McGraw-Hili Australia Pty Ltd Additional owners of copyright are acknowledged in on-page credits. Every effort has been made to trace and acknowledge copyrighted material. The authors and publishers tender their apologies should any infringement have occurred. Reproduction and communication for educational purposes The Australian Copyright Act 1968 (the Act) allows a maximum of one chapter or 10% of the pages of this work, whichever is the greater, to be reproduced and/or communicated by any educational institution for its educational purposes provided that the Institution (or the body that administers it) has sent a Statutory Educational notice to Copyright Agency limited (CAL) and been granted a licence. For details of statutory educational and other copyright licences contact: Copyright Agency limited, l evel 15, 133 Castlereagh Street, Sydney NSW 2000. Telephone: (02) 9394 7600. Website: www,copyright.com.au Reproduction and communication for other purposes Apart from any fair dealing for the purposes of study, research, criticism or review, as permitted under the Act, no part of this publication may be reproduced, dIstributed or transmitted in any form or by any means, or stored in a database or retrieva l system, without the written permission of McGraw-Hili Australia including, but not limited to, any network orother electron1c storage. Enquiries should be made to the publisher via www.mcgraw-hill.com.au or marked for the attention of the permissions editor at the address below. National Library of Australia Cataloguing-In-Publication Data Author: Brukner, Peter. Title: Brukner & Khan's Clinical Sports Medicine I Peter Brukner, Karim Khan. Edition: 4th ed. ISBN: 9780070998131 (hbk.) Notes: Includes index. Previous ed.: Clinical Sports Medicine, 2007. Subjects: Sports medicine. Sports injuries. Other Au thors/Contributors: Khan. Karim. Dewey Number: 617.1027 Published in Australia by McGraw-Hili Australia Pty Ltd Level 2, 82 Waterloo Road, North Ryde NSW 2113 Publisher: Fiona Richardson Senior production editor: Vani Silvana Production editor: Jess Ni Chuinn Publishing and digital manager: Carolyn Crowther Editorial coordinator: Fiona Collison Copy editor: Jill Pope Illustrator: Vicky Earle (anatomical figures) Proorreader: Mary-Jo O'Rourke Indexer: Russell Brooks Cover design: Georgette Hall Internal design: David Rosenmeyer Typeset in 9/11.5 pt Scala by MidlandTypesetters, Australia Printed in China on BOgsm matt art by iBook Printing Ltd

Fo reword to th e fi rst edition (1993) Sport in Australia is ingrained in the national consciousness more widely, deeply, and indelibly than almost anywhere else in the world, When a prominent sportsperson sustains a sporting injury, either traumatically or from overuse, becomes excessively fatigued, or fails to live up to expectations. this assumes national importance. It is even more releva n t nowadays with greater individual participation in sporting activities. The same type of problems occur for recreational athletes, middle-aged people wanting to become fit, or older people wishing to sustain a higher level of activity in their later years. In Clinical Sports Medicine the authors take sport and exercise medicine out of the realm of the elite athlete and place it fairly and squarely where it belongs-as a subspecialty to seIVe everyone in the community who wishes to be active. The book is organized in a manner that is sensible and usable. The chapters are arranged according to the anatomical region of the symptom rather than diagnostic categories. This results in a very usable text for the sports physician, general/family practitioner, physiotherapist, masseur, or athletic trainer whose practice contains many active individuals. Practical aspects of sports medicine are well covered-care of the sporting team and concerns that a clinician might have when traveling with a team. In all, this is an eminently usable text which is timely in its production and will find an important place among clinicians involved in the care of active individuals. JOHN R SUTTON M D, FRACP

Professor of Medicine, Exercise Physiology and Sports Medicin e Faculty of Health Sciences University of Sydm:y Past President, American College of Sports Medicine This foreword was written by th e late Professor fohn Sutton before his untimely death in 1996; it is retained in this textbook out of proJound respect for this champion oj the integration of science, physical activity promotion, and multi· disciplinary patient care.

v

Foreword to the fourth edition Humans were not designed to sit at desks all day and in front of televisions all evening, and this physical inactivity is related to a host of health-related issues. Increasing physical activity is one very powerful way to

mitigate many of the health issues we face today, and programs such as the Healthy People 2020 initiative and the Exercise is Medicine campaign encourage individuals to remain active throughout their lifetime.

As people become more involved in sport and exercise, sports medicine becomes increasingly important, and Clinical Sports Medicine has understandably become what we in the US refer to as the "PDR" (Physicians'

Desk Reference) of sports medicine. For my UK colleagues the translation is "BNF" (British National Pormu· lary). This text is extremely comprehensive, covering fundamental principles of biomechanics, diagnosis and treatment, regional musculoskeletal injuries, and medical problems. The text also addresses those practical issues of sports medicine that are often missing from other texts, such as dealing with athletic teams, covering endurance events, and working with the elite athlete. The organization of the text m akes it remarkably easy to use, including such features as color-coded book sections, flow diagrams to reinforce concepts, and tables that clearly organize information. Vicky Earle's anatomical drawings are truly among the best in the business. All these features put an astounding wealth of information at the reader's fingertips. This information has been assembled by a group of over 100 expe· rienced and world-class physical therapists, physicians, and scientis ts. These co-authors provide up-to-date references when available, and clearly state when evidence is lacki ng. This updated, fourth edition includes zoo new photos/graphi cs and 13 new chapters on current topics, including Integrating evidence into clinical practice, Principles of activity promotion. and Medical emergencies in sport. The edi tors continue to add to the clinically relevant topics with one of my favorites being what I call "How to manage the patient who has seen everyone and wants a cure from you!" (Chapter 41). An innovative and exciting addition to this edition is the integration of the Clinical Sports Medicine master· classes that allow you, through videos and podcasts on the Clinical Sports Medicine website, to learn directly from the experts. These masterciasses, which will be updated regularly, provide a remarkably dynamic component to the text. It is exciting to watch CUnical Sports Medicine evolve substantially with each edition. The editors' focus of this text is to "help clinicians help patients" and they have clearly hit their mark. This book is an absolute musthave for any sports medicine professional. Professor Irene Davis, PT, PhD, FACSM, FAPTA, FASB

Director, Spaulding National Running Center Department of Physical Medicine and Rehabilitation Harvard Medical School Spaulding-Cambridge Outpatient Center CambJidge, MA, USA

vi

Brief contents

Part A

Fundamental principles

Sports and exercise medicine: addressing the world's greatest public health problem

2

2

Sports and exercise medicine: the team approach

6

3 4

Sports injuries: acute

5

Sports injuries: overuse

Integrating evidence into clinical practice to make quality decisions

"

6

Pain: why and how does it hurt?

7

Beware: conditions masquerading as sports injuries

15 25 41 54

8 9

Clinical aspects of biomechanics and sporting injuries

61

Principles of injury prevention

113

10

Recovery

138

145 157

"

Principles of diagnosis: clinical assessment

12

Principles of diagnosis: investigations including imaging

l3

Treatments used for musculoskeletal conditions: more choices and more evidence

164

14 15

Core stability

210

Principles of rehabilitation

227

16

Principles of physical activity promotion for clinicians

254

Part B

Regiona l problems

17

Sports concussion

272

18

Headache

19 20

Facial injuries Neck pain

21

Shoulder pain

Hand and finger injuries

290 300 313 342 390 413 435

Thoracic and chest pain

449

Low back pain

463

22

Elbow and arm pain

23 24 25 26

Wrist pain

27

Buttock pain

492

28

Hip-related pain

510

Groin pain

545

Anterior thigh pain

Leg pain

579 594 626 684 715 735

Calf pain

761

29 30 31 32

Posterior thigh pain Acute knee injuries

33

Anterior knee pain

34 35 36

Lateral, medial, and posterior knee pain

vii

,

:,r::.., :,>

Brief contents

37 38 39 40 41

• 42 43 44 45 46

• 47 48 49 50 51 52 53 54 55 56 57 58 59 60

Pain in the Achilles region Acute ankle injuries

Ankle pain Foot pain The patient with longstanding symptoms: clinical pearls

Parte

viii

776 806 828 844 878

Special groups of participants

The younger athlete Women and activity-related issues across the lifespan The older person who exercises Military personnel

Th e athlete with a disability

888 910 936 943 960

Part D Ma nagement of m edical problems Medical emergencies in the sporting context Sudden cardiac death in sport Managing cardiovascular symptoms in sportspeople Respiratory symptoms during exercise Gastrointestinal symptoms during exercise Renal symptoms during exercise Diabetes mellitus Exercise to treat neurological diseases and improve mental health Joint-related symptoms without acute injury Common sports-related infections

The tired athlete Exercise in the heat Exercise at the extremes of cold and altitude Quick exercise prescriptions for specific medical conditions

PartE 61 62 63 64 65 66 67

·to.

' ••

972 996 1024 1038 1056 1063 1070 1082 1093 1102 111 8 1132 1146 1158

Practica l sports medici ne

The preparticipation physical evaluation Screening the elite sportsperson Providing team care Traveling with a team Medical coverage of endurance events

Drugs and the athlete Ethics and sports medicine

1176 1185 1203 1208 1221 1228 1261

Foreword to the first edition

v

Co-authors

Foreword to the fourth edition

vi

Other contributors

xlii

xxxi

Acknowledgments

xliv

Guided tour of your book

xlv

4

15

Preface About the authors

xxxiii

Editors

xxxv

Fundamental principl es

Sports inj uries: acute

Bone

1 Sport s and exercise med icine: addressi ng the world 's greatest pub lic health prob lem

Fracture

2

Joint

The bu rd en of physical inactivity an d sedentary behavio r The one trillion dollar argument (US alone!)

2 2

Physical fi tness-more health benefi ts than smoking cessation or weig ht loss

Periosteal injury Articular cartilage Dislocation/subluxation Ligament Muscl e Strain/ tear

2

Contusion

The molecular mechanisms that explain the

health benefits of physical activity Putting it all toge ther-the economic imperative Practical challenges The darkest hour is just before the dawn

2 Sports and exercise med icine: the team approac h The sports and exercise med icine team

Multiskilling The sports and exercise medicine model The cha llenges of managemen t Diagnosis Treatment Meeting individual needs The coa ch, the athlete, and t he clin ician "Love t hy sport" (a nd physica l activit y!)

3 Integrating evidence into cli nical practice to make qua lity decisio ns Life before evidence -based practice Sackett and t he McMaster contrib ution ThiS seems obvious-so what is the problem?

2

Myositis ossificans

4

Cramp Tendon

4 4

Bursa Nerve Skin

6

5

6 6 7 7 8 9 9 9 9

Bone stress

Sports inj uries: overuse Mechanism Risk factors Skeletal sites Clinical diagnosis Imaging diagnosis Low-risk and high-risk stress fracture

12 12 13

16 16 17 17 18 18 18 20 20 21 21 22 22 23 23 23 25 25 26 26 28 28 28 29

General prinCiples of stress fracture treatment 30 Ost eitis and periostitis

Apophysitis

11

xxxvi

Articu lar car ti lage Join t Ligament Muscle Focal tissue thickening/fibrosis

31 31 31 31 31 31 32 ix

-

--

Contents Chronic compartment syndrome Muscle soreness Tendon Tendon overuse injury (tendinopathy) A contemporary model of a continuum of tendon pathology

Bu rsa Nerve Skin Blisters Infections Dermatitis Skin ca ncers But it's not that simple .. Pain: w here is it coming from? Masquerades The kinetic chain

6

Pa in: w hy and how does it hurt?

What is pain? What is nociception?

41 41 42 43

The brain decides The bra in corrects the spinal cord When pain persi st s, the brain changes

44 45 45 47

Trea ting someo ne in pain- a complex system requires a comprehensive approach

Radicular pain Somatic pain Clinica l assessment of referred pain Clin ical summary

Disorders of muscle Endocrine disorders Genetic disorders Infection Pai n syndromes

8 Clinica l aspects of biomec hanics and sporting injuries

47

61 61 Ideal neutral stance positio n 64 "Ideal" biomechan ics w ith movement- running 65 Loading (heel strike to foot nat) 66 Midsta nce (foot nat to heel off) 67 Propulsion (heel off to toe off) 68 Initial swing 69 69 Terminal swin g 69 Angle and base of gait 69 Innuence of gai t velocity Comparing heel and forefoot strike patterns 70 Innuence offatigue on running biomechani cs 71 Lower limb joint motion

clini cal sett ing

Condit io ns masquerading as sports Injuries

x

71

Structural ("static") biomechanical assessment

73

Functional lower limb tests- single-leg ajump

77

Dynamic movement assessment

48 49 49 51 52

(e.g. running bi omecha nics) Sport-specific assessment

54

assessment

83

Clinica l assessment of footwear-the Foo twear

Gen eral structure Motion control properties

54 54

82 83

Summary of the lower limb biomechanical

Fit

How to recogn ize a condition masquerading as a sports injury

61

"ldeal" lower limb biomechanics - t he bas ics

Assessment Tool

7 Beware: co nditions masquera ding as sports injuries

54 56 57 57 58 58 59 59 59

stance, heel raise, squat, and landing from

Cl inical approac h to referred pai n- often neglec ted in clin ica l teac hin g

Rheumatological conditions

lower limb biomechanica l assess men t in the

State-dependent sensitivity of spinal nociceptors

Bone and soft t issue tumors

Granulomatous diseases

36 37 37 37 37 37 38 38 38 38 38 38

State-dependent sensitivity of primary nociceptors

_,'

Vascular disorders

33

Other terms associated with overuse tendon injuries

.', _,t>i;' Je'-

. 32 32 33 33

-

'"'

Cushioning Wear pattern s

83 83 83 83 85 85

Conditions rela ted to suboptima l lower limb biomechan ics Management of lower limb biomechan ica l abnormalities Foot orthoses

Tapi ng Biomechanics of cycling Set-up and positioning on the bike Bike set-up in other forms of cycling Aerodynamics and wind resistance Pedaling technique Assessment Rehabilitation Conclusion Upper li mb biomechanics The biomechanics of throwing

102

Abnormal scapular biomechanics and

physiology

103

Clinical significance of scapular biomechanics in shoulder injuries

104

Changes in throwing arm with repeated

pitching

104

Common biomechanical abnormalities

Biomechanics of other overhead sports

105 105 106 107

Prin ci ples of inj ury prevention

113

specific to pitching Biomechanics of swimming Biomechanics of tennis

10 Recove ry

138

Wa rm-down or active recovery

138 139 139 139 140 140 140 140 141 141 142 142

Principles of trai ning Training methods

86 86 91 92 92 96 97 97 97 98 98 98 99

Normal biomechanics of the scapu la in

throwing

Adequate recovery

128 128 130 134

Appropriate trai ning

85

Deep-water runn ing Cold wate r immersion (ice baths) Massage Compression garments Lifestyle factors Nutrit ion Glycogen replacement Protein replacement Co-ingestion of carbohydrate and protein Rehyd ration

Psychology The funct ion of the autonomic nervous system system Techniques that aid psychological recovery

11 Principles of di ag nosis: clinica l assessment Making a diagnos is History Allow enough time

9

Systematic injury prevention Warm-up Ta pi ng and braCing Taping Bracing Protective equ ipment Suitab le eq uipment Runn ing shoes Running spikes

Football boots Ski boots Tenn is racq uets Appropriate surfaces

113 11 6 121 121 122 122 123 123 124 125 125 126 127

143

Effect of exercise on the autonomic nervous

Be a good listener Know the sport Circumstances of the injury

143 143

145 145 146 146 146 146 146

Obtain an accurate descri ption of symptoms History of a previous similar injury Other injuries

General health Work and leisure activit ies Consider why the problem has occurred Training history Equipment Technique Overtraining Psychologica l factors

146 147 147 147 147 147 147 148 148 148 148

xi

Nutritional factors History of exercise· induced anaphylaxis

148 148

Determ ine the importance of the sport to the athlete Exam ination Develop a routine Where relevant, examine the other side Consider possible causes of the injury

Assess local ti ssues Assess for referred pain Assess neural mechanosensitivity Examine the spine Biomechanica l examination Functiona l testing The examination routine

Respiratory invest igations Pu lmonary function tests

148 148 148 148 148

The diagnosis

148 148 149 149 149 149 149 149

Ev idence for t reatment effectiveness is

Attempt to reproduce the patient's symptoms

Card iovascular invest igations

13 Treatments used for m uscu loskeleta l conditions: more choices and more evidence 164 co ntinually changing Acute managemen t Rest Ice Compression Elevation Immobiliza tion and ea rly mobilizat ion Protected mobilization

12 Princip les of diagnosis: investigations incl uding imagi ng Investiga t ions 1. Understand the meaning of test results

Continuous passive motion

157 157 157

2. Know how soon changes can be detected by investigations

157

3. On ly order investigations that will influence management

157

4. Provide relevant clinical findings on the requisition 5. Do not accept a poor quality test

157 157

6. Develop a close working re lationship w ith investigators 7. Explain the investigations to the patient Rad iolog ica l investigation Plain X·ray Computed tomographic (CT) scanning Magnetic resonance imaging (MRI) Ultrasound scan (for diagnosis) Radioisotopic bone scan Neurolog ica l investiga tions Electromyography Nerve conduction studies Neuropsychological testing Muscle assessment Compartment pressure testing

xii

157 158 158 158 158 158 159 160 161 161 161 161 161 161

161 161 161 162

Thera peutic drugs Analgesics Topical analgesics

164 165 165 165 166 166 166 167 167 167 167 168

Nonsteroidal anti-inflammatory drugs (NSAIDs) Topical anti-inflammatory agents Corticosteroids Nitric oxide donor Sclerosing therapy Prolotherapy

168 174 174 176 177 177

Glucosamine su lfate and chondroitin su lfate

178

Hyaluronic acid therapy (Hya lgan, Synvisc, Osteni!, Orthovisc) Antidepressants Local anesthetic injections Traumeel Bisphosphonates Blood and blood products Autologous blood injections Platelet-rich plasma Hea t and cold Cryotherapy Superficial heat Contrast therapy

178 179 179 180 180 180 180 180 181 181 183 184

El ectrotherapy Ultrasound

185 186

TENS (Transcutaneous electrica l nerve

Open surgery

14 Core stabi lity

210

Anatomy

212 212 212 212 213 213 213 213 213 215 215

Interferentialstimulation High-voltage galvanic stimulatio n Low-voltage galva nic stimulatio n Neuromuscular sti mulators Point stimulators Laser Diath ermy Magnetic therapy Extracorporeal shock wave therapy Manual therapy Joint mobilization Joint manipulation Joint traction Soft tissue therapy Muscle energy technique s Neural stretching Acupuncture Dry need ling Hyperbaric oxygen th erapy Surgery Arthroscopic surgery

Osseous and ligamentous structures The thoraco lumbar fascia Paraspinals Quadratus lumborum Abdominals Hip girdle musculature Diaphragm and pelvic floor As sessme nt of core sta bili ty Exercise of the co re musculat ure Decreasing spinal and pelvic viscosity Use of biofeedback and real-time ultrasound in retraining core control Stabilization exercises Functiona l progression Core strengthening for sports

223

Prevention of injury and performance

Conclusion

223 224 224 224

15 Pri nciples of rehabilitation

227

Keys to a successful rehabilitatio n prog ram

227 228 228 228 228

improvement

187 188 188 188 188 189 189 189 189 190 190 191 192 193 193 196 197 198 198 200 200 200 201

stimulation)

Efficacy of core st rengthening exercise

Treatment of low back pain Effectiveness in sports injuries

Explanation Provide precise prescription Make the most of the available facili ties Begin as soon as possible Co mpo nent s of exercise programs for rehabili tat io n Muscle conditioning Cardiovascular fitness Flexibility Proprioception Functional exercises Sport skills Hydrotherapy Deep-water ru nning Correctio n of biomecha nica l abnorma lities Stages of rehabil itation Initial stage Intermediate/preparticipation stage Adva nced stage Return to sport Seconda ry preve nt ion Prog ression of rehabi li ta tio n Type of activity Duration of activity Freq uency In tensity Complexity of activity Monito rin g re habil it at ion programs Psycho logy Emotional responses to injury

228 228 235 235 238 240 240 242 242 243 243 243 243 244 245 246 246 246 246 246 246 246 246 247 247

Psychological strategies to facilitate

216 216 219 223

recovery Conclusion

247 2S0

xiii

16 Pri nciples of physica l acti vity promotion for cl inicia ns

254

Who should receive exercise counse ling ?

255

Migraine Clu ster headache Cervical headache

Mechanism

Are there medical contraind ications to bei ng

active? Executing the presc ription

Practical steps with the consu ltatio n Exe rcise gu id elines

Aerobic activity Defining intensity Resistance training Flexibili ty Follow-up

An overlooked element o f motivati on

Summary

255 256 256 257 257 258 259 267 267 267 268

Cli nical features

Exercise- related causes of headache Pri mary exertional headache Exertional m igraine

Post-traumatic headache Externa l compressio n headache High -altitude headache

Hypercapnia headache

19 Facial injuries

300

Func tional anatomy

300 300 301 303 303 303 303 304 304 304 304 304 305 305

Cl inical assessmen t Soft t issue inj uries Nose

Regional problems

Epistaxis (nosebleed) Nasal fractures

17 Sports concussion

272

Definition of concuss ion

273 273 274 274 274

Prevention of concussion Th e initial impact: app li ed pathop hysiology Management of the concusse d at h lete On·field management safely to competition

277

Risk of further injury Second impact syndrome Concussive convulsions Prolongation of symptoms Chronic traumatic encephalopathy Mental health issues Children and co ncussio n in spo rt

Ear

Auric ul ar hematoma Lacerations Perforated eardrum Otitis externa Assessment of the injured eye Cornea l injuries: abrasions and foreign

Th e risk of p remature return to play and concussion sequelae

Septal hematoma

Eye

Determining when the player can return

281 281 281 281 281 281 282 282

body

Subconjunctival hemorrhage Eyelid injuries Hyphema

Lens dislocation Vitreous hemorrhage Retinal hemorrhage Retinal detachment Orbita l injuries

18 Headache Headache in sport Clin ica l approach to the patient w i th hea dache History Examination Vascu lar headaches

xiv

293 295 295 295 296 297 297 297 298 298 298 299

290 290 291 292 293 293

Prevention of eye injuries Teeth Prevention of dental injuries Fractures of facial bo nes

306 307 307 307 307 307 307 308 308 308 309 309 309

Fractures of the zygomaticomaxil lary com plex

310

Maxillary fractu res Mandibular fractu res Temporomandibular injuries Prevention of facial injLlries

310 311 311 312

Glenoid labrum inju ries Clinically relevant anatomy Making the diagnosis Treatment Dislocation of the glenohu meral joint

20 Neck pain

313

Clinical perspective

313 315 315 317 326 326 326 328 331 332 332 332 332 333 333 334 334 334 335 336

Assessing patient s with neck pain History Physical examination Trea tment of neck pain Education Posture Exercise therapy Manual therapy Soft tissue techniques Neural tissue mobilization Dry needling Stress management Neck pain syndromes Acute wry neck Acceleration-deceleration injury Cervicogenic headache Acute nerve root pain Stingers or burners Conclusion

21 Shoulder pa in

342

Functional anatomy-sta t iC and dynam ic

342 342 343 343 344 344 345 345 352 353 354 354 355 357 357 359

Static stabilizers Dynamic stabilizers

5capulohumeral rhythm Clinical pers pective A practica l approach to shou lder pain History Examination Shoulder investigations Impingement Primary external impingement Secondary external impingement Internal impingement Rotator cuff inj uri es Rotator cuff tendlnopathy Rotator cuff tears

Anterior dislocation

360 360 360 361 362 362

Posterior dislocation of the glenohumera l jOint Shou lder in stabil ity Anterior instability Posterior instability Multidirectional instability Adhesive capsuli tis ("frozen shou lder") Treatment Fracture of the clavicle Middle-third clavicular fracture Distal clavicle fractures AcromioclaviCLd ar joint conditions Acute acromioclavicular joint injuries Chronic acromioclavicular joint pain Referred pai n Less com mon causes of shoulder pain Biceps tendinopathy

Rupture of the long head of the biceps Pectoralis major tears SubscapulariS muscle tears Nerve entrapments Thoracic outlet syndrome

363 364 364 367 367 367 367 368 368 368 369 369 371 372 373 373 373 373 373 373 375

Axillary vein thrombosis reffort"

thrombosis) Fractures around the shoulder joint Principles fo r should er re habilitation Make a complete and accurate diagnosis Early pain reduction

376 376 377 377 377

Integration of the kinetic chain into rehabilitation Scapular stabilization

377 378

Early achievement of 90° of abduction and improved glenohumeral rotation Closed chain rehabilitation Plyometric exercises Rotator cuff exercises

378 381 382 383

Putting it all together-s pecific rehabilitation protocols Acute phase

384 384

xv

Recovery phase Functional phase Criteria for return to play

385 386 387

Subacute onset and chron ic wrist pain History Examination Extra-articular conditions

22 Elbow and arm pain

390

Lateral elbow pain

390 391 393 400 401 401 401 402 403 403 404 404 404 404 405 406

Clinical assessment Lateral elbow tendinopathy Other causes of lateral elbow pain Media l elbow pa in Flexor/pronator tendinopathy Medial collateral ligament sprain Ulnar neuritis Posterio r elbow pain Olecranon bursitis Triceps tendinopathy Posterior impingement Acute elbow injuries Investigation Fractures Dislocations Acute rupture of the medial collateral ligament Tendon ruptures Forearm pain Fracture of the radius and ulna Stress fractures

Forearm compartment pressure syndrome Uppe r arm pai n Myofascial pain Stress reaction of the humerus

Articular causes of subacute and chronic Numbness and hand pain

431 431

24 Hand and fing er inj uries

435

Cli nical eva luation

435 435 436 437 438 438 439 439 439 439 441 442 442 442 442 442 443 443 443 443

w rist pain

History Examination Investigations Pr inciples of treatment of hand injuries Control of edema Exercises Taping and splinting Fractures of the metacarpa ls Fracture of the base of the first metacarpal Fractures of the other metacarpals Fractures of phalanges

407 407 407 407 408

Proximal phalanx fractures Middle phalanx fractures Distal phalanx fractures Dislocation of the metacarpopha langea l joints Dislocat ions of t he finger joints Dislocations of the PIP joint

Entrapment of the posterior interosseous

nerve (radial tunnel syndrome)

Injuries to the distal radial epiphysis

408 409 409 409 409

Dislocations of the DIP joint ligament and te ndon injuries Sprain of the ulnar collateral ligament of the first MCP joint

413

Acute wrist injuries

413 413 415 418 420 420 423 424 425

History Examination Investigations Fracture of the distal radius and ulna Fracture of the scaphoid Fracture of the hook of hamate Dislocation of the carpal bones Scapholunate dissociation

xvi

443

Injuries to the radial collateral ligament of the first MCP joint

23 Wrist pa i n

426 426 426 427 430

Capsular sprain of the first MCP joint PIP joint sprains Mallet finger Boutonniere deformity

444 444 444 445 446

Avulsion of the flexor digitorum profundus tendon Laceratio ns and infections of the hand Overuse co nd iti o ns of the ha nd and fingers

447 447 447

25 Thoracic and chest pa in Thorac ic pai n

Assessment Thoracic intervertebral joint disorders

Costovertebral and costotransverse joint disorders Scheuermann's disease Thoracic intervertebral disk prolapse

T4syndrome

449 449 449 453 454 455 455 455

Postural imbalance of the neck, shoulder and upper thoracic spine Chest pa in

Assessment Rib trauma Referred pain from the thoracic spine Sternoclavicular joint problems Costochondritis Stress fracture of the ribs Side strain Concl usion

456 456 457 458 458 459 460 460 461 461

Concl usio n

480 480 480 481 482 483 483 484 484 484 484 484 485 485 485 487 488

27 Buttock pain

492

Clinical approac h

492 492 494 496 497 498 498 500 501 502 503 503 504 504 504 504 505 505 506 506

Treatment Stress fract ure of the pars in tera rti cularis

Clinical features Treatment Spondylolisthesis

Clinical features Treatment Lumbar hypermobility Structural lumbar instability

Sacroiliac j oint d isorde rs Rehabilitatio n follow ing low bac k pain Posture

Daily activities Sporting technique

Core stability Specific muscl e tightness

History

26 Low back pain

463

Epidemi ology

463 463

Clinical perspective Conditions causing low back pain in which a definitive diagnosis can be made Somatic low back pain

464 465

Functional (clinica l) instability in low back pain History Examination Investigations Severe low ba ck pain

467 468 468 468 472

Clinical features of severe acute low back pain

472

Management of severe acute low back pain Mi ld-to-moderate low bac k pain Clinical features

472 473 474

Treatment of mild-to-moderate low back pain Chronic low back pain Acute nerve root compress ion Clinica l features

474 477 478 480

Examination Investigations Referred pain from t he lumbar spin e Sacroiliac j oint d isorde rs Functional anatomy Clinical features Treatment Iliolumbar ligament sprain Hamstring origin tend in opat hy Fibrous adhesions Ischioglu tea l bu rsitis Myofascial pai n Less common ca uses Quadratus femoris injury Stress fracture of the sacrum Piriformis conditions Posterior thigh compartment syndrome Proximal hamstring avulsion injuries Apophysitis/ avulsion fracture of the ischial tuberosity Condi tions not to be m issed

507 507

xvii

28 Hip-related pain

510

Functional anatomy and biomechan ics

510 511 511 512 513 513

Morphology

Acetabular labrum Ligaments of the hip

Chondral surfaces Joint stability and normal muscle function Clin ical perspective: making sense of a complex

problem Femoroacetabular impingement (FA!) Factors t hat may contr ibute to t he

development of hip-re lated pa in

Extrinsic factors Intrinsic factors Clin ical assessment History Examination Investigations Labra l tears Ligamentum teres tears Synovitis Cho nd ropat hy Re habilitat io n of the inj ured hip

516 516 518 518 519 521 521 522 525 526 527 528 529 530

Unloading and protecting damaged or potentially vulnerable structures

530

Restoration of normal dynamic and neuromotor control

530

Address other remote factors that may be altering the function of the kinetic chain Surgical management of th e inj ured hip Rehabilitation following hip arthroscopy Os acet ab ul are Latera l hip pa in Greater trochanter pain syndrome (GTPS) Gluteus medius tendon tears

534 534 535 536 538 538 540

Factors that increase local bone stress Clin ica l approach History Examination Investigations Acute adductor stra in s Recurrent adductor muscle strain Adductor-related groin pain Earlywarning signs Treatment

Iliopsoas-related groin pain

Epidemiology Clinical concepts Treatment

Abdom inal wall - re lated groin pain Posterior inguinal wall weakness (sports hernia, sportsman's hernia) Gilmore's groin Laparoscopic inguinal ligament release

545

Anatomy

545 547 547 548

Prevalence Risk factors Clin ical overview Local overload causing failure of various structures What role does bone stress play?

xviii

548 549

567 568 568

Tear of the external oblique aponeurosis (hockey groin) Inguinal hernia Rectus abdominis injuries Pubic bone stress-related groin pai n Treatment Less common inj uries Obturator neuropathy Other nerve entrapments Stress fractures of the neck of the femur Stress fracture of the inferior pubic ramus Referred pain to the groin

568 569 569 569 571 572 572 572 572 573 574

30 An te rior thigh pain

579

Cli nical approach

579 579 580 581 582 583 586 587 587 588 589

History Examination

29 Groin pain

550 552 552 553 558 559 559 559 560 560 565 566 566 567 567

Investigations Quad riceps contusion Treatment Acute compartment syndrome of the thigh Myositis ossiftcans Quadriceps muscle strain Distal quadriceps muscle strain Proximal rectus femoris strains

-

I'g.,

.

_ ";'.. . Differentiating between a mild quadriceps strain and a quad ri ceps contusio n Less co mmon cau ses Stress fracture of the femur

Compartment syndrome of the posterior

590 590 590

lateral femoral cutaneous nerve injury ("meralgia paresthetica") Femoral nerve injury Referred pain

591 592 592

31 Posterior thigh pain

594

Functiona l anatomy

594 59S 596 597 599

Cli nical reasoning History Examination Investigations Integrating the clinical assessment and investigation to make a diagnosis Acute hamstring mLlscle strains

Epidem iology Types of acute hamstring strains Management of hamstring injuries Risk factors for acute hamstrin g strain Intrinsic risk factors Extrinsic risk factors Prevention of hamstring st rai ns Nordic drops and oth er eccentric exercises Balance exercises/ proprioception training Soft tissue therapy

Referred pain to po ste rior th ig h Trigger points Lumbar spine Sacroiliac complex Ot her hamstring injuries

Common conjoint tendon tear Upper hamstring tendinopathy lower hamstring tendinopathy Less common causes Nerve entrapments Ischia l bursitis Adductor magnus strains

Vascular

621 621

32 Acute knee inju ries

626

Functional anatomy

626 627

Clinical perspective Does this patient have a significant knee injury?

History Examination Investigations Menisca l injuries Clinica l features Treatment Medial co ll ateral ligament (MCl) inj ury Treatment An te rior crLIciate ligament (ACl) tears Clinical features

627 627 629 633 634 635 635 636 638 638 639 639

Surgical or non·surgical treatment of the torn ACl? Surgical treatment Combined injuries Rehabilitati on after ACl injury

647 650 652 652

Problems encountered during ACl rehabilitation Outcomes after ACL t reatment

656 657

Mechanism of ACL injury as a step toward

617 618 618 618 619 620

Avulsion of the hamstring from the ischial tuberosity

thigh

Rehabilitation after meniscaJ surgery

600 600 600 600 603 615 615 616 616 616 616 617

A promising clinical approach for the

high-risk athlete

Contents

prevention Posteri or cruciate ligament (PCl) tears Clinical featu res Treatment latera l coll ateral ligament (LCL) tears Articular cartilage damage Classification

620 620 620 621 62 1 621 62 1 621

Treatm ent Acute patell ar trauma Fracture of the patella Patellar dislocation less common causes Patellar tendon ruptu re Quadriceps tend on rupture Bursal hematoma

659 668 668 669 669 669 669 671 673 673 674 675 675 675 675

xix

Fat pad impingement Fracture of the tibial plateau Superior tibiofibular joint injury Ruptured hamstring tendon Coronary ligament sprain

677 677 677 677 677

33 Anterior knee pain

684

Clin ica l a pproach History Examination Investigations Patellofemoral pa in

685 685 687 689 689 689 690 690 693 700 700 700 700 701

What is patellofemoral pain syndrome? Functional anatomy Factors that may contribute to pain Treatment of patellofemoral pain Patellofemoral instability Primary patellofemoral instability Secondary patellofemoral instability Patellar tendinopathy Nomenclature Pathology and pathogenesis of patellar tendinopathy Clinical features Investigations Treatment Partial patellar tendon tear Less common causes Fat pad irritation/impingement (insidious onset) Osgood-Schlatter lesion Sinding-Larsen-Johansson lesion Quadriceps tendinopathy Bursitis Synovial plica

34 Lateral, medial, and posterior knee pain Latera l knee pain

Clinical approach Iliotibial band friction syndrome Lateral meniscus abnormality Osteoarthritis of the lateral compartment of the knee

xx

701 701 701 702 707 707 707 708 708 708 709 709

715 715 716 718 722 723

Excessive lateral pressure syndrome Biceps femoris tendinopathy Superior tibiofibular joint injury Referred pain Medial knee pain Patellofemoral syndrome Medial meniscus abnormality Osteoarthritis of the medial compartment of the knee Pes anserinus tendinopathy/bursitis Pellegrini-Stieda syndrome Medial collateral ligament grade 1 sprain Poster ior knee pa in Clinical evaluation

Popliteus tendinopathy Gastrocnemius tendinopathy

Baker's cyst Other causes of posterior knee pain

35 Leg pa in

723 724 724 725 725 725 726 726 727 728 728 728 728 730 731 731 732 735

735 736 738 History 738 Examination 743 Investigations Medial tib ia l stress fractu re 745 746 Assessment 746 Treatment 747 Prevention of recurrence Stress fract ure of the a nterio r cortex of the tib ia 747 747 Treatment Medial tibial stress syndrome 748 749 Treatment Chronic exertiona l compartment syndrome 750 752 Deep posterior compartment syndrome Clin ica l pe rspect ive Role of biomechanics

Anterior and lateral exertional compartment syndromes Outcomes of surgical treatment of exertional compartment syndrome Rehabilitation following compartment syndrome surgery Less common causes Stress fracture of the fibula Referred pain Nerve entrapments

753 754 755 755 755 755 756

Vascular pathologies Developmental issues Periosteal contusion

756 756 756

Autologous blood and platelet-rich plasma

756 757

Surgical treatment

Combined fractures of the tibia and fibula, and isolated fractures of the tibia Isolated fibula fractures

Medications Adjunctive non-operative treatments Electrophysical agents Insertiona l Achill es tend inopathy, ret roca lcanea l b ursit is and Haglund's disease

36 Calf pai n

761

Cli nical perspective

761 763 763 766 766 766 768 769 769 769 770 770 772 772 773 773

History EXamination Investigations Gast rocnemius muscle strain s Acute strain "Tennis leg" Chronic strain Soleus muscle stra in s Accessory sole us Less commo n ca uses Vascular causes Referred pain

Nerve entrapments Superficial compartment synd rome Co nd it ions not to be m issed

Relevant anatomy and pathogenesis Clinica l assessment Treatment

776

Functional ana tomy

776 777 778 778 782

Cl inica l perspective History Exami nation Investigations Midportio n Achi lles tenclinopathy-basic science and clin ica l features

783

Histopathology and basic molecular biology Predi sposing factors-clinica l Clinical features

783 784 784

Practice tips relating to imaging Achilles tendinopathy Midportion Ach illes tend inopathy- treatment

785 785

Targeted eccentric exercise including th e Alfredson program Nitric oxide donor therapy Injections

786 788 788

795 795 796 796

Achi ll es tendon rupture (comp lete)- d iag nosis and init ial man agement

797

Rehabilitation after initial management of Achilles tendon rupture Timing the return to jogging and sports Longer term rehabilitation issu es Posterior impingement syndrom e

Sever's d isease Les s commo n causes Accessory soleus Other causes of pain in the Achilles region

797 799 799 800 80 1 801 801 802

38 Acute ankle inju ries

806

Functional anatomy

806 807 807 808 810 811

Cl inical perspective

37 Pain in the Achilles region

794 794 794 794 795

History Examination Investigations Lateral ligament injuries Treatment and rehabilitation of lateral ligament injuries Less common ank le joint injuries Medial (deltoid) ligament injuries Pott's fracture Maisonneuve fracture

812 816 816 816 817

Persistent pain after ankle sprain - lithe problem an kle" Clinical approach to the problem ankle Osteochondral lesions of the talar dome

817 817 818

Avulsion fracture of the base of the fifth metatarsal Other fractures Impingement syndromes Tendon dislocation or rupture Anteroinferior tibiofibular ligament injury

819 819 822 822 823 xx i

Post-traumatic synovitis Sinus tarsi syndrome Complex regional pain syndrome type 1

824 824 825

Stress fracture of the base of the second metatarsal Fractures of the fifth metatarsal Metatarsophalangeal joint synovitis

39 Ankle pain

828

Medial ankle pa in

828 828 830 832 833 834 835 835 835 836 836 837 838 839 839 839 840 840 841

Clinical perspective Tibialis posterior tendinopathy Flexor hallucis longus tendinopathy Tarsal tunnel syndrome Stress fracture ofthe medial malleolus Medial calcaneal nerve entrapment Other causes of medial ankle pain Latera l ankle pa in Examination Peroneal tendinopathy Sinus tarsi syndrome Anterolateral impingement Posterior impingement syndrome Stress fracture of the ta lus Referred pain Anterior ankle pain Anterior impingement of the ankle Tibialis anterior tendinopathy Anteroinferior tibiofibular joint injury

(AITFL)

First metatarsophalangeal joint sprain ("turf toe") Hallux limitus Hallux valgus ("bunion") Sesamoid injuries Plantar plate tear Stress fracture of the great toe Freiberg's osteochondritis Joplln's neuritis Morton's interdigital neuroma Toedawing Corns and ca lluses Plantar warts Subungual hematoma Subungual exostosis Onychocryptosis

41 The patient with longstanding symptoms: clinical pearls Diag nosis-is it correct? History

842

Examination Investigations

40 Foot pain

844

844 Clinical perspective 846 Plantar fasciitis 847 Fat pad contusion 850 Calcaneal stress fractures 851 Lateral plantar nerve entrapment 851 Midfoot pa in 852 Clinical perspective 852 Stress fracture of the navicular 853 Extensor tendinopathy 855 Midtarsal joint sprains 855 Lisfrancjoint injuries 856 Less common causes of midtarsal joint pain 859 Forefoot pa in 861 Clinical perspective 861 Stress fractures of the metatarsals 862 Rea r foo t pain

xx ii

864 865 866

Time to revisit treatm ent Is there a persisting cause? Obtain details of treatment Make the multidisciplinary team available Keeping profess ional ethics in mind Summary

867 868 869 869 870 872 872 872 872 872 873 874 873 874 875

878 878 879 881 882 883 883 883 885 885 885

Special groups of participant s 42 Th e young er athlete

888

The uniqu eness of th e you ng athlete

888 888 888 889 890 890

Nonlinearity of growth Maturity-associated variation Unique response to skeleta l injury Managemen t o f mu scu loskeletal condi tions Acute fractures

Shoulder pai n Elbow pain Wrist pain Back pain and postural abnormalities Hip pain Knee pain Painless abnormali ties of gait Foot pain

892 893 893 894 895 897 899 900

Guidelines for part icipati on and injury preve nti on Resistance t raining: a specia l case Nutrition for the younger ath lete Energy Protein Carbohydrates Fat Vitamins and minerals Thermoregu lation and hydration Violence in youth sport The "ug ly pa rent " syndrome Coaches' role

43 Women and activity-related issues across the lifespan Overview Sex and gender differences

901 901 902 903 903 903 903 904 904 904 905 905

Girlhood Adolescence

910

Osteoporosis Coronary heart disease The pelvic floor and continence issues Exercise guidelines

926 926 926 928 928 929

44 The older person who exercises

936

Successful aging

936 936 937 937 937

The card iovascular system The respi ratory system Diabetes Osteoarthritis Bone health and prevention of fall-related fractures Psychological function Risks of exercise in the older person Reducing the risks of exercise Exercise prescr ipti o n for the older person The inactive older person The generally active older person in the o lder person

937 937 937 937 938 938 938

system

911 91 1 912

Other cardiac drugs

Beta blockers Diuretics Nonsteroidal anti-inflammatory drugs

939 939 939 939 939

Medications affecting the central nervous system

913

939

Medicati ons affecting the renin-angiotensin

910 910

Effect of the menstrual cycle on performance

Menopause

In tera ction between medication and exercise

The lifespan approach to women and physical activity

Older adu lt

Insulin and oral hypoglycemic drugs

940 940

Menstrual irregularities associated with exercise

914

Complications of exercise-associated menstrual cycle irregularities

916

Treatment of exercise-associated menstrual cycle irregularities

918

Eating disorders and inten se athletic activity Adult women Injuries Breast care Exercise and pregnancy Postpartum exercise

919 919 919 920 922 925

45 Military perso nnel

943

Spec ial cu ltu re among mili tary personne l

943 944 945 946 946 947 948 948 948 949

Epidemiology of mili ta ry injuri es Co mmon military inj uries Overuse injuries of the lower limb Blister injuries Pa rachu ting injuries The ag ing defense forces Inj ury prevention strateg ies in th e m il itary Injury surveillance Fema les and injury risk

xxii i

-

Contents

"

.1>

Body composition Previous Injury Weekly running distance Running experience Competitive behaviors Warm-up/stretching Co ncl usio n

95 1 952 952 953 954 954 954

,

.

f " ......

, ,I'"

':l

Definitive care The prim ary survey in detail Basic life support Airway with cervical spine control Breathing and ventilation Circulation and hemorrhage control

Disability (and neurological status) Exposure and environment control

4 6 Th e a thlet e w ith a d isability

960

Hi stor ical perspect ive

960 961 961 962 962 964 965 965 965

Hea lth be nefits of physical activity Choosing a suitable sport The sportsperson w it h a physica l d isability Spinal cord injury and sports medicine The sportsperson with a limb deficiency The sportsperson with cerebral palsy The sportsperson classified as Les Autres The sportsperson w ith visual impairment The sporrspe rson w ith an in tellec t ual impairment Class ification

Win ter sports and com mo n inj uries An ti-dopi ng iss ues Travel with teams

Recomm end ed general and emergency medical eq uipment

994

48 Sudde n cardi a c deat h in sport

996

Incidence of sudden cardia c death

996 997 998 998 998

Sex and race as risk factors Which sports carry the highest risk Et io logy of sudden card iac death in ath letes Overview SCD due to congenital or genetic structural heart disease

967 968 968 968

1005 SCD due to acquired cardiac abnormalities 1008

SCD due to congenital or genetic abnormalities predisposing to primary electrical disorders of the heart

Evalua t ion of an ath lete for co ndi t io ns caus ing sudden ca rdia c death History Physical examination

12-lead ECG/ EKG Echocardiography

Ma nagem e nt of medical problems

Further investigations

47 Medical emerge n c ies in the spor t in g context

Pu rpose of screen ing

972

Em erg ency care principles Preparation Triage Primary survey Resuscitate and stabilize Focused history Secondary survey Reassessment

xx iv

1008 1008 1009 1009 1009 1009 1013

Primary prevention of SCD in athletespre· participation cardiovascular screen ing

1013

Secondary prevent ion-responding when

Th e role of th e physiotherapis t in emergency care

1000

966 966

Adap ting pe rfo rma nce testin g and trai ni ng for disa bl ed spor tspeo pl e

Appropriate use of analges ia in trauma

976 976 976 977 986 988 991 992 994

972 972 973 973 973 975 975 975 976

an athl ete has co ll apsed Recognition of sudden cardiac arrest Management of sudden cardiac arrest Cardiopulmonary resuscitation

Early defibrillation

1014 1014 1014 1015 1015

,'Z!' • '"'C:: I: 'ii' ,

"I- : . ..,., ... ,

49 Managing cardiovascular symptoms in sportspeople

Contents Pathophysiology

1024

Cardiovas cular symptoms: po tentially life

or death decisions

1024

The clinica l approac h to potentially importan t

ca rd iac symptoms Cli nical approach to sym ptoms associated

1025

1025 Syncope/near-syncope 1026 Unexplained seizure activity 1027 Exertional chest pain 1028 Palpitations 1028 Excessive fatigue or dyspnea with exertion 1029

w ith card iac conditions

Clinical approach to physical examina tion findings Specific physical exami nat ion fi ndings Hypertension Heart murmur Marfan syndrome Non-i nvasive cardiovascu lar testing Electrocardiogram (ECG/ EKG)

1029 1030 1030 1031 1031 1032 1032 1033 1033

Summary

1035 1035

bronchospasm Sin us-related symptoms

Investigations Management of sinusitis Othe r exercise-re lated conditions Exercise-induced anaphylaxis Cholinergic urticaria angioedema

Commo n respi ra tory symptoms Shortness of breath and wheeze Cough Chest pain or tightness Ast hma Epidemiology Clinical features Types of asthma Precipitating factors Risk factors Asthma management Exercise -induced bronchospasm Epidemiology

1049 1051 1051 1051 1052 1052 1052 1052

5 1 Gastrointestinal symptoms during exercise 1056 Upper gastro intestinal symptoms Treatment Gastroin tes tinal bl eed ing Abdominal pai n Treatment Lactose intolerance Celiac disease Irritable bowel syndrome

50 Respiratory symptoms during exercise

1043 1043 1043 1043 1044 1047

Conditions that may mimic exercise-induced

Exercise and gast rointestinal diseases

Temporary and permane nt disquali fication from sports

Bronchial provocation challenge tests

Treatment

Diarrhea

Genetic testing when there is a family history of early sudden cardiac death?

Clinical features Diagnosis

Treatment

Echocardiography and associated tests for structural disease (cardiac CT, MRI)

Etiology

1057 1057 1057 1058 1058 1058 1059 1059 1059 1059 1059

Non -steroidal anti-infla mmatory drug s

1038 1038 1038 1039 1039 1040 1040 1040 1040 1041 1041 1042 1042 1042

(NSAIDs) and the gastrointestinal t ract

1059

Prevention of gastrointestina l symptoms that occur wi th exercise

1060

Limit dietary fiber intake prior to competition

1060

Avoid solid foods during the last three hours prior to the race Select the pre -event meal carefully Prevent dehydration

1061 1061 1061

Avoid fat and protein intake during exercise Sample pre-event diet Consult a sports psychologist

1061 1061 1061

xxv

52 Renal symptoms during exercise

1063

Clin ical anatomy and physiology

1063 1064 1064 1065

Exercise-rela ted renal impa irment Rhabdomyolysis and myoglobinuria Other exercise-related renal impairment

1065

Cli nica l approach to t he ath lete present ing

w it h proteinuria

1065

1082

Effects of physical activity on stroke

mortality

of stroke patients should be used? Parkinson's disease

1066

Exercise and the patient w ith renal im pairment 1066 Exercise for patients with renal Prevention of rena l complications of exercise

53 Diabet es mell itus

1070

Types of diabetes

1070 1070 1070 1070 1070

Clin ical perspect ive Diagnosis Pre-exercis e screen ing for people with diabetes Complications Trea tment Pharmacotherapy in diabetes Dietary management Exercise and diabetes

1071 1071 1071 1071 1072 1073

1074 Exercise and type 1 diabetes 1074 Exercise and type 2 diabetes 1075 Diabetes and competition 1075 Diabetes and travel 1075 High-risk sports 1075 Exercise and the complications of diabetes 1075 Benefits of exerci se

Complications of exercise in the di abetic sp ortsperson

Hypoglycemia Diabetic ketoacidosis in the athlete

1078 1078 1079

Musculoskeletal manifestations of diabetes Concl usion

1083 1083 1083

of Parkinson's disease?

1079 1080

1083

What exercise or physical activity program Multiple sclerosis

1084 1084

Does physical activity prevent the onset of multiple sclerosis or cause exacerbations?

1084

Does physical activity reduce symptoms of multiple sclerosis?

1084

What exercise or physical activity program

should be used?

1085

Special considerations for exercise in patients with multiple sclerosis Dizz in ess

1085 1085

Does physical activity prevent the onset of dizziness

1086

Does physical activity reduce dizziness symptoms

1086

What exercise or physical activity program

should be used Mi ld cogn itive impairment and dementia

1086 1086

Does physical activity prevent the onset of cognitive impairment and dementia

1087

Does physical activity minimize the progression of cognitive impairment and reduce dementia symptoms

1087

Mechanisms that underpin the effect of exercise DepreSSion

1087 1088

Does physical activity prevent the onset of mood disorders?

1088

Does physical activity reduce depreSSion symptoms?

xxvi

1082

Does physical activity prevent the onset of Parkinson's disease?

should be used?

Type 1 diabetes Type 2 diabetes

1082

Does physical activity reduce symptoms

1067 1067

transplantation

Stroke

What exercise or physical activity program

Non-ste roidal anti-inflammatory drugs

(NSAIDs) and th e kidney

1082

Effect of physical activity in the treatment

Clinica l approach to the athlete present in g w ith hematuria

54 Exercise to treat neurological d iseases and improve mental hea lth

1089

.... ,

"',

"

l'

tf

. What exercise or physical activity program

should be used? Anxiety

1089 1089

Does physical activity prevent the onset of anxiety disorders/symptoms?

Does physical activity reduce anxiety symptoms?

1089 1090

What exercise or physical activity program

should be used?

55 Joint-related symptoms without acute injury The pat ient wi t h a single swollen joint

Clinical perspective The patient with low back pain an d stiffness Clinical perspective

1090

1093 1093 1093 1096 1096

The pat ient presenting w ith mUltiple painfu l

1097 Clinica l perspective 1097 The patie nt wi th joint pain w h o "h urts all over" 1099 joints

Ordering and interpreting rheumatological tests Rheumatoid factor Erythrocyte sedimentation rate Antinuclear antibodies

HLA 827 Serum uric acid

1100 1100 1100 1100 1100 1101

56 Common sports-related infections 1102 Exercise and infect ion Exercise and the immune system Exercise and clinical infections Infection and athletic performance Common infect ions in athletes Skin infections

1102 1102 1103 1104 1105 1105

Respiratory and ear nose and throat infections Gastrointestinal and liver infections Ot her infections Human immunodeficiency virus (HIV) Sexually transmitted infections Tetanus

'.,

'

,

"'.' -I'

-...,-".

Contents

57 The tired ath lete

1118

Clinical perspective

1119 1119 1120 1120 1120

History Examination Investigations

Overtraining syndrome Development of the overtraining

1120 Clinical perspective 1121 Central fatigue and overtraining 1124 Monitoring of overtraining 1125 Prevention of overtraining 1125 Treatment of the overtrained sportsperson 1126 Viral illness 1126 Nutritional deficiencies 1126 Depletion of iron stores 1126 Glycogen depletion 1127 1127 Inadequate protein intake Chronic fatigue syndrome 1127 1127 Definition 1128 Etiology 1128 Symptoms 1128 Management syndrome

Chronic fatigue syndrome and the sportsperson

1129

Summary

1129 1129

58 Exercise in the heat

1132

Mechan isms of heat gain and loss

1133 1133

Other ca uses of t ired ness

Clinical perspective Heatstroke-a tempe rature above 41 °C

(106' F) Management of heatstroke Is hospital admission indicated? Complications of heatstroke

1108 1110 1113 1113 1114 11 14

Preventative measures and red ucing risk of infections

- -

Exe rcise-associated co llapse

1135 1135 1136 1136 1137

Management of exercise-associated collapse/exercise-associated postural

hypotension (EAPH) Cramps Management of cramps Fluid overload: hyponatremia

1137 1138 1138 1138

1114

xxvii

r

Contents

_

hyponatremia (EAH) and exerciseEtiology of EAH and EAHE

1139 1139

Other causes of exercise-related collapse in hot weathe r Heat acclimatizat ion

_.

60 Quick exercise prescript ions for specific med ical condition s

Management of exercise-induced associated postural hypotension (EAHE)

'

1141 1142

Introduction Obesity Card iovascu lar disease Myocardial infarction Post- cardiac surgery Cardiac insufficiency

59 Exercise at t he extremes of cold

Hypertension

and alt it ude

1146

Generation of body heat

1146 1146 1146 1147 1147 1147 1147

Chron ic obstructive pulmonary disease

1147 1147 1148

Promotion of bone health and preventio n of

Heat loss Minimizing heat loss Measurement of body temperature Effects of hypothermia Cardiovascular effects Respiratory effects Other effects General principles of managing hypothermia Clinical features of hypothermia Methods to achieve rewarm ing Passive rewarming Active rewarming Other rewarming methods Treatment of hypotherm ia in sport Treatment of mild hypothermia Treatment of moderate hypothermia Treatment of severe hypothermia Treatment of immersion hypothermia Frostbite Superficial frostbite- management Deep frostbite- management Prevention of co ld inj uries Exerc ise and physical activity at altitude Itinerary- ascent rate Previous altitude history

1148 1148 1148 1148 1149 1149 1149 1149 1149 1150 1150 1150 1150 1151 1151 1151

Patient characteristics and previous medical history General preventive measures Prophylactic medications Specific issues for sportspeople Sum mary

xxviii

Hyperlipidemia Asthma Diabetes End-stage renal disease Cancer Arthritis Low back pain

1158 1160 1160 1161 1161 1162 1163 1164 1164 1164 1165 1166 1166 1167 1168

fall-rela ted fractures (for patients d iagnosed wit h osteoporosis) Parkinson's disease Depressive symptoms

1168 1169 1169

Practica l sports medicine 61 The prepart icipation physica l evaluation Obj ectives Setting the tone Specific objectives Who sh oul d underg o t he PP E? Wh o sh ould perfo rm t he PPE? When t o pe rform t he PP E? Where to co nduct t he PP E? What to in cl ude in t he PPE?

1152 1153 1154 1155 1155

1158

History Physical examination Diagnostic tests What is "c lea rance"? Conclusio ns

1176 1176 1176 1176 1178 1178 1178 1178 1179 1179 1179 1179 1181 1182

62 Screening the elite sportsperson Aims of scree ni ng an elite sports perso n

Additional benefits of screening When shou ld sportspeop le be screened?

1185 1185 1185 1186

The screeni ng protocol

1186

The medical screening

1192

Card iovascular screening

1192

Medical health

1193

Baseline data collection

1194

Muscul oskeleta l screen in g

1194

Which tests?

1194

Imaging

1195

Injury prevention

1195

Performance screening

1198

Advantages and disadvantages of sc reen ing

1199

Professional relationship with the sportsperson

1199

Education

1199

Problems

1199

63 Providi ng team care

1203

Th e off-field team

1203

Coaching and fitness staff

1203

Prevention of jet lag

1213

Ti med light exposure and avoidance

1214

Timed me latonin pjlls

1215

sleeping schedule

Synergistic approach Symptomatic treatment for jet lag

1215 1215 1217

The med ica l room

1217

Illness

1218

Traveler's diarrhea

1218

Upper respiratory tract infections

1218

Inj ury

1218

Drug testi ng local contacts

1218

Psycholog ica l sk il ls

1218

Pe rsona! copin g ski lls- susta inabi lity

1218

65 Medica l coverage of end urance events

1221

Ra ce organization

1221

1218

The medica l team

1222

First-aid stations

1222

M ed ica l facility at the race fi nish

1223

Conclus ion

1225

66 Drugs and t he ath lete

1228

Pre-season assessment

1204

Educate team members-healt h literacy

1204

Other essent ials

1204

Non-approved substances at all tim es (i n and

Facilities

1204

ou t of competitio n)

Record-keeping

1204

Prohi bi ted substa nces all times (in and

Confidentiality

1205

out of com pet ition)

1229

The"team clinician's bag"

1205

Anabolic agents

1229

Being part of the "team chemistry"

1206

Peptide hormones, growth factors and

64 Traveling with a team Prepa ration Things to do before travel

1208 1208 1208

Assessing team members' fitness prior to departure

1209

Advice for team members

1209

The medical bag

1210

Clinician's hip bag

1212

Self-preparation

1212

Air t ravel and jet lag

1212

Pathophysiology

1212

1228

related substances

1237

Beta-2 agonists

1241

Hormone antagonists and modulators

1242

Diuretics and other masking agents

1242

Pro hi bited methods at all tim es (in and o ut of com petitio n)

1243

En hancement of oxygen transfer

1243

Chemical and physical manipulation

1244

Gene doping

1245

Prohibited substances in-com pet it ion

1248

Stimulants

1248

Narcotics

1250

Cannabinoids

1251

xxix

GIuco co rticoste raids

1251

Substances prohibi ted in particular sports in-competition Alcohol

Beta blockers

1252 1252 1252

Therapeutic use of a prohibited substance (therapeutic use exemption) Permitted substances Rece ntly deleted drugs Caffeine Non-intentiona l doping in sports Dru g testi ng Testing procedure The ro le of the team clinician

xxx

1252 1253 1253 1253 1254 1254 1254 1256

67 Ethics and sports medicine

1261

Con flict of interest

1261

The clinician's duty: the team or the sportsperson?

1263

Local anesthetic injection and administration of analgesics Short-term gain, long-term pain Informed consent

1263 1264 1264

Guidelines for resolution of conflict of

Ethics in sport

1265 1265 1266 1266 1268 1268

Index

1271

interest Confidentiality The media

Perfo rma nce-enhancing drug s Infectious diseases

Preface "Helping clinicians help patients" has been the clear focus of Clinical Sports Medicine from its inception. This fourth edition (CSM4l builds unashamedly on its 2o-year history. Twenty-year history? The more than 100 contributing authors average 15 years of practical experience each, so you are holding well over 1500 years of distilled clinical wisdom in your hand! If you will permit us some level 5 evidence (expert opinion-see all-new Chapter 3), CSM4 provides clinicians in sports and exercise medicine and physiotherapy/physical therapy at least five major benefits: • The wholehearted commitment from leading clinical faculty from all over the English-speaking world means that CSM4 provides the reader with an authoritative text-you can trust these authors. • At [270 pages and 67 chapters, CSM4 already carries 25% more pages than the best-selling third edition. Our ruthless editing to focus on clinical relevance means this edition contains 40% new material. CSM4 provides a comprehensive base for your clinical library. We provide some specific examples below. • With more than 1000 color images (photos and graphics), the book paints a million words (1000 pictures each painting 1000 word sl) over and above its 1270 pages! More than 200 of those images are new to this edition-customized for CSM4's learners-further extending the book's clarity and usability. • Every copy of CSM4 comes with a code that gives you online access to more than four hours of assessment and treatment video and audio material. Called Clhdcal Sports Medicille masterclasses, this material is integrated with the text and wi ll be free of charge to book owners for 12 months from registration at www.clinicalsportsmedicine.com. You have "the expert in the room. " • Reflecting the expanding evidence base for our field, we include an introduction to evidence-based practice (Chapter 3). All authors aimed to incorporate the best available level of evidence via text, tables, and current references. The online content of CSM4 will benefit from regular updates, adding fur ther to the usefulness of this text for busy clinicians. In short. CSM4 provides excellen t value as an authoritative clinical foundation for physio therapists, medical practitioners, osteopaths, massage therapists, podiatrists, sports/athletic trainers, sports therapists, fitness leaders, and nurses. It has also proven popular for students in sports physiotherapy, medicine. and human movemen t studies/kinesiology.

Editors and authors As the task of editing a book of this magnitude was beyond the two of us, the CSM4 reader now benefits from

the wisdom and productivity of seven sports and exercise medicine greats- Roald Bahr, Steven Blair, Jill Cook. Kay Crossley, fenn y McConnell, Paul McCrory, and Timothy Noakes. The quality of our chapter authors, representing more than 14 countries, grows with each edition. Among our all-star cast, we are particularly grateful to H Il'CimiqlU.'

augmen ted with reverse sixes and calcaneal slings

Wherever thi s icon appears in t he book, go to the website to view a video or listen to a podcast. Access is via the pincode card located in the front of the book.

anchored to lhe lower leg.

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RE C O M M EN DED W E B SITES

Barton q. Bonanno D. M('nz H R. Devdopme nl .lOd

evaluation of:l 1001 for thl' assessmC'nt of foot\IICar characteristics: www.ncbi.nlm.nih.. gol'/pmc/anides/ .. pub med

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First-class content As with previous editions the emphasis is on treatment and rehabilitation. The chapters in Part B. w hich address regional problems, are heavily illustrated with clinica l photos, relevant imaging, and anatomica l illustrations.

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factors

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Fig ure 1.3 Socioecological model of physical activity

Sports an d exercise medic i n e

B

RECOMMENDED WEBSITES

4. Khan KM, Davis Je. A week of physical inactivity has similar health costs to smoking a packet of cigarettes.

British Joumal oiSports Medicine: www.bjsm.bmj.com Exercise is Medicine: www.exerciseismedicine.org International Society of Physical Activity and Health:

Br J Sports Med 2010;44(6):395.

). Blair SN. Physical inactivity: the bigges t public health problem of the 21st century. Br J Sports Med

www.lspah.org

II

200 9 ;43(1) :1- 2.

RECOMMEND ED READ I NG

6. Muller-Rie menschneider F, Reinhold T, Nocon M et al. long-term effectiveness of interven tions promoting

Blair SN. Physical inactivi ty: the biggest public health

physical activity: a systematic review. Prev Med

problem of the 21st century. BrJ Sports Med 2oo9;43{I):I-2, Booth FW, Chakravarthy MV, Gordon SE, Spangenburg EE.

2008;47141'354- 68. 7. Khan KM, Tunaijia H AI. As different as Venus and

Mars: time to distinguish efficacy (can it work?). Dr J

Waging war on physical inactivity: using modern molecular ammunition against an ancient enemy.

J Appl P/IVSio/ 2002;93(1) :3- 30. F-I IlJ;I 1,

Sports Med 2011;45(10):759-60. 8. Booth FW, Chakravarthy MV, Gordon SE el at Waging war on physical inactivity: using modern molecular ammun ition against an ancient enemy. J Appl Physiot

REFERENCES Booth FW, Gordon SE, Carlson

q

2002;93(1):3- 3° ·

et al. Waging

war on modern chronic diseases: primary

9. Morris IN. Exercise in the prevention of coronary heart disease: today's best buy in public health. Med Sci Sports

prevention through exercise biology. J App! Physio/

Exerc 1994;2G (7):807-14.

2000;88(2)774- 87· 2. Katzmarzyk PT, Janssen I. T he economic costs

10, Muller-Riemenschneider F, Reinhold T, Willich SN. Cost-effecliveness of inlelVentions promoting physical

associated with physical inactivity and obesity in Canada: an upda te. Can J Appl Physio/ 2Oo4;29{I):9D-115· 3. Davis Je. Marra CA, Robert:;on MC et al. Economic evaluation of dose-response resistance training in older women: a cost-effectiveness and cost-utility analysis.

Osteoporos Int 201I:22(S):1355-66.

activity. Br) Sports Malzoo9;43(1)7o-G . [I.

Sallis

r. Owen N. Ecological models. In: Glanz K,

Lewis F. Rimer B (eds). Health behavior and healll!

education. San Francisco: Jossey-Bass. 1997:4°3- 24. 12. Khan KM, Weiler R. Blair SN. Prescribing exercise in primary care. 8M) 20 U;343='414I.

5

You may have the greatest bunch of individual stars in the world, but ifthey don't play togethe,; the club wo,,:t be wOlth a dime. Babe Ruth Sports and exercise medicine includes: injury prevention, diagnosis, treatment, and

rehabilitation management of medical problems

exercise prescription in health and in chronic disease

states the needs of exercising in special sub populations the medical care of sporting teams and events medical care in situations of altered physiology, such as at altitude or at depth performance enhancement through training,

nutrition, and psychology ethical issues, such as the problem of drug abuse in

sport.

Because of the breadth of content, sports and exercise medicine lends itself to being practiced by a multidisciplinary team of professionals with specialized skills who provide optimal care for the athlete and improve each other's knowledge and skills.'-7 The adage that a "champion team" would always beat a "team of champions" applies to sports and exercise medicine. This team approach can be implemented in a multidisciplinary sports and exercise medicine clinic or by individual practitioners of different disciplines collaborating by cross-referral.

The sports and exercise medicine team The most appropriate sports and exercise medicine team depends on the setting. In an isolated rural community, the sports and exercise medicine team may consist of a family physician or a physiotherapist/physical therapist alone. In a populous city, the team may consist of: 6

physiotherapist/physical therapist sports physician massage therapist exercise specialist for exercise prescription athletic trainer orthopedic surgeon radiologist podiatrist dietitian/nutritionist psychologist other professionals such as osteopaths, chiropractors, exercise physiologists, biomechanists, nurses, occupational therapists, orthotists, optometrists coach fitness adviser. In the Olympic polyclinic, an institution that aims to serve all 10 000 athletes at the games, the sports medicine team includes 160 practitioners (Table 2.1).

Multiskilling The practitioners in the team have each developed skills in a particular area of sports and exercise medicine. There may also be a considerable amount of overlap between the different practitioners. Practitioners should aim to increase their knowledge and skills in areas other than the one in which they received their basic training. This "rnultiskilling" is critical if the practitioner is geographically isolated or is traveling with sporting teams. The concept of multiskilling is best illustrated by example. When an athlete presents with an

Spo rt s a nd ex e rc ise med ici n e: t he t e a m a p proach Table 2 .1 The clinical team structure for the preparation in advance of the 2012

london Summer Olympic Games

Administration/organ ization (health professional background in brackets) Chief Medical Officer (sports and exercise medicine) medical manager (nursing)

polyclinic manager (nursing)

4 x"duster"venue managers-serving multiple venues (nursing or hospital/health services management) (In addition, for the Games themselves, 30 additional venue medical managers provide administrative/organizational support.)

Clinical consulting Leads in each of: sports and exercise medicine physical therapies (including oversight for massage, chiropractic, osteopathy)

polyclinic (emergency med icine-trained clinical director-with support from dentistry and podiatry) emergency medicine imaging pharmacy veterinary (In addition, for the 3-week period of the Games themselves, 3000 additional clinicians volunteer.)

overuse injury of the 10wer limb. the podiatrist or biomechanist likely has the best knowledge of the relationship between abnormal biomechanics and the development of the injury. in clinical biomechanical assessment, and in possible correction of any biomechanical cause. However. it is essential that other practitioners, such as the sports physician, physiotherapist/physical therapist and sports/ athletic trainer, all have a basic understanding of lower limb biomedlanics and are able to perform a clinical assessment. Similarly, in the athlete who presents complaining of excessive fatigue and poor performance, the dietitian is best able to assess the nutritional state of the athle te and determine if a nutritional deficiency is responsible for the patient's symptoms. However, other practitioners such as the sports physician, physiotherapist/physical therapist, or trainer must also be aware of the possibility of nutritional deficiency as a cause of tiredness, and be able to perform a brief nutritional assessment.

The sports and exercise medicine model The traditional medical model (Fig. 2.r) has the physician as the primary contact practitioner with subsequent referral to other clinicians. The sports and exercise medicine model (Fig. 2.2 overleaf) is different. The athlete's primary professional contact is often with a physiotherapist/physical therapist; however, it is just as likely to be a trainer,

[ Massage therapist

II

Figure 2.1 The traditional medical

Dietitian

model

physician, or massage therapist. It is essential that all practitioners in the health care team understand their own strengths and limitations, and are aware of who else can improve management of the patient.

The challenges of management The secret of success in sports and exercise medicine is to take a broad view of the patient and his or her problem. The narrow view may provide amelioration of symptoms but will ultimately lead to failure. An example of a narrow view is a runner who presents with shin pain, and is diagnosed as having a stress fracture of the tibia, and is treated with rest until free of pain. Although it is likely that in the short term the athlete will improve and return to activity, there remains a high likelihood of recurrence 7

Fundamenta l princ i p l es

I

Dietitian

l:r

)I

Trainer

Athlete-Coach

I I[

I'f.

) t Massa5l,e therapist!

Others Figure 2.2 The sports and exercise medicine model

of the problem on resumption of activity. The clinician must always ask "Why has this injuryJi1lness occurred?" The cause may be obvious- for example, recent sudden doubling of training load-or it may be subtle and, in many cases, multifactorial. The greatest challenge of sports and exercise medicine is to identify and correct the cause of the injury /

illness. The runner with shin pain arising from a stress fracture may have abnormal biomechanics, inappropriate footwear, a change of training surface, or a change in quantity or quality of training. In medicine, there are two main challenges-diagnosis and treatment. In sports and exercise medicine, it is necessary to diagnose both the problem and the cause. Treatment then needs to be focused on both these areas.

Diagnosis Every attempt should be made to diagnose the precise anatomical and pathological cause of the presenting problem. Knowledge of anatomy (especially surface anatomy) and an understanding of the pathological processes likely to occur in athletes often permit a precise diagnosis. Thus, instead of using a purely descriptive term such as "shin splints," the practitioner should attempt to diagnose which of the three underlying causes it could be-stress fracture, chronic compartment syndrome, or periostitis-and use the specific term. Accurate diagnosis guides precise treatment. However, some clinical situ· ations do not allow a precise anatomical and pathological diagnosis. For example, in many cases oflow back pain, it is clinically impossible to differentiate between potential sites of pathology. In situations

8

such as these, it is necessary to monitor symptoms and signs through careful clinical assessment and correct any abnormalities present (e.g. hypomobility of an intervertebral segment) using appropriate treatment techniques. Diagnosis of the presenting problem should be followed by diagnosis of the cause of the problem. The US orthopedic surgeon Ben Kibler has coined the term "victim" for the presenting problem, and "culprit" for the cause. s Diagnosis of the cause often requires a good understanding of biomechanics, technique, training, nutrition, and psychology. Just as more than one pa thological process may con· tribute to the patient's symptoms. a combination of factors may cause the problem. As with any branch of medicine, diagnosis depends on careful clinical assessment, which con· sists of obtaining a history, performing a physical examination, and organizing investigations. The most important of these is undoubtedly the history; unforhmately, this is often neglected. It is essential that the sports clinician be a good listener and develop skills that enable him or her to elicit the appropriate information from the athlete. Once the history has been taken, an examination can be performed. I t is essential to develop examination routines for each joint or region and to include in the examination an assessment of any potential causes. Investigations should be regarded as an adjunct to, rather than a substitute for, adequate history and examination. 9 The investigation must be appropriate to the athlete's problem, and provide additional information; it should only be performed if it will affect the diagnosis and/or treatment.

Spor t s a nd e xe rci se me d icin e : the t e am ap p roach Treatment Ideally, treatment has two components-treatment of the presenting injury (illness and treatment to correct the cause, Generally. the majority of sports and exercise medicine problems will not be corrected by a single fann of treatment. A combination of dif. ferent forms of treatment will usually give the best results. Therefore, it is important for clinicians to be aware of the variety of treatments available and to appreciate when their use may be appropriate. It is also important for clinicians to develop as many treatment skills as possible or, alternatively, ensure access to others with particular skills. It is essential to evaluate the effectiveness of treatment constantly. If a particular treatment is not proving to be effective. it is important firstly to reconsider the diagnosis (Chapter 41). If the diagnosis appears to be correct, other treatments should be considered.

Meeting individual needs Every patient is a unique individual with specific needs. Without an understanding of thi s, it is not possible to manage the athlete appropriately. The patient may be an Olympic athlete whose selection depends on a peak performance at forthcoming trials, or he or she may be a non-competitive business executive whose jogging is an important means of coping with everyday life, or a club tennis player whose weekly competitive game is as important as a Wimbledon final is to a professional. Altematively, the patient may be someone to whom sport is not at all important but whose low back pain causes dis comfort at work. The cost of treatment should also be considered. Does the athlete merely require a diagnosis and reassurance that there is no major injury? Or does the athlete want twice-daily treatment in order to be able to play in an important game? Treatment depends on the patient's situation, not purely on the diagnosis.

The coach, the athlete, and the clinician The relationship between the coach, the athl ete, and the clinician is shown in Figure 2.3. The clinician obviously needs to develop a good relationship with the athlete. A feeling of mutual trust and confidence

Athlete

r - -c-o-. ..... Figu re 2.3 The relationship between the coach, the athlete, and the clinician

will lead to the athlete feeling that he or she can confide in the clinician and the clinician feeling that the athlete will comply with advice. As the coach is directly responsible for the athlete's training and performance, it is essential to involve the coach in clinical decision making. Unforhmately, some coadles have a distrust of clinicians; however, it is essential for the coach to understand that the clinician is also aiming to maximize the performance and health of the athlete. When major injuries occur, professional athletes' agents will be involved in discussions. Involving the coach in the management plan is essential for athlete compliance. The coach win also be valuable in supervising the recommended treatment or rehabilitation program. In addition, discussion with the coach may help to establish a possible technique-related cause for the injury. Ethical issues that arise with respect to patient confidentiality are discussed in Chapter 67.

"Love thy sport" (and physical activity!) To be a successful sports and exercise clinician it is essential to be an advocate for physical activity. A good understanding of a sport confers two advantages. Firstly, if clinicians unders tand the physical demands and technical aspects of a particular sport, it will improve their understanding of possible causes of injury and also facilitate developmen t of sport-specific rehabilita tion programs. Secondly, it will result in the athlete having increased confidence in the clinician. The best way to understand the sport is to attend training and competition, and ideany to participate in the sport. Thus, it is essential to be on site, not only to be available when injuries occur, but also to develop a thorough understanding of the sport and its cul ture.

9

Fundamental p rinciples

II

health problem oflhe 21St century. BrJ Sports Med

RECOMMENDED R E ADING

Batt ME. Maryon-Davis A. Sport and exercise medicine: a timely specialty development. C/ilt J Sport Med

2ooTI7(2):85-6 .

3.

future? Scott MedJ 2.OIO;55(2):2. 4-

Blair SN. Physical inactivity: the biggest pUblic health

problem of the

21St

2OO7:I7(2):85-6. 5.

Cullen M, Batt ME. Sport and exercise medicine in the

2oo5;39(5):25o-I. 6.

Noakes TD. The Tole of the faculty of sports and exercise medicine for public health and elite athlete care. Br J Sports Med.

m I.

2010

2.

10

7.

Hahn A. Sports medicine, sports science: the multidisciplinary road to sports success. ] Sci Mal Sport

8_

2oo4;7(3):275- 7Kibler WB, Sciascia A. Current concepts: scapular dyskinesis. BrJ Sports Mal 2010;44(5):300-5.

Brukner PD, Crossley KM, Morris H et al. Recent advances in sports medicine. Med J Au5t

Harland RW. Essay: Sport and exercise medicine-a personal perspective. Lancet 2005;366 Suppl I:S53-4'

Nm':44(I4):998-IOOl.

REFERENCES

Cullen M, Batt ME. Sport and exercise medicine in the United Kingdom comes of age_ Br J Sports Med

United Kingdom comes of age. Br J Sports Med

2oo5:39(5):25o-I.

Batt ME, Maryon-Davis A. Sport and exercise medicine: a timely specialty development. elinJ Sport Med

century. BrJ Sports Med

2oo9;43{I):I-2.

20°9;43(1):1-2. Robison S. Sports and exercise medidne-a bright

9.

Coris EE, Zwygart K, Fletcher M et al. Imaging in

2006;184(4):188-93_

sports medicine: an overview. Sports Med Arthrosc

Blair SN. Physical inactivity: the biggest public

20°9;17(1):2- 12.

Chapter 3

, I

SI ERRI'NGTON

Randomized trials are for clinicians wlto are uncertain as to wltetlter they are right or notand I am certain I am right. Sir Ian Chalmers, quoting an unnamed orthopedic surgeon This chapter opens with an exercise we use to in troduce the concept of evidence-based practice to final-year students in human movement sciences/ kinesiology (i.e. non-clinicians). If you are an experienced clinician or an expert on evidence-based practice you may want to skip over this chapter! The "'case" for the students to consider involves Mrs J, a 55-year-old woman. Students are told she presents with persistent knee pain due to osteo-

You are asked to advise Mrs J, a 55-year-old woman with knee osteoarthritis, as to whether or not knee arthroscopy is a good idea. You have your own per-

sonal opinion, and you obtain the following four pieces of further information. Which of the four options carries the most weight with you? Would you advise that surgery is a good idea? 1. Dr X, an expert knee surgeon, advises in favor of surgery because "I have done hundreds of these operations and obtained good or excellent results in over 90% of them ." The surgeon offers you and your friend the phone numbers of patients who can provide testimonials. You call a few of these patients and they all vouch for surgery. 2. A published study of cases done by another surgeon, DrY, shows that 75% of patients who have had this type of surgery reported improvements. Overall 7596 of parients had an "excellent or good" outcome. Patients were recruited and interviewed two years after the surgery.

arthritis. The students are given the information in the box (below) and are asked to suggest a treatment for Mrs j. In our student exercise we call for a vote and every year the firs t ballot results in option I (surgery) receiving about 80% of the votes! We then lea.d an open-class discussion and emphasize that the quality of the data should carry more weight than the clinical training of the person providing the advice. Students

3. A published study examined patie nts who had presented with knee pain to a specialist in osteoarthritis two years earHer. One group of patients had undergone arthroscopic surgery, the other had not. Patients who had undergone surgery reported playing more golf and tennis than those who had not undergone arthroscopic surgery. The

paper concluded that surgery was associated with superior outcomes compared to conservative management. 4. A physiotherapy student obtained ethics approval to attend doctors' offices and recruit patients with knee osteoarthritis. The surgeon decided to allocate patients randomly to either "surgery" or "no surgery:'Two years later, the student interviewed the patients again and found that both groups of patients (those who had had surgery and those who had not) had similar levels of pain and function . Both groups had pain scores of around 50 out of 100 where 100 is severe pain.

11

Fundamental princip l es review the options and many begin to see the tions of options It 2, and 3- The evidence in option 4 is designed to mimic an important randomized trial that addressed this question.! (We deliberately avoid the word "randomized" as students are sensitized to this being important, even before they really under· stand study design.) The aim of this introduction to the course is for students to link quality of evidence and decision making. This sounds axiomatic, but our experience over many years reinforces that at first students fail to distinguish "evidence" from "eminence." Students find this practical exercise much more meaningful than a soporific lecture on "research methods." Students are then primed to engage with the literature with a view to making "quality decisions" together with patients.

Life before evidence-based practice Clinicians trained after the year 2000 might be surprised that the term "evidence-based medicine" first appeared in I99I. l Professor Paul McCrory describes that dark period before as a time of "eminence-based practice" but he jests. Nevertheless, a certain amount of clinical training relied on wisdom passing down from mentor to mentor. When clinical trials were few, the opinionated veteran was king. This is understandable in an emerging field.

Sackett and the McMaster contribution Dr David Sackett and colleagues from McMaster University3-5 described a pedagogical approach to evidence·based practice (Fig. Fl. This type of health care reflects "the conscientious, explicit and judicious use of current best evidence in making decisions about the care of individual patients. Evidencebased practice integrates individual clinical expertise with the best available clinical evidence from systematic research."> Since the mid 1990S, evidencebased practice has been facilitated by the Cochrane Collaboration (www.cochrane.org), which conducts and publishes high-quality systematic reviews of randomized trials of effects of interventions to address a wide range of health problems. Applying approach to the case of Mrs J (boxed item p. II), we note that many patients with that clinical presentation have been encouraged to have immediate arthroscopy, based on "expert opinion." They have not been provided with the full range of options that have been evaluated in research. Armed with the information that is freely available through 12

'Evid ence-based practice' is t he integra ti on of best research evidence w it h clinical expertise a nd patient values- Dave Sackett

Figure 3.1 Schematic illustration of how clinical skills, evidence from research, and patient desire should overlap to provide the "quality decision"for the patient * evidence-based practice

PubMed, the "best evidence" is that a well-conducted randomized controlled trial (RCT), systematic review, or meta-analysis (Fig. }2) suggests that arthroscopy is no better than placebo. The pieces of evidence provided in options I to 3 in the boxed item on page II represent a much lower level of evidence-data with much greater potential for bias and, hence, potentially flawed conclusions. However, "evidence" is not synonymous with randomized trials alone. If there is a question about clinical prognosis, or patient experiences, the best evidence comes from other study designs. 6 (See also Recommended reading.) Different study designs provide different quality evidence (Fig. 302). The levels in this figure map

Randomized controlled

trials (RCTs)

Cohort studies Case-controlled studies Case series/reports Background information/expert opinion Figure 3 .2 Hierarchy of study designs

I ntegrat i ng evidence into cli n i ca l practice

closely, but not perfectly, to the Oxford "levels of evid· ence" shown in Table 3.1. We use the Oxford levels of evidence in this book. Table 3 .1 Levels of evidence

Level of evidence Study design Level 1

Systematic review of homogenous RCTs, individual ReT wi th narrow

confidence Interval

Level 2

Individual cohort study or low· quality ReT

level 3

Individual case-control studies, non-consecutive cohort study

level 4

Case series

level 5

Expert opinion

This seems obvious- so what is the problem? Evidence-based practice has in trinsic appeal: however, execution is the challenge. There are not enough individual RCTs, let alone systematic reviews or meta-analyses, to provide a body of evidence for every clinical encounter. For example, your patient might be an elite athlete who earns over US $15 0000 per week; however. unfortunately. the relevant ReT was conducted in recreational athletes whose only reward was pleasure. Also, clinical trials only provide data on "average effects" of interventions; your clinical experience means you can adjust those average effects to mate what might happen in an individual patient. For example, a highly motivated individual might be expected to do better than average with an exercise intervention- where compliance is important. In your office, you need to marry three thingsthe patient's wishes, the clinical evaluation you performed to make a diagnosis, and the evidence (Fig. 3.1). 111ese elements were all part of Sackett's

original definition of evidence-based practice) Unfortunately, some "radical" advocates of pseudoevidence-based practice forget the importance of the patient's wishes and your clinical evaluation, and they focus purely on the evidence component. If given license, those folk (usually disempower clinicians who work with real people; these radicals devalue cli nicians' previous experience and patient wishes. If you are a clinician, don't be disempowered. Embrace evidence-based practice as additional value for your patients. Evidence·based practice helps you distinguish evidence from propaganda (advertisement), probability from certainty, data from assertions, rational belief from superstitions, and, ultimately, science from folklore. 1 By incorporating new evidence, your skills are con tinually updated-you are not stuck in a time warp where you practice today as you did in your year of graduation! In summary, the health professions combine the art of caring for people with the best that science has to offer. The healing part can be likened to the community "shaman" -or healer. The patient's perspective and wishes are critical to reaching a "quality decision," The days of paternalism should be behind us. And remember that the plural of "anecdote" is not "data"! 9 In summary, the purpose of this chapter is to provide a perspective on evidence-based practice and to encourage interested readers to follow up with their own searches on the topic. Use the Recommended reading below. Evidence-based practice and clinical reasoning form key parts of the curriculum fo r students in all health disciplines; this chapter is not meant to provide a comprehensive text for that! Enjoy your evidence-based practice classes and remember that the key is to integrate clinical acumen with the evidence to meet the patient's needs (Fig. J.I)! That way you'll make quality clinical decisions!

13

Fundamenta l p r inc i ples

II

RECOMMENDED WEBS lIES

Centre for Evidence-Based Medicine: www.cebm.net The Cochrane Collaboration: www.cochrane.org

IElI

RECOMMENDED READ I NG

Herbert R, Jamtvedt G, Mead J et al. Practical evidence-based

physiotherapy. Edinburgh: Elsevier, 2005.

m

4.

Sackett DL, Rosenberg WM. On the need for evidence-

5·

based medicine. Health Eeol1 1995;4(4):249-54Sackett DL, Straus S, Richardson WM etal. Evidence-

based medicine: how to practice alld teach EEM. London: Churchill Livingstone, 2000. 6.

7.

REFERENCES

1.

Kirkley A, Birmingham TR, litchfield RB et al.

8.

A randomized trial of arthroscopic surgery 2oo8;359{II):1097-107·

Guyatt G, Evidence-based medicine. ACP Journal Club

3·

Sackett DL Evidence-based medicine. Lancet

I99 I;A-r6:I44_

1995;346 (89 83): Il7I.

14

1996;312(7023):71-2. Dawes M, Summerskill W, Glasziou P et al. Sicily

statement on evidence-based practice. BMC Med Educ

for osteoarthritis of the knee. N Eng! J Med 2.

Herbert R, Jamtvedt G, Mead J et al. Practical evidencebased physiotherapy. Edinburgh: Elsevier, 2005. Sackett DL, Rosenberg WM, Gray JA et al. Evidencebased medicine: what it is and what it isn't. BM]

2005;5(1):1.

9.

McCrory P. Research realpolitik. Br] Sports Med

Chapter 4

There are a lot of myths about my ;.njur;es. They say I have broken every bone in my body. Not true. But I have broken 35 boltes. I had surge,)' '4 times to pilt and plate. [ shattered my pelvis. [forget all of the things that have broke. Evel Kn ievel Sports injuries can occur during any s porting activity. event, or training session. Injuries can affect a varie ty of musculoskeletal struchlres such as muscles, ligaments, and bones. They can b e classified by location, type, body side, and injury event. An injury may be categorized as being either an

acute injury or an overuse injury depending on the mechanism of injury and the onset of symptoms (Table +1). This chapter will review acute inju· ries, while the subsequent chapter (Chapter 5) will describe overuse injuries. Acute injuries may be due to extrinsic causes (such

Ta ble 4.1 Cl assification of spor ting injuries Site

Acute injuries

Overuse injuries (Chapter 5)

Bone

Fracture Periosteal contusion

Stress fracture "Bone

reaction"

Osteitis, periostitis Apophysitis Articular cartilage

Osteochondral!chondral fractures Minor osteochondral injury

Joint Ligament Muscle

Dislocation

Chondropathy (e.g. softening, fibrillation, fissuring, chondromalacia) Synovitis

Subluxation

Osteoarthritis

Sprain/ tear (grades HII)

Inflammation

Strain/tear (grades I-III)

Chronic compartment syndrome

Contusion

Delayed onset muscle soreness

Cramp

Focal tissue thickening/ fibrosis

Acute com pa rtment syndrome Tendon

Tear (complete or partial)

Tendinopathy (includes pararenonitis, t enosynovitis,

Bursa

Traumatic bursitis

Bursitis

Nerve

Neuropra>eia

Entrapment

tendinosis, tendonitis)

Minor nerve inju ry/irritation Altered neuromechanicalsensitivity Skin

Laceration

Blister

Abrasion

Callus

Puncture wound

15

Fundamenta l p r inciples as a direct blow) as a result of contact with another

player or equipment, or intrinsic causes (such as a ligament sprain or muscle tear). As shown in Table 4.1, acute injuries may be classified according to the particular site injured (e.g. bone, cartilage, joint, ligament, muscle, tendon, bursa, nerve, skin) and the type of injury (e.g. fracture, dislocation, sprain. or strain).

(a)

(b)

(c)

(d)

Bone Frachue Fracrures may be due to direct trauma such as a blow, or indirect trauma such as a fall on the outstretched hand or a twisting injury. Frachlres may be closed, or open (compound), where the bony fragment punctures the skin. Fractures are classified as transverse, oblique, spiral, or comminuted (Fig. +1). Another type of fracture seen in athletes, particularly children, is the avulsion fracture, where a piece of bone attached to a tendon or ligament is torn away. The clinical features of a fracture are pain, tenderness, localized bruising, swelling, and, in some cases, deformity and restriction of movement. Fractures are managed by anatomical and functional realignment. Non-displaced or minimally displaced fractures can be treated with bracing or casting. Displaced fractures require reduction and immobilization. A displaced, unstable fracture requires surgical stabilization. There are a number of possible complications of fracture . These include: infection acute compartment syndrome associated injury (e.g. nerve, vessel) deep venous thrombosis/pulmonary embolism delayed union/non-union mal-union.

Infection is most likely to occur in open (compound) fractures. Prophylactic antibio tic therapy is required in the treatment of any open frac ture. Occasionally a fracture may cause swelling of a muscle compartment that is surrounded by a nondistensible fascial sheath, usually in the flexor compartment of the forearm or the anterior comparhnent of the lower leg. This condition-acute muscle compartment syndrome-causes pain out of proportion to the fracture, pain on passive stretch, pulselessness, and paresthesia. This may require urgent fasciotomy, that is, release of the tight band of tissue surrounding the muscle compartment. 16

Fig ure 4.1 Types of fracture (a ) transverse (b) oblique

(e) spiral (d) comminuted

Sports injuries: acute Occasionally, deep venous thrombosis and pulmonary embolism may occur after a fracture. especially a lower limb fracture. This should be prevented by early movement and active muscle contraction. Delayed union. or mal-union of a fractu re causes persistent pain and disability that may require bone grafting, with or without internal fixation. The problems of immobilization are discussed in Chapter 13. If immobilization is required for fracture healing, muscl e wasting and joint stiffness will occur. Muscle wasting can be reduced by the use of electrical muscle stimulation and by isometric muscle contractions. Joint stiffness can be reduced by the use of limited motion braces instead of complete immobili· zation, or by the use of surgical fixation. which allows early movement. Growth plate fractures in children and adolescen ts present a particular problem. These fractures are reviewed in Chapter 42. Soft tissue injury. such as ligament or muscle damage, is often associated with a fracture. and may cause more long-term problems than the fracture its elf. Thus it is important to address the soft tissue components of any bony in; ury. Specific fractures that are common in athletes are discussed in Part B (Chapters '7-4').

1. disruption of the articular cartilage at its deeper layers with or without subchondral bone damage, while the articular surface itself remains intact (Fig. 4.2a) 2. disruption of the articular surface only (Fig. 4.2b) 3. disruption of both articular cartilage and subchondral bone (Fig. 4.2c). Prognosis is related to the depth the injury extends toward the underlying bone. I Factors affecting return to sport include age, duration of symptoms, number of previous injuries, associated injuries. lesion type. size, and location/ Articular cartilage may be injured by acute shearing injuries such as dislocation and subluxation. Common sites of chon dral and osteochondral injuries are the superior articular surface of the talus. the disruption of deep articular cartilage

Periosteal injury Acute periosteal injuries are uncommon. Like frachues, they can be extremely painful. Examples of periosteal injury include the condition known as a "hip pointer," an injury to the periosteum of the iliac crest caused by a direct blow, and periosteal injury of the tibia resulting from a blow from a kick, stick,

Ib)

disruption of articular surface only

or ball.

Articular cartilage Articular cartilage lines the ends of long bones. It provides a low-friction gliding surface, acts as a shock absorber, and reduces peak pressures on underlyi ng bone.I These injuries are far more common than was previously realized. Increased participation in recreational and competitive sports has now been linked to a growing risk of articular cartilage injuries, especially concerning the knee. These injuries ifleft untreated can result in premature osteoarthritis of the joint and in turn affect activities of daily living.l.2. With the advent of MRI a nd arthroscopy, it is now possible to di stinguish three classes of articular cartilage injUIies (Fig. 4-2):

lei i of arti cular cartilage and su bchondral bone

Figure 4.2 The three types of articul ar cartilage injury 17

Fu ndamenta l principles femoral condyles, the patella, and the capitellum of the humerus. Osteochondral injuries may be associated with soft tissue conditions such as ligament sprains and complete ruptures (e.g. anterior cruciate is often normal, ligament injury). As an initial the clinician must maintain a high index of suspicion of osteochondral damage if an apparently "simple joint sprain" remains painful and swollen for longer than expected. These injuries should be investigated with MRI. Arthroscopy may be required to assess the degree of damage and to remove loose fragments or to perform chondroplasty (smooth loose edges of damaged articular cartilage). Acute damage to articular cartilage is present in association with complete ligament ruptures; and may predispose to premature osteoarthri4 Therefore, every attempt should be made to restore the smooth surface of the articular cartilage. Immobilization has a detrimental effect on articular cartilage but continuous passive movement may help counter this effect. Articular cartilage has a limited capacity to regenerate or repair due to its avascular nature. The larger the lesion or defect the lower the probability Treatment aims to restore the structural integrity and function. This is important in athletes whose joints are required to withstand significant stresses during their sport. Currently a range ofinterventions exist to encourage cartilage repair. Interventions can be broadly classified into bone marrow stimulation techniques, joint debridement and drilling, autologous chondrocyte implantation, and osteochondral transplantation (mosaicplasty).l Great debate continues as to which treatment approach for symptomatic chondral and osteochondral defects is most effective. Research is required on the long-term effects of the various treatment options. It is important to identify articular cartilage injuries in children and adolescents before skeletal maturity. Chondral lesions, either diagnosed after MRI or during arthroscopic procedure, are more prevalent than meniscal or ligamentous injuries in skeletally immature patients admitted to hospital following acute knee trauma.'

Joint Dislocation/subluxation Dislocation of a joint occurs when trauma produces complete dissociation of the articulating surfaces of the joint. Subluxation occurs when the articulating 18

{al

(b)

Fi gure 4.3 (a) Subluxation and (b) dislocation of a joint

surfaces remain partially in contact with each other (Fig. +3). The stability of a joint depends on its anatomy. The hip is relatively stable because it has a deep ball and socket configuration, whereas the shoulder is far less stable because it has a small area of bony contact. Less stable joints (such as the shoulder and fingers) are more likely to dislocate. More stable joints (such as the hip, elbow, ankle, and subtalar joints) require much greater forces to dislocate and are, therefore, more likely to be associated with other injuries (e.g. fractures, nerve and vascular damage). All dislocations and subluxations result in injuries to the surrounding joint capsule and ligaments. Complications of dislocations include associated nerve damage (e.g. axillary nerve injury in shoulder dislocations) and vascular damage (e.g. brachial artery damage in elbow dislocations). All dislocations should be X-rayed to exclude an associated fracture. Dislocated joints, in most cases, can be reduced relatively easily. Occasionally muscle relaxation is required and this is achieved either by the use of an injected relaxant such as diazepam or by general anesthetic. After reduction, the joint needs to be protected to aIlow the joint capsule and ligaments to heal. Where possible, early protected mobilization is encouraged. Subsequent muscle strengthening gives the joint increased stability. Management of common dislocations (e.g. shoulder dislocation) is detailed in Part B.

Ligament The stability of a joint is increased by the presence ofa joint capsule of connective tissue, thickened at points of stress to form ligaments. Ligaments are made up

Spo r ts i n j uri e s: ac ut e of closely packed collagen fibers and provide passive joint stability. c. Load is transferred in the direction of the ligament from bone to bone. Injuries occur when a ligament is under excessive load. Ligament injuries range from mild injuries ing the tearing of only a few fi bers to complete tears of the ligament, which may lead to instability of the joint. Ligament injuries are divided into three grades (Fig. 4-4). A grade I sprain represents some stretched fibers bu t clinical testing reveals normal range of motion on stressing the ligament. A grade II sprain involves a considerable proportion of the fibers and, therefore, stretching of the joi nt and stressing the li gament show increased laxity but a definite end point. A grade III sprain is a complete tear of the ligament with excessive joint laxity and no firm end point. Although grade ITT sprains are often painful, they can also be pain-free as sensory fibers are completely divided in the injury. The m anagement of arute ligament sprains is summarized in Figure +5 overleaf. The initial m anagement consists of first aid to minimize bleeding and swelling (Chapter 13). For grade I and grade II sprains, treatment aims to promote tissue healing. prevent joint stiffness, protect against further da mage. and strengthen muscle to provide additional joint stability. The healing of collagen in a partial ligament tear takes several months7 8 However, depending on the degree of damage, rerum to sport may be possible sooner than this. especially with protection against further injury. A recent review of the evidence on acute ankle sprains demonstrated a period of at least six weeks to three months before ligament healing occurred. 9 From six weeks to one year, 31% of subjects continued to have objective mechanical la xity and subj ective ankle instabili ty. Therefore protection for return to physical activity and sport should be considered because of the moderate risk of fe-injury with continual instability. The treatment of a grade III sprain may be either conservative or surgical. For exam ple, the torn medial collateral ligament of the knee and the tom lateral ligament of the ankle may be treated conservatively with full or partial immobilization. Alternatively, the two ends of a tom ligam ent can be reattached surgically and the joint then fully or partially immobilized for approximately six weeks. In celtain instances (e.g. anterior cruciate ligament rup ture), torn ligament tissue is not amenable to primary repair and surgical ligament reconstruction may be required (Fig. 32.10 on page 65 1).

(aJ

(bJ

(eJ

Figure 4.4 ligament sprai ns (a ) grade I (bl grade II (eJ grade III

19

Fundamental p r inc i p l es

L-__

,1

L ! _ _- ,_ _

J

____

First aid management

Electrotherapeutic

J, Surgery-repair

- reconstruction

modalities Joint mobilization

Solt>tissue massage

J.

or Protective bracing

J,

Muscle strengthenrng Proprioceptive training

Functional training Figure 4.5 Management of acute ligament sprains

A number of tissue engineering interventions aim to restore normal function and minimize further joint injury. Examples include the use of growth factors, gene transfer and gene therapy, cell therapy. and the use of scaffolding rnaterials. 6 . ,o However, further research is required on the effectiveness of these interventions.

Figure 4.6 Muscle strains (a) grade I (b) grade II (c) grade III

20

Muscle Muscle injuries are among the most common injuries in sports. The frequency of muscle injuries ranges from 10% to 55% of all sustained sporting injuries and includes muscle strains/tears and contusions."

Strain/tear Muscles are strained or torn when some or all of the fibers fail to cope with the demands placed upon them. Muscles that are commonly affected are the hamstrings, quadriceps, and gastrocnemius; these muscles are all biarthrodial (cross two joints) and thus more vulnerable to injury. A muscle is most likely to tear during sudden acceleration or deceleration. Muscle strains are classified into three grades (Fig. 4-6). A grade I strain involves a small number of muscle fibers and causes localized pain but no loss of strength. A grade II strain is a tear of a significant number of muscle fibers with associated pain and swelling. Pain is reproduced on muscle contraction. Strength is reduced and movement is limited by pain. A grade III strain is a complete tear of the muscle. This is seen most frequently at the musculotendinous junction.

Sports injuri es: acute

The healing of muscle injuries can be divided into three phases which are similar to those in ligament injury healing (Fig. 4.7). Inflammatory phase

Marked hematoma post injury, myofibrils contract

J. Reparative phase

Regeneration of myofibers, production of connective scar tissue

J. Remodeling phase

Maturation of regenerated myofibers, reorganization of scar tissue Figure 4.7 The three phases of muscle injury healing

Acute management of muscle strains should involve:!I·u ea rly ice and compression a short period of immobilization (depending on severity and limited to the first few days after the injury only) early gentle mobilization and range of motion exercises (depending on severity and within pain limits; avoid aggressive stretching techniques) early gentle massage of the affected muscle (massage may be best avoided for the first 24-48 hours depending on severi ty).

Early mobilization in severe cases can cause re-rupture at the original muscle injury point and therefore accurate assess ment of severity is essential. Re-ruptures cause the greatest amount of time los t from sporting activity. ll MRI scans and ultrasound can be helpful in the elite athlete but should not replace importa nt c1ini· cal assessment. Early return to activity and sport can be considered in the elite athlete. u However, return to sport should be determined by extent of muscle strain, muscle group, and demands of the sport placed on the individual athlete. A number of factors predispose to muscle strains: inadequate insufficient joint range of motion excessive muscle tightness fatigue/overuse/inadequate recovery muscle imbalance ll previous injury

faulty tech nique/biomechanics spinal dysfun ction.

Most muscle strains are preventable. Methods of injury prevention are discussed in Chapter 9. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) in the early stages of muscle strai n continues to be widely debated. The analgesic properties ofNSAIDs are not significantly better than paracetamol for musculoskeletal injury.14 However, there are more adverse effects associated with NSAIDs and therefore using paracetamol rather than an NSAID is suggested.

Contusion A muscle contusion usually results from a direct blow from an opposition player or firm contact with equipment in collision sports, such as football, basketball. and hockey. 111e blow causes local mu scle damage with bleeding. The most common site of muscle contusions is the front of the thigh in the quadriceps muscle. This injury is known as a "cork thigh," "charley horse," and also "dead leg." Management of contusion includes minimization of bleeding and swelling, followed by stretching and strengthening. Although most of these injuries are rela tively minor and do not limit participation in sport, a severe con tusion may occasionally result in a large amount of bleeding, especially if the player continues in the game after sustaining the injury. Heat. alcohol. and vigorous massage increase bleed· ing after a contusion and must be avoided. Athletes playing sports with a high risk of contusions in a specific area, such as the thigh in some football codes, should consider the use of protective equipment such as padding. The athlete must weigh up the benefit of reducing injury risk versus the reduction in mobility that may result from wearing the equipment.

Myositis ossificans An occasional complication of a muscle hema toma is myositis ossifica ns. This occurs when the hematoma calcifies. The incidence is highest in high·contact sports, such as the various foo tball codes. Although myositis ossificans is most common following more severe muscle contusions, it may also occur in relatively minor cases. Hemophilia and other bleeding disorders are risk factors. If Myositis ossificans should be suspected in any muscle contusion that does not resolve in the nonnal time frame. An X-ray or 21

Fundamental principles ultrasound performed 10 to £4 days after the injury m ay show an area of calcification. Management of myositis ossificans is conservative and recovery is usually slow.

Cramp Muscle cramps are painful involuntary muscle contractions that occur suddenly and can be temporarily debilitating. Muscle cramp either during or immediately after exercise is commonly referred to "exercise associated muscle cramping" (EAMC). EAMe can be defined as "painful, spasmodic and involuntary contraction of skeletal muscle that occurs during or immediately after exercise,"'s The most common site of muscle cramps is the calf. The enology ofEAMC remains unclear. A leading theory asc ribes its etiology to altered neuromuscular control.!,j· ,6 This theory is based on cramping occurring with repetitive muscle contraction after which increased excitatory and decreased inhibitory signals to the a-motor neuron develop. With continual muscle contraction. excess ive excitation results in a cramp. 111is accounts for immediate effectiveness of inhibitory techniques such as stretching of the muscle or electrical stimulation methods. The fact that elite soccer players rarely cramp during normal 9o-minute games but commonly suffer cramps when extra time is played would appear to support the excessive muscle contraction theory. TIle treatment of cramps is aimed at reducing muscle spindle and motor neuron activity by reflex inhibition and afferent stimulation. Passive stretching reduces mu scle electromyographic activity within IO to 20 seconds, resulting in symptomatic relief. Passive tension should be applied to the affected muscle for 20 to 30 seconds or until fascicu lation ceases, after which the muscle can gradually return to normal length. The effectiveness of passive stretching in treating EAMC offers further support for the hypothesis that abnormal spinal reflex activity is associated with EAMC. rather than a systemic disturbance, such as dehydration or electrolyte depletion. I ' There are no proven strategies for the prevention of exercise-induced muscle cramp but regular muscle stretching. correction of muscle balance and posture. adequate conditioning for the activity, mental preparation for competition. and avoidance of provocative drugs may all be beneficial. Other strategies such as incorporating plyometrics or eccentric muscle strengthening into training programs. maintai ning adequate carbohydrate reserves during competition,

22

or treating m yofascial trigger points require further investigation. 17

Tendon Complete or partial tendon ruptures may occur acutely (Fig. 4-8). Normal tendons consist of tight parallel bundles of collagen fibers. Injuries to tendons generally occur at the point of least blood supply (e.g. with the Achilles tendon usually 2 em [0.75 in.[ above the insertion of the tendon) or at the musculotendinous junction. A tendon rupture occurs without warning, usualIy in an older athlete without a histOlY of injury in that particular tendon. The two most commonly ruptured tendons are the Achilles tendon and the supraspinatus tendon of the shoulder. The main objective of the treatment of tendon injuries is to restore full motion and function. Partial tears are characterized by the sudden onset of pain and by localized tender-

(.)

(b)

Figure 4_8 Tendon rupture (a ) partial (b) complete

Sport s in j u ri e s: a cute

ness but they may be difficult to distinguish from tendinopathy (Chapter 5). When investigation is indicated, ultrasound and MRI can be useful. Bo th modalities can dis tin· guish between a partial or complete tendon ruprnre and overuse tendinopathy. Generally, acute tendon rupture requires surgical treatment followed by pro· gressive rehabilitation.

Bursa The body contains many bursae situated usually between bony surfaces and overlying tendons. Bursae are flat sacs of synovial membrane that contain syno· vial flu id. They are located where moving strucrures are in close proximity (such as between tendon and bone, muscle and bone, and ligament and bone) and facili tate movement by minimizing friction in these areas. Most injuries to bursae are associated with overuse (Chapter 5), but occasionally a direct fall onto a bursa may result in acute traumatic bursitis due to bleeding into the bursa. The management of acute hemorrhagic bursitis involves the application of ice and compression. Aspiration may be indicated if the condition does not resolve.

fibula. Specific peripheral nerve injuries can be as so· ciated with particular sports (e.g. radial nerve palsy with arm wrestli ng). The various codes of foo tball, hockey, baseball, and winter activities are associated with higher risk for these The immediate symptoms are tingli ng, numb· ness , and pa in in the distribution of the nelVe. In minor nelVe injuries the symp toms usually dimi nish quickly but in more severe injuries there will be persistent pain in the area of the distribution of the nerve. Occasionally in severe injuries there will be paralysis or weakness of the muscles innervated by that nerve, in addition to sensory loss in the sensory distribution of the nerve. While this paralysis is present th e area shou ld be supported in a brace or cas t. 111is injury, known as "neuropraxia," usually resolves spontaneously but slowly. There is in creasing awareness that minor nerve injury is a common accompanying feature of many injuries. These nerve injuries are detected clinically by changes in neuromechanical sensitivity and m ay make a significant contri bution to the patient's symptoms. The concept of neuromecharucal sensitivity is discussed more fu lly in Chapter 6.

Skin Nerve Major nerve injuries are unusual in athletes. However, a few nerves are relatively exposed and susceptible to injury from a direct blow. The nerves most often injured in this way are the ulnar nerve at the elbow, and the common peroneal nerve at the neck of the

Acute skin injuries are common in contact sports. Possible damage to underlying structures, such as tendons, muscles, blood vessels, and nerves, should always be considered Open wounds may be abrasions, lacerations, or puncture wounds. The principles of treatment of all open wounds are shown in Table 4.2.

Table 4.2 Principles of treatment of all open wounds Principle

Details

1. Stop any associated

Applya pressure bandage direct ly to the injured part and elevate it. If the wound is open and clean, bring the wound edges togethe r using adhesive strips or sutures. A contaminated wound should not be closed. Remove all d irt and contamination by sim ple irrigation. Extensively wash and scrub with antiseptic solution as required as soon as possible. If the wound is severely conta minated, prophylactic antibiotic therapy shOUld be comm e nced (e.g. nuc!oxacillin 500 mg ora lly four times a day). If anaerobic organisms are suspected (e.g. wound innicted by a bite), add a n antibiotic such as metronidazole (400 mg orally three times a day). This applies when the wou nd is over a constantly moving part (e.g. the ante rio r aspect of the knee). Certain lacerations (e.g. pretibial lacerations) require particular care and strict immobilization to encourage healing. All contaminated wounds, especia lly penetrating wounds. have the potential to become infected with Clostridium teton;. Tetanus immun ization consists of a course of three injections over 6 months given during childhood. Further tetan us toxoid boos ters shou ld be given at 5 to 10 year intervals. In the case of a poss ible contaminated wound, a booster should be given if none has been administe red within the previous 5 yea rs.

bleeding 2. Prevent infection

3. Immobilization (where needed) 4. Check te tanus status

23

Fundame n ta l princ i ples

m I.

REFERENCES

Bhosale AM, Richardson JB. Articular cartilage:

structure, injuries and review of management. Brit Mal

BuI12oo8;8T77-95· 2. Mithoefer K, Hambly K, Della Villa S et al. Return to sports participation after articular cartilage repair in the knee: scientific evidence. Ant J Sports Med 2009;37 Supp1 r:I67S-76S. 3. Engebretsen L, Fritts HM. Osteochondral lesions and cruciate ligament injuries. MRI in 18 knees. Acta Orthop ScaJJd 1993;64:434-6.

4. Myklebust G, BahT R. Return to play guidelines after anterior cruciate ligament surgery. BrJ Sports Med 20°5;39(3):127-31. 5. Oeppen RS, Connolly SA, Bencardino JT et aL Acute

injury of the articular cartilage and subchondral bone: a common but unrecognized lesion in the immature

knee. AJR 2004; r82{I):m-7. 6. Woo SLY, Abramowitch SO, Kilger Ret at Biomechanics of knee ligaments: injury, healing, and repair. ] Biomccll 2006;39(1):r-20. 7. Frank C. Ligament healing: current knowledge

Warnke PH. In-vivo tissue engineering of biological joint replacements. Lancet 2,010;376(9739):394-6.

II.

Jarvinen TAH, Jarvinen TLN, Kaariainen Metal. Muscle injuries: optimising recovery. Best Pmc Res Clin Ritmmatoi2007;2I(2):3I7-31.

12. Orchard IW, Best TM, Mueller-Wohlfahrt I-I-Wet at The early management of muscle strains in the elite athlete: best practice in a world with a limited evidence basis. BrJ Sports Med 2008;42(3):158--9.

13. Croisier J-L, Gantealtme S. Binet J et al. Strength imbalances and prevention of hamstring injury in professional soccer players: a prospective study. Am]

Sports Med 2008;36(8):1469-75' 14. Paoloni lA, Milne C, Orchard JW et al. Non·steroidal anti-inflammatory drugs in sports medicine: gUidelines for practical but sensible use. BrJ Sports Med

20°9:43:863-65.

IS. SchweUnus MP. Cause of exercise associated muscle cramps (EAMC)-altered neuromuscular contro\, dehydration or electrolyte depletion? BrJ Sports Med

200 9;43(6):4°1--8. 16. Schwellnus MP. Muscle cramping in the marathon:

and clinical applications. J Am Acad Ortllor SlIrg

aetiology and risk factors. Sports Med 200T37(4-S):

'99 6 ;474- 83-

36 4-7-

8. Frank C, Shrive N, Hiraoka H et al. Optimisation of the biology of soft tissue repair. J sci Med Sport

1999;2(3):19 0- 210 . 9. Hubbard TI, Hicks-Little CA. Ankle ligament healing

24

10.

17. Bentley S. Exercise-induced muscle cramp. Proposed mechanisms and management. Sports Mal

18. Toth C, McNeil S, Feasby T. Peripheral nervous system

after an acute ankle sprain: an evidence-based

injuries in sport and recreation: a systematic review.

approach. ] Atitl Train 2008:43(5):523-9.

Sports Med 2005:35(8):717-38.

Chapte r 5

And he's got the icepack on his groin there, so possi.bly 11 0t the old shoLdder injury. Ray French , British TV sports commentator Overuse injuries present three distinct challenges to the clinician----ciiagnosis, understanding of why the injury occurred. and treatment. Diagnosis requires taking a comprehensive history of the onset, nature, and site of the pain along with a thorough assessment of potential risk factors; for example, training and technique. Careful examination may reveal which anatomical structure is affected. It is often helpful to ask patients to perform the maneuver that produces their pain. The skilled clinician must seek a cause for every overuse injury. The cause may be quite evident, such as a sudden doubling of training quantity, poor footwear, or an obvious biom echanical abnormality, or m ay be more subt1e, such as running on a cambered surface, muscle imbalance, or leg length discrepancy. The causes of overuse injuries are usually divided into extrinsic facto rs such as training, surfaces, shoes, equipment, and environmental conditions, or intrinsic factors such as age, gender, malalignment, leg length discrepancy, muscle imbalance, m uscle weakness, lack of flexibility, and body compos ition. Possible factors in the development of overuse injuries are shown in Tabl e 5.!. Treabnent of overuse injuries will usually require addressing of the cause as well as specific additional elements such as activity modification, specific exercises to promote tissue repair, soft tissue massage, and pharmacologic agents where appropriate (Chapler I)).

Bone stress Bone stress reactions, which can develop into stress fractures, are fati gue failure injuries of the bone.

Table 5.1 Overuse injuries: predisposing factors

Extrinsic factors

Intrinsic factors

Training errors

MalaHgnment

excessive vol ume

pes planus

excessive intensity

pes cavus

rapid increase

rearfoot varus

sudden change in type

tibia vara

excessive fatigue

genu valgum

inadequate recovery

genu varum

faulty technique

patella alta

Surfaces hard

soft cambered Shoes

femora l neck anteversion tibial torsion Leg length discrepancy Muscle imbalance

inappropriate

Muscle weakness

worn out

Lack of flexibility

Equipment inappropriate Environment al conditions

generalized muscle tightness focal areas of muscle

hot

t hickening

cold

restricted joint range of

humid

motion

Psychological factors

Sex, size, body co mposition

Inadequate nutrition

Other genetic factors endocrine factors metabolic conditions

Stress fractures account fo r 0.7% to 20% of all sports medicine clinic injuries.' Track-and-field athletes have the h ighes t incidence of stress fractures compared with other athletes.'-l There is a continuum of

25

Fundamental princ ip les bone response to stress that ranges from mild (bone strain) to severe (stress fracture) (Fig. 5.1). The clinical features of bone strain, stress reaction, and stress fractures are summarized in Table 5.2. Different sites of stress fractures are associated with particular sporting activities (Fig. 5.2).

Mechanism In a normal environment, musculoskeletal integrity is maintained by a balance of fatigue damage with remodeling activity, stimulated by normal repetitive low-intensity loading forces.! The rate of remod· eling responds to the loads through the bone, which

includes the forces transferred from surrounding muscle activity. High levels of bone stress, through an increase in activity, may lead to higher rates of fa tigue damage where the remodeling response may not be able to cope. This then manifests clinically as a bone stress injury. Overload stress can be applied to bone through two mechanisms: 1. the redistribution of impact forces reSUlting in increased stress at focal points in bone 2 . the action

of muscle pull across bone.

Such overload leads to osteoclastic activity that sur· passes the rate of osteoblastic new bone formation. resulting in temporary weakening of bone. If physical activity is continued, trabecular microfracrures result and these cause early bone marrow edema seen on MRI scanning. In most cases, bone responds to these microfracrures by forming periosteal new bone for reinforcement. However, if the osteoclastic activity continues to exceed the rate of osteoblastic new bone formation, eventually a full cortical break occurs.2 A summary of the histological changes resulting from bone stress is displayed in Figure 5.}

Risk factors CT, X-ray or MRI changes Bone strain Figure 5.1 The continuum of bone stress: from silent stress reaction through to stress fracture. Stress fracture is detected by changes on X-ray, CT scan or MRI

There has been considerable research investigating the association between bone stress injuries and various risk factors (Table 5.3). Two important risk factors are (i) a rapid increase or change in the load on the bone (rapid change in volume or intensity of training), and (ii) an energy imbalance between calories expended and taken in. Energy imbalance

Table 5.2 Continuum of bony changes with overuse Clinical features

Bone stra in

Stress reaction

Stress fracture

Local pain

Nil

Yes

Yes

Loca l tenderness

Nil

Yes

Yes

X-ray appearance

Normal

Normal

Abnormal (periosteal reaction

or cortical defect

in cortical bone, sclerosis in trabecular bone)

MRI appearance

May show increased high

Increased high signal

Radioisotopic bone scan

Increased high Signal ± cortical defect

signal

Increased uptake

Increased uptake

Increased uptake

Normal

Normal

Features of stress fracture

appearance CT scan appearance

(as for X-ray)

26

Spo rt s i njurie s: ov e r us e Site of stre ss fracture

Associated sport/activity

Coracoid prOi:ess of scapula

Tra pshooting

./

Scapula

Running with hand weights

Humerus Olet:ranon Ulna

Throwing; racq uet sports Throwing; pitching Racquet sports (esp. ten nis); gymnastics; volleyball; swimming; softball; wheelchair sp orts

."

Ribs Ribs-2nd- lOth Pars interarticularis

Throwing; pitching Rowing; kayaking Gymnastics; ballet; cricket fast bowling; volleyball; springboard diving

Pubic ra mus' Femur- neck

Distance running; ballet Distance running; jumping; ballet

Femur-shaft

Distance running

Patetl"

Running; hurdling Running

Tibia- plateau

r- 5capu la

f-rlbS , - ••

".,IS I

,

I

5°); a more varus

this, scores of 0 to +5 are considered neutral. A score

rearfoot relative to the floor is given a supinated score

of +6 to +9 is considered pronated, 2:+10 is considered

(- 2 defined by I5 may optimize gait efficiency in a supinated foot (Fig. 9.IOC) . Q

)

Summary of the lower limb biomechanical assessment To iterate how we opened this section, there is no single way to perform the lower limb biomechanical assessment; it varies by clinica l speci alty (e.g. physio· therapy, podiatry, medicine, soft tissue therapy, nurse). Also, the clinical problem influences the order of the assessment, and the relative emphasis on various elements. In this introductory chapter, we ignored the tests used to assess aggravating activities which help identify a link between activity and injury. For teaching purposes, we deliberate ly outlined a simple procedure that would apply for a patient with patella femoral pain.

Forefoot sole flexion point The sale flexion point should line up with the first metatarsophalan geal joint. If the flexion point of the shoe is too proximal. stability is impaired. If the flexion point is too distal, it will impair normal sagittal plane motion of the first metatarsophalangeal joint.

Motion control propeliies Motion control is particularly important for excessive pronators. Footwear properties that influence motion coo trol include the presence or absence of a multiple densi ty sole, heel counter stiffness, midfoot torsional and sagitt al stability, and type affixation (e.g. lacing).

83

Fun d am ent al princip l e s Table 8.4 Sport·specific technique faults that experienced clinicians believe are associated with increased risk of specific injuries (levelS evidence)

Sport Tennis

Technique

Injury

Excessive wrist action with backhand

Extensor tendinopathy of elbow

Service contact made too far back (Le. bait toss

Flexor tendinopathy of elbow

not in front) Swimming

Insufficient body roll

Rotator cuff tendinopathy

Low elbow on recovery

Insufficient shoulder external rotation Diving

Cycling

Shooting at the water too early (backward dives)

Lumbar spine injuries

Incorrect handlebar and seat height

Thoracic/l umbar spine injuries

Toe-in/toe-out on cleats

iliotibial band friction syndrome, pateJlofemoral pain syndrome

Weightlifting

Bar pOSition too far in front of body in clean or

(Olympic)

jerk phase

Lumbar spine injuries Sacroiliac joint injuries

Weightlifting

Grip too wide on bar in bench press

Pectoralis major tendinopathy

(power lifting)

Toes pointing forward on squatting

Patellofemoral pain syndrome, medial meniscus injury

Javelin

Media l elbow pain Poor hip drive

Thoracic/lumbar spine dysfunction

Triple jump

"Blocking" on step phase

Sacroiliac joint/lumbar spine injuries, patellar

Highjump

Incorrect foot plant

Patellar tendinopathy, sinus tarsi syndrome,

tendinopathy, sinus tarsi syndrome

fibular stress fracture Pole vault

Too close on take-off Late plant

Lumbar spine injuries (e.g. spondylolysis) Ankle impringement, talaT stress fracture, shoulder impingement

Running

Anterior pe lvic tilt

Hamstring injuries

Poor lateral pelvic control

Iliotibial band friction syndrome

Cricket bowling

Mixed side-on/front-on action

Pars interarticularis stress fracture

Baseball pitching

Opening up too soon

Anterior shoulder instability, elbow medial collateral ligament sprains, osteochondritis of radiocapitellar joint

Gymnastics

Rowing Ballet

84

Dropped elbowHhanging"

Rotator cuff tendinopathy

Excessive lumbar hyperextension on landing

Pars interarticularis stress fracture

Tumble too short (insufficient rotation)

Anterior ankle impingement

Change from bow side to stroke side

Rib stress fractures

Poor turnout

Hip injuries, medial knee pain

"Sickl ing" en pointe

Second metatarsal stress fracture

Cl in ic a l a spe c ts of bi omec h anics an d spo r t in g inj u r i e s These properties can be quantified using the "Motion Control Properties Scale" outlined below (Table 8.5). Scores range from 0 to II, with II indicating the highest level of motion control.

Cushioning Although evidence is limited, foo twear cushioning is thought to be important for the prevention of lower

Table 8.6 overleaf li sts common lower limb injuries, common clinical considerations. and evidence to support these considerations. It contains the "best available evidence" at January 20Il . The topic of biomechanical risk factors is discussed further in Chapter 9, and in Part B of this book, which covers specific conditions .

limb stress fractures, particularly in more active populations}9 Footwear components to consider include sole density, inner soles, and the presence or absence of cushioning systems such as air and gel pockets. However, the presen ce of cushioning in the heel may have implications for the pitch of the shoe (i.e. increase heel height), with subsequent undesir· able influences on foot strike patterns (Le. inhibit forefoot striking).'

Wear patterns The wear pattern of a shoe can provide insight into the biomechanics of gait. Medial til t of the upper, m edial compression of the midsole (Fig. 8.19a), and greater m edial than lateral wear of the outs ole (Fig. 8.19b) indi cate excessive pronation. Lateral tilt of the upper, lateral compression/collapse of the mid sole. and greater lateral than medial wear of the outsole reflect excessive supination.

Conditions related to s uboptimal lowe r limb biomechanics Conventional wisdom has linked suboptimal lower limb biomechanics with various injuries, but there is a lack of prospective empirical evidence to confirm that biomechanical factors increase risk for lower limb Thus. for now, most biomechanical "risk factors" have only level 3 to 5 evidence (see Chapter 3 for more on levels of evidence).

Figure 8.19 Shoe wear patterns-running shoe With medial compression of the upper

(a)

Tab le 8.5 Motion Control Properties Scale Score

Item

0

2

Midsole density layers

Single density

Dual density

Fixation (upper to foot)

None

Alternative to laces (e.g. strap, Velcro, zip)

laces (at least 3 eyelets)

Heel counter stiffness

No heel counter

Minimal

Moderate

Midfoot sagittal stability

Minimal

Moderate

Rigid

Midfoot torsional stability

Minimal

Moderate

Rigid

3

Rigid

Minimal =>45°; moderate = , ')

Lifestyle factors Adequate rest and sleep are thought to be important in the recovery process, although there has been little research into this area. It has been shown that sleep loss following a match can interfere with performance at training the next day; however, any loss of sleep is likely to be compensated for the next night. '4 It is traditional in certain sports to overindulge in alcohol following a competition. This can have a significant negative effect on recovery. Studies in cyclists showed that muscle glycogen storage was impaired when alcohol was consumed immediately after exercise and displaced carbohydrate intake from the recovery diet.') It is likely, however, that the most important effects of alcohol intake on glycogen resynthesis are indirect-by interfering with the athlete's ability, or interest, to achieve the recommended amounts of carbohydrate required for optimal glycogen restoration.r6 A recent study showed a significant reduction in muscle function during recovery from eccentricinduced muscle damage after alcohol intake.'7

Nutrition Nutrition aids recovery from intense exercise by replenishing glycogen stores and by providing necessary protein and water. Recovery encompasses a complex range of processes that include: refueling the muscle and liver glycogen (carbohydrate) stores replacing the fluid and electrolytes lost in sweat manufacturing new muscle protein, red blood cells, and other cellular components as part of the repair and adaptation process allowing the immune system to handle the damage and challenges caused by the exercise bout.

Glycogen replacement Glycogen is the major energy source for muscular

activity (Chapter )8). Training depletes muscle and liver glycogen stores. Repetitive bouts of activity can cause profound glycogen depletion, and impair sporting performance. The major dietary factor in post-exercise refueling is the amount of carbohydrate consumed. Depending on the fuel cost of the training schedule or the need to fuel up to race, a serious sportsperson may need to consume 7-I2 g of carbohydrate per kg body weight

each day (35'>-840 g per day for a 70 kg athlete) to Figure 10.1 Compression tights

140

ensure adequate glycogen stores.

Re cove ry In the immediate pos t·exercise period, sportspeople are encouraged to consume a carbohydrate· rich snack or meal that provides 1-1. 2 g of carbohydrate per kg body weight within the first hour of finishing, as this is when rates of glycogen synthesis are greatest. This is especially important if the time between prolon ged training sessio ns is less than eight hours. The type and form (meal or snack) of carbohydrate that is suitable will depend on a number of factors , including the sportspersons overall daily carbohydrate and energy requirements, gastric tolerance, acces s and availability of suitable food options, and the length of time before the next training session. Table ]0 .1 gives examples of snacks providing at least SO g of carbohydrate. In general, the immune system is suppressed by intensive training, with many parameters being reduced or disturbed during the hours following a work-out. Th is may place sportspeople at risk of succumbin g to an infectious illness during this time. The most recent evidence points to carbohydrate as one of the most promising nutritional immune protectors. Ensuring adequate carbohydrate stores before exercise, and consum ing carbohydrate during and/or after a prolonged or high-intensity work-out, has been sh own to reduce the disturbance to immune sys tem markers. The carbohydrate reduces the stress hormone response to exercise, thus minimizing its effect o n the immune sys tem, as well as supplying glucose to fuel the activity of many of the immune system white cells.

Protein replacement Intense exercise results in breakdown of muscle tissue. Intake of protein in recovery mea ls is Ta bl e 10.1 Carbohydrate-rich recovery snacks (50 9 (HO portions)

700-800 mL sports drink 2 sports gels 500 mL fruit juice or soft drink 300 mLcarbohydrate loader drink 2 slices roastlbread with jam or ho ney or banana topping 2 cereal bars 1 cup thick vegetable soup + large bread roll 115 g (1 large or 2 small) cake-style muffins, frui t buns or scones 300 g (large) baked potato with salsa fillin g 100 9 pancakes (2 stack) + 30 9 syrup from an Austra lian Institute of Sport fac t sheet

recommended to enhance net protein balance. tissue repa ir, and adaptations involving synthes is of new pro teins. Prolonged and high-intensity exercise causes a substantial breakdown of muscle protein. During the recovery phase, there is a reduction in catabolic (breakdown) processes and a gradual increase in anabolic (build ing) processes, which continues for at least 24 hours a fter exercise. Early intake after exer· cise (within the first hour) of essential amino acid s from good-quality protein foods helps to promote the increase in protein rebuilding. Consuming food sources of protein in meals and snacks after this "window of opportunity" will fu rther promote pro tein syn thesis, although the rate at which it occurs is less. Although research is continuing in to the optimal type (e.g. casein, whey), timing, and amount of protein n eeded to maximize th e desired adaptation fro m the training stimulus , most agree that both resistance and endurance athletes will benefit from consuming 10-2 0 g of high-quality protein in the first hour after exercise. Table 10.2 lists a number of everyday foods that provide approximately IO g of protein.

Co-ingestion of carbohydrate and protein The co·ingestion of protein with carbohydrate will increase the efficiency of muscle glycogen storage when the amount ofcarboh ydrate ingested is below the threshold for maximum glycogen synthesis, or when feeding intervals are more than one hour apart. The effectiveness of protein to enhance muscle glycogen Table 10.2 Foods providing approximately 109 of protein Animal foods

Plant-based foods

40 g cooked lean beef! 120 9 tofu pork/Iamb 4 slices bread 40 g skinless cooked 200 9 baked beans chicken 60 9 nuts 50 9 canned tunal 2 cups pasta/3 cups rice salmon or cooked fish 0.75 cup cooked lentilsl 300 mL milk/glass of kidney bea ns Milo 200 g tub yoghurt 300ml flavored milk 1.5 slices (30 g) cheese 2 eggs from an Australian Inst itute of Sport fact sheet 141

Fundamental princip l es storage appears limited to the first hour after supplementation. It has been shown that glycogen storage during the first 40 minutes of recovery after exercise was twice as fast after a carbohydrate-protein feeding than after an isoenergetic carbohydrate feeding, and four times faster than after a carbohydrate feeding of the same carbohydrate concentration. ,8 This trend also continued following the second feeding two hours into recovery. The co-ingestion of protein with carbohydrate during recovery also increases protein synthesis, and results in a more positive whole-body net protein balance compared with drinks matched for total car· bohydrate,I9 Table 10.3 provides a list of carbohydraterich snacks that also provide at least IO g of protein.

Rehydration Large amounts of fluid may be lost during exertion, particularly with increasing intensity and in hot or humid conditions. It can be difficult for sportspeople to maintain fluid balance in certain environmental conditions. Athletes should weigh themselves before and after exercise and replace the weight lost with water. The majority of sportspeople finish training or competition sessions with some level of fluid deficit. Many fail to drink sufficient volumes of fluid to restore fluid balance. As a fluid deficit incurred Table 10.3 Nutritious carbohydrate-protein recovery

snacks (contain 50 9 (HO + valuable source of protein and micronutrients) 250-300 mL liquid meal supplement 300 g creamed rice 250-300 mL milks hake or fruit smoothie 600 mL low fat navored milk 1-2 sports bars (check labels for carbohydrate and protein content) 1 la rge bowl (2 cups) breakfast cereal with milk 1 large or 2 small cereal bars + 200 g carton flavored yoghurt 220 g baked beans on 2 slices of toast 1 bread roll with cheese/meat filling + large banana 300 g (bowl) fruit salad with 200 9 fruit-flavored yoghurt 2 crumpets with thickly spread peanut butter + 2S0mLmilk 300 g (large) baked potato + cottage cheese filling + glass of milk

from an Australian Institute of Sport fact sheet

142

during one session has the potential to negatively impact on performance during subsequent training sessions, sportspeopJe need to incorporate strategies to restore fluid balance, especially in situations where there is a limited amount of time before their next training session. Athletes should aim to consume 12S-I50% oftheir estimated fluid losses in the 4-6 hours after exercise. The recommendation to consume a volume of fluid greater than that lost in sweat takes into account the continued loss of fluid from the body through sweating and obligatory urine losses. Fluid replacement alone will not guarantee rehydration after exercise. Unless there is simultaneous replacement of electrolytes lost in sweat, especially sodium, consumption of a large volume of fluid may simply result in large urine losses. The addition of sodium, either in the drink or the food consumed with the fluid, will reduce urine losses and thereby enhance fluid balance in the post-exercise period. Further, sodium will also preserve thirst, enhancing voluntary intake. As the amount of sodium considered optimal for re-hydration (50-80 mmoljL) is in excess of that found in most commercially available sports drinks, sports people may be best advised to consume fluids after exercise with everyday foods containing sodium. There is considerable individual variation in sodium concentration of sweat. It may be important in high-level athletes to identify those with high sweat sodium content, and therefore sweat testing may be performed. This is performed with the use of a patch fixed to the forearm during activity (Fig. IO.2). Those with high sodium content may require additional sodium supplementation before and after activity. In considering the type of fluids needed to achieve their rehydration goals, sportspeople should also consider the length of time before their next session, the degree of the fluid deficit incurred, taste preferences, daily energy budget, as well as their other recovery goals. With the latter, athletes can simultaneously meet their refueling, repair, and some of their re-hydration goals by consuming fluids that also provide a source of carbohydrate and protein (e.g. flavored milk, liquid meal supplement).

Psychology As the nervous system controls cardiovascular function, respiration, and metabolism during and after exercise, psychological factors play an important role in recovery.

Recove ry Some organs receive input from both sympathetic and parasympathe tic nerves.

Effect of exercise on the autonomic nervous system

Figure 10.2 Sweat testing

The func tion of the autonomic nervous system After exercise. the nervous system, which functions by releasing neurotransmitters, may be substantially fatigued. The efferent cells of the peripheral nervous system are categorized into those that control skeletal muscle (somatic nerves) and those that control glands, cardiac muscle, and smooth muscle found in the walls of body organs such as the gastrointestinal tract. the blood vessels, and aiIWays (autonomic nerves). Autonomic nerves themselves are div ided in to sympathetic and parasympathetic nerves, according to both anatomical and physiological differences.

The sympathetic nervous system controls the "fight or flight" reaction, which is characterized by an adrenalin rush , tachycardia. increased cardiac outpu t, and bronchodilation. At the same time, blood is shunted away from the gastrointestinal organs to enhance muscle blood flow. Liver glycogen stores are used up to provide blood glucose. After exercise, this automatic effect should be reversed to allow muscles to relax and to replenish body stores of glycogen. If there is insufficient recovery of the nervous system, the sportsperson may remain sym pathetically aroused. This man ifests as increased resting heart rate, muscle tiredn ess, and insomnia. Sympathetic overarousal may delay absorption of nutrients from the gastrointestinal tract, as well as elevating the metabolic ra te. Over time, the sympathetic nervous system can become exhausted, and the patient develops bradycardia, an inability to utilize glycogen, and a diminution in work capacity. This psychological state parallels depression.

Techniques that aid psychological recovery Sportspeo ple who have a good unders tanding of their arousal level are generally calm and stable. They. thus, tend to place less stress on their autonomic nervous system. Specific techniques can lower arousal level. These include the use of soft tissue therapy, spas, warm baths and showers, flotation tan ks, music. visualization and relaxation tapes. As recovery is vital for optimal performance, coaches should be encouraged to incorpora te recovery time into athletes' schedules.

143

Fundamenta l princ i ples from simulated learn post exercise.] Sci Med Sport

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Gill NO, Beaven eM, Cook C. Effectiveness of postmatch recovery strategies in rugby players. Br J Sports

Med 2006;40(3):260-3. 2.

Suzuki M, Umecla T. Nakaji S et al. Effect of

incorporating low intensity exercise into the recovery period after a rugby match. BrJ Sports Med 2oo4:38{4) :436-40.

3. Andersson H. Raastad T, Nilsson J et aL Neuromuscular fatigue and recovery in elite female soccer: effects of active recovery. Mcd Sci Sports Exerc

2008;4°(2):372- 80. 4. Dawson B, Cow S, Modra. S et al. Effects of immediate post-game recovery procedures on muscle soreness, power and Aexiblity levels over the next 48 hours.

] Sci Med Sport 2ooS:8(2):210-.2.I. 5. Spencer M, Bishop D, Dawson B et aL Metabolism and performance in repeated cycle sprints: active versus passive recovery. Med Sci Sports Exerc 2006;8(1): 149 2 -9. 6. Reilly T, Cable NT, Dowzer CN. The efficacy of deep water running. In: McCabe PT, ed. Contemporary

ergonomics. London: Taylor & Francis, 2002:162- 6.

2009;I2,{3):417-2I. II.

Best TM, Hunter R, Wilcox A et a1. Effectiveness of sports massage for recovery of skeletal muscle from strenuous exercise. Oill] Sports Med 2008;r8(5): 44 6 - 60 ,

12. Kraemer Wf, Flanagan SO, Comstock BA et al. Effects of a whole body compression garment on markers of recovery after a heavy resistance workout in men and women. J Strength COlld Res 2010;24(3):8°4- 14. 13. Duffield R, Cannon J, King M. 111e effects of compresion garments on recovery of muscle performance following high-intensity sprint and plyometric exercise. J Sci Med Sport 2010;13(1):136-40' 14. Reilly T, Piercy M. The effects of partial sleep deprivation on weight-lifting performance. Ergollomics 1994:37:107-15. 15. Burke LM, Collier GR. Davis PG et aI. Muscle glycogen storage after prolonged exercise: effect of the frequency of carbohydrate feedings. Am] Clin Nut)" 1996;64: 115-19.

16. Burke LM, Kiens E, Ivy JL. Carbohydrates and fat for training and recovery.] Sports Sci 2oo4;22(1):r5-30.

7. Bleakley CM, Davison GW. What is the biochemical

17- Barnes MJ, Mundel T, Stannard SR. Acute alcohol

and physiological rationale for using cold-water

consumption aggravates the decline in muscle

immersion in sports recovery? A systematic review.

performance foHowing strenuous eccentric exercise.

Er] Sports Med 20ro;44:179-87.

J Sci Med Sport 2010;13(1):189-93-

8. Vaile J, O'Hagan C, Stefanovic B et al. Effect of cold

postexercise muscle glycogen recovery is enhanced

limb blood flow. Br j Sports Med 20II;45(IO):825-9'

with a carbohydrate-protein supplement.] Appl Pl1ysiol

9- Montgomery PG, Pyne DB, Hopkins WG et al. The effect of recovery strategies on physical performance

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water immersion on repeated cycling performance and

2002;93{4):1337-44· [9. Howarth KR, Moreau NA. Phillips SM et aI.

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water immersion methods on post-exercise recovery

1394-4 02 .

11

There is no more difficult art to acquire than the art of observation. The importance of making an accurate, pathological diagnosis cannot be overemphasized. This chapter addresses what physicians call the history and cal examination and what physiotherapists/physical therapists consider the subjective and objective assessment. Chapter 12 addresses investigations. Far too often, sporting injuries are given descriptive labels such as "swimmer's shoulder" or "tennis elbow." These terms do not represent diagnoses. Accurate pathological diagnosis is essential for several reasons: 1. It enables the clinician to explain the problem and the natural history of the condition to the athlete, who will want to know precisely for how long he or she will be affected. A patient may present with an acute knee injury, but the diagnosis of anterior cruciate ligament tear has markedly different implications from the diagnosis of minor meniscal injury. 2. Jt enables optimum treatment. Numerous conditions have similar presentations but markedly different treatments. For example, consider the differences in treatment between lateral ligament sprain of the ankle and osteochondral fracture of the talus, patellofemoral joint syndrome and meniscal tear, hamstring tear and hamstring pain referred from the lumbar spine. 3. It enables optimum rehabilitation prescription. For example, rehabilitation after shin pain due to stress fracture will be more gradual than that after identical shin pain due to chronic compartment syndrome.

....

l!i\f':) h

William Osler

When a patient presents with an overuse injury, an accurate pathological diagnosis must be supplemented by assessment of the etiologic factors underlying the condition, otherwise the injury is likely to be slow to recover and highly likely to recur.

Etiologic factors include training error, malalignment, faulty technique, and inappropriate equipment. An important etiologic factor can sometimes be identified by examining the entire "kinetic chain." Occasionally. it may be impossible to make a precise pathological diagnosis. For example, in a patient with low back pain, the exact source of the pain is often difficult to isolate. In such cases, it is still possible to exclude certain causes of low back pain (e.g. spondylolysis) and identify abnormalities such as areas of focal tenderness, altered soft tissue consistency, or abnormalities of range of motion. Treatment then aims to correct these abnormalities. How treatment affects symptoms and signs can help determine how each particular abnormality contributes to the overall picture.

Ma king a diag nosis Diagnosis relies on taking a careful history, perform. ing a thorough physical examination, and using appropriate investigations. There is a tendency for clinicians to rely too heavily on sophisticated investigations and to neglect their clinical skills. l Keys to accurate diagnosis in patients presenting with apparent musculoskeletal pain include: whether the symptoms are of musculoskeletal origin (Chapter 7)

possible local causes of the patient's symptoms

145

Fundamental princ i p l e s sites that could be referring pain to the site of the symptoms (Chapter 6)

the relevant kinetic chain (e.g. the back and lower limb in a shoulder injury of a tennis player) biomechanics (Chapter 8)

other possible causative factors (e.g. metabolic),

History His tory remains the keystone of accurate diagnosis; it will provide the diagnosis in the majority of cases. At the conclusion of taking the history. it is important to consider the differential diagnosis and the possible etiologic factors. Then proceed to a thorough, focused examination. TIle following principles need to be considered when taking a history.

Allow enough time The patient must feel that the clinician has time available to anow the story to unfold, otherwise important symptoms will not surface.;: In addition to the details of the injmy, there must he time to take the history of the training program or diet as appropriate. Look into possible causes of injury. As a minimum, 30 minutes is required to assess a patient with a new injury; however, in complex chronic cases up to one hour may be necessary.

Be a good listener TI1e clinician must let the story unravel. Appropriate body language and focus on the patient (not the medical record) help this) The sports clinician is in the fortunate position that many patients have good body awareness and are generally able to describe symptoms very well. When seeing inactive patients for exercise prescription, take the time to listen to their goals and fears (Chapter 16).

Know the sport It is helpful to understand the technical demands of a sport when seeing a sports person, as this engenders patient confidence. More importantly, knowledge of the biomechanics and techniques of a particular sport can assist greatly in both making the primary diagnosis and uncovering the predisposing factors.

Circumstances of the in jury The first task in history taking is to determine the exact circumstances of the injury. Most patients will be able to describe in considerable detail the mecha· nism of injury. In acute injuries, this is the single

146

most important clue to diagnosis. For example, an inversion injury to the ankle strongly suggests a lateral ligament injury, a valgus strain to the knee may cause a medial collateral ligament injury, and a pivoting injury accompanied by a "pop" in the knee and followed by rapid swelling suggests an anterior cruciate ligament injury.

Obtain an accurate description of symptoms An accurate description of the patient's symptoms is essential. Common musculoskeletal symptoms include pain, swelling, instability, and loss of function.

Pain Consider the characteristics of the patient's pain: 1. Location: Note the exact location of pain. A detailed knowledge of surface anatomy will enable you to determine the structures likely to be involved. If the pain is poorly localized or varies from site to site, consider the possibility of referred pain. 2. Onset: Speed of onset helps determine whether the pain is due to an acute or overuse injury. Was the onset of pain associated with a snap, crack, tear, or other sensation? 3. Severity: Severity may be classified as mild, moderate, or severe. Assess the severity of the pain immediately after the injury and also subsequently. Was the patient able to continue activity? 4. Irritability: This refers to the level of activity required to provoke pain and how long it subsequently takes to settle. The degree of irritability is especially important, because it affects how vigorously the examination should be performed and how aggressive the treatment should be. 5. Nature: This refers to the quality of the pain. It is important to allow patients to describe pain in their own words. 6. Behavior: Is the pain constant or intermittent? What is the time course of the pain? Is it worse on waking up or does it worsen during the day? Does it wake the patient at night? 7. Radiation: Does the pain radiate at all? If so, where? 8. Aggravating factors: Which activity or posture aggravates the pain? 9. Relieving factors: Is the pain relieved by rest or the adoption of certain postures? Do certain activities

Pri nciples of diagnos is: cl ini ca l assessment relieve the pain? Is the pa in affected by climatic

changes (e.g. cold weather)? 10. Associated features: These include swelling, instability, sensory symptoms such as pins and needles, tingling, or numbness, and motor symptoms, such as muscle weakness. 11. Previous treatment: What was the initial

treatment of the injury? Was ice applied? Was

should always be questioned about spinal symptoms, especially pain and stiffness in the lower back or neck. Past or present injuries in body parts that may at first seem unrelated to the present injury may also be important. For example, a hamstring injury in a throwing athlete can impair the kinetic chain leading to the shoulder, alter throwing biomechanics and. thus. contribute to a rota tor cuff injury.

lirm compression applied? Was the injured part immobilized? If so, for how long? What treatment

General health

has been performed and what effect did that treatment have on the pain?

Is the patient otherwise healthy? TI1e presence of symptoms such as weight loss and general malaise may suggest a serious abnormality (e.g. a tumor). It must be remembered that musculoskeletal symptoms are not always activity-related (Chapter 7)·

Swelling Immediate swelling following an injury may indic· ate a severe injury such as a fracture or major liga· ment tear accompanied by hemarthrosis. Record the degree of swelling-mild, moderate, or severe-and subsequent changes in th e amount of swelling.

Instability Any history of giving way or feeling of instability is significant. Try to elicit the exact activity tha t causes this feeling. For example, in throwing. does the feeling of instability occur in the cocking phase or the follow-through?

Function It is important to know whether the athlete was: able to continue activity w ithout any problems immediately after the injury happened able to continue w ith some restriction

unable to continue. Note subsequent changes in function with time.

History of a previous similar injury If the sports person has had a previous similar injury, record full details of all treatmen t given. response to each type of treatment, and whether any maintenance treatment or exercises have been performed following initial rehabilitation. Previous injury is a major risk factor for recurrence. 4

Other injuries Past injuries may have contributed to the current injury; for example. an inadequately rehabilita ted muscle tear tha t has led to muscle imbalance and a subsequent overuse injury. Because of the importance of spinal abnormali ties as a potential component of the athlete's pain (Chapter 6), the patient

Work and leisure activities Work and leisure activities can playa role in both the etiology and subsequent management of an injury. For example. a patient whose job involves continual bending or who enjoys gardening may aggravate his or her low back pain. It is important to know about these activities and to ascertain whether they can be curtailed.

Consider why the problem ha s occurred Predisposing factors should be considered not only in overuse injuries but also in medical conditions and in acute injuries. In an athlete suffering from exercise-induced asthma, symptoms may occur only during important competition if there is an underlying psychological component. Alternatively, the asthma may occur only at a particular time of the year or at a particular venue if allergy is present. An athlete with an acute hamstring tear may have a history of low back problems or, alternatively, a history of a previous inadequately rehabilitated tear. Recurrence can only be prevented by eli minating the underlying cause.

Training history In any overuse injury. a comprehensive training history is required. This is best done as a weekly diary, as most sportspeople train on a weekly cycle (Chapter 9), It should contain both the quantity and quality oftraining, and describe any recent changes. Note the total amount of training (distance or hours depending on the sport) and training surfaces. Continual activity on hard surfaces or a recent change in surface may predispose to injury. In running sports, pay particular attention to footwear (Chapter 9). For both training

147

Fundamental principl e s and competition shoes. note the shoe type, age. and the wear pattern. Record recovery activities such as massage, spa/sauna, and hours of sleep.

athlete's short- and long-term future sporting commihnents, to schedule appropriate treatment and rehabilitation programs.

Equipment

Examination

Inappropriate equipment may predispose to injury (Chapter 9 ). For example, a bicycle seat that is set too low may contribute to patellofemoral pain.

A number of general principles should be followed in an examination.' At the conclusion of the examination, the differential diagnosis and possible predisposing factors should be considered. If the practitioner is certain of the diagnosis and of the predisposing factors, then counseling and treatment can begin. However, in many cases, further information may be required and the practitioner must decide what, if any, investigations may be needed. The general principles to be followed in an examination are outlined below.

Technique Patients should discuss technique problems that either they, or their coach, have noted. Faulty tech· nique may contribute to injury. For example. a "wristy" backhand drive may contribute to extensor tendinopathy at the elbow.

Overtraining Symptoms such as excessive fatigue. recurrent illness, reduced motivation, persistent soreness, and stiffness may point to overtraining as an etiologic factor (Chapter 9).

Psychological factors Injury can be caused or exacerbated by a number of psychological factors that m ay relate to sport (Le. pressure of impending competition) or may concern personal or business life, The clinician needs to con· sider this possibility and approach it sensitively.

Develop a routine Use a specific routine for exammmg each joint, region, or system, as this forms a habit and allows you to concentrate on the findings and their significance, rather than thinking of what to do next. In Part B, we outline a routine for exami ning each body part.

Where relevant, examine the other side With some aspects of the examination (e.g.ligamentous laxity or muscle tightness), it is important to compare sides using the uninjured side as a control.

Nutritional factors

Con sider possible causes of the in jlllY

Inadequate nutrition can predispose to the overtrain· ing syndrome and m ay playa role in the development of musculoskeletal injuries. In an athlete presenting with excessive tiredness (Chapter 57), a full dietary history is essential.

Try to ascertain the cause of the injury. It is not sufficient to examine the painful area only (e.g. the Achilles tendon). Exam ine joints, muscles, and neural strucrures proximal and distal to the injured area, seeking predisposing factors (e.g. limited dorsiflexion of the ankle, tight gastrocnemius-soleus complex, lumbar facet joint dysfunction).

History of exercise-induced anaphylaxis Exercise-induced anaphyl axis lElA} and food· dependent exercise-induced anaphylaxis (FDEIA) are rare but potentially life-threatening clinical syndromes in which association with exercise is crucial. This is a clinical syndrome in which anaphylaxis occurs in conjunction with exercise. Given the rarity of the condition, our current understanding relies on case studies only)· (,

Attempt to reproduce the patient's symptoms It is helpful to reproduce the patient's symptoms if possible. This can be achieved both by active and/or passive movements and by palpation either locally or, in the case of referred pain, at the site of referral. It may require you to send the patient for a run or some other test of function prior to examination (see below).

Determine the importance of the sport to the athlete

Assess local tissues

The level of commitmen t to the sport. which will n ot necessarily correlate with the athlete's expertise, has a bearing on managemen t decisions. Be aware of the

Assess the joints, muscles, and neural structures at the site of pain for tenderness, tissue feel, and range of motion.

148

Pri nc i p l es of diag n osis: clin i cal assessment

Assess for referred pain Assess the joints, muscles, and neural structures that may refer to the site of pain (Chapter 6).

Assess neural mechanosensitivity Neural mechanosensitivity (Chapter 6) should be assessed using one or more of the neurodynamic tests (on page I50).

Examine the spine Many injuries have a spinal component to the pain or dysfunction. The presence of abnormal neural mechanosensitivity suggests a possible spinal component. In lower limb injuries, examine the lumbar spine and the thoracolumbar junction. In upper limb injuries, examine the cervical and upper thoracic spines. In particular, it is important to seek hypomobility of isolated spinal segments, as this may contribute to distant symptoms.

point in the range, and the presence of abnormal patterns of movement. In many conditions, such as shoulder impingement or patellofemoral pain, the pattern of movement is critical to making a correct diagnosis. If a patienfs pain is not elicited on normal plane movement testing, examine "combined movements" (i.e. movements in two or more planes). By combining movements and evaluating symptom response, additional information is gained to help predict the site ofthe lesion. Other movements, such as repeated, quick or sustained movements, may be required to elicit the patient's pain.

Range of motion testing (passive)

As biomechanical abnormalities are one of the major causes of overuse injuries, it is essential to include this examination in the assessment of overuse injuries (Chapter 8). The biomechanical examination of the lower limb is illustrated in Chapter 8.

Passive range of motion testing is used to elicit joint and muscle stiffness. Injury may be the cause ofjoint stiffness. Alternatively, stiffness may already have been present and predisposed to injury by placing excessive stress on other structures (e.g. a stiff ankle joint can predispose to Achilles tendinopathy). Range of motion testing should include all directions of movement appropriate to a particular joint, and should be compared both with normal range and the unaffected side. Overpressure may be used at the end of range to elicit the patient's symptoms.

Functional testing

Palpation

If a particular maneuver reproduces the patienfs pain, then have the patient perform that maneuver in an attempt to understand why the pain has occurred. This can sometimes be done in the office (e.g. a deep squat) or it may be necessary to watch the athlete perform the activity at a training venue, for example, a long jumper taking off, or a gymnast performing a backward walkover. Video analysis may be helpful.

Palpation is a vital component of examination, and precise knowledge of anatomy, especially surface anatomy, optimizes its value. At times it is essential to determine the exact site of maximal tenderness (e.g. in differentiating between bony tenderness and ligament attachment tenderness after a sprained ankle). When palpating soft tissues, properties of the soft tissue that need to be assessed include:

Biomechanical examination

The examination routine Inspection It is important to observe the individual walking into the office OI walking off the field of play. as well as inspecting the injured area. Note any evidence of deformity, asymmetry, bruising, swelling, skin changes, and muscle wasting. There may, however, be a degree of asymmetry due to one side being dominant, such as the racquet arm in a tennis player.

Range of motion testing (active) Ask the athlete to perform active range ofmotion exercises without assistance. Look carefully for restriction of range of motion, the onset of pain at a particular

resistance muscle spasm tenderness.

Palpate carefully and try to visualize the structures being palpated. Commence with the skin, feeling for any changes in temperature or amount of sweating, infection, or increased sympathetic activity. When palpating muscle, assess tone, focal areas of thickening or trigger points, muscle length, and imbalance. It is important not only to palpate the precise area of pain, for example, the supraspinatus tendon attachment, but also the regions proximal and distal to the painful area, such as the muscle belly of the trapezius muscle. Determine whether tenderness is

149

F undam e n tal p r i ncip l es

focal or diffuse. This may help differentiate between, for example, a stress fracture (focal tenderness) and periostitis (diffuse tenderness). To palpate joints correctly, it is important to understand the two different types of movement present at a joint. Physiological movements are movemen ts that patients can perform themselves. However, in order to achieve a full range of physiological movement, accessory movements are required. Accessory movements are the involuntary, interarticular movements. including glides, rotations, and tilts, that occur in both spinal and peripheral joints during normal physiological movements. Loss of these normal accessory movements may cause pain, altered range, or abnormal quality of physiological joint movement. Pal pation of the spinal and peripheral joints is based on these principles. An example of palpation of accessory movements involves posteroanterior pressure over the spinous process of the vertebra, producing a glide between that vertebra and the ones above and below.

Ligament testing Ligaments are examined for laxity and pain. Specific tests have been devised for all the major ligaments of the body. These involve moving the joint to stress a pi1rticular ligament. This may cause pain or reveal laxity in the joint. Laxity is graded into +1 (mild). + 2 (moderate), and +3 (severe) . Pain on stressing the ligament is also Significant and may indicate, in the absence oflaxity. a mild injury or grade I ligament sprain. A number ofdifferent tests may assess a single ligament: for example. the anterior drawer. Lachman's. and pivot shift tests all test anterior cruciate ligament laxity.

also produce pain. Certain movements require considerable variations in nerve length. Neurodynamic testing examines restriction ofthese nonnal mechanics and their effect on the patient's symptoms. Treatment aims to restore normal nerve mechanics. Neurodynamic tests produce systematic increases in neural mechanosensitivity by successive addition of movements that increase neural mechanosensitivity. The tests may provoke the presenting symptoms or, alternatively, other symptoms such as pins and needles, or numbness. The amount of resis tance encountered during the test is also significant, cially when compared with the uninjured side. The assessment of symptom production and resistance may be affected by each step in the neurodynamics test (Figs 11.1-11.4). This may give an indication of the location of the abnormality. The main neurodynamic tests are: straight leg raise (SLRI (Fig. 11.1)

slump test (Fig. 11.2) neural Thomas test (Fig. 11.3, on page 152) upper limb neurodynamics test (ULTT) (Fig. 11 .4. on page 153). A summary of the tests, the methods, user guidance, normal responses and variations of each test is shown in Table II.! on page ISS. A neurodynamic test can be considered positive if: it reproduces the patient's symptoms the test response can be altered by movements of different body parts that alter neural mechanosensitivity differences in the test occur from side to side and from what is considered normal.

Sh'ength testing Muscles or groups of muscles should be tested for strength and compared with the unaffected side. Muscle weakness may occur as a result of an injury, (e.g. secondary to a cluonic join t effusion), or may be a predisposing factor toward injury.

Testing neural mechanosensitivity Advances in the understanding of neural mechanosensitivity have led to improved awareness of why pain occurs in chronic overuse injuries and pain syndromes. Changes in neural mechanosensitivity are an important component of these disorders (Chapter 6). Just as restrictions of the normal mechanics of joints and muscles may contribute to symptoms. restriction of the normal mechanics of the nervous system may

150

Figure 11.1 Straight leg raise (a l Patient lies supine. The examiner places one hand under the Achilles tendon and the other above the knee. The leg is lifted perpendicular to the bed with the hand above the knee, preventing any knee flexion

Pr i n c i pl es of d i agnos i s: cl i nica l assessment

Figure 11.1 (cont.) (b ) DorsiAexion of the ankle is

added. Eversion and toe extension may sensitize this test further. Other variatio ns can be added (Table 11.1 page 155)

(b ) Patient is asked to put chin on chest and overpressure is applied

Figure 11.2 Slump test (a l Patient slu mps forward and overpressure is applied. The sacrum shou ld remain vertical

(el Patient actively extends one knee

151

Fundamental p rin c i p l es

Figure 11 .3 Neural Thomas test (a) Patient lies supine over the end of the couch in the Thomas position (d) Patient actively dorsiflexes the ankle and

overpressure may be applied

(b) Patient's neck is passively flexed by the examiner, then the examiner passively flexes the patient's (right) knee with his leg

(el Neck flexion is slowly released. Steps (d), (e). and (f) are repeated with the other knee. Other variation s can be added (Table 11 .1 page ISS)

152

Pr i nc ip les o f d i agnosis : clinica l assessm ent

Figu re 11.4 Upper limb neurodynamics test

(a) Patient lies supine close to the edge of the couch. Neck is laterally flexed away from the side to be tested (el Th e forearm is supinated and the wrist and fingers extended

(b) The shoulder is depressed by the examiner's hand (left) and the arm abducted to approximately 11 OCand

(d ) The elbow is extended to the point of onset of

externally rotated

symptoms

153

Fundamental pr i ncip l es

{el The neck position returns to neutral and is then laterally flexed towards the side of the test. Any change in symptoms is noted. Other variations can be added (Table 11.1)

Neurodynamic tests are non-specific but form an extremely useful part of the examination. Abnormalities of neural mechanosensitivity should lead the clinician to examine possible sites of abnormality, especially the spine. Neurodynamic tests can also be used as a treatment procedure. This is discussed in Chapter 13-

Spinal examination Clinical experience suggests that spinal abnormality (e.g. hypomobility) can present in various ways. The presentation may be as pain or injury and this may occur either locally (at the spine) or distantly. Examples for both upper limb and lower limb spinal abnormalities are given in Table 11.2. The pathophysiology underlying these concepts has been discussed in Chapter 6. In patients presenting with upper limb pain, the cervical and upper thoracic spines must be examined. Examine the lumbar spine (including the thoracolumbar junction) in any patient presenting with lower limb pain. An abnormal neurodynamic test strongly indicates a spinal component to the pain.

154

However, a negative neurodynamic test does not exclude the possibility of a spinal component. Begin examining the relevant area of the spine by assessing range of movement with the patient standing. The patient should then lie prone on a firm examination table so the examiner can palpate the vertebrae centrally over the spinous processes and laterally over the apophyseal joints to detect any hypomobility and/or tenderness. Hypomobility or tenderness at a level appropriate to that of the patient's symptoms indicate the site is a possible source of referred pain (Chapter 6). After detecting spinal abnormality on examination, perform a trial treatment (Chapter 13) and then reassess the patient's symptoms and signs. If there is a change in the pain and/or range of movement, then this strongly suggests that the spine is contributing to the symptoms. Occasionally, palpation of a particular site in the spine will achlally reproduce the patient's symptoms distant from the spine. It is important to understand that, even if the symptoms are not produced by palpation of the spine, this does not rule out the possibility of a spinal component.

Biomechanical examination The role of abnormal biomechanics in the production of injuries. especially overuse injuries, is discussed in Chapter 8. Because abnormal biomechanics can contribute to any overuse injury, all clinicians need to perform a biomechanical examination. As with other components of the examination, it is important to develop a routine for the assessment of biomechanical abnormalities. A routine for the assessment of lower limb biomechanics is illustrated in Chapter 8.

Technique Faulty technique is another common cause of injury. A list of technique faults associated with particular injuries is shown in Table 5.1 on page 25. While the clinician cannot be aware of all techniques in various sports, he or she should be able to identifY the common technique faults in popular activities (e.g. pelvic instability while running, faulty backhand drive in tennis). Clinicians should seek biomechanical advice and assistance with assessment from the athlete's coach or a colleague with expertise in the particular area. Video analysis with slow motion or freeze frame may be helpfuL

Prin c i p l es of diag n os i s: cli n i ca l assess men t

Equipment In appropriate equipment predisposes to injury (Chapter 9). Inspect the sportsperson's equipment

(e.g. running shoes, football boo ts, tennis racquet, bicycle, helmet) .

Table 11. 1 Neurodynamic tests Test

Method

Indications

Normal response

Variations

Straight leg ra ise

Patient lies supine

Leg pain

Tigh tness andlor pain in Ankle dorsiflexion

(Fig. 11.1)

Leg ext ended

Back pain

posterior knee, thigh,

Clinician lifts leg

Headache

and calf

Ankle plantarnexionl inversion Hip adduction Hip medial rotation Passive neck flexion

Slump test

Patient sitting

Back pain

Upper thoracic pain

(Fig . 11.2)

Slumps

Buttock pain

Posterior knee pain

Neck flexion

Leg pain

Hamstring pain

Knee extension

Hip medial rotation Ankle and foot alterations

NeuralThomas

Patient lies supi ne

Groin pain

test (Fig. 11.3)

Hip extension

Anterior thigh pain

Quadriceps pain andlor tightness

Neck flexion

test (Fig. 11.4)

Patient supine toward side of couch Cervical contralateral flexion Shoulder girdle depression

Hip abductionl adduction Hip medial/lateral

Knee flexion

neurodynamics

(obturator nerve) Hip adduction

Ankle dorsiflexion Relea se neck flexion

Upper limb

Leg abduction

rotation

Arm pain

Ache In cubital fossa

Forearm pronation

Neck/upper

Tingling in thumb and

Wrist deviation

thoracic pain

lingers

Headache

Should er flexionl extension

Shoulder abducted to 110°

Add straight leg raise

and externally rotated Forearm supination Wrist/fingers extended Elbow extended

Ta ble 11.2 Examples of how spinal abnormality can manifest locally or distantly, with either pain or injury in the upper limb and lower limb Presentation

Local manifestation

Distant manifestation

Upperfimb

Pain

Hypomobllfty of C5--6 joint presenting as neck pain Hypomobility of C5- 6 joint presents as elbow pain Hypomobility of C5-6 jOint predisposing to lateral

Injury

elbow tendinopathy in a tennis player

Lower limb Pain

Hypomobility of LS- S1 joint presenting as lumbosacral pain

Injury

Hypomobility of L5-S 1 joint presents as buttock and hamstring pain Hypomobility of L5-S1 joint predi sposing to a hamstring t ear in a sprinter

155

Fundamental pr i n c iples

m

RECOMM E N DED READING

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Murtagh J. General practice. 4th edn. Sydney: McGraw-HilL 200 7.

iii L

2001;29:300 -3.

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the X-ray': advances in diagnostk imaging do not

treatment. Curr Allergy Asthma Rep 2011;11(1):45- 51.

6.

2.

Vernec A, Shrier I. A teaching unit in primary care sports medicine for family medicine residents. Acad Med 2001;76:293-6.

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Ruusuvuori J. Looking means listening: coordinating displays of engagement in doctor-patient interaction. Soc Sci Med 2001;52:1°93- 108.

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Robson-Ansley P, Toit GO. Pathophysiology, diagnosis and management of exercise-induced anaphylaxis.

replace the need for clinical interpretation. elin J Sport

Med 1998;8:r-4.

Barg W, Medrala W, Wolanczyk-Medrala A. Exercise-

induced anaphylaxis: an update on diagnosis and

REF E RENCES Khan K, Tress B, Hare W et al. 'Treat the patient, not

Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football. Am] Sports Med

Curr Opin AI/ergy CUn ImmunoI201O;1O:31Z-17 .

7·

Plastaras

cr, Rittenberg 10, Rittenberg KE et aL

Comprehensive functional evaluation of the injured runner. Phys Med Rehabil Clin North Am 2005:16:

62 3-49.

-... Ch apter 12

•

CHARLOTTE YONG-HING

•

•

Ii'eat tlte patient, not tlte X-ray. James M Hunter This chapter includes seven principles that may help clinicians maximize the utility of investigations, and which laboratory and special investigations add detail to the sports and exercise medicine diagnosis.

Investigations Appropriate investigations can confirm or exclude a diagnosis suggested by the history and physical examination but should never be a substitute for careful history taking and a comprehensive examination (Chapter II).

Understand the mean ing oftest results

1.

The sports clinician should be able to interpret inves-

tigation results and not rely blindly on the investigation report. A clinician who knows that about a quarter of asymptomatic elite jumping athletes have ultrasound abnormalities in their patellar tendons can reassure the patient that the imaging finding is not an indication for surgery. This is an example of a fa lse positive investigation. Many such examples exist. 2. Know how soon changes can be detected by investigation s

To detect certain abnormalities, the timing of an investigation may need to be appropriate. A female gymnast must have hormone levels tested in the second half of her menstrual cycle to detect low progesterone levels in luteal deficiency. likewise, there is nothing to be gained by repeating a radioisotopic bone scan or a cr scan to assess fracture healing two months after diagnosing a lumbar pars interarticularis defect in a tennis player.

3- Only order investigations that will influence m anagement It is inappropri ate to perform extensive (and expensive) investigations to confirm an already obvious diagnosis. If a stress fracture is seen on a plain X-ray, there is rarely anyth ing to be gained from an MRI scan.

4- Provide relevant clinical findin gs on the requisition Accurate and complete clinical information on requisition form s helps to avoid imaging and reporting errors. ' When particular X-ray views are required they should be requested. If you cannot remember the names of certain views, write that down on the request forms-the radiographer will generally know and, if not, tile radiologist will! It is often helpful to call the radiologist in advance to discuss the best way to image a patient. Remember that weight-bearing views are important to assess suspec ted osteoarthritis at the hip, knee, and ankle. "Functional" views (with the patient placing the joint in the posi tion of pain) are useful for anterior and posterior impingement of the ankle (Chapter 39).

5. Do not accept a poor quality test Inappropriate views or investigations perfonned on inferior equipment can lead to more diagnostic fusion than no investigation at all.

6. Develop a close working relationship with investigators Optimizing communication between colleagues improves the quality o[the service. 1 Regular clinicalradiological rounds or case presentations should be

157

Fundamental principles

encouraged. Digital imaging and telemedicine have made this much easier.

7. Explain the investigations to the patient Give the patient an understanding of the rationale behind each investigation. A sportsperson who complains of persistent ankle pain and swelling several months after an ankle sprain may need an X-ray and MRI. If the patient is merely told that an X-ray is necessary to exclude bony damage, he or she might become confused when told that the X.ray is normal but that further investigations are required to exclude bony or osteochondral damage. Also, be sure to alert patients who are going for a minimally invasive procedure (e.g. MR arthrogram) that this will require an "injection." It is helpful to give the patient a leaflet explaining the investigation, how long it will take, and when he or she should be reviewed with the results of the investigation.

Radiologica l investig ation Plain X-ray Despite the availabili ty ofsophistica ted imaging, plain film radiography often provides diagnostic information about bony abnormalities, such as fractures, dislocations, dysplasia, and calcification (Fig. 12.1).' It is recommended that adult oral doses of paracetamol for the treatment

167

Fundamental princip les of pain or fever be 650-1000 mg every four hours as needed and up to a maximum daily dose of 4 g...'.) At a single dose of 1000 mg, paracetamol reaches its ceiling effect in adults and a further increase to this does not increase its analgesic effects but does, however, increase its toxicity levels. Since the first synthesis of paracetamol in r878 by Morse, its method of action has not been well understood. However, recent laboratory studies have demonstrated that the analgesic effects of paracetamol are the result of the involvement or the cannabinoid --'-4 The cannabinoid system involves a group of neuro-modulatory lipids and their associated receptors, which have influence over physiological processes such as appetite, pain sensation, mood, and memory. It is thought the cannabinoid-I receptors, which are primarily located in the central nervous system, are involved in the analgesic effects of paracetamol. The involvement of this system may now explain some of the strange adverse effects that can be associated with the use of paracetamol, such as mood swings and appetite suppression. These effects are not associated with other analgesics and NSAIDs. The incidence of adverse effects is comparable to placebo!> It is thus safe for use in acute sports injuries at up to )-4 g(day."

Codeine Codeine is a more potent analgesic. It is a narcotic analgesic and was formerly listed as a banned substance by the International Olympic Committee (Chapter 66). This ban was lifted in the mid-r990s.

Topical analgesics Topical analgesics are used extensively by athletes and are known as "sports rubs," "heat rubs" and "liniments." Mostcommerciallyavailable topical analgesics contain a combination of substances such as menthol. methyl salicylate. camphor. and eucalyptus oil. The majority of topical analgesics act as skin counterirritants. Most products contain two or more active ingredients that produce redness, dilate blood vessels, and stimulate pain and temperature receptors. The type and intensity of the effect depends on the particular counterirritant, and its concentration, dosage, and method of application. The exact mechanism of action of counterirritants is unknown. Counterirritants should not be used to replace a proper warm-up as they do not penetrate to deeper muscles. but they may be of use as an adjunct to 168

warm-up. Counterirritants may irritate the skin, causing burning and pain on application. redness, and itchiness, and they occasionally cause blistering or contact dermatitis. They are not appropriate around the groin, mouth, or eye regions, and they should not be used on broken skin. Counterirritants often include a variety of herbal compounds such as capsaicin, camphor, menthol, saIicylates, and eucalyptus oil. Table 1}I outlines the proposed uses and mechanisms of action of these compounds. Previously, the mechanism of action of counterirritants was proposed to be via the stimulation of sensory receptors to dampen painful stimuli.n. JO However, more recent evidence has demonstrated that their mechanism of action is related to their effect on specific ion channels known as the transient receptor potential (TRP) jI These ion channels are thermosensitive (i.e. sensitive to extreme heat or cold). When TRP channels are activated, calcitonin gene-related peptide (CGRP). substance P (SP), and other inflammatory neurotransmitters are released. This causes local irritation and an inflammatory response. Symptoms such as pain, burning, itching, and redness in the skin are due to excitation and senand Cfiber nociceptors. sitization of A delta Prolonged activation of these nociceptors results in a depletion of presynaptic neurotransmitters. This is thought to give rise to the analgesic properties of counterirritants. It is important to note that counterirritants lower or increase the temperature activation ofTRP channels. This explains the cooling and heating effects of heat rubs and ice gels.z7. z8 Figure 1}2 shows a summary of the mechanism of action of counterirritants.

Nonsteroidal anti-inflammatory drugs (NSAIDs) Nonsteriodal anti-inflammatory drugs (NSAIDs) are drugs with analgesic, anti-inflammatory, and antipyretic properties. The term "nonsteroidaY' is used to distinguish this class of drugs from steroids, which, among other effects, produce similar anti.infiammatory effects. Generally, the use of NSAIDs is well accepted in conditions where excessive inflammation is the prime cause of the patient's symptoms (e.g. bursitis); however, the role of NSAIDs in the treatment of other acute and overuse conditions is widely debated.

Trea t me n t s use d for m u sc ul os ke leta l co n d itio n s Tab le 13.1 Common counterirritants: uses and mechanism of action Counterirritant Menthol

Description

Mechanism of action

Uses

Derived from peppermint or

Coug h suppressa nt

other mint oil s

Analgesic

Binds to TRPV3 and k-opioid receptoTs21,28

Coolin g effect

Salicylates

Derived from t he bark o f the

Analgesic

w illow tree

Anti-acne Antipyretic agent

Binds to TRPA 1 27, 29

Cooling effect

Camphor

derived fro m the wood of

Decongestant Cough suppressant

the camphor laurel tree

Antipruritic agent

A sweet smelling compound

(Cinnamomum camph ora )

Binds to TRPV3 receptors2B

Analgesic Heatin g effec t

Capsaicin

The active component in chilli

peppers

Binds to TRPVl receptors 21- 29

Appetite stimulation Heat ing effec t Analgesic Others (treatment of gastric ulcers, rheu matoid, shingles)

Eucalyptus 011

Distilled 011 from the leaf of

Dec:ongestant

the eucalyptu s t ree, native to

Anti-inflam matory

Australia

Analgesic

Binds to TRPMB 28

Antibacterial agent

TRP receptor group activated by: capsaicin StimulatedTRP channels (thermosensitive)

camphor menthol!

. salicylates eucalyptus oil

1 1 Prolonged activation Depletion of pre-synaptic neurotransmitters

Dampened pain perception

Figu re 13.2 M echanism of action of counterirritants

169

Fundamental pr i ncipl es The most common NSAIDs include aspirin, ibuprofen, diclofenac, and naproxen, and at low doses they are available over the counter, making them popular drugs among the general population as well as athletes, especially in terms of self-medicating. These NSAIDs are frequently associated with adverse effects, especially on the stomach, and as a result a different type ofNSAID, the COX-2 inhibitor, which reduces the risk of stomach adverse effects, came into use over the past two decades. However, their association with cardiovascular adverse effects has led to some of these drugs being removed from the market. The frequency of administration ofNSAIDs varies between the different drugs and is related to their half-life (Table IJ_2)_

In spite of the widespread clinical use of NSAIDs, there are no convincing research data proving their effectiveness in the treatment of acute soft tissue injuries. Most studies lacked a placebo group and compared the effectiveness of one NSAID with another,l6 They do not appear to be any more effective than simple analgesics in the management of acute muscle injuries)7. ,8 The lack of scientific support for the use of NSAIDs in acute injury may reflect biological reality, or may be due to the methodological difficulties in performing randomized placebo-controlled trials in the diverse range of acute sporting injuries. A summary of the use of NSAIDs based on research evidence is shown in Table I}4 overleaf.

Use in sport

Adverse effects

Recent studies on the use of NSAIDs in sport have demonstrated an alarming rate of use. A summary of these studies and their findings are displayed in Table IJ.J.

NSAIDs are absorbed by the digestive system, and after entering the blood stream, are metabolized in the liver and later excreted by the kidneys. Adverse effects are associated with the gastrointestinal tract, cardiovascular sys tems, and kidney function. 40 Susceptibility increases with prolonged use/ 6 .j9. 4' In general, the NSAIDs have minimal adverse effects; the most common are gastrointestinal symp· toms, especially epigastric pain, nausea, indigestion, and heartburn. There appears to be considerable individual variation of adverse effect profiles among the different NSAIDs. The risk of dyspeptic adverse effects can be lowered by using the minimum effective dose, taking the drug with or immediately after food or milk, or by the use of antacids. Alcohol, cigarettes, and coffee may aggravate the dyspepsia. To our knowledge, frank peptic ulceration with the short-term use of NSAIDs has not been reported among sportspeople. Occult bleeding may contribute to iron depletion in

Mechanism of action Inflammation occurs at the site of acute injury. A local soft tissue injury such as a ligament tear causes the release ofarachidonic acid from cell walls. Arachidonic acid is converted by a number of enzymes, in particular cyclo-oxygenase (COX), to prostaglandins, thromboxane, and prostacyclins. These substances mediate the inflammatory response. The mechanisms ofaction ofNSAIDs are through the inhibition of the COX system (Fig. IJ.J on page 172). Inhibition of the COX-converting enzyme, specifically through inhibition of prostaglandin, prostacyclins, and thromboxane synthesis, induces anti-inflammatory, analgesic, anti thrombotic, and antipyretic effects)'

Efficacy

Table 13.2 Commonly used NSAIDs Drug

Some trade names

Usual dose (mg)

Half-life

Daily doses

Acetylsalicylic acid

Aspirin

650

30 mins

3-4

CeJecoxib

Celebrex

100- 200

11 - 12hours

1-2

Dic10fenac

Voltaren

25-50

1- 2 hours

2- 3

Ibuprofen

Brufen. Matrin, Advil

400

1-2.5 hours

3-4

Meloxicam

Mabie

7.5-15

20-24 hours

Naproxen

Naprosyn, Anaprox

250-1000

12-15 hours

(ASA)

170

1-2

Tr eatments u sed for muscu l oske l et al condit i ons Table 13.3 Prevalence of NSAIDs use in sport

Study

Sport/event

Gorski

2008 Brazil Iron man

2009 J1

Triathlon

59.9% reported using NSAIDs in the preceeding three months

(3.8 km swim, 180 km cycle,

48.5% without medical prescription

42.2 km run)

Most athletes unaware of adverse effects

Findings 327 athletes in study

Pre-race used mostly for treatment of injuries

During event used mostly for pain relief and injury preventIon

Wharam 2006 H

2004 New Zealand ITonman

330 athletes in study

triath lon

30% reported NSAIOs use

(3.B km swim, 180 km cycle,

NSAJDs use was related to the incidence of hyponatremia

42.2 km run)

NSAIDs users had significa ntly higher plasma K, urea, and creatinine, and lower Na levels

McAnulty

Western States endurance

60 athletes in study

200734

run

Plasma cytokines x2-3 higher in users of NSAIOs

(160km)

NSAIDs users had significa nt amount of delayed onset muscle soreness (OOMS) day 1 post race NSAIDs use during race did not alleviate muscle damage or DOMS and increased oxidative stress markers

Huang

Atlanta and Sydney

257 Canadian athletes in study

2006 13

Olympic Games

Most commonly used drugs were NSAIDs

(1996 & 2000)

NSAIDs use was 33% of athletes in Atlanta and 38% in Sydney The use of NSAIOs was hig hest in softball (60%) in Atlanta and gymnastics (100%) in Sydney

Taioli

Italian Professiona l

2007 19

Football/Soccer League

743 athletes in study 92.6% of players reported the use of NSAIDs in previou s year

(season 2003-04)

86.1 % current users of NSAIDs 22% of players used NSAIDs for >60 days/year

Tscholl

FIFA World Cups

2944 team physicians' reports on players' medication intake

2009 11

(2002 & 2006)

NSAIDs were the most frequently prescribed substances Constituted 46.5% (2002), and 47.7% (2006) of all medications used >50% of players used NSAIDs at least once during

a tournament and

30.8% prior to a match On ave rage, 22.9% of the players used NSAIDs in two out of three matches 10.6% of the players used NSAIDs for every match > 10% of the players used at least 2 forms of NSAIDs and some players used up to 5 different types The use ofCOX-2 inhibitors decreased Significantly from 2002 to 2005 Tscholl 20106 months continued pain and

instability]) Tendon injury

Debatable: •

Chronic tendinopathy has an inOammatory component May be useful in acute presentations for pain relief (use simple analgesics first)

Bone injury

Adverse effect:

(fracture/stress fracture)

Delay bone consolidation •

Avoid especially in the first few weeks of fracture and with stress fractures

Possible b enefit: Reduce incidence of myositis ossilicans and ectopic bone formation joint surgery; whether this beneli! translates to sports injuries is unknown Muscle Injuries (contusion, strain, DOMS)

Possible adverse effect in prolonged use: inhibits protein synthesis, affects remodeling and regeneration phase by reducing myolibrob last proliferation Has demonstrated increased creatine kinase when taken prior to endurance sport events, in turn increasing the extent of muscle injury post event

Impingement synd romes and bursitis

Benefit: Pain relief if requi red for shoulder bursitis, de Quervain's, trochanteriC bursitis (rare, most latera l hip pain is gluteal tendinopathy), ITBFS, Morton's neu roma

172

Tr eatmen t s used for musculoskeletal co n d it i ons

athletes. The clinician should be wary of prescribing long-term use of these drugs in iron-depleted sports people. Other occasional adverse effects include asthma, allergic rhinitis, rashes, tinnitus, deafness, headache, and confusion. The NSAIDs have a number of important drug interactions with anticoagulants. antihypertensives. diuretics, and peripheral vasodilators. Older patients with a history of hypertension, congestive heart failure, or coronary artery disease are at particular risk of adverse cardiovascular events with NSAIDs. Patients with impaired renal function are at risk of fluid retention, hyperkalemia (increased serum potassium level), and hypertension. Prolonged use of NSAIDs is associated with

harmful effects in terms of cell metabolism and growth.3J.J9 NSAIDs have proved to inhibitor decrease the synthesis of extracellular matrix. including collagen turnover and muscle regeneration. and therefore can affect the strength of healing tissue. H . Overall NSAIDs can delay healing in acute ligament. muscle, and tendon injuries. 22 • JHO"H This is thought to be due to their detrimental effect on the cell regeneration phase. as NSAIDs can cause increased fibrosis at the site of injury.4J With an increase in fibrosis. weakness at the injury site can develop. Fibrosis increases with prolonged Slower muscle and ligament recovery increases the risk of re-injury. Therefore, even though NSAIDs may prove to be beneficial in the short term with their analgesic and anti-inflammatory effects, an increased risk of reinjury could potentially impede athletic performance. More studies are needed to investigate the effectiveness of NSAI Ds, particularly in the management of overuse injuries. In the meantime, the precise criteria for the use ofNSAIDs in the management of sporting injuries remain a matter for debate. Things to consider when prescribing NSAf Ds are shown in the box, and a simple guide to the use of NSAIDs is shown in Figure 13.4 overleaf.

COX-2 inhibitors Selective COX-2 inhibitors were introduced in 1999, promising the same anti-inflammatory and analgesic effects as their traditional counterparts but with reduced gastrointestinal adverse effects. 4o.44 Reduced gastrointestinal effects occurred through inhibition of COX I, which has shown to be associated with the upkeep of stomach

.' ..

•

•

The use of paracetamol should be considered for acute and chroniC musculoskeletal pain, due to its Similar analgesiC effects but lower adverse effects than NSAIDs. NSAIOs should be avoided in the first 48 hours post injury. Excessive inflammation, after th e initial 48 hours, may warrant use of NSAIDs. Long-term use (>S days) should be avoided. NSAIDs should be limited to minimal dose and minimal duration. If NSAIDs are required for longer than 5 days, revisit assessment and diagnosis. Use gastro-protective agents for patients at high risk of gastrointestinal problems (e.g. co-administer gastroprotective agents such as misoprosol, Hl antagonist). There is no evidence that prophylactic use of NSAIDs decreases injury risk or improves athletic function. Figure 13.4 overleaf gives a simple guide to the use of NSAIDs. 39

After introduction of these selective COX-2 inhibitors (featured in many "-coxib" drugs such as celecoxib), there was an increase in vascular thrombotic events. COX-2 inhibitors were found to disturb the prostacylin-thromboxane balance, which affects vascular homeostasis. 40 . 44 By 2004 Valdecoxib and rofecoxib were taken off the market, as these drugs specifically were associated with a high number of vascular accidents through the increase in thromboxane.44 Currently, COX-2 inhibitors such as ceJecoxib are widely used particularly in those who have had dyspeptic adverse effects with the use of the traditional NSAlDs.

Ketorolac tromethamine (ToradoI. Acular) Ketorolac tromethamine is a potent analgesic and anti-inflammatory medication that can be administered orally, intravenously, and intramuscularly. It acts by blocking the synthesis of prostaglandins in the cyclo-oxygenase pathway.4S A survey of US National Football League teams revealed that 28 out of the 30 teams that responded to the survey used ketorolac with 93% game-day Adverse effects include headache, vasodilatation. asthma. bleeding. and kidney dysfunction. 173

Fundam e nt al princip l es

¥es

Are inflammatory signs and symptoms

No

present (Le. active swelling, and resting and/or night pain)?

Yes

Previous history of NSAIDs adverse

effects or risk factors for adverse effects?

Recommendation

No

I Noo·NSAIDs

analgesic

NSAIDs combined with

maximum of

protective agent

7 days

NSAIDSfor

NSAIDs not indicated

Figure 13.4 Decision tree for the prescription of NSAIDs to athletes with an acute or chronic musculoskeletal injury FROM WARDEN,g

Of particular concern in the sporting context is the bleeding tendency.

Topical anti-inflammatory agents In light ofthe recent trials demonstrating the harmful cardiovascular effects of some NSAIDs, in addition to the ongoing gastrointestinal concerns, especially with prolonged use, an increased interest in and use of topical NSAIDs has 2i Topical analgesics can achieve similar analgesic effects to oral formu· lations without the systematic adverse effects and safety concerns/i Topical administration ofNSAIDs has several benefits over their oral counterparts. These include lower systemic absorption and hence lower adverse effects, and effective localized analge· sic and anti· inflammatory A number oftopical anti-inflammatory products are available. These include benzydamine, adrenocortical extract, indomethacin, and diclofenac gel. Traditionally these topical drugs have been administered through creams, gels, and sprays, which often required three to four applications per day. More recently, anti.inflammatory drugs have been applied through a patch which releases the drug over 24 hours. There is some evidence of their efficacy. One recent systematic review assessed the effectiveness of topical NSAIDs against a placebo control for chronic musculoskeletal pain. 48 Populations

174

included were predominately knee osteoarthritis. Typical NSAIDs were used for the search strategy, including dicoflenac, ibuprofen, and naproxen. This review identified 25 randomized control trials (RCTs). Minimal adverse events were identified with the highest complication rate found in one study of 6% associated with cutaneous rash. Overall, this review found topical NSAIDs were effective and safe in treating chronic musculoskeletal conditions for a period of two weeks. One recent RCT on the effects of ibuprofen topical gel on muscle soreness resulting from unac· customed exercise found that it was not effective on DOMS after exercise. 49 This trial included re6 par· ticipants of varying ages. Exclusion criteria included occupations that required heavy lifting or strenuous activity, or participation in weight or resistance training programs for the past six months. Subjects performed elbow and knee flexor exercises of 80% (6 sets of 10 reps) ofIRM (repetition maximum).

Corticosteroids The use of corticosteroids, which are potent antiinflammatory drugs, is controversial due to the incidence of adverse effects and concern regard· ing the effect of corticosteroids on tissue healing. Corticosteroids may be administered either by local injection, orally, or by iontophoresis. We found no

Treatments u sed fo r mu sculoske leta l co n di t io ns randomized controlled trials of iontophoresis for sports medicine conditions. A goal of the use ofloea1 corticosteroid injection is to reduce pain and inflammation sufficiently to allow a strengthening program to commence. Corticosteroid injections should be considered a "bridge" treatment that provides immediate symptomatic relief while the underlying cause of the problem is addressed with definitive, disease-modifying therapy.

Local injection for various pathologies Local injection of corticosteroid agents maximizes the concentration at the site of the injury and minimizes the risk of adverse effects associated with systemic administration, Clinicians often use local injection of corticos teroids in conditions that include bursitis, para tenonitis, tenosynovitis, joint synovitis, osteoarthritis, chronic muscle strain, and trigger points. Conditions such as subacromial, olecranon, pre-patellar. and retrocalcaneal bursitis may be resistant to standard physiotherapy jphysical therapy combined with NSAIDs. Intra-articular injections, particularly into weightbearing joints, must be approached with considerable caution because of possible long-term damage to articular cartilage. They should be performed only when the condition h as proven refractory to treahnents such as physiotherapy and NSAIDs. Rheumatologists have long used corticosteroids intra-articularly in acute monoarticular exacerbations of osteoarthritis. An acute attack of gouty arthritis may also respond wen to aspiration and corticosteroid injection as part of the overall management. Apophyseal joint injections have been used in the management of patients with back pain and who have only a short-term response to manual therapy, but the efficacy of such treatment at the lumbar spine is no better than placebo.'i° Controversy surrounds the use of injectable corticosteroid into the epidural space. The role of corticosteroids in the treatment of tendon conditions was systematically reviewed in 2010. 3 As tendinopathy is not associated with inflammatory cells (Chapter 4), corticosteroid therapy is generally falling out of favor for this condition) In lateral elbow pain, corticosteroid injections decrease the likelihood of good outcomes at six months and beyond compared with a "wait and see" approach." See individual regional chapters (Part B) for specific treatment recommendations.

Some clinicians recommend the injection of trigger points with corticosteroid. Soft tissue therapy, dry needling, or local anesthetic injection appear to be equally as effective. Adverse effects of corticosteroid injections include the potential systemic effects of absorbed cortisone, and local effects of injection. Corticosteroids inhibit collagen synthesis and tenocyte-fibroblast cell activity, and thus may impair tissue repairY'» As deleterious effects of corticosteroids appear to be dose-related, repeated injections are discouraged. The main adverse effect of corticosteroid injection, apart from the possible damage to articular cartilage and tendon, is infection. This is a rare occurrence and should be prevented by the use of strict aseptic technique, particularly when performing intra-articular injections. The presence of an overlying skin infection is a contraindication to injection. Corticosteroid injections commonly cause a short-term exacerbation of symptoms, a phenomenon known as "post-injection flare." This may commence soon after injection and usually subsides within 24 hours. This phenomenon is thought to be due to a crystalline synovitis, and is considered by some to be a positive sign of a favorable outcome to the treatment. Patients should always be warned that this may occur. Corticosteroid injections have the reputation of being a particularly painful procedure. but this can be minimized by adding local anesthetic (0.5-I.O mL 1% lignocaine [lidocaine]) to the injection. The abolition of pain after the local anesthetic injection may be diagnostically significant. Traditionally, patients have been advised to rest and minimize activity for three to seven days following corticosteroid injection. There are a number of different fonns of injectable corticosteroid available. They include hydrocortisone, betamethasone, methylprednisolone, and triamcinalone. The main differences are in the speed of onset and half-life of action. There is no convincing evidence that their efficacy differs.

Oral corticosteroids Despite their effectiveness as an anti-inflammatory agent, clinicians have traditionally been reluctant to use oral corticosteroids for the treatment of musculoskeletal inflammation, probably because of potential adverse effects.s4 The most common conditions for which they are used are acute cervical or lumbar radiculopathy jdiskogenic pain, osteitis pubis, 175

Fundament a l principles adhesive capsulitis (frozen shoulder), and chronic tendinopathies. Possible complications include avascular sis of the femoral head. l ) However, the use of short courses (5-7 days) of oral prednisolone (25-50 mg) appears to be associated with minimal detrimental effects. Note that the use of oral corticosteroids is still banned by the International Olympic Committee in competition.

Iontophoresis Iontophoresis is a process by which drugs can be transmitted through the intact skin via electrical potential. Drugs such as corticosteroids, salicylates, local anesthetics, and NSAIDs can thus be administered locally without the traumatic effects of injection, with no pain for the patient, no infection risk, and fewer systemic adverse effects. 56. 57 This process has been shown to deliver the drugs through skin and subcutaneous tissue, and has been in use since the I950s)6 In this way, the drug can reach tissue that may have markedly reduced vascularity (e.g. a bursa or tendon). The results of well-controlled studies suggest that iontophoresis with diclofenac or salicylates improves symptoms in lateral epicondylitis. Iontophoresis with corticosteroid appears to give rapid-onset analgesia in both lateral epicondylitis and plantar fasciitis. Shortterm iontophoresis (two weeks) improves pain and facilitates rehabilitation. 58 Physiotherapists sometimes use iontophoresis to treat inflammatory conditions such as plantar fasciitis, lateral epicondylitis, rotator cuff and Achilles tendinopathy, and bursitis presentations.s 6. 57 A recent laboratory study found that iontophoresis could facilitate the transmission of dexamethasone (a synthetic glucocorticoid steroid) into subcutaneous human tissue.s6 This study reported that some subjects appeared to have good effects, while others showed minimal improvement. This may highlight that iontophoresis may have an individual treatment response. A systematic review on iontophoresis included II articles focusing on common musculoskeletal inflammatory conditions, including plantar fasciitis, epicondylitis, Achilles tendinopathy, and carpal tunnel syndrome.,}7 This review found that the internal validity of most of these studies was compromised in some way, leaving results at high risk of bias. It concluded that research on iontophoresis 176

was limited and called for further studies. In addition to this review, an ReT (level 2 evidence) reported positive effects for iontophoresis in conjunction with low-Dye taping for plantar fasciitis)9 In light of this finding, iontophoresis may currently be best used as an adjunct treatment in the treatment of inflammatory musculoskeletal conditions.

Nitric oxide donor Glyceryl trinitrate (GTN), or nitroglycerin, is a nitric oxide donor used for over 100 years as a vasodilator and for symptomatic treatment of angina. The mechanism of action of organic nitrates is through the production of nitric oxide, a highly reactive free radical that is an important mediator in many physiological and pathophysioogical processes. One action of nitric oxide is to stimulate collagen synthesis by wound fibroblasts, so it is proposed that nitric oxide may modulate tendon healing by stimulating fibroblasts to repair collagen. Thus, organic nitrates such as GTN may be viewed as prodrugs of endogenous nitric oxide, an endothelial cell-derived relaxing factor. Transdermal GTN patches are a simple way of applying and dosing nitric oxide. Paoloni et a1. provided level 2 evidence that use of nitric oxide donor (GTN patches applied locally I.25 mg/day) was an effective treatment for noninsertional Achilles, supraspinatus and lateral elbow tendinopathy.6o-z About 20% more patients prescribed the GTN patches were asymptomatic at six months than control group participants who received "best-practice" care (i.e. rehabilitation alone) (Fig. I).5). A recent ReT (level 2 evidence) included 40 subjects with non·insertional Achilles tendinopathy.6) Both groups received standard physiotherapy treat· ment and one group incorporated the use of a daily GTN patch at a dose of 2.5 mgj24 h. This study found conflicting results to the Paoloni study in that at six months there was no significant difference in pain or disability scores between groups. Headaches occurred in 4 (20%) of subjects. Another ReT (Ievelz evidence) included I54 sub· jects with lateral epicondylosis, divided into four groups.64 All four groups performed wrist extensor strengthening and stretching exercises. The groups included one control and three GTN patch groups of different pharmaceutical strengths (0.72 mgjz4 h; 1.44 mgj24 h; ).6 mgj24 h). This trial, in contrast to the previous ReT on lateral epicondylosis, did not demonstrate significant findings for the use of GTN

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6-12 weeks)-such as significantly delayed recovery and 62% greater recurrences than if the patient was advised to adopt a wait-and-see approach);' }6 Thus, it is prudent to consider using this injection within a more comprehensive ment framework as illustrated in Figure 22.13.

Prior to any Injection, the clinician should fully inform the patient of likely short- and long-term outcom es, as adopting a wait-and-see policy will result in approximately 80% success rate at 12 monthsY When corticosteroid and local anesthetic agents are injected, the aim should be around the extensor carpi radialis brevis tendon, directly over the point of maximal tenderness, but not into the tendon substance itself.

"JU'l/';.

Acomprehensive program fo r man agement of lateral elbow pain (Fig. 22.13) would include first implementing a graduated progressive exercise program over 8 weeks, pain rel ief if required, ergonomic advice, and activity modification.)7

Advice Activity modification and ergonomics Self-admini stered pain relief (TENS. meds)

r--- OR --+ 1_ forB-12.weeks Wait and see .j.

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Nitric oxide do nor th erapy

Initial studies of lateral elbow, Achilles, and supraspinatus tendinopathies provided level 2 evidence that nitric oxide donor therapy (glyceryl trinitrate [GTN J patches applied locally 1.25 mg/day) improved outcomes within three to six months l :! (Fig. 22.14). One mechanism by which this treatment might work is through enhanced collagen synthesis. However. a recent dose-ranging clinical trial for lateral elbow tendinopathy failed to confirm the initial findings, and highlighted that type of exercise (strengthening as opposed to stretching) is a significant consicleration. l 9 Pragmatically, the practitioner and pa tient need to be aware that 4-5% of patients using a GIN patch will develop head aches or skin rash that are severe enough to discontinue treatment, and that this seems to be dose·dependent. Thus it is important to carefully meter the dose and monitor the response. Botulinum t oxin Historically used for neuromuscular conditions, botulinum toxin (Botox) injection is a new and unproven treatment for tendinopathy. There is evidence that it produces short·term improvement in pain when compared to placebo;Ju.4 0 however, it is important to counsel the patient prior to the treatment that there will be a high likelihood (92% at 8 weeks post injection)4 1 of an extensor muscle lag. Autologous blood inject ion It has been suggested that the introduction of auto· logous blood or platelet-rich plasma (in which autologous blood is first concentra ted via centrifugation and isolation of the platelet fraction) may re-initiate

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,

Not lateral elbow tendinopathy: Other treatment

l Lat eral elbow tendinopathy confi rmed : Counsel regarding injections (corticosteroids, PRP), surgery, job reassign.ment (usually only in recalcitrant cases)

Figure 22.13 Treatment algorithm

Figure 22.14 Nitric oxide donor therapy- one-qua rter of a 0.5 mg/24 hr glyceryl trinitrate (GTN) patch in place over the most tender site of extensor tendinopat hy

399

or enhance a presumably deficient inflammationrepair response, thereby promoting healing. There is conflicting evidence, with one high-quality trial showing no difference from a placebo,l6 two others showing superiority to corticos teroid injection,4 2 .4l and a number of case series indicating it is beneficial in the short term44 and long term.4; Correct predisposing factors Probably the most important factor to be avoided is excessive or unaccustomed activity. In tennis players, a major cause is a faulty backhand technique with the elbow leading (Fig. 22.15). Other technique faults that may predispose to the development of extensor tendinopathy include excessive forearm pronation while attempting to hit top-spin forehands and excessive wris t flick (flexion) movement while serving. Correction of these faults requires assistance of a qualified tennis coach. Other factors, such as racquet type, grip size, string tension. court surface, and ball weight, may influence the amount of shock imparted to the elbow (Chapter 9). A mid-sized, graphite racquet with a large "sweet spot' and a grip size that feels comfortable should be used. Care should be taken to avoid using racquets with excessively large or, especially, small grips.

Figure 22.15 Backhand technique (al Incorrect

Surgery Surgery might be considered occasionally in the case with a long history (e.g. >r8 months) of severe lateral elbow pain that is recalcitrant to the treatment strategies outlined above. Surgery is varied, but most approaches involve some degree of excision of the degenerative tissue within the common extensorf extensor carpi radialis brevis tendon and release of the tendon from the lateral epicondyle. A recent systematic review has concluded that there is a dearth of quality evidence to recommend one surgical approach over others.4-6 (b )

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Return to activity

Other causes oflateral elbow pain

As with all soft tissue injuries, it is important to return gradually to activity following treatment. The tennis player should initially practice backhand techniquewithout a ball, then progress slowly from gentle hitting from the service line to eventually hitting full length shots (Chapter IS). Depending on tile severity of the condition and the length of the rehabilitation program, this graduated return should take place over a period of three to six weeks.

Other causes of lateral elbow pain may occur in isolation or in conjunction with the previously mentioned conditions. Radiohumeral bursitis is occasionally seen in sportspeople. TI1is may be distinguished from extensor tendinopathy by the site of tenderness, which is over the radiohumeral joint and distal to the lateral epicondyle, maximally over the anterolateral aspect of the head of the radius. The presence of this

400

bursitis may be confirmed on ultrasound examination. Injection with a corticosteroid agent is the most effective fonn of treatment. Os teochondritis of the capitellum or radial head may occur in younger sportspeople (Chapter 42) involved in throwing sports. This is a significant condition as it can cause an enlarged, deformed capitellum that may predispose to the development of osteoarthritis. The treatment of this condition involves avoidance of aggravating activities. The lateral elbow is a common site of referred pain, especially from the cervical and upper thoracic spine and periscapular soft tissues. Most patients with chronic lateral elbow pain are likely to have some componen t of their pain emanating from the cervical and thoracic spine (Chapter 20). Any associated abnonnalities of the cervical and thoracic spine should be treated and the patient's signs reassessed immediately after treatment. If there is a noticeable difference, this may indicate a significant component of referred pain .

Medial elbow pain Patients who present with medial elbow pain can be considered in two main group s. One group has pain associated with excessive activity of the wrist flexors. This is the medial equivalent of extensor tendinopathy, with a similar pathological process occurring in the tendons of pronator teres and the flexor group. This condition can be referred to as "flexor/pronator tendinopathy." The second group of patients have m edial elbow pain related to excessive throwing activities. Throwing produces a valgus stress on the elbow that is resisted primarily by the anterior oblique portion of the medial collateral ligament of the elbow and secondarily by the stability of the radiocapitellar joint. Repetitive throwing, especially if throwing technique is poor (Chapter 9), leads to stretching of the ligament and a degree of valgus instability. A fixed flexio n deformity of the elbow may develop as a result of scarring of the medial collateral ligament. Subsequently, there may be some secondary impingement of the medial tip of

the olecranon onto the olecranon fossa, producing a synovitis or loose body forma tion. With valgus stress, the compressive forces may also damage the radio" capitellar joint. Several of these pathological entities may be present in combination. In children and adolescents, repetitive valgus stress may result in damage to the medial epicondylar epiphysis with pain and tenderness in this region. This usually responds to a period of rest followed by a gradual rerum to throwing activity, but may progress to avulsion with continued activity. This condition, commonly known as "little leaguer's elbow," is considered in Chapter 42. The causes of medial elbow pain are shown in Table 22.2.

Flexor/pronator tendinopathy This condition is not as common as its lateral equivalent; it accoWlts for 9- 20% of all epicondylalgia diagnoses,47 It is seen especially in golfers ("golfer's elbow") and in tennis players who impart a lot of top spin on their forehand shot. The primary pathology exists in the tendinous origin of the forearm fl exor muscles, particularly in the pronator teres Ultrasound is sensitive and specific fo r detecting clinically defined medial epicondylitis, with focal hypoechoic areas of tendinosis being the most common finding, followed by partial tears (i. e. these are identical to lateral epicondylalgia ultrasound findings). On exami nation, there is usually localized tenderness just at or below the medial epicondyle, with pain on res isted wrist flexion and resisted forearm pronation (Fig. 22.16 overleaf). Treahnent is along the same lines as treatment of extensor tendinopathy (Fig. 22.13). Particular atten· tion should be paid to the tennis forehand or the golf swing technique. Due to its close proximity to the medial epicondyle. the ulnar nerve may become irri· tated or trapped in scar tissue. This should be treated with neural mobilization.

Medial collateral ligament sprain Sprain of the medial collateral ligament of the elbow may occur as an acute injury, or as the resu lt of

Ta ble 22 .2 Causes of medial elbow pain Common

Less common

Not to be missed

Flexor/pronator tendinopathy Medial collateral ligament sprain Acute

Ulnar neuritis

Refe rred pain

•

Apophysitis (children and adolescents)

Ch ronic

Avulsion fra cture of the medial epicondyle (children and adolescents)

40 1

Figure 22.16 Medial elbow pain reproduced with resisted wrist flexio n and forearm pronation chronic excessive valgus stress due to throwing. It occurs particularly in baseball pitchers and javelin throwers. The repeated valgus stress. especially in throwers who "open up too soon" (Le. become fronton too early in the throwing motion). leads initially to microtearing and inflammation of the ligament. then scarring and calcification and, occasionally ligament rupture. The biomechanics of throwing is discussed in Chapter 8. On examination. there is loca1ized tenderness over the ligament and mild instability on valgus stress (Fig. 22.17a). There are often associated abnormalities. such as a flexion contracture of the forearm muscles. synovitis and loose body formation around the tip of the olecranon. as well as damage to the radiocapitellar joint. However. many throwers demonstrate a flexion contracture without concurrent medial collateral ligament pathology.49 Treatment in the early stages of the injury involves modification of activity, correction of faulty technique. local electrotherapeutic modalities (possibly as for lateral elbow tendinopatby, as little research exists for the medial equivalent), and soft tissue therapy to the medial ligament. Medial strapping of the elbow may offer additional protection (Fig. 22.17b). Specificmusde strengthening should be commenced, concentrat· ing on the forearm Hexors and pronators (Fig. 22.r8). Advanced pathology may require arthroscopic removal oflaase bodies and bony spurs. Occasionally, significant instabili ty develops and requires ligament reconstruction; this should be avoided if possible, as the results of surgery are often disappointing.

Figure 22.17 (a) Assessment of integrity of the medial collateral ligament

(b) Elbow stability tape

Ulna r neuritis The ulnar nerve pierces the intermuscular septum in the middle of the upper arm then passes deep to

402

Figure 22.18 Strengthening exercises for the forearm flexors and pronators

Elbow and arm pa i n the medial head of the triceps muscle to locate in a superficial groove (the ulnar sulcus) between the ole· eranon and the medial epicondyle. It then enters the forearm between the humerus and the ulnar heads of the flexor carpi ulnaris muscle. Inflammation of the ulnar nerve can occur as a result of a combination of any of [our 1. Traction injuries to the nerve may occu r because of t he dynamic va lgus forces of throwing, especially when combined with valgus instability of the elbow.

2. Progressive compression can occur at the cubital tunnel secondary to inflammation and adhesions

from repetitive stresses, or where the nerve passes between the two heads of the flexor carpi ulnaris due to muscle overdevelopment secondary to resistance weighHraining exercises. 3. Recurrent subluxation of the nerve can occur due to acquired laxity from repetitive stress or direct trauma. 4 . Irregularities within the ulnar groove (such as spurs) commonly result from overuse injuries in throwers.

The patient presents with posteromedial elbow pain and sensory symptoms such as pins and needles or numbness along the ulnar nerve distribution on the ulnar border of the forearm and the ulnar one and a half fingers. The nerve may be tender behind the medial epicondyle (Fig. 22.19), and tapping over the nerve may reproduce symptoms in some cases. Placing the elbow in maximum flexion, the forearm in pronation and the wrist in full extension for one minute may reproduce medial elbow pain and tingling/ numbness in the ring and little finger if ulnar n euritis is present. Patients with clinical features of ulnar nerve involvement should undergo neIVe conduction studies:*' Reports of a snapping sensation

Fig ure 22. 1 9 Palpation of the ulnar nerve

should lead to the suspicion of ulnar neIVe subluxation, which can be confirmed with dynamic ultrasound exnmination. 5! Treatment of ulnar neuritis depends on the initiating factor. 1. Traction injuries related to valgus instability from throwing are best served by treating the instabi lity to reduce the ongoing irritation of the ulnar nerve. 2. If adhesions are felt to be present, treatment may include local soft tissue therapy to the nerve in the ulnar groove, to mobilize soft tissue that may be compressing or tethe ring the nerve and restricting its free movement. Neural mobilisation is often beneficial. 3. Recurrent subluxation of the uln ar nerve should be referred to a neurologist or neurosurgeon experienced in managing this condition in active individuals. Management will depend on the degree of symptoms, electrophysiological evidence of nerve injury, and local management expertise (in relation to nerve transposition surgery). 4. Bony irregularities may be amenable to arthroscopic debridement.

Posterior elbow pain The main causes of posterior elbow pain are olecranon bursitis, triceps tendinopathy. and posterior impingement. Gout should always be considered.

Olecranon bursitis Olecranon bursitis may present after a single episode of trauma or, more commonly, afte r repeated trauma , such as fa lls onto a hard surface affecting the posterior aspect of the elbow. This is commonly seen in basketball players "taking a charge." It is also seen in individuals who rest their elbow on a hard surface for long period s of tim e when it is known as "s tudent's elbow." The olecranon bursa is a subcutaneous bursa that may become filled with blood and serous fluid (Fig. 22.20 overleaf). Treatment consists initially of NSAIDs, rest, and firm compression. If this fails, aspiration of the con ten ts of the bursa and injection with a mixture of corticosteroid and loca l anesthetic agen ts are usually effective. The needle should be inser ted at an oblique angle to reduce the risk of sinus formation. Although this is considered a straightforward procedure among experienced clinicians, there is a trend to use ultrasound imaging support to increase the accuracy of needle insertion. Ifrecurrent bursitis

403

Posterior impingement

Figure 22.20 Olecranon bursa (a ) Palpation site of bursa

Posterior impingement is probably the most common cause of posterior elbow pain. It occurs in two situations. In the younger sportsperson there is the "hyperextension valgus overload syndrome." Repetitive hyperextension valgus stress to the elbow results in impingement of the posterior medial corner of the olecranon tip on the olecranon fossa. Over time this causes osteophyte formation, exacerbating the impingement and leading to a fixed flexion deformity. In the older patient, the most common cause is early osteoarthritis, which often predominantly affects the radiocapitellar joint. Generalized osteophytes form through the elbow. Impingement of these osteophytes posteriorly results in posterior pain. The main clinical feature in sportspeople with posterior impingement is a fixed flexion deformity of some degree and posterior pain with forced extension (Fig. 22.21). Physiotherapy may include strategies to minimize hyperextension forces such as taping or bracing, along with a strength and flexibility program, and graduated return to sport or activity. If conservative measures fail, arthroscopic removal of the impinging posterior bone and soft tissue is very effective in relieving symptoms and improving extension.

Acute elbow injuries Acute elbow injuries include fractures, dislocations, and ligament or tendon ruptures. (b) Olecranon bursitis

does not respond to aspiration and injection, surgical excision of the bursa is required. Occasionally, olecranon bursitis can become infected. This is a serious complication that requires immediate drainage, strict immobilization, and antibiotic therapy. Osteomyelitis and septic arthritis can fonow. Excision of the bursa is occasionally required.

Investigation Given the nature of an acute elbow injury, radiography is often used as an initial assessment. In an

Triceps tendinopathy Tendinopathy at the insertion of the triceps onto the olecranon is occasionally seen. Standard conservative measures for treatment of tendinopathy should be used. Soft tissue therapy including self-massage with a styrofoam roll, and dry needling to reduce excessive tightness of the triceps musculotendinous complex may be helpful. 404

Figure 22.2 1 Posterior impingement. The elbow is forced into end-range extension. If posterior pain is produced, then posterior impingement is present

El bo w and arm pa i n attempt to reduce unnecessary use of such investigations, which are not without implications to both the patient and the healthcare system, an assessment protocol has been deve10pedY' B Patients who cannot fully extend their elbow after injury should be referred for X ray, because there is a 50% chance of fracture. Those who are fully able to extend the elbow are unlikely to have a fracture, although they should be followed up in 7 - IO days if symptoms have not resolved.

treated with multiple surgical procedures. Thus, surgery should be performed in the first 24 hours after injury or after five to seven days. Long-term follow-up of bicolumnar fractures of the distal humerus, capitellum/trochlear fractures, or elbow fracture·dislocations is recommended. A five year study has shown that 75 of 139 patients with elbow fractures exhibit radiographic evidence of moderate to severe arthrosis.s" This is not the case for fractures of the olecranon and radial head.

Fractures

Supracondylar fractures

As the complication rate for elbow fractures is higher than with fractures near other joints, it is essential that fractures in this region are recognized and treated early and aggressively. Unstable fractures, usually those associated with displacement, should be referred early for orthopedic management. When the articular or cortical surface has less than 2 mm (0.1 in.) ofvertical or horizontal displacement, the fracture can be regarded as stable and treated conservatively.5o! The most common complication of elbow frac· rures is stiffness, particularly loss of terminal extension. Promp t diagnosis and treatment that includes an early rehabilitation program can help avoid this outcome. Thus, treatment of elbow fractures must be aggressive. Surgically stabilizing an adult elbow frachIre allows early commencement of a postoperative range of motion program. A stable fracture that involves no significant comminution, displacement, or angulation may be treated conservatively. In adults. immobilizing the arm for a few days, even up to a week, is generally well tolerated. Then the arm should be placed in a removal splint and early motion commenced. The fracture should be protected for a further six to eight weeks, with early and frequent radiographic checks to ensure the reduction stays anatomical. The other main complication of elbow fractures, particularly in high-energy injuries, is heterotopic ossification. This usually appears within the first month after surgery and plateaus after four to six months. Traumatized elbows that are forcefully or passively manipulated may also be at greater risk of this complication. 55 Therefore, gentle, active assisted range of motion and pain free stretching exercises are preferred. Mobilization with movements. applied correctly in a pain-free manner, may be helpful in restoring motion ..>7 Heterotopic bone formation has also been associated with elbow fractures treated surgically between one and five days after injury or

Supracondylar fractures are more common around the age of 12 years than in adults. They often occur from a fall on an outstretched arm, either from a height or from a bicycle. Because they are rotationally unstable and have a high rate of neurovascular complications, these fractures should be regarded as an orthopedic emergency. For fractures that are unstable, displaced, or that cannot be reduced without jeopardizing the blood supply. the treatment of choice is dosed reduction in the operating room under general anesthesia. Percutaneous pins placed across the fracture main· tain the reduction and prevent late slippage. The arm is initially placed in a splint and then several days later in a cast. The pins are removed after four to six weeks. Stiffness is typically not a problem in children recovering from fractures.

4

4

Olecranon fractures Olecranon fractures occur from a fall onto an outstretched hand or from direct trauma to the elbow. If the fracture is non-displaced and stable, the patient should be able to extend the arm against gravity. Treatment consists of immobilizing the arm for two to three weeks in a posterior splint, then in a removable splint and a range-oC-motion program commenced. If the patient is unable to extend the elbow against gravity or if radiographs show significant displacement, open reduction with internal fixation by tension-band wiring is preferred. Early motion is started within one week of surgery.

Radial head fracture The most common fracture around the elbow in sports people is the radial head fracture, almost always resulting from a fall onto an outstretched hand. Most radial head fractures are minimally placed or non-displaced (type II and are velY difficult

405

Reg ional pr ob lems to see on radiographs. Sometimes the only clue is the fat pad sign, which appears as a triangular radiolucency just in front of the elbow joint. Early aspiration, splinting with an easily removable device, and early commencement of a range of motion program yields excellent results. Complete healing can be expected within six to eight weeks. For displaced radial head fractures (type 2), surgical intervention with operative fixation or excision is preferred. Comminuted fractures (type 3) are treated by excision. Type 4 fractures occu r in the presence of a dislocation and can be very unstable. They always require surgical treatment.

Dislocations Posterior The most serious acute injury to the elbow is posterior dislocation of the elbow. This can occur either in contact sports or when falling from a height such as while pole vaul ting. There is often an associated fracture of the coronoid process or radial head. The usual mechanism is a posterolateral rotatory force resulting from a fall on an outstretched hand with the shoulder abducted, axial compression, forearm in supination then forced flexion of the elbow.'; The major complication of posterior dislocation of the elbow is impairment of the vascular supply to the forearm. Assessment of pulses distal to the dislocation is essential. If pulses are absent, reduction of the dislocation is required urgently. Reduction is usually relatively easy. With the elbow held at 45", the clinician stabilises the humerus by gripping the anterior aspect of the distal humerus, and traction is placed longitudinally along the forearm with the other hand (Fig. 22.22). The elbow usually reduces

with a pronounced clunk. If vascular impairment persists after reduction, urgent surgical intervention is required. Following reduction , the stability of the collateral ligaments should be assessed (Fig. 22.17a). A postreduction X-ray should also be performed. Small fractures of the coronoid process or undisplaced fractures of the radial head only require conservative treatment with support in a sling fo r two to three weeks. Large coronoid fractures, however, may result in chronic instability and should be reduced and fixed surgically. Large fractures of the radial head may be difficult to manage but in most cases can be internally fixed. Occasionally, a large fracture of the capitellum may occur. This also requires internal fixation. Sometimes a piece of bone becomes trapped in the joint after reduction. This needs to be excluded with good-quality post-reduction X-rays. Long-term loss ofextension is frequently a problem following elbow dislocation. Immediate active mobilization under supervision has been shown to result in less restriction of elbow extension with no apparent increase in instability,58 Professional sportspeople with a simple dislocation with no associated fracture or instability are able to return to sport relatively quickly after an accelerated rehabilitation program. Verrall described three cases of stable dislocations in professional footballers who returned to sport after 13, 21 and seven days respectively with no further complications)9 Joint mobilization (Fig. 22.23) may be required as part of the treatment. Surrounding muscles should also be strengthened. Elbow stability taping should be applied on return to sport (Fig. 22.17b). Heterotopic ossification occasionally occurs following elbow dislocation. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) for a period of three months following the injury may reduce the incidence of this complication. Some patients may develop chronic instability of the elbow following an acute dislocation. This is classically posterior lateral instability. If symptoms are unacceptable, then a reconstruction of the lateral ulnar collateral ligament may be indicated.

Other dislocations Figure 22.22 Technique for reduction of posterior dislocation of the elbow

406

Elbow dislocations in directions other than posterior occur occasionally. These are often associated with severe ligamentous disruption, and patients should be referred to an orthopedic surgeon immediately.

El bow an d a rm p a i n

Acute rupture of the medial collateral ligament Acute rupture of the medial collateral ligament may occur in a previously damaged ligament or in a normal ligament subjected to extreme valgus stress (e.g. elbow dislocation). The degree of instability should be assessed by applying valgus stress to the elbow at )0" of flexion (Fig. 22.17a). If complete dis· ruption is present with associated instability, surgical repair of the ligament is required. Incomplete tears should be treated with protection in a brace and muscle strengthening for a period of three to six weeks, followed by graduated return to sport.

Tendon ruptures

Figu re 22.23 Examples of mobilisation with movement techniques that use a glide out of the plane of extension to improve extension (a) Sustained lateral glide applied through a belt while

assisted active extension is performed

Acute avulsion of the biceps or triceps tendons from their insertions is a rare condition. Rupture of the biceps tendon insertion occurs males predominantly in young or engaged in strength activities (e.g. weightlifting). Partial ruptures are more painful than complete tures, due to mechanical irritation of the remaining intact tendon. Early surgical repair of complete tures would be expected to lead to better outcomes, as complete rupture of tendons leads to degenerative processes due to the loss of mechanical load. Rupture of the triceps tendon occurs most monly with excessive deceleration force, such as during a fall or by a direct blow to the posterior aspect of the elbow. Partial and complete triceps rup" tures are seen in American National Football League linemen. Partial tears tend to heal well without surgery. Acute complete nlptures at the insertion of either of these tendons should be treated surgically.

Forearm pain

Fracture of the radius and ulna

(b) Sustained internal rotation 27

The bones of the forearm are commonly injured by a fall on the back or front of the outstretched hand. It is usual for both bones to break, although a single bone may be fractured in cases of direct violence or in fractures of the distal third where there is no shortening. A displaced fracture is usually clinically obvious. X-rays should be taken for post-reduction comparison and for exclusion of a concurrent dislocation. Two types of dislocation occur-the Monteggia injury (fractured ulna with dislocated head of the radius at the elbow joint) and the Galeazzi injury (fractured

407

radius with dislocated head of the ulna at the wrist joint)_ In children. angulation ofless than ID" is accepta· ble. Other fractures should be reduced under local or general anesthesia depending on the age of the child. The usual position for immobilization is in prona· tion. although in proximal radial fractures and in Smith's fractures at the wrist. the forearm should be held in supination. The plaster should extend above the elbow and leave the metacarpophalangeal joints free. Depending on the age of the child. immob" ilization should last four to six weeks. The position should be checked by X·ray every one to two weeks depending on stability. In adults, perfect reduction of radial and ulnar fractures is necessary to ensure future sporting function. Most of these fractures are significantly displaced and require internal fixation by plate and screw. Depending on the accuracy of the reduction, either a cast or crepe bandage support is required postoperatively for 8-10 weeks. Isolated fracture of the ulna is treated conservatively by an above-elbow cast in mid"pronation for eight weeks. Monteggia and Galeazzi injuries are usually displaced and should be referred to an orthopedic surgeon for reduction.

Sh-ess fractures

posterior interosseous nerve may occur at one of four sites: fibrous bands in front ofthe radial head recurrent radial vessels arcade of Frohse tendinous margin of the extensor carpi radialis brevis muscle.

It is often difficult to differentiate between exten· sor tendinopathy and the early stages of posterior interosseous nerve entrapment. Posterior interos" seous nerve entrapment is seen in patients who repetitively pronate and supinate the forearm, whereas extensor tendinopathy is more frequently associated with repetitive wrist extension. Symptoms of posterior interosseous nerve entrapment include paresthesia in the hand and lateral forearm, pain over the forearm extensor mass, wrist aching, and middle or upper third humeral pain. Maximal tenderness is over the supinator muscle, four finger-breadths below the lateral epicondyle (distal to the area of maximal tenderness in extensor tendinopathy). Reproduction of symptoms by manual palpation of these local structures, and the relief of such palpation"induced symptoms by injection of local anesthetic. should be considered as part of the physical examination.6 Nerve entrapment also causes !

Stress fractures of the forearm bones occur occasion· aUyin sportspeopleinvolved in upper limb sports (e.g. baseball, tennis, swimming). Treatment involves rest and correction of the possible predisposing factors, such as faulty technique.

Entrapment of the posterior interosseous nerve (radial hmnel syndrome) The radial nerve divides into the superficial radial and the posterior interosseous nerve at the level of the radiocapitellar joint (Fig. 22.24). The posterior interosseous nerve passes distal to the origin of the extensor carpi radialis brevis and enters the arcade of Frohse. Prior to entering the arcade, it gives off branches to the extensor carpi radialis brevis and supi. nator muscles. The arcade is a semicircular fibrous arch at the proximal head of the supinator muscle, which begins at the tip of the lateral epicondyle and extends downward, attaching to the medial aspect of the lateral epicondyle. The posterior interosseous nerve then emerges from the supinator muscle distally, where it divides into terminal branches that innervate the medial extensors. Compression of the 408

supinator

ulna

extensor

pollicis brevis

Figure 22.24 Anatomy of the posterior interosseous

nerve 60

El bow and a rm pain

marked pain on resisted supination of the fo rearm with the elbow flexed to 90° and the forearm fully pronated. Another sign is pain with resisted extension of the middle finger with the elbow extended, although this can be positive in extensor tendinopathy as well. Neurodynamic tests may reproduce the patient's symptoms and nerve conduction studies may be performed to confirm the diagnosis. Treabnent consists of soft tissue therapy over the supinator muscle at the site of entrapment and neural tissue mobilisation, along with exercises targeting strength and endurance deficits in the forearm muscles. If this is unsuccessful, decompression surgery may be required.

. _"u : l J

delto,d mfraspmatus

?x x x

•

x

•

Figure 22.25 Myofascial trigger points around the shoulder region that refer pain to the upper arm

Forearm compartment pressure syndrome Forearm compartment pressure syndromes have been described in kayakers. canoeists. motor cyclists (popularly termed "arm pump" in motor cross), and weight-training athletes. The flexor compartment is most usually affected. Symptoms include activity-related pain that is relieved by rest. Diagnosis requires compartment pressure testing (Chapter II). Treatment consists of local soft tissue therapy. Surgical fasciotomy may be required.

Attention should also be paid to the lower cervical and upper thoracic to mid-thoracic spine. Increased muscle tone and trigger points may be found in the paraspinal muscles, and hypomobility of the intervertebral segments may be present. TI1ese abnormali· ties must also be treated with heat and soft tissue techniques.

Stress reaction of the humerus Upper arm pain An aching pain in the upper arm is a common complaint, especially among manual workers (e.g. bricklayers. carpenters) and sportspeople. The most common cause is myofascial pain, but stress fracture of the humerus needs to be considered.

Myofascial pain A dull non-specific pain in the upper ann is most likely to be myofascial in nahire. The most common source of the upper arm pain is trigger poin ts in and around the infras pinatus muscle (Fig. 22.25). Firm palpation of these trigger points often reproduces the pain. The cervical spine and glenohumeral joint need to be assessed for their possible involvement. and treatment directed accordingly. Treatment consists of heat. and digital ischemic pressure or dry needling to the trigger points.

Stress reactions and frachlres of the humerus have been described in baseball pitchers, tennis players. javelin throwers, bodybuilders, and weightlifters. In a group of symptomatic elite tennis players. MR I of the humerus demonstrated bone marrow edema and/or periostitis, and the extent ofimaging changes was related to the severity and duration of symptoms.(i; Most of the fractures occurred in adolescents and were associated with a recent increase in activity. In a number of cases, the diagnosis was made retrospectively when an acute fracture occurred and the patient acknowledged symptoms leading up to the acute episode. Recommended treatment follows the general principles of management of simple stress fractures, involving avoidance of the aggravating activity until symptom-free and no local tenderness. then gradual resumption of the activity.

409

CLINICAL SPORTS ME D ICINE

epicondylalgia. Arch Phys Med Relwbil2006;87(4):

MASTERC L AS S ES

49 0-5. Andersson G, Forsgren S, Scott A et a1. Tenocyte

www cl jnjca lsp o rtsm e d jcj o e com

II.

Listen to the podcast with chapter authors Vicenzino and

hypercellularity and vascular proliferation in a rabbit

Scott. They provide practical tips on:

model oftendinopathy: contralateral effects suggest

confirming the diagnosis oflateral elbow pain

the involvement of central neuronal mechanisms.

choosing among the many treatment options.

Br} Sports Med 2on;45(5):399-406. 12. Pienimaki IT, Kauranell K, Vanharanta H. Bilaterally

m

RECOMMENDED READING Vicenzino B, Hing W, Rivett D, Hall T. Mobilisatiott with movement: the art and the science. Sydney. Churchill Livingstone,2on.

decreased motor performance of arms in patients with chronic tennis elbow. Arch Phys Med Relwbil

1997;78 (10): 1°9 2-95. 13. Waugh EJ, Jaglal SB. Davis AM. Computer use associated with poor long-term prognosis of conservatively managed lateral epicondylalgia.) Orthop

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...

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Conservative treatments for tennis elbow-do

can reduce postoperative analgesic consumption.

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pa tients with chronic refractory lateral epicondylitis.

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Roelllgel101.2o06; r87(4):90 1-4·

,.

";.sJt'

..., ., . •

AU this year I've been wanting to avoid surgery with different treatments but evidently the injUly is more serious. The recove,y time is prolonged but it depends on many factors that can't be measured today. Juan Martin Del Potro, Argentinian tennis player and US Open Champion

announcing surgery for a wrist flexor tendon injury." May, 2010 guo ted in Guardian.co.uk.

2 009,

The wrist is frequently injured during sport.! Distal radial fractures are the most common fracture seen in emergency departments,l and scaphoid frachues are the most common carpal fracture) Men are more likely to sustain a hand or wrist injury:"I children and adolescents are more likely to have a wrist injury compared with adults.s Injuries to the wrist range from acute traumatic fractures (such as occur during football, hockey, and snowboarding) to overuse conditions (which occur in racquet sports, golf, and gymnastics). If wrist injuries are not treated appropriately at the time of injury. they can lead to future impairments that can affect not only sporting endeavors but also activities of daily living.(j In this chapter we address two common clinical scenarios: the acute wrist injury (usually as a resu lt of a fall onto the outstretched hand) the longer-term (chronic, or subacute) wrist pain that has developed gradually with or without a clear history of a past injury.

Acute wri st injuri es The wrist joint has multiple axes of rnovementflexion-extension and radial-ulnar deviation occur at the radiocarpal joints. and pronation-supination occurs at the distal radioulnar joint (in conjunction with the proximal radioulnar joint). 111ese movements provide mobility for hand function. If

Injuries to the wrist often occur due to a fall on the outstretched hand IFOOSH). In sportspeople, the most common acute injuries are fractures of the distal radius or scaphoid, or damage to an intercarpal ligament. Intercarpal ligament injuries are becom· ing more frequently recognized and, if they are not treated appropriately (e.g. including surgical repair where indicated), may result in long·term disability. The causes of acute pain in this region are shown in Table 2).[ overleaf. The anatomy of the wrist is complex (Fig. 23.1 overleaf). It is helpful to know the surface anatomy of the scaphoid tubercle. hook of hamate. pisiform, Lister's tubercle, and anatomical snuffbox. The bony anatomy consists of a proximal row (lunate, triquetrum, pisiform) and a distal row (trapezium, trapezoid, capitate, hamate), which are bridged by the scaphoid bone. Normally, the distal carpal row should be stable; thus, a ligamentous injury here can greatly impair the integrity of the wrist. 'The proximal row permits more intercarpal movement to allow wrist flexion/extension and radial and ulnar deviation. Here a ligamentous injury disrupts important kinematics behveen the scaphoid, lunate, and trio quetrum, resulting in carpal instability with potential weakness and impairment of hand function.

History It is essential to determine the mechanism of the injury causing wrist pain. A fall on the outstretched

Del Potro returned to competition nine months after surgery.

41 3

"""

Table 23 .1 Causes of acute wrist pain Common

less common

Not to be missed

Distal radius fracture (often

Fracture of hook of hamate Triangular fibrocartilage complex tear Distal radioulnar joint instability Scapholunate dissociation

Carpal dislocation Anterior dislocation of lunate Perilunar dislocation Traumatic ulnar artery aneurysm or thrombosis (karate)

intra-articular in the athlete) Scaphoid fracture Wrist ligament sprain/tear Intercarpal ligament Scapholunate ligament Lunotriquetral ligament

(el Surface anatomy, volar view

Figu re 23.1 Anatomy of the wrist (a) Carpal bones (MC= metacarpal) fibrous flexor sheaths

brachioradialis

tendon

flexor pollicis longus

(bl Surface anatomy, dorsal view

414

(d) Volar aspect

i 1&

Ta bl e 23.2 Clinical distinction between dorsal and volar pain in acute wrist pain Causes of dorsal wrist pain Causes of volar wrist pain

adductor

extensor carpi

ulln,,'II' tendon

extensor retinaculum

(e) Dorsal aspect

hand may be severe enough to fracrure the scaphoid or distal radius, or damage the intercarpal ligaments and/or triangular fibrocartilage complex. These injuries are commonly encountered in highvelocity activities such as snowboarding,7 rollerblading,B. 9 or falling off a bike. A patient may fracture the hook of hamate while swinging a golf club,1O tennis racquet, or bat, or while striking a hard object (e.g. the ground). Rotational stress to the distal radioulnar joint, and forced ulnar deviation and rotation may tear the triangular fibrocartilage complex. It is very useful to detennine the site of the pain; the causes of volar pain are different from those of dorsal wrist pain (Table 23.2). Other important aspects of the history may include: hand dominance occupation manual labor, food service industry) degree of reliance on hands in occupation/recreation history of past upper extremity fractures, including childhood fractureslinjuries history of osteoarthritis, rheumatoid arthritis, thyroid dysfunction, diabetes any unusual sounds (e.g. clicks, clunks, snaps)

Carpal instability Scaphoid fracture Hook of hamate fracture Scaphoid impaction syndrome Fracture dislocation of carpus Lunate fracture Distal radius fracture Scapholunate ligament tear Kienb6ck's disease (acute onset) Lunotriquetralligament tear Distal radioulnar joint injury Carpometacarpal dislocation

recurrent wrist swelling, which raises the suspicion of wrist instability musician (number of years playing, hours of practice per week, change in playing, complex piece, etc.) gardening, crafts, hobbies.

Examination Examination involves: ,. Observation (Fig. 23.2a overleaf) 2. Active movements (a) flexion/extension (b) supination/pronation (c) radial/ulnar deviation (Fig. 23.2b overleaf) 3. Passive movements (a) extension (Fig. 23.2c overleaf) (b) fiexion (Fig. 23.2d overleaf) 4. Palpation (a) distal forearm (Fig. 23.2e overleaf) (b) radial snuffbox (Fig. 23.2f overleaf) (c) base of metacarpals (d) lunate (Fig. 23.2g overleaf) (e) head of ulna (Fig. 23.2h overleaf) (f) radioulnar joint 5. Special tests (a) hamate/pisiform (Fig. 23.2i overleaf) (b) Watson's test for scapholunate injury (Fig. 23.2j on page 418) (c) stress of triangular fibrocartilage complex (Fig. 23.2k on page418)

415

(d)

ulnar fovea sign for foveal disruption and ulnar triquetralligament injury (Fig. 23.21on page 418) (e) grip-Jamar dynamometer (may be contraindicated if a maximal effort is not permitted [e.g. after tendon repair]) (f) dexterity-Purdue pegboard (Fig. 23.2m on page419) (g) dexterity-Moberg test (h) sensation- Semmes Weinstein monofilament testing (il sensation- temperature (j) nerve entrapment-Tinel's sign 6. Standardized rating scales

(el Range of motlon-the"prayer position:' Normal range of motion in wrist extension is 70"

Figure 23.2 Examination of the patient with an acute wrist injury (a) Observation. Inspect the wrist for obvious deformity suggesting a distal radial fracture. Swelling in the region of the radial snuffbox may indicate a scaphoid fracture. Inspect the hand and wrist posture, temperature, COIOf, muscular wasting, scars, normal arches of the hand

(b) Active movement-radial/ulnar deviation. Normal range is radial 20° and ulnar 60", Pain and restriction of movement should be noted. Always compare motion with that of the other hand

416

(d) Range of motion-the"reverse prayer position:' Normal range of motion in wrist flexion is 80"_90°

W ri s t pa in

(e) Palpation-the distal forearm is palpated for bony tenderness or deformity

(h) Palpation- head of ulna and ulnar sn uffbox. Swelling and tende rness over the dorsal ulnar aspect of the wrist is present with fractures of the ulnar

styloid. Distal to the ulnar head is the ulnar snuffbox. The triquetrum lies in this sulcus and can be palpated with the wrist in radial deviation. Tenderness may indicate triquetral fracture or triquetrolunate injury. The triquetrohamate joint is located more distally. Pain here may represent triquetrohamate ligame nt injury

If} Palpation-radial snuffbox. The proximal snuffbox is the site of the radial styloid, the middle snuffbox is the site of the scaphoid bone, while the distal snuffbox is over the scaphotrapezial joint

(i) Palpation-the pisiform is palpated at the flexor

crease of the wrist on the ulnar side. Tenderness in this region may occur with pisiform or triquetra I fracture. The hook of hamate is 1 cm (0.5 in.) distal and radial to the pisiform. Examination may show tenderness over the hook or on the dorsal ulnar surface

(9) Palpation-the lunate is palpated as a bony prominence proximal to the capitate sulcus. lunate tenderness may correspond to a fracture. On the radial side of the lunate lies the scapholunate joint. which may

be tender in scapholunate ligament sprain. This is a site of ganglion formation

Several valid and reliable assessment scales can quantify function of the wrist specifically, or the upper extremity, after an injury. These include the Patient Rated Wrist Evaluation (PRWE),"'" the Disability of the Arm, Shoulder and Hand (DASH and Quick DASH),'I"4 and the Mayo wrist score measurements.') The Mayo and DASH scores can conveniently be completed online at the following website for various orthopedic scores (www.orthopaedicscore.com).

41 7

U) Special test-Watson's test for scapholunate instability. The examiner places the thumb on the scaphoid tuberosity as shown with the wrist in ulnar deviation. The wrist is then deviated radially with the examiner placing pressure on the scaphoid. If the athlete feels pain dorsally (over the scapholunate ligament) or the examiner feels the scaphoid move dorsally, then scapholunate dissociation is present

(k) Special test- triangular fibrocartilage complex integrity. The wrist is placed into dorsiflexion and ulnar deviation and then rotated. Overpressure causes pain and occasionally clicking in patients with a tear of the triangular fibrocartilage complex

Investigations Plain radiography Following trauma, routine radiograph views should include a PA with the wrist neutral as well as PAs with both radial and ulnar deviation. If ligament injury is suspected, also obtain a PA view with clenched fist. A straight lateral view of the wrist, with the dorsum of the distal forearm and the hand forming a straight line, permits assessment of the distal radius, the lunate, the scaphoid, and the capitate and may reveal

subtle instability. Undisplaced distal radial and scaphoid fractures, however, are often difficult to see

418

0) Ulnar fovea sign forfoveal disruption and ulnar triquetralligament injury. The ulnar stylOid process is easily palpated with the forearm in neutral rotation. The fovea lies between the ulnar styloid (US) process and the flexor carpi ulnaris (FeU) tendon. Distally it is bounded by the pisiforn (P) bone and proximally by the volar surface of the ulnar head, which in this photo is under the examiner's finger pulp. The tip of the examiner's index finger points to the location of the fovea on initial radiographs; clinical suspicion of fracture warrants investigation with other modalities (see

"Special imaging studies" below). The normal PA view is shown in Figure 23.3a. Inspect each bone in turn. Note the line joining the proximal ends of the proximal row of the carpus and

the "C" shape of the midcarpal joint (Gilula's arcs). If these Hnes are not smooth, a major abnormality is present. Assess the size of the scapholunate gap and look for scaphoid flexion (the signet ring sign) as these are signs of scapholunate instability. The lateral radiograph of the normal wrist can be seen in Figure 23.3b. The proximal pole of the lW1ate fits into the concavity of the distal radius, and the

Wris t pa in

(m) Special test-Purdue pegboard dexterity test. This measures dexterity for activities that involve gross movements of the hands, fingers, and arms, and also those that require"fingertip" dexterity convex head of the capitate fits into the distal concavity of the lunate. These bones should be aligned with each other and with the base of the third metacarpal. A clenched fist PA view should be taken if scapholun. ate instability is suspected. This is indicated by a widened gap of 3 mm (o.! in.) or greater between the scaphoid and lunate on the PA view; however, this may not present until some time after a scapholunate tear. ? Rile-

'0""

Figure 23.3 Radiograph of the wrist (a ) PA view-Gilula's arcs

Scapholunate instability cannot be ruled out on initial plai n radiographs, as it may take some months forthe scaphoid and lunate to separate significantly radiographically.

Special imaging studies The combination of the complex anatomy of the wrist and subtle wrist injuries that can cause substantial morbidity has led to the development of specialized wrist imaging techniques. Special scaphoid views should be requested if a scaphoid fracture is suspected. A carpal tunnel view with the wrist in dorsiflexion allows inspection of the hook of hamate and the ridge of the trapezium. For suspected mechanical pathology (such as an occult ganglion, an occult fracture, non-union, or bone necrosis), several modalities are useful (e.g. ultrasonography, radionudide bone scan, cr scan, MRI). Ultrasonography is a quick and accessible way to assess soft tissue abnormalities such as tendon injury, synovial thickening, ganglions, and synovial cysts. Bone scans have high sensitivity and low specificity; thus, they can effec tively rule out subtle fractures.

(b)

Lateral view

419

MRI may be equally sensitive to and more specific than a bone scan. CT scanning is particularly useful for evaluating fractures that are difficult to evaluate fully on plain films, but MRI can also provide information about soft tissue injuries. Thus, a complete scapholunate ligament tear is more effectively identified with MRI than with CT. Arthrography of the wrist is no longer used as an investigative tool except in combination with MRI-"MR arthrogram' or MRA. If all imaging results are negative but clinically significant wrist pain persists, the clinician should refer the patient to a specialist for further evaluation.

Fracture of the distal radius and ulna Distal radial fractures (Fig. 23.4) are very common peripheral As the force required to fracture young adults' bones is great, sportspeople may simultaneously incur an intra-articular fracture and ligamentous strain or rupture. The higher the forces involved (e.g. in high-velocity sports), the greater the likelihood of a complex injury involving articular structures. TI1US, thorough assessment

of ligamentous injury is essential when fractures occur. Initial treatment of the fracture is anatomical reduction and immobilization for up to six weeks in a cast that covers the distal half of the forearm, the wrist, and the hand, leaving the metacarpophalangeal joints free. 16 Radiographs are required every two weeks during healing to ensure that satisfactory reduction is maintained. Inaccurate reduction, articular surface angulation, radial inclination, or inadequate restoration oflength all require early internal fixation with fixed anglevolar plating. 16 . 17 While it is sometimes not possible to achieve perfect reduction because of dorsal comminution, every effort should be made to restore anatomical alignment to avoid ongoing functional impairment. Overall, there is a trend to more aggressive treatment using volar plating, and this has led to improved functional outcomes, especially in the young active adult.

Fracture of the scaphoid Carpal fractures account for many hand/wrist fractures. The most common carpal fracture involves the scaphoid;4 the usual mechanism is a fall on the outstretched hand. As the patienfs pain may settle soon after the fall, he or she may not present to a clinician until some time after the injury. The key examination finding is tenderness in the anatomical snuffbox (Fig. 2}2f on page 417). This may be accompanied by swelling and loss of grip strength. Snuffbox tenderness should be compared with the other wrist, as some degree of tenderness is normal. Swelling in the snuffbox should also be sought. A more specific clinical test for scaphoid fracture is pain on axial compression of the thumb toward the radius or direct pressure on the scaphoid tuberosity with radial deviation of the wrist. Plain radiographs with special scaphoid views will usually demonstrate the fracture (Fig. 23.5). If a scaphoid fracture is suspected clinically but the radiograph is normal, a fracture cannot be ruled out. MRI is an ideal diagnostic test for an acute injury that may be cost-saving in some settings. 11 Bone scan also has excellent sensitivity for scaphoid fracture. Note that it can take 24 hours for the injury to be revealed on MRI or bone scan. I' R4 ('

Figure 23.4 Colles' fracture, a speCific type of distal radial fracture

420

'brry

If a scaphoid fracture is susp ecte d cli nically butthe rad iograph is norma l, a fracture can not be ru led out.

Figure 23.6 Two types of treatment of scaphoid fractures (a) Cast immobilization

Figure 23.5 A subtle scaphoid fracture

In cases where these imaging modalities are not available, the wrist should be immobilized for 12 days as if a fracture were present, and followed by clinical examination and repeat radiograph. Note that scaphoid fracture is the most commonly missed fracture leading to litigation. If there is no bony damage, scapholunate instability should also be considered (see below).

Traditional treatment of stable and unstable scaphoid fractures A stable scaphoid fracture should be immobilized for eight weeks in a scaphoid cast extending from the proximal forearm to, but not including, the interphalangeal joint of the thumb (Fig. 23.6a). On removing the cast, re-evaluate the frachtre clinically and radiologically. As with all fractures, clinical union precedes radiological union and determines readiness to return to sport. Absence of pain on palpation, and comfort when the wrist is rotated and angulated by the examiner indicate clinical union. Radiological union of the scaphoid should occur before finally discharging the patient from follow-up. Overall, in excess of 90% of scaphoid fractures heal without problems. Unstable, angulated (>I5-20Q) or significantly displaced fractures (diastasis in the fracture gap >I.S mm) require immediate percutaneous fixation (Fig. 2}6b) or open reduction and internal fixation.

(b) Surgical fixation. This is increasingly being used for uncomplicated scaphoid fractures (see also box overleaf)

Emerging treatment of stable scaphoid fractures By early 20n, new data emerged surrounding the management of "routine" scaphoid undisplaced or minimally displaced fracture. Until then, meta-analyses indicated that there was no evidence to determine whether non-surgical or surgical management was superior. However, publication of four new randomized controlled trials (RCTs) in 2007 and 2008 led Buizje and colleagues to conclude in a 2010 meta-analysis that surgical treahnent provides superior functional outcome and requires less time off work (see box overleaf).l)\ Surgical treahnent, however, was associated with a higher rate of complications 42 1

management

Operative

Study or subgroup Arora

Mean

4

Dias

3.9

McQueen

6.3

Vinnars

4.5

Conservative

SD

Total

4.2

21

7.9

TOTAL (95% (I) Heterogeneity:

uncomplicated

Mean

13

SD 14.1

Std. mean difference IV, random, 95% (I

Total

Weight

23

17.6%

-0.83 [- 1.45, - 0.21J

39

5.2

1.8

42

31.3%

-0.88 [-1.33, -0.42J

23

12.3

19.2

24

20.0%

-0.40 [-0.98, 0.18J

40

5

1.5

35

31.1%

-0.39 [-0.85, 0.06J

124

100.0%

-0.62 [-0.89, -0.36J

123 = 0.00; Chi2 = 3.16; df = 3 (P = 0.37);

Std mean difference

12=5%

IV, random, 95% ( I

Test for overall effect: Z = 4.62 (P :;o shown to be associated with low back pain.

(e) Sitting with lumbar roll

An important component of rehabilitation ofpatients with low back pain is to correct deficiency of core

485

Figure 26.17 Standing posture

Figure 26.18 lifting technique

(a) Hyperlordotic

(a) Incorrect

(b) Correct

(b) Correct

486

Lo w ba ck p ai n stability. A core stability program is described in Chap terI 4· Once activation of the spine stabilizers (transversus abdominis and lumbar multifidus) has been achieved, global muscle strengthening should commence. In patients with low back pain, particular emphasis should be placed on strengthening the gluteal and hamstring muscles. Adequate gluteal strength is required for pelvic control. Lack of pelvic control may lead to anterior tilting of the pelvis and increased stress on the lumbar spine. It is important that the gluteal muscles are activated during lifting and bending. Gluteal strengthening exercises should be performed while controlling pelvic movement (Fig. 26,[9). The single· leg squat (Fig. 26.20 overleaf) is an excellent rehabilitation exercise combining motor control and strengthening.

rectus femoriS, and gastrocnemius. Tigh tness of these muscles affects the biomechanics of the lumbar

Specific muscle tightness Specific muscle tightness or shortening is commonly found in association with low back pain. Commonly shortened muscles include the erector spinae, psoas, iliotibial band, hip external rotators, hamstrings, (b) Bending with gluteals but using lumbar flexion

Figure 26.19 Gluteal strengthening (al Bending at the knee without using gluteals

(el Bending with gluteals and braced lumbar spinethis is the recommended exercise

487

spine. These tight muscles should be corrected as part of the rehabilitation program. The various techniques are shown in Figure 26.2I. Muscle tightness may be corrected by the use of therapist-assisted exercises, home exercises, soft tissue therapy to the muscles, and dry needling of trigger points.

Con cl u sion

Figu re 26.20 and motor control

squat-gluteal strengthening

Muscle

Self-exercise

The clinical approach to the sportsperson with low back pain is relatively straightfonvard. It involves initial assessment of abnormalities of the joints, muscles, and neural structures. These abnormalities are then systematically corrected by the use ofmanual therapy techniques. Associated with this correction of abnormalities, a comprehensive rehabilitation program must be performed, including correction of any biomechanical factors that place increased stress on the lumbar spine in the particular sportsperson. This requires individual assessment of abnormalities of technique, muscle weakness, muscle tightness, or

Assisted exercise

Myolascfal release

Erector spinae

Patlent is side·lying. Therapist's wrists are crossed over each other to provide traction.

Psoas

.

m

backvertical- -/

Iliotibial band

I

" ,-.

rj

Therapist's hand is over the psoas. Hip is extended from the flexed position.

n

Patient is side.lying and facing away. Hip is extended and adducted.

Figure 26.21 Techniques used to treat tightness of individual muscles

488

Patient is side· lying and facing away. Therapist uses elbowiforearm \0 perform release

Low b ac k pa i n poor muscle control There is now considerable evi· dence that inability to use the stabilizing muscles. transversus abdominis and lumbar multifidus, are important features of patients with low back pain,

Muscle

Self· exercise

and a specific rehabilitation program must be instituted to correct these deficits. Low back pain provides another example of the integrated approach required in the m anagement of sporting injuries.

Assisted exercise

MyofasciaJ refease

•

Hip external rolators

Hip into adduction with treatment leg crossed over opposite leg .

Patient is side.lying. Therapist stands behind and lakes the lop

i

reg backward.

Hamstrings

Palienl is prone. The e lbow or forearm is kepi stationary arld the kn ee passively extended.

Rectus femoris

.

'.,

Keep pelvis down wtli!e exlending hip and fl exing knee .

Therapist uses Iorearm 10 massage up the thigh 01 the leg which is hanging al f Ihe table.

•

Gastrocnemius

Therapi st uses thig h 10 oblaln pa ssive ankle dorsiflexion.

Pressu re on back leg.

•

•

Soleus

Pressure on Irani Jeg.

Therapist uses mesl la as sist ankle dorsiflexio n.

Figure 26.21 (cont.) Techniques used to treat tightness of individual muscl es

489

ED

RECOMMENDED WEBSITFS

7.

An educational tool about low back pain can be found at www.iowbackpain.tv

2002.

S.

m

RECOMMENDED READ I NG

4th edn. Edinburgh: Churchill Livingstone, 2005. maHllal medicine. Stuttgart, Germany: Georg Thieme

Verlag, 2008, Ucciardone

Je. BrimhallAK, King LN.

pain. A predictor of symptomatic discs and anular

muscle strength in male and female collegiate athletes,

CUlt] Sport Med 2000;10(2):89-97, Richardson C, Jull G, Hodges P et aL 71u:rapeutic exercisefor

spillal segmental stabilization ill lolV back pnill. 2nd edn, Edinburgh: Churchill Livingstone, 2004.

m

Hides JA, Stokes MJ, $aide M et al. Evidence oflumbar

Furlan AD, van Tulder M, Cherkin D et al. Acupunchlre and dry· needling for low back pain: an updated systematic review within the framework of the cochrane collaboration. Spine (Phi/a Pa 1976) 2005:30(8):

944- 6 3. 12. Shen FH, Samartzis D, Andersson GB. Nonsurgical management of acute and chronic low back pain. ] Am

Acad Orthop Surg 2006;14(8}:477-87. 13. Lord SM, Bamsley L, Bogduk N. The utility of comparative local anesthetic blocks versus placebo· zygapophysial joint pain. CIiIlJ Pain 1995;n(3):208-13 . 14. Dreyfuss P, Halbrook B, Pauza K et al. Efficacy and

multifidus muscle wasting ipsilateral to symptoms

validity of radiofrequency neurotomy for chronic

in patients with acute/subacute low back pain_

lumbar zygapophysial joint pain. Spine (Phila Pa 1976)

Carlson C. Axial back pain in the athlete:

2000:25(1O): 1270- 7· 15. van KleefM, Barendse GA, Kessels A et ai.

pathophysiology and approach to rehabilitation.

Randomized trial of radio frequency lumbar facet

Curr Rev Musculoskelet Mal 2oo9;2(2}:88-93,

denervation for chronic low back pain. Spine (Phila Pa

Freeman MD, Woodham MA, Woodham AW. lhe role of the lumbar multifidus in chronic low back pain: a review. PM R 2010:2(2):142-6.

1976) 1999;24(18):1937-42.

r

16. Yin W, Willard F, Carreiro et a!. Sensory stimulationguided sacroiliac joint radiofrequency neurotomy:

Hodges PW, Richardson CA. Inefficient muscular

technique based on neuroanatomy of the dorsal sacral

stabilization of the lumbar spine associated with low

plexus. Spine (Phila Pa 1976) 2003:28(20):2419-25.

back pain. A motor control evaluation of transversus

17. Pauza KJ, Howell S, Dreyfuss P et a1. A randomized,

abdominis. Spille (Phi/a Pa 1976) 1996;21(22):

placebo·controlled trial of intra dis cal electrothermal

26 4 0 -50

therapy for the treatment of discogenic low back pain.

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Hodges PW, Richardson CA. Delayed postural contraction of transversus abdominis in low back pain associated with movement of the lower limb. ] Spinal

Disord 1998;II(I}:46-56. Sihvonen T, Lindgren KA, Airaksinen 0 et al. Movement disturbances of the lumbar spine and abnormal back muscle electromyographic findings in recurrent low back pain. Spine (Phila Pa 1976) 1997: 22 (3): 28 9-9 ).

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Spille (Phi/a Pa 1976) 1994;19(2):165-72.

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Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? A randomized clinical

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manipUlative treatment for low back pain: a systematic

Maitland GO. Vertebral numipulatiol1. 5th edn. London:

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Donelson R, Aprill C, Medcalf R et a1. A prospective study of centralization oflumbar and referred

Bogduk N. Clinical alJatOIl1V oftlte lumbar spine alld sacrum. Dvorak J, Dvorak V, Gilliar \V et at eds. Musculoskeletal

McGill S. LolV back disorders: evidence-based prevention and rehabilitation. Champaign, IL: Human Kinetics,

Spine] 20°4:4(1):27-35. 18. Carragee EJ. The surgical treatment of disc degeneration: is the race not to the swift? Spine] 200 5:5(6):5 8 7-8. I9. Deyo RA, Nachemson A, Mirza SK. Spinal-fusion surgery-the case for restraint. N EnglJ Med 20°4:35°(7)722-6. 20. Brukner P, Bennell K, Matheson G. Stressfractures. Melbourne: Blackwells Scientific Asia, 1999.

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controlled trial of manual therapy and specific ad juvant exercise for chronic low back pa in. Clin J Pain 20 0 ):21(6):46 3-70 . 26. Green JP. Grenier SG . McGill SM. Low·back stiffn ess is altered with wann-up and bench rest: implications for athletes. Med Sci Sports Exerc 2002;34(7) : 1076- 8 1.

Joint Surg Br20Io:92(G)751-9 .

491

I can't hit a ball more thalt 200 yards. I have no butt. You need a butt if you're going to hit a golf ball. Dennis Quad, American actor and producer Buttock pain is most commonly seen in athletes involved in kicking or sprinting sports. It can occur in isolation or it may be associated with low back or posterior thigh pain. Buttock pain or injuries such as pressure sores are also common in wheelchair ath· letes. Diagnosis of buttock pain can be difficult, as pain may arise from a number aflocal structures in the buttock or can be referred from the lumbar spine or sacroiliac joint (SIn. The causes of buttock pain are shown in Table 27.1. The anatomy of the buttock region is shown in Figure 27.1.

Clinica l approach When assessing a patient with buttock pain, the clinician should attempt to determine whether the pain

is local or referred. Clues can be obtained from the nature and location of the athlete's pain. Examination may then identifY which of the local or the potential pain.referring structures are causing the buttock pain. Investigation is of limited usefulness in the assessment of the patient with buttock pain.

History A deep aching diffuse pain that is variable in site is an indication of referred pain. Buttock pain associ· ated with low back pain suggests lumbar spine abnormality. Buttock pain associated with groin pain may suggest SIJ or hip involvement. When the patient is easily able to localize pain of a fairly constant nature, the source is more likely to

Table 27.1 Causes of buttock pain Common

less common

Not to be missed

Referred pain • lumbar spine • Sacroiliac joint

Quadratus femoris injuries Piriformis conditions

SpondyJoarthropathies Ankylosing spondylitis Reiter's syndrome (reactive arthritis) Psoriatic arthritis Arthritis associated with inflammatory bowel disease Malignancy Bone and joint infection

Hamstring origin tendinopathy Ischiogluteal bursitis Myofascial pain

492

• Impingement • Muscle strain Fibrous adhesions around sciatic nerve Prolapsed intervertebral disk (Chapter 26) Chronic compartment syndrome of the posterior thigh Stress fracture of the sacrum Proximal hamstring origin avulsion Apophysitis/avulsion fracture • Ischial tuberosity (children) Gluteus medius tendinopathy (Chapter 28)

be in the buttock region itself. Pain constantly localized to the ischial tuberosity is usually due to either tendinopathy at the origin of the hamstring muscles or ischiogluteal bursitis. Pain and tenderness more proximally situated and medial to the greater trochanter may be from the piriformis muscle. Pain aggravated by running, especially sprinting, is not diagnostic, as most conditions causing buttock pain may be aggravated by sprinting. Increased local pain on prolonged sitting may be an indication that ischiogluteal bursitis is the cause of the problem, although lumbar spine problems can be aggravated by sitting. The timing of the buttock pain is important in establishing the nature of the diagnosis. Inflammatory pains such as those experienced in sacroiliitis as part of a spondyloarthropathy are typically worst in the morning and improve with light exercise. Such "morning stiffness" lasts at least 30 minutes. Other features that strongly suggest the presence of a spondyloarthropathy include associated enthesopathy such as Achilles tendinopathy or plantar fasciitis and multiple joint problems. Figure 27.1 Anatomy of the buttocks (a)

Surface anatomy

gluteus medius (cut)

gluteus minimus

maximus (cut)

adductor minim us

gracilis mag nus

biceps femoris

long head (cut) iliotibial

band

biceps femoris

short head

(b) Muscles of the buttock: superficial (left) and deep (right) 493

Examination The slump test is an important part of the examination in attempting to differentiate between local and referred pain. However, not all cases of referred pain win have a positive slump test result. The lumbar spine should always be carefully examined, particularly for evidence of hypomobility or hypermobility of one or more intervertebral segments.

5. Resisted movements (a) hip internal rotation (Fig. 27.20 (b) hip external rotation (Fig. 27.2g) (e)

knee nexion (Fig. 27.2h)

6. Palpation {al sacroiliac joint (Fig. 27.2i) (b)

gluteal muscies (Fig. 27.2j on page 496)

(cl

ischial tuberosity

1. Observation (a) (b)

from behind (Fig. 27.2a) from the side

2. Active movements-lumbar spine (Chapter 26) (a) flexion (b) extension (e) lateral flexion (d) combined movements

3. Active movements-hip joint (a)

flexion/extension (Fig. 27.2b)

(b) abduction/adduction (e) internal/external rotation 4. Passive movements (al hip movements (b) hip quadrant-pain provocation test (Fig. 27.2c) (el external rotator stretch (Fig. 27.2d) (d)

(b) Active movement-hip flexion/extension

hip extension (Fig. 27.2e)

{el Passive movement-hip quadrant (pain provocation test). The hip joint is placed into the quadrant position, which consists of flexion, adduction and internal rotation

Figure 27.2 Examination of the patient with buttock pain (a) Observation from behind may detect asymmetrical muscle wasting. Observation from the side may detect the presence of a lumbar lordosis or anterior pelvic tilt

494

(d) Muscle stretch-external rotators

Bu ttock pa i n (d) sacrotuberous ligament (e)

iliolumbar ligament

(0

anterior superior iliac spines 7. Special tests la) slump test IFig. 27.2k overleaf} (b)

lumbar spine examination (Chapter 26)

(e)

sacroiliac tests (i)

stork test (Fig. 27.21overleaf)

(ii)

active straight leg raise (ASLR) (Fig. 27.2m overleaf)

(iii) Patrick or FABER test-flexion, abduction,

rotation (Fig. 27.2n on page 497) (g) ReSisted movement- external rotation . Resisted

external rotation from a position of internal rotation is used to isolate the piriformis muscle

(h) Resisted movement-knee flexion. This should be performed both concentrically and eccent rically to reproduce hamstring origin pain

{el Passive movement-hip extension. With the examiner's hand stabilizing the pelvis, the hip is passively extended

(fl Resisted movement-internal rotation

(i) Palpation-sacroiliac joint. The patient should be palpated in a posteroanterior direction over the region of the SUo This area also includes the iliolumbar ligament

495

(j) Palpation-buttock. The patient should be lying prone with a pillow under the knee to place the hip into slight passive extension and relax the hip extensor muscles. Palpate from the hamstring origin across to the greater trochanter. Palpation of the gluteus medius, piriformis, and the external rotators should be performed in varying degrees of hip rotation

Stork test. The pelvis should not anteriorly! posteriorly/laterally tilt nor rotate in the transverse plane as the weight is shifted to the supporting limb

(I)

(m) Active straight leg raise (ASLR). This test involves the patient lying supine and lifting his leg to a height of Scm

Investigations

(k) Neurodynamic test- slump test (see also Fig. 11.2 on page' 51). Reproduction of the patient's buttock pain in the starting position shown and relieving the pain with cervical extension is consistent with a positive slump test

496

A plain X-ray may demonstrate a stress fracture of the pars interarticularis, which may refer pain to the buttock. Spondylolisthesis may be evident. The presence of spondylolisthesis does not necessarily mean, however, that the slip is causing the patienfs pain (Chapter 26). X-ray may also show degenerative changes in the SIT in the older athlete. Inflammatory sacroiliitis with loss of definition of the SI) strongly suggests

Referred pain from the lumbar spine Buttock pain may be referred from the lumbar spine in the presence or absence of low back pain. Any of the somatic, innervated structures of the lumbar spine may refer pain to the buttock. Abnormalities are found most often in the intervertebral disks and the apophyseal joints. Spondylolysis and spondy· lolisthesis may also cause buttock pain. The patient usually gives a history of a diffuse ache in the buttock that may vary in severity. The slump test (Fig. 27.2k) may reproduce the butlock pain with relief of pain on cervical spine extension. It has been shown that 80% of normal individuals reporting a sensory response from the slump test have relief of this response with cervical extension. A positive slump test result indicates increased neural mechanosensitivity. This may be due to damage to the nerve itself. or it may be secondary to lumbar spine abnormalities. Failure of the slump test to reproduce the patient's buttock pain does not necessarily rule out the possibility of referred pain as the cause of pain. Normative data on the slump test demonstrates that buttock pain is not a normal response to the slump test in healthy individuals. Palpation of the lumbar spine may reveal areas of tenderness and hypomobility of intervertebral segments. The best means of assessing whether a lumbar spine abnormality is the cause of buttock pain is to improve mobility of the stiff segments by mobilization or manipulation, and to reassess the symptoms and signs, both immedia tely after treatment and prior to the next treatment. Local areas of buttock tenderness may occur with referred pain. In cases of longstanding referred pain, soft ti ssue abnormalities are usually found. especially in the gluteal muscles, external rotators. and lumbar multifidus. These include taut fibrous bands within muscles, and general muscle tightness. Active trigger points may refer pain in a characteristic distribution. The treatment of lumbar disorders has been described in Chapter 26 and requires an integrated approach. Local electrotherapy can reduce pain and inflammation. Mobilization or manipulation may restore full mobility to stiff intervertebral segments. Soft tissue therapy and dry needling may be used to treat chronic muscle thickening both around the lumbar vertebrae and in the gluteal region. Specific stretching of the gluteal muscles and hip external rotators should be commenced if there is any evidence of tightness. Z

Z

(nl FABER test- flexi on, abduction, externa l rotation. Pai n in the buttock with this test is suggestive of sacroiliac origin

a spondyloarthopathy. A recent consensus statement of rheumatologists and radiologists notes that a clear presence of bone marrow edema on MRI is essential for defining active sacroiliitis. [ X-rays of the ischial tuberosity in cases of chronic hamstring origin tendinopathy are usually normal; however, occasionally erosions can be d emonstrated. In the adolescent, apophysitis or avulsion of the ischial tuberosity may be demonstrated. Iso topic bone scan may show increased uptake in the region of the SIJ, or identify a stress fracture of the ischium. sacrum. or pubic ramus. Soft tissue ultrasound examination or MRI may image an enlarged or inflamed ischiogluteal bursa, or show evidence of chronic scarring at the hamstring origin. Blood tests may indicate the presence of systemic disease. Useful screening tests are a full blood examination looking for a raised white cell count (suggesting possible infection). and erythrocyte sedi· mentation rate (which may be elevated in the presence of an inflammatory condition) (Chapter 55).

497

Neural mobilization such as the slump stretch should be included if there is evidence of restriction, but they should be used with caution. A recent systematic review found inconclusive evidence for the use of slump stretching for low back pain) The patient should be shown an exercise program involving stretching and strengthening of the muscles supporting the lumbar spine (Chapter 26).

Sacroiliac joint disorde rs The concept of the SIT as a pain generator is now well established." However, the evaluation and treatment of SIT dysfunction remains controversial. One issue is the broad categorization and terminology utilized for the anatomical etiologies of the pain by various health professionals. Controversy also exists because of the complex anatomy and biomechanics of the SI). There is no specific symptom or cluster of symptoms, nor any specific examination technique, that is both sensitive and specific for the diagnosis of SIJ abnormalities. However, two recent studies have demonstrated that positive findings on a combination of pain provocation and motion palpation tests reliably indicate SI) dysfunction .',6 There are no imaging studies that distinguish the asymptomatic from the symptomatic patient. 4 Traditionally, local anesthetic blocks were considered the gold standard for diagnosing the SI) as a source of pain.' However, it is possible that anesthetic diffuses out of the joint in some cases and may affect surrou nding ligaments and nerve roots, including the lumbosacral trunk. This may reduce the specificity of SIT anesthetic blocks as a diagnostic tool. 8 In patients with low back pain, the prevalence of sacroiliac pain, diagnosed by local anesthetic blocks, is IS%.9. 10 The incidence may be even higher in high level sportspeople. One study showed an incidence of over 50% in elite rowers. II

Functional anatomy The SIT is diarthrodial (synovial anterior and fibrous posterior). Its joint surfaces are reciprocally shaped but no t congruent, have a high friction coefficient, and have two large elevations allowing interdigitation with the reciprocal surface. Age changes begin to occur on the iliac side of the joint as early as the third decade. The joint surface irregularities increase with age and seem to be related to weight-beari ng. The capsule becomes more thickened and fibrous 498

with age. The ligaments of the SI) are shown in Figure 27.3. SII motion is best described as a combination of flexion and extension, superior and inferior glide, and anterior and posterior translation. SIT motion is minimal, with approximately 2.5 of rotation and 0.7 mm (0.3 in.) of translation.' and it is best regarded as a stress-relieving joint in conjunction with the pubic symphysis. In the nonnal gait cycle, combined movements occur conversely in the right and left innominate bones, and function in connection with the sacrum and spine. Throughout this cycle, there is also rotatory motion at the pubic symphysis, which is essential for normal motion through the joint. In static stance, when one bends forward and the lumbar spine regionally extends, the sacrum regionally flexes, with the base moving forward and the apex moving posteriorly. During this motion, both innominates go into a motion of external rotation and out-flaring. 'Ibis combination of motion during forward flexion is referred to as nutation of the pelvis. The opposite occurs in extension and is called counternutation. SII dysfunction refers to an abnormal fWlction (e.g. hypomobility or hypermobility) at the joint, which places stresses on structures in or around it. Therefore, SIT dysfunction may contribute to lumbar, buttock, hamstring, or groin pain. The precise etiology of sacroiliac dysfunction is uncertain. Osteopaths describe a number of dysfunctions associated with hypomobility, including: 12

0

innominate shears, superior and inferior innominate rotations, anterior and posterior innominate in-flare and out-flare sacral torsions, flexion and extension unilateral sacral lesions, flexion and extension. Vleeming and colleagues'l have described their integra ted model of joint dysfunction. It integrates structure (form and anatomy), function (forces and motor control), and the mind (emotions and awareness ). Integral to the biomechanics of SIJ stability is the concept of a self-locking mechanism. The ability of the SI) to self-lock occurs through two types of closure-form and force. Form closure describes how specifically shaped. closely fitting contacts provide inherent stability independent of external load. Force closure describes how external compression forces add additional stability. The fascia and muscles within the region provide significant self-bracing and self-locking to the SI) and

Buttock pa in

supraspino us ligament

---fi"'---t

iliolumbar ligament

( sacrospinous ligament ischiofemoral

.' Z

.

superficial dorsal sacrococcygeal ligament

ligament

la) iliolumbar ligament

anterior sacroiliac ligament

Ib)

Figure 27.3 ligaments of the sacroiliac joint (a) posterior view (b) anterior view

499

its ligaments through their anatomical configuration. As shown in Figure 27-4, this is formed ventrally by the external abdominal obliques, linea alba, internal abdominal obliques, and transverse abdominals; dorsally the latissimus dorsi, thoracolumbar fascia, gluteus maxim us, and iliotibial tract contribute significantly. The fibers of the internal oblique and transversus abdominus muscles are entated perpendicular to the SIJ and are hence best positioned to provide force closure.'4·I5 Vleeming et aL further proposed that the posterior layer ofth e thoracolumharfascia acted to transfer load from the ipsilateral latissimus dorsi to the contralateral gluteus maximus. 'J This load transfer is thought to he critical during rotation of the trunk, helping to stabilize the lower lumbar spine and pelvis. A connection has also been shown between the biceps femoris muscle and the sacrotuberous ligament, allowing the hams tring to play an integral role in the intrinsic stability of the SIJ. The biceps femoris, which is frequently found to be shortened on the side

Figure 27.4 The cross-li ke configuration demonstrating the force closure of the sacroiliac joint

500

of the SIJ dysfunction, may act to compensate to help stabilize the joint.

Clinical features The patient with SIJ pain classical1y describes low back pain below LS. The pain is usually restricted to one side but may occasionally be bilateraL SIJ disorders commonly refer to the buttock, groin, and posterolateral thigh. Occasionally, SIJ pain refers to the scrotum or labia. Broadhurst lG describes a clinically useful description of pelvic/SI) dysfunction. Clinically. the patient has deep-sea ted buttock pain, difficulty in negotiating stairs, and problems rolling over in bed, with a triad of signs-pain over the SIJ, tenderness over the sacrospinous and sacrotuberous ligaments, and pai n reproduction over the pubic symphysis. Precipitating factors for the development of SI} disorders may include muscle imbalance between the hip flexors and extensors or behveen the external and internal rotators of the hip, leg length imbalance, and biomechanical abnormalities (such as excess ive subtalar pronation). The physical examination should begin by obser· vation of the sportsperson both statically and dynamo ical1y. The patient should be evaluated in standing, supine, and prone positions, and symmetry assessed in the heights of the iliac spines, anterior superior iliac spines, posterior superior iliac spines, ischial tuberosities, gluteal folds, and greater trochanters, as well as sym metry of the sacral sulci, inferior lateral angles, and pubic tubercles. Leg length discrepancy should be assessed. True leg length discrepancies will generally cause asymmetry and pain, whereas a functional leg length discrepancy is usually the result of SIJ and/or pelvic dysfunction. Dynamic observation may reveal a decrease in stride length with walking, leading to a limp, or a Trendelenburg gait due to reflex inhibition of the gluteus medius. Muscle strength and flexibility should be assessed. Full assessment of the hips and lumbar spine should also be performed. The presence of trigger points in surrounding muscles, particularly gluteus medius, should be noted. Palpation over the SIJ may reveal local tenderness. Numerous clinical tests have been described to assess SI J function; however, individually these tests are often unreliable. Posi tive findings on multiple SI} tests are a more reliable indication of SIJ dysfunction.s· G Some of the more popular tests

include standing and seated flexion tests, the stork test (Fig. 27.21), the AS LR test (Fig. 27.2m), and the Patrick or FABER test (Fig. 27.2n). The ASLR test is thought to test the quality ofload transfer through the lumbopelvic region. I? This test involves the patient lying supine and lifting his or her leg to a height of 5 cm. A subjective feeling of heaviness in the leg. and observations of excessive abdominal muscle bracing and altered respiratory patterns may indicate SIT instability. A positive ASLR test is recorded if these observations improve with manual compression of the ilia. 17 There is no specific gold standard imaging test to diagnose SIT dysfunction due to the location of the joint and overlying struchlres that make visualization difficult. 4

Treatment To reflect the complex narure of the SIT and its surrounding structures, a multirude of treatment techniques have been advocated and described in the literature. In an athletic population, treatment should focus on the entire abdomino-lumbo-sacro-pelvic-hip complex, addressing articular, muscular, neural, and fascial restrictions, inhibitions, and deficiencies.4 Initial treatment may focus on symptom reliefbut ultimately treatment should address the underlying pathology. For example, if a true leg length discrep' ancy is assessed, then shoe inserts may be appropriate to distribute loads evenly across the pelvis. Core stability training (Chapter '4) should be included. One study has suggested that the clini· cal benefits incurred with training the transversus abdominis muscle may be due to significantly reduced laxity in the SIT.'8 Exercise rehabilitation is an integral part of recovery from SI] dysfunction. Pelvic or 511 dysfunction should be considered with the lumbar spine in any program designed to improve the overall control of the lumbopelvic area. Stretching and soft tissue therapy are useful in correcting pelvic/Sl , imbalance. The most common soft tissue abnormalities found with unil ateral anterior tilt are tight psoas and recrus femoris muscles. A technique to reduce psoas tightness is shown in Figure 27.5. Muscle energy techniques (Chapter I3) may also be helpful, as may osteopathic-, chiropractic-, and physiotherapy-based manipulation techniques. These techniques are often used to address altered gait mechanics and spine malalignment issues. Sacroiliac belts may be useful in the initial phases

Figure 27.5 Soft tissue therapy-psoas. Sustained longitudinal pressure is app lied to the psoas muscle fibers, superior to th e inguinal ligament, with th e hip initially flexed and slowly moved into increased extension of management, but not in the long term. Once soft tissue abnormalities have been resolved, contributing facto rs such as posture, lifestyle habits, or training errors should also be addressed, to prevent recurrence. If these manual techniques fail to control the sacroiliac pain, injection therapy may prove useful. A combination of local anesthetic and corticosteroid agents may be injected into the region of the SII, as shown in Figure 27.6 overleaf, preferably under fluoroscopic or ultrasound guidance. Sclerosants are occasionally used when hypermobility is present, sometimes referred to as prolo therapy. Prolotherapy usually involves the injection of a sclerosing agent into the extra-articular ligamen ts, such as the dorsal interosseous ligament. The aim of prolotherapy is to reduce pain by reducing excessive joint movement (refer to Chapter 13 for more information) . A recen t prospective case study reported significant improvements in subjective and clinical outcomes at a two-year follow-up, after three 50 1

Useful techniques to mobilize the soft tissues and joints of this region are shown in Figures 27.7 and 27.8. These can be combined with passive hip extension.

Hamstring origin tendinopathy

Iliolumbar ligament sprain

Tendinopathy of the hamstring origin may occur near the ischial tuberosity after an acute tear that is inadequately treated or, more commonly, as a result of overuse.'" It is frequently seen in sprinters and middle- to long-distance runners. It is often difficult to treat and is characterized by lower gluteal pain which is aggravated with sporting activity, especially sprinting and acceleration with running. There may be a sudden onset of sharp pain; however, more often there is an insidious onset after a session of sprinting. On examination, there is local tenderness with pain on hamstring stretch and resisted contraction around the ischial tuberosity. The lesion may be found at the attachment

The iliolumbar ligament extends from the transverse process of the fifth lumbar vertebrae to the posterior part of the iliac crest. Sprain of this ligament may cause sacroiliac pain, particularly at its iliac attachment. It is almost impossible, however, to differentiate clinically between pain from this ligament and pain from the SI] and its associated ligaments. Slouching involves a combined movement of posterior pelvic tilt and lumbar spine forward flexion. The dorsal spinal muscles are thought to have a protective role both statically and dynamically around the lumbar spine and pelvis during this position. However, in the case of muscle fatigue, wasting, or delayed muscle response (such as in the presence of pain), the forces impact on passive structures such as the iliolumbar ligament, and therefore make it susceptible injury. Consequently sportspeople should be advised to avoid slouching in the presence oflow back injury/pain to avoid further injury. There is level I evidence that the iliolumbar ligament, as well as the other extra-articular SIT ligaments (sacrospinous, sacrotuberous, dorsal, and ventral sacroiliac) may sometimes be a source of pain in provocative SIr tests. s Therefore, in addition to their biomechanical roles, these ligaments should be considered as a potential source of pain. The same study concluded that corticosteroid injections may diffuse within these ligaments, providing pain relief.8 Injection of a mixture oflocal anesthetic and corticosteroid agents to the insertion of the iliolumbar ligament at the iliac crest may also be effective.

Figure 27.7 Ischemic pressure with the elbow to the origin of the hip external rotators and associated passive internal and external rotation ofthe hip

Figure 27.6 Corticosteroid injection to the region of the SIJ.lnjection is directed inferolaterally

prolotherapy injections were administered six weeks apart. I')

502

Butt ock p ai n

Figure 27,8 Ischemic pressure with the elbow to the hip abductors in the position of increased neural

mechanosensitivity

site, within the tendon, or at the musculotendinous junction. The slump test may reproduce the pain, but cervical extension makes little or no difference to the degree of pain. Pain can also be reprodu ced around the ischial tuberosity after prolonged sitting. MRI is more sensitive than ultrasound investiga. tions in diagnosis and ruling out other pa thologies, zl In one surgical shtdy of 90 sportspeople, semi· membranosis involvement was most commonly found on MRI." Initial treatment of this condition should include soft tissue therapy (Fig. 27.9), specifically deep transverse friction to the area of palpable abn ormality after reduction of inflammation with ice and nonsteroidal anti-inflammatory drugs (NSAIDs). Initial friction treatment should be relatively light. As the inflammation settles, treatment can be more vigorous. Abnormalities within the musculotendinous unit can be treated with stretching, su stained myofascial tension, and dry needling if trigger points are present. An exercise program incorporating progressive eccentric hamstring and core stability exercises is integrated late in

Figure 27.9 Ischemic pressure with the knuckles to the hamstring origin in the position of in creased length

Percutaneous corticosteroid injection can relieve symptoms but may not give long-lasti ng results. 11 H Recalcitrant cases may benefi t from a course of shock wave treatment to the region ,l4 or injection of autologous blood. Surgical intervention may be considered only when conservative measures have failed. 21 Tenotomy of the semimembranosis muscle, 3-4 em distal to the origin, may have good functional outcomes and return to sport after 2- 12 In longstanding cases of hamstrin g origin tendinopathy, there will be marked muscle tightness and weakness of the hamstring muscles, which may be corrected by stre tching and progressive strengthening (Chapter 31). Successful rehabilitation also requires stretching of the shortened antagonist muscles such as psoas and rectus femoris.

Fibrous adhesions Occasionally, in cases of chronic tendinopathy of hamstring origin, fibrous adhesions develop and irritate the sciatic nerve as it descends from medial to lateral just above the ischial tuberosity and then 503

passes under the biceps femoris muscle. This condition has been termed the "hamstring syndrome.""5 Hamstring syndrome is characterized by poorly localized buttock pain which radiates distally to the popliteal fossa.,,6 Pain from sitting or hamstring stretching is caused by traction, compression, and/or irritation of the sciatic nerve. Adhesions around the sciatic nerve may fail to respond to manual therapy, particularly if they have been present for some time. On these occasions, exploration of the sciatic nerve may be required with division of the adhesions and bands of fibrous

Ischiogluteal bursitis The ischiogluteal bursa lies between the hamstring tendon and its bony origin at the ischial tuberosity. This bursa occasionally becomes inflamed. It may exist in isolation or in conjunction with hamstring origin tendinopathy. Clinically, it is almost impossible to differentiate between ischiogluteal bursitis and hamstring origin tendinopathy, as both may present as pain aggravated by sitting or sprinting, and both are associated with local tenderness and pain on muscle contraction. One indication that ischiogluteal bursitis may be the diagnosis is that deep friction therapy fails to relieve the pain. Ultrasound examination may reveal a fluid-filled bursa. In this case, an injection of corticosteroid and local anesthetic agents into the bursa may be appropriate. As a result of pain-induced muscle inhibition, there is usually associated hamstring muscle weakness that requires comprehensive rehabilitation.

Myofascial pain The gluteus medius and piriformis muscles are two of the most common sites at which trigger points develop. Active trigger points in these muscles may present as buttock and/or posterior thigh pain (Fig. 27.ro). These muscles are often shortened as a result of pain (Fig. 27.2d). Careful palpation of these muscles should be performed, palpating for taut bands and exquisitely tender points that may be just tender locally or may refer pain distally into the posterior thigh. Dry needling may be an effective treatment method that can result in immediate analgesic effects and lengthening of the muscles with increased hip rotation and hamstring stretch on Electrotherapy, 504

Figure 27.10 Site of trigger points that commonly refer pain to the buttock

such as ultrasound, may also be useful treatment adjunct. 30 It is important to remember that trigger points are a secondary phenomenon. There is some evidence that there is a relationship between trigger points and joint dysfunction, mechanical low back pain, SIJ dysfunction, biomechanical abnormalities of the lower limbs, and psychological stress. 2B. JO In an athletic population, muscle imbalances, muscle weakness, fatigue, and/or injury can contribute to the development of active trigger This can be related to high training loads, reduced game fitness, and concurrent injuries. Therefore the clinician needs to be aware of the possible underlying causes, and aim to address these issues to enhance management and for injury prevention purposes.

less common causes Quadratus femoris injury The quadratus femoris (QF) muscle originates at the ischial tuberosity and inserts onto the quadrate tubercle on the femur. Its main action involves external rotation and adduction of the hip. Additionally the QF can act as a stabiliser of the hip joint. Due to its close proximity to the origin of the hamstring muscles, QF injuries are often misdiagnosed as hamstring pathologyY-ll Only a few cases of QF injury have been reported in the literahtre, mainly in sports such as badminton and tennisY· II

Buttock pa in Clinically, athletes can present with buttock pain. or groin pain, or both. Hip pain has also been described.!' Symptoms can radiate down the posterior thigh due to sciatic nerve irritation from a result· ant hematoma,l" P Pain can be aggravated by sporting activity such as running. hip stretches (flexion and adduction), and sitting. Palpation arowld the ischial mberosity and along the muscle onto its insertion on the femur can reproduce painy-n Hip flexion, and internal and external rotation can also reproduce pain. Investigations may not pick up any abnormalities on X-ray or ultrasound; however, MRI may show the correct diagnosis Y Treatment for QF strains can include electrotherapy (TENS), a hip-stretching routine, and a progreso sive hip rotator strengthening program.J'-1l Return to sport can be anywhere from five weeks to three

in the sciatic nerve passing through the piriformis Two piriformis conditions are muscle (Fig. commonly seen in sportspeople-impingement and muscle strain.

Piriformis syndrome Although known as the "piriformis syndrome, n this would be better referred to as "piriformis impinge· ment."!9 1t results from pressure on the sciatic nerve. usually as a result of its aberrant course through, or above, the piriformis muscle. This condition presents as local and referred pain, and abnormal neuro10gical symptoms in the posterior thigh and calf. Conservative treatment can consist of NSA I Ds, botulinum toxin injections, stretdling, arupuncture and dry needling, and soft tissue therapy, and can

months. (cur)

Stress fracture of the sacrum Sacral stress fractures are rare but occur most frequently in female distance runners. They may be associated with osteopenia secondary to menstrual and/or eating disorders, such as seen in the female

obturator internus

athletic triad (Chapter 43).

Athletes describe unilateral non-specific low back, buttock, or hip pain exacerbated by weight-bearing activity, without a history of trauma}4. 35 Palpation often reveals an exquisitely tender area on the sacrum. The diagnosis of stress fracture may be confirmed with bone scan or MRI, but may not always been sensitive in the early phases)6. )7 Treatment consists ofnon-weight-bearing until free of pain (one to two weeks), then a gradual increase in activity-initially non-weight-bearing (e.g. swimming, cycling, water running), and then graduated

quadratus femoris

Figure 27.11 Course of the sciatic nerve in the buttock (a)

Normal

weight-bearing. Athletes may not be pain·free until

six: months and return to sport may not be possible until eight months post-diagnosis)S However. a closely monitored and structured rehabilitation program focusing on slow progression of increasing loads can accelerate rerum to sport in 7 to 8 weeks. J \

Piriformis conditions The piriformis muscle arises from the anterior surface of the sacrum and passes posterolaterally through the sciatic notch to insert into the upper border of the greater trochanter. The sciatic nerve exits the pelvis through the sciatic notch and descends immediately in front of the piriformis muscle. In 10% of the population, anatomical variations result

nerves emerging mid-piriformis

(b)

Aberrant 505

include an adjunct core stability exercise program. 4 Surgery may be required.

(>

Piriformis muscle strain Pirifonnis muscle strain may be acute, which is often associated with muscle spasm, or chronic and may be associated with chronic muscle shortening, such as seen in long-distance walkers and runners.4! Athletes may complain of deep buttock pain aggravated by sitting (especially greater than 20 minutes),'}! climbing stairs, squats, and internal rotation of the leg such as in cross-legged sitting. On examination, there is often tenderness, either in the belly of the pirifonnis or, more distally, near its insertion into the greater trochanter. Spasm-a sausage-like palpable area-of the pirifonnis may also be felt. Passive internal hip rotation is reduced, and resisted abduction with the hip adducted and flexed may reproduce the pain over the piriformis. Pain may also be reproduced by resisted external rotation with the hip and knee flexed, beginning from a position of internal rotation so that end range is tested (Fig. 27.2g). Chronic cases may reveal muscle atrophy. The hip joint should be excluded as a source of symptoms. Treatment can involves stretching of the exter· nal rotators (Figs 27.12a, b), strengthening of the hip muscles (rotators, abductors, and adductors) , electrotherapeutic modalities (e.g. ultrasound, laser, high-voltage galvanic stimulation), muscle energy techniques, and soft tissue therapy to the tender area in the piriformis muscle. Longitudinal gliding combined with passive internal hip rotation (Fig. 27.12C) can be an effective technique, as is transverse gliding and sustained longirudinal release with the patient side-lying. Acupuncture and dry needling may also be considered.

Figure 27.12 Treatment of tight piriformis muscle

(a) Muscle stretch- hip external rotators. The hip is placed into flexion, adduction and then alternated into external and internal rotation

Posterior thigh com partment syndrome Posterior thigh compartment syndrome is an unusual condition that presents with the typical symptoms of a compartment syndrome-that is, pain increasing with exercise and a feeling oftightness. Posterior thigh compartment syndrome has been repDrted in a basketball player following a biceps femoris muscle strain, and after complete hamstring avulsion Pain is typically in the buttock and posterior thigh, and treatment involves range of movement exercises, massage therapy and, occasionally, surgery. Limited fasciectomy involving the ischial htberosity and upper 5 cm (2 in.) of the posterior fascia-can be performed. It is important to diagnose early and commence

506

(b) Muscle stretch-external rotators

appropriate management in a time-efficient manner to avoid adverse effects such as nerve injury.

Proximal hamstring avulsion injuries Proximal hamstring avulsion injuries can occur when the hip is forced into flexion with the knee relatively fixed at full extension, which has been cited in water Other mechanisms of injury include direct trauma, falling injuries, and doing the "splits." Subjectively, a popping or tearing sensation

But tock pa i n In chronic presentations, continual hamstring tightness, muscle atrophy, and prolonged functional deficits can also indicate the need for surgery.'H Surgery for the treahnent of hamstring avulsion injuries has shown good r esults.H .';(}

Apophysitis/avulsion fracture of the ischial tuberosity

(e) Soft tissue therapy-piriformis. Sustained longitudinal pressu re to the belly of the piriformis

muscle, initially in passive external rotation and then moving into internal rotation

in the gluteal and proximal posterior thigh region are reported; this is followed by an inability to weight· bear. 44 • 45 Aggravating factors include knee extension, weight·hearing. and sitting. After several days, there is often a significant amount of swelling and bruising extending down the posterior thigh toward the popliteal fossa. Active

Avulsion fracture of the ischial tuberosity is similar in presentation to muscle avulsion injury, but is more commonly seen in adolescents where, instead of the ham string muscle tearing, muscle traction separates a fragment of bone from its ori gin at the ischial tuberosity. This fragmen t of bone is clearly demonstrated on plain X- ray (Fig. 27.13). Management of this condition is generally conservative. The patient should be treated as for a severe (grade III) tear of th e hamstring muscle (Chapter 31). However, if th ere is marked separation (greater than 2.5 em (I in.]) of the fragment, then surgery is indio cated. There have been a number of reports of this injury in adults. The results of late surgical repair have been goOd. 47..18

Conditions not to be missed Buttock pain m ay be the presenting symptom of systemic dis orders, most commonly, sacroiliitis associated with spondyloarthropathies, such as ankylosing spondylitis.

knee flexion often reveals a significant deformity when performed in the pron e position;H Chronic conditions can reveal a slow·to-resolve hematoma, which complicates the healing and encourages the scarring process;l; Irritation of the sciatic nerve can result. prolonging functionalimpainnent. X-rays are often nonsignifican t. Ultrasound and/ or MRI can aid diagnosis. with MRl being more sensitive to the extent of the in jury.H.4s ConselVative treatment includes off..loading the hamstrings by non-weight-bearing on crutches, gentle compression. and RICE (refer to Chapter 13 for more information). Once the sportsperson can mobilize comfortably without crutches. range of movement exercises. and progressive strengthening exercises can begin. Surgery is indicated for acute presentations in the young and highly active populations. A complete hamstring group retraction of greater than 2 cm, seen on MRI. can also be an indication for surgery.4';

Figure 27.13 Avulsion of the ischial tuberosity

507

II

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Bogduk N. Clinical anatomy oItlie lumbar spine (md sacrum.

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Edinburgh: ChurchilIlivingstone, 1997. 14. Hoek van DGA, Snijders q, Stoeckart R et a1. A biomechankal model on muscle forces in the

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509

Eo says he felt his hip come out of the socket, so he popped it back in, but that's j"st impossible,

no one's that strong. Bo Jacksons trainer after the American football and baseball All·Star dislocated his hip when tackled during the '990 NFL playoffs Until recently, the hip joint was not thought to be a significant cause of problems in the athletic population. although hip disorders have long been recognized in the pediatric population (Perthes disease, slipped femoral epiphysis) and older people (osteo· arthritis). It was not until the advent of, firstly, MRI, and then hip arthroscopy, that it was realized that the incidence of hip labIal and acetabular rim pathology was high, and that anatomical variants such as femoroacetabular impingement (FAI) were a common underlying cause of groin pain. Hip pain is a common cause of activity restriction in sportspeople. Hip and groin pain is the third most common injury reported in the Australian Football League (AFL)/ accounting for between 5 and 15% of all football-related it is also prevalent in many other sports, including tennis, football of all codes, and hockey. The likelihood of a sportsperson sustaining an injury to the hip joint can be increased by the demands of the sport, in particular, sports that require repetitive hip flexion, adduction, and Hip joint injury can also be caused by the inherent individual anatomical variations within the joint, such as FAlor developmental dysplasia of the hip (DDH).'-" The range of motion of the hip is critical in determining the likelihood of intra-articular damage during sporting activity. The demands of range of motion vary between all sporting activities and the levels of activity. As range of motion decreases, the risk ofimpingement-related damage increases, especially with contact sports. Intra-articular hip pathologies contribute to both

510

a reduced ability to participate in sporting or physical activities as well as pain and also reduced function during activities of daily living. There is also considerable evidence that hip pathologies are sh'ong contribuI; tors to hip, groin, and pelvic pain in young Burnett et al. 14 demonstrated that 92% of patients with an arthroscopically confirmed labral tear complained of moderate to severe groin pain. Philippon et al.1a described labral tears and FAI in 100% of professional National Hockey League (NHL) ice hockey players presenting for hip arthroscopy or the treatment of longstanding hip and groin pain. Injury to the ligamentum teres of the hip has been cited as the third most common cause of hip and groin pain in the sportsperson. 'S- 17 In this chapter, we: review the functional anatomy of the hip provide a clinical approach to assessment of what is often a longstanding problem detail the pathologies and management of the many important conditions that are now recognized to cause pain around the hip region.

This chapter should be read in conjunction with the chapter on groin pain (Chapter 29).

Functional anatomy and biomechanics TIle hip has three functions: It allows mobility of the lower limb. Ittransmits loads between the upper body, trunk, and lower limb. It also proVides a stable base in activities.

H i p-r elated pa in The anatomical structure of the hip allows it to perform these fun ctions. The hip joint is supported by a number of dynamic and passive supports-these include its bony morphology, passive restraints such as capsule and ligaments, and a complex system of interplayi ng muscle groups. The biomechanics of the hip joi nt are generally under-reported in the literature and so are poorly understood. An appreciation of the functional anatomy of the hip and the role of the various structures surrounding the hip will assist in this understanding (Fig. 28.1).

Morphology The hip joint (femoroacetabular joint) is a tri-planar synovial joint, formed by the head of femur inferiorly and the acetabulum superiorly. The acetabulum sits within the bony pelvis and is normally antevened (forward-facing) by approximately 23°,8 (Fig. 28.2a overleaf). The acetabulum also faces inferiorly and laterally. The head and neck of the femur are also anteverted- this refers to th.e most superior aspect of the femoral head and the femora l neck (Fig. 28.2b overleaf). This angle is normally between 10° and ]5° in adults. The head of femur also faces superiorly and medially. A reduction in either femoral Of acetabular anteversion is considered to increase the risk of hip pathology. The relationship between the head and neck of the femur, called the head-neck offset, is also very important when discussing the hip joint. TIlis refers to the difference between the greates t diameter of the s pherical femoral head and the diameter of the neck measured around the femoral neck axis in any plane (Fig. 28.2C overlean and is normally approximately 20 mm in people without hip pain.1! A reduced head-neck offset '') (also referred to as a cam lesion) is considered to increase the risk of hip p athology and will be discussed in detail below. The morphological struc ture of the hip joint allows the hip to achieve its three planes of movement, being flexion and extension, adduction and abduction, and external and internal rotation.

Acetabular labru m The acetabulum forms the socket of the hip joint. and is lined with articular cartilage. The acetabular labrum (Fig. 28.3 on page 513) is a ring of fibrocartilage and dense connective tissue which is attached

Figure 28.1 Anatomy of the hip and groin area (a) Plain X-ray of the pelvis

femoral head

greater troc:hanler

femora l neck

(bl The hip joint to the bony acetabular rim. The acetabular labrum is thinnest in its anterior aspect. The blood supply of the labrum enters though the adjacent joint capsule. Only the outer one· third of the labrum is vascularized.!O Nocioceptive free nerve endings are distributed throughout the acetabular labrum, suggesti ng a pain-producing capacity.ll.lz

511

Figure 28.2 (a) (T showing acetabular anteversion 18

Normal offset (between lines 1 and 2)

(b) Transverse views of a normal hip (upper figure) and a dysplastic hip (lower figure)19 (1) Angle of torsion - rotation of the femoral neck relative to the shaft (transcondylar axis), normally 10-1 S° of anteversion. Dysplastic hips usually have increased angle (2) Acetabular anteversion angle- the anterior direction of the acetabulum, is normally 20-40° of anteversion. Dysplastic hips usual[y have increased angle but it may be decreased

The acetabular labrum has several functions. These are primarily to deepen the acetabulum, to distribute the contact stress of the acetabulum over a vvider area (increasing contact area by 28%);'.J and assisting in synovial fluid containment and distribution. n-24

Decreased offset

(e) Femoral head-neck offset 19 The head- neck offset is the distance between the most superior aspect of the femoral head (line 1) and the femoral neck (line 2). Line 3 is first drawn through the long axis ofthe neck, then parallel lines are drawn representing the superior aspect of the femoral head (line 1) and the femora [ neck (line 2). The offset is the distance between lines 1 and 2. A decreased offset (lower figure) leads to reduced clearance and subsequent impingement

Ligaments of the hip The transverse acetabular ligament (Fig. 28.3) traverses the acetabular notch, connecting the anterior and posterior edges of the labrum. The deepest layer of labral tissue blend into this ligament. The

512

transverse acetabular ligament is under greatest load in weight-bearing, widening the acetabular notch and placing the transverse acetabular ligament under a tensile load. 24

H i p - re l ated pa i n

iliac spine

ilioremoral ligament

reclus femoris ligament

ischiofemoral ligament

teres

Figure 28.3 Transverse acetabular ligame nt, acetabular labrum, and ligamentum teres (resected)

The ligamentum teres (Fig. 28.3) is an intraarticular ligament, arising from the fovea of the head of the femur, becoming triangular in shape, with an anterior and posterior branch, which insert into the anterior and posterior aspect of the transverse acetabular ligament respectively."s It is covered by the synovium within the hip. IS The ligamentum teres is also rich in free nerve endings, which are mechanoreceptors. J6 The ligamentum teres was originally thought to be a histological vestige which becomes redundant early in childhood; however, it is now assumed that the liga mentum teres plays an important proprioceptive role, especially in weigh t-bearing activities. ' 5 The iliofemoral ligament (Y ligament of Bigelow) reinforces the anterior capsule and originates from the anterior iliac spine, fanning into an inverted Y shape to insert into the intertrochanteric line (Fig. 28-4). It is taut in hyperextension and also provides stability in relaxed standing. The pubofemoral ligamen t arises from the anterior surface of the pubic ramus and inserts into the intertrochanteric fossa (Fig. 28-4). It is taut in abduction and extension, and also reinforces the anterior caps ule.

Figure 28.4 Capsular ligaments of the hip

The ischiofemoral ligament arises from the posterior surface of the acetabular rim and labrum. and extends into the femoral neck just proximal to the greater trochanter (Fig. 28.4). Its fibers run in a spiral pattern and are also taut in hyperextension. The iliofemoral, pubofemoral, and ischiofemoral ligaments act to res train hyperextension, which is of particular relevance in relaxed standing.

Chondral surfaces Both articular surfaces of the hip are lined with articular cartilage. These chondral surfaces rely upon adequate function of the synovium and movement of synovial fluid within the joint to provide nutrition, because articular cartilage is avascular. As both the acetabular labrum and ligamentum teres have been reported to attach to the synovium, they may also play a role in the nutrition and normal function of articular cartilage within the hip joint.

Joint stability and normal muscle function The bony morphology, acetabular labrum, ligamentum teres, other ligaments, and capsule of the hip 513

joint all provide passive stability to the hip joint. Dynamic stability is provided by a complex interplay between various muscles surrounding the hip joint. The concept of deep hip stabilizers, the "hip rotator cuff," has been present for some years/7 but has grown in popularity in recent years. In particular, the primary hip stabilizers are thought to provide a posterior, medial, and inferior force on the femur to control the position of the head of femur within the acetabulum. Ultimately, the dynamic control provided by the deep hip stabilizers has potential to minimize stress on vulnerable structures, such as the anterosuperior acetabular labrum, and the anterosuperior acetabular rim (Fig. 28.5). Recent reports have described the roles of hip muscles, with respect to muscle morphology, primary action of joint movement, and lines of action in relation to the axes of joint movementr.o) generate large forces over small length changes and, hence, are considered to be joint stabilizers? MRI can differentiate between musculotendinous injuries and tendon avulsion injuries, which has an impact on management options-namely, surgical interventions. 5; An imaging study of subjects presenting with groin pain found 98% had positive findings on MRI

558

be given to both reducing the physical training load and commencing treatment. 51 Absolute values vary, but one study showed mean sphygmomanometer pressures at 00 and 30° hip flexion of >210 mmHg in patients without groin pain, and 5% may be appropriate criteria. that could be suggestive of cause of groin pain)!'> Compared with surgical results, MRI had good sensitivity and specificity for rectus abdominis and adductor tendon injury, and these two clinical entities were the most common. A review on diagnosis in sportspeople presenting with longstanding groin pain. This review revealed the following results for imaging studies: 55 Abnormalities were found on X-ray in 76% of sportspeople with a history of groin pain, compared with 45% in controls. Significant changes have been observed in the sacroiliacjoint{s) on X-ray, which can be suggestive ofthe involvement of the whole pelvic ring in longstanding groin pain presentations. 50% of sports people demonstrated positive signs on herniography on the asymptomatic side compared with 84% on the symptomatic side. This may suggest either poor sensitivity of herniography or the global involvement of the abdominal/ inguinal region. Additionally, one reviewed study demonstrated that only 27% of hernias were detected on herniography. Increased abnormalities have been observed on the symptomatic side at the site of the adductor tubercle on bone scan. However, bone scans have shown poor validity and therefore have questionable usage in longstanding groin pain presentations. Abnormalities have been consistently found at the adductor tendons on MRI when groin pain was experienced for longer than one year. However, this was not consistently seen in groin pain of lesser duration. This could be suggestive of adductor tendinopathy having a secondary, progreSSive nature. A secondary cleft, interpreted as adductor microtear at symphyseal enthesis on MRI, has been observed in 70% and 88% of sportspeopJe presenting with

Gr o i n pa i n longstanding groin pain in two studies. Both studies observed no signs of secondary deft in their matched control groups, suggesting this finding had good validity. Abnormalities have been consistently observed at the adductor enthesis on the symptomatic side on ultrasound investigations. Abnormalities were found to be easily detectable when the same anatomical site was compared to the asymptomatic side. On ultrasound investigation, normal inguinal canal could be diagnosed when some canal closure was observed under"stress:' Abdominal wall deficiency could be diagnosed when an increase in area was observed. Additionally, an association was observed between increased groin pain and bilateral abdominal wall deficiency. Interestingly, there was no correlation with side of wall deficiency and side of groin symptoms. Pubic bone marrow edema has shown strong correlation with groin pain symptoms in one study but not in another. Additionally, one study observed bone marrow edema in both groin pain groups and matched controls. This could be suggestive of a normal bone process in relation to high intensity athletic training. Attenuation was observed in the abdominal wall musculofascial layers in 90% of groin pain subjects. 100% of positive findings correlated to side of symptoms.

Acute adductor strains Adductor muscle strains are a common injury in sports that involve sudden changes of direction and are characterized by a history of the sportsperson feeling a "pull" or a strain in the groin region. They training. S9 It are more likely to occur in is important for the clinician to localize the injury to the muscle belly, tendomuscular junction or bony attachment, as management and prognosis can differ depending on site of injury. Adduction of the hip involves six muscles, includ· ing adductor longus, magnus, brevis, and gracilis, pectineus, and obturator externus. S Within an openchain environment, these muscles act as adductors of the hip, whereas in a closed-chain environment their function changes to more of a stability role of the hip on the pelvis. In acute presentations the pain is usually well localized, either to the belly or the proximal musculotendinous junction of one of the adductor tendons near their origin on the inferior pubic ramus. It is

well established that the adductor longus muscle is the most frequently injured adductor muscle. H Examination often reveals localized tenderness, pain on passive abduction, and pain on resis ted adduction or combined flexion/adduction. Current evidence supports initial conservative treatment with exercise therapy for groin pain in sportspeople.l. 6 0 . 61 A progressive strengthening program around the hip, pelvis, and abdominals seems to have most effect.'·6 1 Treatment usually commences with initial tion of bleeding and swelling using the RICE (rest, ice, compression, exercise) regimen (Chapter 10). Due to concerns that early stretching may predispose to the development of chronic tendinopathy, stretching does not playa significant role in the management of adductor muscle strains. Progressive strengthening exercises should not be commenced until at least 48 hours after injury. The rehabilitation program for acute adductor strains corresponds to the basic adductor rehabilitation program described below, once the acute signs have settled.

Recurrent adductor muscle strain Recurrent adductor muscle strains are commonY A review of I292 hockey players found that those with

a past history of groin pain had double the risk of injury. For a veteran player, the risk increased to five times that of a rookie. I ) This may be due to inadequate rehabili tation of the initial injury, resuming sport too quickly, or not resolving associated problems such as lumbar spine stiffness, hip restrictions, core stability, or pelvic imbalances. If untreated, these injuries can lead to chronic exercise-related groin pain.

Adductor-related groin pain Longs tanding adductor-related groin pain is localized medially in the groin and may radiate down along the adductor muscles. The key examination features that distinguish this clinical entity from others are maximal tenderness at the adductor tendon tion and pain with resisted adduction (squeeze test) (Fig. 29.Se and box pages 556-8). Weakness of the adductor muscles is common, and palpation of the adductor longus insertion at the pubic bone reveals tenderness. Generally, increased muscle tone with trigger points along the adductor longus is often found as well. The pubic symphysis is frequently tender, but this does not help to differentiate the four clinical entities (Table 29.2).

559

Historically many of these patients were diag· nosed as having an "adductor tendinopathy." A true tendinopathy is quite unusual, and an enthesopathy with associated adductor myofascial tightness is the more common clinical scenario.

Early warning signs Unfortunately most patients with adductor·related groin pain continue to train and play until pain prevents them from running. When the condition has reached that stage. a lengthy period of rest and rehabilitation is usually required. However, if early warning signs are heeded, appropriate measures may prevent the development of the full-blown syndrome. These early clinical warning signs are (from most common to least common): tightness/stiffness during or after activity with nil (or temporary only) relief from stretching loss of acceleration loss of maximal sprinting speed loss of distance with long kick on run vague discomfort with deceleration.

If pain is experienced during any of the rehabilita· tion activities, or after them, that activity should be reduced or ceased altogether. Experienced clinicians use absence of pain on the key provocation tests (e.g. squeeze test and Thomas test position) as a guide to progress the rehabilitation program and minimize the mechanical stress on injured tissues (see progression of program below).

Identify and reduce the sources of increased load on the pelvis As discussed previously, it is essential to identifY and reduce the sources of increased load on the pubic bones. This may involve: reducing adductor muscle tone and guarding with soft tissue treatment (Fig. 29.7a) and/or dry needling correcting iliopsoas muscle shortening with local soft tissue treatment (Fig. 29.7b), neural mobilization (Fig. 29.7c), and mobilization of upper lumbar intervertebral joints (Chapter 26)

Treatment Traditional treatment for most types of groin pain was "rest;" however, this usually resulted in a return of symptoms on resumption of activity. Compared with rest and passive electrotherapy, active rehabilita· tion provides more than IO times the likelihood of pain·free successful return to sport. 6z The treatment protocol outlined below combines the latest research evidence with the authors' experience. 6o• 6l Five basic principles underpin a treatment regimen: 1. Ensure that exercise is performed without pain. 2. Identify and reduce the sources of increased load on the pelvis. 3. Improve lumbopelvic stability. 4. Strengthen local musculature using proven protocols. 5. Progress the patient's level of activity on the basis of regular clinica[ assessment. These are outlined below.

Ensure that exercise is performed without pain The first and most important step is for the patient to cease training and playing in pain. Painfree exercise is absolutely crucial for this rehabilitation program.

560

Figure 29.7 Treatment techniques used in related pain (a) Soft tissue therapy- sustained myofascial tension to the adductor muscle group

reducing gluteus medius muscle tone and myofasciaJ shortening with soft tissue treatment andlor dry needling identifying and correcting any hip joint abnormality (Chapter 28) mobilizing stiff intervertebral segments (Chapter 26) improving core stability (Chapte r 14), especially activation of transversus abdominis and anterior pelvic floor muscles.

Improve lumbopelvic stability Research has demonstrated a delayed onset of action, IS and reduced thickness I; of transversus abdominis activity in patients with longstanding groin pain, sugges ting that impaired core or lumbopelvic stability (Chapter 14) plays a role in the development of this condition. In our clinical experience, a core stability program has proven to be an important component of the rehabilitation program for longstanding groin pain. This program has been described in Chapter 14. (b) Soft tissue therapy-sustained myofascial tension to the iliopsoas muscle. The hip should be slowly passively extended from the flexed position shown to increase the tension

Strengthen local musculature using proven protocols Once pain has settled and muscle shortening has been corrected in the adductor, ilio psoas, and gluteal muscles. then a graduated pain-free muscle strengthen ing program can be commenced. A random ized clinical trial found an active training program aimed at improving muscle strength and coordination of the muscles acting on the pelvis, in particular the adductor muscles, was more effective in the treatment of a group of sportspeople wi th longstanding groin pain than a physiotherapy program consisting of laser, TENS, friction massage, and stretching without active This program is described in the box (overleaf). A similar pre-season adductor muscle strengthening program reduced the incidence of adductor muscle strains in ice hockey players who were identified as at ri sk.>' 64

Progress the patienfs level of activity on the basis of regular clinical assessment (cl Neural mobilization-Thomas position. Commence in the iliopsoas stretch positio n, then add passive cervical/upper thoracic tension, and then passive knee flexion to elicit a stretch

The aim of the graded exercise program is to gradu· ally increase the load on the pubic bones and sur· rounding tissues. Once the patient is pain-free (see above), pain-free walking can begin and be gradually increased in speed and distance. 56 1

Exercise rehabilitation program groin pain in sportspeopie"

.

I

••

aimed at improving the muscles stabilizing the pelvis

In the same starting position as for the sit-ups but clamping a soccer ball between the knees,

and the hip joints, in particular the adductor muscles. The program consists of two parts:

the player does a combination of a sit-ups while pulling the ball towards the head.

This program consists of static and dynamic exercises

(d)

•

adductor activation

The exercise is performed rhythmically and with accuracy to gain balance and coordina-

Module 2: More demanding exercises with heavier

tion. Five sets of 10 with 15 second recovery

Module 1: Two-week familiarization program -

resistance training, and balance and coordination.

The training program is performed three times a week and the exercises from Module 1 are per-

(e) (f)

formed on the days in between the treatment

periods. Wobble board training for 5 minutes. Adductor lateral slide. Using a sliding board with an extremely smooth surface (or a very smooth floor) and wearing a low-friction sock on the sliding foot, one foot is positioned next

days. The total length of the training period is 8-12 weeks. Sports activities are not allowed in the

to the sliding board and the other foot on the board parallel to the first one. The foot

treatment period. Pain-free bike riding is allowed. After 6 weeks, pain-free jogging is allowed. Return to sport is allowed when neither treatment nor

on the board slides out laterally and is then pulled back to the starting position. The foot

jogging causes any pain. Stretching of the adductor muscles is not advised, but stretching of the other lower extremity muscles, par-

should be pressed against the surface through the whole exercise with as much force as tol -

ticularly the iliopsoas, is recommended.

erated within the patient's threshold of pain (Fig. 29.8c overleaf). Perform continuously for

Module 1: Static and dynamic exercises (2-week base training program)

(g)

Static 1. (a)

Adduction for 30 seconds against a soccer ball

done with the foot on the board placed in a 90° angle to the foot outside the board.

placed between the feet when lying in the

Perform continuously for 1 minute with each

supine position with the knees fully extended and the first toe pointing straight upwards

leg in turn. All the above exercises should be commenced carefully, and the number of sets and range of motion

(fig. 29.8a). (b)

Adduction for 30 seconds against a soccer ball placed between the knees when lying in the supine position with the knees and the hips flexed at 45° and the feet flat on the floor

pointing straight ahead (Fig. 29.8b). Exercises 1(a) and (b) should be repeated 10 times with'5 second recovery periods between each contraction. The force of the adduction should be just sufficient to reach the point where pain begins.

gradually increased, respecting pain and exhaustion. Module 2: Dynamic exercises This entire module is done twice at each training

session for three training sessions per week with a day in between. Module 1 is done on alternate days, so players are training a total of six days per week. Exercises 2{a} to (e) are done as five sets of 10 repetitions. 2. (a) Lying on one side with the lower leg stretched

Dynamic (c)

and the upper leg bent and placed in front of the lower leg, the lower leg is moved up and

Sit-ups from the supine position with the hip and knee joints flexed at 45° and the feet against the floor. The sit-ups are performed

(b)

down, pointing the heel upwards. Lying on one side with the lower leg bent

quarter twist towards the opposite knee. Five

and the upper leg stretched, the upper leg is moved up and down, pointing the heel

sets of' a with' 5 second recovery periods.

upwards.

as a straight abdominal curl and also with a

562

1 minute with each leg in turn. Forward slide. The same procedure is also

Gro i n pa in

(c)

Begin by standing at the end of a high couch

and then lie prone so that the torso is supported by the couch. The hips are at the edge of the couch at 90° of flexion and the feet are

on the floor. From this position, both hips

are slowly extended so both legs are lifted to the greatest possible extension of hips and

spine; legs are then lowered together. (d)

Standing abduction/adduction using ankle pulleys. Begin with a low weight and gradually

(el

increase the weight but keep it submaximal. Standing on one leg, the knee of the supporting leg is flexed and extended rhythmically and

in the same rhythm, swinging both arms back and forth independently ("cross-country skiing

on one Jeg

n )

(Fig. 29.8d overleaf), The non-

weight-bearing leg is not moved. The balance and position are kept accurately, and the exercise is stopped when this is no longer possible. Progression of the exercise is obtained by holding a 1 kg (2.2Ib) weight in each hand. (f) nFitter"training for 5 minutes. (g) Standing on the sliding board, side-to-side skating movements on the sliding board are done as five sets of 1 minute training periods with 15 second recovery. Practical tips Supervision is important-the patient should be instructed by a physiotherapist, a physician, an

Figure 29.8 Static and dynami c exercises to improve the muscles stabilizing the pelvis and the hip joints (a) Static exercise - adduction for 30 seconds against a soccer ball placed between the feet

athletic trainer, or another qualified person who has been train ed in the details of the program. Exercises such as 1(d) and 2(e) are very important, especially at the end of the training period, but they are technically difficult. The athletes can do the program at home or at the gym or the fitness club. but we recommend physiotherapist supervision for three to four times within the first 2 weeks, and after that a visit every 10-14 days to check the technique and ensure progression. Patience is the key to success. Patients often make good progress in th e first few weeks, but symptoms can plateau from that pe riod until the 6-9 week period, when there is a positive "breakthrough.n It is important to use pain as a guide to how much to do. Muscle soreness similar to that after a regular practice in the sports field is not a problem, but if the patient experiences pain from the injury, the intensity of the exercises should be adju sted. Pain medication including NSAIDs should be avoided. Athletes should continue with some of the exercises on a regular basis (one to two times a week) for at least a year after total recovery and return to sport. The athlete must appreciate that su ccessful rehabilitation of chronic groin pain takes a minimum of 8-12 weeks.

(b) Static exercise-adduction for 30 seconds against

a soccer ball placed between the knees whe n lying in the supine position with the knees and the hips flexed at45"

563

(c) Static exercIse-adductor lateral slide. The foot on the slippery surface slides out laterally and is then pulled back to the starting position in contact with the surface and with as much force as tolerable

(d) Dynamic exercise-cress-country skiing on one leg. Note that the non-weight-bearing leg is not moved

564

Gro i n pa i n The criteria for when the patient may return to running are when: brisk walking is pain-free resisted hip flexion in the Thomas position is painfree there is no "crossover" sign (p. 553) there is minimal adductor guarding. Various progressive running regimens can be used. One effective program is described here: 61 100 m run-throughs with 10m acceleration and deceleration phases with walk recovery. Patient should commence with six to eight repetitions on alternate days. Key criteria (adductor guarding, squeeze test) should be assessed immediately after each session and again the next morning. The running program can be progressed further by replacing walk recovery with jog recovery. The aim should be to build up to 20 x 100 m run-throughs and jog back. Lateral running (gradual change of direction such as figure eight) can be commenced when the above running program is completed pain-free, the hip flexion test is still pain-free with no crossover sign, there is no adductor guarding, and the squeeze test is pain-free. Figure-of-eight running should commence slowly with very gradual change of direction, then gradually increase both speed and sharpness of change of direction. In kicking sports, short stationary kicking can be commenced when hip flexion tests are pain-free without crossover. The player may gradually increase the kicking distance and then start shorter kicking on the run. The last stage in the kicking program is long kicks at full pace and kicking around the body.

Key clinical signs suggestive of "excessive loading" during rehabilitation The therapist must continually guard against the player "overdoing" rehabilitation. The following signs appear to suggest excessive loading and deterioration during rehabilitation: pain on passive hip abduction adductor muscle"guarding"with increased muscle tone on passive combined hip external rotation and abduction pain and weakness with resisted adductor contraction pain on the squeeze test (Fig. 29.Se)

pain on resisted hip flexion (Fig. 29.Sd) pain on resisted hip flexion and adduction in the Thomas test position positive crossover sign.

Other non-surgical treatments Compression shorts have been advocated for those with mild pain who insist on continuing to train and play, and for those returning to sport after rehabilitation. 6s- 67 The shorts substantially reduce pain when worn during exercise. 6s The mechanism of action of compression shorts remains unclear.

Failure of conservative management Conservative management as outlined above might fail for a number of reasons. These include: incorrect diagnosis (hip joint pathology, hernia, stress fracture, referred pain) inadequate period of rest poor compliance exercising into pain inappropriate progressions inadequate core stability persistent lumbar intervertebral hypomobility persistent adductor guarding.

Surgery If persistent adductor shortening/guarding is a problem that does not respond to soft tissue treatment and/or dry needling, a partial adductor tendon release may help. 69·7° Abolition of the patient's symptoms and signs with a trial injection of local anesthetic is advocated by some as an indication that the release will be successful in alleviating symptoms. One technique advocated is to release the superficial section of the normal adductor longus tendon at a point distal to the insertion. It is posrulated that this may have the effect of transferring stress from the superficial section of the tendon to the stressshielded deeper portion)l Anecdotally, these patients often make a quick recovery and rerum to high-level sport after four to six weeks.

Iliopsoas-related groin pain The iliopsoas muscle is the strongest flexor of the hip joint. The iliopsoas muscle is shown in Figure 29.9 overleaf. It arises from the five lumbar vertebrae and the ilium, and inserts into the lesser trochanter of the femur. It is occasionally injured acutely; however, it frequently becomes tight when there is neural

565

Reg i ona l problems

Clinical concepts psoas minor

- -flfj:4O However, there was a significant recurrence of pain in the following months. The relevance of the secondary symphyseal cleft remains unclear and requires further investigation. The pubic bones are subjected to considerable forces by the various pelvic structures mentioned above. It may be that pubic bone abnormalities are the cause of pain in a small group of patients, or they may simply be a sign of increased bone stress when the other clinical entities (e.g. adductor-related) are affected.

Treatment In addition to the management of factors that contribute to pubic overload, a variety of treatments have focused on the symphysis pubis and bony abnormalities. The use of corticosteroids both as a local injec· tion into the symphysis pubis ,01 and in oral form (25-50 rug/day for 7 days) has been anecdotally helpful, but no control1ed trial has been reported. We have found a short (5-7 days) course of oral prednisolone (So rug/day) helpful in settling pain, thus enabling the patient to commence the rehabilitation program earlier. Dextrose prolotherapy injections have been shown to be helpful in one study. Monthly injections of 12.5% dextrose and 0.5% lignocaine (lidocaine) into the adductor origins, suprapubic abdominal inser· tions, and symphysis pubis were given until resolu· tion of symptoms. An average of 2.8 treabnents were required. Three· to six-monthly courses of intravenous injection of the bisphosphonate pamidronate were found to be helpful in one report of three cases.IO J Some physicians are advocating the use of extracorporeal shock wave therapy, but there is no evidence to support this. Surgery has been advocated by some clinicians. In the chronic stage of the condition, where imaging shows erosions and cystic changes in the pubic symphysis (Fig. 29.IIC), surgical exploration and debridement of the symphysis may be indicated. ,o4 Symphyseal wedge resection is out of favor as it can give rise to progressive sacroiliac arthrosis and ultimately posterior pelvic instability requiring major pelvic stabilization. to(; Arthrodesis of the pubic symphysis by bone grafting and a compression plate has been used successfully in patients with proven pubic instability. ,o7 I02

lO

(e) MRI of the pubic symphysis at a point just posterior to the adductor longus insertion. Symphyseal degenerative changes and a "secondary cleft" sign (solid white arrows) are demonstrated. Note the reactive oedema tracking through the cleft and into the adjacent obturator externus muscle (white open arrow)

)

57 1

Less common injuries

Obturator neuropathy Obturator neuropathy is a fascial entrapment of the obturator nerve as it enters the adductor compartment. Obturator neuropathies have been reported to occur in Aus tralian Rules football and rugby. It has distinct clinical feahtres that separate it from other causes of groin pain. loS. 1°9 Obturator neuropathy presents as exercise-related groin pain, which initially is concentrated on the proximal groin, but with increasing exercise radiates towards the distal medial thigh. There may be associated weakness or a feeling of a lack of propulsion of the limb during funning, but numbness is very rarely reported. At rest, examination findings can be nonspecific, with pain on passive abduction of the hip, and pain and weakness on resisted hip adduction. The ipsilateral pubic tubercle is often tender. The essential component of the physical examination is to exercise the patient to a level that reproduces his or her symptoms, and then immediately examine the patient. This examination will reveal weakness of resisted adduction and numbness over the distal medial thigh. Bone scan in this condition often shows increased uptake over the ipsilateral pubic tubercle, frequently called "osteitis pubis" by the reporting radiologist. The diagnosis is confirmed by needle EMG (electromyogram), which shows chronic denervation patterns of the adductor muscle group. Conservative treatment of this condition, including sustained myofascial tension massage over the adductor compartment, neural stretches, spinal mobilization, and iliopsoas soft tissue techniques, is generally unsuccessful. The definitive treatment of this condition is surgical. An oblique incision is made in the proximal groin. The plane between the adductor longus and pectineus is identified and dissected, revealing the obturator nerve under the fascia over the adductor brevis. This fascia is divided and the nerve is freed up to the level of the obturator foramen. The fascial anatomy (Fig. 29.12) here is very important, with the fascia of the adductor longus curving around the muscle medially and passing back deep to the muscle to become the fascia over the adductor brevis, which is thought to be responsible for the fascial entrapment of the obturator nerve. Postsurgical management includes wound management, soft tissue techniques, and a graduated return to full activity over a period of four to six weeks.

572

(

I

)

I

adductor brevis m. Fig ure 29.12 Obturator neuropathy-fascial

arrangements

Other nerve entrapments A number of superficial nerves in the groin may become entrapped and should be considered as possible causes of groin pain. The ilioinguinal nerve supplies the skin around the genitalia and inside of the thigh, and may produce pain as a result of entrapment. The genitofemoral nerve innervates an area of skin just above the groin fold. The lateral cutaneous nerve of the thigh is the most common nerve affected. This nerve supplies the outside of the thigh. This condition is known as "meralgia paresthetica." This condition is described in Chapter 30. Diagnosis of pudendal nerve entrapment requires the presence of the following criteria- pain in the territory of the pudendal nerve from the anus to the penis or clitoris, pain being predominantly experienced while sitting, pain that does not wake the patient at night, pain that has no objective sensory impairment, and pain that is relieved by diagnostic pudendal nerve block. 1I0 Treatment of these conditions is usually not necessary as they often spontaneously resolve. Meralgia paresthetica is sometimes treated with a corticosteroid injection at the site where the nerve exits the pelvis, I em (0.5 in.) medial to the anterior superior iliac spine. Occasionally, the nerve needs to be explored surgically and the area of entrapment released.

Stress fractures of the neck of the femur Stress fracture of the neck of the femur is another cause of groin pain. The usual history is one of gradual onset of groin pain, which is poorly localized and aggravated by activity. Examination may show some localized tenderness; however, often there is relatively little to find other than pain at the extremes of hip joint movement, especial1y internal rotation. X-ray may demonstrate the fracture if it has been present for a number of weeks but this investigation should not be relied on to rule out the condition; iso-

topic bone scan and MRI (Fig. 29.13) are the most sensitive tests. Stress fractures of the neck of the femur occur on either the superior or tension side of the bone, or on the inferior or compression side (Fig. 29.14). Stress fractures of the superior aspect of the femoral neck should be regarded as a surgical emergency and treated with either urgent internal fixation or strict

bed rest. The concern is that such stress fractures have a tendency to go on to fun fracture, which compromises the blood supply to the femoral head. Stress fractures of the inferior surface of the femoral neck are more benign and can be treated with an initial period of non-weight-bearing rest followed by a period of weight-bearing without running. They require at least six weeks of rest and usually considerably longer. Following the period of rest, a further six weeks of progressive loading will take the patient back to full training. Biornechanical (Chapter 8), nutritional, and endocrine risk factors (Chapter 43) should be assessed and treated as appropriate.

Stress fracture of th e inferior pubic ramus

Figure 29.13 MRr showing stress fracture of the neck

of the femur

Stress fracture of the inferior pubic ramus, especially in distance runners, is an important differential diagnosis of adductor tendinopathy. There is usually a his tory of overuse and localized tenderness, which is not aggravated by passive abduction or resisted adduction. In this condition, pain is often referred to the buttock. A stress fracture may not be visible on plain X-ray for several weeks, whereas a radionuclide bone scan will demonstrate a focal area of increased activity within hours (Fig. 29.15) and an MRI will show a focal area of bone edema. As with any stress fracture, etiological factors must be considered. Stress fractures of the inferior pubic ramus in females may be associated with reduced bone density, low initial aerobic fitness, and nutritional insufficiency. Prolonged amenorrhea is also linked with this stress fracture (Chapter 431.

compression

Figure 29.14 Stress fractures of the neck of the femur- superior or tension fracture on the superior aspect of the femoral neck, and inferior or compression fracture on the inferior side

Figure 29 .15 Radionuclide bone scan demonstrating

stress fracture of the inferior pubic ramus

573

Treatment consists of relative rest from aggravating activities (such as running) until there is no longer any local tenderness. Fitness should be maintained with swimming or cycling, with gradual return to weight-bearing over a number of weeks. Predisposing factors such as a negative energy intake, muscular imbalance, or biomechanical abnormality also need assessment and intervention. Preventive strategies can be incorporated, especially in the female military population. Strategies may include pre-training interventions focusing on improving aerobic fitness to reduce fatigue fractures, and calcium and vitamin D supplementaFemale recruits who report no menses in tion. the year prior to recruitment should also be observed closely. (]! IlI

•

I1

;O

Referred pain to the groin The possibility of referred pain to the groin should always be considered, especially when there is little to find on local examination. A common site of referral

574

to the groin is the sacroiliac joint, and this should always be assessed in any examination of a patient with groin pain. The sacroiliac joint, may also refer pain to the scrotum in males and labia in females. The assessment and treatment of sacroiliac problems have been discussed in Chapter 27. The lumbar spine may refer pain to the groin. The lumbar spine and thoracolumbar junction should always be examined in a patient with groin pain. Neurodynamic tests, such as the slump and neural Thomas test position should be performed as part of the assessment (Chapter II). Variations such as the addition of adduction or hip rotation may reproduce the patient's pain. A positive neurodynamic test result requires further evaluation to determine the site of the abnormality. The position of reproduction of pain can be used to correct neural tightness by neural mobilization. Active trigger points may also refer to the groin and should be treated with soft tissue therapy.

-

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As strol1g as my legs are, it is my mind that has made me a champion.

Midlael Johnson. four times Olympic Gold Medal winner who suffered from a very publicized quadriceps strain The anterior thigh (Fig. 30.1) is the site of common sporting injuries such as quadriceps muscle contusion and strain of the quadriceps muscle. Referred pain from the hip, sacroiliac joint (SIJ) and lumbar spine can also cause anterior thigh pain. l Stress fracture of the femur is an uncommon, but important diagnosis. The causes of anterior thigh pain are shown in Table 30.1 overleaf.

Figure 30.1 Anatomy of the anterior thigh (a l Surface anatomy

Clinical a pproach History The two most important aspects of the history of a patient with anterior thigh pain are the exact site of the pain and the mechanism of injury. The site of the

(b ) Muscles orthe anterior thigh

579

Reg io n a l p rob lems Table 30.1 Causes of anterior thigh pain Common

Less common

Not to be missed

Quadriceps muscle contusion

Referred pain upper [umbarspine sacroiliac joint hip joint Stress fracture of the femur Sartorius muscle strain Gracilis strain

Slipped capita! femoral epiphysis

("cork thigh:' "charley horse;'

"dead leg', Quadriceps muscle strain distal rectus femoris •

proximal rectus femoris

Myositis osslncans

Perthes'disease Tumor (e.g. osteosarcoma of the femur) Acute compartment syndrome of the

thigh

Avulsion of the apophysis of rectus femoris Nerve entrapment

lateral cutaneous nerve •

femoral cutaneous nerve

pain is usually well localized in cases of conmsion or muscle strain. Contusions can occur anywhere in the quadriceps muscle but they are most common anterolaterally and in the vasms medialis obliquus. Muscle strains generally occur in the midline of the thigh anteriorly. The mechanism of injury may help differentiate between the two conditions. A contusion is likely to be the result of a direct blow, whereas a muscle strain usually occurs when an athlete is striving for extra speed when running or extra distance when kicking. In contact sports, however, the athlete may have difficulty recalling the exact mechanism ofinjury. Whether the athlete was able to continue activity, the present level of function, and the degree of swelling are all guides to the severity of the condition. Determine whether the RICE regimen was implemented initially and whether there were any aggravating factors (such as a continued activity). Gradual onset of poorly localized anterior thigh pain in a distance runner worsening with activity may indicate stress fracture of the femur. If the pain is variable and not clearly localized, and if specific aggravating factors are lacking, consider referred pain. Bilateral pain suggests the pain is referred from the lumbar spine.

motion and muscle strength. Functional testing may be necessary to reproduce the symptoms. 1. Observation (a) standing (b)

walking

(c)

supine

2. Active movements (a) hip flexion (b) knee flexion (c) knee extension 3. PaSSive movements (a) hip and knee (e.g. hip quadrant) (b) muscle stretch (e.g. quadriceps) (Fig. 30.2a) 4. Resisted movements (a) knee extension (Fig. 30.2b)

Examination In anterior thigh pain of acute onset, the diagnosis is usually straightforward, and examination can focus on local strucmres. In anterior thigh pain ofinsidious onset, diagnosis is more difficult and examination should include sites that refer pain to the thigh-the lumbar spine, SIr, and hip. The aim of the examination is to determine the exact site of the abnormality and to assess range of

580

Figure 30. 2 Examination of the patient with anterior thigh pain (a) Passive movement-quadriceps stretch. A passive stretch of the quadriceps muscles is performed to end of range. Passive hip extension may be added to increase the stretch on the rectus femoris, which may reproduce the patient's pain

An t e ri or t h i gh pa i n (b) straight-leg raise (el hip fiexion (Fig. 30.2cl 5. Functional tests

(al squat (Fig. 30.2dl (bl jump (el hop (dl kick 6. Palpation (al quadriceps muscle (Fig. 30.2e overleaf) 7. Special tests {al femoral stress fracture (Fig. 30.2f overleaf) (b) (e)

neurodynamic testing (Fig. 30.29 overleaf) lumbar spine (Chapter 26)

(dl SIJ (Chapter 271 {el knee jerk reflex

Investigations Investigations are usually not required in sportspeople with anterior thigh pain. If a quadriceps contusion fails to respond to treatment, X-ray may demonstrate myositis ossificans. This is usually not evident WltiI at least three weeks after the injury. Ultrasound examination Of MRI will confinn the presence of a hematoma. and may demonstrate early evidence of calcification.

(el Resisted movement- hip flexion

(b) Resisted movement-knee- extension. With the hip and knee flexed to 90°, the knee is extended against resistance

(dl Functional movements-squat. If the previous activities have failed to reproduce the patient's pain, functional movements should be used to reproduce the pain. These may include squat, hop, or jump

58 1

(el Palpation. The anterior thigh Is palpated for tenderness, swelling, and areas offocal muscle thickening. A focal defect in the muscle belly may be palpated, especially with active muscle contraction

(g) Special tests-neurodynamic test (modified Thomas test). The patient is placed tn the psoas stretch position. Cervical and upper thoracic flexion is added and then the clinician passively bends the patient's knee (using his or her own leg). Reproduction of the patient's symptoms indicates a neural contribution

If a stress fracture of the femur is suspected, plain X.ray is indicated. If this is normal, MRI is the inves· tigation of choice. When thigh pain is associated with restricted or painful hip motion, imaging is indicated. Although hip pathology most often refers to the groin (Chapter 28), it can refer to the anterior, and occa· sionally lateral, thigh. In adults, osteoarthritis is a likely diagnosis; in adolescents, consider a slipped capital femoral epiphysis (Chapter 42) or avulsion fracture.

Quadriceps contusion

(f) Special tests- for the presence of a femoral stress fracture. This is performed with pressure over the distal end of the femur. Reproduction of the patient's pain may be indicative of a femoral stress fracture

582

If the patient suffered a direct blow to the anterior thigh, and examination confirms an area of tender· ness and swelling with worsening pain on active contraction and passive stretch, thigh contusion with resultant hematoma is the most likely diagnosis. In severe cases with extensive swelling, pain may be severe enough to interfere with sleep. Quadriceps contusion is an extremely common injury and is known colloquially as a "charley horse," "cork thigh," or "dead leg." It is common in contact sports such as football and basketball. In sports such as field hockey, lacrosse, and cricket. a ball traveling at high speed may cause a contusion. Assess the severity of the contusion to deter· mine prognosis (which can vary from several days to a number of weeks off sport) and plan appropri· ate treatment. The degree of passive knee flexion after 24 hours is a clinical indicator of the severity of

the hematoma. For optimal treatment and accurate monitoring of progress, it is important to identify the exact muscle involved. MRI will show significant edema throughout the involved muscle (Fig. )0.)). Blood from contusions of the lower third of the thigh may track down to the knee joint and irritate the patellofemoral joint.

Treatment The treatment of a thigh contusion can be divided in to four stages: Stage l-control of hemorrhage Stage 2-restoration of pain-free range of motion Stage 3-functional rehabilitation Stage 4-graduated

return to activity.

A summary of the types of treatment appropriate for each stage is shown in Tables 30.2 and 30.3 overleaf. Progression within each stage, and from one stage to the next, depends on the severity of the contusion and the rate of recovery. The most important period in the treatment of a thigh contusion is in the first 24 hours following

Figure 30 .3 MRI appearance of severe hematoma (arrow) of the vastus intermedius muscle

the injury. A player who suffers a thigh contusion should be removed from the field of play and receive the RICE regimen (Chapter I)). Iffull weight-bearing is painful for the sports person, crutches can help unload the muscle and it emphasizes the serious nature of the condition.

Table 30.2 Grading and treatment of quadriceps contusion

Grading

Clinical features

Mild

Mayor may not remember incident

Ice, stretch, and bandage for first 24-48 hours

Usually can continue activity

Then should regain full ROM and start functional

Sore after cooling down or next morning

Treatment

strengthening- bike, running, swimming

May restrict full ROM (stretch) (by S-20%)

Strengthening may be required

Tender to palpa tion

Soft tissue therapy and electrotherapy are effective

Minimal loss of strength Moderate

Usually remembers incident but can continue

See Table 30.3 overleaf

activity although may stiffen up with rest (e.g. half·time or full-time) Moderate restriction of ROM (by 20-50%) Some pain on restricted contraction Tender to palpation May have tracking Usually FWB, but often limp Severe

Usually remembers incident

Ice regularly over 2-3 days

May not be able to control rapid onset of swelling/

Stretches (active after 2-3 days)

bleeding Very restricted ROM (loss of>50%) Difficulty with FWB

No massage/ultrasound No overpressure with passive stretching for 7-10days

Tender over large area (tracking) Obvious bleeding Functional loss of strength ROM = range of motion; FWB -= ful' weight-bearing.

583

'" co -I'

Table 30.3 Treatment of moderate quadriceps co ntusion or grade I[ muscle strain Stage

Aim Contro l of hemorrhage

Weight-bearing

RICE

Crutches if unable

RICE, compression

toFWB

to Include knee

joint if lower third of thigh (fig. 30.4)

Electrotherapy

Electrical

Soft tissue therapy

Stretching

Strengthening

Contraindicated

Gentle stretch to

Static muscle contraction if

stimulation

onset of pain (fig.30.5a)

Magnetic field

possible

therapy Laser if superficial

Pulsed ultrasound

2

Restore and

maintain pain-free ROM

Progress to PWB and FWB as tolerated

and muscle

strength

Maintain compression

As for stage 1 Higher dosages

bandage when

for thermal effect

limb is dependent. Ice after exercise

(ultrasound)

Grade I- II

Increase stretches

longitudinal gliding

Static muscle contrac tion inner range through range (Fig. 30.6a on page 586)

away from site of

Stationary exercise: bike Pool (walk/swim/kick)

injury Grade II transverse gliding away from

Concentric and eccentric exercise (Fig. 30.6b on

site of injury

page 586)

3

FUnctional

fW8

rehabilitation

Usually not required

Longitudinal gliding Transverse gliding

Maintain stretch (Fig. 30.5b)

All stage 2 exercises gradually increasing repetitions, speed and resistance Include pulleys, rebounder, profitter, wall squats, step-downs (Fig. 30.6c on page 586) Hop/jumping, running Increase eccentric exercises

4

Gradual return

Myofascial tension in knee flexion

to sports

Kicking action with pulleys Multidirectional activities

(fig. 30.7 on

Figure of eight

page 587)

Jumping Plyometrics Graduated specific sporting activities Must complete full training before return to sport Heat-retaining brace m ay be helpfu)

PWB = partial weight-bearing; FWB

=full weight-bearing; ROM =range of motion.

'"3

A n t e rior t high pa in

RAe 7tJ\I""?o

In the acute man agement of a thigh contusion, ice should be applied in a position of maximal pain-free quadriceps stretch (Fig. 30.4). Immobilizing the knee in 120 degrees offlexion immediately after injury and for the first 24 hours may be beneficial. l • l This is done by bandaging the entire lower limb. Th e patient then mobilizes with crutches

After the restriction, active pain-free isometric exercises can be started and the use of crutches can· tinues until the athlete is able to resume full athletic activity. It is important that this management tech· nique is not recommended for severe contusions. This technique may reduce time away from sport, improve pain-free range of movement, and reduce the rate of re-injury) The patient must be careful not to aggravate the bleeding by excessive activity, alcohol ingestion, or the application of heat. Loss of range of motion is the most significant finding after thigh contusion, and range of movement must be regained in a gradual , pain-free progress ion before return to athletic activity is considered. After a moderate-te-severe contusion, there is a considerable risk of re-bleed in the first 7-10 days. Therefore, care must be taken with stretching, electrotherapy, heat, and massage. The patient must be careful not to overstretch. Stretching should be pain-free. Soft tissue therapy is contraindicated for 48 hours following contusion. Subsequently. soft tissue therapy may be used. but great care must be taken not to aggravate the condition. Treatment must be ligh t and it must produce absolutely no pain (Fig. 30.7 on page 587). Excessively painful soft tissue therapy will cause bleeding to recur and is never indicated in the treatment of conhtsion.

Figu re 30.4 RICE treatment of an acute thigh contusion in a position of maximal pain-free stretch

Figure 30.5 Quadriceps stretching exercises {a J Standard quadriceps stretch while sta nding . It is important to have good pelvic control and not to lean forward while performing the stretch

(b ) Passive stretch. The tension of the stretch can be altered by adding hip extension

585

Reg i ona l problems

Figure 30.6 Quadriceps strengthening exercises

(al Active quadriceps exercises. Initially inner range quadriceps strengthening is performed with a rolled towel under the knee as shown. The range is slowly increased, depending on symptoms, until range quadriceps contraction can be performed

pain-free

(c) Functional exercises A variety of functional exercises can be performed in the late stage of rehabilitation: squats, wall squats, stepdowns (illustrated), shuttle. Most of these involve both eccentric and concentric contraction of the quadriceps

in American football 0; may sustain a series of minor contusions during the course of a game. These appear to have a cumulative effect and may impair performance later in the game. Protective padding helps to minimize this effect.

Acute compartment syndrome of the thigh (b) Resisted quadriceps Concentric and eccentric exercises are performed

against gradually increased resistance. Knee extension involves concentric contraction of the quadriceps muscle, while lowering the foot from extension involves eccentric quadriceps contraction

It has been suggested that athletes in high-risk sports should consider wearing thigh protection routinely,4 Players such as ruckmen in Australian Rules football, forwards in basketball, and running backs

586

Intramuscular hematoma of the thigh after a blunt contusion may result in high intracompartment pressures and a diagnosis of compartment syndrome of the thigh. Symptoms often include pain and paresthesia, and occur with intra-comparhnental pressures greater than approximately 20 mmHg.6 Pressures of greater than 30 mmHg over a duration of more than six hours can lead to irreversible damage. 6 Unlike other acute compartment syndromes, this condition does not usually need to be treated by surgical decompression. This recommendation is based

Ante r i or thigh pain

Myositis ossificans

In myositis ossificans, osteoblasts replace some of the fibroblasts in the healing hematoma one week fonowing the injury and lay down new bone over a number of weeks. After approximately six or seven weeks, this bone growth ceases. At this stage, a lump is often palpable. Slow resorption of the bone then occurs, but a small amount of bone may remain. Why some contusions develop calcification is not known. Incidence rates range from 9% to 20% in athletes with a thigh contusion.? The more severe the contusion, the more likely is the development of myositis ossificans.7 Intramuscular contusions appear to be more susceptible than intennuscular. Inappropriate treatment of the contusion, such as heat or massage, may increase the risk of myositis ossificans arising. 9 The risk is especially high if the contusion results in prone knee flexion of less than 45° two to three days after the injury. Thus, particular care should be taken when managing these severe contusions. A significant re-bleed may also result in the development of myositis ossificans. The dence of myositis ossificans appears to be increased when a knee effusion is present. Symptoms of developing myositis ossificans include an increase in morning pain and pain with activity. Patients often also complain of night pain. On palpation, the developing myositis ossificans has a characteristic "woody" fee1. Initial improvement in range of motion ceases with subsequent deterioration. Once myositis ossificans is established, there is very little that can be done to accelerate the resorptive process. Treatment may include local electrotherapy to reduce muscle spasm and gentle, painless range of motion exercises. Shock wave therapy has been suggested to improve nmction.IO Indomethacin, which reduces new bone formation, R has been prescribed as a preventative measure in high-risk presentations} Corticosteroid injection is absolutely contraindicated in this condition. Surgery is contraindicated in the early stages and only considered when the margins of the ectopic bone are smooth on investigations, suggesting bone maturity.;

Occasionally after a thigh contusion, the hematoma calcifies. This is known as "myositis ossificans" and can usually be seen on a plain a minimum of three weeks after the injury. If there is no convincing history of recent trauma, the practitioner must rule out the differential diagnosis of the X-ray-bone tumor (Chapter 7)-"

Strains of the quadriceps muscle usually occur during sprinting, jumping, or kicking. In football, quadriceps strains are often associated with over-striding when decelerating during running, or under-striding during the deceleration phase of the kicking leg when

Fig ure 30.7 Soft tissue therapy-sustained myoFascia[ tension in the position of maximal hip extension and

knee flexion

on clinical evidence from cases where surgery was performed. When the muscle was viewed during surgery, there was no evidence of necrotic tissue. Also, there were no subsequent adverse effects ofthe compartment syndrome, such as restricted motion or loss of function. 6 In a case study of an amateur soccer player who sustained a high impact injury from an opposing player,' conservative treatment included rest from any lower limb activity for the first 48 hours, followed by gentle range of motion exercises of the hip and knee. This routine was slowly progressed over the following months and the athlete returned to soccer after six months. 6

Quadriceps muscle strain

587

kicking a football on the run. Fatigue, weakness, and muscle imbalances can impact on performance, and are therefore risk factors for muscle strains. Strains are seen in all the quadriceps muscles but are most common in the rectus femoris, which is more vulnerable to strain as it passes over two joints- the hip and the knee. I1

':!.."1 l,.,. 711

The most common site of strain is the distal musculotendinous junction of the rectus femoris (see below). Management of this type of rectus femoris strain and of strains of the vasti muscles is relatively straightforward; rehabilitation time is short. Strains of the prox imal rectus are not as straightforward and are discussed on page 589.

Distal quadriceps muscle strain Like all muscle strains, distal quadriceps strains (Fig. )0.8a) may be graded into mild (grade I). moderate (grade II), or severe, complete tears (grade III). The athlete feels the injury as a sudden pain in the anterior thigh during an activity requiring explosive muscle contraction. There is local pain and tenderness and, if the strain is severe, swelling and bruising. Grade I strain is a minor injury with pain on resisted active contraction and on passive stretching. An area oflocal spasm is palpable at the site of pain. An athlete with such a strain may not cease activity at the time of the pain, but will usually notice the injury after cooling down or the following day. Moderate or grade II strains cause significant pain on passive stretching as well as on unopposed active contraction. There is usually a moderate area of inflammation surrounding a tender palpable lesion. The athlete with a grade II strain is generally unable to continue the activity. Complete tears of the rectus femoris occur with sudden onset of pain and disability during intense activity. A muscle fiber defect is usually palpable when the muscle is contracted. In the long term, they resolve with conservative management, often with surprisingly little disability.

Figure 30.8 There are two types of quadriceps strains (a) The more common occurs at the distal musculotendinous junction of rectus femoris and has a better prognosis

Treatment The principles of treatment of a quadriceps muscle strain are similar to those of a thigh contusion. The various treatment techniques shown in Table 30.3 are also appropriate for the treatment of quadriceps strain; however, depending on the severity of the

588

(b) The less common occurs in the proximal rectus femoris and takes longer to recover ADAPTED FROM HASSELMAN ET Al. PA9S

strain, progression through the various stages may be slower. Although loss of range of motion may be less obvious than with a contusion. it is important that the athlete regain pain-free range of movement as soon as possible. Loss of strength may be more marked than with a thigh contusion and strength retraining requires emphasis in the rehabilitation program. As with the general principles of muscle rehabilitation. the program should commence with low-resistance. high-repetition exercise. Concentric and eccen tric exercises should begin with very low weights. General fitness can be maintained by activities such as swimming (initially with a pool buoy) and upper body training. Functional retraining should be incorporated as soon as possible. Full training must be completed prior to return to sport. Unfortunately, quadriceps strains often recur, either in the same season, or even a year or two

Proxim al rectus femoris strains With the advent of MR I, a second type of rectus femoris strain injury was recognized occurri ng proximally. apparently with in the belly of the muscle (Fig. 30.8b). This has been termed a "bulls·eye" lesion'; (Fig. 30.9) and seems to contradict the basic tenet that muscle strain occurs at the muscle- tendon junction. Cadaveric'" and M studies of symptomatic and asymptomatic individuals showed that the proximal tendon of the rectus femoris muscle has two components-the direct (straight) and indirect (reflected) heads (Fig. 30.8b). The tendon of the direct head originates from the anterior inferior iliac spine; the tendon of the indirect head arises from the superior acetabular ridge and the hip joint capsule, initially deep to the direct head. 1>!-'! The two heads then form a conjoined tendon. As it progresses along the muscle it flattens out, laterally rotates, and migrates to the middle of the muscle belly. This has been termed the "central tendon." Complete tears are uncommon, which is thought to be due to the extreme length of the musculotendinous junction (approximately two-thirds of the muscle belly).'s Diagnosis is often difficult, because the pathology is deep and the physical assessment findi ngs are non·specific. R-4('

7/iV-"

In three series of proximal thigh strains,11.16.11 the ol'>! average time to presentation was 5- 7 months.

Figure 30.9 MRI of the proximal rectus femoris musculotendinous junction (a) MRI of a proximal rectus femoris tear in a 19-yearold man shows the characteristic "bull's-eye" si gn; this is made up by a ha lo of increased signal (white signal highlighted by white arrows) around the deep tendon (black tendon highlighted with a black arrow)

(b) A comparable MRI of a similar injury, which differs only in the tendon having a low-signa l intensity inside the bright halo (arrow). This is consistent with fatty atrophy in the tend on- the results of the injury having occurred a reasonable time in the past (chronic)

Patients complained of a tender anterior thigh mass and/or weakness and pain with activi ties such as running and kicking. Initial injury was described 589

as a "deep tearing sensation." The anterior thigh mass may be associated with muscle retraction.'5 These signs and symptoms are likely to be due to the indirect and direct heads of the proximal tendon acting independently, creating a shearing phenom· enon, in contrast to what occurs in the normal rectus femoris.' Unlike typical strains which present as focal lesions on MRI, rectus femoris proximal musculotend· inous junction injuries have a longitudinal distribution ofincreased signal along the tendon (Fig. 30.9).'\

strain; however, the distinction needs to be made as an athlete with a thigh strain should progress more slowly through a rehabilitation program (Table 30.3) than should the athlete with a quadriceps contusion. The athlete with thigh strain should avoid sharp acceleration and deceleration movements in the early stages of injury. Some of the features that may assist the clinician in differentiating these conditions are shown in Table 30.+ MRI or ultrasonography may also help differentiate the two conditions.

Treatment

Less common ca uses Stress fracture of the femur

Management of proximal rectus femoris strains depends on the severity of the injury and the athletic demands ofthe individual. Conservative management aimed at symptom relief and avoidance of re-injury is recommended for grade I and II strains. Surgical intervention is typically reserved for grade III strains, which can involve resection of scar tissue. One series diagnosed on MRps showed an average return to full training in professional footballers after a comprehensive rehabilitation program of 27 days for central tendon lesions, compared to nine days for peripheral rectus femoris strains and 4-5 days for strains of tlle vasti muscles.

Differentiating between a mild quadriceps strain and a quadriceps contusion Occasionally, it may be difficult to distinguish between a minor contusion and a minor muscle

Femoral stress fractures can occur around the femoral neck, intertrochanteric and subtrochanteric regions, and the femoral shaft.'9 Stress fractures in the femur can occur following anterior cruciate ligament (ACL) surgery using transfemoral fixation. and are associated with accelerated rehabilitation programs. 20 Stress fracture of the shaft of the femur. although uncommon, should be suspected in an athlete, especially a distance runner. who complains of a dull ache, poorly localized in the anterior thigh. Risk factors for developing femoral stress fractures include training errors, hard training surfaces, and poor footwear.'9 Intrinsic risk factors include leg length discrepancies, and excessive foot pronation or supination. Pain may be referred to the groin or knee, and the

Ta bl e 30.4 Distinguishing features of minor quadriceps contusion and grade I quadriceps muscle strain Diagnostic features

Quadriceps contusion

Grade I rectus femoris muscle strain

Mechanism

Contact injury

Non-contact

Pain onset

Immediate or soon after

After cool·down (next day)

Behavior of pain (24 hours post trauma)

Improves with gentle activity

Painful with use

Location

Usually lateral or distal

Rectus femoris muscle belly (proximal or middle th ird)

Bruising/swelling

May be obvious early

May be absent or delayed

Palpation findings

Tenderness more obvious, lump may feel ovoid or spherical, becomes progressively harder

May be difficult to find, or may be a small area of focal tenderness with a characteristic ring of innammation surrounding it Muscle spasm in adjacent fibers proximally and distally

Effect of gentle stretch

May initially aggravate pain

Not associated with pain

No loss of strength except pain inhibition

Loss of strength (may need eccentric or functiona l testing to reproduce pain)

Strength testing

590

Ant e ri or th igh pain athlete may present with an antalgic gait (especially in the case of femoral neck stress

-

? R-l

b'"

71l

There may be tenderness over the shaft of the femur that (an be aggravated if the patient sits with the leg hanging over the edge of a bench, particularly if there is downward pressure placed on the dista l femur, the so-called "hang test" or"fulcrum test" (Fig. lO.2f).

Because X-ray is limited in detecting changes in bone structure. isotopic bone scan or MRI (Fig. 30.IO) is usually required to make the diagnosis. Treatment depends on location and type of fracture. and generally involves rest from painful activities, and maintenance of fitness by cycling or swimming for at least four weeks. Predisposing factors such as excessive training, biomechanical abnonnality and. in females. m enstrual disturbance should be sought, and corrected where possible. Surgery is indicated where a fracture h as become displaced. When the hang test is completely negative (on average after seven weeks), it is thought to be safe to rehtrn to sport gradually.n Stress fractures are more prevalent among female athletes, particularly if they h ave insufficient calorie intake (Chapter 43). Sports nutritionist input is an important part of the management plan. 19 . 1 ) . l 4 Female military recruits have susceptibility to lower limb stress fractures when entering with

Figure 30.10 MRI of a stress fracture of the shaft of the femur

poor aerobic fitness and a history of amenorrhea (Chapter 45). Prevention strategies include identifying recruits with limited aerobic fitn ess and including nutritionist advice for recruits with menstrual issues.

Lateral femoral cutaneous nerve injury ("meralgia paresthetica") Lateral cutaneous nerve of thigh injury. also known as "meralgia pares th etica," can be a cause of anterolateral thigh pain. The lateral femoral cutaneous nerve is a purely sensory nerve and originates from the lumbar plexus (L2. LJ). The nerve runs along the lateral border of the psoas major muscle. across the iliacus muscle, and exi ts the abdomen under th e inguinal ligament close to the anterior superior iliac spine (AS IS). It then crosses the sartorius muscle and divides into an anterior and a posterior branch. The posterior branch p ierces the fascia lata and runs distally, supplying the skin of the lateral thigh from the greater trochanter to the mid-thigh region. The anterior branch supplies the skin approximately 10 em below the inguinal ligament and distally to the proximal knee. This nerve is susceptible to injury via blunt trauma around the ASIS and the anterior thigh . especially in contact sports such as rugby.2(l Repeated falls from a balance beam in gymnasts may cause injuryY Obesity, pregnancy, and surgical procedures around the nerve are risk factors for nerve injury, irritation. and en trapment.s. 18 Repeated hip flexion and extension during sporting activity (e.g. gymnastics) can irritate the nerve. 16 Entrapment can occur around the ASIS between the ilium and the inguinal ligament. Symptoms include pain, numbness. and paresthesia of the anterolateral thigh without loss of reflex or motor contro1. 27. 18 Sporting activity can aggravate symptoms.: 6 . 19 Tight-fitting garments and athletic compression garments can lead to symptoms. Entrapment as a result of wearing weight belts in scuba divers has also been reported. ;).7 Treatment is often conservative, with a period of res t until symptoms have res olved. Antiinflammatory medications can be beneficial in the early phases. 28 If symptoms do not settle quickly, other interventions su ch as local an es thetic injection can be trialed. Thigh and hip pads can be used as preventive strategy in high contact sports. 26 If conservative treatment fails, surgical decompression of the nerve is ind icated.J° 59 1

Regiona l p r ob l ems

Femoral nerve injury The femoral nerve passes between the psoas major and the iliacus muscles and exits the abdomen deep to the inguinal1igament through the femoral canal. In the upper thigh, the nerve gives offmotor branches to the quadriceps. sartorius, and pectineus muscles. The sensory branches supply the skin of the anterior thigh. The femoral nerve then continues distally as the saphenous nerve. Injury to the nerve can occur secondalY to hyperextension of the hip, such as seen in gymnasts, dancers, football players, basketball players, and long Gymnasts and dancers performing maneuvers that involve extreme hip extension coupled with knee flexion are susceptible to injury of the femoral nerve. 27 Previously, injury was thought to be due to trac· tion placed on the nerve. However, it is now thought to be secondary to strain of the iliopsoas muscle, where a local hematoma causes compression of the Psoas bursitis can also lead to compres· sian and irritation.17 Pain is often located around the inguinal region. Reduced power of the knee extensors and/or reduced knee jerk may also be Sometimes, despite motor changes, sensation can be Conservative treatment is normally trialed first until symptoms settle. Return to sport is possible when strength in the lower limb is regained.

extension) affects the pain, the lumbar spine and psoas muscle should be examined carefully. Any area(s) of abnormality should be treated, and both the local signs (e.g. reproduction of pain with func· tional testing) and neurodynamic tests should be repeated to assess any changes. As with any soft tissue injury, local and referred factors may combine to produce the patient's symptoms. Commonly there is hypomobility of the upper lumbar intervertebral segments on the affected side, associated with a tight psoas muscle. Mobilization of the hypomobile segments will often significantly reduce symptoms. Deep soft tissue treatment to the psoas muscle may also be effective (Fig. 30.n).

Referred pain Referred pain may arise from the hip joint, the SIJ, the lumbar spine (especially upper lumbar) and neural structures. Patients with referred pain may not have a history of injury and may have few signs suggesting local abnormalities. An increase in neural mechanosensitivity may suggest that referred pain is a contributing to thigh pain. The modified Thomas test (Fig. 30.2g) is the most specific neurodynamic test for a patient with anterior thigh pain. If the modified Thomas test reproduces the patient's anterior thigh pain, and altering the neural mechanosensitivity (e.g. passive knee flexion/

592

Figure 30.11 Deep soft tissue treatment to the psoas

muscle

Anterior t high pain 16. Rask MR, Lattig GJ. Traumatic fibrosis of the rectus

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Beatty K. Mclntosh A, Savage T et a1. Biomechanics

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2007;25=18-2 3. 12. Orchard JW Intrinsic and ext rinsic risk fa ctors for muscle strains in Australian football. Am J Sports Med 200 1;29:3°0-3. 13. Hughes C, Hasselman

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Herring SA, Akutho la V. Kaufman MS, eds. Nerve and vascular injuries in sporlS mcdicine. New York: Springer 2009:16I-7°. 28. Toussaint Cp, Perry EC, Pisansky MT et ai. Whars new in the diagnosis and treatment of peripheral ne rve entrapment neuropathies. Neurol CUn 20IO;28(4): 979-10 °4. 29. Ulkar B. Yildiz Y, Kunduracioglu B. Meralgia paresthetica: a long·standing performance-limiting cause of anterior thigh pain in a soccer player. Am J

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593

It comes on suddenly like a cyclist getting a puncture. It was like someOlte getting up and

slapping me around the face. Derek Redmond describing the hamstring injury he suffered in the 1992 Olympic 400 m semi-final. Redmond famously got up and hobbled the remaining 250 meters of the race with the aid of his father Pain in the "hamstring region" can prove very frustrating for recreational and amateur athletes and may even be career threatening for professional sportspeople. Hamstring muscle strains are the most common cause of posterior thigh pain, but referred pain to this area is also common. The average number of days until rehUll to sport for hamstring injuries ranges from 8 to 25 days.' The incidence of recurrence is high. Up to one-third of hamstring injuries will recur, with the greatest risk being during the initial two weeks following return to

two heads-a long head and a short head. The long head is innervated by the tibial portion of the sciatic nerve (LS, 51-3). whereas the short head is innervated by the common peroneal portion (L5. 51-2). The proximal hamstring complex (Fig. 31.lc) is a common site of much pathology and it has an intricate

This chapter focuses on: the relevant anatomy, which is critical to diagnosis, prognosis, and management the clinical distinction between the major pathologies that cause posterior thigh pain the increasingly appreciated ro le for diagnostic imaging for this injury treatment approaches fo r the two types of acute hamstring injuries and for referred pain the indications for considering early or late surgical treatment how to make the, often difftcult, decision preventing the rightfully feared setback-hamstring strain recurrence.

Functiona l anato my The hamstring muscle group (Fig. 31.I) consists of three main muscles-biceps femoris. semimernbranosus. and semitendinosus. Biceps femoris has

594

Fi gure 31.1 Anatomy of the posterior thigh Surface anatomy

(a )

Pos terio r thi gh pa in

crest

gluteus

medius gluteus

maximus

I i tract

gracilis

••

adductor mag nus

biceps femoris (JongheadJ

semimembranosus

'

(b) Muscles of the posterior thigh

/

architecture.! The long head of biceps femoris and semitendinosus share a common proxlmal tendon that arises from the medial facet of the ischial tuberosity. Semitendinosus muscle fibers originate from the ischial tuberosity and the medial aspect of the common tendon; muscle fibers from the long head of bicep femoris originate from the lateral aspect of the common tendon approximately 6 em (2'l.f in.) below the ischial tuberosity. The proximal semimembranosus tendon arises from the lateral facet of the ischial tuberosity and, moving distally. extends medially, passing ventral (deep) to the semitendinosus/biceps femoris long head common proximal tendon. The short head of biceps femoris arises from the linea aspera and thus only functions on the knee joint. Semitendinosus inserts onto the anteromedial surface of the proximal tibia (as part of the pes anserine muscle group). whereas semimembranosus inserts onto the medial tibial epicondyle (Fig. 34.IOb on page 726). Biceps femoris long head and short head form a common distal tendon that has several insertions. including the lateral femoral epicondyle. fibula head. popliteus tendon. and arcuate popliteal ligament (Fig. J4.lb on page 715).4 The posterior portion of the adductor magnus functions as if it were a "hamstring" due to its anatomical alignment and innervation. Adductor magnus is a strong hip extensor muscle, especially when the hip is flexed; it is innervated by the tibial portion of the sciatic nerve, like the majority of the hamstring group.

Clinical reasoning

semitendinosus muscle

The key to effective management of posterior thigh pain is correct diagnosis. The clinician must determine whether the injury to the posterior thigh is an acute muscle strain or pain referred from elsewhere (e.g. lumbar spine). This can be challenging. In healthy individuals. a strain to a large muscle group such as the hamstrings is the result of substantial force. The sportsperson typically recalls precisely when the incident occurred, and whether a significant force was applied to the muscle. The incident may be related to an eccentric contraction (e.g. sprinting) or it may be associated with an excessive stretch (e.g. ballet dancing). 't' RIl

Q,orr,

(e) Proximal hamstring origin

Clinicians should be reticent to diagnose an acute muscle strain in the absence of a convincing history of injury. Without a strong history of injury, consider referred pa in.

595

Tethering of neural structures and fascial strains in the posterior thigh can also occur as an incident; however, skillful examination will reveal whether the injury has a neuromechanical or fascial component. Although the clinical examination for referred pain may not be different from a low-grade strain, the absence of evidence of muscle injury on MRI (10- 20% of posterior thigh pain presentations 5-7) should make the clinician highly suspicious of a referred cause of pain. The causes of posterior thigh pain are listed in

History

1&'IJ'l;.

2. Occupation/lifestyle (al What factors other than sport could be aggravating the condition (e.g. prolonged sitting at work, repetitive bending over with young

3. Incident (a) Yes-consider strain, fascial/neural trauma.

Because there are different causes of posterior thigh pain, the clinician should use the history to develop a differential diagnosis, which can then be refined further with a physical examination that is then appropriately structured. Important points that experienced clinicians consider are shown in the box. This list is not the complete history.

'0'"

(a) Has a change in training coincided with injury? (b) Is there an adequate base of training?

children)?

Table 31.1.

'i' RI1 ('

,. Level of activity

Of the points in the bOK, point 5-the ability to waJkpain-free within 1 day of the injury- and point ll-whether it is a recurrent problem-are particularly important.

(b) No-consider overuse, referred pain, alternative abnormality. 4. Progress since injury (a) Slow-indicates a more severe injury. (b) Erratic-strain is being aggravated by activity or injury is not a strain.

5. Ability to walk pain free within' day following injuryB (a) Yes- sign of better prognosis (b) No-suggests longer rehabilitation time (4 times more likely to require >3 weeks to return to AFL football compared with those who could walk pain-free within a day).

Tab le 31.1 Causes of posterior thigh pain Common

less common

Not to be missed

Hamstring muscle strains

Referred pain

Tumors

Type I • Type II

Tendinopathy Biceps femoris

• Recurrent Hamstring muscle contusion Referred pain •

Sem im emb ra nos us/sem [tend i nos us Bursitis Semimembranous

Lumbar spine

Neural structures

•

•

Fibrous adhesions

Gluteal trigger points

lschiogluteal

"Hamstring syndrome" (Chapter 27) Chronic compartment syndrome of the posterior thigh Apophysitis/avulsion fracture of the ischial tuberosity (in adolescents) Nerve entrapments Posterior cutaneous nerve of the thigh Sciatic Adductor magnus strains Myositis ossificans, hamstring muscle

596

Bone tumors

Sacroiliac joint

Vascular •

Iliac artery endofibrosis

6. Aggravating factors (a) Incident-related: useful for specificity of rehabilitation (e.g. acceleration injuries require acceleration in the rehabilitation program). (b) Non-incident-related: eradication or modification for recovery and prevention (e.g. sitting at a computer causing back/hamstring pain requires ergonomic modification). 7. Behavior with sport (a) Increases with activity; worse afterinflammatory pathology. (b) Starts with minimal or no pain, builds up with activity but not as severe after-daudicant, either neurological or vascular. (c) Sudden onset-mechanical (e.g. strain). 8. Night pain (a) Sinister pathology. (b) Inflammatory condition. 9. Site of pain tal Posterior thigh and/or lower back-lumbar referral or neuromotor/biomechanical mediator. (b) Buttock, sacroiliac joint without lower back symptoms-gluteal trigger points. (cllschial: tendinopathy/bursitis/apophysitisl avulsion. 10. Presence of neurological symptoms (a) Nerve involvement. 11. Recurrent problem (al Extensive examination and rehabilitation required.

3. 4.

5.

6.

7.

(c) knee flexion (active prone knee bend) (d) active knee extension (Fig. 31.2b overleaf) Passive movements (a) hamstring muscle stretch (Fig. 31.2c overleaf) Resisted movements (a) knee flexion in isolation (b) hip extension in isolation (cl combined contraction single-leg bridge (Fig. 31 .2d overleaf) Functional tests (a) running (b) kicking (c) sprint starts Palpation (a) hamstring muscles (Fig. 31.2e overleaf) (b) ischial tuberosity (e) gluteal muscles (Fig. 31 .2f on page 599) Special tests (a) neurodynamic test: slump test (Fig, 31.2g on page 599)

(b) History of prior biceps femoris injury is a strong predictor of risk of recurrence (20 times more likely among football players who had had such an injury within the previous 12 months)!

Examination The examination further refines the distinction between local injury (Le. acute muscle strain), referred pain, or other unusual causes. A practical approach to assess various factors that commonly cause posterior thigh pain is outlined below. 1. Observation (a) standing (Fig. 31.2a) (b) walking (c) lying prone 2. Active movements (a) lumbar movements (b) hip extension

Figure 31.2 Examination of the patient with posterior thigh pain (a) Observation. look for wasting, bruising, or swelling of the posterior thigh. Observation of gait is also important, Observation of the lumbar spine may show the presence of an excessive lordosis or relative asymmetry. A late ral view may demonstrate excessive lumbar lordosis, or anterior pelvic tilt

597

Regional problems (b) (e) (d) (e)

lumbar spine examination (Chapter 26) sacroiliac joint (Chapter 27) assessment of lumhopelvic stability (Chapter 14) biomechanical analysis

See biomechanical analysis in (/inicalSports Medicine masterclasses at www.clinica lsportsmedicine.com.

(d) Combined contraction-single-leg bridge. A widely used "quick" clinical assessment of hamstring resisted contraction is the single-leg bridge. This can be done with the knee fully extended or flexed to 900 (or any angle in between these two positions).

(b) Active movement-active knee extension. The hip is actively flexed to 90° with the knee initially at 90° also. The knee is then slowly extended until pain is felt and

then to the end of range

(el Passive movement-hamstring muscle stretch. The leg is raised to the point where pain is first felt and then to the end of range, pain permitting. Movement should be compared with the uninjured side

598

(e) Palpation. Palpate carefully bearing the underlying anatomy in mind to determine the location of an acute muscle strain (e.g. medial vS.lateral hamstring, proximal vs. distal)

Pos t er io r t h igh pa in (Fig. 3I.3b). and at times. computerized tomography. MRI is the most popular option (especially for the elite-level athlete) because it is non-invasive and capable of providing high-resolution images. MRI can help identify injury location, contribute to

RIj

,..-

n determ ining the likely prognosis, and help predict

C'"

'b""

7fJ'(?

recurrence for certain inju ries. This is a major new step in clinical care in the 20105.

(f) Palpation-gluteal muscles. Palpate the gluteal muscles for trigger points that are taut bands, which are

usually exquisitely tender loca ll y and may refer pain into the hamstring muscle

Figure 31 .3 Imaging of hamstring injuries (a) Ultrasound showing hypoechoic area (between

electronic ca lipers, +)

(g) Special tests-slump test. The slu mp test (Chapter 11) is an essential part of the examination of the patient with posterior thigh pain. It helps the clinician differentiate between hamstring muscle injuries and referred pain to the hamstring region from the lumbar spine

Inves tigations Investigations of posterior thigh pain can be very useful. but clinicians must interpret these findings together with the rest of the examination. Appropriate imaging may include ultrasound (Fig. 3I.3a), MRI

(b) MRI demon strating edema in hamstring region consistent with biceps femoris muscle tear

599

Integrating the clinical assessment and investigation to make a diagnosis Table 31.2 summarizes elements of the history. physical examination, and investigations that point to whether the diagnosis is likely to be an acute hamstring muscle injury, or referred pain to the posterior thigh.

Acute ham string muscle stra ins Before outlining type I and type II hamstring injuries, the epidemiologies of these injuries are outlined together. As the differentiation of acute hamstring injuries into two types has only occurred in the past few years, it is not possible to provide separate epidemiological data with confidence. 'i'RA ('

'0'" )(j'rj".)

In the large majority of hamstring strains, the injured muscle is biceps femoris (reported as 76- 87%).5Semimembranosus injury is uncommon; semitendinosus inj ury is rare.

Epidemiology Acute hamstring strains are common injuries in many popular sports, including the various football codes, field hockey, cricket. and track and field. For example, hamstring strains are the most common injury in Australian Rules football, constituting 15% of all injuries, with an incidence rate of six injuries per club (approximately 40 players) per season, and

a prevalence rate of 21 missed matches per club per season.9 Similarly, in British soccer, hamstring strains make up 12% of all injuries, with an incidence rate averaging five injuries per club per season, resulting in 15 matches and 90 days missed.lO· lJ The average injury causes the loss of three to four matches. 9 .!2 Hamstring injuries in ballet have not been captured as well as in football codes, but estimates of lifetime prevalence of hamstring injury are as high as 51% (34% acute, 17% overuse).!J With respect to epidemiology of recurrence, acute hamstring strains have the highest recurrence rate of any injury, a rate of 34% in Australian Rules football 9 and 12% in British soccer.12

Types of acute hamstring strains There are at least two distinctly different types ofacute hamstring strains (type I and type II), distinguished by different injury situations. The more common, type I, hamstring strains occur during high-speed running7' '2, '4- '9 (Fig. 31.4a). Type II hamstring strains occur during movements leading to extensive lengthening of the hamstrings when in more hip flexion, such as high kicking. sliding tackle, sagittal split; these may occur at slow speeds (Fig. 3I.4b). 'j- 7 These are often seen in gymnasts and banet dancers. Type I strains (the high-speed running type) usually involve the long head of biceps femoris, most commonly at the proximal muscle-tendon junction 1

Ta ble 31 .2 Clinical features of hamstring muscle tear and referred hamstring pain Clinical feature

Acute hamstring strain (type I or III

Referred pain to post erio r thigh

Onset

Sudden

May be sudden onset or gradual feeling of tightness

Pain

Moderate to severe

Usually less severe, may be cramping or"twinge"

Ability to walk

Disabling-difficulty walking, unable to run

Often able to walk/jog pain-free

Stretch

Markedly reduced

Minimal reduction

Strength

Markedly reduced contraction with pain against resistance

Full or near to full muscle strength against resistance

Local signs

Hematoma, bruising

None

Tenderness

Marked focal tenderness

Variable tenderness, usually non-specific

Slump test

Negative

Frequently positive

Trigger points

May have gluteal trigger points

Gluteal trigger points that reproduce hamstring pain on palpation or needling

Lumbar spinel SIJ signs

May have abnormal lumbar spine/SIJ signs

Frequently have abnormal lumbar spine/SIJ signs

Investigations

Abnormal ultrasound/MRI

Normal ultrasound/MRl

600

Poster ior thig h pain

Figure 31.4 (a ) Sprinting is the classic activity that causes type I hamstring strains

(b) Type II hamstring strains occur with maximal stretching (e.g. dancer's sagitta l split and soccer kicking)

(Fig. 31.53 overleaO,14· 17 In contrast. type II injuries (the stretching type) are typically located close to the ischial tuberosity and involve the proximal free tendon of semimembranosus (Fig. 31.5b overleaf).(}· W The proximal free tendon of semimembranosus has a length of more than IO em; thus the stretching type ofharnstring strain can in fact be considered a tendon Type I strains (high-speed running type) generally cause a more marked acute decl ine in function but typically require a shorter rehabilitation period than the type II stretching type of ham string strains (Fig. 3I.6 overleaf);'" The injury mechanism and location give important informa tion about the prog· nosis of the injury. I).'" The injury location can be determined both by maximal pain palpation and by

MRI during the first two weeks after injury occurrence. The closer the site of maximum pain palpation to the ischial tuberosity, the longer the rehabilitation period.'4. 16. 17 MRI should always be obtained when a total rupture is suspected.

Type I acute hamstring strain: sprinting-related Although there are a variety of sports skills that can potentially heavily load tl,e hamstrings (e_g. kicking. twisting, jumping, hurdling), sprinting is the most commonly reported mechanism of type I acute hamstring muscle strain.7. 19 Why do hamstrin gs fail during sprinting? Case studies suggest that hamstrings are most vulnerable to injury during the terminal swing phase of 60 1

........ 100

.q

-"'"

80

_ c

=c.-

proximal muscle belly

proximal

60

I -£ 40

'0

lendon junction

.t

20

2 distal muscle belly

42

10 21 Time after injury (days)

Figure 31.6 Comparison of hamstring injuries in

Figure 31.5 (a) Type I strains (the high-speed running type) are mainly located to the long head of biceps femoris and typically involve the proximal musdetendon junction 17

sprinters (type I) and dancers {type 11)2° (al Hip flexibility (range of motion) of the injured leg expressed as a percentage of the uninjured leg in the sprinters (n :::: 18) and dancers (n = 15). The sprinters' injuries (type I) resulted in more reduction in flexibility, but Similar times to return to near flexibility levels

>0"" .
1 day = 4 times more likely to take >3 weeks),

Subsequent Stretching

Combining this with a past history of hamstring

Hamstrings (Fig. 31.1 0 on page 607)

injury within 12 months resulted in a 93% chance

Antagonist muscles

of taking longer than 3 weeks to return in elite AFL

-

footballers.8 Days to jog pain-free is the strongest predictor of

Soft tissue treatment • Hamstrings (Fig. 31.12a, b on pages 607-608)

time to RTP] , -2 days = 5 days = significantly longer than 4 weeks to RTP

MRI-negative "hamstring strains" are associated with relatively rapid time to RTP and are relatively

Gluteal trigger points (Fig. 31.13 on page 608) Hamstrings (Fig. 31.14 on page 609) (a) Standing single-leg hamstring catches with theraband

The more proximal (closest to the ischial tuberosity

(b) Single-leg bridge catch (c) Single-leg ball rollouts

in a biceps femoris injury) the site of maximal

(d) Bridge walk-out

common (10-20%).1.5-7

tenderness, the more prolonged the time to return to

(e) Nordics

pre-injury level. 16

(f) Single-leg dead lifts with kettle bell

Injury to the proximal free tendon of biceps femoris is associated with a very long return to pre-injury

(g) Yo-yo

level in sprinters (more than twice as long as those not involving the proximal free tendon).Hi A "kicking" or "slow-stretching" mechanism of injury

(h) Askling's gliding (Fig. 31.15 on page 610) Gluteals and adductor mag nus (Fig. 31.16 on page 611) Neuromuscular control exercises (Figs 31.17 and 31.18 on page 612)

is associated with a much more prolonged return

Spinal mobilization

to pre-injury level than a high-speed running

Cross-training bike

mechanism, even though initial signs and symptoms may actually present as far less severe.

10

Length of tear (>60 mm) and cross-sectional area (>55% of total) on MRI are correlated with prolonged return to play.5.6.2B.29

Running program Sprinting technique drills Advanced agility drills Sport-specific training drills

Acute management phase Rehabilitation programs require a basic structure, but should be a "recipe." Treat each case on its merits. TIle management guideline (Table 31.3) captures many experienced clinicians' recommendations.'·H Progression through phases of the rehabilitation program must not be time-dependent. Sometimes what initially appears to be rather minor injury can J;; take an extended period to fully recover, and vice 7!j \j --;. b versa. Progression must be based on successfully achieving key funct ional and/or clin ica l criteria (see box on page 606).

604

Acute injuries should always be assessed thoroughly before any treatment is administered. The fundamental objective of the acute management phase is to facilitate myofiber regeneration and to minimize fibrosis. If strategies aimed at minimizing scar tissue formation are instituted immediately, this may reduce the chances of injury recurrence. RICE Traditionally, the most common treatment in the first few days following type I acute hamstring strain is the rest. ice, compression, elevation (RICE) program. For example, applying ice for IO-I5 minutes using a

Poste ri o r t hi g h pa i n

cold pack, every three to four hours, for the first few days until acute symptoms settle. Compression can be achieved in between times via an elastic bandage or tubigrip stocking. Muscle activation Although RICE is the recommended initial approach, recent research in cell therapy and tissue engineering is indicating an additional role for controlled and monitored exercise (or muscle contraction) regimens. Muscle contraction promotes angiogenesis (i.e. the formation of new blood vessels and the expansion of existing vascularity) and in doing so increases the likelihood of deliveri ng muscle-derived stem cells to the injured region. These cells are likely derived from the vascular endothelium and offer great potential for providing long-term myofiber regeneration. Note that "mechanotherapy" also provides a scientific underpinning for early muscle contraction)S In this light, the commencement of frequent (e.g. 3-4 times per day) low-grade pain-free muscle contractions (e.g. simple isometric hamstring contractions or active prone knee bends) immediately following injury would appear advantageous (Fig. 31.9). Such muscle contractions could be done immediately prior to the application of ice. Medical therapies Despite the widespread use of nonsteroidal antiinflammatory drugs (NSAIDs) in the treatment of hamstring injuries, the two randomized controlled studies8• 36 failed to show beneficial effects of NSA IDSs compared with analgesics or pJacebo on acute muscle strain injuries. It is likely that simple analgesics are just as effective, and do not have the long-term risks on skeletal muscle and the gas trointestinal system associated with NSAI Ds. One study showed favorable results with intramuscular corticosteroid inj ection in American football players with acute hamstri ng injuries. fl Previously, the use of corticosteroids in acute muscle strains had been clearly contraindicated because they were thought to delay elimination of hematoma and necrotic tissue, as well as retarding muscle regeneration. There are concerns regarding the retrospective nature of the National Football League (NFL) study and lack of control group, so we caution against the use of corticosteroids in this situation, particularly as there have been no further studies confirming these results There is increasing interest in the use of growth fac tors to accelerate healing after muscle and tendon

Figure 31.9 Early pain-free muscle contraction (a) hip exte nsion exercise with whole leg a few centimeters (1 in.) off the plinth

(b) Active prone knee bends

injury.18 Animal studies have demonstrated clear benefits in terms of accelerated healing. There are various methods of delivery of the growth factorsall involving the release of growth factors from platelets. These include plasma-rich platelets (PRP) and autologous blood)? Clinical studies in humans are very limited at this stage, but are promising in some settings. The combined injection of Traumeel Sand Actovegin, a deproteinized calves' blood hemodialysate, immediately after a hamstring muscle injury and again at day 2 and day 4 post-injury to the area of the muscle strain and the lumbar spine, is common practice in sports medicine in Germany. It is becoming increasingly popular among eli te sports people elsewhere, despite the lack of any controlled trials supporting its use,l8. 4 0

605

Reg i onal p r ob lems

71J ' Consequen tly, to prevent long-term loss of range of motion (e.g. perhaps from significant scar tissue), a controlled stretching program can be instituted. However, in our clinical experience, most sportspeople regain their normal range of motion without the need for excessive or aggressive hamstring stretching regimens. It may be more important to focus on stretching of other structures. For example, tight hip flexor muscles may place the sportsperson at increased risk of hamstring Soft tissue treatment A comprehensive clinical examination of the lumbar spine, sacroiliac, and buttock regions should be insti tuted at an early stage to assess whether not these regions have any contribution to the presenting injury. For example, Cibulka et al}' reported that mobilization of the sacroiliac joint was of some benefit in the treatment of acute hamstring strains. Neural mobility restriction is frequently present in hamstring injuries secondary to bleeding around the sciatic nerve. Neural mobilizing exercises should be perfo rmed to reduce adhesions. Neural mobilizing can be performed in the hamstring stretch position (Fig. 3I.IOb) by adding gentle cervical flexion (Fig. j I. II).

of: hamstring

• I

Key criteria

1. Begin running and active rehab (i.e.

Pain-free walking

begin subacute/conditioning phase) 2. Return to full activities (i.e. begin

Adequate force with resisted muscle contraction Comp lete resol ution of any symptoms with maximal resisted muscle

functional phase)

contraction Equivocal tenderness upon palpation (left = right) Full and symptom-free range of movement/flexibility (left = right) Successful completion of a structured running program (i.e. time for middle 20 meter port ion of runn ing program (page 613); time comparable to previously determined time for maximum effort recorded when uninjured) Successful completion of appropriate rehabilitation exercises Successful completion of controlled functional (sports-related) tasks,

3. Return to play

specific to original injury mechanism Successful completion of sufficient period of normal training activities (e.g. one full week) with no adverse reaction of any clinica l and/or functional signs and symptoms Additional tests (isokinetic strength testing, Askli ng's H-test on page 614)

606

Figure 31.10 Hamstring stretches (al Hamstring stretch with contralateral knee flexion. The lower leg can be placed in different degrees of external an d internal rotation to maximize the effectiveness of the stretch

Figure 31.1 1 Ne ural mobilizing. Neural mobilizing can be perfo rmed in the hamstring stretch position (Fig. 31.1 Obi by add ing gent le cervical nexion

(b) Hamstring stretch with bent knee results in maximal stretch to the upper hamstrings Soft tissue techniques can be used in the treatment of hamstring strains. Digital ischemic pressure and sustained myofascial tension (Figs 31.12a, b overleaf) are used, gently at first and then more vigorously. Longitudinal massage along the muscle may assist in scar reorganization. Abnormalities of the gluteal muscles may be associated with ham string strains. These regions may be treated in a s ide·lying position using elbow ischemic pressure with the tissue on stretch and the muscle contracting (Fig. 31.13 overleaf) .

Figure 31.12 Soft tissue techniques in the treatment of hamstring injuries (a) Sustained co mp ress ion force to hamstring

607

Reg i ona l p r ob l em s

(b) Sustained myofascial tension combined with

passive knee extension. The hand or the elbow (illustrated) is kept stationary and the release is performed by passively extending the knee (arrow)

Strengthening for hamstring muscles Strengthening is an essential component of the rehabilitation and prevention of hamstring injuries. Muscle strengthening should be specific for deficits in motor unit recruitment, muscle bulk, type of contraction (e.g. eccentric/concentric) and ability to develop tension a t speed. Most hamstring researchers believe that the strains occur when the hamstring muscle group are extensively lengthened, especially in the stretch· ing type of injury.!6. but also in the sprinting type It is also generally accepted that retrain¥ ing needs to be specific to muscle function. 4,-4G Based on this concept, training programs for prevention and rehabilitation of hamstring injur· ies should include exercises emphasizing eccentric muscle contractions and extensive lengthening. Since three of the four hamstring muscles span two joints, both hip and knee joint positions need atten· tion. When prescribing exercises, it is recommended to use exercises that involve simultaneous hip and knee flexion.

Figure 31.13 Treatment of the gluteal region in a lying pOSition using elbow ischemic pressure with the muscle contracting

Numerous exercises fulfill these criteria and we recommend: standing single-leg hamstring catches wi th theraband (Fig.31.14a) single-leg bridge catch (Fig. 31.14b) Single-leg ball rollouts (Fig. 31.14c) bridge walk-outs (Fig. 31.14d) Nordic drops (Fig. 31.14e) single-leg dead lifts with dumb bell (Fig. 31.14f

overleaf) yo-yo (Fig. 31.149 overleaf).

2 .'.

608

One study has confirmed the efficacy of Nordic drops in developing hamstring strengthY Other studies have shown that Nordic exercises were effective in preventing recurrence of hamstring injury (see below).4s.49 The Nordic strengthening program shown in Table 31.4 overleaf is based on the Mjolsnes and Arnason studies.47. It is designed for a 5- 10 week pre·season training program. Introduce this with at least a day between sessions, as the eccentric load can cause delayed onset muscle soreness (DOMS). Adjust

Poster i or thigh pa in

(d ) Bridge walk-outs

Figure 31 .14 Strengthening exercises (a) Standing single-leg hamstring catches with theraband

(e) Nordic eccentric hamstring exercise (drops)patients allow them selves to fall forward and then resist the fall for as long as possible using their hamstrings

(b) Single-leg bridge catch

the load in response to any soreness to encourage compliance. If the program is performed in-season, then one session per week is appropriate. Another exercise that imposes high loads during extensive lengthening of the hamstring is the 50called ''Askling's gliding exercise," described below and shown in the CSM masterclass video (see Fig. 31.15 overleaf). This exercise can be used early in the rehabilitation phase, but should be used with caution (pain-free) because of the high loads exerted on the hamstrings.

le i Sing le-leg ball rollouts

Askling's gliding exercise is shown in (finical Sports Medicine masterdasses at www. cI in ica Is portsme di cin e. (0 m.

609

(f)

Single-leg dead lifts with dumbbell

Figure 31.15 Askling'5 gliding exercise

The exercise starts in a neutral position with all the body weight on the front leg. The gliding (backwards of the other leg) starts and goes on until a posi-

(g) Yo-yo machine

Table 31.4 Pre-season training protocol for Nordic hamstring exercises

Sessions per Week

week

Sets and repetitions

2x5 2

2

2x6

3

3

3

4

3

3x8- 10

5-10

3

3 sets, t 2, 10, B repetitions(O)

x 6--8

= range of motion (a) Load is increased as subject can withstand the forward fall longer. When managing to withstand the whole ROM for 12 repetitions, increase load by adding speed to the starting phase of the motion. The partner can also increase loading further by pushing at the back of the shoulders ROM

610

tion is reached where the sportsperson is not able to go further because of pain, weakness, or limited flexibility. The upper body should be flexed fOlWard during the gliding of the leg backwards. This exercise is intended to be mainly an eccentric one, and therefore the movement returning to the neutral position should be supported by both the arms pulling on a hand rail. For the exercise to be progressive, movement velocity of the gliding can be increased. It is very important to perform the exercise with high concentration and not allow pain. A suitable training session might consist of 3 sets with 3 repetitions, repeated twice a week. Generally, low-grade or minor hamstring injuries or first-time injuries progress quickly; therefore functional strength may be adequate to allow return to sport. Functional exercises could be added to ongoing training and include an exercise such as bridge walkouts (Fig. 3I.14d). More severe or recurrent injuries require more extensive strength work and high-level eccentric load (e.g. theraband catches in standing, Nordic drops, single-leg dead lifts with a weight). Eccentric muscle training results in muscle damage and delayed onset muscle soreness in those unaccustomed to it. Therefore. any eccentric strengthening program should allow adequate time for recovery, especially in the first few weeks. Strengthening for hamstring synergists Rehabilitation must not be restricted to the hamstring alone-it must also include the muscles that assist

Pos t e ri o r th igh pa i n the activity of the hamstring. The gluteal muscles contribute at least 50% to isometric hip If gluteal strength is inadequate the hamstring muscles can be overloaded and susceptible to injury. This is especially true during sprinting activities. The gluteus maximus acts during running to control trunk flexion of the stance leg. decelerate the swing leg. and extend the hipY Any alteration in gluteus maximus activation. strength, or endurance places greater demand on the hamstrings. Overa ll the gluteus maximus provides powerful hip extension when sprinting, and the hamstrings help to transfer the power behveen the hip and knee jointsY To improve gluteus maximus activation. strength, and endurance it is important to initially teach good motor patterns (coordinated, well-timed movement). Isolating the gluteus maximus from hamstring exercises should be an early priority. Progression can be made through bridging exercises (Fig. JI.16a). In the final stages, reintegrate the gluteus maxim us with the hamstrings with exercises such as singl e-leg dead-lifts and lungesY· The adductor magnus is also an important hip extensor. Therefore, strengthening of the hamstring group should always include specific work to ensure adequate gluteal and adductor magnus conditioning (Fig. JI.16)."

Ibl Squat

Neuromuscular control exercises

Neuromuscular control of the lumbopelvic region , including anterior and posterior pelvic tilt. may be needed to promote optimal function of the

lei Splitsquat

Fig ure 31.16 Gluteals and adductor mag nus strengthening exercises (a) One-legged bridging

hamstrings in spnntlng and high·speed skilled movement. Changes in pelvic position can lead to changes in length-tension relationships or forcevelocity A rehabilitation program focusing on progressive agility, neuromuscular control, and lumbopelvic stability exercises (Fig. 31.17 overleaf) was more 6 11

effective in preventing injury recurrence than exer' cises involving a more traditional stretching and simple strengthening exercise programY It is also important to consider motor control exer· cises for deep lumbar spine stabilizers (e.g. multi· fidus). Such exercises can involve isolated activations in prone lying; then progress to functional postural control exercises against gravity (e.g. sit to stand by flexing trunk forward at the hip and maintaining optimal lumbar spine lordotic angle).I4· 1\ Advanced neuromuscular control exercises for the lumbopelvic region and entire lower extremity are discussed in Chapter 1+ Exercises might include side stepping, grape·vine stepping, single-leg stand windmill touches (Fig. JI.I8), fast feet drills etcY

Functional progression Early commencement of a progressive running program is an important part of a rehabilitation program following a hamstring muscle injury.

:;;

Figure 31 .17 Lumbopelvic stability exercises- single leg balance. A quarter squat can be added

Athletes rehabilitating from hamstring strain should run on a day on/day off basis.

711V"':).'O

The basic principles of the running program and an example are shown in the two boxes opposite.

Criteria to progress to return-to-sport phase Once the foIIowing criteria are met, the rehabilitation can progress to the next stage-the return to com· petition phase:

Figure 31 .18 Neuromuscular control exercise Single-limb balance windmill touches with dumbbells. Begin in (a) single-limb stance position with dumbbells overhead and perform windmill motion under control with end position of (b) touching dumbbell to floor 6 12

Poster ior th igh pa in

1. A formal funning program could commence when the sportsperson is comfortable running at approx. 50% intensity (e.g. is able to do a sub maximal stride without pain). Prior to this, running would likely

comprise jogging, progressing to some low-grade fartlek-type running.

2. SportspeopJe rehabilitating from hamstring strain should run on a day on/day off basis (thus three

runs per week). The advantage of a day off is that the clinician can assess key signs and symptoms and

thus make a judgment as to whether the person

1. 2 km jog 2. 2 km varying pace up to 75% of maximum 3. Run-throughs- accelerate 40 m, constant speed

20 m (in 3.5 seconds), decelerate 40 m (x3) 35m

20m

30m

20m

25m

20m

20m

20m

15m

20m

4. Run-throughs-accelerate 40 m, constant speed

20 m (in 2.5 seconds), decelerate 40 m (x3)

has coped with or reacted adversely to the load. The

35 m

20m

structure and intensity of the ne)(t running session

25 m

20m

can then be planned accordingly.

20m

20m

15 m

20m

10m

20m

3. It is advisable to intermingle the running program

with intervals (e.g. repetitions 150 meters/200 meters at tolerable intensity) rather than using the running program as the only type of running done at all stages of the rehabilitation process. Start with the structured running program, determine the pace the sports person can handle without pain, then do a few sessions of repetition running, return to the running program and reassess pain-free pace etc. Finish with the running program to ensure the intensity of the mid-20 m is dose to what you know the sportsperson could do prior to the injury. 4. The warm-up prior to running should start with jogging, then progress to footwork and agility drilisY 5. Sprinting technique drills should be included in the rehabilitation program (e.g. as part of warm-up). A purpose-developed sprint technique training program has been shown to result in a significant improvemen t in lower joint position sense, in a test position similar to the range of movement of the lower limb during the late swing and early stance phase of running gait.56 Poor movement discrimination ability has been shown to be related to susceptibility to future hamstring stra in injury in Australian Rules football players.57 6. Sport-specific training drills sB should also be added in the late stages of rehabilitation.

absence of clinical signs (e.g. full power with contraction, normal ROM, tenderness with palpation equal to uninjured side)

35 m (x3) 30 m (x3) 25 m (x3) 20 m (x3) 15 m (x3)

35 m (x3) 25 m (x3) 20 m (x3) 15 m(x3) 10m(x3)

5. Running out to catch ball-uncontested (x5) 6. Running out to catch ball-contested (xS) 7. Running and picking up ball-contested (xS) successful completion of running program (Le. 20 m time comparable to previously determined time recorded when uninjured) successful completion of appropriate rehabilitation exercises successful completed at least two normal duration training sessions at maximal exertion . In severe or recurrent cases, isokinetic dynamometer assessment may be helpful. Key parameters include hamstring length at which peak torque is developed, and concentric/eccentric hamstring strength ratio)')

Rehlrn-to-competition/sport phase It is extremely difficult to decide when the sportsperson is ready to return to sport after a hamstring strain." This difficulty may be the reason that there is a conspicuously high injury recurrence rate, particularly within a few weeks after the retum.'s, 60 This vulnerability to strain persists, although gradually reduces, for many weeks following return to play.'l Return-to-sport rehabilitation programs that only rely on subjective measures such as "pain-free movements" may result in deficits in neuromuscular control, strength. flexibility, ground reaction force attenuation and production, and lead to asymmetries betvveen the legs during normal athletic movementsY These deficits and deficiencies could

613

Regional problems

persist into sport practice and competition, and ultimately increase the risk of re-injury and limit athletic performance. A criteria-based approach to rehabilitation that includes objective and quantitative tests has the potential to identify deficits and address them in a systematic progression (Le. algorithm) during the stages of returning to sport. However, further research is needed (Le. prospective, retrospective, and training studies) to validate the criteria-based progressions in each phase: completion of progressive running program full range of movement (equal to uninjured leg)

-

slow passive61 . 62 active straight-leg raises 63

pain-free maximal isometric contraction full strength (equal or almost equal to uninjured leg) - measured by manual testing, hand-held

-

dynamometer, or isokinetic machine 90%64-95% 65,6(iof eccentric strength of uninjured

leg

functional tests -

sprinting from a standing start

-

abrupt changes of pace during run

-

side stepping

-

bending to catch ball at full speed (if appropriate for the sport)

successful completion of a full week of maximal training.

Askling's H-test is a complement to the clinical examination before return to sport. 67 Notably, this active test must not be performed before the time of rehabilitation at which all clinical tests, including those of passive flexibility, indicate complete recovery (see box below).

IW ,wwJ

Askling's hamstring apprehension test (H-test) is shown in (finical Sports Medicine masterclasses at www.elinicalsportsmedieine.co m.

It does not appear that MRI appearance is a good indicator of readiness to return to play. Abnormalities

During the test, the subject should be positioned on a bench in a supine position with the contralateral leg and the upper body stabilized with straps (Fig. 31.19). A knee brace ensures full knee extension of the tested leg, and the foot of the tested leg should be kept slightly plantarflexed. No warm-up exercises are to be performed before the test. The uninjured leg is tested before the injured leg. The instruction to the subject is to perform a straight-leg raise as fast as possible to the

Figure 31.19 Askling's hamstring apprehension test

highest point without taking any risk of injury. A set

{a} Starting position

of three consecutive trials are performed, preceded by one practice trial with submaximal effort. After the three active test trials, the subject is to estimate experience of insecurity and pain on a VAS scale, from 0 to 100. In the study by Askling et al.67 the athletes noted an average insecurity estimation of 52 for the injured leg and 0 for the uninjured leg. The new active test seems to be sensitive enough to detect differences both in active flexibility and in insecurity after acute hamstring strains at a time when the commonly used clinical examination fails to reveal injury signs. If insecurity persists, the test should be repeated until no insecurity is reported. The athlete is then allowed to return to sport.

614

(b) Maximal hip flexion

Poste ri o r th i gh pa i n on MRI tend to persist well after sportspeople are back to full sport. s The length of time until return to sport is proportional to the severity of the injury. In most cases a sportsperson with a mild hamstring strain would achieve the return-ta-play criteria (page 606) in 12-18 days if optimally treated (Table )r.)). A practical tip to reduce the incidence of reCUTrenee is to restrict game time when first returning from hamstring injury to minimize fatigue. In this way, return to sport can be progressed.

\' RA '0'" 71J\{?

It is important to persist with a well-structured strength and neuromuscular control exercise program after return to sport, to lessen the likelihood of recurrence. This should be continued until there are no longer any significant asymmetries or hamstring/quadriceps ratio deficits. These sessions must be carefully schedu led to allow recovery time before exposure to high-risk activity.

Risk factors for acute hamstring strain Risk factors for acute hamstring strain are discussed here because patients rarely present for "primary prevention"-to avoid hamstring injuries before they have one. Some risk factors may be mitigated. Risk factors for acute hamstring strains may be intrinsic (person-related) or extrinsic (environment-related) factors (as they are with all injuries [Chapters 4 and 5]). There have been two published systematic reviews on this topic to date. G8. 6 ') Factors that appear to predict risk of hamstring strain are discussed below. Other factors have been evaluated, but do not appear to be risk factors; these include body mass index (BMI),'il. 70. 7 height/8.70-71 weight,'I>· 7° . 7' , 71 and functional performance tests (e.g. countermovement jump. 40 m sprint tests, Nordic hamstring strength test, hamstring length measurement).7 1

1

Intrinsic risk factors Age A number of studies have shown that sportspeople of older age are at increased risk of acute hamstring strain, even when the confounding factor of previous injury is removed.7Q-74 Australian Rules footballers aged 23 years or more were almost four times as likely as younger players to sustain an acute hamstring strain during the season,7;}. Older sports people may be at heightened risk due to increased body weight and reduced hip flexor

ftexibility.4:J. It has also been speculated that the high risk of older sportspeople to acute hamstring strain is related to degenerative changes at the lumbosacral junction»

Past history of injury Past history of injury is a critical factor for the development of a/another hamstring injury. A prior history of acute hamstring strain is a significant risk for future injury)0.7I.7J.74 In comparison to injury-free sportspeople, those with a past history of hamstring injury do not appear to display appreciable differences in running mechanics;7(i.7J however, they do display differences in musculotendon morphology (differences in muscle volume, presence of scar tissueFR and contraction mechanics)') It may be that the presence of scar tissue creates abnormally high rates of localized tissue strains in the immediately adjacent muscle fibers, and thus the risk of further injury.77 Therefore strategies to reduce the development of scar tissue following initial injury are critical in terms of minimizing future risk of re-injury. Sports people with a history ofinjury to other areas of the lower limb also have an increased likelihood of acute hamstring strain. These include: knee- major knee injury (e.g. anterior cruciate ligament [ACL] reconstruction, patellar dislocation)25, B groin-history of osteitis pubis (bone marrow edema on MRl)73 calf muscle strain 74 lumbar spine-"major" injury (Le. episode which required radiological investigation with a specific recorded clinical diagnosis).73

Hamstring strength Numerous studies have evaluated whether strength quantified via an isokinetic dynamometer is a risk factor for hamstring strain. While, intuitively, reduced muscle strength would appear to predispose to hamstring strain, the evidence is mixed. Such conflicting findings may relate to the difficulty in quantifYing muscle strength in a systematic manner (Le. what type of contraction [isometric, concentric, eccentric], what strength parameter or index to measure [peak torque, knee angle at which peak torque occurs, hamstring/quadriceps ratio, hamstring to hip flexor ratio, strength asymmetry], as well as the level of motivation of the sportspeople).

615

Reg io n a l pro b le ms Current evidence indicates that knee flexor peak torque is not a risk factor for hamstring strainY' 6J, 80 Increased knee extensor torque was a risk factor for hamstring strain in one study" but not in other studies. c,j, 80, 81 Hamstring to quadriceps ratio has also been extensively investigated. A reduced hamstring to quadriceps ratio (i.e. weaker hamstrings and/or stronger quadriceps muscles) has been shown to be a risk factor for hamstring strain in some studies'" ,9· 81, 82 but not in other studies. (> \ . Ho

Other factors Other intrinsic risk factors for acute hamstring strain which have only limited supporting evidence include (but are not limited to): ethnicity12.73 reduced ankle dorsiflexion lunge range of motion l9

reduced quadriceps f1exibilit y 19. ti2 poor lower limb joint posi tion sense. 57

There is conflicting evidence regarding whether or not reduced hamstring flexibility (e.g. assessed via the active and/or passive knee extension tes t) is a risk factor for hamstring strain. Most studies cate that reduced hamstring flexibility is not a risk factor;'')· 7 0 -72 however, two studies have reported the opposite. 61 . 62

Extrinsic risk factors Fatigue It has long been speculated that fatigue is a risk factor for an acute hamstring strain, but there is very little evidence to support or refute this claim. Verrall et aU found that 85% of acute hamstring strains occurred after the first quarter of a competitive match or after the first 15 minutes of a training session. Furthermore, Woods et al. I l found that 47% of their acute hamstring strains occurred towards the end (during the linal third) of the first and second halves of a match. Such observations suggest fatigue may be a factor, but further research is required.

and defensive secondary, as well as players on the special teams units, are most commonly injured. xl

Prevention of hamstring strains A recent Cochrane systematic review concluded that there is insufficient evidence from randomized con· trolled trials to draw conclusions on the effectiveness of interventions used to prevent hamstring injuries in people participating in football or other activities for these injuries. X4 However, some recent studies have suggested that Nordic exercises, a balance program, and soft tissue therapy may help prevent hamstring injuries.

Nordic drops and other eccentric exercises There is evidence from a number of shldies4x. 4')· 8, that an eccentric strengthening program can reduce the incidence of hamstring injUly. In Petersen's study,49 there was a significant reduction (approximately in the "total" number of hamstring injuries (i.e. new plus recurrent injuries), and a sig' nificant reduction (approximately seven-fold) in the number of recurrent injuries for the intervention group, which undertook a lo·week progressive preseason eccentric training program of Nordic cises (Fig. J'.'4e on page 609) followed by a weekly seasonal program. There was also an approximate reduction in number of new hamstrings injuries in the intervention group, but this did not reach statistical significance. Amason's study also showed a reduction in s tring injuries with a Nordic exercise program. 48 An eccentric/concentric strengthening program using a prone leg curl machine in soccer players also prevented hamstring injuries. 8) Two other studies have looked at the effect of Nordic exercises and shown a minimal positive effect in one study, I') and no effect in the other. 86 However, both these studies suffered from poor compliance, which may explain the differences between their studies and those that showed a positive effect.

Balance exercises /proprioception training Player position There is limited evidence that different playing posi. tions is associated with higher risk of hamstring strain. Goalkeepers have a significantly lower risk for hamstring strain than outfield players in soccer, lZ and rugby forwards have a reduced risk of hamstring strains compared with backs.'l\ In American football, the speed position players, such as the wide receivers

6 16

Proprioceptive exercises or balance training may be an effective strategy for preventing hamstrings injuries. X7-X') A positive effect was found in one study,H,) whereas MO other studies failed to show any effect. X.7· xx In the German study,8') 24 elite female soccer players of a German premier league soccer team formed an additional soccer'specific proprioceptive

Poster io r t hig h pa in multistation training program over three years. Progression in level of difficulty from easy to complex was a main feature of the exercises. The duration of each exercise was between 15 and 30 seconds. The exercises that were implemented were: 1. single-foot stand on right and left foot 2. jump forward in single-foot stand with flexed knee at landing and balancing 3. jump backward in si ngle -foot stand and bal anci ng

4. row jumping single foot 5. row jumping bipedal 6. obstacle course forward and backward

7. obstacle course sideways 8. bipedal jumping on forefoot 9. sideways jumping in single-legged stand

10. sitting on a wobble board with balancing torso 11 . jumping forward over a line, landing with flexed

knees, and balancing 12. standing on both hands and feet with diagonal

balancing. All exercises were performed with no additional weight; tha t is, players had to bear only their own body weight on one or two legs or all extremities depending on the exercise. In addition, balance training was implemented in soccer-specific match-play training on balance boards. At the end of the three-year proprioceptive balance training intervention, non-contact hamstring injury rates were reduced from 22.4 to 8.2/1000 hours. Furthermore, the more minutes of balance training performed, the lower the rate of hamstring injuries.

monitored during the season (e.g. follow ing games) for signs of adverse reaction to load (e.g. palpation. pain/weakness with isometric maximum voluntary contraction IMVC] tests ).

A promising clin ical approach for the h igh -risk athlete One test that may be helpful in screening or monitoring the state of a player's hamstrings during the season is an isometric maximum voluntary contraction (MVC). In this tes t the player is positioned with his or her hips and knees flexed to 900 and both heels resting on a firm plinth of adjustable height (Fig. ) 1.20). The cuff of a digital sphygmomanometer is pre-inHated to 10 mmHg and placed under one heel. The player pushes their heel into the cuff as hard as possible by Hexing their knee without lifting their buttocks off the ground. The contraction is held for three seconds, and the peak press ure recorded. The process is repeated for the opposite leg. The test is performed weekly one or two days post-match and any reduction in MVC is taken as a warning sign. and trai ning load is reduced until the test returns to normal This lest may be particularly useful in those who have had a previous ham string injury and are therefore at risk of a recurrence.

Soft tissu e th erapy Hoskins and Pollard90 demonstrated that a soft tissue therapy program reduced the incidence oflower limb muscle strains, but not specifically hamstring strains. in a group of semi-eli te AFL footballers. Treatment for the intervention group was individually determined and could involve manipulation/mobilization and/or soft tissue therapies to the spine and extremity. Minimum scheduling was one treatment per week for six weeks, one treatment per fortnigh t for three months, and then one treatment per month for the remainder of the season (three months). No positive effect on hamstring injury prevention was found with stretching plus warm-up/cooldown.?1 Another way of preventing hamstring injuries is to identify those at high risk of injury and modify their activity accordingly. Players can be regularly

Figure 31.20 Schache's hamstring maximum voluntary contraction (MVC) test. The used to measure an isometric maximum voluntary contraction (MVC) of the hamstrings with the digital sphygmomanometer 617

Referred pain to posterior thigh The possibility of referred pain should always be considered in the athlete presenting with posterior thigh pain. Hamstring pain may be referred from the lumbar spine, the sacroiliac joint or from soft tissues (e.g. the proximal fibers of the gluteus maximus and, especially, gluteus medius and the piriformis muscle) (Fig. 31.21). Often, there is a history of previous or current low back pain. The slump test (Fig. lI.2g) should be used to detect neural mechanosensitivity. The test is positive when the patienfs hamstring pain is reproduced with knee extension during neck flexion and subsequently relieved by neck extension. Examination may reveal

reduced range of movement of the lumbar spine, tenderness and/or stiffness oflumbar intervertebral joint(s), or tenderness over the area of the sacroiliac joint. A positive slump test is strongly suggestive of a referred component to the patient's pain. However, a negative slump test does not exclude the possibil. ity of referred pain, and the lumbar spine should

) XX -+X'

gluteus mediu s

tensorfascia \ " lata

X

piriformis

§:\ _ \

biceps femoris semImembranosus & semitendinosus

,---")F' Figure 31 .21 Pattern of referred pain to the hamstrings from trigger points

618

be carefully examined to detect any intervertebral segment hypomobility. The slump stretch (Fig. 31.2g) has been advocated as a method of treatment of hamstring pain in Australian Rules footballers. 91

Trigger points Trigger points are common sources of referred pain to both the buttock (Chapter 27) and posterior thigh. The most common trigger points that refer pain to the mid-hamstring are in the gluteus minimus, gluteus medius, and piriformis muscles. The clinical syndrome associated with posterior thigh pain without evidence ofhamstring muscle injury on MRI and reproduction of the patient's pain on palpation of gluteal trigger points is now well recognized and extremely common. 9l The clinical features are described in Table 31.2 on page 600. The patient often complains of a feeling of tightness, cramping, or "twinge," or a feeling that the hamstring is "about to tear." On examination, there may be some localized tenderness in the hamstring although it is usually not focal, and there is restriction in hamstring and gluteal stretch. Firm palpation of the gluteal muscles will detect tight bands that contain active trigger points, which when firmly pal. pated are extremely tender, refer pain into the ham· string and elicit a "twitch response." Treatment involves deactivating the trigger point either with ischemic pressure using the elbow (Fig. 31.22a) or dry needling (Fig. 31.22b). Following the local treatment, the tight muscle groups-the gluteals and hamstrings-should be stretched.

Lumbar spine The lumbar spine is a source of pain referral to the posterior thigh. Unfortunately, it is difficult to distinguish between sources based on the behavior and distribution of the pain. Pain may be referred from the disk, zygoapophyseal joints, muscles, ligaments, or any structure that can produce pain locally in the lumbar spine. 94 Nerve root compression may also be a cause of hamstring pain. Diagnostic blocks and provocation injections have been advocated to isolate sources of pain in the lumbar spine. However, in the clinical setting, this is often not possible. It is important to examine the lumbar spine carefully (Chapter 26). This will assist in the identification of the lumbar spine as a source of hamstring pain. Remember also that the lumbar spine may be a cause oflumbar pain indirectly. For example, the lumbar spine may cause

Poster i o r th i g h pa i n

Figure 3 1.22 Treatment of gluteal trigger points {a} Elbow pressure

a biomechanical block to hip extension, resulting in overload of the sacroiliac joint and referred pain to the hamstring group. True nerve root compression is usually more definitive in its presentation. The patient may have associated neurological symptoms, such as numbness and loss of foot eversion. The management of these injuries usually involves an extended period of rest and. in certain cases, an epidural injection. In extreme cases, surgical decompression of the nerve root may be warranted. Spondylolisthesis and spondylolysis (Chapter 26) have both been associated with hamstring pain and tighhless.')6 Examination findings of positive lumbar quadrant tests or single-leg standing lumbar extension are suggestive of these conditions; these spinal pathologies can be confirmed on MRI or CT scan. Stabilization programs are the treatment of choice, as the deep abdominal muscles are deficient in people with back pain as a result of spondylolisthesis and spondylolysis.')? In severe cases, clinicians have resorted to corticosteroid injection (+j- neuroablation using pulsed radiofrequency) under X-ray control into the deficient pars interarticularis. 0

I&"J"'> 0

An effusion that develops after a few hours or, more commonly, the following day represents reactive synovitis and is a feature of meniscal and chondral injuries. There is usually little effusion with collateral ligament injuries. If a patient volunteers having heard a "pop;' a "snap;' or a "tear;'the injury should be considered an ACl tear until proven otherwise.

Patients presenting with a sensation of something having "moved" or "popped out" in the knee should not be assumed to have suffered a patellar dislocation. This symptom is more commonly associated with an ACL rupture. There may be associated "elicking" or "locking," and this is often seen with meniscal injuries. "Locking" is classically associated with a loose body or displaced meniscal tear. Locking does not mean locked in one knee position; the tenn is used when significant loss of passive range of motion is present, especially loss of full extension. It is helpful to ask the patient in what "position' the knee locks. If the patient reports that the knee locks when it is straight, and does not bend, this usually is a manifestation of patellofemoral pain and injury- the kneecap is unable to engage in the groove secondary to pain. The symptom of "giving way" can occur with instability, such as in ACL deficiency. Instability may also occur with meniscal tears, articular cartilage damage, patellofemoral pain (Chapter 33) and severe knee pain. In the latter cases of knee pain instability, a careful history will reveal more of a "jack-knife" (collapsing) phenomenon in flexion rather than a true "giving way" in extension. Patients with recurrent patellar dislocation and those with loose bodies in the knee can describe similar sensations. If a patient reports feeling unstable on steps, this is most often a reflection of quadriceps weakness and/or pain, and rarely represents true kneecap instability. The comprehensive history will also include:

the initial management of the injury the degree of disability

Table 32.2 Time relationship of swelling to diagnosis Immediate {O-2 hours} (hemarthrosis)

Delayed (6- 24) hours (effusion)

No swelling

ACl rupture Patellar dislocation Major chondral lesion

Meniscus Smaller chondral lesion

MCl sprain (superficial)

628

Ac ut e k n ee i nju ri es a history of previous injury to either knee or any previous surgery

D. Palpation 1. patellofemoral joint (including patellar and

the patient's age, occupation, type of sport and leisure activities, and the leve l of sport played.

If the patient is a good historian, the diagnosis will be obvious in most cases.

Examination Each structure that may be injured must be examined. Important clues to diagnosis include the presence or

absence of effusion or hemarthrosis, the range of motion, and tests of the ligaments and m enisci.

quadriceps tendons, medial and lateral retinaculum)

2. 3.

MCl lCl

4.

medial joint line (Fig. 32.2d overleaf)

5.

lateral joint li ne

6.

posterior structu res (e.g. ham string tendons, Baker's cyst, gastrocnemius origins)-best done in the prone position

Knee examination is demonstrated in detail in the Clinical Sports Medicine masterclasses at www.dinicalsportsmedicine.co m. Examination includes: A. Observatio n

2.

1.

standing walking

3.

supine (Fig, 32.2a)

B. Active movements

1.

flexion

2. 3.

extension straight-leg raise

C. Passive movements 1. fiexion (Fig. 32.2b) 2.

extension (Fig. 32 .2c) (b) Passive movement- flexion Assess range of motion, end feel. and presence of pain

Ie) Passive movement-extension. Hold both legs Figure 32.2 Examination of the patient with an acute

by the toes, looking for fi xed flexion deformity or

knee injury (a) Observation-supine. Look for swelling, deformity,

hyperextension in ACL or peL rupture. Overpressure

and bruising

provoke pain in meniscal injuries

may be applied to assess end range. This proced ure may

629

E. Special tests 1. presence of effusion (Fig. 32.2e) 2. stability tests (a) MCl (Fig. 32.2f) (b) lCL(Fig.32.2g) (c) ACl (i) lachman's test (Figs 32.2h-k) (ii) anterior drawer test (Fig. 32.21 overleaf) (iii) pivot shift test (Fig. 32.2m overleaf) (d) PCl (i) posterior sag (Fig. 32.2n overleaf) (ii) reverse lachman's test (iii) posterior drawer test (Fig. 32.20 overleaf) (iv) external rotation test-active and passive (e) patella (i) medial and lateral patella translation (or mobility) 3. flexion/rotation (a) McMurray's test (Fig. 32.2p on page 633) (b) Apley's grind test 4. patellar apprehension test (Fig. 32.2q on page 633) 5. patellofemoral joint (Chapter 33)

(d) Palpation-medial joint line The knee should be palpated in 300. of flexion

630

6.

functional tests (al squat test (helps to assess functional valgus collapse of knee) (b) hop test (c) pelvic bridge/plank arrow (helps assess core strength)

(e) Special tests-presence of effusion

Manually drain the medial subpatellar pouch by stroking the fluid in a superior direction. Then "milk" the fluid back into the knee from above on the lateral side while observing the pouch for evidence that fluid is reaccumulating. This test is more sensitive than the "patellar tap:' It is important to differentiate between an effuSion and an hemorrhagic bursitis

(t) Stabilitytest-MCl This is tested first with the knee in full extension and then also at 30" of flexion (illustrated). The examiner applies a valgus force, being careful to eliminate any femoral rotation. Assess for onset of any pain, extent of valgus movement, and feel for end point. If the knee "gaps" at full extension, there must be associated posterior cruciate injury

(9) Stability test-LCL The LCL is tested in a simi lar manner to the Mel except

with varus stress applied

(hI Stability test-Lachman's test Lachman's test is performed with the knee in 15" of flexion, ensuring the hamstrings are relaxed. The examiner draws the tibia forward, feeling for laxity, and

assessing the quality of the end point. Compare with the uninjured side

' Lachman's test

(i)

-}

0)

(k)

(i) The ACL is slightly slack in the start position

(j) When the ACl is inta ct, the ligament snaps tight and the examiner senses a "firm"/"sudden" end feel (k) When the ACL is ruptured, the Lachman's test results in a

end feel

631

(I) Stability test-anterior drawer test This is performed with the knee in 900 of flexion and the patient's foot kept stable. Ensure the hamstrings are relaxed with the index finger on the femoral condyles. The tibia is drawn anteriorly and assessed for degree of movement and quality of end point. The test can be performed with the tibia in internal and external rotation to assess anterolateral and anteromedial instability respectively

(m) Special test-pivot shift test With the tibia internally rotated and the knee in full extension, a valgus force is applied to the knee. In a knee with ACl deficiency, the condyles will be subluxated. The knee is then flexed, looking for a "clunk" of reduction, which renders the pivot shift test positive. Maintaining this position, the knee is extended, looking for a click into subluxation, which is called a "positive jerk test"

632

(n) Stability test-posterior sag With both knees flexed at 90 0 and the patient relaxed, the position of the tibia relative to the femur is observed. This will be relatively posterior in the knee with PCl deficiency

(0) Stability test-posterior drawer test With the knee as for the anterior drawer test, the examiner grips the tibia firmly as shown and pushes it posteriorly. Feel for the extent of the posterior movement and quality of end point. The test can be repeated with the tibia in external rotation to assess posterolateral capsular integrity

Acute knee in juries

(p ) Flexion/rotation test-McMurray's test The knee is Aexed and, at various stages of Aexion, internal and external rotation of the tibia are performed. The presence of pain and a palpable "clunk"is a positive McMurray's test and is consistent with meniscal injury. lfthere is no clunk but the patient's pain is reproduced, then the meniscus may be damaged or there may be a patellofemoral joint abnormality

(q ) Special tests-patellar apprehension test The knee may be placed on a pillow to maintain 20-30° of Aexion. Gently push the patella laterally. The test is positive if the patient develops apprehension with a sensation of impending dislocation

Investigations X-ray

Tab le 32.3 Criteria for knee X-ray based on Ottawa knee rule la)

Clinicians often wonder whether or not to perform an X-ray in cases of an acute knee injury. More than 90% of radiographs ordered to evaluate knee injuries are normal. A set of decision criteria known as "the Ottawa knee rule" was developed in an adult emergencymedicine setting in the mid-1990S (Table 32.3).2 Also, surgeons always wish to see preoperative films so there are no intraoperative surprises_ The main aim of performing an X-ray in cases of moderate and severe acute knee injuries is to detect a fracture:

A knee radiograph is indicated after trauma only when at least one of the foHowing is present: patient age more than 55 tenderness at the fibular head tenderness over the patella inability to flex the knee to 90° (this captures most hemarthrosis, fractures) inability to weight-bear for four steps at the time of the injury and when examined. To these, we suggest a high index of suspicion for: high-speed injuries children or adolescents (who may avulse a bony fragment instead of tearing a cruciate ligament) if there is clinical suspicion of loose bodies.

a tibial avulsion fracture associated with an ACL or pel injury a tibial plateau fracture following a high-speed kneeloading injury an osteochondral fracture after patellar dislocation.

The Ottawa knee rule was designed for use in the emergency department setting

10)

633

Magnetic resonance imaging (MRI)

Ultrasound examination

MRI is reliable, safe, and accurate in the diagnostic work-up of acute knee injuries. Even when a ligament disruption is diagnosed by physical examination, MRI can add value by demonstrating the extent of associated injury to cartilage and meniscus. Patellar injury and quadriceps tendon injury can also be assessed.

In the setting of an acute knee injmy, a complete patellar tendon rupture will be obvious clinically. High-quality ultrasound examination can demonstrate partial tears of this tendon. Ultrasound examination can also detect the size and location of bursal swelling, and differentiate intra- from extra-articular swelling if necessary.

I' R04 ('

'0'" 71J'{'?

MRI should never be ordered in the absence of a thorough history and physical examination.

MRI findings that are not clinically relevant should be interpreted with caution. For example, meniscus tears were recently shown to be present in a relatively high proportion of asymptomatic knees.) Thus, such an injury presenting on MRI but not associated with relevant clinical features might be a "red herring" (irrelevant) not in need of treatment. MRT can be very useful when a primary patellar dislocation is suspected clinically. MRI can help to detect osteochondral avulsion fractures that require surgical assessment. As the avulsed fragment swells (and deteriorates), there is a limited window of time for surgical fixation ofthe fragment. Usually it needs to be identified and treated within IO-I4 days of the injury. The advent ofMRI brought the discovery that significant knee injuries are associated with edema in the subchondral region. This phenomenon is known as a bone bruise or bone marrow lesion (BML). Clinically, a bone bruise is associated with pain, tenderness, swelling, and delayed recovery. The presence of a bone bruise indicates substantial articular 5 but the clinical relevance of a cartilage bone bruise is still to be determined.

Meniscal injuries Acute meniscal tears occur when the shear stress generated within the knee in flexion and compression, combined with femoral rotation, exceeds the meniscal collagen's ability to resist these forces. (, The medial meniscal attachment to the medial joint capsule decreases its mobility, thereby increasing its risk for injury compared with the more mobile lateral meniscus. 7 Degenerative meniscal tears occur in the older popUlation frequently without an inciting event and also without symptoms) The different types of meniscal tear are shown in Figure )2.). posterior horn

anterior horn vascular supply

The role for diagnostic arthroscopy In the developed world, arthroscopy is rarely used for diagnosis. However, in rare cases, when the clinical picture is unclear and the patient has persistent pain and swelling not responding to other treatment alternatives, diagnostic arthroscopy may be usefuL It is then used to confirm the presence or absence of pertinent intra-articular pathology. This can be particularly useful in cases of cartilage injury; MRI is imperfect in revealing cartilage damage. Performing a knee arthroscopy for pain without other objective signs or symptoms is not advocated.

634

longitudinal

degenerative

nap

cross- I section

radial

bucket handle

horizontal cleavage

Figure 32.3 Meniscus tear orientation and zones of vascularity; these drawings are of a medial meniscal tear

Acute knee in juries

Clinical features The history can provide a mechanism and a sense of the severity of meniscal tears. The clinical features are as follows: The most (ommon mechanism of meniscal injury

is a twisting injury with the foot anchored on the ground; this rotational force is often caused by another player's body.

The twisting component may be of comparatively slow speed. This type of injury is commonly seen in football and basketball players. The degree of pain associated with an acute meniscal injury varies considerably.

Some patients may describe a tearing sensation at the time of injury.

A small meniscal tear may cause no immediate symptoms; it may become painful and cause knee swelling over 24 hours. Small tears may also occur with minimal trauma in the older sportsperson as a result of degenerative change of the meniscus. Patients with more severe meniscal injuries (e.g. a longitudinal (" bucket handle"] tear) present with more severe symptoms. Pain and restriction of range of motion occur soon after injury. Intermittent locking may occur as a result of the torn flap, the "bucket handle;' impinging between the articular surFaces. This may unlock spontaneously with a clicking sensation. This often occurs in association with ACL tears. In these patients, a history of locking may be due to either the ACL or the meniscal injury.

On examination, the signs of a meniscal tear include: joint line tenderness (palpated with the knee flexed at 45-90') joint effusion- this is usually present, although absence of an effusion does not necessarily rule out meniscal damage pain-usually present with knee hyperflexion (such as squatting), especially with posterior horn tears restricted range of motion of the knee joint-this may be due to the torn meniscal flap or the effusion.

EJ

www These tests are demonstrated in the Clinical Sports Medicine masterclasses at www. cI in ica Is portsmed ici ne .com.

The flexion/rotation (McMurray's) test (Fig. J2.2p) is positive when pain is produced by the test, and a clunk is heard or felt that corresponds to the torn flap

being impinged in the joint. However, it is not neces· sary to have a positive McMurray's test (i.e. a clunk) to make a diagnosis of a torn meniscus. The hyper· flexion portion of the McMurray's test provokes pain in most meniscal injuries. Pain produced by flexion and external rotation is often indicative of medial meniscal damage, whereas pain on internal rotation indicates lateral meniscal pain. Asking patients where they feel pain during hyperflexion maneuvers gives a suggestion of the location of the tear-medial or lateral. MRI is the investigation of choice. This can aid management if the MRI shows either a complex tear (rather than minimal damage) or, more rarely, a peripheral meniscus tear. If meniscal tearing is minimal and stable without displacement, clinical progress remains the best measure of non·operative management. Peripheral meniscus tears, depending on the length of the tear, may be fixed surgically.

Treatment The management of meniscal tears varies depend· ing on the severity of the condition. At one end of the spectrum, a small tear or a degenerative menis· cus tear, presenting with pain but not with mechan· ical symptoms such as locking or range of motion (ROM) restriction, should initially be treated non· surgically.8 On the other hand, a large painful "bucket handle" tear causing a locked knee requires urgent arthroscopic surgery. The majority of meniscal inju· ries fall somewhere between these two extremes, and the decision on whether to proceed immediately to arthroscopy must be made on the basis of the sever· ity ofthe symptoms and signs, as well as the demands of the sportsperson.

f; 1:>

In the challenging situation where a patient has both early osteoarthritis and a meniscal tear, physical examination features and MRI together can help predict which patients might benefit from arthroscopic surgery.

The highest likelihood of benefi t from arthroscopic partial menisectomy is in patients with clinical find· ings of increasing pain (as distinct from stable pain) as well as locking, when these were complemented by MRI findings of a displaced meniscal tear but no marrow lesions. 9 Table 32.4 overleaf provides some clinical guid. ance for choosing either non·surgical or surgical treatment.

635

Table 32.4 Clinical features of meniscal injuries that may affect prognosis Factors that may indicate non-surgical treatment is

Factors that may indicate surgery will be

likely to be successful

required

Symptoms develop over 24-48 hours following the injury

Severe twisting injury, sportsperson is unable to continue

Minimal injury or no recall of specific injury Able to Minimal swelling

playing l ocked knee or severely restricted ROM Positive McMurray's test (palpable clunk)

Full range of movement with pain only at end of ROM

Pain on McMurray's test with minimal knee flexion

Pain on McMurray's test only in inner range of flexion Previous history of rapid recovery from similar injury

Presence of associated ACL tear

Early degenerative changes on plain radiographs

Little improvement of clinical features after three weeks of non-surgical treatment

ROM = range of motion

Non-surgical management of meniscal injuries Non-surgical management of relatively minor meniscal injuries is often successful, particularly in a person whose sport does not involve twisting activities. The principles of non-surgical management are the same as those following partial menisectomy (Table 32.5). although the rate of progress may vary depending on the clinical features. The criteria for return to sport following meniscal injury. treated surgically or non-surgically, are shown below. If appropriate rehabilitation principles have been followed. then the criteria will usually all be satisfied: absence of effusion

As the outer one-third of the meniscus rim has a blood supply, tears in this region can heal. The tear with the best chance of a successful repair is an acute longitudinal tear in the peripheral one-third of the meniscus in a young patient. JO Degenerative. flap. horizontal cleavages, and complex meniscal tears are poor candidates for repair.7 Young patients have a higher success rate of healing the meniscus. Peripheral meniscus tears in otherwise stable knees without concomitant ligament damage have a reduced success rate. Partial tears may require removal of the damaged flap of the meniscus. Patients with degenerative tears with no or minimal cartilage wear are less symptomatic than those patients with concomitant cartilage damage.

full range of movement normal quadriceps and hamstring function

Rehabilitation after meniscal surgery

normal hip external rotator function

Rehabilitation should always commence prior to surgery. and in some cases surgery can be avoided because "prehabilitation" leads to full recovery. For patients scheduled for surgery. it is important to:

good proprioception functional exercises performed without difficulty training performed without subsequent knee symptoms Simulated match situations undertaken without subsequent knee symptoms.

reduce pain and swelling with the use of electrotherapeutic modalities and gentle range of motion exercises maintain strength of the quadriceps, hamstrings,

Surgical management of meniscal injuries The aim of surgery is to preseIVe as much of the meniscus as possible. Some meniscallesions are suitable for repair by arthroscopic meniscal suture. The decision as to whether or not to attempt meniscal repair is based on several factors. Repair is favored if: the tear occurred recently (within weeks) the patient is younger the knee is stable the tear is peripheral.

636

and hip abductor and extensor muscles protect against further damage to the joint (patient may use crutches if necessary) explain the surgical procedure and the postoperative rehabilitation program to the patient.

The precise nature of the rehabilitation process depends on the exten t of the injury and the surgery performed (Table 32.5). Arthroscopic partial menisectomy is usually a straightforward procedure followed by a fairly rapid return to activity; some sports people

Table 32_5 Rehabi litation program for both non-surg ical management of meniscal injury and following arthroscopic partial menisectomy Functional/ sport-related Phase

Goal of phase

Time post injury

Physiotherapy

Exercise program

activity

Phase 1

Control swelling Maintain knee extension Knee flexion to 100°+ 4/5 quadriceps strength 4+/5 hamstring strength

0-1 week

Cryotherapy Electrotherapy Compression Manual therapy Gait re-education Patient education

Gentle ROM (extension and nexion) QuadricepsNMO setting Supported (bilateral) calf raises Hip abduction and extension Hamstring pulleys/rubbers Gait re-education drills

Progress to FWB and normal gait pattern

light exercise bike Phase 2

Eliminate swelling

1- 2 weeks

Full ROM

4+15 quadriceps strength SIS hamstring strength

Phase 3

Full ROM

'"w "

Full strength, ROM. and endurance of affected limb Return to sport-specific d rills and restricted training and match play

ROM drills QuadricepsNMO setting Mini-squats and -lunges leg press (double, then sing le leg) Step-ups Bridges (double-, then single-leg) Hip abduction and extension with rubber t ubing Single-l eg calf raises Galt re-education drills Balance and proprioceptive drills (sing le leg)

Swi mming (light kick) Exercise bike

Walking

l>

2-3 weeks

Manual therapy Exercise/activity modification and supervision

As above-increase difficulty, repetitions and weight where appropriate Jump and land drills Agility drills

Running Swimming Road bike Sport-specific exercises (progressively sequenced) (e.g. running forwards, sid eways, backwards, sprinting, jumping, hopping. changing direction, kicking)

3-5 weeks

As above

High-level sport-specific strengthening as required

Retu rn to sport-specific drills, restricted training and match play

Full strength Full sq uat Dynamic proprioceptive training Return to running and restricted sport-specific drills

Phase 4

Cryotherapy Electrotherapy Compression Manual therapy Gait re-education Exercise modification and supervision

FWB = full weight-bearing; ROM = range of motio n; VMO = vastus medialis obliquus

"c

."

with a small isolated medial meniscal tear are ready to return to sport after four weeks of rehabilitation. \' RA

'orr,

l /i -V-;

The rehab ilitation process usually takes longer if there has been a more comp licated tear of the meniscus, especia ll y if the latera l men iscus is inju red.

The presence of associated abnormalities (such as articular cartilage damage or MCL or ACL tears) also slows down the rehabilitation process. If the sportsperson returns to play before the knee is properly rehabilitated, he or she may not experience difficulty during the first competition, but may be prone to develop recurrent effusions and persistent pain. 'i' RIl

_

Ie.

'orr,

11:J'f-;

Asuccessful return to sport after meniscal knee surgery should not be measured by the time to play the first match but, rather, the time to play the second!

Close monitoring is essential during postmenisectomy rehabilitation, while the remaining meniscus and underlying articular cartilage slowly increase their tolerance to load-bearing activities. Constant reassessment after progressively more difficult activities should be performed by the therapist monitoring the rehabilitation program. The development of increased pain or swelling should result in the program being slowed or revised accordingly.

Me dial collate ral lig a m e nt (MCL) injury Injury to the MCL usually occurs as a result of a valgus stress to the partially flexed knee. This can occur in a non·contact mechanism such as downhill skiing, or in contact sports when an opponent falls across the knee from lateral to medial. MCL tears are classified on the basis of their severity into grade I (mild, first degree), grade II (moderate partial ruptures, second degree) or grade III (complete tears, third degree). In patients with a grade I MCL sprain, there is local tenderness over the MCL on the medial femoral condyle or medial tibial plateau but usually no swelling. When a valgus stress is applied at 30" of flexion, there is pain but no laxity (Fig. 32.2f on page 630). Ligament integrity is intact. A grade II MCL sprain is produced by a more severe valgus stress. Examination shows marked tenderness, sometimes with localized swelling. A valgus stress applied at 30° of knee flexion causes pain. Some laxity (typically

In summary, both surgical and non ·surgical treatment improve self'reported knee fu nction after ACl injury. There exists no scientific evidence to support supe ri ority of one treatment over the other.

Two years after injury, ACL-injured patients report worse outcomes than an age-matched communitybased sample, which indicates that none ofthe current treatment options succeed in restoring full knee function from the patients' perspective.

Return to sport One of the major aims of treatment of ACL injury is to restore the knee and to get the sportsperson back in pre-injury activity. This is also the main argument for surgical treatment. Reports of rehtrn to sports foI· lowing ACL injury do not use a consistent definition and thus results should be interpreted with some caution. One frequent source of misinterpretation is that the definition of return to pre-injury activity is vague and includes one, and sometimes two, levels below the actual pre-injury activity level on a 10 graded scale. Following ACL reconstruction, there is a large variation in reports on the rate of return to sport, with variations from 65% to 88% being able to return to sport within the first year.5,-\G In a metaanalysis of 392 patients, 72% (n=28r) had returned to their pre-injury activity level hvo years after ACL reconstruction. 57 A recent report on national elite soccer players showed a rate of return to sport of 94% after ACL reconstruction. 18 The authors speculate that one of the main contributing factors might be the extraordinary care and rehabilitation provided by the team physiotherapists in these professional soccer clubs. In contrast, another recent publication showed that only 63% of National Football League (NFL) sportspeople returned to NFL game play at an average of 10.8 months after ACL surgery.>9 A success rate around 70% is not excellent for a surgical treatment option, but it should be noted that some of these sportspeople do not return to sports for reasons other than knee problems. The proportion of such individuals is, however, not well described. Among patients treated non-operatively, the rate of return to sports varies even more widely than among those treated surgically. Scientific reports suggest a range from 19% to 82% for return to preinjury activity." 60

658

TIlliS, there is no firm data to support that return to pre-injury sport is more likely after ACL reconstruction than after non-surgical treatment. However, individuals active on a professional or sub-professional level often lack the possibility to wait and see, and thus most undergo surgery. Sportspeople who successfully return to sport after non-operative treatment could represent a group gaining functionally stable knees without a fully restored stability at rest. Factors associated with success after non-surgical treatment need to be better explored. There is some evidence that those rehtrning to sports after ACL injury may stop playing earlier than their non-injured counterparts. 6 ,- 6, In the only study in which the reduction in sport participation can be related to a control group, Roos et al. Ga

found that only 30% of those who had ACL injury were active after three years compared with 80% of controls, and that after seven years none of the elite injured players were active regardless of the type of treatment. In addition, previously injured sports people retire at a higher rate than sportspeople without previous ACL injury.' The reason for this may be that many of the sportspeople who return to sport experience significant knee problems such as instability. reduced range of motion, and/or pain.

Re-injury rate In most studies, among those treated with ACL reconstruction, the incidence of graft failure is generally of the order of 3- 6%.64. 6S There is some evidence from a meta-analysis that the failure rate may be lower in patellar tendon autografts,GG although another systematic review failed to show a difference,lo There is an increased risk of rupture of the contralateral ACL in patients who have already had an ACL injury. This may be particularly true for females. Ci7

7&'0

Data from Dr Anthony Beutler's JUMp·ACL study indicate that, for military cadets who suffer an ACL rupture, the risl{ of ACL rupture in the ipsilateral (operated) or contra lateral knee may be as high as 5- 10 times that of an uninjured control

Data from non-surgically treated individuals are lacking, but "giving way" is likely to occur with a higher frequency than graft ruptures. A "give way' episode might produce a trauma similar to the original trauma and thus cause additional meniscus damage, cartilage

Ac ute knee i n j uries

lesions, and collateral Iigamentinjury. The importance of such re-injuries needs to be investigated. Following ACL injury, there may also be an increased risk of other knee injuries (e.g. menisca1. articular cartilage injury) due to the nature of the sporting activity. Re-injury appears to be most likely in the first 12 months after surgery)O

Osteoarthritis ACL rupture is associated with a significant risk of the development of osteoarthritis, with reports suggesting a frequency of osteoarthritis in 20--50% of individuals 10-IS years after injury.IlIl,69 Although it was recognized that ACL injuries treated non-operatively were associated with an increased risk of osteo· arthritis, it had been hoped that ACL reconstruction. by restoring knee anatomy and reducing instability, would eliminate, or substantially reduce, the incidence of osteoarthritis. At this time, however. there is no evidence that ligament reconstruction prevents the future development of osteoarthritis. 62. Long-term follow-up studies of patients who have undergone ACL reconstruction with more modern techniques have shown that nearly all patients develop radiological signs of osteoarthritis after 15-20 years. 52. 511. 7) Many of these patients are, however. asymptomatic. The mechanisms driving osteoarthritis development are not well unders tood. but the traumatic impact suffered by the subchondral bone. the cartilage, and the meniscus has been suggested as a potential initiator of the di sease';·1The extent of the traumatic impact can be visualized by MRI where post-traumatic bone marrow lesions (BML)- a footprint of the injury mechanism-occur with practic· ally all ACL tears.4 BML are strongly associated with articular cartilage damage, chondrocyte apoptosis, and osteocyte death. 5 Meniscal injury is found in 75% of cases of ACL tears and these injuries are also suggested to predispose the development of osteoarthritis.75 A related, important sports medicine question is. "Does returning to active sport increase the likelihood of developing osteoarthritis, or does it bring this even t on more quickly?" No studies have evaluated this phenomenon, but it is reasonable to assume that intense weight-bearing activity involvin g pivoti ng would accelerate the degenerative process, compared with someone who remains sedentary or takes up a non-weight-bearing sport (e.g. cycling, swimming).

We and others'·.,u propose that sports people who have undergone an ACL reconstruction should receive advice about the likelihood of developing osteoarthritis, and the possibility tha t returning to active sports participation will accelerate its development. Many professional and dedicated sportspeople may decide to continue thei r sport in spite of that advice, but it is the du ty of health professionals to enable them to make an informed decision.

Gender difference Because of the increased prevalence of ACL injuries in female athletes. researchers have studied the possible differences in outcome after ACL reconstruction between males and females. The majority of studies show increased postsurgical laxity in females. but previous studies reported no difference in graft failure. activity level, Of subjective or functional n-8,

However, a recent study of several thousand patients from the Swedish ACLregistry who had been treated with ACL reconstruction showed significant gender differences in the self-reported outcome one and two years after surgery.5 The authors reported that female patients showed worse outcomes than male patients before surgery, and at one and two years after ACL reconstruction, and the authors suggested that possible sex differences should be analyzed in future studies on evaluation after ACL injury/reconstruction. Thus it is possible that previous reports were underpowered and that a clinically important gender difference might exist. 1

Mechanism of ACL injury as a step toward prevention As 60-80% of ACL injuries occur in non-contact situations, it seems likely that the appropriate prevention efforts are warranted. Tn ball sports, two common mechanisms cause ACL tears: a cutting maneuver8 2-84 one-leg landing.

Cutting or sidestep maneuvers are associated with drama tic increases in the varus-valgus and internal rotation moments, as well as deceleration. The typical ACLinjuryoccurs with the knee externally rotated and in 10-3 0° of flexion when the knee is placed in a valgus position as the sports person takes off from the planted foot and internally rotates their upper body with the aim of suddenly changing direction (Fig. 32.1Ia overleaf).I!'j·1I6 The ground reaction

659

force falls medial to the knee joint during a cutting maneuver and this added force may tax an already tensioned ACL and lead to failure. Similarly. in the landing injuries the knee is close to full extension. High-speed activities such as cutting or landing maneuvers require eccentric muscle action of the quadriceps to resist further flexion. It is hypothesized that vigorous eccentric quadriceps muscle action may playa role in disruption of the ACL. Although this normally may be insufficient to tear the ACL, it may be that the addition of a valgus knee position and/or rotation could trigger an ACL rupture. One question that is often asked is why the ACL tears in situations and maneuvers that the sportsperson has performed many times in the past. Frequently, there is some external factor that renders the person susceptible. The sports person could be off balance, be pushed or held by an opponent, be trying to avoid collision with an opponent, or have adopted an unusually wide foot position. These perturbations may contribute to the injury by causing the sportsperson to plant the foot so as to promote unfavorable lower extremity alignment; this may be compounded by inadequate muscle protection and poor neuromuscular controI.1I6 Fatigue and loss of concentration may also be relevant factors. What has become recognized is that unfavorable body movements in landing and pivoting can occur, leading to what has become known as the "functional valgus" or "dynamic valgus" knee-a pattern of knee collapse where the knee falls medial to the hip and foot. This has been called by Ireland the "position of no return," but perhaps it should be termed the "injury-prone position" since there is no proof that one cannot recover from this position (Fig. 32.nb).Hj Intervention programs aimed at reducing the risk of ACL injury are based on training safer neuromuscular patterns in simple maneuvers such as cutting and jump-landing activities. The mechanism of ACL injury in skiing is different from that in jumping, running, and cutting sports such as football and basketball. In skiing, most ACL injuries result from internal rotation of the tibia with the knee flexed greater than 90", a position that occurs when a skier who is falling backwards catches Intervention the inside edge of the tail of the programs in skiing are aimed at increasing the skier's awareness of patterns that are injurious to the knee, and giving alternative strategies in the hope of avoiding these patterns altogether. 660

Figure 32.1 1 Abnormal pOSitions that may lead to ACL injury {al The typical pOSition during the cutting maneuver which leads to ACL injury

Why do females tear their ACLs at three times the rate of males The rate of non-contact ACL injury among female sportspeople is considerably higher (x2-8) than that in males at comparable risk (exposure) and in comparable activities. At present, four main areas are being investigated to explain this discrepancy: 1. anatomical 2. hormonal 3. shoe- surface interface 4. neuromuscular. Anatomical differences

A number of anatomical differences between women and men have been proposed as contributing factors to the greater rupture rates of ACLs in females. These differences in females include: smaller size and different shape of the intercondylar notch 69. 90 smaller ACL within the smaller notch 9t . n wider pelvis and greater Q angle greater ligament laxity,93

mu scles

involved

Position of safety

back

bod y positio n norma l lordosis

body position

Point of"no return"

muscles

involved

forward flexed,

rotated opposite side

hips

extensors

flexed

abductors

neulrdl abduction a dduction, neutral rOlation

gluteals

knee

flexors hamstring

tibial rotation

plantar flexors

landing pattern

gastrocnemi us posterior tibialis

fle xed

neutral

both feet in contro l

balanced

adduct ion inte rna l ro tation

less flexed, valg us

flexors adductors iliopsoas

extensors

quadriceps

internal or external

one foo t out of contro l

unbalanced

pe ro neals tibia lis ante rior

(b) The pOSitions of safety and oruno return"

Although anatomi cal differences may playa role in ACL injury risk, since there is litt1e that one can change in one's anatomy, focus has turned to that which may be able to be chan ged. Hormonal differences

Females have a unique hormonal cycle, and estrogen has long been implicated as a risk factor in the higher ACL injury rates in fema les. Estrogen receptors can be detected in the human AC L;94 relaxin receptors are found on female but not male ACLs.91 Research examining a possible relationship between phase of the menstrual cycle and ACL injury has shown conHitting results.9:" 0.3 in.) of posterior translation is indicative of a pe l tear. MRI has a high predictive accuracy in the diag· nosis of the acute pel injury. 'l' but a lesser accuracy in chronic injuries. If an injury to the pos terolateral corner is suspected. MRI can be helpful; however. to view this region properly a specific imaging protocol is usually required. When the MRI requisition states that injury to the posterolateral corner is suspected, the radiologist can optimize the imaging protocoL Treatment peL ruphlre can generally be managed non-surgically with a comprehensive rehabilitation program. A suggested program emphas izing intensive quadriceps exercises is shown in Table 32.10 overleaf. More severe in juries (grade III) should be immobilized in extension for the first two weeks.

Results show that patients with isolated PCl tears have a good functional result despite ongoing laxity, after an appropriate rehabilita tion program. Regardless of the amou nt oflaxity. half ofthe patien ts in one large shldy returned to sport at the same or higher level. one- third at a lower level. and one-sixth did not return to the same sport.'\! Surgical reconstruction is indicated when the pel in jury occurs in combina tion wi th other posterolateral struchlres or where significant rotatory instability is present.

latera] collateral ligament (lCl) tears LCL tears are much less common than Mel tears. They are usually due to a severe, high-energy. direct varus stress on the knee and are graded in a similar fashion to Me l sprains. Differential diagnosis may be an avulsion of the biceps femoris tendon. Clinicians should be awa re tha t local tenderness on the posterolateral corner of the knee may also occur with AC l tears. Complete tears of the LeL are usually associated with other instabilities (such as pel ruphlre), and may result in posterolateral rotatory instability of the knee. These tears are best treated by acute surgical repair in conjunction with repair of other damaged ligaments. late or delayed reconstruction of the lel is difficult and results are poor. A varus knee with lateral and/or posterolateral instability is associated with worse results. An osteotomy is necessary fo r surgical treatment of this ligament injury, wi th or without a reconstruction of the li gament itself.

Articu]ar cartilage damage Since the introduction of arthroscopy and MR I, considera ble insight has been gained in to the role of articular cartilage (chondral) damage as a cause of symptoms and signs in the knee join t. Articular cartilage damage may occur as an isolated condition in which chondral or subchondral damage is the primary pathology, or in association with other inj uries, such as ligamentous instability resulting from a MCl. ACl, or peL injury, or patellar dislocations. Articular car tilage damage may also be seen in association with meniscal injury and patenar dislocation.

Classification Chondral injury is gradedaccording to the Outerbridge classification and more recently the International Cartilage Repair Society (ICRS) grading system

669

a-

"a

Table 32.10 Rehabilitation of a pel tear (see Figs 32.5 and 32.6)

Ph ase Phase 1

Goal of phase

Time post injury

PWB-FWB

0-2 weeks

Eliminate swelling

0- 100° ROM 4+15 quadriceps strength 515 hamstring strength Phase 2

No swelling

Physiotherapy treatment

Exercise program

Cryotherapy Electrotherapy

Gentle flexion ROM Extension ROM to 00 QuadricepsNMO setting Supported (bilateral) calf raises Hip abduction and extension Hamstring pu lleys/rubbers Gait drills

Nil

ROM drills QuadricepsNMO setting Mini-squats and -lunges

Walking

Compression

Manual therapy Gait re-education Patient education 2-4 weeks

Full ROM

4+/5 quadriceps strength 5/5 hamstring strength

Cryotherapy Electrotherapy Compression Manual therapy Gait Exercise modification

activity

Exercise bike

Leg press then single-leg) Step-ups Bridges then si ngle-leg) Hip abduction and extension with rubber tubing Single-leg cal f raises Gait re-education drills Balance and proprioceptive drills (singleleg)

Phase 3

Full ROM Full strength and power Return to jogging, running, and agility Return to restricted sport-specific drills

4-6 weeks

Manual therapy Exercise/activity modincation and supervision

As above-increase difficulty, repetitions, and weight where appropriate Jump and land drills Agility drills

Phase4

Return to sport

6-10 weeks

As above

High-level required

FWB = full weight-bearing; PWB = partial weight-bearing; ROM

=range of motion; VMO =vastus medialis obliquus

strengthening as

Straight line jogging Swimming (light kick) Road bike Straight line running Progressing to running and agility (progressively sequenced) (e.g. running forwards. sideways, backwards. sprinting, jumping, hopping, changing directions. kicking) Progressive return to sport (e,g. restricted training, unrestricted training, match play, competitive match play)

Acu t e knee i njuries (Tables 32.1I and p.I2). Articular cartilage damage varies from gross, macroscopically evident defects in which the underlying bone is exposed (grade IV). to microscopic damage that appears normal on arthroscopy but is soft when probed (grade I). Articular cartilage damage in the knee has both short-term and long-term effects. In the short term, it causes recu rrent pain and swelHng. In the longer term, it accelerates the development of osteoarthritis.

Treatment Various methods have been used to encourage healing of articular cartilage defects.'}}

Microfracture (bone marrow stimulation) Microfracture (less commonly known as bone marrow stimulation) is the most frequently used technique for treating small symptomatic lesions of the articular cartilage in the knee. '14 The procedures are technically straightforward. and the costs are low compared with those of other treatment modalities. Microfracture involves perforation of the subchondral plate to recruit m esendtymal stem cells from the bone marrow space into the lesion. TIle mesenchymal stem cells are able to differentiate into fibrochondrocytes, which contribute to fibrocartilage repair of the lesion. However, the overall concentration of the mesenchymal stem cells is quite low and declines with age. The formation of a stable blood clot that m aximally fills the chondral Ta b le 32 .11 Outerbridge classification of chondral defects

1. Softening 2. 1 cm (>0.4 in.) defect, deeper 4. Subchondral bone exposed Table 32.1 2 International Carti lage Repair Society (lCRS) classification

of chondral defects

1. Superficiallesions

A. Soft indentation B. Superficial fissures or cracks

2. lesions 50% depth B. Down to calcified layer

C. Down to but not through subchondral bone D. Blisters 4. Very abnormal into subchondral bone

defect is importan t, and it has been correlated with the success of bone marrow stimulation procedures. Reparative fib rocartilage consists of type- I, type-II. and type-I ll collagen in varying amounts. The fibrocartilage does not resemble the surrounding hyaline cartilage and has less type-II collagen. The postoperative regimen after micro fracture is demanding and has been reported to be a critical aspect of the ultimate efficacy. I II Patients with a femoral condyl:lf lesion are initially treated with continuous passive motion with a a" to 60 e range of motion for six weeks postoperatively. The patient typically remains non-weight-bearing with the use of crutches for six weeks. Patients who have undergone microfracture of a patellar or trochlear defect are allowed to bear weight as tolerated postoperatively, but knee motion is restricted by a brace allowing movement from oOto 40°. Continuous passive motion is initiated immediately and used, within this arc of motion, for approxi mately six to eight hours daily. At two mon ths, unrestricted motion is typically allowed and closed chain exercises are initiated. Short·arc closed chain concentric and eccentric muscle strengthening is effective and protects the patellofemoral articulation. Typically, a return to full activities is permitted at three months after a full, painless range of motion is achieved There are various adjuncts to improve the stability of the clot. These include various growth factors as weII as hyaluronic acid viscosupplementation.

Platelet-rich plasma TIlere has been a remarkable increase in the use of platelet-rich plasm a to facilitate healing in a variety of pathological musculoskeletal conditions. The theoretical advantage of this autologous blood product rests in the concentrated platelets and associa ted quantity of platelet-derived growth factor and other mi togenic factors that m ay promote the healing of chondral injuries. Despite these encouraging preliminary results, however, to our knowledge, no clin ical studies have proven the efficacy of platelet-rich plasma injection for focal chondral inju ries of the knee.

Autologous osteochondral transplantation Autologous osteochondral mosaicplas ty, sometimes referred to as "OATS" (osteoarticular transfer system), is an effective method for resurfacing osteochondral defects of the knee. I Il The technique 67 1

involves transplantation of multiple small cylindrical autogenous osteochondral plugs harvested from the less weight-bearing periphery of the articular surface of the femoral condyle; these are transferred to create a congruent and durable resurfaced area in the defect. The procedure offers several advantages over other repair techniques, including transplantation of viable hyaline cartilage, a relatively brief rehabilitation period, and the ability to perform the procedure in a single operation. The limitations of autologous osteochondral mosaicplasty include donor site morbidity, and a limited availability of graft that can be harvested from the patellofemoral joint or the zone adjacent to the intercondylar notch. The outcomes of autologous mosaicplasty for symptomatic chondral defects have been encouraging, and the procedure has been used with success. IJ6

Osteochondral allograft transplantation Osteochondral allograft transplantation is a cartilage resurfacing procedure that involves transplantation of a cadaver graft consisting of intact, viable articular cartilage and its underlying subchondral bone into the defect. The size, depth, and location of the defect are all critical factors in the tailoring of the donor graft. Advantages to the use of osteochondral allografts include the ability to achieve precise surface architecture, immediate transplantation of viable hyaline cartilage as a single-stage procedure, the potential to replace large defects or even hemicondyles, and no donor site morbidity. Use of a large dowel osteochondral transplant in this capacity eliminates the dead space that is encountered between the smaller cylindrical grafts that are used with autologous mosaicplasty. Limitations of osteochondral allografting include limited graft availability, high cost, risk of immunological rejection, possible incomplete graft incorporation, potential for disease transmission, and the technically demanding aspects of machining and sizing the allograft.

logous chondrocyte implantation is the development of hyaline-like cartilage rather than fibrocartilage in the defect, presumably leading to better longterm outcomes and longevity of the healing tissue. However, the procedure is not without limitations. Autologous chondrocyte implantation involves a minimum of two operations, one for tissue harvest and the other for cell implantation. Furthermore, autologous chondrocyte implantation is technically demanding, and complications related to the perio· steal graft have been reported.

Cell-based and scaffold treatment Although cell-based therapies for inducing cartilage regeneration, such as autologous chondrocyte implantation,havedemonstrated progress, the results have not been highly predictable or reproducible. In addition, limitations have included a requirement for a two-stage procedure and a technically demanding operation that fails to provide structural support for cells during the postoperative healing and incorporation phase. So-called second-generation techniques in which harvested autologous chondrocytes are delivered on absorbable scaffolds that support the cells during the preimplantation culturing and postoperative healing phases have evolved. Essential properties of these scaffolds include biocompatibility and biodegradability through safe biomechanical pathways at suitable time intervals. In the matrix-associated chondrocyte implantation procedure. chondrocytes are incorporated into a porcine type-IJIII collagen membrane. One surface has a relatively higher density of collagen fibers that creates a smooth low-friction surface, while the other has a rough appearance because oflarger interstices between the collagen fibers to allow for seeding of chondrocytes. Hyaluronan-based scaffolds deliver the autologous chondrocytes in a scaffold of hyaluronan derivatives. Advantages of these procedures over autologous chondrocyte implantation include a more even cell distribution, avoidance of periosteal harvest and implantation, and increased technical ease without the need for suturing to adjacent articular cartilage. Il7

Autologous chondrocyte implantation Autologous chondrocyte implantation, originally described in 1994, is an innovative, novel technique to restore cartilage cells into full-thickness chondral defects. The primary theoretical advantage of auto672

Tissue-engineered collagen matrices seeded with autologous chondrocytes Tissue-engineered collagen matrices seeded with autologous chondrocytes provide a promising new

technology with which to address chondral lesions of the knee.'ll This procedure involves harvesting of the autologous chondrocytes from non-weight·bearing aspects of the knee in a manner analogous to conventional autologous chondrocyte implantation. The cells are then loaded onto a type-I bovine collagen honeycomb matrix and are cultured ex vivo. In distinction to second-generation techniques, however, the cell-scaffold construct is subsequently subjected to mechanical stimulation with the use of a proprietary bioreactor that applies hydrostatic pressure to the chondrocytes for a minimum of seven days. A lack of mechanical stimulation may be responsible for chondrocyte dedifferentiation and inferior mechanical properties, and the application of a mechanical load stimulates chondrocytes to produce increased amounts of type-I I collagen. aggrecan, and other critical components of a hyaline extracellular matrix.

Summary of treatments for articular cartilage defects There is currently considerable debate as to the efficacy of the various treatments and as yet no consensus on optimal treatment has been reached.' ll There is a lack of high-quality studies (Table )2.I)). Tabl e 32.13 Grades of recommendation for cartilage repair procedures Gradelo 728

Medial collateral ligament grade I sprain A grade I medial collateral ligament sprain or bursitis often presents without a history of any major trauma. The medial collateral ligament can also become inflamed as a result of activities that put a constant valgus strain on the knee, such as swimming breaststroke. This condition is commonly referred to as "breaststroker's knee" and is actually a first-degree sprain of the medial collateral ligament, or inflammation of the medial collateral ligament bursa due to excessive stress.

Posterior knee pain Accurate and specific diagnosis of pain about the posterior knee (Fig. 34.12) may be difficult. Posterior knee pain is a common site of referred pain from the lumbar spine and from the patellofemoral joint. Alternatively, local structures (e.g. popliteus, biceps femoris tendon) may cause posterior knee pain. A knee effusion is a common cause of pain and tightness of the back of the knee. The causes of posterior knee pain are shown in Table 3+ 3-

Clinical evaluation History Posterior knee pain precipitated by acceleration or deceleration (e.g. downhill running, kicking, sprinting) is likely to be biceps femoris or popliteus tendinopathy. Pain described as a poorly localized dull ache not directly related to activity suggests it may be referred. The presence of low back pain or patellofemoral symptoms provides a diagnostic clue. A previous acute knee injury may have caused an effusion with the development of a Baker's cyst.

Examination In the examination ofthe posterior aspect of the knee, it is important to differentiate between local and referred causes of pain. The slump test (Fig. 3+2i) may indicate whether the pain is referred from the lumbar spine or neural structures. It is also important to detect the presence of an effusion, as this may be the cause of the posterior knee pain. 1 . Observation (a) standing (Fig. 34.13a overleaf) (b) prone 2. Active movements (a) flexion (b) extension (c) tibial rotation

Lat er al, m ed i al , a n d p os t e ri o r k n ee p a in

(b ) An atomy ADAPTED FROM THE CJBA COLLECTION OF MEDICAL

Figure 34.12 Posterior aspect of the knee

IlLUSTRAnONS. REPRODUCED BY COURTESY OF OBA·GEIGY LIMITED,

(a) Surface anatomy

BASEL, SWITZERLANO. ALL RIGHTS RESERVED

Tab le 34.3 Causes of posterior knee pain Common

Less common

Not to be missed

Knee joint effusion

Popliteus tendinopathy Baker's cyst

Claudication

Gastrocnemius tendinopathy

Posterio r crudate ligament sprain

Referred pain lumbar spine

Deep venous thrombosis

Patellofemoral joint Neural mechanosensjtivity

Biceps femoris tendinopathy

3. Passive movements

6. Special tests (a) knee effusion

(a)

flexion

(b)

extension (with adduction and abduction)

(b) examination of knee jOint (Chapter 32)

(c)

tibial rotatio n

(e)

(d)

m uscle stretch-ha mstrings

4. Resisted movements (a)

knee flexion

(b)

knee flexion in externa l t ibial rota tion (Fig. 34.13b overlea f )

(e)

external tibial rotation (Fig. 34.13c overleaf)

5. Palpation (Fig. 34.13d overleaf) (a)

hamstring tendons

(b)

popliteus

(c)

joint line

(d)

gastrocnemius origin

neurodynamie test-sl ump test (Fig. 34.2i on page 71B)

(d)

eXamination of lumbar spine (Chapter 26)

(e)

biomechanical examination (Chapter 8)

(f)

squat

Investigations Investigations may not always add to the clinical diagnosis for posterior knee pain in a sports person, and may not be appropriate. However. ul trasound may be used to confirm the presence of a Baker's cyst and to identify a tendinopathy. MRI or arthroscopy are the investigations of choice if the initial diagnosis does not respond to treatment. 729

(c) Resisted movement-popliteus. With the patient supine, hips and knees flexed to 90 0 and the leg internally rotated, the patient is asked to "hold it there" while the examiner applies an external rotation force

Figure 34.13 Examination of patient with posterior knee pain (a) Observation-standing. Obvious swelling or fullness of the posterior aspect of the knee joint suggests a Baker's cyst. Inspection may reveal a biomechanical abnormality

(b) Resisted movements-knee flexion in external tibial rotation. Resisted contraction of the popliteus tendon

Popliteus tendinopathy The popliteus muscle arises from the posteromedial border of the proximal tibial metaphysis and travels proximally beneath the lateral head of

730

(d) Palpation. This should be performed with the knee in flexion. Tenderness can be elicited over the hamstring tendons (shown), gastrocnemius origin, or popliteus. It is helpful for the patient to gently contract and relax individual muscles that are being palpated in order for the examiner to precisely pinpoint the site of pain

the gastrocnemius to insert onto the lateral femoral condyle. It also has attachments to the fibula and the posterior horn of the lateral meniscus. The popliteus tendon limits external and internal rotation. knee varus stresses, and anterior translation of the femur (acts with the quadriceps and posterior cruciate ligament).IT Additionally, the popliteus has a role in unlocking the knee during initial flexion from an extended position, and aids retraction of the posterior horn of the lateral meniscus to minimize compressive forces during knee flexion. With its role in knee stability, the popliteal tendon could be thought of as the fifth ligament of the knee,sl therefore should be assessed of tibial rotation during a routine knee stability assessment.

Lat e r a l, med i al, and posterio r k nee p ai n Pain associated with the popliteus region may arise from the popliteus muscle. its tendon, or the popliteus-arcuate ligament complex. Due to their close proximity, differentiation is difficult. Isolated popliteal muscle injuries are rare. Popliteal muscle injuries associated with lateral meni scus and posterior cruciate ligament injuries are more Posterior lateral instability is often associated with some degree of popliteal pathology. Twisting activities can res ult in popliteal injuries. Impingement of the popliteus tendon can occur with knee rotational instab ilities (e.g. following pos terior capsule-arcuate ligament strain), and overuse in jur. ies are often associated with repetitive or prolonged acceleration/deceleration activities (e.g. downhill running). Sportspeople typically present with posterior knee pain and may report some instability. The main clinical finding is tenderness on palpation along the proximal aspect of the tendon (Fig. J4.I Jd). With the athlete prone, palpation should begin near the posterolateral corner medial to the biceps tendon and then progress along the m edial joint line. Resisted knee flexion in external tibial rotation may reproduce the athlete's pain (Fig. J4.IJb). Garrick and Webb ll describe a test for the popliteus with the patient supine, hips and knees flexed to 90°, and the leg internally rotated. The patient is asked to "hold it there" while the examiner applies an external rota tion force (Fig. 34.I3c). It is important that the clinicia n assesses both active and passive tibial rotation. Excessive rotati on may be a result of repeated strain to the area. Knee flexion and extension range of motion at the end of range may be limited, and also may reproduce pain. Lower limb biomechanics should be assessed in terms of varus. valgus, and rotational forces around the knee. Soft tissue techniques and mobilization may improve any restriction of tibial rotation or knee flexion or extension. Rehabilitation should focus on strengthening of the tibia l rotators (Fig. 34-14) and hamstring muscles. Any weakness or fati gue in the quadriceps can add excessive strain on the popliteus and should be addressed (e. g. wi th an eccentric strengthening program). Patien ts who fa il to respond to initial treatment may benefit from corticosteroid injection posteriorly into the point of maximal tenderness, or into the popliteus itself guided by ultrasound.14. 55

Figure 34.14 Strengthening of the tibial rotato rs. This may be performed against manual resista nce (illustrated), with pulleys, rubber tubing resistance, or w ith isokinetic machines

Gastrocnemiu s tendinopathy The origin of the medial gastrocnemius at the posterior femoral condyle is occasionally susceptible to painful overuse injuries, especially in runners. This may result from excessive hill runnin g or a rapid increase in mileage. Examina tion may reveal local tenderness and associated trigger points in the medial gastrocnemius muscle belly. Pain may be reproduced on resisted knee flexion, calf raises with the knee in extension, jumping, and hopping. Occasionally. stretching the gastrocnemius muscle can reproduce the athlete's pain. Possible biomechanical factors should be assessed including muscle imbalances around the hip, knee and ankle. Knee stability, footwear, and foot function should also be assessed. Initial treatment may consist of activity modification, ice, electrotherapy, and local and generalized soft tissue therapy. A graduated stretching/strengthening program (Chapter J6) should be incorporated to ensure positive long-term results.

Baker's cyst A Baker's cyst (popliteal cyst) can be defined as "a synovial fluid filled mass located in the poplitea l fossa."I(' The mas s is often an enlarged bursa located beneath the medial gastrocnemius or semimembranosis muscles or both. It can be thought of as a chronic knee joint effusion (Fig. 34.15 overleaf) that herniates between the two heads of the gastrocnemius. In children, the mass is often isolated, asym p· tomatic, and resolves spontaneously. In adults, the mass almost always communicates with the knee joint and is secondary to intra-articular pathologyY' 731

Figure 34.15 Baker's cyst (arrowed)-knee joint effusion herniating posteriorly; usually secondary to degenerative or meniscal pathology

Intra-articular pathology includes meniscal tears (most common), ACL deficiencies, cartilage degeneration, and arthritis. The size of the mass may fluctuate. Observation of an athlete's knee in standing often reveals a palpable, swollen, tender mass over the posteromedial joint line. End-oFrange knee flexion may be restricted and painful. Deep squats and kneeling

732

may also produce posterior knee pain. Due to its high association with intra-articular pathologies, a full assessment of the knee is warranted. X-ray may be of little use in the assessment of Baker's cyst, but may rule out other pathologies (e.g. calcification, loose bodies). Ultrasound can visualize the cyst: however, it cannot assess intra-articular structures, which may be the underlying cause.l G MRI will both confirm the presence of the cyst and may identify the underlying intra-articular cause; it is considered the gold standard.s G. ,7Aspiration can differentiate between inflammatory, infectious, and mechanical etiologies. Occasionally the cyst may rupture, leading to lower leg swelling simulating venous thrombosis. A ruptured cyst usually displays a "crescent sigrt'an ecchymotic ("bruised") area around the malleoli. Initial treatment should involve addressing the underlying cause (e.g. meniscal tear). Aspiration together with steroid injection may be useful in the short term. IG. 5H Surgery may be indicated in symptomatic athletes presenting with a large, symptomatic mass. However, unless the underlying pathology is addressed, it is more than likely the mass will reform.

Other causes of posterior knee pain Deep venous thrombosis usually presents as calf pain (Chapter 36) but may occasionally present as posterior knee pain. It usually occurs after surgery or following a period of immobilization. Claudication can occasionally present as posterior knee pain. It can occur in young adults, not only in the older person. Popliteal artery entrapment syndrome usually presents as calf pain (Chapter 36).

I§I

RECOMME N D E D R E ADING

14. Zenz p. Huber M , Obenaus CH et a1. Leng thening of the iliotibial band by femoral detachment and multiple

Beals RK. The iliotibial tract: a review. CUrr Orlhop Pmc

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20°9;20(1):87-91. Ellis R, Hing W. Reid D. Iliotibial band friction syndrome-a systema tic review. Mlln The.r 2007;I2.{J):200-8. Fredericson M. WolfC.ll iotibial band syndrome in runners .

Sports Med 20°5;35(5):451-9-

m 1.

Beals RK. TIle iliotibial tract: a review. Cllrr Orthop Prac

Alii 2003;34(3):329-4° . 16. Willis RH. Meniscal injuries in children and

adolescents. Op Teel! Sports Med 2006;14(3): 197-202.

Fairclough

I.

J. Felson DT et aI. The role of knee

Hayashi K. Toumi H et al. Is iliotibial

decline in knee osteoarthritis. JAMA 2001;286(2): 188-95· 18. BJQuwer

eM. Ta l AWV. Bergink AP e t a l. Association

band syndrome really a friction syndrome? j Sci Med

between valgus and varus alignment and the

Sport 20°7;10(2):74- 6.

develo pment and progression of radiographic

3. Ellis R, Hing W, Reid D. Iliotibial band friction

syndrome-a systematic review. Man Ther 2oo7;IZ{ 3):2oo-8.

4. Falvey Ee, Clark RA, Franklyn-Miller A et al. Iliotibial band syndrome: an examination oflhl' evidence behind a n umber of treatmen t options. Scand J Med Sci Sports

5. Orchard J. Fricker PA. Abud AT e t al. Biomechanics of iliotibial band friction syndrome in runners. Am J

Sports Med 1996;24(3):375-9. 6. Noehren B. Davis 1. Hamill

J. Prospective study o r the

biomechanical factors associated with iliotibial band syndrome. Clill Biomecll 200T22(9):95I-6. 7. Frede ricson M. Cookingham CL, Chaudhari AM et al. Hip abducto r weakness in distance runners with iliotibial band syndrome. Clill J Sport M,d 2000;10:16 9-75. 8. FrederiC$on M, Wolfe. Iliotibial band syndrome in runners. Sports Med 2°°5;35 (5):451-9. 9. Messier SP. Edwards DG. Martin DF et a1. Etiology of iliotibial band frictio n syndrome in distance runners.

Med Sci Sports Exerc 1995;27(7):951- 6o. 10 . Nishimura G, Yamato M, Tarnai K et al. MR findings in iliotibial band syndrome. skeletu/ Rudiol

'997;26(91:533-7· Martens M, Librecht

osteoarthritis of the knee. Arth Rheum 2OO7;56(4): 1204-11 . 19. Altman RD. Moskowitz R. Intraarticular $odium hyaluronate (Hyalgan) in the treatment of patients with osteoarthritis of the knee: a randomized clinical trial.

J RheumatoI1998;Z5=2203- IZ. RJ . Bartha C. Home based exercise therapy fo r

20. Petrella

2 010:20:5 80-7.

JI.

Kocher MS, Klingele K, Rassman SO. Meniscal d isorders: normal. discoid, and cysts. Orthop elill Nortll

alignment in disease progression and functional

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17. Sharma L. Song

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r. Burssens A. Surgical treatment

older patients with knee osteoarthritis: a randomized clinical trial. J RhClIInatol 2000:27(9):22 IS- ZI. ZI. Squire MW. Callaghan

JJ, Goetz DD et a1.

Unkompartmental knee replacement. A minimum

IS year followup s tudy. eli» Orthop 1999;36,:61-72. 22. Merican AM. Amis AA. Anatomy of the la teral retinaculum of the knee. J Bone Joint Surg Br 2008: 9°.8(4):5 2 7- 34. 23. Shellock FG . Sto ne KR. ernes 'V. Develo pme nt and clinical application of kinematic MRI of the patellofemoral joint using an extremity MR sys tem.

Med Sci Sports Exert 1999;3I(S):788-9I. 24. Panni AS, Ta11arolle M. Patricola A et al. Long·term result$ oflatera l retinacular release. Arthroscopy 2005:2 1(5):526- 31. 25. Chance-Larse n K. lilliewood C, Garth A. Prone hi p extension with lower abdom inal hollowing improves the relative ti ming of glulcus maxim us activation in relation to biceps femoris. Mall TIler 2010;15(1):61- 5. 26. Longo UG. Garau G. Denaro V et al. Surgical

of the iliotibial band friction s yndrome. Am J Sports

management of tendinopathy of biceps femoris tendon

Med '989: TIle patient with medial tibial stress syndrome complains of diffuse pain along the medial border of the tibia (the junction of the lower third and upper two thirds of the tibia), which usually decreases with wa rming up. More focal pain should alert the examiner to the possibility of a true stress fracture. The sports person can often complete the training session but pain gradually recurs after exercise and is worse the following morning. Historically the tibialis posterior was thought to be the source of the pain, but more recently the soleus and flexor digitorum longus have been The incidence of medial tibial sb-ess syndrome has been reported to be between 4% and 35% in military personnel and

Risk factors number of factors may contribute to the increased stress and traction on the posterior medial aspect of the tibia. These include excessive pronation (fla t feet). training errors. shoe design, surface type, muscle dysfunction . fatigue. and decreased flexibility. Other risk factors that have been reported include

A

female gender, higher body mass index (BMI) , greater

(b ) Plain X-ray appearance of multiple "dreaded black lines"

Medial tibial stress syndrome As noted previously, there has been a tendency in the past to categorize all shin pain, especially that which is not a stress fractu re, under the term "shin splints."Z-! Indeed, shin splints is more of a vague symptom sportspeople describe for leg pain most

748

in ternal and external rotation of the hip, increased calf girth, and a history of previous stress fractures or use of orthotics. 2 C>, 29 TIle biomechanics of medial tibial stress syndrome relates to the sequence of even ts that occurs with walking and running}O During midstance, foo t pronation provides shock absorption and an accommodation to the varied terrain. The medial soleus is the strongest plantar flexor and invertor of the foot. The soleus muscle eccentrically contracts to resist pronation. Excessive pronation due to pes planus or overuse combined with repetitive impact loading leads to chronic traction over its insertion onto the periosteum on the posterior medial border

of the tibia, leading direc tly to medial tibial traction stress syndrome and medial tibial stress syndrome. Metabolic bone health may also contribute. Sportspeople with pain related to medial tibial stress syndrome were found to have lower bone mineral density at the affected region compared with control and athletic control subjects)' Bone mineral density was also decreased on the unaffected side in subjects with unilateral symptoms. These sportspeople regained normal bone mineral density after recovery from their symptomsY Reduced bone density or bone conditioning to stress may contribute to the increased risk of medial tibial stress syndrome seen in female miHtary recruits. A study examining possible risk factors for the development of medial shin pain in military recruits showed that females were three times as likely to develop the syndrome. u Beyond gender, no other risk factors of statistical significance were noted, but increased hip range of motion (both internal and external rotation), and lower lean calf girth were associated with medial shin pain in the male recruits.n Radiographs are routinely negative with medial tibial stress syndrome; however, with careful inspection some periosteal reaction can be seen in rare patients, and localized swelling can be seen in others. Isotopic bone scan may show patchy, diffuse areas of increased uptake along the medial border of the tibia as shown in Figure 35.5b. This is in contrast to stress fractures, which should show focal uptake. In early stages, however. the bone scan appearance may also be normal. MRI was found to have similar sensitivity and specificity to isotope bone scan.? Int erestingly there were a number of abnormal bone scan and MRI appearances in the asymptom atic control group in that study.7

Treatment Most sportspeople will present with a long his tory of complaints. having tried a number of home remedies, stretches, medicines, or cold treatment. Assessing previous treatments in terms of what provided relief and what exacerbated the problem is beneficial. While heat or whirlpool may improve flexibility and warm up the muscles, it also increases the circulation to the region, which can increase symptoms of inflammation. The fo undation of treatment is based on symptomatic relief, identification of risk factors, and treating the underlying pathology. Symptomatic treatment begins with rest, ice, and analgesia if needed.

Switching to pain-free cross-training activi ties (such as swimming or cycling) can keep the sportsperson active. Craig has suggested that no current method of treatment is better than rest alone; yet she still suggests that the use of shock-absorptive insoles is H In resistant cases, immobilization and protected weight-bearing may be necessary to rest the chronic tension placed on the soleus insertion with repeated weight-bearing. A critical facet of treatment is based on a careful assessment of foot alignment and gait mechanics. Taping techniques are only effective if they control foot pronation. Permanent relief can occasionally be achieved through appropriate shoe wear and the application of cushioned orthotics (for shock absorp. tion assistance) with a semi-rigid medial arch support (to support the pronated foot). We have found positive results in our patients, at least in the initial phase, by treating them with the same knee high pneumatic splint that we use for stress fractures (Air-Stirrup Leg Brace, Aircast, New Jersey, USA). Alternative modalities can be effective in relieving pain and should be considered. The entire calf muscle should be assessed for area s of tightness or focal thickening that can be treated with appropriate soft tissue techniques (Chapter 35). Digital ischemic pressure should be applied to the thickened muscle fibers of the soleus, flexor digitorum longus, and tibialis posterior adjacent to their bony attachment, avoiding the site of periosteal attachment, which may prove too painful (Fig. 35.8a overleaf). The effect may be enhanced by adding passive dorsiflexion and plantarftexion while digital ischemic pressure is applied. Transverse friction should be used on focal regions of muscle thickening in the soleus and flexor digitorum longus. Abnormalities of the tibialis posterior may be treated through the relaxed overlying muscles. Sustained myofascial tension can be applied paraHel to the tibial border, releasing the flexor digitorum longus , and along the soleus aponeurosis in the direction of normal stress with combined active ankle dorsiflexion (Fig. 35.8b overleaf) . Vacuum cupping techniques can be effective but it is important to remain clear of the tibial border to avoid causing capillary damage (Fig. 35.8c overleaf). Physical therapy programs have focused on motor strengthening and flexibility, especially proprioceptive neuromuscular facilitation (PNF) stretching. Electrical stimulation, iontophoresis, and ultrasound have been attempted with mixed results. Prolotherapy (injection with agents intended

749

Re g io nal pro b lems

Fig ure 35.8 Soft tissue therapy in the treatment of

inflammatory shin pain (a) Digital ischemic pressure to the medial soleus aponeurosis and flexor digitorum longus. This can be performed with passive and active dorsiflexion

(e) Vacuum cupping

the superficial and posterior compartments off their conjoined insertion onto the posteromedial border of the tibia can be performed with a projected success rate of 70% improvement in high-performance elite sportspeople.;q'lS

Chronic exertional compartment syndrom e

(b) Sustained myofascial tension along the soleus aponeurosis in the direction of normal stress combined with active ankle dorsiflexion

to accelerate the healing process), and platelet-rich plasma injections have also been performed but very little quality research is available to validate their efficacy. In resistant cases, surgical release (with or without periosteal tissue resection or ablation) of

750

Compartment syndrome is defined as increased pressure within a closed fibro-osseous space, causing reduced blood flow and reduced tissue perfusion, which subsequently lead to ischemic pain and possible permanent damage to the tissues of the compartment. l6 It may be acute, chronic (exertional), or convert from chronic to acute. Chronic exertional compartment syndrome (CECS) with stress fractures, and medial tibial stress syndrome are key components of the differential diagnosis of leg pain in sportspeople, especially in distance runners and those sportspeople in aerobic training. The syndrome is frequently bilateral. When the pain is in the calf, the clinician should also consider popliteal artery entrapment syndrome in the differential diagnosis (Chapter )6).

Leg pain

Pathogenesis Even though. classically, exertional compartment syndrome was felt to be an ischemic phenomenon like acute compartment syndrome, the exact etiology of chronic exertional compartment syndrome is stilI unclear. Repetitive overuse followed by asso· ciated inflammation may lead to fibrosis and therefore reduced elasticity of the fascia surrounding the muscle compartments. As a result, when the patient exercises, the muscles attempt to expand but are unable to do so. Biopsies have revealed abnormally thickened, non-compliant fascia. A series of biopsies at the fascial-periosteal interface revealed varying degrees of fibrocytic activity. chronic inflammatory cells, and vascular proliferation as well as a decrease in collagen irregularity, suggesting an attempt at remodeling. 1i As a result of this stiffened, abnormal fascial compartment, when the patient exercises, the muscle attempts to expand but is resisted by a less compliant fascia. 111is results in increased pressure, soft tissue ischemia, and, therefore, pain. Although ischemia is likely to playa role this has not been substantiated. It is probable that, within a tight fascial compartment, the normal consequence of metabolic activity during exercise would lead to an increase in pressure sufficient to compromise tissue perfusion at the capillary level. Birtles et al.J x induced similar symptoms to those of compartment syndrome by restricting venous flow during exercise. In a more recent biopsy study, Edmundsson et ai,9 noted that, when patients with chronic exertional compartment syndrome had muscle biopsies at the time of their fascial release, laboratory analysis revealed lower capillary density, lower number of capillaries around muscle fibers, and lower density of capillaries per muscle fiber area. Researchers concluded that the reduced microcirculation capacity was a likely contributor to the development of, or secondary to, the chronic exertional compartment syndrome. There is, however, conflicting evidence via nuclear magnetic resonance spectroscopy shtdies,4 0 MIBI perfusion imaging,4! and T2-weighed and arterial spin-labeling MRI shtdies. 4 !

Clinical features Typical clinical feahtres of chronic exertional comparhnent syndrome are the absence of pain at rest, and increasing achy pain and a sensation of tightness with exertion. Symptoms usually resolve or significantly dissipate within several minutes of rest.

Rarely, sportspeople develop paresthesias or motor weakness with exertion. At rest, physical examination is usually unremarkable. When the patient aims to reproduce the symptoms with exertion, the examiner may be able to palpate the increased tension in the compartment. There may be a muscle bulge or small herniation. The most common compartment involved is the anterior compartment, presenting with anterolateral pain with exertion. The other two common compartments are the lateral compartment, which may present with paresthesias in the distribution of the superficial peroneal nerve to the dorsum of the foot, and the deep posterior compartment, usually associated with posteromedial tibial pain. Involvement of the superficial posterior compartment is quite rare.

Investigations Investigations and screening should always include an assessment of limb and foot alignment, evaluation of the biomechanical demands of the specific sport including court surface and shoe-wear, a history of previous injuries or trauma, and a screen for overlapping pathology such as stress fractures, medial tibial stress syndrome, and metabolic and nutritional factors. In one study, diabetes mellitus was implicated as a risk factor for developing chronic exertional compartment Radiographs are frequently obtained as an inexpensive screening tool for associated bone pathology. The definitive diagnosis is made on the basis of intracompartmental pressure measurements (Table 35.3). The use of near-infrared spectroscopy has shown promise as a non-invasive alternative but it is expensive and has not yet become commonly used. 7 In a comparison shtdy using near-infrared spectroscopy compared with MRI and intracompartmental pressure measurements, van den Brand 7 argued that the sensitivity of near-infrared spectroscopy (85%) was superior to both MRI and intracompartmental pressure measurements (both 77%). More recently, Williams et aI. and associates have suggested that nonpainful neurosensory testing can be performed using a Pressure Specified Sensory Device pre- and post-exertion; this can guide the clinician regarding the presence of chronic exertional compartment syndrome or the efficacy of previous release. 4l Other investigators have looked more deeply into advanced imaging techniques including TC-99m tetrofosmin single photon emission 751

CT, and a novel dual birdcage coil and in-scanner MRI protocol to assist with making a diagnosis using non-invasive means.44. 45 Nonetheless, intracompartmental pressure measurements remain the gold standard.

Deep posterior compartment syndrome Deep posterior compartment syndrome typically presents as an ache in the region of the medial border of the tibia or as chronic calf pain. Beware the multiple other causes of calf pain including popliteal artery entrapment syndrome (Chapter )6). The deep posterior compartment contains the flexor hallucis longus, flexor digitorum longus, and tibialis posterior (Fig. 35.1). Occasionally, a separate fascial sheath surrounds the tibialis posterior muscle, forming an extra compartment that may provoke symptoms independent of the other compartments. Active, passive, or resisted motion of these muscles may exacerbate pain. The patient describes a feeling of tightness or a bursting sensation. Pain increases with exercise. There may be associated distal symptoms (e.g. weakness, pins and needles on the plantar aspect of the foot), which may be indicative of tibial nerve compression. Small muscle hernias occasion· ally occur along the medial or anterior borders of the tibia after exercise. On examination. there may be tenderness along the medial aspect of the tibia; however. this is often relatively mild. Due to the deep nature of the compartment, palpable fascial tightness is less obvious in comparison with anterior or lateral compartment syndromes. Nonetheless, the experienced clinician may be able to discern the difference between palpable tightness in the deep compartment and fascial thickening and induration found in association with medial tibial stress syndrome. Routinely all four compartments should be measured pre- and post-exertion in sportspeople suspicious for chronic exertional compartment syndrome. To measure deep posterior compartment pressures, the needle or catheter is inserted from the medial aspect through two layers of fascia aiming posterior to the tibia (Fig. 35.9). Exercises including running or jumping, stair-climbing, use of pulleys in plantarflexion and dorsiflexion or repeated calf raises, or isokinetic resistance machines can be used to exacerbate complaints. Routinely, we ask patients to run five minutes into their pain to ensure a valid test. It is important to reproduce the patient's pain, otherwise the test is not considered valid.

752

Figure 35.9 Compartment pressure testing-deep posterior compartment. The Stryker catheter is inserted into the deep posterior compartment

Post-exertional measurements must be obtained immediately after ceasing exercise and may be repeated again after 10 minutes. Normal compartment pressures are regarded as being between 0 and 10 mmHg. For the diagnosis of chronic compartment syndrome, maximal pressure during exercise of greater than 25 mmHg, an elevation of pressures greater than 10 mmHg, or a resting post-exercise pressure greater than 25 mmHg is necessary (Table 35.3). If the elevated pressure takes more than 5 minutes to return to normal, this may also be significant.

Treatment Treatment of isolated deep posterior exertional compartment syndrome usually begins with a conservative regimen of reduced exercise and deep massage therapy. Careful analysis of all contributing factors and overlapping diagnoses must be considered. Longitudinal release work with passive and active dorsiflexion is performed to reduce fascial thickening (Fig. 35.10). Transverse frictions are used to treat chronic muscular thickening. Dry needling of the deep muscles or prolotherapy may also be helpful. Assessment and correction of any biomechanical abnormalities, especially excessive pronation, must be included. Isolated deep posterior exertional compartment syndrome is uncommon and may be confused with medial tibial stress syndrome, popliteal artery entrapment syndrome. vascular claudication, and stress fractures. Indeed it is not surprising that initial treatment is the same as that for medial tibial stress syndrome. Unfortunately, if associated diagnoses or contributing factors cannot be identified

Leg p ai n may avoid the increased complication risk that occurs when releasing the posterior compartmen ts. 46

Anterior and lateral exertional compartmen t syndromes

Figure 35.10 Soft tissue therapy in the treatment of deep posterior compartment syndrome-longitudinal release to reduce fascial thickening. Active or passive dorsiflexion improves the release

and if pressures are elevated, symptoms are usually refractory to treatment, and surgical release may be necessary. The surgical approach is along the posterior medial edge of the tibia and may be performed through one or two small incisions. The saphenous vein lies directly along the path to the fascial insertion onto the posteromedial border of the tibia. Extreme care must be used to (cntm} all bleeding at the time of surgery, as injury to one of the branches is common and increases the risk of postoperative hematoma or cellulitis. 4G Some authors have suggested a benefit of fasciectomy (removal of a portion of fascial tissue) over fas ciotomy (simple incision) due to concerns that the fascial insertion and sheath reforms. 8 They argue that this periosteal stripping serves an added role of treating any associated medial tibial stress syndrome. as well as assuring release of any anatomic variations of tibialis posterior compartments. Due to the extensive nature of the procedu re, which requires longer incisions and the increased risk of complications, we recommend this ex tensive approach only in revision cases. In addition. in patients who have positive an terior or lateral compartment pressures but only borderline pressures in the deep compartment, recommendations to restrict releases and treatment to the affected compartment are prudent. This approach

The anterior compa rtment contains the tibialis anterior. extensor djgitorum longus. extensor hallucis longus. and peroneus tertius muscles, as well as the deep peroneal nerve; the lateral (peroneal) compartment contains the peroneus lon gus and brevis tendons as well as the superficial peroneal nerve. For anterior compartment pathology. pain during exertion is felt just lateral to the anterior border of the shin, and paresthesias may present in the first web space. For lateral compartment pathology. pain is palpated just anterior to the fibula, and paresthesias may occur over the dorsum of the foot. The int ermuscular septum (raph e) between the two compartments can be visualized in thin individuals by looking for the indentation of skin when you squeeze the soft tissues between the anterior border of the tibia and fibula. dinical examination at rest is usual1y normal, or there may be palpable generalized tightness of the anterior or lateral compartment with focal regions of excessive muscle thickening. It is also important to assess the plantar flexors, especially the soleus and gastrocnemius. If these antagonists are tight, they may predispose to anterior compartment syndrome. Muscle herniation may be palpable with exertion, most commonlyoccuHing 5-7 em (2-3 in.) proximally to the distal tip of the fibula where the superficial peroneal nerve penetrates the lateral compa rtment fascia. Diagnosis of anterior and lateral exertional compartment syndrome is confirmed with pre- and post·exertional compartment testing (Table 35.3).

Treatment Treatment is based on the same principles as for the deep posterior compartment. All contributing factors should be assessed and treated. Lowering the heel in the sportsperson's shoe or orthotics may reduce the load of the anterior muscles and alleviate pain. Sustained myofascial tension techniques combined with passive and active plantarflexion may restore fascial flexibili ty (Fig. 35.U3 overleaf). Focal regions of muscular thickening should be treated with transverse friction or dry needling. In addition, because the anterior and lateral compartments are superficial, vacuum cupping may be attempted (Fig. 35.nb overleaf). Accurate cup placement is required to avoid capillary and periosteal damage. It is also

753

Figure 35 .1 1 Soft tissue therapy in the treatment of anterior compartment syndrome (a) Sustained myofascial tension with active or passive plantarflexion

helpful to treat tightness of the posterior compart· ment (antagonist muscles) with sustained myofascial tension (grade III) combined with passive and active dorsiflexion. Unfortunately, when the diagnosis is pressure pos· itive and there are no obvious precipitating factors, conservative treatment frequently fails, and surgical release is required. Fasiectomy is rarely necessary, as success rates with anterior and lateral compartment releases with minimal incision, and percutaneous and endoscopically assisted releases approach 90%. Newer equipment including balloon catheters and endoscopic vein harvesting retractors have been used to make endoscopic assisted techniques even saferY Special care is essential to visualize the superficial peroneal nerve at the time of surgery to avoid iatro· genie injury. Acute compartment syndromes are usually associated with trauma. Intracompartmental pressures are significantly elevated and do not subside with rest. Emergency surgical release is essential to avoid ischemic injUlY to the extremity. This emergency is covered more completely in Chapter 47; however, it is important to be aware of a number of case reports in which acute anterior compartment syndromes were brought on by exercise and overuse. 41(.4'.1 In many of these cases the patient or sportsperson continued to exercise through the initial pain that may have represented an exertional compartment syndrome which would have otherwise gone away with rest. When pain does not settle in an appropriate time frame, conversion of an exertional compartment syndrome to an acute compartment syndrome should be considered.

Outcomes of surgical treatment of exertiona! compartmen t syndrome

(b) Vacuum cupping

754

Fasciotomy with or without fasciectomy is the standard surgical treatment for both anterior and deep posterior compartment syndromes. The majority of patients undergoing this procedure (80-90%) have a satisfactory result, with many being able to return to their previous level of sport.')o However, there is a significant percentage that either fail to improve after surgery or, after a period of improvement, have a recurrence of symptoms. Some studies suggest that failure and recurrences are more common in the deep posterior compartment,5°· 5' possibly due to failure to release the tibialis posterior compartment,'O while another study showed a more negative outcome with the anterior compartment releases.

Leg pa in Micheli et a1. compared outcomes by gender and noted a slightly decreased rate of successful outcomes in female patienlsY In a study of 18 patients who underwent revision surgery,S! increased pressure was found only in a localized area at the site of the scar in 60% of patients. whereas 40% had high pressures through· out the compartmen t. They found that the exuberant scar tissue was thicker, denser, and more constricting than was the original fascia. Eight of the 18 patients had entrapment of the superficial peroneal nerve with numbness and paresthesia over the dorsum of the foot with exertion (a posi tive Tinel's sign) and localized tenderness over the nerve, exacerbated by active dorsiflexion and eversion. as well as passive inversion and plantar flex ion. All those with peroneal nerve entrapment had a good result from the revision surgery, whereas only 50% of those without nerve entrapment had a satisfactory outcome. Slimmon et aU4 reported a 60% excellent or good outcome after a minim um of two years in 50 patients who underwent fasciectomy. Of the 50 patients, 58% were exercising at a lower level than before the injury, and, of those, 36% cited the return of their compartment syndrom e or the development of a different lower leg compartment syndrome as the reason for the reduction in exercise levels. The foundation of a successful surgical result begins with a proper anatomic diagnosis. Care is important to confirm the diagnosis preopera tively with intracompartmental pressure measurement, as well as treatin g any associated or contri buting factors. Surgery should target the specific anatomical pathology. Avoiding the release of all four compartments in every patient- unless preoperative testing provides definitive indication-reduces the risk of surgical complication s. Meticulous control of intra·operative bleeding will reduce the risk of postoperative hematoma and cellulites. Due to the extensive subcutaneous dissection. postoperative cellulitis or infection is more common than som e other procedures. Perioperative antibiotics and postoperative cryotherapy can reduce this risk. If identified in the postoperative period, the surgeon should have a relatively low threshold to return to the operating room and perform early irrigation. The absolute indication for fasciectomy in contrast to fasciotomy is not clear, as the former may increase the risk of bleeding and postoperative stiff.. ness. Perhaps the most common complication is

postoperative stiffness, which can be avoided by early and aggressive postopera tive mobilization.

Rehab ilitation following com pa rtment syndrome surgery The following protocol is Perioperative antibiotics and cryotherapy to reduce complications of infection, hematoma, and celluli tes. Range of motio n exercises of the knee and ankle in the immediate postoperative period. Full plan tar and dorsiflexion is encouraged. Three to five days of limited weight-bearing on crutches, then full weight-bearing as tolerated. Once the wounds have healed. a strengthening program includ ing cycling and swimming should commence. Gradual return to light jogging at about 4- 6 weeks after surgery. Full sports participation is anticipated at 6- 8 weeks if one compartment released, and 8- 12 weeks if both legs and multiple compartments released. The sportsperson should be pain-free wi th 90% strength regained prior to full sports participation.

Less common causes Stress fracture of th e fi bula Stress fractures of the fibula are not seen as frequently as stress fractures of the tibia. As the fibula plays a minimal role in weight-bearing. this stress fracture is usually due to muscle traction or torsional forces placed through the bone. In the sportsperson with excessive subtalar pronation. the peroneal muscles are forced to contract harder and longer during toe·off. Examination may reveal local tenderness and pain in springing the fibula proximal to the site of the stress fracture. This injury is usually not as painful on weightbearing as is stress fracture of the tibia. It is treated symptomatically with rest from activity unti l bony tenderness settles. Due to poorer rotational control, knee-high pneumatic braces may not be as effective as on the tibia. There should then be a gradu al increase in the amount of activity. Soft tissue abnormalities should be corrected. This injury is often associated with a biomechanical abnormality such as excessive pronation or excessive supina tion.

Referred pai n Referred pain is not a common cause ofleg pain in sports people but should be considered in cases with persistent and atypical pain. Pain may be referred 755

from the lumbar spine, proximal nerve entrapment, the knee joint (Baker's cyst, meniniscal cysts), the superior tibiofibular joint (instability or ganglion cyst), and, occasionally, the ankle joint (instability, Maisonneuve fracrure).

surgical release for pressure positive chronic exertional compartment syndrome was I2 years old and it is unclear whether this patient would have grown out of the problem at maturity.

Periosteal contusion Nerve entrapments Within the leg itself. nerve entrapment of either the superficial peroneal nerve in the lateral compartment or the deep peroneal nerve in the anterior compartment can occur due to trauma or a tight brace or cast. Fascial entrapment at the level of the fibular head is also seen occasionally. The tibial nerve in the deep posterior compartment is less commonly involved with entrapment but can be injured with trauma. Pain and sensory changes may occur. The diagnosis is suggested by the presence of motor or sensory changes, and is confirmed with nerve conduction studies performed pre and post exercise. Surgery may be required to alleviate these conditions.

Vascular pathologies Popliteal artery entrapment syndrome usually presents with calf pain and is therefore more fully described in Chapter 36; however, it may rarely present as pain in the anterior compartment» It can be misdiagnosed as anterior compartment syndrome as they both present with daudicant-type pain. However, the pain from popliteal artery entrapment disappears immediately on cessation of exercise, whereas compartment syndrome pain often persists for approximately 30 minutes as an aching sensation. While deep venous thrombosis is most commonly posterior, chronic venous stasis changes can occur anteriorly and may be evidence of systemic disease.

Developmental issues Juvenile tibia vara (Blount disease) usually presents due to deformity rather than pain. Osgood-Schlatter's disease is a traction apophysitis at the insertion of the patellar tendon onto the tibial tuberosity; it is seen commonly among adolescent sportspeople. Patients usually present with pain and tenderness at the tibial tuberosity (Chapter 42). "Growing pains" may affect the leg and are usually a diagnosis of exclusion. Intermittent achy pain exacerbated by periods of active growth with completely negative imaging and work-up are characteristic. The youngest reported patient treated with 75 6

Periosteal contusion occurs as a result of a direct blow from a hard object such as a football boot. It can be extremely painful at the time of injury. however, the pain usually settles relatively quickly. Persistent pain may occur because of a hematoma having formed under the periosteum. There will be local tenderness and bony swelling. Treatment consists of rest and protection.

Combined frachues of the tibia and fibula , and isolated fractures of the tibia Various patterns of tibia, fibula, or combined tibia and fibula fractures can cause leg pain. These patterns range from complete to incomplete fracrures, stress fracrures, open or closed fractures, simple or comminuted fractures, to displaced and non-displaced [racrures. In sport, combined fractures of the tibia and fibula may be related to indirect violence in landing from a jump onto a twisted foot but may also occur with direct trauma in collision sports. Pain is the most common clinical finding. Weight-bearing is virtually impossible with a displaced fracture of the tibia.

Management When managing combined fractures of both the tibia and fibula. treatment is primarily guided by the stability and fracture pattern of the tibia. Strucrurally the tibia is responsible for 90% of the load across the leg. Its stability is of primary importance. Open fracrures in which the bone is exposed or has puncrured the skin are orthopedic emergencies. The wound must be aggressively irrigated, usually in the operating room, and the patient should be started on appropriate antibiotic therapy. With careful scrutiny, many closed tibial fractures can be treated conservatively but angulation must be minimal (see Practice pearl opposite-surgical management). Specifically, minimal angulation is defined as less than 5" to roO in the frontal plane, 10" to IS" of anterior/posterior bowing on the lateral view, and 3" to i' of rotation deformity. If closed management is appropriate, immobi· lize the limb in an above-knee plaster with the knee slightly flexed and the ankle in 90° of dorsiflexion. Elevate the limb for 3-7 days until swelling subsides.

It is imperative that check X·rays are viewed by the clinician weekly for the firs t few weeks to ensure that there is not progressive angulation of the fracture. At 6-8 weeks the patient may be able to switch into a hinged knee cast. Bony union requires 8 to 12 weeks, and 16 to 20 weeks are required for con solidation. TIle length of time required for complete healing to occur has led some surgeons to proceed with surgical fixation, which can allow earlier mobilization and rehun to play in some fractures. Physiotherapy after removal of the plaster is aimed at regaining fuJI range of knee flexion and quadriceps muscle strength. Activities such as swim· ming can be resumed immediately after removal of the piaster, but multidirectional running sports must wait until range of movement and muscle strength have returned to normal. \" R,.,

r b.....

Isolated fibula fractures Twisting or a direct blow can cause an isolated fracture of the fibula. TIle patient may report only local tenderness. 111e ankle and knee joints must be carefully examined for associated inju ries. A Maisonneuve injury comprises an unstable liga· mentous ankle injury, tearing of the syndesmosis and the interosseous membrane connecting the tibia and fibula, and a proximal fibula fracture. This rela· tively benign appearing proximal fibula frac ture actually represents an unstable ankle injury that should not be missed as it requires surgical stabilization. As long as the fracture does not involve the ankle joint, treatment is symptomatic-prescribe analgesia appropriately and provide crutches/walkin g stick as needed.

Note thatthere is a strong trend toward early surgical fi xation of unstable tibia l fractures, with intramedullary nailing. This allows sportspeop le earlierweight·bearing, and earlier conditioning activities and return to sport; it also obviates the risk of potential malunion.

757

Reg i ona l prob l ems

CLINICAL SPORTS MEDICINE MASTERCLASSES

11. Zadpoor AA. Nikooyan AA. 111e relationship between lower-extremity stress fractures and the ground reaction force: a systema tic revie\v. elin Biomec/J (Bristol. Avon)

www cl i ojca lsportsmed j cjoe com

2011:26(1):23-8.

Listen to the podcast \\'ilh the chaptcr authors. Watch the assessment of the patient with shin pain.

12. Crowell HP, Davis IS. Gait retraining to reduce lower extremity loading in runners. eli" Biomech (Bristol.

See a video explanation of compartment pressure

Avon) 2011:26(1):78-83.

testing.

I@I I.

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Table 37.7 continued Comparative/additional intervention

Author, year

Outcome measure

length of follow-up

athletic level)

Conclusion

Notes

Surgical treatment VS. eccentric

Alfred son et

Muscle st rength

12 w eeks

n = 30 (2317)

Surgical treatment was observed to have no

All patients w ho underwent

al.,19981

exercise (EE)

(Biodex Isokine tic

Population (n (M / FJ

All recreational athletes

Dynamometer), pain

benefit over EE and took

(Visual Analog Scale

double the amount of

(VASil

time to return to preinjury level of activity

surgery attempted conventional treatments and

opted to have surgery

EE was unsupervised but a quality check was done at 6 weeks

Topical g lyceryl trinitrate (GTN)

+ eccentric exercise (EE) vs. placebo patch

Paoloni et al., 2004 48

+ eccentric

Pain scores (rest,

2,6, 12,and

activity, nig ht),

24 weeks

clinical assessment of

n = 6S (40/2S) Level of activity not disctosed

tendon tenderness,

exercise

Treatment using GTN in

EE was not supervised.

conjunction with EE was Patients administered their observed to be a more

own GTN or placebo patches

effective treatment than EE alone

functio nal hop test,

Pain during activity and

ankle p lantar flexor peak force and total

at night. functional

work (Orthopaedic

mea sures and patient

Research Institute

outcomes were all

- Ankle Strength

significantly better in

Testing System )

the GTN t reatment group

Steroid injection

+ eccentric

exercise (EE) vs. placebo injection

+ eccentric exercise

Fredberg et at, 2004 4'1 C'.....

In clinical practice, it is Widely agreed that all grade III ankle injuries warrant a trial of initial conservative management over at least a six· to twelve-week period, irrespective of the caliber of the sportsperson.

If, despite appropriate rehabilitation and protection, the patient complains of recurrent episodes of ins tability or persistent pain, then surgical reconstruction of the lateral ligament is indicated. The preferred surgical method is anatomical reconstruction using the damaged ligamen ts; this produces good functional results, with low risk of complications. The ligaments are shortened and reinserted to bone, and only if the ligament tissue is extremely damaged or even absent may other methods such as tenodesis, in most cases using the peroneus brevis tendon, be considered. Following surgery, it is important to undertake a comprehensive rehabilitation program to restore full joint range of motion, strength, and proprioception. The principles of rehabilitation outlined on page 812 816

are appropriate. The anatomical reconstruction produces good clinical results in more than 90% of patients. There is, however, increased lisk of inferior results in cases of very longstanding ligament insufficiency and generalized joint laxity. In case of anatomic reconstruction, both the antelior talofibular ligament and calcaneofibular ligament should be reconstructed simultaneously. Post-operatively, early range of motion training, e.g. using Aircast stirrup, is recommended.

Less common ankle joint injuries Medial (deltoid) ligament injuries Because the deltoid ligament is stronger than the lateral ligament, and probably because eversion is a less common mechanism of ankle sprain, medial ankle ligament injuries are less common than lateral ligament injuries. Occasionally, medial and lateral ligament injuries occur in the same ankle sprain, however, not commonly. Medial ligament injuries may occur together with fractures (e.g. medial malleolus, talar dome, articular surfaces). Medial ligament sprains should be treated in the same manner as lateral ligament sprains, although return to activity takes about twice as long (or more) as would be predicted were the injury on the lateral side.

Pot! s fracture A fracture affecting one or more of the malleoli (lateral, medial, posterior) is known as a Pott's ture. It can be difficult to distinguish a fracture from a moderate- to-severe ligament sprain, as both conditions may result from similar mechanisms of injury and cause severe pain and inability to weight-bear. Careful and gentle palpation can generally localize the greatest site of tenderness to either the malleoli (fracture) or just distal to the malleolus to the liga. ment attachment (sprain). X-ray is often requiredthe Ottawa rules (Fig. 38.3) are useful in these cases. The management of Pott's fractures requires restoration of the normal anatomy between the superior surface of the talus and the ankle mortise (inferior margins of the tibia and fibula). If this relationship has been disrupted with dislocation of the joint surface, internal fixation is almost always required. Stable internal fixation is used; early range of motion training is recommended. Isolated undisplaced spiral fracht res of the lateral malleolus (without medial ligament instability) and posterior malleolar frachtres involving less than 25% of the articular surface are usually stable. These

Acute ankle injuries

fractures can be treated sym ptomatically with early mobilization, using crutches only in the early stages for pain relief Lateral malleolar fractures associated with medial instability, hairline medial malleolar fractures. and larger undisplaced posterior malleolar fractures are potentially unstable, but may be treated conservatively with six weeks of immobilization using a below-knee cast with extension to include the metatarsal heads. In cases of undisplaced or minimally displaced fractures, the immobilization time may be shortened considerably, using an ankle brace and early range of motion training. A walking heel may be applied after swelling has subsided (3-5 days). Displaced medial malleolar, large posterior malleolar, bimalleolar or trimalleolar fractures, or any displaced fracture that involves the ankle mortise require orthopedic referral for open reduction and internal fixation. A comprehensive rehabilitation program should be undertaken following surgical fixation or removal of the cast. The aims of the rehabilitation program are to restore full range of motion, strengthen the surrounding muscles and improve proprioception. Guidelines for ankle rehabilitation are provided on page 8 12.

Maisonneuve fra cture Maisonneuve fractures are found more commonly in patients presenting to emergency departments than in the sports setting, but occasionally highimpact sports injuries can cause this variant of the syndesmosis sprain. The injury involves complete rupture of the medial ligament, the anteroinferior tibiofibular ligament (see below) and interosseous membrane, as well as a proximal fibular fracture. Surprisingly, non-weight-bearing X-rays may not demonstrate the fracture, as the unstabl e ankle can

reduce spontaneously. Urgent referral to an ortho· pedic surgeon is

Pe rs ist e nt pain after ankle sprain"th e proble m ankle" Most cases of ankle ligament sprain resolve satisfac· torily with treatment-pain and swelling settle and function improves. However, as ankle sprain is such a common condition, there remains a substantial number of patients who do not progress well and complain of pain, recurrent instabili ty, swelling, and impaired function three to six weeks after injury, or even longer. TIlis is a very common presentation in a sports medicine practice and the key to successful management is accurate diagnosis. The ankle may continue to cause problems because of an undiagnosed fracture or other bony abnormality (Table 38.2). Alternatively, there may be Hgament, tendon, synovial, or neurolog· ical dysfunction (fable 38.3 overleaf). In the remainder of this chapter, we discuss a clinical approach to managing patients with this presentation, and then detail management of specific conditions.

Clinical approach to the problem ankle The clinician should take a detailed history that clarifies whether the problem has arisen following an ankle sprain (the true "problem ankle") or whether the patient has longstanding ankle pain that arose without a history of injury (see Chapter 39). The patient who has had inadequate rehabilitation usually complains of persistent pain, reduced range of motion, and limitation of function with increasing activity. Determine whether the rehabilitation was adequate by asking the patient to show you the exercises he or she performed in rehabilitation. Did therapy include range of motion exercises

Table 38.2 Fractures and impingements that may cause persistent ankle pain after ankle injury Fractures and chondral lesions

Bony impingements(OI

Anterior process calcaneus

Anterior impingement

Lateral process talus

Posterior impingement

Posterior process talus (or, rare, as trigonum fracture)

Anterolateral impingement

Osteochondral lesion TIbial plafond chondral lesion Base of fifth metatarsal (0)

Although impingements are included here in the bony causes, pain commonly arises from soft tissue impingement

between bony prominences. Also, impingements most commonly present as ankle pain of gradual onset but are included here as they can present and fail

[0

resolve aft er acute injuries

817

Table 38.3 Ligamentous, tendon, and neurological causes of persistent ankle pain after ankle injury Other soft tissue and neural Atypical sprains

Tendon injuries

abnormalities

Chronic ligamentous instability Medial ligament sprain Syndesmosis sprain (AITFL sprain) Subtalar joint spra in

Chronic peroneal tendon weakness Peroneal tendon subluxation/rupture TIbialis posterior tendon subluxation/ rupture

Inadequate rehabilitation Chronic synovitis Sinus tarsi syndrome Complex regional pain syndrome

type 1 (particularly dorsiflexion), strengthening exercises (with the foot fully plantarflexed to engage the peroneal tendons/muscles) and possibly proprioceptive retraining?15 Examination of the inadequately rehabilitated ankle reveals decreased range of motion in the ankle joint (especially dorsiflexion), weak peronealmuscles, and impaired proprioception. These findings can be reversed with active and passive mobilization of the ankle joint (Fig. 38.5), peroneal muscle strengthening (Fig. 38.6). and proprioception training (Fig. 38.7). Other abnormalities can also cause this constellation of examination findings- remember that the ankle may be inadequately rehabilitated because of the pain of an osteochondral lesion of the talus. If rehabilitation has been appropriate and symp· toms persist, it is necessary to consider the presence of other abnormalities. Was it a high·energy injury that may have caused a fracture? Symptoms of intraarticular abnonnalities include clicking, locking, and joint swelling. The clinician should palpate an the sites of potential fracture very carefully to exclude that condition. Soft tissue injuries that can cause persistent ankle pain after sprain include chronic ligament instabiI· ity, complex regional pain syndrome type I (formerly known as reflex sympathetic dystrophy [RSD]) and. rarely, tendon dislocation or subluxation, or even tendon rupture (partial or total). Inflammation of the sinus tarsi (sinus tarsi syndrome) can be a cause of persistent ankle pain, but this syndrome can also occur secondary to associated fractures. Thus, even if the patient has features of the sinus tarsi syndrome, the clinician should still seek other injuries too. Appropriate investigation is a key part of manage· ment of patients with the problem ankle. Both radio· isotopic bone scan and MRI are able to distinguish soft tissue damage from bony injury; MRI is preferred in most cases. In soft tissue injuries. isotope activity in the bone phase is normal. Ifbony damage is present, isotope activity in the bone phase is increased. MRI

818

can detect bony and soft tissue abnormalities but the clinician must remember that a subluxing tendon can appear normal on MRI. The conditions that are associated with the various findings on MRI and bone scan are listed in Figure 38.10.

Osteochondral lesions of the talar dome It is not uncommon for osteochondral fractures of the talar dome to occur in association with ankle sprains, particularly when there is a compressive component to the inversion injury, such as when landing from a jump. The talar dome is compressed by the tibial plafond, causing damage to the osteochondral surface. The lesions occur most commonly in the superomedial corner of the talar dome, and much less commonly on the superolateral part. Large fractures may be recognized at the time of injury. The fracture site will be tender and may be evident on X-ray. Usually, the lesion is not detected initially and the patient presents some time later with unremitting ankle aching and locking or catching, despite appropriate treatment for an ankle sprain.

? RAl 0'"

7/1 ' ,?R -'1 ('

'0.'""

Technique correction is important in ballet dancers with flexor hallicus longus tend in apathy.

Surgical treatment should be considered when persistent synovitis or triggering prevents dancing en pointe. Surgery involves exploration of the tendon and release of the tendon sheath. This can be accomplish ed in almost all cases u sing the a rtInoscope. with a posterior approach. The fibrous band around the tendon is cleaned off and the tendon released.

Tarsal tunnel syndrome Tarsal tunnel syndrome occurs as a result of entrap· ment of the posterior tibial nerve in the tarsal tunnel where the nerve winds aroun d the medial malleolus. IQ It m ay also involve only one of its term inal branches distal to the tarsa l tunnel. Pain and sensory disturbance are felt in the medial part of the heel.

Causes The causes of tarsal tunnel syndrome are: idiopathic- in approximately 50% of cases trauma (e.g. inversion injury to the ankle, or direct blow to the ankle with large bleeding, for instance in soccer) overuse associated with excessive pronation less common causes - ganglion - talonavicular coalition - va ricose veins - synovial cyst - lipoma - accessory muscl e-flexor digitorum a ccessorius longus

- tenosynovitis-often correlated with arthritis (seronegative rheumatoid arthri tis) - fracture of the di stal tibia or calcaneus.

Clinical features Poorly defined burning, tingling, or numb sensation on the plantar aspect of the foot, ohen rad iating into the toes. Pain is usually aggravated by activity and relieved by rest. Pain is usua lly the reason patients see k help; the location of th e pain can be diffuse and poo rly defined. In some patients the sym ptoms are worse in bed at night and relieved by getting up a nd moving o r massaging the foot. Swelling s, varicosities, or thicken ing s may be found on examination around the medial ankle or heel. A ganglion or cyst may be palpable in the tendon sheaths around the medial ankle. Tenderness in the region ofthe tarsal tunnel is common. Tapping over the posterior tibial nerve (TInel's sig n {Fig 39.2d)) may e licit the patient's pain and very occasionally cause fasciculations; however, this "classic" sign is not commonly seen. There may be altered sensation along the arch of the foot. The distribution of the sensory changes in the foot needs to be differentiated from the typical derma tomal distribution of 51 nerve root compression.

Investigations Nerve conduction studies should be performed."· U These not only help to confirm the diagnosis but they can also guide the surgeon as to the location of the nerve compression. Nevertheless tarsal tunnel syndrome is primarily a clinical diagnosis and nerve conduction studies a re negative in approximately 50% of patients. Ultrasound or MRI may be required to assess for a space-occupying lesion as a cause of the syndrome. An X-ray and, if required. a CT scan should be performed in the case of excessive pronation or if a tarsal coalition is suspected.

Differential diagnosis Differential diagnosis includes entrapment of the medial and/or lateral plantar nerves, or both, plantar fasciitis, intervertebral disk degeneration and other causes of nerve inflammation or degeneratio n.

833

The diagnosis of tarsal tunnel is often difficult and the symptoms and signs are often vague. This is important to bear in mind, at least before surgical in tervention is decided upon.

(Fig. 39.5a). If the X-ray is normal, a radioisotopic bone scan, MRI is the preferred investigation and CT scan is also good for imaging bony lesions (Fig. 39.Sb).

Treatment Non-surgical treatment should be attempted in those with either an idiopathic or biomechanical cause. If neurodynamic tes ts prove positive, appropriate neural gliding treatments are indicated. If excessive pronation is present, an orthotic may prove helpful. Surgical treatment is required if there is mechanical pressure on the nerve. A decompression of the posterior tibial nerve and its branches may be indicated in selected cases, but only after both the diagnosis and site of nerve entrapment have been confirmed. If' R4('

Su rgery should be reserved as the last resort. lH'Ii">c

Surgery should be reserved as the last resort, if all other treatment fails, symptoms are severe, and the clinician is confident of mechanical pressure on the nerve. Results of surgery have not been encouraging,') with a high perioperative complication

Stress fracture of the medial malleolus Stress fracture of the medial malleolus is an unusual injury but should be considered in the runner or soccer player presenting with persistent medial ankle pain aggravated by activity.'" " Although the fracture line is frequently vertical from the junction of the tibial plafond and the medial malleolus, it may arch obliquely from the junction to the distal tibial metaphysis.

Figure 39.5 (a) X-ray of stress fracture of medial malleolus

Clinical features Sports people classically present with anterior and medial ankle pain that progressively increases with running and jumping activities. Often they experience an acute episode, which leads to their seeking medical attention. Examination reveals tenderness overlying the medial malleolus, frequen tly in conjunction with a mild ankle effusion. Symptoms may also develop slowly over a period of weeks to months.

Investigations In the early stages. X-rays may be normal, but with time a linear area of hyperlucency may be apparent, progressing to a lytic area and fracture line

834

(b) (T scan of stress fracture of the medial malleolus

Treatment

Investigations

If X-ray reveals no fracture or an undisplaced fracture, treatment requires non-weight-bearing rest with an Aircast brace until local tenderness resolves, a period of approximately six weeks. If, however, a displaced fracture or a fracture that has progressed to non-union is present, surgery with internal fixation is required. Following [raemre healing, the practitioner should assess biomechanics and footwear. A graduated return to activity is required and usually takes around 12 weeks.'7 Even in the case of undisplaced fracture, surgical intervention with internal screw fixation (percutaneous sc rew fixation) followed by immobilization in plaster for three weeks and Aircast for a further three weeks is advisable.

Nerve conduction shldies can help confirm the diagnosis. Injection of local anesthetic at the point of maximal tenderness with a resultant di sa ppearance of pain will confirm the diagnosis. The diagnosis may often be difficult to establish.

Medial calcaneal nerve entrapment The medial calcaneal nerve is a branch of the pas· tedor tibial nerve arising at the level of the medial malleolus or below and passing superficially to innervate the skin of the heel. Occasionally it may arise from the lateral plantar nerve, a branch of the posterior tibial nerve. It has been theorized that a valgus hindfoot may predispose joggers to compression of this nerve branch. This nerve entrapment is often termed "Baxter's nerve."

Clinical features Pain is burning; it is over the inferomedial aspect of the calcaneus. Pain often radiates into the arch of the foot. Pain is aggravated

by funning.

Tenderness over the medial calcaneus. Tinel's sign is positive (Fig. 39.2d), There is often associated excessive pronation of the hindfoot.

Treatment Treatment involves minimizing the trauma to the nerve with a change of footwear or the use of a pad over the area to protect the nerve. Use afloca! electrotherapeutic modalities and transverse friction to the painful site may help to settle the pain. If this is not successful, injection of corticosteroid and local anesthetic agents into the area of point tenderness may be helpful. Surgery may, in selec ted cases, be required to decompress the nerve.

Other causes of medial ankle pain Two conditions that generally cause foo t pain but may present as medial ankle pain are stress fractures of the calcaneus and the navicular bone (Chapter 40). Referred pain from neural structures may occasionally present as medial ankle pain. Entrapment of the medial plantar nerve generally causes midfoot pain but may present as medial ankle pain.

Lateral ankle pain Lateral ankle pain is generally associated with a biomechanical abnormality. The two most common causes are peroneal tendinopathy and sinus tarsi syndrome. The causes oflateral ankle pain are listed in Table 39,2. The anatomy of the region is illustrated in Figure 39.6 overleaf.

Tab le 39.2 Causes of lateral ankle pain Common

Less common

Peroneal tendinopathy

Impingement syndrome

Stress fracture of the distal fibula

Sinus tarsi syndrome

•

Anterolateral

Cuboid syndrome

Posterior

Complex regional pain syndrome

Recurrent dislocation of peroneal tendons

Not to b e missed

type 1 (following knee or ankle trauma)

Stress fracture of the talus Referred pain Lumbar spine Peroneal nerve Superior tibiofibular joint

835

Figure 39.6 Lateral aspect of the ankle (a) Anatomy of the lateral ankle

Figure 39.7 Examination of the patient with lateral ankle pain (a) Resisted movement- eversion (peroneal muscles)

(b) Sinus tarsi

Examination Examination is as for the patient with acute ankle injury (Chapter 38), with particular attention to testing resisted eversion of the peroneal tendons (Fig. 39.7a) and careful palpation for tenderness, swelling and crepitus (Fig. 39.7b).

Peroneal tendinopathy The most common overuse injury causing lateral ankle pain is peroneal tendinopathy-almost always peroneus brevis tendinopathy. The peroneus longus and peroneus brevis tendons cross the ankle joint within a fibro-osseous tunnel, posterior to the lateral malleolus. The peroneus brevis tendon inserts into the tuberosity on the lateral aspect of the base of the fifth metatarsal. The peroneus longus tendon passes under the plantar surface of the foot to insert into the lateral side of the base of the first metatarsal and medial cuneiform. The peroneal tendons share a common tendon sheath proximal to the distal tip of the fibula, after which they have their own tendon sheaths. The peroneal muscles serve as ankle dorsiflexors in addition to being the primary evertors of the ankle.

836

(b) Palpation-the peroneal tendons are palpated for tenderness and crepitus

Causes Peroneal tendinopathy may occur either as a result of an acute or recurrent ankle inversion injury, or secondary to an overuse injury. Soft footwear may predispose to the development of peroneal tendinopathy. Common causes of an overuse injury include: excessive eversion of the foot, such as occurs when running on slopes or cambered surfaces 18 excessive pronation of the foot secondary to tight ankle plantarflexors (most commonly soleus) resulting in excessive load on the lateral muscles excessive action of the peroneals (e.g. dancing, basketball, volleyball).

An infiammatOlY arthropathy may also result in the development of a peroneal tenosynovitis and subsequent peroneal tendinopathy. It has been suggested that peroneal tendinopathy may be due to the excessive pulley action of, and

abrupt change in direction of, the peroneal tendons at the lateral malleolus (e.g. in skiers and soccer players). In some cases, peroneal tendinopahy is correlated with peroneal tendon instability in the retromalleolar groove of the lateral malleolus. There are three main sites of peroneal tendinopathy. posterior to the lateral malleolus (most common) at the peroneal trochlea at the plantar surface of the cuboid.

Clinical features l ate ral ankle or heel pain and typical retromalleolar swelling. which is aggravated by activity and relieved by rest. local tenderness over the peroneal tendons on examination, sometimes associated with swelling and crepitus (a true para tenonitis). Painful passive inversion and resisted eversion, although in some cases eccentric contraction may be required to reproduce the pain. Calf muscle tightness may be present. Excessive subtalar pronation or stiffness of the subtalar or midtarsal joints is demonstrated on biomechanical examination.

Investigations MRI is the recommended investigation and shows characteristic features of tendinopathy- increased signal and tendon thicken ing and longihldinal rupture (Fig. 39.8)." If MR I is unavailable. an ultrasound may be performed, with similar good results. If an underlying infiammatolY arthropathy is suspected, obtain blood tes ts to assess for rheumatologi. cal and inflammatory markers.

Treatment Treatment initially involves settling the pain with rest from aggravating activities, analgesic medication if needed, and soft tissue therapy. Stretching in con· junction with mobilization of the subtalar and midtarsal joints may help. Footwear should be assessed and the use of lateral heel wedges or orthoses may be required to correct biomechanical abnormalities. Strengthening exercises should include resisted eversion (e.g. rubber tubing. rotagym), especially in pla ntarflexion as this position maximally engages the peroneal muscles. In severe cases, surgery may be required, which may involve a synovectomy. tendon debridement. or

Figure 39.8 Sagittal oblique MR image of a

longitudinal rupture of the peroneus brevis tendon at the lateral malleolus level. The rupture causes high signal (two brIght regions) in black tendon (solid arrowhead points to peroneus brevis). The peroneus longus tendon (open arrowhead) is normal (homogenous black signal on MR)

repair ofthe tendon in case oflongitudinal rupture.>o If peroneal tendinopathy is associated with tendon instability, ligament reconstruction should address the instability of the tendon at the same time as the tendon is repaired.

Sinus tarsi syndrome TIle sinus tarsi (Fig. 39.6b) is a small osseous canal running from an opening anterior and inferior to the la teral malleolus in a posteromedial direction to a point posterior to the medial malleolus. The inter· osseous ligamen t occupies the sinus tarsi and divides it into an anterior portion, which is parl of the talocalcaneonavicular joint, and a posterior part, which represents the subtalar joint. It is lined by a synovial membrane and in addition to the ligament, it contains small blood vessels, fat and connective tissue.

Causes Although injury to the sinus tarsi may result from chronic overuse secondary to poor biomechanics (especially excessive pronation), approximately 70%

837

of all patients with sinus tarsi syndrome have had a single or repeated inversion injury to the ankle. It may also occur after repeated forced eversion to the ankle, such as take off. The sinus tarsi contains abundant synovial tissue that is prone to synovitis and inflammation when injured. An influx of inflammatory cells may result in the development of a low-grade and longstanding inflammatory synovitis. Other causes of sinus tarsi syndrome include chronic inflammation in conditions such as gout, inflammatory arthropathies, and osteoarthritis.

Clinical features Pain may be poorly localized and vague but is most often centered just anterior to the lateral malleolus. Pain is often more severe in the morning and may diminish with exercise. Pain may be exacerbated by running on a curve in the direction of the affected ankle-the patient may also complain of ankle and foot stiffness, a feeling of instability of the hindfoot, and occasionally weakness, Difficulty, often marked, walking on uneven ground. Full range of pain-free ankle movement on examination, but the subtalar joint may be stiff. Pain occurs on forced passive eversion ofthe subtalar joint; forced passive inversion may also be painful due to damage to the subtalar ligaments. Tenderness of the lateral aspect of the ankle at the opening ofthe sinus tarsi and occasionally also over the anterior talofibular ligament; there may be minor localized swelling,

Diagnosis

Figure 39.9 Local anesthetic injection under fluoroscopic gUidance. The needle is introduced into the lateral opening ofthe sinus tarsi with the foot in passive inversion. The needle should be directed medially and slightly posteriorly

subtalar joint is essential (Fig. 39.10). Rehabilitation involves proprioception and strength training. Biomechanical correction may be indicated. Direct infiltration of the sinus tarsi with corticosteroid and local anesthetic agents may prove therapeutic; however, it is important that all underlying abnormalities are also corrected. Surgery is rarely indicated.

Anterolateral impingement Causes Repeated minor ankle sprains or a major sprain involving the anterolateral aspect of the anlde may cause anterolateral impingement. An inversion sprain to the anterior talofibular ligament may

The most appropriate diagnostic test is injection of I mL of a short-acting local anesthetic agent (e.g. 1% lignocaine Ilidocaine}) into the sinus tarsi; this can be done using fluoroscopic to ensure correct location (Fig. 39.9). In sinus tarsi syndrome, this injection will relieve pain so that functional tests, such as hopping on the affected leg, can be performed comfortably (for diagnosis). An ankle X-ray may be performed to exclude so-called "four-corner syndrome" or degenerative changes of the subtalar joint. MRI may show an increased signal and fluid in the sinus tarsi, but is not often helpful.

Treatment Non-surgical management includes relative rest, ice, and electrotherapeutic modalities. Mobilization of the

838

Figu re 39.10 Mobilization of the subtalar joint is performed by medial-to-lateral transverse glide of the calcaneus on the talus with the patient side-lying and the ankle dorsif[exed

promote synovial thickening and exudation. Usually this is subsequently resorbed, but sometimes this is incomplete and the res idual tissue becomes hyali· nized and molded by pressure from the articular sur· faces ofthe talus and fibula, where it may be trapped during ankle movements. A meniscoid lesion thus develops in the anterolateral gutter. It has also been suggested that rneniscoid les ions may result from tears of the anterior talofibular ligament (or aberrant ligament structure) in which the torn fragment becomes interposed between the lateral malleolus and the lateral aspect of the talus. Another postulated cause of anterolateral ankle impingement is chondromalacia of the lateral wall of the talus wi th an associated synovial reaction.

Clinical features The classic presentation is pain at the an terior as pect of the lateral malleolus and an intermittent catching sensation in the ankle in a sports person with a previous history of a single ankle inversion injury. or multiple inversion injuries (such as in soccer players). Examination may reveal tenderness in the region of the anteroinferior border of the fibula and ante· rolateral surface of the talus. The pain is relieved by tightening the tibialis posterior tendon and releasing the peroneal tendons. Proprioception may be poor.u

Investigations Clinical assessment is more reliable than M RI to diagnose this lesion. ll An arthroscopic examination confirms the diagnosis.

Treatment Corticosteroid Il1Jechon may be helpful initially but, frequently, arthroscopic removal of the fibrotic. meniscoid lesion is required. Generally results after arthroscopic removal of the im pinged tissue are encouraging. and soccer playe rs return to sport after a short period (three to four weeks) of rehabilitation. Even though anterolateral impingement limits dorsiflexion. it takes ballet dancers about three months to regain full pointe position (plantarflex ion) afte r this operation.

Posterior impingement syndrome Pos terior impingement syndrome sometimes pre· sen ts as lateral ankle pain but more commonly as pain in the posterior ankle (Chapter 37) .

Stress fra cture of the talu s Stress frac tures of the posterolateral aspect of the talus have been described in track and field athletes, triathletes. and Australian Rules footballers.l l

Causes These stress fractures may develop secondary to excessive subtalar pronation and plantarflexion. resulting in impingement orthe lateral process of the calcaneus on the posterolateral corner of the talus. lr• In pole vaulters, this injury is usually acute and is attributed to "planting" the pole too late.

Clinical features latera l ankle pain of gradual onset. Pain is made worse by running and weight-bearing. Marked tenderness and occasionally swelling in the region of the sinus tarsi or posterior aspect of the ankle.

Diagnosis

Typical isotopic bone scan and cr scan appearances are shown in Figure 39. 1[ overleaf. MRI will also reveal the fracture, with the STIR (short TI inversion recovery) sequence being most helpful.

Treatment Treatment requires cast immobiliza tion for six to eight weeks, and then a supervised graduated rehab· ilitation. In elite sportspeople, when a rapid recovery is required in a few selected cases, or in the case of failure of non-surgical management, surgical removal of the lateral process has been shown to produce good results. ? RAe

,fIt--""" -::n Biomechanical correctio n with orthoses is requ ired 0""

before activity is resumed.

As this injury is invariably associated wi th excessive pronation, biomechanical correction with orthoses is required before activity is resumed.

Referred pain A variation of the slump test (Chapter II) with the ankle in plantarRexion and inversion can be perfo rmed to detect increased neural mechanosensitivity in the peroneal nerve. If the test is positive, this position can be used as a stretch in addition to soft tissue therapy to possible areas of restriction (e.g. around the head of the fibula). 839

.

L T I'IED

.'

.,....... ' ....

'

::.

....

Figure 39.1 1 Stress fracture of the talus Isotopic bone scan

(a)

Figure 39.12 Surface anatomy of the anterior ankle showing tendons (b) CT scan

Anterior ankle pain Pain over the anterior aspect ofthe anlde joint without a history of acute injury is usually due to either lis anterior tendinopathy or anterior impingement of the ankle. The surface anatomy of the anterior ankle is shown in Figure 39.12.

Anterior impingement of the ankle Anterior impingement of the ankle joint (anterior tibiotalar impingement) is a condition in which additional soft or bony tissue is trapped between the tibia and talus during dorsiflexion; it may be the cause of chronic ankle pain or may result in pain and disability persisting after an ankle sprain. Although this syndrome has been called "footballer's ankle," it is also seen commonly in ballet dancers.

Causes Anterior impingement occurs secondary to the development of exostoses (bone spurs) on the anterior rim of the tibia and on the upper anterior surface of the

840

Fig ure 39.13 X-ray showing bony exostosis on the anterior talus neck of talus (Fig. 39.I3). The exostoses were initially described in ballet dancers and were thought to be secondary to a traction injury of the joint capsule of

the ankle that occurs whenever the foot is repeatedly forced into extreme plantarflexion. Subsequently the development of the exostoses has been attributed to direct osseous impingement during extremes of dorsiflexion, as occurs with kicking in football and performing the plii (lunge) in ballet. As these exos toses become larger. they impinge on overlying soft tissue and cause pain. Ligamen tous injuries and thus instability following inversion injuries to the ankle may also result in anterior ankle impingement; it has been shown that the distal fascicle of the anterior inferior tibiofibular ligament m ay impinge on the anterolateral aspect of the talus and cause local pain.

Clinical features Anterior ankle pain initially starts as a vague discomfort. Pain ultimately becomes sharper and more localized to the anterior aspect of the ankle and footespecially on dorsiflexion of the foot. Pain is worse with activity, particularly with running, descending pfie (lunge) in classical ballet. kicking in football, and other activities involving dorsiflexion. Ankle stiffness occurs as the impingement develops. Loss of take-off speed is noticed as the impingement develops. Tenderness along the anterior margin of the talocru ral joint. Palpable exostoses (if they are large). Restricted dorsiflexion. Painful dorsiflexion. The anterior impingement test (Fig. 39.14a), where the patient lunges forward maximally with the heel remaining on the floor, reproduces the pain.

Investigations Lateral ankle X-rays in flexion and extension show exos toses and abnormal tibiotalar contact. Ideally perform ed weight-bearing in the lunge position, X-ray shows bone-an-bone impingement that confirms the diagnosis (Fig. 39.14D).

Treatment In milder cases, non-surgical treatmen t consists of a heel lift, rest, modification of activities to limit dorsiflexion, nonsteroidal anti-inflammatory drugs (NSAIDs), and physiotherapy, including accessory anteroposterior glides of the talocrural joint at the

Figure 39.14 The anterior impingement test (a) The patient lunges forwa rd maximally and, if thi s reproduces the pain, the test is positive and suggests the diagnosis of anterior impingement

(b) The same position is used to take a lateral A positive test reveals bone-on-bone impingement (a rrowed) when the patient adopts the lunge position that reproduces pain end of range of dorsiflexion. Taping or orthoses m ay help control the pain if they restric t ankle dorsiflexion or improve join t insta bility (as join t insta bili ty has been shown to contribu te to the development of anterior impingement). More prominent exostoses m ay require surgical removal arthroscopically. The clinical results after arthroscopic removal are encouraging and the ma jority of patien ts become pain·free. with increased range of ankle motion.

Tibialis anterior tendinopathy The tibialis anterior tendon is the primary dorsiflexor of the foot; it also adducts and supina tes (inverts)

84 1

the foot. It passes medially over the anterior ankle joint and runs to insert into the medial and plantar aspects of the medial cuneiform bone and the adjacent base of the first metatarsal.

Causes

anterior tendon, especially over the anterior joint line. There is pain on resisted dorsiflexion and eccen· tric inversion. Longstanding and non-treated tendinopathy may eventually lead to partial or even total rupture of the tendon (under the extensor retinaculum).

Tendinopathy of the tibialis anterior may result from:

Investigations

overuse of the ankle dorsiflexors secondary to; - restriction in joint range of motion (as may occur with a stiff ankle) - downhill running playing racquet sports involving constant change of direction excessive tightness of strapping or shoelaces over the tibialis anterior tendon.

Clinical features The main symptoms are pain, swelling, and stiffness in the anterior ankle, which are aggravated by activity, especially running, and walking up hills or stairs. On examination, there is localized tenderness, swelling, and occasionally crepitus along the tibialis

842

Ultrasound or MRI may be used to confirm the diagnosis and exclude tears of the tendon.

Treatment Eccentric strengthening, soft tissue therapy and mobilization of the ankle joint are common treatments. Correction of biomechanics with orthoses may be helpfuL In case of partial or total rupture, surgical reconstruction may be required.

Anteroinferior tibiofibular joint injury (AITFL) This injury is discussed in Chapter)8 (pages 82)-41 because it results from an acute anlde injury (and often a fracture). Ifmissed, it will present as persistent pain and loss of function after an ankle sprain.

iii

13. Skalley TC, Scho n LC, Hinton RY et al. Clinical results

REEER E NC E S

following revisio n tibial nerve release. Foot Ankle Int

L Gluck G $, Heckman OS, Parekh SG. Tendon disorders of the foot and ankle, part 3: the posterior tibial tendon.

1994;15(7):3 60-7. 14- Pfeiffer WH, Cracchiolo A. 3rd. Clinical results after

Am j Sporls Med 201 0:38{IO):2133-44-

2. Bowring B, Chockalingam N. Conservative treatment

of tibialis posterior tendon dysfunction- a review.

tarsal tunnel decompression . ] BOlle joint Surg Am 1994;7 6 (8):1222- 3°. 15. Brukner P, BenneU K. Ma theson G. Stress!ractures.

Foot (Edillb) 2010;20{I):18-2 6. 3. Hutchinson BL, O'Rourke EM . Tibiali s posterior

Me lbourne: Blad.-weJls Scie ntific Asia. 1999·

16. Kor A, Saltzman AT. Wempe PD. Medial m alleolar

tendon d ysfunction and peroneal tendon subluxation.

stress fractures. Lite rature review. diagnosis, and trea tment. J Am Podilltr Med Assoc 2003:9}(4):

Clin Podiatr Me(l SIIrg 199pz(4J:703- 23· 4 . Landorf K. Tibialis posterior tendon dysfun ction .

Ea rly identification is the key to success. Aust Podialr

29 2-7. 17. lowett AI. Birks C L Blackney Me. Medial

1995 ;29:9- 14.

m alleolar s tress fra cture secondary to ch ronic ankle

5- Premkumar A. Perry MB , Dwyer AJ et al. So nography and MR imaging of posterior tibial ten dinopathy.

impingemen t. Foot Ankle f lit 2008;29 (717 16-21. 18. Clarke H D. Kitaoka H B. Ehman RL Peroneal tendon

AJR Am) Rocn tgmof 2002: 178(T}:223-32. 6. Kulig K. Lederhaus ES, Reischl S ct al. Effect of

injuries. Foot Ankle Int 1998:t 9 (5):280-8. 19. T jin A. Ton ER. Schweitzer ME et OIL M R imaging

eccen tric exercise program for early tibialis posterior te ndinopatlly. Fool Allkle

rll' 20°9:3° (9 ):877-8 , .

7. Lo LD, Schweitzer ME , Fan JK et al. MR imaging

findings of entrapment of the fl exor hallu ci s longus

of peroneal tendon disorders. Aj RAm j Roelltgenal 1997;168(1):135-4°· 20. Maffulli N. Ferran NA. Oliva F e t OIL Rerurrent subluxation of the peroneal tendons. Am j S/Jorts Med

tendon . AjR Am j Roenlgello/ 200 1:176(5) :1145- 8.

8. Simpso n MR, Howard TM. TClldinopa thies of the foot

2006;34(6):9 86- 9 2 . 2 1.

and ankle. Am Fum Physiciu n 2009:80 (IO):1l07- 14· 9. Khan K. Brown J, Way S e t al. Oventse injuries in classical balle t. Sports Med 199P9(SJ:34I-57· 10. RotiIiguez D , Devos Bevernage B. Maldague P et a!. Tarsal tunnel syndrome and fl exor h allucis longus

II.

resonance imaging and clinical examination (Lette r).

Sports Med 1998:26: rS2-3· Liu SH. Nuccion Sl., Finerman G. Diagnosis of

Alii j 22.

anterolateral a nkle impingement. Comparison

tendon hypertrophy. Ol1liop Traumat a! Surg Res

betv.'een magnetic resonance imaging and clinical

2010:9 6 (7): 82 9- 31. Pa tel AT. Gaines K, Malamut R e t at. Usefulness of

examination [sec comments]. Am j Spal1 s Med

eiectrodiagnostic techniques in the evaluation of

12.

Highet RM, Diagnosis of anterola teral an kle impingement: comparison between magne tic

' 997'25(3):3 8 9-93. 23 . Bradshaw C, Khan K, Brukner P. Stress fracture of

suspected tarsal tunnel syndIOme: an evidence·based

the body of the talus in athletes demo nstrated with

review. Muscle Nrn1e 200;:32(2):236- 4°.

computer to mography. elin J Spo rt Med 199 6 :6 (1):

Oh

51. Meyer RD. Entrapment neuropa thies of the

48-5 1,

tibial (posterior tibial) ne rve. Neural Clill 1999;17(3):

;93- 615, vii.

843

Houston Rockets center Yao Ming has elected to have extensive sU/'ge,'y on his ji-actured left foot ... After consultation with a battery of doctors, Yao, 28, has decided to undergo a bone graft to heal the existingji-acture and have his arch surgically lowered to "educe the stress Or! his foot. ES PN NBA n ews reporting Yao Ming's navicular stress fracture management plan. fuly 1 8 , 2009 , Yao Ming an nounced h is retirement from basketball, fuly 8, 20 11. Many practitioners consider the foot a difficult region to treat, largely because the anatomy seems rather complex (Figs 40.1, 40.2). If the foot is considered in its three distinct regions (Fig. 40.I)-the rear foot (calcaneus and talus), the midfoot (the cuneiforms and navicular medially, the cuboid laterally), and the forefoot (the metatarsals and phalanges)-the bony anatomy is greatly simplified. Soft tissue anatomy can be superimposed on the regional division of the foot (Figs 40.2c-e). In keeping with this anatomical division of the foot, clinical assessment of foot pain is most conveniently considered in three anatomical regions (Fig. 40.1):

Rear foot pain The most common cause of rear foot (inferior heel) pain is plantar fasciitis. A lay term for this condition is "heel spur(s)." This condition occurs mainly in runners and the older adult, and is often associated with a biomechanical abnormality, such as excessive pronation or supination. In non-athletic populations, limited ankle dorsiflexion range of motion and high body mass index (BMI) should be considered predisposing factors.' Another common cause of heel pain is the fat pad syndrome or fat pad contusion. This is also known as a "bruised heel" or a "stone bruise." Less common causes of heel pain are stress fracture of the calcaneus and conditions that refer pain to this area such as tarsal tunnel syndrome (Chapter 39) or medial calcaneal nerve entrapment (Chapter 39). Causes of rear foot pain are listed in Table 40.1 overleaf.

heel pain (arising from the rear foot) midfoot pain forefoot pain.

rear foot

midfoot

II

forefoot

II

Figure 40. 1 The regions of the foot-rear foot, mid foot and forefoot

844

cuneiforms

calcaneus

5th metatarsal

Figure 40.2 Anatomy of the foot (a) Lateral view ofthe bones of the foot

fibrous flexor tendon sheaths

talonavicular joint

& lateral heads of nexor haJlucis brevis

flexor hall ucis longus tendon

(b) Medial view of the bones of the foot

hallucis

peroneus

longus tendon

tibialis anterior

flexor digiti minimi brevis flexor digitorum brevis abductor digiti minimi

aponeurosis (cut)

(d) Plantar view of the soft tissues of the foot-first

extensor

digitorum longus

layer

inferior

extensor

retinaculum extensor hallucis brevis

extensor digitorum longus tendons

",. t-lll- extensor hallucis lon gus t endon

(e) Dorsal view of the 50ft tissues of the foot

(e) Plantar fascia

845

Table 40.1 Causes of rear foot and inferior heel pain Common

Less common

Not to be missed

Plantar fasciitis Fat pad contusion

Calcaneal fractures • Traumatic • Stress fracture Medial calcaneal nerve entrapment (Chapter 39) Lateral plantar nerve entrapment Tarsal tunnel syndrome {Chapter 39} Talar stress fracture (Chapter 39) Retrocalcaneal bursitis (Chapter 37)

Spondyloarthropathies Osteoid osteoma Regional complex pain syndrome type 1 (after knee or ankle inj ury)

Clinical perspective History The pain of plantar fascii tis is usually of insidious onset, whereas fat pad damage may occur either as a result of a single traumatic episode (e.g. jumping from a height onto the heel) or from repeated heel strike (e.g. on hard surfaces with inadequate heel support). Plantar fasciitis pain is typically worse in the morning, improves with exercise at first and is aggravated by standing.

Isotopic bone scan or MRI are the investigations of choice for stress fracture. MRI and ul trasound can each be used to confirm the presence and severity of plantar fasciitis. MRI reveals increased signal intensity and thickening at the attachment of the plantar fascia to the calcaneus (Fig. 4z.d on page 845) at the medial calcaneal hlberosity, often with edema in the adjacent bone. Ultrasound reveals a characteristic region ofhypoechogenicity. In plantar fasciitis, bone

Examination Examination of the rearfoot is shown in Figure 40.3. The windlass (or Jack's) test (passive dorsiflexion of the first metatarsophalangeal joint) is a quick and highly specific test for the plantar fascia 2 (Fig·4 0 .Jc). Biomechanical assessment is an important componen t of the examination and must include ankle, subtalar, and midtarsal joint range of motion. Functional assessment of forefoo t and first metatarsophalangeal joint range of motion can provide information on overall foot function. Inspection of footwear is also important. Close inspection of the soles of shoes can highlight asymmetrical wear, which may indicate biomechanical problems.

Figure40.3 Examination of the rear foot (a) Palpation- medial process of calcaneal tuberosity. Palpate plantar fascia attachment

Investigations X-ray only contributes to the clinical work-up of rearfoot pain in a small proportion of cases. It may reveal a calcaneal spur but, as this mayor may not be symptomatic, it does not add clinical utility. Plain X-ray is generally normal in stress fractures of the calcaneus, but if the injury has been present for many weeks, there may be a line of sclerosis (increased opacity). This appearance is characteristic of stress fracture in trabecular bone.

846

(b) Palpation- heel fat pad

Thus, the pathology resembles that of tendinosisj tendinopathy (Chapter 5) and the condition should be more correctly referred to as "plantar fasciosis"l or "fasciopathy." However, as nei ther of these terms is in common usage, we continue to use the traditional term, "plantar fasciitis," in this book.

Causes

(e) The windlass (or Jack's) test- passive dorsiflexion of the first metatarsalphalangeal joint

scan may demonstrate an increased up take at the attachment of the plantar fascia at the medial calcaneal tuberosity as an incidental finding; it is not usually done for that purpose.

Plantar fasciitis The plantar fascia plays an important role in normal foot biomechanics. The plantar fascia is composed of three segments, all arising from the calcaneus. The central, and clinically most important, segment arises from the plantar aspect of the posteromedial calcaneal tuberosity and inserts into the toes to form the longitudinal arch of the foot. The fascia provides static support for the longitudinal arch and dynamic shock absorption. Normal walking and running biomechanics involve subtalar joint supination at heel contact, pronation at midstance (to allow shock absorption), and re-supination at late stance. Tension in the plantar fascia in late stance, caused by dorsiflexion of the metatarsophalangeal (MTP) joints, helps to stabilize the foot and reduce tension in plantar ligaments and neural structures. Plantar fascii tis, an overuse condition ofthe plantar fascia at its attachment to the calcaneus, is due to collagen disarray in the absence of inflammatory cells.

Individuals with pes planus (low arches or flat fee t) or pes cavus (high arches) are at increased risk of developing plantar fasciitis. Pes planus places an increased strain on the origin of the plantar fascia at the calcaneus, as the plantar fascia attempts to maintain a stable arch during the propulsive phase of the gait. Excessive movement into pronation, or a lack of re-supination in late stance may also predispose to plantar fasciitis .4 In the cavus foot, there may be excessive strain on the heel area because the foot lacks the ability to evert, absorb shock, and adapt itself to the ground. Plan tar fasciitis commonly results [rom activities that require maximal plantarflexion of the ankle and simultaneous dorsiflexion of the MTP joints (e.g. running, dancing). In the older patient, it may be related to excessive walking in inappropriate or nonsupportive footwear) The American Physical Therapy Associations 2008 guidelines on heel pain and plantar fasciitis state that clinicians should consider reduced ankle dorsiflexion and increased BMI as risk factors for plantar fasciitis, especially in non-athletic populations.' Obesity and work-related weight-bearing are also independent risk factors} Plantar fasciitis is commonly associated with tightness in the proximal myofascial structures, especially the calf, hamstring, and gluteal regions) Tightness in these muscle groups can predispose to plantar fasciitis by altering the normal foot biomechanics outlined above. Hip muscle strength imbalances can also predispose to plantar fasciitis. A case-control study of 30 recreational runners with unilateral overuse injuries including plantar fasciitis, found significant reductions in hip Hexor and abductor strength compared with the uninjured side.G No significant sideto-side differences were found in uninjured control subjects.

Clinical features The pain is usually of gradual onset and felt classically on the medial aspect of the heel. Initially, it is worse in the morning and decreases with activity, often to

847

ache post-activity. Periods of inactivity during the day are generally followed by an increase in pain as activity is recommenced. As the condition becomes more severe, the pain may be present when weight-bearing and worsen with activity. 111ere may be a history of contralateral leg or foot problems in patients with abnormal biomechanics. Examination reveals acute tenderness along the medial tuberosity of the calcaneus, and this may extend some centimeters along the medial border of the plantar fascia. The plantar fascia is generally tight, and stretching the plantar fascia may reproduce pain, such as during the windlass test (Fig. 40.3c). Assessment of the patient's gait may reveal excessive supination or pronation. Both an abducted gait and calf tightness may reduce the sportsperson's ability to supinate, increasing the strain on the plantar fascia. Assessment of the patient's motor control through the single-leg squat test may reveal excessive subtalar and midfoot pronation, tibial internal rotation, and internal rotation and abduction of the hip. Individual assessment oflower limb muscle strength may reveal weakness in the tibialis posterior, calf, and hip abductor musculature. Assessment of the patient's single-leg balance may reveal toe clawing or reduced proximal muscle control. Toe clawing (excessive activity of the long toe flexors) can be an indication of weak intrinsic foot musculature or foot instability.

Investigations Ultrasound is the gold standard diagnostic investigation for plantar fasciitis, with swelling of the plantar fascia the typical feature. The thickness of the fascia may also be measured. X-rays are often performed but are not essential for the diagnosis. X-ray may show a calcaneal spur (Fig. 40.4); however, Lu et al. have confirmed that the spurs are not causally related to pain) X-ray appearances were unrelated to pain; it is important to explain these findings to patients.

Figure 40.4 Although calcaneal spurs can be rather large, they are not causally associated with plantar fasciitis. They are also found in asymptomatic individuals, as in this case, on both feet when only one is symptomatic, and they can enlarge even after symptoms have resolved self-massage with a frozen bottle or golf ball (Fig.40.5b) nonsteroidal anti-inflammatory drugs (NSA1Ds), which provide pain relief in some patients9 taping-two types of taping have been advocated: - taping the foot into inversion (Fig. 40.Sc) - low-Dye taping (Fig. 40.Sd) involves the application of rigid tape to the plantar aspect of the foot, with the aim of supporting the plantar fascia. Low-Dye taping can provide good

Treatment Treatment op tions for plantar fasciitis can be divided into two groups-those for the short term, and those for the long term. Treatment options for the short term include: avoidance of aggravating activity cryotherapy after activity stretching of the plantar fascia (Fig. 40.5a),3 gastrocnemius, and soleus

848

Fig ure 40.5 Treatment of plantar fasciitis (a) Stretching the plantar fascia

short-term pain relief and improved function for plantar fasciitis 10.1 1 silicone gel heel pad (Fig. 40.5e) corticosteroid injection 12 (Fig. 40.5f)-leve I2 evidence supports the use of corticosteroid injection in the short term.B It must be combined with other treatments such as stretching, biomechanical correction, and motor control re-education to prevent recurrence; there is some concern that

(b) Self-massage with a golf ball

injection is associated with an increased risk of rupture H 15 and fat pad atrophy iontophoresis 16-dexa methasone or acetic acid administered via iontophoresis can provide shortterm improveme nts to pain and fun ction extracorporeal shock wave therapy-this has been used for chronic cases but research evidence of its efficacy has been confl icting.17- lo

(d) LOW-Dye taping

(e) A silicone gel heel pad and heel cup

(e) Taping. The foot is placed into inversion by taping from the lateral aspect of the dorsum of the foot and across the plantar aspect before anchoring the tape to the skin over the medial arch

(f ) Corticosteroid injection

849

(9) Strasbourg sock

surgery-this is sometimes required in patients who remain symptomatic despite appropriate treatment; this is needed more in patients with a rigid, cavus foot whose plantar fascia tends to be shortened and thickened rather than in those with a pes planus foot type. - plantar fasciectomy-in an uncontrolled case series of plantar fasciectomy with neurolysis of the nerve to the abductor digiti quinti muscle, 92% of patients had a "satisfactory functional outcome"; time from surgery to return to work averaged nine weeks 18 - minimally invasive endoscopic plantar fascia release-this is a promising procedure that is gaining acceptance among foot surgeons.29, 30 R,s. 6J all of which could impact on stress fracture development.

The ocp is now used by many sportswomen and can be administered safely from the age of 16 years or three years past menarche. OCPs have numerous beneficial effects for the sportswoman in addition to contraception and cycle control-reduction in dysmenorrhea, premenstrual syndrome, menorrhagia, and iron deficiency anemia secondary to excessive mon thly blood loss." Women takin g the OCP have decreased frequency of dysfunctional uterine bleeding, functional ovarian cysts, pelvic inflammatory disease, benign breast disease, and ectopic pregnancies. The risks of ovarian and endometrial cancers are also reduced. However, optimal levels of bone density are achieved through natural menstruation physiology. Initial high-dose pills were associated with a high incidence of adverse effects, such as weight gain. The advent of low-dose pi11s reduced adverse effects. Most population studies indicate no overall effect on body weight while taking the OCp61L 6

Acomprehensive evaluation should include assessment of exe rcise behaviors, nutritional intake, weight control measures, psychological factors, and laboratory or diagnostic testing as approp riate.

Adult women TIle adult woman exerciser obtains num erous health benefits from her activity; however, she should be aware of some injuries that she is at increased risk of, and also should be aware of ongoi ng mai ntenance of care for specific women's issues.

Injuries Musculoskeletal injuries Three musculoskeletal injuries tha t occur more frequently in females than males are stress fractures, pateUofemoral problems, and anterior cruciate ligament repuhtre. Stress fractures Stress fractures occur more frequently in amenorrheic women than in those who are men struating normally, and menstrual status should be assessed in all sportswomen who present with stress fractures. However, stress fractures can also be related to training error, overuse, malalignment, and hard runn ing surfaces. (See also Chapter 5 and discllssion of stress fractures at specific skeletal sites, e.g. navicular stress fracture in Chapter 40.)

919

Special groups of part ic ipants Patellofemoral pain syndrome The increased Q angle at the knee caused by slanting of the femur may increase susceptibility of sportswomen to patel1ofemoral pain. This biomechanical abnormality may also increase susceptibility to the development of other overuse injuries of the lower leg (e.g. medial tibial stress syndrome). See detailed discussion of patellofemoral pain syndrome in Chapter 33 as well in the (finical Sports Medicine masterc1asses at www. dinicalsportsmedicine.com.

Anterior cruciate ligament rupture Women are two to eight times more likely to sustain an anterior cruciate ligament rupture than males,711 There are many theories as to why this difference in injury rate exists. These include both intrinsic and extrinsic factors. Intrinsic factors include joint laxity, hormonal influences, limb alignment, notch dimensions. and ligament size; extrinsic factors include type of sport. conditioning. and equipment/II Female athletes may be more predisposed to anterior cruciate ligament injuries during the ovulatory phase of the menstrual cycle.7,). 80 Sportswomen taking oral contraceptives demonstrate lower impact forces and reduced torques at the knee, increased hamstring to quadriceps strength ratios, increased stability on one leg, and decreased knee laxity relative to sportswomen not using the ocr. The use of the ocr in combination with neuromuscular training may increase the dynamic stability of the knee joint and may decrease injury risk in female athletes. Interventional measures such as these may perhaps reduce the risk of anterior cruciate ligament injury in this high-risk population.'')· ko Chapter 32 has a detailed discussion of this problem and relevant pre· ventive strategies,ill

Vulval injuries I njuries to the female genital organs occur occasion· ally and usually are associated with blunt trauma or repetitive impact. Vulval conhlsions and lacerations can occur from trauma related to falls and traumatic impact. Women performing sports requiring equipment that is in close contact with the body {such as gymnastics} are vulnerable. as are women performing sports such as water-skiing where sudden impact can lead to tissue damage. Contusions should be treated with the application of ice; lacerations may require surgical repair.

920

Breast care The breast is composed primarily of fatty tissue. Breast size and shape is largely determined by genetic predisposition but may be affected by general weight loss or weight gain. Breast changes are common in the premenstrual period. when the breast may increase in size up to 40%. The nipple contains smooth muscle fibers that respond to cold or tactile stimulation. Recommendations for breast care in sport are shown in Table 4}}

Trauma Breast trauma is not common but a contusion may occur as a result of a direct blow from a ball. racquet, or opponent. The contusion is associated with bleed· ing and swelling. It should be treated with ice, analgesics. and support. Occasionally. a deep hematoma wi11 require aspiration. It is important to reassure the sportswoman that there is no evidence that trauma to the breast causes tumors.

Nipple problems "Runners' nipples" is a common condition in which the nipples are irritated by rubbing against clothing during prolonged activity. This condition is common in both men and women. and is more likely to occur in cold weather where the nipple is more prominent and harder. It may be prevented by the use of petro· leum jelly, tape over the nipples, or a seamless bra. Cyclists also commonly develop nipple problems as a result of a combination of perspiration and cold. TIlis can be prevented by the use of appropri· ate clothing, especially a wind-breaking material over the chest.

Sports bras Excessive movement of the breasts, particularly in an up-and-down motion. can occur during exercise. This may lead to pain and discomfort, and affect sports performance. A number of specialized sports bras are now available. Sports bras should give support from above, below, and the sides. They should be made of a material that is firm, mostly non-elastic, non-abrasive. and of good absorptive quality. The straps should be of non·stretch material and, ideally, crossed or Y·shaped at the back There should be no seams or ridges in the nipple area, and no fasteners or hooks. The sports bra should be individually fitted and be comfortable both at rest and with vigorous activity. There should

Women and activ it y- related iss u es ac ross t h e lifespa n Tab le 43 .3 Recommendations for breast care in sport Issue

Garment solution

Increased physical

Advise garment suited to type of exercise: Advise exercise fo r health: impact- supportive, compression, seamless, include bra advice awareness that chaffing, bruising, irritation, sweat absorbent and pain are not normal and should be endurance-ventilated, scapu lar reinforcement, porous fabric addressed contact-protective padding refer to physician jf further evaluation

activity

Healthcare practitioner role

required Bruising

shoulder strap • anterior breast

Shoulder strap: wider shoulder straps, can add strap pads Anterior breast:

Address the co ntact component of sport: techn ique changes shell chest protectors

less anterior compression, separate cup style

game conduct

may help Nipple chafing

Hygiene issues:

Bra cups: seamless cups

dry nipples (change out of sweaty or wet

ensure proper size and fit

garments)

sweat absorbent material

air dry after showering moisturizers such as vitamin E cream or lanolin lubricants such as Bodyglide or Vaseline educate on signs of infection

Controlling breast movement

Advise proper posture:

Compression style garment:

rhomboid and scapular stabilization, and

full figure support Spandex body suit for additional support

strengthening to reduce forward posture

proper sizing and fit

gait and footwear to ensure co rrect movement patterns

also be provision for the insertion of padding for use in contact sports. Various degrees of padding can be added to the bra. In certain sports, such as martial arts and foot· ball, a plastic cup bra may be placed over the normal sports bra. Protective chest pads should be worn in softball and ice hockey, and are available in designs specific for women. A large proportion of women living with breast cancer experience bra discomfort while they exercise.Jt• The chest band has been identified as the bra compo· nent which causes the most discomfort to the patient with breast cancer. Band tightness is usually the acute cause of this discomfort, particUlarly for lumpectomy patients. Women living with a breast cancer diagnosis are particularly susceptible to fluctuating tissue edema during both treatment and exercise. A woman undergoing a lumpectomy experiences the partial removal of a breast, which can lead to asymmetrical breast mass. As bras are fitted to the larger breast, the smaller, treated breast frequently does not adequately

fill the bra cup, and may experience greater motion and consequently greater breast pain. This may be addressed by having bras personally customized. Breast sensitivity may also be seen in women with other conditions, such as following traumatic injury to the thorax or following open heart surgery.

Posture and therapeutic exercise It is not uncommon clinically to see women, particu·

larly younger women, with poor posture related to breast size. Anecdotally this is particularly common in swimmers and women with larger breasts. The women may present clinically with insidious onset of back or neck pain; alternatively they may present with an injury or other medical condition. Posture may be related in part to psychosocial factors. They may be presenting for treatment of back pain, or they may report increased sensitivity to the wea ring of a bra. In all of these situations, practitioners play a key role in educating women about posture and related breast care.

921

..•....

1llIAlUlJi'.iC&:

Spec i a l groups o f pa r t i cipa nts

For many women, education and exercise alone are sufficient to correct posture. Further assessment ofmobility and movement through the thorax, ing ribs and thoracic vertebrae, should be undertaken if a woman is reporting pain or dysfunction. Trigger points within the intercostal muscles may benefit from soft tissue techniques to restore normal muscle tone and function. Manual therapy can restore joint mobility and rib mechanics. Breathing disorders or

abnormal breathing mechanics must be addressed in order to normalize movement and any reported sensitivi ty. Education and individualized exercise prescription should be provided for posture, scapulothoradc stability, and normal breathing. Women recovering from any condition that involves the thorax (e.g. breast cancer, post-open heart surgery, post-thoracotomy) can benefit from such therapeutic interventions. Most women, including those with large breasts, can maintain a healthy active lifestyle with the correct fitting of a supportive sports bra. Despite this, some women report discomfort with high-impact exercises such as running. Deep-water running is a strenuous but more comfortable form of exercise for women with large breasts relative to running on a treadmill. This is sometimes part of the exercise prescription for women with large breasts. s;:

Exercise and pregnancy The prescription of exercise during pregnancy is an effective tool for improving general emotional wellbeing, maintaining optimal weight management, and controlling blood glucose. The PARmed-X is a validated screening tool to assess readiness for physical activity and screen for contraindications while providing current exercise education. S3 The current guidelines for exercise prescription during pregnancy refer to low-risk single The guidelines are listed on pages 923-24> after the box on the contraindications to exercise in pregnancy. In general there is good evidence to support regular moderate low-impact exercise in a low-risk pregnancy. Contact sports carry a high risk in the second and third trimester because direct trauma to the pelvis and lower abdominal area may occur. At that time the uterus is thinning with fetal growth and migrating to the abdominal cavity where there is less protection. For this reason, contact sports or sports with a high risk of collision should be avoided after the first trimester.

922

Potential risks of maternal exercise to the fetus Changes in fetal heart rate may occur in response to exercise; this seems to be related to gestational age and the duration, intensity, and type of exercise. Blood flow to the uterus during exercise is maximal at the area of attachment of the placenta, therefore minimizing the hypoxic effect on the fetus. Generally, increases in fetal heart rate ofbetween IO and 30 beats per minute are found fonowing maternal exercise. s, Occasionally, bradycardia (slowing of the heart rate) is observed. s6 The clinical significance offetal tachycardia or bradycardia is uncertain. The average birth weight of babies whose mothers have exercised intensively and very frequently during pregnancy is lower than that of babies born to sedentary mothers.S7 There do not appear to be any shortor long-term adverse sequelae as a result of this difference in weight between groups. There is a theoretical risk of premature labor associated with maternal exercise due to increased levels of noradrenalin (norepinephrine), which may cause increased uterine irritability and subsequent premature labor. This has not been observed in practice. The other major area of concern for the health of the fetus with maternal exercise is the risk of hyperthermia. Animal data suggests that a core temperature in excess of 39°C (rozOF) may result in neural tube defects in the fetus. This malformation is the result of failure of closure of the neural tube, a process that occurs approximately 25 days after conception. This has not been confirmed in humans. Pregnant women, however, should avoid hyperthermia during the first weeks of their pregnancy. Moderate exercise in normal environmental conditions results in only minimal increases in core temperature.

Risks to the mother The pregnant woman shows an increased susceptibility to musculoskeletal pain, especially the devel· opment of pain in the low back, sacroiliac region, or pubic symphysis. The mechanism of the development of low back and pelvic girdle pain in the pregnant woman probably relates to a combination of factors, including a change in the center of gravity upwards and forwards associated with forward tilting of the pelvis, an increase in lumbar lordosis, and loosening of ligaments associated with increased levels of the

Women and act i vity - re l ated i ssues ac r oss the li fespan

hormone relaxin. 88 The incidence oflow back pain can be reduced by careful attention to posture and avoidance of sudden movements as well as strengthening of the abdominal and back muscles. Pelvic girdle pain can be reduced by advice, and the use of a sacroiliac belt, stabilizing exercise, and acupuncture.8 ". 9 0 Another possible problem affecting the pregnant woman is hypotension. Postural hypotension results from prolonged standing whereby there is a decrease in cardiac output due to slowed venous return. Supine hypotension can occur with lying or exercising in the supine position. In the supine position, the uterus compresses the major blood vessels, resulting in reduced blood return to the heart and thus hypotension.

Restrictive lung disease Incompetent cervix/cerclage Multiple gestations at risk for premature labor Persistent 2nd or 3rd trimester bleeding Placenta previa after 26 weeks of gestation Premature labor during the current pregnancy Ruptured membranes Pre-eclampsia/pregnancy-induced hypertension

RelatiVe contraindications Severe anemia Chronic bronchitis

The advantages of exercise during pregnancy relate more to the general physical and psychological wellbeing of the mother rather than to effects on the pregnancy itself. Women who exercise prior to pregnancy and continue to do so during pregnancy, weigh less, gain less weight, and deliver slightly smaller babies than sed· entary women. Increased fitness may enable women to cope better with labor. Even overweight pregnant women who commence an aerobic exercise program can improve fibless throughout pregnancy.9 There is no evidence that women who have exercised during pregnancy have shorter or easier labors. Exercise during pregnancy is also valuable for the prevention and treatment of conditions such as ges· tational diabetes. The activation of large groups of muscles allows for an improved glucose utilization while simultaneously increasing insulin sensitivity.9 I

2

It appears that women who engage in

f:

Hemodynamically significant heart disease

Unevaluated maternal cardiac arrhythmia

Advantages of exercise during pregnancy

\'.!.,'l ('......

Absolute contraindications

recreational physical activity during pregnancy have approximately 50% reduction in the risk for gestational diabetes compared with inactive women. 9l

Active women also have approximately 40% reduction in pre-eclampsia risk.9}-9)

Contraindications to exercise during pregnancy Exercise is contraindicated in women with any serious or potentially serious complication of preg· nancy. A list of these contraindications is shown in the box. 96

Poorly controlled type 1 diabetes Morbid obesity Extreme underweight (BMI< 12) History of extremely sedentary lifestyle Intrauterine growth restriction in current pregnancy Poorly controlled hypertension Orthopedic limitations Poorly controlled seizure disorder Poorly controlled hyperthyroidism Heavy smoker IOIAs listed in the American College of Obstetricians and Gynecologists COG Committee Opinion No. 267. Exercise during pregnancy and the p05tpartum period 2002"" I!>lAdditional contraindications should be left for the physician to individualize

Guidelines for exercise during pregnancy The majority of women are able to perform exercise during pregnancy to benefit their health and wellbeing. Serious sportswomen who wish to continue intense training during pregnancy should he counseled on an individual basis. In most cases, providing the pregnancy progresses normally, they are able to maintain a reasonably high level of training until dis· comfort forces them to reduce their training, usually around the sixth month. Guidelines for exercise during pregnancy are listed beloW:96, 97 1. Prior to participating in an exercise program, it is recommended that women meet with their healthcare provider to fill out the PARmed-X for Pregnancy83 to determine any possible contra indications to exercise.

923

Spec i a l groups of part i c i pa n ts 2. Accumulate 30 minutes Of more of moderate exercise between three and five times a week. If a

woman has been sedentary prior to pregnancy, then new exercise regimens should be avoided until the

second trimester. All exercise should be gradually in low-impact aerobic introduced and

forms. 3. Avoid prolonged exercise in the supine position after

the first trimester. 4. Avoid exercise in hot weather.

5. It is recommended that an additional 1250 kJ (300 kca1) of nutrition be consumed for every exercise session including 250 mL (8 oz.) of fluid

Yoga is an excellent means of maintaining flexibility and relaxation. Excessive stretching should be avoided because the hormone relaxin loosens ligaments. Cycling has the advantage of being a non.weightbearing activity. In the middle and later stages of pregnancy, it may be advisable to use a stationary bike because of balance problems caused by the shift in the center of gravity. Cycling should be avoided in high temperatures or humidity. Water activities are popular during pregnancy because of the support provided by the buoyancy of the water.

intake.

6. Perform a good warm-up and cool-down. 7. Avoid excessive or ballistic stretching. 8. Wear a firm supportive bra.

9. Cease activity immediately if any abnormal symptoms develop (see Table 43.4).

Type of exercise

There is no one recommended type of exercise during pregnancy. Readers are referred to published guidelines for safe exercise during pregnancy.

Practical suggestions for the older person include parking further away at malls and shopping centers, taking the stairs instead of the elevator, or taking a 5. to 10·minute walk several times a day.

The aphorism "start low, go slow" applies in this population as it does in exercise prescription in generaL 1be clinician should set easily attai nable short-term goals and increase time spent pe rforming moderate activities by no more than 5% per week. The eventual goal is to accumulate 30 minut es a day of moderately intense physical activity on most days of the week (see also Chapters 16 and 60) that

93 8

includes a combination of aerobic, strength, and balance training.

The generally active older person For older people who are generally active, begin by increasing the volume of aerobi c exercise or resistance training. Aerobic exercises that are ticularly attractive to older individuals are cycling on a statio nary bicycle, brisk walking, swimming, and water aquatics. TIle person should warm up (e.g. slow walking) for 5 minutes and stretch slowly for 5- 10 minutes before exercising at a moderate level--one at which a conversation ca n be easily maintained. The person about to undertake res ista nce ing should also perform a warm-up and stretch first. Free weights and commercially available equipment are suitable for the older person exercising. Proper breathing consists of exhaling during the lift for 2-4 seconds followed by inhaling during the lowering of the weight for 4- 6 seconds, working through the entire range of motion (or as tolerated for those with arthritis). The Valsalva maneuver should be avoided, particularly in older people who are more prone to postural hypotension and syncope than their younger counterparts. The lifts should be separated by 2 seconds of rest. The goal is to perform one or two sets of 8-15 repetitions per set with {- 2 minutes of res t between sets. TIle patient should aim to lift a weight that is 70-80% of a one repetition maximum (IRM) or the most that he or she can lift th rough a full ran ge of motion at one time. The resistance should be increased no more frequently tha n monthly. Strength exercises should be followed by a cool-down and a stretch. Current evidence suggests that participants who undertake th is type of program twice weekly or more obtain benefi ts. Only the very unfit benefi t from a once-weekly program. Ie. The principles offoll ow-up and praise fo r progress, as ou tlined in the principles of exercise prescription (Chapter 16), apply particularly to older people, who may feel less confident about their ca pacity for activity. Please also see Chapter 54 (for exercise prescription for neurological conditions) and Chapter 60 (for exercise prescrip tion for va rious other conditions), which have relevance to the older person.

T he o l d er pe r son who exerci ses

Interaction between medication and exercise in the older person Many older people have at least one chronic medical condition, and m any have multiple ch ronic conditions for which medication is warranted. As a result, many older peopl e consume multiple medications. There are poten tial problem s associated with exercise and some of these drugs,

Medica tions affecting the reninang iotensin system Drugs affectin g the renin-angiotensin system (such as angiotensin -converting enzyme [ACEI inhibitors and angiotensin 11 receptor b lockers) lower peripheral vascular resistance. They are widely used to treat hypertension, sys tolic heart failure, and chronic kidney disease.

These drugs are suitable for the hypertensive athlete as they do not limit maximal oxygen uptake. Although the risk of dehydration among young people may have been over-represen ted in recen t years (Chapter 58). older peopl e who are taking these m edica tions may have an increased susceptibility to the effec ts of exercise-rela ted dehydra tion. The vasodilator effect may combine with fluid losses to cause hypotension and dizziness.

Beta blockers Beta blockers are used to treat hypertension, angina , heart failure, and cardiac dysrhythmias, as well as tremor and migraine; however, they may be less effective in older people than in middle-aged pa tients. These drugs are often prescribed after acute myocardial infarction . Beta blockers reduce cardiac rate and outp ut, and attenuate the normal physiological response to exercise. The lack of a tachycardia induced by exercise bothers some dislike the absence of th e "adrenalin surge." Older athletes who are taking beta blockers have a restricted exer cise capaci ty, particularly in endurance events. Adverse effects include postural hypotension, exacerbation of peripheral vas cular disease, excessive tiredness. impotence, and hyperkalemia. as well as the potential of masking hypoglycem ia in people with diabetes taking older n onselec tive agents.

Diuretics Systematic reviews and clinical guidelines recommend thiazide diuretics as a firs t-line therapy for hypertensionY' \H Diuretics are also used in the

treatmen t of heart fa ilure and flui d retention to increase urinary excretion of excess salt and fl uid. Older athletes who exercise in warm-to-ho t condition s and take diuretics are at a particular risk of dehydration. Less common adverse effec ts of thiazide diuretics include in creased blood sugar levels l9 and increas ed uric acid levels, which can be sufficient to precipi tate gout. A combina tion of an tihypertensive medication and vigorous exercise with associated dehydration may decrease the intravascular volume and cause postural hypotension , which may manifest itself as Jigh theadedness or fain ting. Prevention includes maintainin g adequate hydra tion and avoiding standing still immediately after exertion. Alternatively, other m edications may be availa ble. By defini tion. diuretics lead to increased fluid excretion through the renal tract and the diuresis occurs in relatively close proximity to oral ingestion. Older exercise participants attending classes or undertaking exercise ou tdoors may wish to delay the intake of their diuretic until after exercise to avoid the need to urinate excessively. This should be unde rtaken in co nsultation with th eir medical practitioner.

Other cardiac drugs Calcium-channel blockers and nitra tes (glyceryl trinitrate/nitroglycerin) are lIsed to treat hypertension and angina. TIley may impair cardi ac ou tput in exercise and cause peripheral vasodi latation, thus reducing performance. Peripheral venous pooling and the vasodi lata tion can lead to pos tura l hypotension. partiCUlarly during the cool-down period of exercise. These adverse effec ts should, h owever, be weighed up agai ns t the drug's direct effect on improving exercise tolerance by improving blood Bow to the heart. Antiarrhythmic drugs may also reduce cardiac output.

Non steroidal anti-inflammatory drugs Nonsteroidal anti-inflammatory drugs (NSA IDs) are commonly used for the treatment of arthritis and musculoskeletal problems in the older athlete. Adverse effects of these medications incl ude hyperten sion, fluid retention, renal impairment, and the developm ent of peptic ulceration and bleeding. The risk of bleedin g is grea tly increased when NSAIDs are prescribed in conjunction with warfarin. The risk of cardiac events in those taking certain NSAIDs wa s discussed in Chapter J3. The drugs should be used cautiously in older people and

939

discontinued if the patient complains of adverse effects. To minimize the risk of gastric irritation, these m edications should be taken with food or an acid-lowering medication (Chapter 13). Topical anti-inflammatory medications may be a useful alternative.

Medications affecting the central nervous system Hypnotic medications such as the benzodiazepines (including nitrazepam, diazepam, oxazepam, and temazepam) may affect fine motor skills, coordination, reaction time, and thermoregulation. This may lead to an increased risk of injury, especially in contact sports.

940

Often, people who commence exercise can reduce their need for these medications, as exercise can improve sleep patterns.

Insulin and oral hypoglycemic drugs The dosages of insulin and the oral hypoglycemic drugs may need to be reduced prior to exercise to avoid hypoglycemia (Chapter 53). Early symptoms of insulin resistance in older people can be postpran· dial hyperglycemia. Close monitoring of glycemic control and symptoms during exercise is necessary when initiating an exercise regimen in order to minimize the risk of hypoglycemia during exercise.

Th e o l de r pe r so n w h o exe r cises

m I.

performance: results of th e Lifestyle In terventions and

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Pain is weakness leaving the body. The principles of SpOlt and exercise medicine apply to a large extent when caring for military personnel. However, there are also important differences between military and athletic populations (Fig. 45.1). In this chapter, we discuss additional issues that are relevant when taking care ofmilitary personneL For those inex· perienced in working in this setting we introduce: the special culture of the military environment the epidemiology of military injuries common military injuries.

Figure 4 5. 1 Physical training in the military takes place within a unique culture and environment

US Marine Corps

Special military culture Providing primary care in a military setting offers unique challenges to the clinician. With regards to sports medicine. there are many special feahtres which influence the type and severity of injuries seen, and multiple factors which have an impact on the rehabilitation process. The clinician must become well versed in these unique factors in order to ensure appropriate diagnosis, treatment, and, mately, timely and effective return to full duties. One of the most important differences between civilian and military practice is the compulsory nature of physical training. To prepare a recruit for the ultimate goal of being fit for deployment, all military recruits undergo exercise regimens that are designed not only to improve their fitness, but also to prepare them physically and psychologically for extreme environments, discomfort, and pain. Furthermore, trainees have not always had a background of physical training, unlike an elite sportsperson who has come up through the junior ranks. With training in the military, it is the same goal whether a soldier is training to become a paratrooper, a weapons technician, or an administrator. It follows that most militaries encourage personnel to continue exercising despite early warning signs of pain that would normally cause civilian sportspeople to stop or slow down. Many recruits conceal the nature and extent of their injuries until graduation, for fear of medical "back squadding" (recruits held back in training), and a degree of derision from fellow recruits and their superiors. A soldier who fin· ishes a forced march by walking on a broken ankle for 12 miles with a funy weighted mcksack receives accolades and respect from peers and superiors.

943

Further to the drive toward pushing through pain. soldiers with a history of previous injury or who are diagnosed with post-traumatic stress demonstrate an increased threshold of pain-meaning they feel less pain for a given stimulus compared with controls." Pain thresholds may be related to environmental and psychological factors (for example, the common experience of WWII soldiers reporting no pain during the heat of battle despite severe injuries).l As a consequence of these changes in experiencing or reporting of pain, military members often present to military clinics with musculoskeletal injuries that are severe and debilitating, requiring longer periods of rehabilitation. Clinicians must keep this in mind when assessing injured patients, who may present stoically, making it challenging to determine the severity of pain or injury. A general tendency in medicine is to attribute a patient's symptoms to a unifying, single diagnosis. Because of the cultural overlay and late presentation, it is common for military patients to present with multiple concurrent pathologies. It is therefore very important to perform a thorough history and examination at the initial presentation, although time pressures may mitigate against this. Concurrent pathology should always be considered in a patient whose progress is slow or who does not respond to treatment considered appropriate for the initial diagnosis.

Epidemiology of military injuries Military populations undertake sh'enuous physical training and have high rates of injury compared with most sportspeople. Recruit populations have especially high incidence of injury and attrition. In New Zealand, the injury rate for recruits was more than five times that of trained personnel:1 High attrition rates represent a significant cost and a reduced return on investment. An injured soldier cannot perform his or her duties even if physically fit, and a moderate level of injury can impinge on the combat readiness of individual units. US military studies have shown that injury inci· dence rates range from 120 to 144 injuries/loo sol· diers/year' in infantry. special forces, and Ranger units. and 36o/IOo/year for Naval Special Warfare training. 1i A comparison of injury incidence and annual injury rates between different military recruit populations is shown in Table 45.1. Types and incidence of injuries by country are shown in Table 45.2, and cause of injuries in Table 45-3Injuries are not just a problem within a barracks setting. Non-battle injuries in US service personnel have been a major cause of medical evacuation from Iraq and Afghanistan. As at December 2006, 35% of all medical evacuations from Iraq and 36% from Afghanistan were due to non-battle injury.7 These constituted the largest single category of evacuations for both operations. Historically. lower limb comprised the bulk of

Table 45.1 Comparison of injury incidence and annual injury rates between different military recruit populations Gender

Incidence

Rate per 100/year

8

Fema le

42%

252

8

Male

23%

138

9

Male

31%

179

4415

9

Fema le

22%

127

9500

9

Male

11%

63

N

Year

M ilitary

1982

US Army

767

1982

US Army

3437

1994

South African Army

1261

1995

US Navy

1995

US Navy

Weeks

1995

US Marine Corps

1498

11

Female

49%

232

1995

US Marine Corps

396

11

Male

29%

137

1995

US Air Force

5250

6

Female

33%

285

1995

US Air Force

8656

6

Male

15%

130

1999

Australian Army

154

12

Female

35%

140

1999

Austra lian Army

554

12

Male

22.5%

90

2008

British Army

1480

12

Female

13.6%

58

2008

British Army

11937

12

Male

4.6%

19

944

M i l it ary p e r so nn e l Tab le 4 5.2 Types and incidence of injuries by country

Australian

Australian

South African

New Zea land

Body part

US infantry!

US military 14

recruits!!

army9

recruits 10

recruits 4

Ankle/foot

11,6%/20.8%

13%

18.3%/11.9%

3S%

Knee/lower leg

17.6% /15.1%

22%

32.1%n.3%

16%

low back

10.2%

20%

Spine

15.2%

Lower limb

39.6%

Upper limb

19.4%

80%

Table 4 5.3 Cause of injuries by country

Afghanistan/ Iraq Cause

US infantry 8

medical evacuations ll

Training-related

47%

19-21%

Falls/jumps

1B%

Motor vehicle-related

12-16%

Australian

New Zealand

recruits 12

recruits 4

19.2%

Runn ing

36.6%

Obstacle cou rse

14.6%

Basic training

Norwegian

28%

20-25%

Acute overexertion

37%

Team sports

25%

injuries (Table 45.2), but in Afghanistan and Iraq the back. knee, and wrist/hand were the most common body regions affected in those medically evacuated. This pattern of military injuries (i.e. being primarily lower limb in nature) presents in contrast to the Australian civilian workplace, where back injury is reported as the most common single injury (25%). followed by other injuries (37%), the hand (14.3 %) and. finally, lower limb injuries (10.8%).11Overuse is the most common cause of military training injuries reported in the Injuries cause disproportionate morbidity in young military populations. In a US mili tary population. injuries accounted for 56% of sick-call diagnoses. but caused nearly IO times the number of limited.duty days as illness. Soldiers with lower extremity running injuries spent seven times more days on a restricted duty profile than those with non-runn ing injuries. '4 In outpatient cl in ics, between 80-90% of all limited-duty days accrued by US Army trainees and infantry soLdiers were the Australian studies result of training-related have similarly found morbidity to be proportionately larger than the percentage ofinjuries.'> 10

Common military injuries The range of injury and illness facing clinicians who serve the m ilitary greatly exceeds that usually seen in civilian medicine. Mili tary members may be exposed to anything from extremes in temperature to biological and chemical agents. to communicable disease-including sexually transmitted and tropical illnesses. Traumatic injuries can result in concussion or traumatic brain injury, spinal cord injury. limb amputation, and a myriad of other injuries that can affect mUltiple systems and often require urgent care. For example, significan t risk for injUly occurs in diving operations, includin g submariner evacuation and rescue. However. the majority of the injuries tend to be related to environmental exposure (e.g. barotrauma, decompression illness, cold exposure. marine life exposure) rather than to mechanical mechanisms of injury. and thus most injuries are of a non-musculoskeletal nature. ,6.1, Psychosocial factors can influence the recovery trajectory of military sports injuries. Experienci ng deployment can affect emotional and psychological health. even in situations of peace-keeping missions, resulting in anything from fatigue and exhaustion to 945

depression, post-traumatic stress disorders. and suicidal ideation. Counter insurgency and peace-keeping operations have confused lines between friend and foe. Decisions affecting the lives of civilians. soldiers' team members. and the enemy may have to be made rapidly and in confused situations. The stress of the battle situation and post hoc analysis of alternative outcomes add to the risk of post-traumatic stress disorders. Coping strategies may involve high rates of substance use. such as smoking and alcohol dependency. Social support networks can be affected. These and other complicating factors may not be obvious but need to be considered when assessing and treating members presenting to the clinic. The following discussion addresses musculoskeletal and sports injuries; however, the reader is encouraged to maintain a broad perspective when assessing sports injuries. as often these other factors present comorbidly. Many "injury" chapters (Part B) in this book are relevant to the military population; the focus of this chapter is to highlight common specific militalY issues. and to highlight treatment approaches that are particular to this population.

Overuse injuries of the lower limb There are three peaks of overuse lower limb injuries in the military. The first and greatest is among recruits. the second in trained soldiers preparing for special forces selection. and a third in older soldiers training to pass annual fitness assessments. The syndromes of medial tibal stress syndrome, exertional compartment syndromes, and bone stress spectrum can coexist. All personnel presenting with lower limb injuries should be evaluated for spinal or discogenic pathology as well. The most common lower limb overuse injury is "leg pain due to medial tibial stress syndrome" (MTSS) (Chapters 5 and 35). Early identification with correction of training errors and biomechanical factors often leads to rapid resolution. Recalcitrant MTSS may require appropriate orthoses, corticosteroid injection, and rarely medial tibial fascial release. A significant proportion of recalcitrant MTSS has underlying exertional compartment syndrome. We have encountered resting compartment pressures >50 mmHg (normal resting , Jo nes BH e t al. Impact of

investigation idenlify a rubber matting ha2ard for anterior crudatc ligament rupture on an obstacle course. Mil Med 2002;r67{4) :359- G2.

sock systems on frequency and severity ofblisler injury in a Marine recruit population. Natick MA: USAR IEM, 1993· 33. Quinn

46. Pope RP. Rubber ma ttin g on an obs tacle course causes ante rior cnldate ligament ruptllres and its remova l

J. The effe such as sublingual nifedipine. RJI

Thermoregulation People with spinal cord injury are vulnerable to hea t injuryq due to a reduction in peripheral receptor and cooling mechanisms; sweating is impaired below the level of the spinal injury. SportspeopJe need to hydrate appropriately and acclimatize. Cooling and pre-cooling strategies offset the risk of heat illness and enhance endurance of These techniques include misting fans on the bench, ice packs to axillae and neck, and pre-cooling with iced "slurpee" drinks or ice baths. There is also an increased inability to maintain body temperature in a cold environment beca use of lack of sensory input and shivering response. Thus, adequate preventive measures, including appropriate clothing, are particularly important for the person with disabilities. (Chapters 58 and 59 have mOfe information on exercising in hot and cold climates.)

Pressure sores The insensible areas of skin below the level of the lesion are susceptible to unnoticed skin abrasions or pressure sores fro m prolonged sitting. Once esta blished, a pressure sore can entail months out of normal activities for th e individual. RAe-

0.... 71:J'40"C (!04' F), which is a recognized trigger in BrS.('5 Affected individuals aTe advised to abstain from chronic or prolonged intensive exercise. The leD is the only established treatment to preven t seD and is reserved for survivors of aborted SeD, and those with sustained ventricular arrhythmias and unheralded syncope_

Catecholaminergic polymorphic ventricular tachycardia Catecholaminergic polymorphic ventricular tachycardia (CPYI) is a hereditary ion channel disorder characterized by adrenergically mediated polymOl·· phic ventricular tachyca rdia due to mutations within genes encodin g the ryanodine receptor calsequestrin or the ankyrin-B proteins. Intensive physical exercise (e.g. swimming) or emotional stress are well recognized triggers for seD particularly in childhood and adolescent sportspeople.Cry Stress-induced syncope is one clinically recognized manifestation. 61 . 68 Typically, the baseline ECG/EKG is norm al; however, exercise stress testing may demonstrate multifocal ventricular premature beats, which. in the context of unheralded syncope, should raise clinical

1007

,

suspicion of the condition in individuals with a structurally normal heart. Ventricular tachycardia with a beat-to·beat 180 alternating QRS axis (bi-directional ventricular tachycardia) is considered to be highly characteristic of CPVT; however, this is an exceptionally rare manifestation of the disorder. Prevention of SCD includes medical therapy with beta blockers and avoidance of moderate- to high-intensity exercise. 68 0

SCD due to acquired cardiac abnormalities Myocarditis Myocarditis is usually due to a viral illness. It accounts for 7% of all SCDs in sportspeople. The inflammation and subsequent focal necrosis of the myocardium is thought to be the substrate for malignant ventricular tachyarrhythmias causing sudden death. Most affected individuals experience coryzal symptoms and a mild febrile illness; however, sudden death in a relatively asymptomatic athlete is the commonest presentation. Overt cardiac symptoms are rare and include chest pain, dyspnea, and palpitation. The ECGjEKG usually reveals non-specific ST and T wave abnormalities but may be normal. Echocardiography may also be normal in mild cases. A raised serum cardiac troponin is useful in confirming the diagnosis in an athlete with a febrile illness associated with chest pain, palpitation, and non-specific ECGjEKG abnormalities. 69 Athletes with proven myocarditis should abstain from strenuous exertion and competitive sport for six months,J.o. 3'

Commotio cordis Commotio cordis refers to SCD from ventricular fibrillation resulting from blunt trauma to the chest wall. The precise frequency of the problem is unknown but it has been reported with increasing frequency in the past decade. The incidence is more common in children and adolescents due to their relatively thin and compliant chest walls. Sports usually associated with commotio cordis include baseball, field hockey, lacrosse, ice hockey, karate, and judo. The victim is often struck by an innocentappearing blow or a projectile object regarded as a standard implement of the game. Sudden death due to ventricular fibrillation is instantaneous. 70

1008

Animal experiments in a juvenile swine model have provided insights into the mechanism responsible for ventricular fibrillation. Induction of ventricular fibrillation occurs folIowing chest wall blows during a vulnerable window just before the peak of the T wave. A rapid rise in left ventricular pressure follows which is thought to activate ion channels via mechano·electric coupling. The generation of an inward current via mecllanosensitive ion channels results in augmentation of repolarization and nonuniform myocardial activation, and is the cause of premature ventricular depolarizations that trigger ventricular fib rillation in commotio cordis. Survival after commotio cordis is only 15% and only possible with prompt cardiac defibrillation. The velocity and hardness of the projectile object are recognized determinants of ventricular fibrillation. Several measures to prevent commotio cordis have been suggested, which include use of softer bans than traditional standard hard balls in hockey and baseball, and the use of chest barriers in sports vulnerable to commotio cordis?' Use of automated external defibrillators (AEDs) in young athletic individuals vulnerable to such trauma has saved lives.

Evaluation of an athlete for conditions causing sudden cardiac death History, examination, and investigations help in the evaluation ofan athlete at risk ofsudden cardiac death. The box on pages 1010-12 contain three common diagnostic conundrums facing the clinician.

History Most athletes are evaluated as part of cardiovascular programs implemented by sporting organizations to exclude potentially lethal inherited or congenital cardiac disorders prior to clearance for competition. Rarely, cardiovascular evaluation may be triggered because of symptoms of cardiovascular disease or a family history of premature cardiovascular disease or SCD in a first-degree relative (parent, sibling). In many situations, athletes are investigated at centers with expertise in conditions capable of causing SeD in athletes (particularly cardiomyopathy) as well as knowledge regarding the impact of cardiovascular training on cardiac size in order to enable the differentiation between physiological adaptation and cardiac pathology (see Chapter 49 for more information on the differentiation).

Sudd en ca rdia c de a th in s port Most athletes are asymptomatic but the presence of chest pain, dyspnea disproportionate to the exercise performed, palpitations, dizziness, or syncope during exercise are ominous symptoms and warrant thorough evaluation (Chapter 49). It is prudent to ascertain any family history of premature cardiac disease or SeD in first-degree relatives as most conditions discussed above are hereditary. Ventricular arrhythmias in family members m ay present as syncope. epilepsy, or unexplained drowning, and inquiry into these circumstances may provide further important information regarding serious familial cardiac disease. Where possible, it is important to obtain post-mortem reports on first-degree relatives who suffered premature SeD as this may prove useful in differentiating death from a hereditary disorder (such as HCM) and a sporadic disorder (such as CCAA).

Physical examination General physical examination may prove useful in identifYing signs of Marfan syndrome (Fig. 48.7) and peripheral stigmata of familial hypercholesterolemia (Fig. 48.8). Cardiac auscultation may raise suspicion of aortic stenosis and HCM (of which approximately 25% have resting left ventricular outflow obstruction).

12-lead ECG/EKG The I2-lead ECG/EKG permits the diagnosis ofWPW and congenital LQTS, and the presence of certain repolarization patterns provides vital information regarding the possibility of an underlying cardiomyopathy; the ECG/E KG is abnormal in over 90% of individuals with HCM. The presence of deep (>-0.2 m V) T-wave inversions in leads other than III, aVR, and VI should result in further investigation for cardiomyopathy. Contrary to previously published literature, our experience suggests that deep T·wave inversions are a rare manifestation of cardiovascular adap· tation in adult and adolescent athletes 71 but are common in HCM and may be present in almost any lead (Fig. 48.9 panel A). Additional electrocardiographic abnormalities in HCM include voltage criteria for left atrial enlargement, extreme leftward axis, ST-segment depression. pathological Q waves, and left bundle branch block. Although individuals with HCM commonly exhibit high voltage QRS complexes, the presen ce of isolated Sokolow- Lyon

voltage criterion for left ventricular hypertrophy is rare in HCM and more suggestive of physiological cardiac adaptation. T-wave inversion beyond VI (and up to V4) may be normal in juvenile athletes and Afro-Caribbean athletes but their persistence in Caucasian athletes aged >16 year s should prompt furth er investiga· tion for ARVC (Fig. 48.9 panel B) P T-wave inversion may also be identified in athl etes with dilated cardiomyopathy an d LQTS.

Echocardiography Echocardiograph y is the gold standard investigation for the diagnosis of HeM and valvular heart disease; however, it only proves diagnostic in relatively advanced cases of ARVC. The echocardiographic assessment of an athlete with chest pain or syncope should also involve identification of the origins of the coronary ostia to rule out the diagnosis of anomalous coronary origins, as exercise testing lacks sensitivity and is invariably normal in these conditions.

Further investigations Some sportspeople require further electrocardiographic, imaging, and invasive electrophysiological investigations for the purposes of diagnostic clarification and risk stratification for SCD. Exercise testing and 24-hour Holter monitoring provide prognostic information in HeM and diagnostic information in ARVC and LQTS. Cardiac magnetic resonance facilitates the diagnosis of ARVC and HeM , and magnetic resonance coronary angiography is the investigation of choice for confinning the diagnosis of CCAA. Electrophysiological studies provide prognostic information in WPW. In the past two decades, there have been major advances in the m olecular genetics of HCM, ARVC, and LQTS. However, marked genetic heterogeneity and incomplete knowledge of causal mutations do not currently allow timely diagnosis in the majority of affected individuals. Additionally, failure to identifya genetic abnormality when screening for known mutations for a particular disorder such as HeM cannot be regarded as exclusion, as many mutations are yet to be identified. Continuing advances in molecular genetics and refinement of genetic analytic techniques hold promise and may prove invaluable in facilitating diagnoses in difficult clinical scenarios.

1009

Athlete's heart vs hypertrophic cardiomyopathy (HeM) Regular participation in sport is associated with modest increases in ventricular wall thickness and cavity size as well as enhanced diastolic filling. This reversible physiological cardiac remodeling enables enhanced left ventricular filling and the augmentation of a large stroke volume even at rapid heart rates for sustained increases in cardiac outpUt. 14 A small proportion of male athletes, predominantly involved in endurance sports, demonstrate extreme phYSiological adaptation with left ventricular wall thickness measurements of 13- 15 mm.75 Although the majority of individuals with HCM have a mean left ventricular wall thickness of 18- 20 mm, approximately 8% have morphologically mild hypertrophy in a lower range. Therefore a male athlete with a wall thickness of 13-15 mm falls into a grey zone where the differentiation between physiological left ventricular hypertrophy (LVH) is crucial, since diagnostic errors have the potential for serious consequences In the majority of athletes, the differentiation between athlete's heart and HCM is possible with echocardiography alone. Physiological LVH is homogeneous and associated with enlarged chamber size and normal indices of diastolic function. In contrast, individuals with HCM often show bizarre patterns of LVH, small chamber size, and impaired diastolic function. End-diastolic LV dimensions (LVEDD) >55 mm are common in trained athletes but rare in HCM where LV cavity size is most often 1 mm in depth from baseline in two or more adjacent leads not including aVR orVl

5T-Segment depression

2:1 mm in depth in two or more adjacent leads

Pathologic Q waves

>3 mm in depth or >0.04 sec in duration in two or more leads

Complete left bundle branch block

QRS >0.12 sec, predominantly negative QRS complex in lead Vl (QS or r5t and upright monophasic R wave in leads I and V6

Complete right bundle branch

QRS >0.12 sec, terminal R wave in lead V1 (rsR'), and wide terminal S wave in leads

block

1 andV6

Intra-ventricu lar conduction delay

Non-specific, ORS >0.12 sec

Left atrial enlargement

Prolonged P wave duration of >0.12 sec in leads 1or II w ith negative portion of the P wave 2:1 mm in depth and 2:0.04 sec in duration in lead Vl

Left axis deviation

-30· to - 90·

Right atrial enlargement

High/pointed P wave 2:2.5 mm in leads II and III orVI

Right ventricular hypertrophy

Right axis deviation 2:120·, tall R wave in Vl + persistent precordial 5 waves (R in V1 +SinV5 >10.Smm)

MobitzType 11 second degree AV

Intermittently non-conducted P waves not preceded by PR prolongation and not

block

followed by PR shortening

Third degree AV block

Complete heart block

Ventricular pre-excitation

PR interval

in whom there is a documented genetic disease in the family.

Temporary and permanent disqualification from sports Careful activity recommenda.tions involving temporary or permanent sports disqualifica tion for sportspeople with identified cardiovascular disease should be made in consultation with a cardiologist. Exercise recommendations in sports peop le with underlyin g cardiovascular disease susceptible to s udden ca rdiac death are predicated on th e likelihood that in tense athl etic training a.nd competition act as a trigger to in crease the risk of death or disease progression. l6 The 36th Bethesda Conference sponsored by the American College of Cardiology J6 and the European Society of CardiologySI provide eligibility recommendations for competitive sportspeopJe with cardiovascular ab normalities. Th ese expert consensus recommendations provide a framework on which to base clea rance decisions once a cardiovascular abnormality is identified, taking into account the severity of disease, potential for sudden death or disease progression, and the type and intensity of exercise involved in a particular sport. Withdrawal from athletic training and competition can reduce

----

Ch L'l, pter; 49

the exposure risk in sportspeople who have disorders predisposing them to sudden cardiac death:;" Low intensity competitive sports such as golf and bowling are still allowed. Individuals disqualified from competitive sports should be guided to engage in recrea tional exercise considered to be safe in order to maintain general health. The American Hea rt Association provides recomm endations for physical activity and recreational sports participation for young patients with genetic cardiovascular diseases, which is a useful s tarting point)) Many experts suggest that the level of exertion be guided by the ability to converse during the activity. If an individual is so dyspneic that they can no longer talk, th e level of exertion is too intense. In some cases, early detection of clinically significant cardiovascular disease may permit timely therapeutic interventions, such as implan table cardioverter-defibrillators (I CD) , that alter clini cal course and significantly prolong life. Although there is controversy about sportspeopJe with ICDs competing, the Bethesda guidelines do not advise itY' The implantation of an IC D should not allow a return to sport in those with underlying structural hea rt disease that would oth erwise prohibit com petition. There is concern about sports triggering ventricular arrhythmias, heightened sympathetic tone which may make arrhythmias more resis tant to defibrillation , and damage to the ICD system.

Summary Cardiovascular symptoms in sportspeople warrant a comprehensive diagnostic evaluation to rule out conditions that pred ispose to sudden dea th . While not all sports people with underlyin g heart disease manifest symptoms, prodromal symptoms such as syncope. exertional chest pain, excessive dyspnea/fatigue, and unexplained seizure ac tivity may occur in some sports people as warning events prior to sudden cardiac death. Careful evaluation of sportspeople with cardiovascular symptoms can detect po tentially leth al cardiovascular disease and, through appropri. ate treahuent and ac tivity modification, reduce the risk fo r sudden death in s port.

1035

--"

m t.

when screening for inherited cardiac pathologies:

REFERENCES

Maron BJ, Doerer

n, Haas TS et a1. Sudden deaths

in young competitive athletes: analysis oft866 deaths in the United States, 1980-2006, Circulation 2009; 119 (8): 108 5-92. 2.

Maron BJ. Sudden death in young athletes. N EnglJ

Med 2003;349(1l):roG4-75. 3. AsifI, Hannon K, Drezner J et aI. Incidence and etiology of sudden death in NCAA athletes. elin J Sport Med 2010;20(2):136,

4. Campbell RM, Berger S, Drezner

J. Sudden

cardiac arrest in children and young athletes: the

importance of a detailed personal and family history in the pre-participation evaluation. Br J Sports Med 20 °9:43(5):33 6 -41.

5. Maron 81, Shirani

J, Paliae LC et al. Sudden death in

young competitive athletes. Clinical, demographic, and

pathological profiles.JAMA 1996;276(3):199-204. 6. Basso C, Maron BI, Corrado 0 et at Clinical profile of congenital coronary artery anomalies with origin from the wrong aortic sinus leading to sudden death in young competitive athletes. J Am Coli Cardiol 2000;35 (6): 14 9 3-5 01. 7. Tester OJ, Spoon DB. Valdivia HH et al. Targeted

recommendations: a Dutch experience. Br J Sports Med 2°°9;43(9):7°8-15. 15. Hevia AC, Fernandez MM, Palacio JM et aL ECG as a part of the preparticipation screening programme: an old and still present international dilemma. Br J Sports

Med 20n;45(10):776-9. 16. Baggish AL, Hutter AM Jr, Wang F et a1. Cardiovascular screening in college athletes with and without electrocardiography: a cross-sectional shtdy. An11 Intem

Med 2010;152(5):269-75. 17. Orezner J, Corrado O. Is there evidence for re Twenty per cent of patients with established reflux consider exercise to be the major contributor to their symptoms. The mechanism by which exercise causes reflux is not wen understood, as reflux is normally associated with relaxation of the lower esophageal sphincter. This has not been described with exercise. Reflux appears to be more common when exercise is performed after a meal. Importantly, exercise does not appear to have any effect on gastric acid secretion.

? R4('

0'""

II:J"$'>,

Distinguishing between chest pain due to gastroesophageal reflux or esophageal muscular spasm, and chest pain due to chest wall or cardiac causes can be difficult. Any sportsperson presenting with chest pain on exertion must be thoroughly assessed to exclude cardiac causes.

Much attention has been paid to the factors that may affect the gastric emptying rate. Exercise at a very high intensity reduces the gastric emptying rate. However, as this level of exercise intensity cannot be maintained for long periods, its effect on the gastric emptying rate may be fairly insignificant. Increased volume in the stomach results in an initial rapid emptying, followed by a phase of reduced emptying once the volume of the stomach has decreased to about 30% of its initial content. Until recently, it was thought that osmolality was an important factor in the rate of gastric emptying. While it is true that liquids empty more quickly than solids, there does not appear to be significant differences in the gastric emptying rate for liquids of different osmolality.4.) Other factors that may be involved include gastrointestinal hormone levels, particle size, meal volume, dietary fiber, gastric acidity, and the sportsperson's anxiety level.

Treatment The treahuent of upper gastrointestinal symptoms associated with exercise is aimed at reducing the contents of the stomach during exercise. This is achieved by avoiding solid foods for at least three hours before intense exercise. The pre-exercise meal should be high in carbohydrate and low in fat and protein.

If additional measures are required. the use of antacid medication, in either tablet or liquid form, may reduce the incidence of heartburn and upper abdominal pain. Antacids usually remain in the stomach for 30 minutes. If this is not sufficient, the use of histamine H 2 -receptor antagonists (such as ranitidine and cimetidine) may occasionally be necessaly. Domperidone 10-20 mg I hour before meals may also be effective. Sportspeople in prolonged endurance events (over 4 hours' duration), who need to consume food while exercising, are particularly susceptible to upper gastrointestinal symptoms. Chewing gum is a mechanical means of stimulating gastric emptying and avoids possible complications of medications. Always trial any chosen intervention before "race day."

Gastrointestina l bleeding An occasional bloody stool is frequently noted by runners 6 and the incidence of occult bleeding is high.i As the amount of bleeding in most cases is small, most sportspeople are not affected clinically; however, occasionally iron-deficiency anemia may occur. Reduced iron stores are denoted by a low serum ferritin level. The most frequently reported site of exerciseassociated gastrointestinal hemorrhage is the fundus of the stomach. The mechanism underpinning this transitory hemorrhagic gastritis is uncertain. Ischemia may playa role, as may direct trauma from the diaphragm. In susceptible individuals, the gastritis may result in part from the general stress of competition along with the associated rise in key stress hormones such as adrenalin (epinephrine) and cortisol. Nonsteroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal bleeding in runners. 6 . 7 A Mallory-Weiss tear secondary to forceful vomiting may present with signs of upper gastrointestinal bleeding. No examples of bleeding from the small intestine have been reported. However. colonic bleeding has been observed, particularly from the proximal colon. The etiology of gastrointestinal bleeding associated with exercise is uncertain and is likely to be multifactorial. During exercise, blood flow is diverted from the splanchnic bed to the exercising muscles. Blood flow to the gastrointestinal tract may be reduced by as much as 75% during intense exercise. s A number of other factors may contribute to a reduction of blood flow. Such factors include exercise in the fasted state, as the absence of nutrients within

1057

Management of med ical pro b lems the intestine reduces the blood flow to that area. Also, high thermal stress, dehydration, and high exercise intensity playa role. It must be remembered that gastrointestinal bleeding in a sportsperson is not necessarily ated with exercise, and the sports person with obvious gastrointestinal bleeding should be fully investigated to determine the source of the bleeding.

Treatm ent If no obvious cause of the bleeding is established, ensure adequate hydration to prevent aggravation of the relative ischemia. As the mechanical effect of jarring while running is thought by some to be a contributory fac tor to gastrointestinal bleeding, the amount of jarring should be reduced by using appropriate footwear and avoiding running on hard surfaces. Those sportspeople with a known tendency for gastrointestinal bleeding and those who complain of fatigue should have the state of their iron stores assessed by measurement of their serum ferritin levels. Serum ferritin levels of less than 30 ngjmL in women and 50 ngjmL in men indicate reduced iron stores.

Abdominal pain Many sportspeople complain of a sharp, colicky pain in the left: or right upper quadrant during strenuous exercise. This is commonly referred to as a "stitch." The exact cause of this common phenomenon is unknown but it may be due to muscle spasm of the diaphragm or trapping of gas in the hepatic or splenic flexure of the colon. This condition has often been thought to be associated with exercise undertaken soon after eating a solid meal. There is no proof of this; however, avoiding a solid meal prior to exercise may be an appropriate treatment. Exhaling on foot-strike on the opposite side to the pain may be helpful. Occasionally, athletes get a "claudication-type" abdominal pain. This occurs in association with intense, endurance exercise and is thought to occur as a consequence of relative ischemia due to shunting of blood away from the gastrointestinal tract to the exercising muscles. 8 This effect is aggravated by dehydration. A rare cause of abdominal pain is "cecal slap" on the right psoas muscle. The possibility of abdominal pain being referred from the thoracic spine should always be considered. 1058

A thorough examination of the thoracic spine should be performed in any sportsperson who complains of abdominal pain. Hypomobility detected in one or more intervertebral segments should be corrected by manual therapy techniques, and the effect on the sportsperson's symptoms noted.

Dia rrh ea Diarrhea appears to be more frequent with exercise,,) especially with long-distance running; as a result the terms "runner's trots" and "runner's diarrhea" have been coined to describe the condition. Sportspeople may complain of an urge to defecate while running, and approximately half of those who experience this urge to defecate achtally complain of episodes of diarrhea during running. The incidence of runner's diarrhea seems to be related to the intensity of the exercise and occurs more commonly in competition than in training. The anxiety associated with competition may be a contributory factor. The exact cause of runner's diarrhea is uncer· tain. Relative intestinal ischemia, described previously, may be a contributory factor. An increase in intestinal motility may also contribute. Studies of the relationship between intestinal transit time and exercise have shown conflicting results; however, it would appear that intestinal motility is increased with intense exercise. This increase in gut motility and changes in intestinal secretion and absorption may be related to the increased level of endorphins associated wi th exercise. When faced with a patient with diarrhea, the clinician should also seek a history of vitamin and mineral supplementation, or ingestion of caffeine or artificial sweeteners prior to exercise. Each of these may contribute to runner's diarrhea. R4 (' '0"'"

Acute diarrhea is usually due to an infective ca use and may be viral or bacterial.

ler",'" Acute diarrhea is a particular problem for sportspeople when they are traveling away from home and is further considered in Chap ter 6+ In the 24 hours prior to major competition, team physicians generally prescribe norfloxacin (800 mg) or ciproftoxacin (I g) with loperamide (4 mg) to try to provide rapid symptom relief Sportspeople with chronic diarrhea should be fully investigated to exclude any other abnormal-

---r!',

I

':

G astro i ntestinal symptoms dur i ng exer cise ity (e.g. inflammatory bowel disease. malabsorptive disorders).

Treatment The treahnent of sportspeopJe with exercise-related diarrhea is often diffic ult. Dietary changes should include reduction of the fiber content of the diet in the 24 hours prior to intense competitive exercise. If the problem persists, prophylactic antidiarrheal medication (such as loperamide) may be used; however, this should not be llsed on a regular basis. Antispasmodics (e.g. mebeverine) may be useful.

Exercise and gastrointestina l diseases Lactose in tolerance A limited number of people lack the enzyme lactase, which is necessary for the digestion oflactose or milk sugar. Asian and African populations typically display an absence of lactase. Al so, adult lactase has only about 5% of the activity of childhood lactase. Lactose intolerance leads to gastrointestinal disorders resulting in cramps, flatulence, and diarrhea. Sportspeople sufferi ng from lactose intolerance need to avoid dairy products. with the possi ble exception of yoghurt. The lactose in yoghurt is la rgely broken down by the bacterial cultures present. It is important that sports people who avoid lactose ensure an adequate dietary intake of calcium and protein via alternative sources such as soy-based products (including milks, yoghurts. cheeses, and ice-crea ms). An often unrecognized source of lactose is highprotein drinks and sports supplements. Also, temporary lactose intolerance may follow acute infective diarrhea (particularly if caused by rotavirus). Therefore, milk-based products should be among the las t to be reintroduced to the sports person's diet after such an episode.

Celiac disease Celiac disease is characterized by abnormal mucosa in the small intestine induced by a component of the gluten protein of wheat. Barley, rye. and oats also con tain gluten. Anemia is often seen in sport'speople with celiac disease due to malabsorption of iron and folate. Howell-Jolly bodies may be seen on the blood film due to folate deficiency. Prevalence data suggest that symptomatic or latent celiac disease affects up to I in 200 people in most Western countries. It may not always present with the classic symptoms of diarrhea and bloating; tiredness is a common presentation (Chapter Laboratory

I

C!lia,Bs .er51

testing may show high levels of IgA antien domysial and IgA tissue transglu taminase antibodies. However, any of the IgA tests may be falsely negative in up to 3- 5% of celiac patients. mainly in those with associated IgA deficiency_" Definitive diagnosis is via multiple sm all bowel biopsy, showing typical mucosal changes of subtotal villous atrophy. Sportspeople diagnosed with celiac disease are given comprehensive lists of alternative high· carbohydrate food sources and shou ld consult a dietitian for ass istance in planning a nutritionally adequate diet. Unfortunately, m any people selfdiagnose their symptoms as being due to gluten intolerance. They may reduce their gluten intake and note an improvement. It then becomes very difficult to convince these people that they need to go back onto a die t containing gluten for one month prior to having a small bowel biopsy to definitely prove the diagnosis.

Irritable bowel syndrome Irritable bowel syndrome is a very common gastrointestinal disorder that causes lower abdominal pain and constipation alternating wi th diarrhea. The cause is not known but there seems to be a strong association between this condition and the intestinal res ponse to emotional stress (e.g. sport· ing competition). Treatment includes a balanced fiber diet together with antispasmodic agents (e.g. dicyclomi ne).

Non-steroidal anti-inflammatory drugs (NSAIDs) and the gastrointestinal tract NSAIDs are used by up to 35% of sportspeople in competition. 'l During exercise. the reduction of gastrointestinal blood flow increases the potential for gut toxidty. Gastrointestinal adverse effects are the most common reason for cessation of use of these medicines both in the general and the athletic population. They can affect any portion of the gastrointestinal tract as ind icated in Table 51.3 overleaf. There are two groups of sports people who present for clinical evaluation. By far the most common are healthy individuals who experience dyspepsia with NSAID use. This affects about 1 0 % of the population. Strategies which ca n be include: using a tradi tional (non-specifi c) NSAIO under cover of a proton pump inhibitor (PPJ) B using a cydooxyge nase (CQX)-2 agent

1059

,

Table 51.3 Gastrointestinal related adverse effects of NSAIDs !(j' Only use NSAIDs for conditions with inflammation.

1060

Limit dietary fib er intake prior to competition To ensure that the gut has minimal food content prior to racing, it is necessary to reduce the fiber content of the diet in the days preceding the race. This means, in the two days prior to the competition, change from wholemeal and wholegrain varieties of rice, breads, and cereals to the more refined alternatives. Avoid fresh fruit and vegetables with skin, legumes, and heavy seasonings such as garlic, pepper, and curry. Runners who regularly suffer from diarrhea or the urge to use their bowels regularly during a race may

Minimizing gastrointestinal tra ct exercising-advice for

lien _

1. Train and compete with your upper gut as empty as

possible (at least 3 hours after a meal). 2. Limit the fat and protein content of your last meal

before exercising. 3. Prevent dehydration- get used to drinking during

training and long events. foods prior to competition. Only take tablets (NSAIDs) on the advice of a doctor, if you have an injury where inflammation plays a large role. Otherwise, use paracetamol (acetaminophen). Always take NSAIDs on a full stomach. If you have a family history of bowel or stomach cancer, consider regular screening examinations. If you develop "red flag" symptoms (e.g. upper or lower gastrointestinal bleeding, unintended weight loss), see your doctor and get these properly evaluated. If nerves are a likely cause of gut symptoms, consult a sports psychologist.

4. Avoid S.

6,

7.

8.

9.

exercise

benefit from a liquid nutrition supplement during the last days preceding the competition. This will ensure that the gastrointestinal contents are minimized prior to the race. An alternative approach is to consume only fluids prior to competition on the day of the event.

liquid meal replacements a useful option. Boiled white rice, pasta, pancakes with syrup, canned fruit, peeled potatoes, plain dry biscuits, and plain rolls or bread all make good choices. Practice food intake during training.

Avoid solid foods during the last three hours prior to the race

A sample 24-hour pre-race diet that will help minimize gastrointestinal problems during a race is shown in the box below. This plan provides approximately '4700 kJ (l500 kcal) with 76% of the energy from carbohydrate and less than 20 g of clietary fiber.

Sample pre-event diet To ensure that the stomach is empty, it is important that the pre-event meal is consumed at least three hours before the race begins. However, in some sportspeople with a low gastric emptying rate. the pre-event meal may need to be accompanied by a prokinetic agent (e.g. domperidone) and eaten up to four to six hours prior to competition. Fluids, however, should still be consumed in the period leading up to the race.

Select the pre-event meal carefully The pre-event meal should contain negligible amounts of fat and protein so that it will be easily digested by the time the event begins. Select from low-fiber high-carbohydrate foods such as white rice, white bread, plain pastas, plain breakfast cereals (e.g. cornflakes, rice bubbles), and avoid adding any fats such as margarine, butter, or creamy sauces. Simple carbohydrates such as honey, jam, and syrup may be used to increase the energy value of the meal. Note that high-fructose foods (e.g. dried fruit, fruit juices, jam, soft drinks/pop) are absorbed slowly, so large volumes may not be well tolerated if the sportsperson has a tendency for gastrointestinal upset.

Consult a sports psychologist If pre-race nerves are a likely cause of gastro· intestinal problems, it may be helpful to discuss race build-up with a sports psychologist. Proper management of anxiety can not only improve stomach and bowel problems but may also help maximize race perfonnance. /

...,

"

A sample 24-hour pre.-race:cl!et • ;a

._

Breakfast 1 large bowl (2 cups) breakfast cereal with skim milk 2 slices white toast spread with honey 1 cup canned peaches 1 glass 100% apple juice

Snack 3 pancakes (made with low-fat milk) topped with golden syrup 300 mL flavored mineral water

Lunch

Prevent dehydration It is important to drink small amounts frequently during the event, aiming to prevent thirst. During long events (more than 90 minutes) the sportsperson should choose a drink that contains some carbohydrate (up to 10% solution) and low concentrations of sodium and potassium. Concentrated drinks are more likely to cause symptoms. Practice drinking during training so that it becomes a habit in competitions.

2 white bread rolls filled with low-fat cheese 1 tub low-fat fruit yoghurt 2 glasses water

Snack 2 toasted crumpets spread with honey 1 glass 100% pineapple juice

Dinner 2 cups boiled white pasta topped with sauce made from tomato paste and fresh mushrooms 1 slice white bread

Avoid fat and protein intake during exercise During ultra-endurance events where food may be consumed during the event, select items that contain minimum quantities of protein and fat. Fiber intake needs to be kept low and some runners may find

1 serve rice pudding (white rice) 3 glasses water

Snack 300 mL nutrition supplement 1 glass lemonade

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R E ADI N G

5. Rogers L Summers RW, Lambert GP. Gastric emptying and intestinal absorption of a low-carbohydrate sport

Peter:; HP, De Vries WR, Vanberge-Henegouwen GP et a1. Potential

and hazards of physical activity and

exercise on the gastrointestinal tract. Gilt 200r;48:

drink during exercise. IntJ Sport Nutr Exert Mctall 2005:15 (3):·2.20-35· 6. Simons SM, Kennedy RG. Gastrointestinal problems in

435-9Carter MJ, Lobo AJ. Travis

sr, IBD section, British Society

runners. Curr Sports Med Rep 2004;3(2):Il2- 16.

7. Smetanka RD , Lambert GP, Murray R et al. Intestinal

of Gastroenterology. Guidelines for the management

permeability in nmners in the 1996 Chicago marathon.

ofinAammatory bowel disease in adults. Gut 2004;53(SUPPI. 5):VI- r6.

Jnt J Sport

Ng V. Millard WM. Competing with erahn's disease.

Gastrointestinal profile of symptomatic athletes at

Management issues in active patients. Phys SporJsmrd 200S;33{u):47-53·

Pitsis

ce, Fallon KE, Fallon SK et al. Response of soluble

rest and during physical exercise. EurJ Appl Physiol 20 °4;9 1 (4):4 2 9- 34. 9. Rao 55, Beaty J, Chamberlain M et a!. Effects of acute

transferrin receptor and iron-related parameters to iron

graded exercise on human colonic motility. Am J Physiol

supplementation in elite, iron-depleted, nonanemic female ath letes. ClinJ Sport Med 2004;14(5) :300-4.

R EF E RE NCE S I.

1999:276{5 Pt I):G1221-6. 10.

Green HR, Cellier C. Celiac disease. New Engl J Med

II.

2007;357:173 1-43. Gastroenterological Society of Australia. Professional

Casey E, Mistry OJ, MacKnight JM. Training

guidelines. Coeliac disease. Available online: http://

room management of medical conditions: sports

gesa.blissmedia.com.au/files/editoLupioad/File/

gastroenterology, Gin Sports Med 2005:24(3):

52 5-4 o ,viii. 2. de Vries E, Soer jomataram 1, Lemmens VE et al.

Professional/CoeIiac.....Disease4Ed07·pdf. 12. Tscholl P, Junge A, Dvorak J. The use of medication and nutritional supplements during FIFA World Cups

Lifestyle changes and reduction of colon cancer

2002 and 2006. Br J Sports Mal 2008;42:725-30.

incidence in Europe: a scenario s tudy of physical

13. Gupta M, Eisen GM. N5AIDs and the gastrointestinal

activity promotion and weight reduction. fur J Cancer 2010;46 (14):26°5- 16. 3. Shawdon A. Gastro·oesophageal reflux and exercise. Important pathology to consider in the athletic population. Sports Med 1995:20(2):109-16. 4. Brouns F, Senden J, Beckers EJ et a1. Osmolarity does

1062

Nutr 1999;9(4):426-33.

8. van Nieuwenhoven MA. Brouns F, Brummer RJ.

tract. CUrrCllt GastroCllt.erol Rep 2009;11 :345- 5314. Riendeau D, Percival MD, Br ideau C et al. Etoricoxib (MK-0663): preclinical profile and comparison with other agents that selectively inhibit cyclooxygenase·2.

J Phannacol Exp T1Jerap 2001;296:558--66. 15. Paoloni JA, Milne C, Orchard J et al. Non-steroidal

not affect the gastric emptying rate of oral rehydration

anti-inflammatory drugs in sports medicine: guidelines

solutions. ] Parmter Enteral Nutr 1995:I9{5):

for practical but sensible use. Br J Sports Med

4 0 3- 6 .

2009:43:863-5.

Ch a pter 52

If you want this j ersey, you've got to piss blood Jor it.

Attributed to All Black rugby player Mark Shaw in conversation with h is successor Mike Brewer

The kidneys are important but often neglected organs. Exercise can h ave significant effects on renal

func tion. The m ost serious renal problem is rhah· domyolysis. Other common renal problem s include post-exercise protein/ hemoglobinuria. and nonsteroidal anti-inflammatory drug (NSAID)-induced renal dysfunction and/or inju ry. Renal trauma can result from sports-related abdominal injury.

Clin ica l anatomy and physiology Ordinarily, the kidn eys are paired organs that lie under well·developed flan k muscles." Kidneys receive high blood flow (approxim ately 2 0 % of the total cardiac

output at rest) and are composed of metabolically

active cells. These cells are suscepti ble to hypoxia, and tolerate this poorly. The tubular arrangement within the kidney uses a countercurrent mechanism to produce hypertonic urine. The four ma jor functions of kidneys are: to maintain salt and water balance to excre te nitro gen, mainl y as urea to produce e rythropoeitin and th e vitam in 0 metabolite 1,2S-dihydroxycholecalcife rol to regul ate blood pressure via the renin-angio tensinaldostero ne system.

Normal values for renal function at rest and with exercise are listed in Table 52.1.

Table 52.1 Renal fun ction- normal values

At rest

During exercise

Renal blood now mUmin>'

1200

300

Glomeru lar filtration rate (GFR) mUm in-I

120

60

Concen trating ability:

100-1200 mOsmol/kg water -I 280-295 mOsmollkg water -1 Dail y urine volume 400-4000 mL

Urine osmolality

Serum osmolality

Obligatory water loss 840 mL.Jt.

.Jt.Assumptiom: For each 3 g of pro tein ingested, about 1 9 of urea wiff be produced. 1 g of urea equals approximately 17 mmol. Urine osmolality can be up to three times that of plasma. It fo/{ows that 120 9 of protein ingested per day provides 40 9 of urea for excretion. This is about 680 mmo!. At a urine osmolality three times that of plasma, 840 mL of obligatory water loss per day is required to excrete that nitrogen.

1063

During exercise, physiological changes that have been observed are: increased glomerular permeability increased excretion of red blood cells and protein into the urine renal vasoconstriction, especially of efferent arterioles increased filtration pressure relative stasis of blood in glomerular capillaries. Collectively, these changes result in a degree of hypoxic damage to the nephron. In addition to the above, there is also: decreased urine flow, mainly due to antidiuretic hormone (ADH) secretion.

Exercise-related renal impairment Exercise-related renal impairment usually occurs as a result of dehydration. Exerciseresults in fluid losses of 1-2 Llhr, particularly in hot conditions. Replacement rarely matches this fluid loss, so a cascade of events may occur as depicted in Figure 52.I. In some cases, overly aggressive fluid replacement during exercise, especially in events lasting over four hours, can result in hyponatremia. Prolonged exercise is known to cause non-osmotic release of ADH. The non-osmotic release of ADH in combination with salt loss from sweat and excessive fluid intake causes hyponatremia. Hyponatremia occurs in slow athletes in long events. Up to 30% of long-distance runners may develop mild hyponatremia (serum sodium in range 125-135 mmol/L). This is usually asymptomatic, but more severe drops (below 120 mmol/L) can result in

Dehydration and hypovolemia

Decreased renal perfusion with hypoxia of renal cells

Possible acute renal failure Figure 52.1 The cascade of events that can lead to renal impairment 1064

cerebral edema, seizures, and even death. Until quite recently, sportspeople were encouraged to drink according to a predetermined schedule in endurance events. The obsessional sportspeople that rigorously stuck to these schedules were consequently at the greatest risk of developing hyponatremia. Current expert opinion on hydration is based on the proceedings of the Second World Conference on Hyponatremia in 2007.) Recommendations suggest starting any event well hydrated, and drinking according to thirst rather than to a predetermined schedule (see also Chapter 58).

Rhabdomyolysis and myoglobinuria Rhabdomyolysis is the most serious renal condition associated with exercise. It is characterized as "muscle cell meltdown."'; As a consequence of the breakdown of muscle cells, plus increased glomerular permeability, myoglobin (an oxygen transport protein) leaks into the urine. Serious sequelae may occur; in some cases the condition is fatal. More commonly, acute renal failure with associated hyperkalemia may ensue. Acute compartment syndrome is another recognized complication. Rhabdomyolysis is predictable to some degree. Recognized risk factors include unaccustomed extreme exertion, especially in the heat, where dehydration and hypovolemia are more common. Eccentric exercise is associated with greater damage to muscle fibers and Z bands, and in military reports the condition is referred to as the "squat jump syndrome." Viral illnesses, metabolic disorders (e.g. diabetes), and certain drugs (e.g. statins, diuretics), are associated with the condition. It is more common in sports people with the sickle cell trait.' Awareness of the above risk factors can be used to guide training to ensure an orderly progressive introduction of any eccentric exercise. Repeated bouts of the same type of exercise provoke less damage than the first bout. .....

J(j'of":. b

Rhabdomyolysis is a potentially fatal condition, and requires hospital admission for dose observation and active management.

Diagnosis relies on the history including risk factors listed above, plus examination findings which include marked tenderness of the affected muscle groups, and possibly hypovolemia. Signs of serious causes of exercise-related collapse include altered mental status, systolic blood pressure less than roo mmHg, and heart

Renal symptoms during exercise rate greater then ICO bpm. The characteristic labora· tory findings are of a grossly elevated serum creatine kinase (CK) level (over 10 000 lUlL) and myoglobin in the urine with a positive dipstick test. Management consists of hospital admission, aggressive fluid replacement (4-II L in the first 24 hours), cation exchange resins, forced diuresis, and careful alkalinization of the urine. Phosphate binders are also of benefit. In some cases, dialysis may be needed. Fasciotomy is indicated if associated compartment syndrome is present.

Other exercise-related renal impairment Footstrike hemolysis Hemoglobinuria may occur as a result of footstrike

hemolysis when running, and also with karate. Solutions for runners include well cushioned shoes, use of viscoelastic inserts. and running on soft surfaces. Karate exponents may need to modify their training.

Athletic pseudonephritis Gardner identified a condition he termed "athletic pseudonephritis."G Up to 20% of marathon runners presented with transient microhematuria and proteinuria. In football players, red blood cells were identified in post-match urine samples. Repeat urine testing a few days later usually shows resolution of any abnormality.

Abrasions of the bladder wall in long-distance runners A seminal investigation by Blacklock in 1977 reported hematuria in long-distance runners.7 Cystoscopy showed abrasions of the bladder wall around the trigone. The postulated mechanism of damage was repeated impact of the flaccid posterior bladder wall against the trigone. TIle observed time course was of recovery over several days. Preventive strategies include exercising with a partially full bladder, and attention to pre-exercise fluid intake.

Renal trauma Renal trauma can occur from a direct blow in boxing or a collision sport such as Rugby Union. Running can also cause transmitted shock to the kidneys. Most renal trauma can be managed non-surgically, but damage to the pedicle requires urgent surgical treatment to restore an adequate blood supply to the kidney.s

Clinical approach to the athlete presenting with hematuria The presence of blood in the urine is an alarming symptom for any sportsperson. When assessing a patient, ask about any recent trauma in the flank or urethral area, and any past history of renal stones. The sports person should be questioned about any recent sore throat that could be a precursor of poststreptococcal glomerulonephritis. On examination, look for evidence of edema or hypotension. Check for flank tenderness or evidence of urethral trauma. Investigations can usually be confined to urinalysis to check for cell casts and urine culture. No other investigations are required unless the clinical picture suggests it. At follow-up two to three days from the first sighting of blood in the urine, in most cases the hematuria will have settled. This tends to suggest that the hematuria is related to a benign exercise-related cause (see above). Further evaluation should be reserved for those with persistent urinary abnormalities or a suspicious history. Testing should aim to identify the site of bleeding and the nature of the pathology causing bleeding. Relevant investigations include renal ultrasound (or intravenous urography [IVU] in some circumstances), urine cytology. and cys toscopy. The sportsperson with microscopic hematuria can resume normal activity. If macroscopic hematuria is present, the individual should rest until it clears. Management of renal disorders depends on the particular condition present. A discussion of management strategies is beyond the scope of this chapter.

Clinical approach to the sports person presenting with proteinuria Proteinuria in sportspeople is typically picked up at a periodic medical screening examination. A small amount of proteinuria is normal (up to 200 mg/day). Dipstick testing usually registers "trace" proteinuria at urinary protein levels of roo mg/L. Orthostatic proteinuria is common in patients below the age of 30 (Le. the majority of those sportspeople having their first medical screening). If the protein:creatinine ratio is less than 0.2. and urinalysis is otherwise normal. then the diagnosis of orthostatic proteinuria is confirmed.9 With exercise. there is increased filtration of macro-molecules, especially albumin, and decreased tubular reabsorption of small molecular weight

1065

Ma n ageme n t of medical prob l ems proteins. However, in most cases the proteinuria is transient, and resolves within four hours of stopping exercise. Standard protocols recommend a repeat urinalysis 24-48 hours later. If the urine still contains protein then a 24-hour urine should be collected for protein. creatine, and proteiD electrophoresis. Senlrn creatinine, urea, electrolytes, and glucose should be checked. If proteinuria exceeds 3 g/day. nephrology referral is indicated, as the likelihood of serious renal disease is high. Lesser grades of exercise-related proteinuria are thought to be due to a variety of factors. These may include metabolic acidosis, some renal hypoxia, renal arteriole vasoconstriction, and loss of the negative charge on the glomerular membrane.IO Proteinuria appears to be proportional to exercise intensity, and

is more common with running than cycling or swimming at a given exercise intensity.H

Non-steroidal anti-inflammatory drug s (NSAIDs) and th e kidney The effects ofNSAIDs on the kidney are outlined in the box below.

Exercise and the patient w ith renal impai rm ent People with varying degrees of renal impairment can benefit from exercise provided they adhere to a few simple rules: Firstly, depending on the degree of renal impairment, there will be some reduction in the homeostatic functions of the kidneys. The ability

Rarely, NSA1Ds can cause interstitial nephritis and the nephrotic syndrome. It can occur from 2-75 weeks after commencing the NSAID, and resolves up to one year after stopping it. There is no eVidence that NSAIDs cause papillary necrosis, which is typically associated with phenacetin. Low-dose aspirin decreases platelet aggregation, and this could conceivably contribute to hematuria. The counsel of perfection is to never use NSA1Ds when exercising. The fact that NSAIDs are in widespread use by people who exercise, with relatively few serious adverse consequences, attests to their relative safety. However, the clinician should be mindful that, the longer and more intense the exercise bout, and the hotter the environmental conditions, the more risky it is to use NSAIDs when exercising. The renal effects of NSAlDs are often overlooked, but exercise can amplify them and cause clinical problems. NSAJDs inhibit prostaglandin synthesis. This in turn causes renal vasoconstriction, with reduced urine output, and salt and water retention. The sportsperson who becomes dehydrated and is taking NSA1Ds Is at special risk. The prostaglandin inhibition may abolish the normal protective vasodilatation of afferent arterioles and contribute to acute oUguric renal failure. In addition, there is potassium retention due to decreased plasma renin activity and decreased aldosterone. 12

1066

The risk of renal impairment following exercise is exacerbated by NSAID use. Risks are greater err, with prolonged or high-intensity exercise, both of 7&'11"-' which significantly compromise renal blood flow. \' RA('

IIJiiia

Any decision to use NSAIDs should be made by a well· informed sportsperson after discussion with their doctor, and will depend on the clinical scenario and a careful consideration of the benefits and risks. If NSAID use is justified, then a preparation with a short halflife (e.g. ibuprofen) is likely to be safer than one with a long half-life.

Ren al sy mptoms du ri n g exercise to excrete nitrogen and compensate for extremes dec reases in proporti on to the decline in renal fun ction. We therefo re advise against protein

supplementati on in any exe rcising individual wi th rena l impairm ent.

Secondly, as re nal fun ction d ecreases there may be associated hypertensio n. Thi s needs good control, otherwise there will be an accelerated loss of t he remain ing fu nction ing nephrons. Thirdly, w ith sign ifi cant rena l impairm ent th ere is a

drop in erythropoe it in prod uction, which will res ult in anemia. This, in tu rn, w ill restrict exercise ca pacity. V R-'l ("

IIJ-

Renal impa irment reduces protein excretion

;; and therefore we advise against protein 'b""

supp lementation in exercising indiv iduals with this condition.

The most common cause of renal function decline is increase in age. Most organ systems, including the renal system, function at an optimal level in young adulthood (age 20- )0 years). Witl, each passing decade over 30 yea rs there is approximately a 10% loss of function. Additional pathology such as hypertension or diabetes (type J or type z) can accelerate th is age-related decline. Collectively, these changes mean tha t the average 80-year-old has an estimated one-quarter of the renal function of a young adu lt. Advanced renal disease is ass ociated with fluid overload, electrolyte disturbances, m uscle weakness, cardiac dysfunction, peripheral neuropathy, and renal osteodystrophy. Dialysis m ay ameliorate some of these. bu t the definitive treatment is renal transplantation.

Exercise for pati ents with renal transplantation Most nephrologists encourage regular exercise after kidney transplantation. The Cleveland Clinic Foundation (CFC} I3 recommends warm-up stretches followed by aerobic activity that progressively increases in duration and intensity as physical capabilities improve. That founda tion also suggests that more vigorous activities are followed by a proper cool· down. They counsel against exercising in extreme climatic condi tions or in the presence of intercurrent illness. Chest pain, weakness, and ligh theadedness are indications 10 stop exercising and rest. Most trans plant units encourage partici pation in a wide variety of sports but counsel against boxing. martial arts, and collision sports {e.g. rugby or American football) .14 There are reported cases of

professional sporlspeople in collision sports making a successful return to play. and these sportspeople are mana ged on a case-by-case basis in cons ultation with their nephrologist and transplant surgeon. For sports people wishing to return to col1ision sports, the transplanted kidney should be placed in a less vulnerable position (e.g. up under the ribcage). Immunosuppressive dru gs will need to be continued on a lifelong basis. Similar to recommendations for exercise after kidney transplantation, traditional expert advice for individuals with one kidney has been to avoid contact (collision) sports. IS However, more recent investigations indicate that individuals with one kidney have a low risk of fur ther renal injury fro m contact sports and their restr iction from play is unsupported by available evidence.' Patients' participation in contact sports remains a controversial issue and may be best determined by a thorough, ind ividualized assessment. l

Prevention of renal complications of exercise Most causes of exercise-related renal impairment are preventable. Simple measures that athletes can adopt to minimize their risk are listed in the box (below).

Remain well hydrated from day to day. Know your "wet weigh t," part icularly in hot weather, and regard any sudd en weight loss as an indication of dehydration. Start any exercise bout well hydrated. During exercise, drink according t o thi rst. After exercise, drin k freely in th e first hour or two to replace fluids lost. Avoid anti-inflam ma tory drugs in the 48 hours prior to prolonged strenuous exercise. Weigh yourself daily. If you do not pass any urine in t he 12 ho urs after an exercise bout, seek urg ent medical advice. Do not ignore blood in t he urine-it may have a se rious cause. Iftraveling from a cool to a hot environment. acclimatize grad ually to the conditions. Exercise initially in the coolest pa rt of th e day. If you exercise vigorous ly, do not restrict your sa lt intake.

1067

Ma n agement of medica l p r oblems

Jonah Lomu (Fig. 52.2) All Black international rugby

player from New Zealand of Tongan descent developed nephrotic syndrome at the height of his career. Despite treatment with immunosuppressive drugs,

he developed progressive renal impairment with anemia. He received dialysis t reatment, but developed severe peripheral neuropathy and had to stop playing rugby. Subsequently he received a live donor kidney

transplant and the peripheral neuropathy resolved. He was able to return to playing professional rugby

and has been a very public supporter of initiatives to reduce the effect of kidney disease, particularly in children.

Figure 52.2 Jonah Lornu of New Zealand eludes an England player on his way to the tryline during the Rugby World Cup before he developed nephrotiC syndrome

1068

Renal sym ptoms du ri ng exercise

II

RECOMMENDED WEBSITES

7. Blacklock NJ . Bladder trauma in the long-distance runner: "10.000 metres

Cleveland Clinic Foundation. Exercise guidelines after kidney transplant: http://my.clevelanddinic.org/

serviccs/Kidney_Trans piantation/hicExercise_ GuidelineLaftec Kidney_Transpianl.as px

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8. Bernard

Rayner B, Schwellnus M P. Exercise and the kidney. rn:

98-1°3· 9. Batt M. Nephrology in sportspeople. In: Fields K. Fricker P. eds. Medical problem s ill athletes. Malde n; Blackwell Science. 1997:209-15. to. Rayner B. Exercise and the kidney. In: Schwellnus M.

ed. Ol},mpic Jextbook of medicine ilt sport. London:

Schwellnus M, ed. Olympic textbook oj medicine in sport.

Blackwell. 2008:375- 89.

London: Blackwell, 2.008: 375-89

m

RE E ERE NC E S

I.

Grinsell MM . Showaher S, Gordon KA et al. Single kidney and sports participation: perception versus

2..

JJ. Renal trauma: evaluation. management.

and return 10 play. ellrr Sports M,d Rep 2009;8(2) :

Poortmans JR. Exercise and renal function. Sp{))1S Mal

19 84;1: 125-53

Br J Urol

1977;49(2); r2 9-3 2 .

II.

Poortmans JR. Exercise and renal function. Sports Med 19 84;1(2): 12 5- 53.

12. Walke r

RI . Fawcett JP. Flannery EM et al.

Indomethacin potentiates exercise· induced reduction

reality. Pediatrics 2o o6; 1I8(3}:IOI9-27.

in renal hemodynamics in athletes. M,d Sci Sports Extrc

Holmes Fe, HuntJ], SevierTL. Renal injury in sport.

1994;26(Il):1302 - 6 .

Curr Sports Med Rep 20°3:2(2):103-9_ 3. Hew-ButlerT, Ayus re, Kipps C et 31. Statement of the

13. develand Oinic Foundation. Exercise guidelines after kidney transplant. 2009. Available: http://

Second International Exercise-Associated Hyponatrem ia

my.d evelandc1inic.org/services/ Kidney_

Consensus Development Conference. New Zealand.

Transplanlation/ hiLExercise_Guidelines_afte r_

2007. Cli" J Sport Med 2008;18(2):m -2I. 4. Knochel J. Risks and benefits and myoglobinuria.

Semi" N'phrol 1981;18:75- 86. 5. Eichner ER. Sickle cell trait in sports. CurT Sports Med Rep 2010;9(6):347-51. 6. Gardner KD. Jr. Athletic pseudonephritis; alte ration of

Kidney_Transplant.aspx. 14. Heffernan A, Gill D. Sporting activity follow ing kidney transplanta tion. Pedialr Nephrol 1998;12(6):

447-8 . IS. Dyment PG. Goldberg B, Haefele SB et al. American Academy of Pediatrics Committee on Sports Medicine.

urine sedimenl by athletic competition. J Am Med Al:soc

Recommendations for participation in competitive

1956;161(17): 16 13-7.

s ports. Pediatrics 1988;81:737-9.

1069

It took me about 12 months to come to terms with diabe tes. It was very You want your body to do what you tell it to do. Sir Stephen Redgrave, English rower who won his fifth Olympic gold medal in 2000, three years after being diagnosed with diabetes In this chapter we examine two aspects of the tionship between diabetes mellitus and exercise: the adjustments the person with diabetes might make if he or she wishes to exercise short-term and long-term risks and benefits of exercise to the patient with diabetes.

British rower Sir Steven Redgrave (chapter opening quote) provides a remarkable story of sporting success despite having diabetes mellitus. I Many other athletes with diabetes have also been exh'emely successful: Jay Cutler, a National Football League (NFL) quarterback who was diagnosed with type I diabetes in 2008, continued his successful playing career. 111ere are two distinct types of diabetes mellitustype I and type 2.

Types of diabetes Type I diabetes Type 1 diabetes, previously known as "juvenile-onset diabetes," is though t to be an inheri ted autoimmune disease in which antibodies are produced against the beta cells of the pancreas. This ultimately results in the absence of endogenous insulin production, which is the characteristic feature of type 1 diabetes. The incidence of type 1 diabetes varies throughout the world but represents approximately 10-15% of diabetic cases in the Western world. The onset commonly occurs in childhood and adolescence but can become symptomatic at any age. Insulin administration is essential to prevent ke tosis, coma, and death. The aims of treatment are 1070

tight control of blood glucose levels and prevention of microvascular and macrovascular complications.

Type 2 diabetes Type 2 diabetes, previously known as "maturityonset" or "adult-onset" diabetes, is a disease oElater onset, linked to both genetic and lifestyle factors. It is characterized by diminished insulin secretion relative to selUm glucose levels, in conjunction with peripheral insulin resistance, bo th of which result in chronic hyperglycemia. Approximately 90% of individuals with diabetes have type 2 diabetes and it is thought to affect 3-7% of people in Western countries. The prevalence of type 2 diabetes increases with age. The pathogenesis of type 2 diabetes remains unknown but it is believed to be a heterogeneous disorder with a strong genetic factor. Approximately 80% of individuals with type 2 diabetes are obese. Type 2 diabetes is characterized by three major metabolic abnormali ties: impairment in pancreatic beta cell insulin secretion in response to a glucose stimulus reduced sensitivity to the action of insulin in major organ systems such as muscle, liver, and adipose tissue excessive hepatic glucose production in the basal state.

Clinical perspective Diagnosis Both type I and type 2 diabetes are diagnosed by detection of a fasting (>8 hours) plasma glucose

--,

I

Diabetes mel li tu s level that exceeds 7 mmol/L (126 mg/dL). a plasma glucose level greater than II mmol/L (200 rug/dL) at 2 hours after an oral glucose challenge (oral glucose tolerance test). a glycosylated HbAlc level of 6-5% or higher, or by the appearance of other classic symptoms of diabetes."

_I

has had type 1 diabetes for more than 15 years is over 35 years of age has any coronary artery disease risk factors has any microvascular or macrovascuJar disease, or peripheral vascular disease.

Complications Pre-exercise screening fo r people with diabetes Prior to the commencement of, or an increase in the intensity of, an exercise program in patients with diabetes, a full clinical examination should be performed with particular attention to the potential sites of diabetic complications-the cardiovascular system. the feet, and the eyes. Ideally patients should have reasonable diabetic control before considering exercise. Long-term diabetic control indicators such as glycosylated hemoglobin (HhAIC) and fructosamine allow an objective measure. The HbAI C level allows assessment of the diabetes control in the preceding two to three months, and fructosa mine in the preceding three weeks. The actual levels of these markers that indicate reasonable con trol depend on the laboratory used. The ideal HbAl c level for participating in competi tive sports should be ::;;7% for adults and ::;;7.5% for adolescents. A blood glucose level diary should be kept, with measurements taken at variable times during the day. Fasting cholesterol and triglyceride levels should also be measured. Assessment of renal function measuring urea, creatinine, and electrolyte levels, and urina ry protein excretion and creatinine clearance, should also be performed. Examination should focus on: cardiovascular system-blood pressure including postural drop, heart, presence of carotid or renal bruits, peripheral pulses eyes-retinopathy, glaucoma, cataracts peripheral neuropathy- with emphasis on the feet.

Pre-exercise cardiac screening should be thorough. Ischemic heart disease is present in up to 50% of patients with type 2 diabetes at the time of diag· nosis. Chest pain is not always present in diabetic patients because silent ischemia can occur secondary to autonomic neuropathy. Exercise stress testing should be performed if the patient: will be undergoing vigorous activity (heart rate >60% of maximum) has had type 2 diabetes for more than 10 years

Both type I and type 2 diabetes may result in plications that affect multiple end-organ systems. In particular, diabetes is associated with accelerated atherosclerosis formation, which results in the risk of acute myocardial infarction increasing by two to three times) Peripheral arterial disease incidence is elevated dramatically and the risk of cerebral stroke doubles. In addition, diabetes can cause retinopathy. nephropathy. and autonomic neuropathy (leading to complications such as impaired gastric emptying, altered sweating. and potential silent myocardial ischemia), all of which can have serious implications for exercise. The risk of sllch complications is associated with both the duration of the diabetes and the diabetic control.

Treatment The trea tment of both type I and type 2 diabetes focuses on the maintenance of near normal blood glucose levels. For those patients with type I diabetes, exogenolls insulin is essential, in conjunction with management through diet and close monitoring of blood glucose levels. In contrast, only patients with poorly controlled type 2 diabetes require insulin, the majority being managed with a combination of diet, exercise, and weight loss. If, however, this is not adequa te, a patient with type 2 diabetes may require the use of oral hypoglycemic agents. These agents are used in preference to insulin- insulin being reserved only for patients in whom adequate control cannot be achieved. For people with either type I or type 2 diabetes, a low-fat, carbohydrate-controlled diet with an emphasis on an increased intake of complex carbohydrates and reduced simple carbohydrates is recommended.

Pharmacotherapy in diabetes Four principal types of insulin are available for patients with type I diabetes: rapid acting - very fast onset (within 5-15 minutes with a peak of action within 1 hour) and short

1071

Management of med i cal problems reduced or even stopped. If an HbArc ofless than 7% is not achieved after three months of monotherapy, combination therapy should be considered.

duration (3- 5 hours). Examples include insulin lispro,

aspart, and glu1isine short acting-rapid onset of action (within 30 minutes with peak of action between 2-3 hours) and longer duration (5-8 hours). Examples include

Dietary man agement

regular insulin

The importance of a high-carbohydrate. low-fat diet for optimal diabetic control is now well established. Fortunately, this conforms to the guidelines for maximizing athletic performance. Carbohydrate requirements for exercise vary considerably among individuals. People with diabetes should monitor their blood glucose levels to determine their carbohydrate needs before, during, and after exercise (Table 53.1). Individuals vary considerably in their responses to exercise. Only blood glucose monitoring before. during, and after training determines individual needs. Table 53-I should be used as a starting point or guide only_ Sportspeople involved in endurance events who are carbohydrate-loading prior to competition may need to increase their insulin dosage to cope with the increased carbohydrate intake. It is then important that carbohydrate is ingested before, during. and after the event.

intermediate acting-slower onset (may take 1-2 hours with peak of action between 4-10 hours) and longer duration (6- 18 hours). Examples include

lente (Monotard), NPH, and Protophane long acting-slow onset (2+ hours with peak at 6-20 hours) and long duration (at least 24 hours) allowing a background level of insulin (e.g. ultralente).lnsulin glargine and detimiT are other

long-acting insulins that are "peakless:' with onset in about 1.5 hours and a maximum effect at 4-5 hours that is maintained for 17- 24 hours.

Only patients with poorly controlled type 2 diabetes require insulin. If a trial of a healthy lifestyle for two to three months is unsuccessful in controlling the blood glucose level, oral agents can be used. Several classes of oral agents are available, each with differentent pharmacologic properties. 4 If weight continues to be lost while exercising, the dose may be

Tabl e 53.1 Adjustment of food intake recommended to permit the person with diabetes to exercise Duration of

Blood glucose level

Activity

exercise

(mmollL [mg/dLlI

Adjustment

Low level

Y2 hour

5.5 (>100)

No extra food

Moderate intensity

1 hour

16.5 (>300)

No extra food. Preferably do not exercise as blood glucose level maygo up

Strenuous activity

Varying intensity

1-2 hours

Long duration

16.5 (>300)

Preferably do not exercise as blood glucose level may go up Insulin may be decreased (conservatively estimate the decrease in insulin peaking at time of activity by 10%. A 50% reduction is not common)

Y2-1 day

Increase carbohydrate before, during, and after activity 10- 50 g (HO per hour, such as diluted fruit juice

(HO = carbohydrate

1072

Di abet e s m e l lit u s

While it is advised that all insulin-dependent diabetic sports people seek individual counseling from appropriate clinicians to arrange a s pecific dietary and training program , there are some important points that all diabetic sportspeople should be aware of: Sports peo ple need to learn the effects of different types of exercise, under different environmental

cond itions, on their blood glucose levels. It is important to always have carbohydrate foods available suc h as fruit, fruit juice, barley sugar, or biscuits. After vigorous exercise, blood glucose levels may continue to drop for a number of hours. It

is important that carbohydrate is ingested when exercise is completed to ensure replenishm ent of glycogen stores and to prevent hypoglycemia. Diabetic sportspeople have simila r micronutrient need s to non-diabetic sportspeople.5 A sports nutritionist can assist in creating an eating plan that ensures adequate amounts of calcium, vitamin 0, and micro nutirents.

The box below can be u sed by patients as a reminder of dietary tips.

Exercise and diabetes All clinicians engaged with a pa tient with diabetes should work together closely when considering exercise prescription for the diabetic patient. The targe t for an adult should be to achieve at least 30 minutes of continuous or intermittent moderate aerobic activity, equivalent to brisk walking, fi ve or six days a week for a total of 150 m inutes of aerobic activity per weekf' Additionally, 2-3 sessions of resistance exercise per week should be included';':! In long-standing diabetics, heart rate may be an unreliable indicator of exertion because of autonomic neuropathy, and the rating of perceived exertion scales may be more useful. Alth ough exercise in conjunction with a proper diet and medications is the cornerstone in the treatment of diabetes, s pecial care must be taken in those ta king insulin. Both insulin and exercise independently facilitate glucose transport across the mitochondrial membrane by promoting GLUT4 transporter proteins from intracellular vesicl es.9 The action of insulin and exercise is also cumulative. As such, an exercising type I diabetic will have lowered insuli n requirements, and may notice up to a 30% reduction in insulin requirements with exercise. importantly, in

For diabetic patients: to consider when exercisi ng

••

Before exercise

During exercise

After exercise

Know the effects of different

When exercising intermittently,

After vigorous exercise. blood

t ypes of exercise. and different

ingest carbohydrates in

glucose levels may continue

environments. on your blood glu cose level.

between to control blood

to drop. Ingest carbohydrate

Have quick-d igesting

glucose levels. Regular carbohydrate intake is

carbohydrates available (e.g.

usually necessary for long-

barley sugar. fruit juice etc.).

duration exercise.

Eat 1-2 hours prior to exercise to ensure ideal glucose leve ls.

Hyd rate.

when exercise is complete to replenish glycoge n stores. Alcohol consumption is discouraged after exercise as

it dehydrates and lowers the blood glucose level. Hydrate.

Hydrate (dehydra tion can be confused with hypoglycemia). If insulin is injected prior to exercise, use a site away from the muscle group being exercised so that it is not metabolized too quickly.

1073

Management of medical problems the person with type I diabetes, glycemic control may

Exercise and type I diabetes

not be improved with regular exercise if changes in

Control of blood glucose is achieved in a patient with type 1 diabetes through a balance in the carbohydrate intake, exercise, and insulin dosage. The meal plan and insulin dosage should be adjusted according to the patient's response to exercise. A degree of trial and error is necessary for people with type I diabetes taking up new activities. Frequent self-monitoring should occur, at least until a balance is achieved among diet, exercise, and insulin parameters. The ideal pre.exercise blood level is 6.6- 10 mmol/L (120180 mgjdL).< Sportspeople who have blood glucose concentrations exceeding II mmoljL (200 mg/dL) and ketones in their urine, or a blood glucose level of more than 16.5 mmoljL ()OO mgjdL) regardless of ketone status, should postpone exercise and take supplemental insulin. Those with blood glucose levels less than 5.5 mmoljL (100 mgjdL) require a pre-exercise carbohydrate snack (e.g. sports drink, juice, glucose tablet, fruit). Exercise of 20-30 minutes at less than 70% VO ,max (e.g. walking, golf, table tennis) requires a rapidly absorbable carbohydrate (15 g fruit exchange or 60 calories) before exercise, but needs minimal insulin dosing adjustments. More vigorous activity of less than 1 hour (e.g. jogging, swimming, cycling, skiing, tennis) often requires a 25% reduction in pre-exercise insulin and 15-)0 g of rapidly absorbed carbohydrate before and every 30 minutes after the onset of activity. Strenuous activity of longer than I hour (e.g. marathon running, triathlon, cross·country skiing) may require a 30-80% reduction in pre·exercise insulin and ingestion of two fruit exchanges (30 g or 100-120 calories) every 30 minutes. If early morning activity is to be performed, the basal insulin from the evening dose of intermediate· acting insulin may need to be reduced by 20-50%. The morning regular·acting insulin dose may also need to be reduced by 30-50% before breakfast, or even omitted if exercise is performed before food. Depending on the intensity and duration of the initial activity and likelihood of further activity, a reduction of 30-50% may be needed with each sub· sequent mea1. Post·exercise hyperglycemia will occur, especially after high-intensity, short·burst activity,!2. but insulin should still be decreased by 25-50% (because insulin sensitivity is increased for 12-15 hours after activo ity has ceased). Consuming carbohydrates within 30 minutes of exhaustive, glycogen·depleting exercise

the individual's diet and insulin dosage do not appropriately match exercise requirements. In the absence of exercise, even for a few days, the increased insulin sensitivity begins to decline, It is of extreme importance that those with dia-

betes monitor their blood glucose levels before and after every work-out. If the work-out is prolonged, or symptoms occur, the blood sugar level should also be taken during the exercise session. If no means exist to identify blood glucose levels before a work-out, then the work-out should be of short duration and low intensity with a glucose supply readily available.

Certain environmental conditions, such as extreme heat or strong winds, should be taken into consideration, as supplemental glucose may be required while exercising under such conditions. In contrast, if exercising when unwell or with a low· grade infection, glucose levels need to be monitored as relative hyperglycemia may occur. All patients with diabetes should carry an iden· tification card or bracelet identifYing themselves as having diabetes. They should be educated to be alert to the early signs of hypoglycemia for up to 24 hours after exercise. It is essential that they carry glucose tablets or an alternative source of glucose with them at all times. Dehydration during exercise should be prevented by adequate fluid consumption. It is also recommended that the diabetic sportsperson exercise with somebody else, if possible, in case of adverse reactions.

Benefits of exercise TIle benefits of exercise in type I diabetics include improved insulin sensitivity, improved blood lipids, decreased resting heart rate and blood pressure, decreased body weight, and possibly decreased risk of coronary heart disease.1O In type I diabetes, exer· cise does not improve glycemic control per se, but it reduces the risk factors for development of cardiovas· cular disease. It is well recognized that exercise reduces the risk of developing type 2 diabetes. There are also con· siderable benefits for those with type 2 diabetes. 11 A program of regular aerobic and resistance exercise can reverse many of the defects in metabolism of both fat and glucose that occur in people with type 2 diabetes; this will improve the HbAIC.7 1074

Di a betes me llitu s allows for more efficient restoration of muscle glycogen, This will also help prevent post-exercise. lateonset hypoglycemia, which can occur up to 24 hours followi ng such exercise. If exercise is unexpected. insulin ad justment may be impossible. Instead, supplementation with 20- 30 g of carbohydrate, at the onset of exercise and every 30 minutes thereafter, may p reven t hypoglycemia. In elite sportspeople and with intense bouts of exercise, reductions in insulin dosage may be even hi gher than those listed above. During periods of inactivity (e.g. holidays. recovery from injury),

increased insulin requirements are to be expected. A practical guide for patients with diabetes is shown in the box overleaf.

Exercise and type 2 diabetes Those patients with type 2 diabetes who are managed with diet therapy alone do not usually need to make any adjustments for exercise. Patients taking oral h ypoglycemic drugs may need to halve their doses on days of prolonged exercise or withhold them altogether, depending on their blood glucose levels. They are also advised to carry some glucose with them and to be able to recognize the symptoms of hypoglycemia. Hypoglycemia is a par-

ticular risk in those people with diabetes taking sulfonylureas due to their long half-lives and increased endogenous insulin production.

Diabetes and competition Every diabetic sportsperson sh ould develop an individual diabetes care plan for both training and competition.'! As competition may require interstate travel and altered eati ng patterns, the diabetic sportsperson should practice the match day routine at home and have snacks available as necessary. Good control of blood glucose levels may require regular access to carbohydrate-containing drinks. This not only serves to improve the glucose profile but also aids rehydration during prolonged exercise.

Diabetes and travel A physician's letter should accompany diabetic travelers stating that they carry ins ulin , needles, and blood glucose testing equipment. Copies of prescriptions should be taken, with medications in their original packaging. Insulin should no t be packed into checked luggage as there is a risk of it being misplaced, and freezing and thawing in the luggage hold. Insulin will generally keep fo r a m onth at room

temperature. Additional supplies should include those needed to treat hypoglycemia (including snacks). supplies for urine or blood ketone testing, a sharps container for used needles, and spare batteries an d palis [or meters and pumps. General recommendations for travel can be reviewed at several wehsites.1.I Traveling in a north-south direct ion generally requires no alteration to insulin doses. Eas t to west travel of more than five hours generally requires insulin dose adjustment. East-bound travel results in a shorter day, and west-bound travel a longer one. Travelers should check blood glucose levels at leas t every six hours on the flight. Omitting long-acting insu li n for the flight duration and using quick-acting insuli n approximately every six hours around average meal times is one technique. Once at the destination, quick-acting insuli n is used until bedtime, whe n long-acting insulin is recommenced. Continuous insulin pumps usually require 110 adjustment. with the pump's dock being adjusted to the destination time on arrival.

High-risk sports Diabetic patients are at increased risk of complications while participating in high-risk sports. Hypoglycemic attacks, characterized by inattenti on or lack of concentration, in sports such as rock and mountain climbing and skydiving have the potential for serious if not fatal injury. The suitability of scuba diving for diabetics has been studied. Military diving is not allowed in Great Britain for those with type I diabetes, and in the US, people with diabetes can not join the military at all.') Scu ba diving may be safe with adequate preparation and a skilled partner who can handle trouble with di abetes during the dive.

Exercise and the complications of diabetes Exercise is often neglected when the secondary complications of diabetes occur. Some unique concerns for the patient with diabetes th at warrant close scrutiny include autonom ic and peripheral neuropathy, retinopathy, and nephropathy.

Autonomic neuropathy Abnormal autonomic function is common among those with diabetes of long duration. The risks of exercise when autonomic neuropathy is present incl ude hypoglycemia. abnormal heart rate and blood pressure responses (e.g. postural drop). impaired

1075

I .

Preparation It is very important prior to exercise that a full assessment by a health care professional is performed to identify possible risks associated with diabetes while exercising. Special attention should be paid to understanding how your body and blood glucose levels respond to different types of physical activity. Previously sedentary individuals are recommended to gradually build into an exercise regime. Nutrition Exercise 1-2 hours after eating a meal to ensure ideal glucose level during activity. Hydration before, during, and after exercise is important as dehydration can be confused with hypoglycemia. Have fast-acting carbohydrates (foodlfJuid) accessible during and immediately after exercise. Generally, carbohydrates should be ingested following exercise, but depending on the intensity and duration, adjustments may be required (Table 53.1 outlines a general guide for blood glucose adjustments, but it is advised that individual blood glucose is tested before, during, and after to identify personal nutrition needs): - short-burst high-intensity-carbohydrate may not be necessary after exercise as glucose production may exceed uptake endurance or intermittent exercise-carbohydrate should be consumed before, during, and after. Be sure to understand personal insulin requirements when ingesting more carbohydrate than usual (i.e. "carb"loading prior to an event). Insulin and blood glucose monitoring Individuals differ greatly in their insulin requirements. Duration and intensity of exercise, as well as type of diabetes, should all be considered. A personal protocol should be developed with a healthcare professional; this can be modified based on experience and consistency of exercise. If possible, avoid injecting insulin into the body part that will be exercised. Monitor blood glucose before, during, and immediately after exercising.

1076

Additional blood glucose monitoring 4-6 hours after aerobic exercise should be performed to monitor for low blood sugar (hypoglycemia). Physical activity/exercise A combination of aerobic and resistance exercises provides the most benefit to those with diabetes. A healthcare professional and exercise specialist will be able to tailor a program to suit each individual, but general recommendations follow. Aerobic - A minimum of 150 minutes per week (spread over at least 3 days) of moderate to vigorous aerobic exercise. ExerCise may be split into smaller time increments (3 x 10 minutes pared to 30 minutes continuous).

Intensity

Example

Moderate-50-70% of maximum heart rate

Biking, walking, swimming, dancing, water aerobics

Vigorous- > 70% of maximum heart rate

Jogging, aerobics, hockey, basketball, hiking

Resistance Resistance exercise 2-3 times per week has been proven to improve insulin sensitivity and glycemic control (see Figures 53.1 and 53.2 for examples). - Initial instruction and periodic supervision by an exercise specialist is recommended.

Progression

Exercises

2-3 times per week1al

Shoulder press Bicep curls Push-ups Leg press Knee extension Hamstring curl

Start with 1 set/l 0-12 reps with moderate weight Progress to 2 sets/1 0-12 reps Progress to 3 sets/8-10 reps with heavier weight

'100 mm/h) may indicate malignancy, sepsis, or vasculitis (e.g. giant cell arteritis), normal levels do not exclude disease. Confounding factors in the interpretation of the ESR include anemia, polycythemia, abnormal red

cell morphology, and congestive heart failure. ESR testing is not useful as a screening test in asymptomatic individuals.

Antinuclear antibodies Autoantibodies that react with various components of the cell nucleus are called "antinuclear antibodies" (ANAs). Almost 100% of patients with systemic lupus erythematosus will be ANA positive but, as with RhF, ANAs are found in individuals with other conditions, such as scleroderma, Sjogren's syndrome, rheumatoid arthritis, infiammatOlY myositis, Hashimoto's thyroiditis, chronic liver or lung disease, druginduced lupus, and in 15% of healthy older persons. The ANA test should no t be used to screen patients with join t pain or presumed systemic illness.

H LA B27 HLA B27 is a gene found in up to 7% of normal individuals. HLA B27 is often associated with ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and enteropathic arthritis (the spondyloarthropathies). The prevalence of this allele in different populations is shown in Table 55.6. Also, 12% ofHLA B27 pos itive siblings of patients with ankylosing spondylitis will develop the condition." In sports people with low back pain, HLA B27 should no t be ordered routinely as there is a 7% prevalence ofHLA B27 positive alleles in the general population, whereas the prevalence in patients with spondyloarthropathy is approximately 95%. Given these pre-test probabilities, the test is more likely to produce a false positive than a true positive result. It is diagnostically valuable when the incomplete syndrome is present or when the pre-test probability that Ta bl e 55.6 Prevalence ofthe HLA B27 allele Frequency of

Population

Table 55.5 Conditions w ith an RhF association Cond it ion Sjogren's syndrome

RhF association (% )

90

Ankylosing spondylitis Ankylosing spondylitis with iritis Reactive arthritis (Reiter's syndrome)

90 >95

75-80

Psoriatic arthritis

Rheumatoid arthritis

75- 80

SystemiC lupus erythemat05us

25-50

Pu lmonary diseases

10-25

Ankylosing spondylitis/gout

5- 10

•

Spondylitis

Healthy young individuals

8-,0 The term "heat cramps" should be abandoned as it clouds understanding of the possible neural nature of this connection.

Man agement of cramps Stretching out the muscle to length is one effective therapy. Application of ice and physiotherapy of the affected muscle may also help. The Boston Marathon medical team treats muscle cramps with intravenous normal saline, and intravenous magnesium therapy has been used in the Hawaiian

1138

Ironman Triathlon; however, clinical trials of either treatment have yet to be published. More recently, evidence has accumulated that the ingestion of pickle juice may expedite recovery from cramps by a central neural mechanism,J2 since recovery occurs before there is any chance that the ingredients could have acted at a peripheral site (e.g. in the skeletal muscles}.ll

Fluid overload: hyponatremia Hyponatremia is perhaps the most important differential diagnosis in sportspeople who seek medical attention at an event undertaken in the heat, particularly in endurance events lasting four or more hours. Thus, any sportsperson who becomes unconscious during or after ultra-distance running or triathlon races and whose rectal temperature is not elevated should be considered to have symptomatic hyponatremia (exercise associated hyponatremic encephalopathy-EAHE) until measurement of the serum sodium concentration refutes the diagnosis. We emphasize that dehydration does not cause unconsciousness until it is associated with renal failure with uremia or hepatic failure.'4 To achieve such a weight loss as a result of dehydration, a 50 kg sportsperson would require 10 hours of high-intensity exercise at a sweat rate of 1 L per hour without any fluid replacement. Such a performance seems improbable in modern sporting events in which fluid is provided usually every 1-3 km and sportspeople are typically advised to drink "as much as tolerable during exercise." In contrast, the !Kung San have been known to exercise for six hours in 45°C (lI3°F) desert heat without fluid replacement and without obvious detrimental effects other than some evidence of fatigue. 2 Indeed a recent study found that the current world record in the 42 km marathon was set by a sportsperson who lost IO% of his body weight during his record-setting perfonnance.>4 It is much more likely that sportspeople encouraged to drink "as much as tolerable" during exercise in order to prevent "dehydration" will present with fluid Sports people with EAHE and serum sodium concentrations below 129 mmol/L (129 mEq/L) are rhydrated by between 2 Land 6 L,7.)6 The physician should be alerted to this diagnosis in a patient with an altered level of consciousness. If the patient is conscious, he or she may complain of feeling bloated or "swollen." A helpful clinical sign is that rings, race identification bracelets, and watchstraps feel and are

noticeably tighter. The race bracelet is a particula rly useful indicator, as it is usually loose fitting before a race. A feeling of intes tinal fuIlness or vomiting of clear fluid is another indicator of prolonged excessive fluid ingestion.

Etiology of EAH and EAHE RA ('

b'"

Managem ent of exercise-induced hyponatremia (EA H) and exerciseassociated postural hypotension (EAI-oIE) Under no circumstances should any hypotonic or isotonic fluids be given to unconscious or semiconscious sportspeople with EAH or EAHE. Rather, patients with EAH require some or all of the follow· ing interventions dependent on the degree to which they have developed encephalopathy secondary to cerebral edema: fluid restriction diuretics intravenous hypertonic (3-5%) saline at rates of about 100 mUhr.lt;

As the condition is due in part (see below) to abnormal secretion of arginine/vasopressin (an tidiuretic h ormone [ADH)) in the face of hypotonicity and fluid

overload, diuresis may be delayed even in patients with quite mild EAH. The use of a diuretic may be justified to initiate diuresis . Providing hypotonic or isotonic fluids to patients who are unconscious because of cerebral edema delays recovery and may produce a fatal result, as appears to have happened in isolated cases in recent years.l7- 19 In summary, it is essential that physicians carin g for sportspeople with EAH and EAHE are aware of the correct management of this condition. The current management includes: bladder catheterization to monitor the rate of urine production during recovery-spontaneous recovery will occur if adequate amounts of urine (>500 mUhr) are passed. (Note: A high urine sodium concentration in the face of EAH is diagnostic of inappropriate secretion of arginine/vasopressin [ADH], one of the three cardinal requirements for the development of this condition, see below) no fluids by mouth-salt tablets and sodiumcontaining foods can be given high sodium {3-S %} solutions given intravenously proVided they are infused slowly (50-1 00 mUhr) use of diuretics.

llJ'1 1160

Thus, regular exercise with a goal of weight management has the potential to prevent significant pain and disability as one ages. Consequently exercise should focus not only on body weigh t management (for the prevention of osteoarthritis), but rather on enhancing overall health through the same mechanisms that benefit all individuals regardless of body composition. [, II. [6 The amount of exercise required to achieve a healthy, stable body weight varies among individuals. Exercise prescription targeting weight loss is generally orientated toward maximum energy expendihtre. Therefore, individuals who aim to lose weight must increase activity above the recommended guidelines for healthy adults (Table 60.1). In this context. aerobic exercise will provide the bulk of energy expenditure. However, resistance exercise also has an important role in maintaining overall health and has been linked to improved mortalities in men. 16 . '7 Resistance training can influence body composition favorably with improved lean body mass, despite not having direct influence on body weight.[F. Table 60.3 serves as a guide to people living with obesity who wish to reduce their body weight. Note that with regards to resistance training, the guide suggests beginning with "low intensity" training. However, clinicians should consider patients individually, as many will both tolerate and enjoy higher intensities of training.

Cardiovascular disease If an individual with cardiovascular disease (CVD) risk fac tors or known CVD is ready to begin an exercise program, a thorough pre-screening is indicated. This includes a detailed history, medical examination, and risk stratification. Relevant investigations should be reviewed, particularly if a graded exercise stress test has been completed. The results should be used to help guide initial exercise prescription. It is of particular importance that exercise programs are done under supervision or guidance of appropriately qualified clinicians. and for some individuals it is recommended that programs be completed in a facility with access to appropriately trained medical staff and varying levels of monitoring (e.g. ECC monitoring). Patients should be educated early on methods for monitoring their exercise intensity (e.g. perceived exertion, the talk test, heart rate monitor) and should be aware of specific signs and symptoms pertaining to their individual condition.

Quic k exercise prescriptions for spec ific medical condit ions Ta b le 60.3 Exercise prescription: obesity Exercise type

Frequency

Intensity

Time

Aerobic (e.g. large-muscl e activities such as walking.

Appropriate exercise prescription includes balance training, aerobic weightbearing exercise, and resistance training. (,0-6) As with other clinical populations. the ideal program for managing osteoporosis has not been determined.c'l Moderate intensity exercise that does not cause pain should be encouraged. In people with osteoporosis, exercises that cause heavy twisting or bending of the spine may cause compression frachIres.'> The Otago Exercise Program can help guide clinicians in developing a tailored exercise program for the prevention of falls. 6 .. , 65

Quick exe rcise Tab le 60.14 EXercise prescription: low back pain (acute and chronic) Exercise type

Frequency

Aerobic (e.g. low-impact

5-7 days/week

large-muscle activities such

Intensity

Time

11 - 16/ 20 RPE, 60-80%

150-300 mins/week

limited by symptoms

Empha size duration over

as walking, swImming,

intensity

cycling, rowing, water aerobics) Resistance (e.g. abdominal

Daily

As tolerated

strengthening/back

Age 50, 8- 12 reps/day

extensions)

Involving 8-10 muscle groups

Flexibility (e.g. exercise not

Daily

exacerbating low back pain)

To level of tension, before

2 min/muscle group, 3 reps

discomfort

Resources: Guidelines (or exercise testing ond prescription;9 Exercise management (or persons with chronic diseases and disabilities;19 ACSM's resources for clinical exercise physiology: musculoskeletal, neuromuscular, neoplastic, immunologic, and hematologic conditions5 1 RPE = rating of perceived exertion; HR-. = m aximum heart rate

Table 60.15 overleafhas exercise prescriptions for bone health and fracture prevention.

Parkinson's disease The effect ofexercise in people with Parkinson's disease is variable due to the varying disease states. Because of the chronic, progressive nature of Parkinson's disease, it is particularly important to evaluate exercise programs regularly. As outlined in Chapter 54, exercise in people with Parkinson's disease improves cognitive, motor, and functional ability.66 Exercise prescription targets range of motion and flexibility exercises, balance and gait training, mobility, and/or coordination exercises to assist with functional ability. Evidence for aerobic activities and resistance training remains limited. ('7,68

Specific exercise training that targets speech and motor deficits in Parkinson's disease appears to be beneficiaL 6 9 Techniques tha t can improve the ability to initiate movem ents or resume movements during bouts of akinesia include rocking (side to side), rhythm, use of music, or counting.

Depressive symptoms Studies have also shown links between exercise and mental wellbeing (Chapter 54). Dunn et aU" studied the effects of exercise on major depressive disorders and found that meeting recommended doses of aerobic exercise was as effective as medica tion or cognitive behavioral therapy in treating m ild to moderate major depressive disorders. Exercise that did not meet recomm ended doses was ineffective.7°· 71

1169

Manage m en t of med i cal pr ob le m s Table 60.15 Exercise prescription: bone health. frac ture prevention

Exercise type

Frequency

Intensity

Time

Aerobic (e.g. large-muscle activities such as walking, swimming, cycling, rowing,

3- 5 days/week

11 - 16/ 20 RPE

Limited by symptoms

150-300 mins/week Emphasize duration over intensity

60- 80% lRM

8- 12 reps/day

water aerobics)

Resistance (e.g. free

2-3 days/week

weights, machine weights,

Involving 8-10 muscle

calisthenics)

groups

80- 90% lRM

5-6 reps/day Involving 8- 10 muscle groups

Flexibility (e.g . ROM

3- 7 days/ week

exercises)

Balance training (static and dynamic)

To level of tension, before

1 min/muscle group. 3 reps

discomfort

4-7 days/week

Safe but individually

2-4 exercises, 3 reps each

challenging

Resources: ACSM's Guidelines for exercise testing and ACSMj Exercise management for persons with chronic diseases and disabilities;19ACSM3" resources for clinical exercise physiology: musculoskeletal, neuromuscular, neoplastic, immunologic, and hematologic conditions S1 RM = repetition max; RPE = rating of perceived exertion; HR",.. = maximum heart rate

1170

Quick exercise prescr i ptions for spec i fic medic al cond i tio n s

CLINICAL SPORTS MEOICINE

w. Nelson ME. Rejeski Wj, Blair SN et 011. Physical activity

MA S TERCLASSES

and public health in older adults: recommendation

www cljojcalsportsmedjc j ne com

from the American College of Sports Medicine and

Usten to the podcasl by Karim Khan on exercise

the American Heart Association. M,d Sci Sports Exerc

prescription for bone health and falls prevention.

2007:39(8) :1435-45· II.

I!lI

Huang Y, Macera CA. Blair SN et al. Physical

RECOMMENDED RE AD I N G

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Clin Gastrocllttro/ 2004;18(6):lO09-29. 19. Durstine IL, Moore GE. Painter PL et aI., cds. ACSM's

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18. Donnelly JE. Smith B. Jacobsen OJ e t al. The role of

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Sports Excrc 2009 ;41(2):459-71. 21. Taylor RS. Brown A. Ebrahim S et al. Exercise·based reh abili tation for patients with coronary hea rt disease: system atic review a nd meta-analysis of randomized controlled trials . Am j Med 2004;116(10):

682-92. 22. Ehrman J et al., cds. ACSM's Resource manual for

g1.lidelinesfor exercise testing and prescriptioll. 6 th ed:

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Philadelphia PA: Lippincott Williams & Wilkins, 200 9, 23. Hambrecht R. Walther C, Mobius-Winkler S et a1. Patients with stable coronary artery disease: a randomized trial percutaneous coronary angioplasty compared with exercise training, Circulation 2004;1°9:1371-8, 24. Jessup M, Abraham WI: Casey DE et aL 2009 Focused

exercise in asthma: relevance to etiology and treatment.

J Allergy Clin InllntmoI2005;ll,(5):928-34· 36. Church TS. Blair SN. Cocreham S et aI. Effects of aerobic and resistance training on hemoglobin AlC levels in patients with type 2 diabetes: a randomized controlled trial. JAMA 2010;3°4(20):2253-62.

update: ACCF/AHA Guidelines for the diagnosis and

37. Sigal RJ, Kenny GP, Boule NG et al. Effects of aerobic training. resistance training, or both on glycemic

management of heart failure in adults: a report of the

control in type 2 diabetes: a randomized trial. Alln

American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines:

Inten! Med 20°7;147(6):357-69. 38. Church TS. Cheng YJ, Earnest CP et aI. Exercise

developed in collaboration with the international

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mortality among men with diabetes. Diabetes C(lrc

2009;119:1977-2016. 25. Pifta IL, Apstein CS, Balady GJ et al. Exercise and heart failure: a statement from the American Heart

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Barlow CE et a1.

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Can Respir J 2007:14{SUppl B):5-32B. 33. Reid WD, Chung F. Cli/tical management noles alld case

Curr Omeer 'I11er Rev 2006;2:351-60. 43. Ness KK, Wall MM. Oakes JM et al. Physical performance limitations and particpation restrictions among cancer survivors: a population-based study. Anll

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histories ilt cardiopulmollary physical therapy. Thorofare,

Impact of physical activity on cancer recurrence and

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survival in patients with stage III colon cancer: findings

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11 72

35. Lucas SR. Platts-Mills TAE. Physical activity and

from CALGB 89803. J Clill OncoI2006;24(22):

3535-4'48. Schmitz KH. Ahmed RL. Troxel AB et al. Weight lifting for women at risk for breast cancer-

Quick exerc i se prescript i ons for spec i f ic medica l conditions

related lymphedema: a randomized trial.JAMA 2010:3°4(24): 26 99-7°5. 49. Bicego D, Brown K, Ruddick M et al. Exercise for women with or at risk for breast cancer-related lymphedema. Phys 71wr 2006;86:1398-405. 50. Kushi LH, Byers T, Doyle C et al. Am erican Cancer Society guidelines on nutrition and physical act ivity for cancer prevention: reducing the ris k of cancer with healthy food choices and physical activity. CA Cancer j

Clill 2006;56(5):254-81; quiz 313-4. 51. Myers I, Nieman D, eds, ACSM's resou )'cesfor clinical

t!xercist I'Jlysi%gy: musculoskeletal. neuromuscular, neoplastic, immunologic, a"d il(!malologjc co"ditions. znd ed. Philadelphia PA: Li ppincott Williams & Wilkins, 20lO, 52. Sch mitz KH, Courneya KS, Matthews C et al. American College of Sports Medicine round table on exercise gUidelines for cancer survivors. Med Sci Sports Exerc 2010:42(7): 14°9-26. 53 . Bennell K, Hinman R. Exercise as a treatment for

osteoarthri tis. Curr Opfll Rlteumato/ z ooS:I](5):634- 40. 54. Fritz JM, Clelan d JA, Brennan GP. Does adherence to the guideline recommendation for active treatments improve the quality of care for patients with acute low back pain delivered by physical therap ists? Med Care 20°7:45(10):973-80. 55. Airaksinen 0, Brox fl , Cedraschi C et al. Chapter 4. European guidelines for the management of chronic nonspe50 lux (Ix) can cause some melatonin inhibition and light intensity Of>2000 Ix com· pletely suppresses it. Therefore, sum mer's long days and short nights will suppress melatonin secretion despite the 12-hour SNC "on' signal. The I2-hour SNC "on ' signal despite melatonin inhibition by light is considered an operational definition for biological n ight. Therefore. the nocturnal SNC signal synchronized to h ome nigh t time (biological night) may result in melatonin secretion if an un-adapted jet traveler is placed in a dimly lit room. Melatonin can be measured in saliva, plasma, and

(Fig. 64.r). The symp toms of jet lag di ssipate as the circadian clock gradually resets (adjus ts) to the time cues at the n ew destination time zone.7· 8, Although there is considerable individual variability, it is estimated that it takes about one day per time zone for the biological clock to resynch ronize with the sleep/wake schedu le.'>, 'l fJ,

Prevention of jet lag The faster th e biological clock adapts to th e new time zone the shorter the symptomatic period. Thus speeding up the adaptation is the primary goal. 17 Traveling (>3 time zone) for a stay longer than five days, circadian adaptation is desirable.'7. 18 Prefli ght adjustment to travel may speed up A summary of the general guidelines and principles are presented in Table 64-3 and Table 64.4 overleaf.

urine.I] The circadian rhythm is regularly synchronized to the 24-hour day by the environmental time cues termed Uzeitgebers," such as alternation ofli gh t and darkness, ingestion of m elatonin, sleep/ awake sch edules, as well as activity and meal timing. /1. 17 Traveling across multiple time zones (>3 time zones ) causes a temporary misalignment betwee n the circadian clock (lag) and the sleep/wake sch edu le at the destination time zon e th at is slow to reset

Ath letes shou ld spend time outdoors, rather than c ....... -::. indoors, during the sun light hou rs particularly I '0"" on arrival at the destination. Natural light resets }1JIoJ? circadian rhythm. 'i'R 4

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1216

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Race organization Specific pre-race strategies to enhance the safety of the competitors include the following: 1. Schedule the race at a time of year and day when environmental co nditions will not adversely affect performance or health. The medical director of the race shou ld have the authority to cancel the race should adverse weather conditions preva il. The American Co llege of Sports Medicine position statement recommends that if the wet bulb globe temperature index is above 28 C (B2° F) or if the ambient dry bulb temperature is below _20°C (_4°F), organizers shou ld consider ca nceling o r rescheduling the event.1 2. Ensure adequate provision of carbohydratecontaining fluids e n route, as th is is essential. 3. Plan the race course 50 that the start and finish are in an area large enough to accommodate all spectators, participants, and medical facilities, and allow quick get-away routes for emergency vehicles. Place first-aid stations along the route Q

122 1

4.

5.

6.

7.

at points allowing for rapid access by emergency vehicles and ideally about 3-5 km apart. Set screening and qualification standards to ensure that unfit and inexperienced sports people do not place themselves at undue medical risk during the event. Provide seminars for participants by medical personnel, as this can reduce the number of casualties. Advice may include: (a) correct training (b) consumption of sufficient carbohydrate before the race (cl eating a breakfast and drinking approximately 500-800 mL of a 4-7% carbohydrate solution every hour during the race (d) warning of the dangers of competing during or shortly after a febrile illness or while taking medications. Ensure registration forms include questions regarding past and present medical history. This enables identification of, for example, sportspeople with diabetes, asthma, or coronary artery disease. Such sportspeople could be sent specific information advising them on safety precautions such as wearing a medical bracelet. Implement an "impaired competitor" strategy. Strategically positioned helpers should be permitted to stop sportspeople who appear ill and unable to finish the course. There should be vehicles to transport these competitors to the finish Jine. Advise the local hospital emergency department ofthe forthcoming race and the likely number and nature of casualties. Hold meetings between the various members of the medical team (see below). Ensure an emergency transport service is available to bring problem cases to the central medical facility or to the nearest hospital emergency facility. Helicopter evacuation has proven invaluable for prompt treatment of sportspeopJe suffering cardiac arrest and other life-threatening conditions.

The medical director is responsible for the pre» paration of medical services and the supervision of the medical team on the day of the event. As endur» ance events are commonly held over a large area, communication between the different members of the medical team is the highest priority. The medical director should ensure adequate means of communication are available through the use of a two-way radio system or cellular network system. The medica1 team shou1d consist of appropriately trained doctors (sporting injuries and medical emergencies), physiotherapists, sports/athletic trainers, nurses, podiatrists, and masseurs. For an endurance event with 1O00 competitors, the medical team should number approximately 20, of which at least one-third should be doctors. Approximately 60% of the medical team should be situated in the medical areas near the finishing line, 10% of the medical team should be at the finish line itself, 20% of the medical team should be distributed at the first-aid stations along the route, and 1O% of the medical team should be patrolling the route in road cars, bicycles, or ambulances. In shorter events, a greater proportion of the medical team should be situated near the finish line. ? RA(' 0""

11;JV?

The medical team should practice perform ing emergency procedures, sportsperson evacuation, and rapid assessment of the collapsed sportsperson prior to the event.

The me dica l t ea m

At peak periods in a large race of IO 000-20 000 competitors, it is common to have four to six sportspeople requiring attention every minute-a much faster rate of admission than even the busiest innercity trauma centers. Thus, the medical team must have procedures well rehearsed. The preparation period also provides the medical director with the opportunity to ensure that all caregivers are using the most recent, evidence-based guidelines for the management of casualties) In large even ts (>3000 competitors) and in adverse environmental conditions. at least one fully equipped mobile intensive care ambulance should be in attendance near the finish line. In small events, the ambulance service should be notified that the event is taking place.

A medical director with appropriate expertise should be appointed a number of months prior to the staging of an endurance event to work closely with the event director. Early appoinhnent of a medical director permits him or her to implement the pre-race strategies outlined above.

First-aid stations should be placed en route at strategic positions, providing a stretch and massage facility for cramping muscles, first aid (sticking plasters) for chafing skin and blistered feet, and identification of

S.

9. 10.

1222

First -aid station s

Medica l coverage of endurance events drink is preferred in order to improve endurance and to prevent hypoglycemia.

the at-risk runner who is confused or deliriou s. These stations provide a center from which Spofts peopl e can be transported to the central medical facility or to a nearby hospital emergency department. Thus, stations should be positioned in areas that have good access to exit routes as needed. In running events. first-aid stations should be about 3-5 km apart. Clinicians skilled in treating common musculoskeletal problems and administering emergency firs t aid should staff these. All first-aid stations should be in communication with the medical director. In larger events, a road car or ambulance should patrol the course with a doctor in attendance. Drink stations are usually situated next to fi rstaid stations. It is important tha t the two be separated by at least 50 m so that the large crowds passing through the drink station s do not interfere with first-aid management. Additional drink stations should be sihtated at approximately 2-2.5 km intervals in events such as a m ara thon. For events las ting less than one hour, water is the fluid of choice fo r rehydration. For longer events, a glucose-electrolyte

Medical facility at the race finish The layout of the central medical station depends on the facilities available to the race or ganizers. Figure 65.1 shows the floor plan of the medical facility at the end of the 56 km Two Oceans ultram arathon foot race held annually in Cape Town, Sou th Africa. ' The green and red zones are for non-severe and severe cases, respectively. Other areas are allocated for the diagnostic laboratory, physiotherapy, medical supplies, and toilets. Note that the red zone for em ergencies such as cardiovascu lar collapse, hypothermia. and heatstroke is bes t loca ted immediately adjacent to the triage station . The red zone can be constructed to afford a degree of privacy for di stressed or seriously ill patient'S and permit discreet measurement of rectal temperatures. This area should be staffed by emergency-trained doctors and nurses. An ambulance should be located next to the red zone to allow rapid transport of emergency cases.

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Figure 65.1 Floor plan of the medical facility located at the finish line of the 56-km Two Oceans ultra marathon foot race held in Cape Town, South Africa

1223

Practical sports med i cine The benefit of this type of system over the undifferentiated medical tent that was prevalent in the past is that potentially lethal emergencies are much less likely to be overlooked in the general hustle and bustle of sportspeople with numerous important but not life-threatening musculoskeletal problems. Figure 65.2 provides guidelines for the activities that need to be completed in each of the areas. The equipment needs for a race medical center include the following:

3. Blankets for each stretcher. These allow for discreet measurement of rectal temperature (Chapter 58) and treatment of hypothermia (Chapter 59). 4. Plastic baths large enough to accommodate the torso of 40-90 kg (6.3-14.5 stone) sports people. These are filled with ice water and are used to treat heatstroke (Chapter 58). 5. Refrigerator facility-a mobile refrigerator truck is ideal for large races. 6. Computer terminal linked to the race finish. 7. Blood electrolyte and sodium analyzers, Ideally, serum sodium and potassium concentrations should be measured in all patients; however, this is essential in all subjects who are diagnosed as "dehydrated" and in need of intravenous fluids, A serum sodium concentration below 130 mmollL (130 mEq/L) indicates that the sportsperson is more likely overhydrated rather than underhydrated,'l's 8. Bins for rubbish and "sharps." 9. Toilet facilities. 10. Medications and equipment. Table 65.2 lists the resuscitation and medical equipment and Table 65.3 lists the medications required to

1. Chairs and tables for the computer operator at the admission area, the laboratory technologist and the diagnostic equipment, and for the other medical equipment and drugs. 2. Stretchers for transporting collapsed sports people from the race finish to the medical facilities. These are also used for sportspeople to lie on in the green and red zones. Stretchers must be rigid so the foot can be elevated and so collapsed sportspeople can be nursed, at least initially, in the head-down position (Chapter S8). Some A-frame stands are needed to elevate the foot of the stretcher. These are removed once the sportsperson's cardiovascular status has normalized.

Admission area

Triage area

• given medical card • race number recorded • time of entry to facility recorded

• • • • •

BP, pulse, temperature, state of consciousnesS blood glucose concentration information recorded on card diagnosis made aSSigned to zone (see Table 58.1 for criteria)

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J.

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+--

----+

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Within each zone • · • • Discharge area • record time out offacility • check medical card filled out satisfactorily • record discharge and diagnosis on computer

record vital signs regularly check serum electrolyte and glucose concentrations record method oftreatment intermittent assessment of progress on therapy

! Satisfactory progress • discharge home

Figure 65.2 Suggested flow chart for the management of sports people once they enter the central medical facility

1224

Medica l coverage of endurance events Tabl e 65 .2 Essential resuscitation and diagnostic tools for an endurance sporting event w ith 1000 competi tors

Resuscitation tools

Diagnostic tools

Oral airways (sizes 6-8)

Stethoscopes (5)

Resuscitation masks (disposable)

Sphygmomanometers for blood pressure measurement (5)

Defribrillator

Rectal thermometers (5; with disinfectant)

Oxygen cylinder/mask (2)

Torches

Ophthalmoscope and otoscope Glucometers for blood monitoring (2)

Reflex hammer

Blood electrolyte analyzer Urine sticks Peak flow meter (1)

cope with the expected emergency conditions. A pharmacist should be present to control the distribution of medications.

Additional supplies required for the medical tents and firs t-aid stations are shown in the boxes overleaf.

11 . Given that over 60% of runners requiring attention after a marathon require physiotherapy services,

Conclusion

it is ideal if a separate physiotherapy area ca n be

The risks associated with endurance events can be reduced with adequa te preparation, good medical coverage on the day of the event, and, liost importantly, education of the competitors. Educating the competitors regarding some of the pitfalls of competing in an endurance event improves their performance and reduces the risk of any major problems.

set aside from the central medical facility. Many endurance events also provide a massage tent for sportspeople. As there are

ohen a large number

of minor foot injuries associated w ith endurance running events, the presence of a podiatri st is also of great assista nce.

Tab le 65 .3 Basic med ications required in the medical facility at an endu rance sporting event w ith 1000 competitors

Mode of administration Injectab le

Medication Atropine (0.4 mg/mL) Dexamethasone (4 mg/mL) Morphine sulfate (1 5 mg/ mL) Dextrose 50% Adrenalin (epinephrine) (1:1000) (1 mg/mL) Salbutamol for nebulizer Metoclopramide Cardiac resuscitation drugs-atropine, lignocaine (lidocaine). frusemide Xylocaine (local anesthetic) Tetanus toxoid

Inhalation Oral

Salbutamol inhaler Paracetamol (acetaminophen) (500 mg) Sublingua l glyceryl trinitrate (nitroglycerin) (OA mg) Isordil spray Chlorzoxazone tablets (500 mg) Loperamide capsules (2 mg)

Topica l

Propacaine (0.5%) eye anesthetic Water-soluble lubricant Povidone iodine Tincture of benzoin

1225

Pract ical spor t s medicine

• Surgical instruments and disposables Scissors Latex gloves Syringes (3 mL, S mL, 10 mL) Needles (1 8, 21, 2S gauge) Steri-strips, sticking plasters Skin disinfectant Adhesive bandages Gauze pads Suture equipment (disposable) Fluid administration sets; cannulas, poles, giving sets (10) Normal saline for intravenous use (10 x , L) 5% dextrose for intravenous use (2 x 1 L) Haemaccel for intravenous use (2 x 1 L)

Ice and plastic bags (100 kg of ice) Water (500 L) Glucose- electrolyte drink (to make 250 L) Cups (2000) Towels Blankets (10) Rigid-frame stretchers (1 OJ Nebulizer (2) Inflatable arm and leg splints (2 each) Slings (5) Rigid strapping tape (various sizes) Elastic bandages (various sizes) Tape scissors Dressing packs (10) Eye pads Petroleum jelly

Supplies required at a first-aid station along al with 1000 competitors Stretchers (S) Blankets (5) 10 cm (4 in.) and 15 cm (7.5 in .) elastic bandages (6 each)

Pens and paper for record collection Laptop computer for data entry Athletic trainer's kit Podiatrist's kit (scalpel, sharp scissors, disinfectant, skin care pad, adhesive felt)

Gauze pads Rigid strapping tape Dressing packs (5) Skin disinfectant Inflatable arm and leg splints (1 each) Athletic trainer's kit Petroleum jelly Pen and paper for record collection

Medical input into the planning of the event is essentiaL The risk of thermal injury is reduced if the event is held at a time that is likely to avoid extremes

1226

of heat or cold. Events held in warmer climates should be commenced early in the morning or in the evening. Adequate facilities and equipment should be provided with well-stocked, regular drink stations along the route. The presence of experienced, trained medical and paramedical staff to deal with any emergency dramatically reduces the risk of serious problems. A functional layout of the medical facility can permit rapid, appropriate care of all race participants.

Medical coverage of endurance events CLINICAL SPORTS MEDICINE ON L INE MASTERCLASSES ww w c li n jcalsportsme d jc jne com

mI

hyponatremia. Med Sci Sports Exerc 2001; 33(9):

14}4-4 2. Winger 1M, Dugas

JP, Dugas LR. Beliefs about hydration

See the supporting podcast with author Professor

and physiology drive drinking behaviours in runners.

Timothy Noakes

BriJ Sports Mcd, 2011 (45)8;646-9,

R EC OMMENDED READING

McGarvey J, TIlompson

J, Hanna C et al. Sensitivity

m

REEERENCES

I.

Ho ltzhausen LM , Noakes TO. Collapsed

and specificity of clinical signs for assessment of

ulttaendurance athlete: proposed mechanisms

dehydration in endurance athle tes. Br j SpO,1S Mcd

and an approach to management. Gill] Sport Med

1997;7(4):29 2- 3° 1.

201 O;44{10 ):71 6--19. Maughan RI, Watson P, Shirreffs SM. Heat and cold: what

2.

Armstrong LE, Epstein Y. Greenleaf JE et al. American

does the environment do to the marathon runne r?

College of Sports Medicine position stand. Heat and

SpO/1S Med 20°7:37(4'5):396- 9-

cold iUnesses during d istance nmning. Mal Sci SJX'rts

Exerc 1996;28(12):i-:-:,

Noakes T. Mekler T, Pecioe DT. Jim Peters' collapse in the 1954 Vancouver Empire Games marathon. S AJr Mea J

3.

s tatement of the

2008 Aug;98{8):S96-Goo.

2012

4.

triathlon. cUn J Sport

Speedy DB, Noakes TD, Kimber NE et at Fluid ba lance 200 1: 11(1) :

44-50,

Speedy DB. Noakes TD, Boswell T et al. Response to a fluid load in athletes with a his tory of exercise induced

200P 5(4) :208-13. Speedy DB, Rogers JR, Noakes TO et al. Diagnosis

and prevention of hyponatremia at an ultradistance

(in press) .

during and after an ironman triathlon . Gill j Sport Med

International Exercise·Associated

Cape Town. South Africa 2005, Gill j Sport Mcd

Z003 .

Noakes TO. Waterlogged. Why the sciwce ofhydralioll Ja ils to fit thejacts. Champaign, II: Human Kinetics Publishers.

lSI

Hyponatremia Consens us Development Conference.

Noakes TO. TIll: lore of nmning. 4 th ed. Cha m paign. II: Human Kinetics Publishers.

Hew·ButlerT, Almond C. Ayus JC et al. Consensus

5.

Mea 2000;10(1):52-8·

Reid SA. Speedy DB. 111Ompson 1M et OIL Study of hematological and biochemical parameters in runners completing a standard mara thon. Clin j Sport Med

2004;14(6):344- 53.

1227

J don't kiww. [ "ever smoked Astl"OTwf

Tug McG raw, when asked if he preferred grass or artificial turf, ' 974

The use of performance-enhancing drugs is prob· .bly the m.jor problem facing sport today. Despite intense efforts by sporting bodies and the medical profession to eliminate the problem, to

In addition, WA DA monitors certain other sub· stances (in 2 011. stimulants and narcotics) to detect patterns of misuse; this may lead to these substances

assist sports performance remains widespread.

Athletes may have i1lnesses or conditions that require the m to take banned medications. In these cases. the athlete may apply for a Therapeutic Use Exemption (TUE) from their National Anti-Doping Organization or their International Federation to obtain authority to use the substance. WADA does not gran t TUE s but may consider appeals relat ed to

The Intern.tional Olympic Committee's (IOC) definition of doping is: The use of an expedient (substance or method) which is potentially harmful to an athlete's health and/or capable of enhancing their performance, or the presence in the athlete's body of a prohibited substance or evidence of the use thereof or evidence of the use of a prohibited method.

The World Anti·Doping Agency (WADA) is responsible for producing and maintaining the World Anti.Doping Code con taining the Prohibited List of Substances-subs tances and methods that are banned either at all times or in· competition on ly.

Subst. nces will be . dded to the list if they s.tisfY

being . dded to the prohibited list in the futu re.

the gr. nting or denying of. TUE. The proh ibited list is shown in the box opposite. A summary of the prohibited classes of drugs , and their m edical usage, effect on performance, and adverse effects is shown in Table 66.1 on pages 1230 to 1232 .

Non-approved substances at all times (in and out of competition)

an y two of the followin g three criteria: ,. the potential for enhanced performance 2. the potential for being detrimental to health

3. they violate the spirit of sport. The list is reviewed annually and an updated list commences on I January each year. The list that took effect on I January 2 0 II contains five classes of substances that are prohibited both in and out of competition . another four classes of substances prohibited in competition only. three methods prohibi ted in and out of competition , and two substa nces prohibited in particular sports (see box at top of page 1229).

1228

so: NonMapproved substances 1 Any pharmacological substance which is not addressed by any of the subsequent sections of the List and with no current approval by any governmental regulatory health authority for human therapeutic use (i.e. drugs under pre-clinical or clini cal development or discontinued) is prohibited at all times.

Drugs and the ath lete

Substances and methods prohibited at all times (in and out of competition) SO. Non-approved substances Prohibited substances 51. Anabolic agents

52. Peptide hormones, growth factors, and related substances 53. Beta-2 agoni5t5 54. Hormone antagonists and modu lators 55. Diuretics and other masking agents Prohibited methods

M2. Chemical and physical man ipulation M3. Gene doping

Substances and methods prohibited Prohibited substances 56. Stimulants 57. Narcotics 58. Cannabinoids 59. Glucocorticosteroids Substances prohibited in particular sports pt. Alcohol P2. Beta blockers

Ml. Enhancement of oxygen transfer

Prohibited substances all times (in and out of competition) Anabolic agents Prohibited anabolic agents are shown in the box. 51 : Anabolic agents 1 Anabolic agents are prohibited. 1. Anabolic androgenic steroids (AAS) (a) Exogenous AAS including: l-androstenediol, l-androstenedione, bolandiol, bolasterone, boldenone, boldione, calusterone. dostebol,

danazol, dehydrochlormethyltestosterone, desoxymethyltestosterone, drostanolone, ethylestrenol, fiuoxymesterone, formebolone, furazabol, gestrinone, 4-hydroxytestosterone, mestanolone, mesterolone, metenolone, methandienone, methandriol, methasterone, methyldienolone, methyl-l-testosterone, methylnortestosterone, methyltestosterone, metribolone, mibolerone, nandrolone, 19-norandrostenedione, norboletone, norclostebol, norethandrolone, oxabolone, oxandrolone, oxymesterone, oxymetholone, prostanozol, quinbolone. stanozolol, stenbolone, l -testosterone, tetrahydrogestrinone, trenbolone, and other substances with a similar chemical structure or similar biological effect(s) (b) Endogenous AA5 when administered exogenously: androstenediol, androstenedione, dihydrotestosterone, prasterone, testosterone, and their metabolites and isomers 2. Other anabolic agents: e.g. clenbuterol, selective androgen receptor modulators (5ARMs), tibolone, zerano!, zilpaterol.

Anabolic androgenic steroids Androgens are steroid hormones that are secreted primarily by the testes but also by the adrenal glands and ovaries. Testosterone is the principal androgen responsible for the development of the primary sexual characteristics in utero and during the neonatal period. It is also responsible for the development of the pubertal secondary sexual characteristics and it contributes to the increase in height and amount of skeletal muscle at that time. Tes tosterone promotes aggressive behavior, which is possibly due to direct stimulation of brain receptors. It also plays a role in sexual orientation. Anabolic androgenic steroid (AAS) hormones are derivatives of testosterone. The structure of the testosterone molecule can be adjusted to maximize either the androgenic or the anabolic effect. Athletes generally abuse those agents that have maximum anabolic effect while minimizing the androgenic adverse effects. A large number of different AAS hormones have been synthesized. Examples of prohibited AASs are shown in the box on the left. The exogenous AASs are synthetic analogs of testosterone; the endogenous ones are naturally occurring and are involved in the metabolic pathways of testosterone. The clinical uses of anabolic steroids are limited. They may be used as hormone replacement for primary and secondary hypogonadism, Klinefelter's syndrome, and. occasionally, delayed puberty. They have also been used to treat disturbances of nitrogen balance and muscular development, and several other non-endocrine diseases, including forms of 1229

w '" 0

Ta bl e 66. 1 Prohibited drugs and their effects Medical usage

Effe ct on performance

Adverse effects

Methandrostenolone

Hypogonadism Severe osteoporosis Breast carcinoma

Increased muscle bulk Increased muscle strength Possibly improving anticataboli( effect. recovery

Acne

Stanozolol

Type of drug

Examples

Anabolic steroids

Nandrolone

Baldness Gynecomastia Decreased sperm production, testes size, and sex drive Increased aggression

",

Liver abnormalities

"'" "'"

Hypertension

-0

Hyperchol esterolemia

rl

0 rl

Peptide hormones, growth

factors, and related substances

Beta-2 CJgonists

Erythropoietin (EPO)

Human growth hormone (hGH)

Anemia secondary to chronic renal disease

Increased endurance

Increased blood viscosity Myocardial infarction

Dwarfism Short stature

Anecdotal evidence only

Allergic reactions Diabetogenic effect Acromegaly

Insulin-like growth factor ClGF-1)

Dwarfism Diabetes mellitus type 2

Anecdotal evidence only

Acromegaly Organomegaly Hypoglycemia

Insulin

Diabetes

Anecdotal evidence only

Hypoglycemia

Human chorionic gonadotrophin (HCG)

Hypogonadism

May increase endogenous production of steroids

Gynecomastia

Adrenocorticotropic hormone (ACTH)

Steroid-responsive conditions

Euphoria

As in glucocorticosteroids

Salbutamol (oral) Terbu taline

Asthma Exercise-induced bronchospasm

Possible anabolic effects

Tachycardia Tremor Palpitations

3

'"

"n

:J

'"

Type of drug

Examples

Medical usage

Effect on performance

Adverse effects

Hormone anatgonists and modulators

Aromatase inhibitors (anastrozole,

Breast cancer

Used to counter gynecomastia

Joint aches

Breast cancer,

Males: used with AAS to prevent

aminoglutethamide) Selective estrogen receptor modulators (SERMS) (tamoxifen)

Stiffness

osteoporosis

gynecomastia

Females: masculinization Deep venous thrombosis

Females: muscle bulk (anecdotal evidence) Clomiphene

Anovulatory infertility

CYciofenii

Increases gonadotrophinreleasing hormone (GnRH)

Bloating Stomach pains

and endogenous testosterone

Blurred vision

(anecdotal evidence)

Headaches Nausea Dizziness

Diuretics and other masking agents Stimulants

Frusemide

Hypertension

Rapid weight loss

Hydrochlorothiazide

Edema

Decreases concentration of drugs Dehydration

Chlorothiazide

Congestive cardiac failure

Amphetamines (dexamphetamine,

Narcolepsy

May delay fatigue

Anxiety

ADHD (attention deficit

Increased alertness

Insomnia

dimethylamphetamine)

in urine

hyperactivity disorder)

Electrolyte imbalance Muscle cramps

o C

Impaired concentration

Glucocorticosteroids

Prednisolone

Widely used antiinflammatory Severe asthma

Enhancement of oxygen transfer

Blood doping

Nil

Euphoria

Cushingoid symptoms

Provide rapid blood

oxygen carriers, perfluorocarbon

volume expansion

emissions)

following acute blood loss

AAS = anabolic androgenic steroids

o

Some evidence of performance enhancement Improves endurance

3

Transfusion reaction Increased blood viscosity

Artificial oxygen ca rriers (hemoglobin

"0

Improved endurance (no evidence as yet)

",

a.

,..,

::> ",

Drugs a nd t he at hl ete anemia, hereditary angioneurotic edema, and breast carcinoma. Steroids increase lean body mass in patients with chronic obstructive pUlmonary disease (COrD) and HIV, and they may have a role in the treatment of muscular dystrophy and several dermatological diseases.""

The use of AASs in certain sports, particularly power sports such as weightHfting, power lifting, \ sprinting, and throwing, is widespread, as is their use by body builders.4111e use of AASs in footballers varies in the different codes of football. There would appear to be a high incidence of use in players of American football, with a lower incidence in players of other football codes,

7lJV? '0

While the incidence of AAS use is highest in elite athletes, there is a disturbingly high incidence among recreational and high school athletes. I - 8

This may be related to a desire to increase sporting performance or to improve body image. In 1987. the first US national study of AAS use at a high school level found that 6.6% of male seniors had used the drugs; 38% of those users had commenced before turning 16 years of age.> Subsequent studies have confirmed that 4-6% (range 3-12%) of US high school boys have used AASs at some time, as have 1-2% of US high school girls.'> AASs are taken orally or by intramuscular injection. More recently, transdermal patches, buccal tablets, nasal sprays, gels, and creams are being used as the delivery mechanisms.''" AASs are usually used in a cyclical manner with periods of heavy use, generally lasting six to 12 weeks. alternating with drug-free periods lasting from one to 12 months. The aim of the drug-free periods is to reduce the adverse effects of the drugs; whether this is the case remains unknown. AAS users follow a "pyramid" regimen, which commences with a low daily dose and gradually increases to a high dose then back down to a lower dose, and/ or a "stacking" regimen, in which several different types of anabolic steroids, oral and/or injectable, are taken simultaneously. The purpose behind the "stacking" regimen is to achieve receptor saturation with a lower total androgen dose than would be required if only one compound were used. Users hope that this regimen may reduce the incidence of adverse effects. Commonly, a combination known as "pyramid stacking" is used. TIle dosages taken by AAS users varies but those wishing to bulk up frequently use dosages 10-100 times the physiological dose.

Different AASs are used at different times of the training program depending on the phase of activity being performed. Certain AASs are regarded by their users (e.g. body builders) as more appropriate for specific aims, such as increased muscle definition. AAS users may use other dntgs (e.g. diuretics. anti-estrogens, human chorionic gonadotrophin [HCGJ and anti-acne medications) to counteract the common adverse effects of AAS. Most AASs are obtained through a black market that exists through gymnasiums, health centers, and, increasingly, on the internet. Information (and misinformation!) is readily available in pamphlets, nichemarket magazines, and. of course, on the internet. Testosterone precursors (e.g. dehydroepiandrosterone [DHEAJ) and designer steroids (e.g. tetrahydrogestrinone ITHG]) have recently received considerable publicity (page 12)6). Effect on performance

Anabolic steroids have a threefold effect: 1. Anabolic effect. This is due to the induction of

protein synthesis in skeletal muscle cells. AASs attach to specific cytoplasmic receptors in muscle cells and this complex then activates the nucleus to synthesize ribosomal and messenger RNA and initiate the process of protein synthesis. This anabolic effect continues during steroid treatment. An additional anabolic effect may occur indirectly through increased levels of endogenous growth hormone aSSOCiated with AAS administration. 2. Anticatabolic effect. This is mediated in two ways. AASs may reverse the catabolic effects of glucocorticosteroids released at times of training stress, and they may improve the utilization of ingested protein, thereby increasing nitrogen retention. This effect depends on adequate protein intake. Athletes in heavy training, especially weight training, are in a catabolic state. This is associated with the release of glucocorticosteroids and increased nitrogen utilization. When intense training is combined with insufficient recovery time or inadequate protein intake, a chronic catabolic state may develop. This can be aSSOCiated with impaired training and competition performance and the development of oVeruse injuries. Anabolic steroids may reverse this catabolic state, and permit an increased training load. AAS use appears to increase muscle size and muscle strength but only when certain conditions

1233

Practical sports medicine are met. For anabolic steroids to be effective in increasing muscle size and strength, the athlete taking the steroids must perform intense weight training and have an adequate protein intake. If these conditions are met, an increase in muscle size and strength will result. 3. Enhancement of aggressive behavior. Increased aggression may encourage a greater training

intensity and may also be advantageous during competition in sports such as weightlifting and contact sports. However, there may also be negative psychological effects (as discussed below).

111ere is considerable evidence that testosterone administration combined with weight training leads to an increase in lean body mass and a decrease in body fat." -ll This effect appears to be dose-related. The change in muscle mass with testosterone use is due to muscle fiber hypertrophy and increased numbers of myonuc1ei. '4 Studies have demonstrated a 5-20% increase in baseline strength, depending on the drugs and dose used as well as the administration period .. : While the majority of anabolic steroid use has been by athletes in power events, there is anecdotal evidence of a positive effect of anabolic steroids on endurance exercise. Firstly, the anti-catabolic effect may improve recovery from heavy training, thus reducing the likelihood of injury and allowing the athlete to undertake a greater volume and intensity of training. Secondly, anabolic steroids have a stimula tory effect on bone marrow, which may result in an increased production of red blood cells, thus improving the oxygen-carrying capacity of the blood. Long-term treatment of certain anemias with AASs has shown an increase in hemoglobin concentrations, but the majority of shIdies have failed to show any improvement in endurance performance with The above effects of anabolic steroids occur in both males and females. Adverse effects Adverse effects of anabolic steroid usage are extremely common and can be particularly significant in women. The majority of adverse effects are reversible on cessation of the drug{s). However, a number of serious adverse effects have been reported with anabolic steroid use, in some cases leading to death. The mortality rate among elite power lifters suspected of

1234

steroid abuse was significantly higher (12.9%) than that of a control population (}I%).'> Another study investigating the deaths of 34 known users of the drugs concluded that AAS use was associated with an increased risk of violent death from impulsive, aggressive behavior or depressive symptoms. ,(, An additional health risk associated with the use of AASs is that of infection associated with needle sharing. HIV, hepatitis Band C, and abscesses have been documented among anabolic steroid injectors who share needles'j and one study found that 25% of adolescent AAS users shared needles. 'j The long-term effects of prolonged anabolic steroid

i'.!...A (',.,. usage are unknown. However, as athletes who abuse It} 't}? '0

these compou nds often ad minister doses as high as 100 times the usual therapeutic dose, there is a hi gh risk of adverse effects and toxicity.

As well as this, a number of violent crimes, including domestic violence, which have resulted in death, have been attributed to "roid rage." A lis t of the common and less common adverse effects of anabolic steroid usage is shown in Table 66.2. Toxicity in both sexes Liver As many as 80% of individuals using those androgens that have a I7-methyl substitution on the steroid molecule have developed liver disorders, including hyperbilirubinemia and elevated liver enzyme levels. ,H These changes can be reversed with cessation of the drug. However, continued administration can lead to biliary obstruction and jaundice. This may take up to three months to reverse when steroid use is ceased. The responsible steroid compounds are mainly oral and include stanozolol and oxymethalone. Intermittent administration of these compounds has been shown to lower the incidence of these symptoms. The carbon-I7 esters, such as testosterone and nandrolone, are not associated with these liver problems as these substances are administered by injection and bypass the liver. The use of anabolic steroids to treat various medical illnesses has been occasionally associated with the development of other liver abnormalities, such as peliosis hepatis (blood-filled cysts in the liver),'')' and benign and malignant hepatic tumors. ) prescription drugs - athletes must inform clinicians that they are subject to drug testing and ensure that the

125 6

clinician confirms that the medication being prescribed does not contain any banned substance - if the clinician is uncertain, suggest contacting the national anti-doping agency for confirmation inadvertent doping - checking the contents of all medications, especially over-the-counter substances and supplements - if uncertain, contact the national anti-doping agency for confirmation drug testing protocols - especially the importance of listing all medications including supplements travel - be aware while traveling in foreign countries that drugs with the same or similar brand names may have a different composition in different countries - always ensure that you take your own regular medications with you.

Drug s and the ath le te

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