Brukner and Khan’s Clinical Sports Medicine, 4th Edition

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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

~ 61 62 63 64 65 66 67

viii

' ••

Pain in the Achilles region Acute ankle injuries

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

Parte

'~,

·to.

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

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

Preface About the authors

xxxiii

Editors

xxxv

Fundamental principl es

Sports inj uries: acute

4

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

15 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)

32 32 33 33

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

Bone and soft t issue tumors Rheumatological conditions 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

_,' ,~ti~~

lower limb biomechanica l assess men t in the

State-dependent sensitivity of spinal nociceptors

-

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'-

.

A contemporary model of a continuum of tendon pathology

-~~-

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 racquets 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 stimulation)

Open surgery

14 Core stabi lity

210

Anatomy

212 212 212 212 213 213 213 213 213 215 215

Interferentialstimulation 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

High-voltage galvanic stimulatio n

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

Migraine

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

254

Who should receive exercise counse ling ?

255

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

290

Prevention of eye injuries Teeth

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

290 291 292 293 293

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

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

xx ii

864 865 866

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

-

,

.

f " ......

, ,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

~'~ii::1 ':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

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 athletes-

972

pre· 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 ptom s 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 Exercise ~ induced

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 ho "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'

:~::;r

-...,-".

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

~-:;t~

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

Pre~travel

1215

sleeping schedule

Synergistic approach Symptomatic treatment for jet lag

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 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

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)

to departure

1212

1228

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.

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Skin cancers Although not technically overuse injuries, we include skin cancer here as it is a critical pathology and sports and exercise clinicians are in a position to save lives by being aware of this condition, which has greater incidence in certain sports)6 Ultraviolet light exposure is the most important risk factor for cutaneous melanoma and nonmelanoma skin cancers. Nonmelanoma skin cancer includes basal cell carcinoma and squamous cell carcinoma. Constitutive skin color and genetic factors, as well as immunological factors, playa role in the development of skin cancer.

But it's not that simple""" Although it is important to have a good understanding of the conditions outlined in this chapter and in Chapter 4. three important additional components are necessary for successful management of patients with sporting injuries.

Pain: where is it coming from) The pain your patient feels at a particular site may not necessarily be emanating from that site. It is essential to understand the concept of "referred pain," which is the topic of Chapter 6.

38

Masquerades There are many medical conditions whose presentation may mimic a sporting injury. While many of these conditions are relatively rare, it is nevertheless important to keep them at the back of your mind. If the clinical pattern does not seem to fit the obvious diagnosis, then think of the conditions that may masquerade as sporting injuries. These are described in Chapter 7.

The kinetic chain Every athletic activity involves movements of joints and limbs in coordinated ways to perform a task. These activities include running, jumping, throwing. stopping, and kicking. The tasks may include throwing a ball, hitting a ball, kicking a ball, jumping over an object, or propelling the body through air or water. Individual body segments and joints, collectively called "links," must be moved in certain specific sequences to allow efficient accomplishment of the tasks. The sequencing of the links is called the "kinetic chaiti' of an athletic activity.J7 Each kinetic chain has its own sequence but the basic organization includes proximal to distal sequencing, a proximal base of support or stability, and successive activation of each segment of the link and each successive link. The net result is generation of force and energy in each link, summation of the developed force and energy through each of the links. and efficient transfer of the force and energy to the terminalIink. Injuries or adaptations in some areas of the kinetic chain can cause problems not only locally but distantly. as distal links must compensate for the lack of force and energy delivered through the more proximal links. This phenomenon, called "catch-up," is both inefficient in the kinetic chain, and dangerous to the distal link because it may cause more load or stress than the link can safely handle. These changes may result in anatomical or biomechanical situations that increase injury risk, perpetuate injury patterns, or decrease performance. For example, a tennis player with stiffness of the lumbar spine may overload the rotator cuff muscles while serving to generate sufficient power and. thus, develop a tear of the rotator cuff muscles. These deficits in the kinetic chain must be identified and corrected as part of the treatment and rehabilitation process. We will be constantly returning to the theme of the kinetic chain throughout the following chapters.

Sports i njuries: o v eruse

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REFERENCES

'- Bntkner PO, Bennell KL, Matheson GO. StressfraclJlrcs, Melbourne: Blackwells Scientific Asia, 1999. 2. Diehl JL Best TM , Kaeding CC. Classification and

'7· van Zoest WJF, HoogeveenAR, Scheltinga MRM eta!. Chronic deep pos terior compartment syndrome of the leg in athletes: postoperative results of fasciotomy. Int J

Sports Med 2008:29(5):419-23. ,8. Piasecki DP, Meyer 0, Bach BR. ExertionaJ

retum·to·play considerations for stress fractures.

compartment syndrome of the forearm III an

Clill Sports Med 2006;25( 1): I7-z8.

elite fl atwa ter sprint kayaker, Am J Sports Med

3· Rome K, Handol! HHG. Ashford R. Interventions for preventing and treating stress fractures and stress reactions of bone of the lower limbs in young :ldults.

2008;}6(11):Z222- S'

'9· Blackman PC, Simmons LR, Crossley KM . Trea tmen t of chronic exertional anterior compartm en t syndrome

Cochrane DMabase Sys / Rtv zo09(z):CDoo0450.

with massage: a pilot study. Clin J Sport Med

4· Manore MM, Kam, LC, Loucks, AB. The female athlete triad: components. nutrition issues, and health consequences.] Sports Sci 2oo7;z5 (1):S61-715· Macera CA. Lower extremity injuries in runners: advances in prediction. Sports Med f99Z; I3=50-7. 6. Johanson MA. Contributing factors in microtrauma injuries of the lower extremity. J Back MI/sculoskelet RchabH f992;2:12 - Z5.

7· Giladi M, Milgrom C. Simkin A et a!. Stress fractures and tibial bone width. A risk factor. J Bone Joint Su'1l' '9 87;69· B:j26-9· 8. Bennell KL. Malcolm SA. Thomas SA et a!. Risk factors for stress fractures in track and fidd athletes: a 12-month prospective s tudy. Am J Sports Mea 1996;24:810-18. 9· Brukner PD, Bradshaw C. Khan KM et a1. Stress fractures: a series of I80 cases. Clin J Sport Mea

'99 6 ;61 21: 8 5- 9. '0.

Baquie p. Brukner PD. Injuries presenting to an Australian Sports Medicine Centre: a Iz·month study.

H.

').

!99 8 ;8:t4- !7· Herbert RD , de Noronha M. Stretching to prevent or reduce muscle soreness after exercise. Cochrane

".

DattlMse Sysl Rev 2oo7(4):CDo04577. Howatson G, van Someren KA. The prevention and trNtment of exercise-induced muscle damage. Sports

Med 2008;38(6) :483-503.

22. Barnett A. Using recovery modalities between training sessions in elite athletes: does it help? Sports Meci 2006;3 6 1917 8 '-9 6 . 2). Cook JL, Purdam CR. Is tendon pathology a continuum ? A pathology model to explain the clinical presentation ofl oad·induced lendinopalhy. Dr] S,)ort5

Med 200 9;43(6):4°9-16. 24· Koh ES, Lee Ie, Healy)e. MRI of overuse injury in elite athletes. CUll Radiolzo07;6z(II):1036- 43. 25· Kong A. Van der Vliet A. Zadow S, MRI and US of gluteal tendinopathy in greater trochanteric pain syndrome. Eur Radiol Z007;IT I772--8326. Benjamin M, Kaiser E, Milz S. Structure·function

din J Sport Med 1997;7(1):28-3 I.

relationships in tendons: a review.] Anal

Datir AP. Stress·related bone injuries with emphasis on

2008;2f2:211- 28.

MRI. Clin Radiol 20°7:9:828-36.

".

20.

27· Hariri S. Savidge E, Reinold MM et al. Treatment of

Moran OS. Imaging oflower extremity stress fracture

recalcitrant iliotibial band friction syndrome with open

injuries. Sports Med (All ckland) zo08;38(4):345- 56.

iliotibial band bursectomy: indications. technique, and

E'redericson M, Jennings F, Beaulieu C, Matheson GO. Stress fractures in athletes. Top Magn Reso/l Imaging zo06; IT309 - 25·

'4· Khan KM. Fuller PI , Brukner PD et al. Outcome of conservative and surgical management of navicular stress fracture in athletes. Eighty·six cases proven with computerized tomography. Am] Sports Meci '99 Z;20(6):657- 66 . '5· Harada M, Takahara M, Mura N et al. Risk factors for elbow injuries among young baseball players. J Sh.oulder

Elbow SlUg 2010 jun;19(4):S02-7.

,6. Parks ED. Ray TR. Prevention of overuse injuries in young baseball pitchers. Sports Health: A Multidisciplinary Approacli Z009;1:514-

clinical outcomes. Am J Sports Med 2009:37 (7):14 17-24. 28. Ellis R. Hing W, Reid D. Iliotibial band friction syndrome--a systematic review. Man TIler 2oo7;1z(3):200--8.

29· Seroyer ST, Nho SJ, Bach BR et aL Shoulder pain in the overhead throwing athlete. Sports Healtli: A MultidiscipJil!ary Approach Z009; I:ro8-zo. 3°· Werd MB. AchiUes tendon sports injuries: a review of classification and treatment. J Am Podia!r Med Assoc zo07;97(1):37-48.

3'- Banky J, McCrory PR oMouthguard use in Australian foo tball.] Sci Med Sport 1999;z(I):20-9. 32. Van Tiggelen 0 , Wickes S, Coorevits p. Dumalin M, Witvrouw E. Sock systems to prevent foot blis ters

39

Fundamenta l princip l es

and the impact on overuse injuries of the knee joint.

Mil Med 20°9;174(2):183---9. 33. Yavuz M, Davis BL Plantar shear stress distribution in

cancer in athletes. Sp01is Healtli 2009:r(4):335- 40' 37. Kibler WB. Determining the extent orthe functional

athletic individuals wi th frictiona l foot blisters. JAm

deficit. In: Kibler WB , Herring SA, Press JM (eds).

Podiatr Medt Assoc 2010;100(2):116-20.

Functional Rehabilitation of Sports and Musculoskeletal

34. Adams BB, Skin infections in athletes. Dennatol Nurs 2008;20(1):39- 44· 35. Kockentiet E, Adams BB. Contact dermatitis in athletes. JAm Acad Dennata! 2oo7:SG(G}:I048- 55.

40

36. Harrison SC, Bergfeld WF. Ultraviolet light and skin

Injuries. Gaithersburg, MO: Aspen Publishers, 1998: 16-1 9_

Chapte r 6

witu G -LORIMER MOSELEY

Thelt, [Mr Hammerhead Shark}, his shirt covered in blood, sp'''' around and hit his knee Olt the table, at which point he swore and yelled "My knee! My knee!," the whole time unfussed about the hammer stuck in his neck. G Lorimer Moseley. Painful yams. Metaphors (l[ stories to help ""derstand the biology of pai". Canberra: Dancing Giraffe Press, 2007 Even the simplest biological organisms can protect

themselves from threatening stimuli-by altering their path of movement away from the source of the threat. I As evolution has honed us into more and more sophistica ted creatures, we have also honed this fundamental capacity to protect ourselves from threat. Indeed, humans have very sophisticated methods of protection, perhaps none more sophisti. cated than pain. This chapter includes: some examples of the "fearful and wonderful

complexity" of pain, which are conveyed by

- proposing a contemporary definition of pain that is contrary to conventional definitions but which integrates the huge amount of research that has been undertaken since our conventional definitions were established introducing the idea of nociception and describing some of what is known about the biological mechanisms that underpin nociception - providing a conceptual framework with which to make sense of pain within the context of clinical practice a very practical clinical approach to considering referred pain when managing patients.

What is pain? Almost everyone experiences pain. Those who do not experience pain as the rest of us know it are at a distinct disadvantage in life and are likely to die young without living fast. Pain is an unpleasant sensory and emotional experience that is felt in the body and that

COURTESY OF MALCOLM WILLEn

motivates us to do something to escape it. These two characteristics of pain-its unpleasantness and its anatomical focus-are what makes it such an effective protective device. Pain alerts us to tissue damage or the threat thereof. Pain makes us seek attention. Pain changes our behavior. Pain stops us competing, keeps us seeking a cure, and compels us to prioritize pain relief above almost everything else. In fact. if the brain concludes that there is something more important than protecting a body part, then it makes the executive decision to not produce pain. Therein lies the key to really understanding pain-it is as simple 41

Fundamental principle s and as difficult as this-if the brain concludes that a body part is in danger and needs protecting. and you, the organism, ought to know about it, then the brain will make that body part hurt.' This concept of pain integrates a vast body of basic, applied. and clinical research. It differs greatly from conventional theories, which have changed little since the seventeenth century when Rene Descartes was ridiculed for suggesting that we were not made from four bodily humors) ~ ('/I The critical concept is that pain is not a measure of tissue damage, but an indicator of the brain's 1Ii 'Ii"> 0 conviction about the need to protect certain tissue.

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To better understand pain as the protective output of the brain, not as a marker of tissue damage, let us consider several contrasts between the two models (Table 6.1).

What is nociception? Nociception is not pain. "Nociception" refers to the detection, transmission, and processing of noxious stimuli. A noxious stimulus is one that is actually or potentially damaging. The neurons that detect noxious stimuli and transmit a nociceptive message to the spinal cord are called "nociceptors" ("danger receptors"). Nociceptors are high-threshold neurons, which means that a stimulus needs to be of sufficient intensity to evoke a response. The intensity of the stimulus is usually approaching or surpassing that which is damaging to the tissue in which the neuron

resides. Nociceptors are thinner than other peripheral neurons and many of them are not myelinated. They fall into two classes-C fibers (unmyelinated, slow conducting neurons) and AS fibers (myelinated, slow conducting neurons). Although all nociceptors are C or AS neurones, not all C and AS fibers are nociceptors (see Meyer et a1. 4 for review). Nociceptors are located in almost all the tissues of the body (with the notable exception of the brain). This network of neurons can be considered a very thorough surveillance system. Of course, the surveillance function of the peripheral nervous system is much more comprehensive than nociceptors alonehowever, nociceptors are always surveying the anatomical landscape for dangerous events. All such events fall into one or more of three categoriesthermal, chemical, or mechanical. Thus, nociceptors have specialized receptors that are cold-sensitive, hot-sensitive, chemosensitive, or mechanosensitive. In addition to these high-threshold neurons, humans have low-threshold neurons that are solely interested in one modality or another, such as thermosensitive A~ fibers, which inform brainstem areas of even tiny fluctuations in tissue temperature- fluctuations that are well within a safe operating range. In contrast to low-threshold single-modal neurons, nociceptors are bimodal or multimodal. That is, they are responsive to thermal and mechanical input, or to thermal, mechanical, and chemical input. These nociceptors, situated in the tissues of the body, are called primary nociceptors (see Bevan' and Butler & Moseley6 for reviews).

Table 6.1 Contrasts between pain as a protective output of the brain and pain as a marker of tissue damage Pain as a protective output of the brain

Pain as a marker of tissue damage

Pain is in consciousness.

Damage IS in the body.

One can not be in pain and not know about it.

One can be severely damaged and not know about it.

No brain, no pain.

No body, no damage.

Pain is affected by who is in the area.

Damage is not.

Pain is affected bywhat else is at stake.

Damage is not.

Pain is affected by beliefs.

Damage is not (well, not directly).

Pain can occur in a body part that does not exist.

Damage cannot.

Pain can occur in a body part that is not damaged.

Damage can occur in a body part that is not painful.

Pain can occur without activation of nociceptors {see belowl.

Damage cannot (excepting local anesthetic or pre~ injury nociceptor death).

42

Pa i n : w h y a n d h ow d oes i t h u r t ? Primary nociceptors are also different from other peripheral neurons in that they project to neurons in the dorsal horn of the spinal cord, not to thalami c or cortical structures. The neurons with which primary nociceptors synapse in the spinal cord are called "secondary" or "spinal" nociceptors and the synapse is open to modulatory input from other peripheral inputs and to descending input (see below). That the nociceptive system is polymodal and has a "relay station" in the spinal cord raises two very important issues. That primary nociceptors are multimodal and only project as far as the spinal cord clearly shows that the nociceptive system, per se, is not able to transmit modality-specific information. That is, the nociceptive system does not tell the brain that some thing is "dangerously hot," or ~dangerously cold," or "dangerously squashed." Rather. the nociceptive system has the apparently simple task of telling the brain that something is "dangerous." It is the non-nociceptive inputs that provide critical information about the nature of the danger. The polymodal characteristic also means that, if a stimulus is both dangerously hot and dangerously squashing, it evokes quicker firing of primary nociceptors, which effectively tells the spinal nociceptor that something is "doubly dangerous." To consider a clinical example, if a primary nociceptor is activated by chemicals released by an inflammatory event and the tissues are then poked and prodded, the addition of a mechanical input to the chemical input will increase firing of nociceptors. That primary nociceptive input is open to modulation at the spinal relay station means that other peripheral input can decrease noxious input. Peripheral input at the spinal relay station is from interneurons that are activated by activation of wide diameter peripheral neurons (AP fibers) from the same or adjacent areas. This is why one can, for example, "rub it better" or, in a more sophisticated way, put TE NS on it. In fact, TENS was born from Melzack and Wall's famous gate control theory of 1965.7 Moreover, the spinal relay station can be modulated by descending input from suprapinal structures and it is this descending input that arguably represents a more important and potent modulatory influence. s

chemical irritants are generated by the tissues themselves when they are injured. Together, these tissues are called "inflammatory soup" becaus e there are many chemicals involved and the exact ingredients of any particular soup is individual. Figure 6.1 depicts typical inflam mation-mediated sensitization of primary nociceptors. This "peripheral sensitizationn is exac tly that-nociceptors become responsive to stimuli that are not normally evocative. One

State-dependent sensitivity of p rimaly

(normal) and red (sensitized) bars depict nociceptor

nocicepto r s Primary nociceplors become sensitized in the presence of chemical irritants. The most common

responses to test stimuli (yellow bars). When there is peripheral sensitization (red bars), even tiny stim uli evoke responses

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43

Fundamental principles obvious example is that of sunburn-sunburnt skin hurts when you get into a shower of 40°C (104°F) because nociceptors are sensitized sufficiently to be activated by a thennal stimulus 4-5'C i7-9'F) cooler than that which would normally be required. That peripherally sensitized tissues are heat-sensitive is a very important phenomenon for the reasoning clinician because, as will be mentioned later, centrally sensitized tissue is not heat-sensitive. Therefore, if one has concluded that there is a peripheral problem and one can heat the culprit tissues to 42°C, one can confirm the conclusion, or question it, by determining whether the tissues are more sensitive in the presence of thermal stimuli that would normally be too cool to activate nociceptors (see also Fig. 6.2). Another aspect of sunburn, the reddening of the skin, is an important aspect of peripheral sensitiza~ tion. Reddening of the skin is a sign of neurogenic

inflammation (see also Figs 6.1 & 6.2). When noci~ ceptors are activated, an impulse is transmitted along every branch of the nociceptor. If an impulse transmits "in the wrong direction" and arrives at another terminal branch, then it causes the release of chemi~ cals that in themselves are inflammatory and cause vasodilation. 4 This mechanism is responsible for the flare that occurs around a skin wound or scratch. It is an important mechanism if the nociceptor is being activated proximally (e.g. in the dorsal root ganglion or in the spinal cord), because it means that the tissues become inflamed even though the problem is not in the tissues.

State-dependent sensitivity of spinal nociceptors When spinal nociceptors are active for some time, they too become sensitized. Many biological processes that can contribute to "central sensitization" 10

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Figure 6.2 Peripheral and central sensitiZation. Presuming an injury within the lightly shaded zone, the presence of inflammation in the area and activation of primary nociceptors will lead to peripheral sensitization. This will manifest as primary allodynia and hyperalgeSia, as represented by a shift in the thermal pain threshold so that pain is evoked at lower temperatures than normal (a), and a similar shift in the mechanical pain threshold so that pain is evoked at lower pressures than normal (b). If central sensitization ensues, the surrounding area, here represented by the dark shaded zone, will become mechanically sensitive (d) but will not be thermally sensitive (c)

44

Pain: w h y and ho w do e s it h urt? have been uncovered. (In-depth discussion is beyond the scope of this chaptel~ however, there are several resources that discuss central sensitization in more detail listed at the end of this chapter.) The manifestation of central sensitization is mechanical sensitivity beyond the area ofinjury and peripheral sensitization (Fig. 6.2). In short , central sensitization means that the spinal cord "upregulates" nociceptive input at the spinal cord (see Woolf & Salter,s Doubell, Mannion & Woolf,') and Fields & Bashaum J O for reviews) . This has implications for the biopsychosocial model of pain perception which is outlined in Chapter 20 (Fig. 20 .2, on page 315).

The brain decides As was emphasized earlier, pain emerges from the brain and reflects the brain's evaluation of threat to body tissue and the need for action. Spinal nociceptors are important informants in this regard, but, ul timately, nociception is neither sufficient nor necessary for pain (see Table 6_1 on page 42). Modern conceptual models of pain highlight this critical role of the brain. One fra m ework that makes this clear is that of cortical represen tations (see Butler & Moselel' for a clinician-friendly review). According to this framework, an indivi dual will experience, for example, ankle pain, when a network of brain cells, distributed across the brain, is activated. That network of brain cells, then, is considered the neural representation of that ind ividual's ankle pain. As it is a unique and distributed network, one might call it a neurotag.(' Each of the brain cells that constitute this ankle pain neurotag also contributes to other neurotags, and activation, or otherwise, of this ankle pain neuro tag is open to modu1ation at every synapse of every constituen t brain ce11. This brings an enormous complexity to the neurophysiology of pain, although pain is simply one expression of the neurophysiology of consciousness, which no one fu lly understands. This conceptual framewo rk means that anything that is represented by that individual's brain , and which provides credible evidence about the danger to which the ankle is curren tly exposed, should modulate activity of the ankle pain neurotag. In more clinical terms, anything that provides credible informa tion about the likely danger level should modulate ankle pain. Credible information may rela te to likely consequences of damage-for example, ankle damage is more dangerous to a top-level dancer than it is to an archer, a fact that will upregulate the ankle

pain neurotag. However, a top-l evel dancer migh t have the long-held belief that her body is indestructible, which would downregulate the ankle pain neurotag. Credible information might relate to other sensory cues-for example. damaging one's ankle on the bend in the final of a 200 m race in fro nt of a screaming crowd may very well lead to those same cues upregulating the ankle pai n neurotag when those sensory cues occur again. Clearly, this neural complexity has clear implications for rehabilitation. in that the neuroscience of pain and protection suggests that rehab ilitation of this individual with ank1e pain is not co mplete until the athlete has been exposed to every credible byte of informa tion that implies danger to the ankle. Hopefully you can now appreciate why Descartes' idea, tha t we have pain receptors in the tissues and pain signals are transmitted to the brain,l is inadequate (although popular). The simplicity of Descartes' idea is seductive, but it simply does not hold up. If, as a clinician or patient, one is to accept the true complexity of pain as evidenced by a huge amount of experimental and clinical litera ture and as conceptualized by the represen tation framework, then one must also accept that activity in primary nociceptors is one of many contributors to pain. The truly modern-day clinician should be open to nontissue contributions (i.e. central sens itization or central downregulation) and be alert to evidence of their influence. Charles Darwin suggested that young scientists should write down the results that do not support their current beliefs because these are the results they are most likely to [orget." Perhaps clinicians should do the same. With regard to pain, this would mean writing it down when the same mechanical input flares a condition one day and not the next, when pain is worse in competition than it is in training, when strength, endura nce, control. and flexibility are exemplary but the sportsperson still tweaks a hamstring runnin g at 90%. Some such findings might be squeezed into a Descartian framework, but, arguably, they fit more easily into a modern knowledge-based framework.

The brain corrects the spinal cord The brain has several hundred projections to the spinal nociceptor. Projections originate throughout the brain and have both facili tatory and inhibitory effects. Structures within the brainstem (e.g. the periaqueductal gray [PAG matter)) are important relay stations 45

Fundamental pr i nciples between the brain and the spinal

nociceptort~'!3.

The

effect of such a powerful modulatory capacity is, not surprisingly, powerful modulation. There are many experiments that have investigated how the brain modulates the spinal nociceptors. We can

easily summarize them here using the same language

as above: once the brain evaluates the true danger level and need for action, it corrects the spinal cord by either inhibiting spinal nociceptors or facilitating them.

Going back to the example of ankle pain, on a neurophysiological level. activation ofthe brain's ankle

pain neurotag sends a copy to a virtual comparator,

which also receives a copy of the ascending spinal nociceptive input. The two inputs are compared and the comparator sends a correction to the midbrain and thence to the distal terminal of the spinal nocic· eptor (Fig. 6.)). This kind of feedback loop is embedded in theoretical and experimental investigations of many aspects of human physiology. For example, in motor control the idea of reafference and sensory-motor feedback loops is wen established-a motor command is thought to generate an efferent copy that is then compared to sensory feedback of the movement

Previous exposure

How dangerous is this really?

What is at stake? Who is around? What is around? Cultural, social meaning

Thoughts, beliefs, logic, knowledge

COOJparatoJ

Injury

Inflammation

Neurogenic inflam.mation

• PAG [periaqueductal gray matter)

Figure 6.3 Feedback loops within the nociceptive system and the endpoint of pain: injury excites primary nociceptors.lnjury·induced inflammation activates and sensitizes primary nociceptors (peripheral sensitization). Activation of nociceptors causes neurogenic inflammation in nearby areas and excites spinal nociceptors. Spinal nociceptors project to thalamic nuclei, which then project to the brain. A complex evaluative process occurs within the brain, whereby every byte of information that provides credible evidence about the actual danger faced by the tissues in question is able to upregulate or downregulate the pain neurotag. This process permits the brain to determine"How dangerous is this really?"The final /ldecision/lleads to activation of the pain neurotag and pain emerges into consciousness. Simultaneously, as though a bifurcation of a single neural output, the determined danger level is sent to a /lcomparator;'where it is used as a reference for the spinal nociceptor input. This comparator then modulates midbrain structures and thence in turn the spinal nociceptor to /lcorrectl/its activation level. Thus, descending modulation can be facilitatory or inhibitory. The broken line from spinal nociceptor towards neurogenic inflammation refers to the possibility of tissue inflammation evoked by descending facilitation. That is, excessive facilitation of the spinal nociceptor in the absence of primary nociceptor activity activates the primary nociceptor antidromically, which induces neurogenic inflammation in the periphery.

46

Pai n: w h y and ho w doe s it hu r t ? (from proprioceptors). and any discrepancy between the predicted and actual outcome is used to correct the motor command,I4

If the brain concl udes that the need to protect tissues is greater than spinal nociceptor activity t.ii-~ ~ would suggest, it will facilitate the spinal ~ b'" nociceptor. If the brain concludes the need to protect )11 '' Specifically, it increases navicular and medial longitudinal arch height, reduces tibial internal rotation and calcaneal eversion, alters patterns of plantar pressure, and reduces activity of particular leg muscles. lIZ Techniques such as patellar taping may also alleviate symptoms associated with patellofemoral joint biomechanics.' ll. 114 It is important to be aware of skin breakdown associated with prolonged use of tape (particularly in sportspeople involved in vigorous activity), and to implement appropriate strategies to prevent this.

Biomechanics of cycling with EMMA COLSON

Cycling is unique due to the combination of extreme postural inertia of the upper and lower body together with excessive, repetitious load on the lower limbs. A competitive road cyclist sits in the same posi~ tion for 25-35 hours per week and cycles at a rate of

92

Incorrect seat height has several sequelae. If the seat is too high, power is diminished because lower limb muscles must work beyond their optimal lengthtension range. Also, there is excess stress on the posterior structures (hamstrings, gastrocnemius, and posterior knee joint capsule). Furthermore, compensatory excessive hip extension causes loss of the stable pelvic core. Ili In this situation, the rider often rocks the pelvis from side to side to maintain stability on the bicycle, and this fatigues struchtres such as the adductors, gluteals, spine, and even upper body musculahlre. Conversely, a low seat increases knee flexion throughoutthe pedal cycle and increases patellofemoral and suprapatellar bursalloading. Il8 It also places the hamstring, gluteal, and gastrocnemius muscles in a suboptimal length- tension relationship.1l7 Measurement Foot at bottom stroke (Fig. B.23a). With the elite cyclist, measurements are a guide, but in the end this is the desired "look:' In-seam measurement (Fig. B.23b). A useful rough guide is the Le Mond method first described by US cyclist Greg Le Mond. This measurement multiplied by a factor of 0.88 will roughly approximate the measurement of the center-to-top height (see Fig. 823cJ. Center-to-top measurement (Fig. 8.23c). This height should be equal to the in-seam measurement multiplied by 0.88 (Le Mond method).

Cl inical aspects of b i omechanics and sporting injur i es

Figure 8.23 Measurement of seat height (al Elite rider extension of stroke

(e) Center-ta-top measuring

Variations to seat height measurement will depend on: seat type and weight distribution cleat position-movement fore or aft will effectively

alter leg length deat stack height- will affect relative leg length personal preference- excessively plantarflexed riders might like a high seat seat fore/aft-a set-back seat may need to be lower crank length-smaller cranks will require a higher

seat shoe thickness-thicker soles increase relative leg

length rider experience-for the recreational cyclist or one new to the sport, the first priority is the ability to safely dismount, so this type of cyclist might ride with the seat at lower than optimum height. (b) In-seam measuring

Seat fore/aft position Fore/aft position is important for knee loading. IIs A seat too far forward will result in increased patellofemoral compression forces. The seat fore/aft position also affects hip flexion and gluteal-hamstring 93

Fundamental principles

muscle length. If the seat is too far back, the hamstring and gluteal muscles will be overlengthened, which appears to inhibit force production. If the seat is too far forward, the knees become more flexed, the hips more extended, and the muscles of the lower limb are at a less than optimal length-tension relationship. In addition, the more upright position is less aerodynamic. Seat inclination can also be varied from 0° of anterior tilt (i.e. a "flaf' seat) to about ISQ; inclination beyond this angle causes the rider to slip off the seat. Traditionally, it has been recommended that the seat be flat. A biomechanical study suggested that 10-IS of anterior inclination reduces low back pain. II') Further study of this matter is required. Q

Measurement

Plumb bolt method for saddle fore/aft measurement (Fig. 8.24). Here the bike is level and the plumb bolt is dropped from the posterior part ofthe tibial tuberosity to land either over the pedal axis or behind it. Landing in front of the axis will result in increased patellofemoral joint loading.

The amount of seat set-back is a personal choice and will relate to the following: rider size-a larger cyclist will be more comfortable further back hip flexibility-a cyclist with poor hip range will need to be further forward bike handling- moving behind the bottom bracket may lighten the front end a Ilttle, which could feel unbalanced and less stable for a road bike but allow a mountain biker to lift the front and push the front wheel into corners more event type-time trial and triathlon cyclists are usually very far forward, as they lean down and stretch out in front of the bike into an extreme aerodynamic position; this sort of riding is not comfortable for long -distance endurance training rider stability and flexibility-a cyclist needs flexibillty and also stability to sustain a set-back seat position; this comes with years of cycling experience and can be assisted by specific exercises.

Reach Reach measurement probably has the most variability with set-up. There is no measurement for reach as it will depend on rider flexibility, experience, comfort, desired bike-handling and desired aerodynamics. In Figure 8.25, it is clear that the same setting of reach can look right if the cyclist has the flexibility and control to maintain the position (Fig. 8.25a), or look wrong if the cyclist is stiff or unable to maintain the desired position (Fig. 8.2Sb). Measurement Bar reach and drop- good positioning (Fig. B.2SaJ, With good positioning, the set-up allows the cyclist to attain an anteriorly tilted pelvis, a flat unkinked back, retracted scapulae, unlocked elbows, and relaxed upper limbs. Bar reach and drop-poor positioning (Fig. 8.25bJ. Poor positioning results when, for the same settings as those used in Figure B.2Sa, the cyclist has poor flexibility through the pelviS, hip, and hamstrings, This pulls the cyclist backward and makes the bike reach look too extreme.

Figure 8.24 Measurement of seat fore/aft positionplumb bolt over axis

94

Variations to reach will be dependent on the type of cycling. Track riders and time trial cyclists will be very stretched out. whereas a mountain biker will be more upright, reflecting less aerodynamic demand and more focus on handling and maneuverability.

Cl i nica l aspects of biomechanics and sporting i nju ri es

Cleats/pedal interface Cleats are the most finicky part of elite cycling. Effective force transference, and hence less injury potential, is gained with a cleat with a low stack height. This places the foot doser to the pedal.

Float has become a popular and controversial part of cleat design. 1he desired outcome of float is motion that allows the cyclist to move the foot unrestrained if required. Getting out of the seat is one such example. If the foot were fixed rigidly to the pedal, the knee would be strained excessively. Float, however, should not be confused with slop. "Slop" is undesired motion of the foot while applying power to the pedals. Hence. a good cleat design has a midpoint that the foot will sit a t mos t of the time, with a small amount of force required to move off that midpoint. Figure 8.2 5 Measurement of bar reach and drop

{al Good positioning

Cleat positioning Fore/aft. The cleat should allow the base of the first metatarsal to sit over the pedal axis. This facilitates maximum leverage though the foot (Fig. 8.26a). Medial and lateral. Most cleats allow adjustment toward the inside or outside of the shoe. Riders with narrow hips would place the cleats to the maximum outside position, thus allowing their legs to be close together-mimicking their standing alignment. Riders with wide hips or a wide natural stance would do the opposite. Rotation. In general, the feet should be pointing straight ahead. However, if the cyclist has a natural toe~out position, then the cleat needs to be rotated in to accommodate that. Many cyclists ride quite comfortably hitting the crank with their heel slightly on each pedal stroke.

(b) Poor positioning

Cranks Crank size is proportionate to trochanteric height (leg length). In general, the issue is really only for small

riders. Riders under about 165 on (5 ft 5 in.) should be on cranks of 170 cm length or less. Very small riders

ofr6o on (5 ft 3 in.) orless could be better on 167.5 or even 165 em cranks. If there is any issue ofknee prob. lems in a smaller cyclist, this is one point to give early consideration to. Conversely, very tall riders should be on 175 em cranks and those over 180 em (6 ft) might consider 177.5 em cranks. Crank size seems unimpor· tant for people of average height.

Figure 8.26 {al Cleat position. Note the therapist's thumb is over the base of the first metatarsal, which lines up with the center point of the pedal spindle

95

Fundamenta l pr i ncip l es aerobar use or for someone with limited hip motion. Seats should be narrow enough to allow the legs to pedal freely without impingement (Fig, 8.27),

Shoes Many road shoes have a poor foot bed and may require the addition of an orthotic, especially for riders with pronation. Also assess the differen t shoe shapes. Recreational cyclists riding "street wear" bike shoes sacrifice rigidity, and will overload the knees if they do any substantial distance in them.

Handlebars Handlebars come in different shapes and sizes. The addition of aerobars to a road bike without any adjustment to seat position will probably create over· stretching and neck problems.

Bike set-up in other forms of cycling Other forms of riding follow this basic bicycle set·up, but some aspects are altered because of the specifics of the sport. In mountain biking, the aerodynamic positioning is less important than control (depending on the

Figure 8.26 (cont.) (b) limb alignment. Note the alignment of the hip, knee, and ankle

The main aim of cleat setting is to align the hip, knee, and ankle (Fig. 8.26b). However, should the natural stance of the cyclist be poorly aligned, the cleats will need to be set to allow for this. Pedal and cleat systems mostly go together. The size of the pedal platform might be relevant for very tall cyclis ts who find smaller cleat systems too unsta¥ ble. Similarly, very small riders might find a large pedal platform reduces their foot leverage. Cyclists with narrow hips may also have problems with the increased Q angle of some pedal systems that are set a long way out from the crank. This situ· ation is aggravated by a wide bottom bracket (on many mountain bikes) and also cranks that angle outward at the pedal end.

Seats Comfort on the seat is imperative to endurance cycling. Seats should be set horizontal, as mentioned above. A slight downward tilt can be useful with

96

Figure 8.27 Seat width. Note how the narrow seat allows the cyclist's legs to drop down unimpeded

Cl i n ica l aspects of biomec h an i cs and spo r t i ng i n ju ri es technical difficulty of the course) . Thus, the rider is

more upright, and maneuverability of the bicycle becomes paramount. Hence, the frames tend to be small in comparison to the rider, and reach is often shortened to make the front end easier to position and lift over objects.

For the same reason, trick/ trial bikes look ridiculously small for the rider. For downhill mounta in biking, power generation is not as important as stability and control, so the seat is positioned to maintain a center of gravity as low as poss ible. Downhill cyclists usually have another bike with a "correct" seat set-up for fitness training, as dis tance training with their competition bike set-up would predispose to knee problems. For time trial. track sprinting and tria thlons, the relative height of the sea t to handlebars is sometimes increased to improve aerodynamics. These cyclists need good flexibili ty and excellent stability. Aerobars are added in triathlons to enhance aerodynamics. Triathletes tend to ride with the seat positioned higher and further forward than recommended, a nd hence "toe" more (i.e. paddle using the toe rather than dipping the heel to plantar grade). This most likely increases the contribution of their quadriceps at the expense of underutilization of the hamstring, gastrocnemius, and gluteal muscles. '17 Anecdotally, triathletes report that their hamstrings feel better for the running section after us ing this position in the ride.

Aerodynamics and wind resistance Wind resistance is the primary retarding force in road cycling. TIle single most important factor in reducing the effect of wind resistance is the fronton surface area that the cyclist exposes to the wind. This becomes particularly important for the cyclist involved in time trial even ts. The rider must be able to position the pelvis in an anterior tilt to flatten out the lumbar spine and so redu ce his or her fro nt-on surface area. It appears that there is a metabolic cost fo r the cyclist to attain such a position, but this is fa r outweighed by the aerodynamic power savings. l 2 ! Road bikes are des igned with this ideal in mind, and hence an inability to attain an aerodynamic posture ca n result in injuries. Phys ical assess· m ent and rehabilitation of the road cycl ist should be directed toward the cycl ist attaining an efficient aerodynamic posture without placing strain on his or her body to do so. This requires flexibility, s trength, and motor control. Should the cyclist be W)

unable to con trol a posture to fit the bike, then the setting of the bicycle needs to b e modifi ed to ensure injury-free cyclin g.

Pedaling technique Motion of the pedal s troke needs to appea r (and sound) sm ooth and continuous. Tryin g to create an upstroke can be injurious to the cycl ist. Cleats aid proprioception, to stop the foot fallin g off the pedal during high-intensity pedaling. u~ An upstroke utilizes the psoas and hamstrings at their less than optimal length- tension range, and so will destabilize the pelvis, providing an ineffective base for generation ofleg muscle power. The last "up" phase of the pedal cycle is very short. It corresponds to the power phase of the opposite pedal in steadystate riding. The momentum of the ascending leg and drive of the opposite leg create a nega tive torque situation that drives the ascending leg through to the top stroke.

Assessment The practi tioner needs to understand th e cycling discipline of the injured a thlete. Cyclist experience, phase of training program, and current goals must be established. As always, the history of the injury is important, with special attention to recent crashes, equipment modifica tions, training spikes, or training variations. The important components of the physical assessment are: body type and size-big sprinters will have very different issues to small hill climbers; very small females are often riding equipment designed for much larger people physical alignment (or malalignm ent) and how that might relate to the injury flexibility and stability-to attain the on-bike posture (Fig. 8.28 overleaf), the cyclist needs to be flexible through: ~ arm overhead - thoracic sp ine - pelvis anterior til t - hamstring s in tilt pOSition - glutea ls/hips (tightness here will affect knee tra cking) - iliotibial band - knee range - ankle dorsiflexion range. The cyclist also needs the appropriate muscle strength to hold the on-bike position (Fig. 8.28), and

97

Fundamenta l principles

",~

.

Figure 8.28 Cyclist in "on~bike" posture. Maintenance

of this posture requires both flexibility and stability. The ability to deliver power in the posture requires

Figu re 8.29 Strengthening exercises for cyclists (a) Scapular strengthening exercises. Cyclists with neck problems should strengthen the scapular retractors while maintaining an anterior pelvic tilt

dissociation of the hips from a stable pelvis and trunk

dissociation of the hip motion from the pelvis and trunk to deliver power. Strength imbalances in cycling can result in the overloading of one leg or other regions of the body. Assessment should be made of right versus left leg, the lower nerve roots, the vastus medialis obliquus, gluteus maximus, gluteus medius, erector spinae, pelvic floor, transversus abdominis, pelvic floor, the upper body stabilizers (the retractor group), and also single-leg balance and control.

Rehabilitation The key to the management of cycling injuries is to identify and treat the cause. It is important for the cyclist to continue riding, in a modified form, if at all possible. Rehabilitation exercises should, as much as possible, mimic the on-bike demands. Hence, working the body while maintaining an on-bike anterior tilt position is useful. Examples of important rehabilitation exercises for the cyclist are shown in Figure 8.29.

98

Conclusion An appreciation of the posturaljbiomechanical and physical demands of the sport of cycling will enhance the practitioner's ability to diagnose and manage cycling injuries.

Upper limb biomechanics with \V. BEN KIB LER

Correct biomechanics are as important in upper limb activities as they are in lower limb activities. For example, repeated throwing places tremendous stresses on the upper limb, especially the shoulder and elbow joints.III Throwing, however, is a "whole body activity," involving the transfer of momentum from body to ball.

The biomechanics of throwing Throwing is a whole body activity that commences with drive from the large leg muscles and rotation of the hips, and progresses through segmental rotation of the trunk and shoulder girdle. It continues

Cl i n ical aspec t s o f b i o m echa n i cs an d spo r t i ng injur ies

-

,i

f

Figure 8.29 (cont.) (b) Gluteal strengthening exercise.

A weak gluteal muscle can be worked in this on·bike position. Thus, the rehabilitatio n aims of stability (holding the pelvis in single-leg stance), strength ening of the gluteals, and re hea rsing dissociation of the limb from the pelvis are incorporated

with a "whip_like" transfer of momentu m through eJbow extension and through the small mu scles of the forearm and hand, transferring propulsive [orce to the ball. The skilled clinician should assess both the scapulohumeral and the truncal mechanics in a throwing sportsperson. The role of the scapula in throwing is discussed in more detail below. and th e back, trunk, and hips serve as a cen ter of rotation and a transfer link from the legs to the shoulder. Throwing can be divided into four phases: ,. 2. 3. 4.

preparation/wind-up cocking acceleration deceleration/follow-through

80% time sequence 2% time sequence 18% time sequence

Wind-up Wind-up (Fig. 8.)0 overleaf) establishes the rhythm of the pitch or throw. During wind-up, the body rotates so that the hip and shoulders are at 90" to

(c) High box step-ups, Strength imbalances in the right quadriceps are addressed in this high stepping activity. The cyclist maintains an anterior tilt to mimic the on-bike position

the target. The m ajor forces arise in the lower half of the body and develop a forward-moving "controlled fall." In pitch ing, hip flexion or the lead leg raises the center of gravity. The wind-up phase lasts 500-1000 milliseconds. During this phase, muscles of the shoulder are relatively inactive.

Cocking The cocking movement (Fig. 8.31 overleaf) positions the body to enable all body segments to contribute to ball propulsion. In cocking, the shoulder moves into abduction through full horizontal extension and then into maximal external rotation. When the scapula is maximally retracted, the acromion starts to elevate. With maximal external rotation, the shoulder is "loaded," wi th the anterior capsule coiled tightly in the apprehension position, storing elastic energy. The internal rotalors are stretched.I:lo! At this stage, anterior joint forces are maximal and can exceed )50 newtons (N).

99

Fundamental princip les

Figure 8.30 Throwing-wind-up

these structures can become attenuated and lead to subtle instability. 12 5 In the trunk, tensile forces increase in the abdomen, hip extensors, and spine, with the lead hip internally rotating just prior to ground contact. The cocking phase ends with the plan ting of the lead leg, with the body positioned for energy transfer through the legs, trunk, and arms to the ball. This phase also lasts 500-1000 milliseconds. The wind-up and cocking phases together constitute 80% of the duration of the pitch (approximately 1500 milliseconds). Shoulder cocking continues with the counterclockwise rotation of the pelvis and trunk (when viewed from above), which abruptly places the arm behind the body in an externally rotated position. Lateral trunk flexion determines the degree of arm abduction. When viewed in the coronal plane, the relative abduction of the humerus to the long axis of the trunk is a fairly constant 9 0-100", regardless of style. The overhand athlete leans contralaterally, while the side-arm or submarine thrower actually leans toward the throwing arm. Rotation of the trunk also aids in abduction. Although the muscles of the shoulder produce little abduction during the early cocking phase of a wen-executed throw. the periscapular muscles are quite active. The force couple between the upper trapezius and serratus anterior initiates acromial elevation. and the lower trapezius maintains elevation at abduction angles greater than 65°.

Acceleration

Figure 8.3 1 Throwing- cocking

Toward the end of cocking, the static anterior restraints (anterior inferior glenohumeral ligament and anterior inferior capsule) are under the greatest strain. Because of the repetitive nature of throwing,

100

The acceleration phase (Fig. 8,32) is extremely explosive. It consists of the rapid release of two forces-the stored elastic force of the tightly bound fibrous tissue of the capsule, and forceful internal rotation from the in ternal rotators (subscapularis, pectoralis major, latissimus dorsi, teres major). This generates excessive forces at the glenohumeral articulation'26 and, thus, the cuff musculature remains highly active to keep the humeral head enlocated in the glenoid. Large muscles outside the rotator cuff are responsible for the subsequent acceleration of the arm. This includes muscles of the anterior chest wall, as well as the muscles and fascia that surround the spine. The critical role of the muscles controlling scapulothoracic motion-scapular positioning and stabilization against the thorax-is discussed below. At the shoulder, acceleration is the shortest phase of the throwing motion. lasting only 50 milliseconds

Clinica l aspect s of b iome ch a n ics an d sporting injuri e s

Figure 8.32 Throwing-acce leration

Figure 8.33 Throwing- deceleration/ follow-through

(2% of the overall time). In both the acceleration and

the properly thrown pitch, the spine and its associated musculature have a significant role as a force attenuataI'. Toward the end of the pitching motion, the torso, having decelerat ed so the arm could acquire kinetic energy in the arm acceleration phase, begins to rotate forward. The forward rotation of this larger link segment helps to reacquire some of thi s energy. This theoretically reduces the burden on the serratus anterior and other stabilizers, which are attempting to eccentrically maintain the position of the scapula and maintain the humeral head within the glenoid. In addition to the high stresses on the posterior shoulder structures, this phase places large stresses on the elbow flexors that act to li mit rapid elbow extension. This phase lasts approximately 350 milliseconds and constitutes approximately 18% of the total time. The role of the trunk in throwing is clear. When trunk motion is inhibited, or the potenlial ground reaction force reduced, throwing velocity is markedly lower. In one study, with a normal overhead throw rated at 100%. peak velocities d ropped to 84% when a forward stride was not allowed. and dropped to 63.5% and 53.1% when the lower body and lower body plus trunk were restricted, respectively.'n Peak baIl-release velocities attained by water polo players are approximately half the velocity that a thrown

the late-cocking phases, muscle fatigue (which is accelerated if there is mild instability due to attenuated static restrains) can lead to loss of coordinated rotator cuff motion and, thus, decreased anterior shoulder wall support. The acceleration phase concludes with ball release, which occurs at approximately ear level. The movements involved in acceleration place enormous v3:2 ratio) strong in swimmers. Swimmers strive to have a long stroke as this improves propulsion, but the resultant prolonged shoulder adduction and internal rotation may lead to hypovascularity of the supraspinatus muscle and increased risk of tendinopathy. This is exacerbated if hand paddles are used. Therefore, the stroke may need to be shortened to decrease injury risk. Other technique factors that predispose to impingement are an excessively straight arm during the recovery phase and insufficient body roll. Body also increases the efficiency of fonvard propulsion in freestyle and backstroke by allowing the shoulder to act in a more neutral position relative to the coronal plane, balancing the adductors and abductors. To prevent shoulder injury in a swimmer. the practitioner should:

Table 8.10 Common technical errors in specific swimming strokes that predispose to injury

Swimming stroke Butterfly

Common technical error that predisposes to shoulder injury Entering the arms into the water too far outside the line of the shoulders or with the arms too close together

Backstroke

Pull-through with elbows extended, which results in a straight pull-through instead of an S-shaped pull-through

ron

Insufficient body roll Freestyle

A line of pull-through that crosses far beyond the midline Striving for too much length in the stroke Insufficient body roll

Breaststroke

Excessive elbow extension

ensure that the swimmer has adequate strength and control of the scapular stabilizing muscles ensure that the internal to external rotator strength ratio is normal (forthe sport)130 ensure the swimmer stretches the scapulohumeral muscles, including the infraspinatus, teres minor, and subscapularis muscles correct cervical and thoracic hypomobillty.

When assessing swimming technique to prevent injury, the practitioner should look for good elbow height during the recovery phase of the stroke and adequate body roll. (A bilateral breathing pattern increases body roll.) Common technical errors in specific swimming strokes that predispose to injury are shown in Table 8.IO.

Biomechanics of tennis Tennis places great stress on the shoulder and elbow. The shoulder receives maximal loads during the serve and overhead strokes, and rotator cuff impingement may arise from a mechanism parallel to that in throwers and swimmers. The tennis service begins with 90° abduction and external rotation in the cocking phase. The shoulder then moves rapidly from external to internal rotation and from abduction into forward flexion. The deceleration or followthrough phase is controlled by the external rotators. Impingement is exacerbated by increased internal rotation of the shoulder in forward flexion. Over 50% of the to tal kinetic energy and total force generated 106

in the tennis serve is created by the lower legs, hips, and trunk. In many tennis serving motions, the feet and body are actually off the ground when this rotation reaches its maximum peak. The entire stable base of the arm, in this situation, rests on the scapula rather than on the feet or the ground. Therefore, stability of the scapula in relationship to the entire moving arm is the key point at this important time in the throwing sequence. If we compare the biomechanics of serving to those of pitching, we find that the forces transmitted to the shoulder are lower in serving, as the tennis racquet dissipates much of the impact force. This enables the tennis player to serve more than roo times daily, whereas the pitcher can only pitch approximately every fourth day. Because of the racquet. tennis serving requires a smaller range of internal/external rotation than pitching. Nevertheless, shoulder instability may develop over time.

Tennis biomechanics and elbow pain Elbow pain (Chapter 22) is extremely common among tennis players. This may be due to the dominant activity of the wrist extensors. Poor backhand technique is a major predisposing factor. 'j' The role of racquets in the development of increased force through the elbow is discussed in Chapter 9. Commencing tennis late in life also appears to be a risk factor for elbow pain.

Cl in ica l aspects of biomec h a ni cs and sport i ng i nju ri es

Tennis racquets Tennis racquets can play an important role in injury and, although they could be categorized as a factor in tennis biomechanics, we discuss them in Chapter 9.

Biomechanics of other overhead sports Any sport involving overhead activity may lead to the development of shoulder and elbow problems. Many of the principles of biomechanics discussed above apply to these sports. Water polo and volleyball provide the clinician with some specific challenges.

Water polo Water polo players are particularly susceptible, as the sport involves a combination of swimming and throwing. Shoulder impingement commonly occurs in association with anterior instability. Instability may be atraumatic or traumatic (e.g. as a result of a block). Water polo players are susceptible to imbalance between internal and external rotators and they may have poor scapular contro1. Prevention ofinjury may be enhanced by prophylactic strengthening of the external rotators and scapular stabilizers. Water polo players have a restricted throwing action due to the large ball size, the presence of the water, and the lack of a base of support. This leads to poor throwing biomechanics-shoulder stabilizers

must generate more forces and there is reduced elbow angular acceleration. They may attempt to overcome this by angling their bodies to become more horizontal in the water when shooting, thus enabling them to throw with the shoulder at 90" of abduction, reducing the likelihood of impingement.

Volleyball The overhead spike in volleyball is associated with a high incidence of shoulder injury. The technique is similar to the throwing action. There is limitation in the amount of follow-through available with a spike due to the proximity of the net. Another potential hazard for the "spiker" is that the spike may be blocked by an opponent. Internal and external rotator muscle balance must be maintained to prevent injury, and the practitioner should also ensure that sportspeople have adequate scapular contro1. An injury that is unique to volleyball, and results from specific biomechanics in association with an anatomical predisposition, is suprascapular nerve entrapment at the spinoglenoid notch. Il~ Players who use the "float" serve and who have a suprascapular nerve that turns sharply after passing through the spinoglenoid notch are predisposed to tractioninduced palsy of the suprascapular nerve (see Fig. zI.z8 and page 373 in Chapter ZI).

107

Fundamental principles

CLINICAL SPOR T S MEDICINE MASTERCLASSES www cl j njca ! spo(tsmedjc j ne

+

com

Listen to the interview with chapter authors.

Acta Physiol Scand [989; 136(2):217-27. 5. Franz JR, PayIo KW, Dicharry J et ai. Changes in the coordination of h ip and pelvis kinematics with mode of

See demonstration ofbiomechanical assessment.

locomotion. Celit Postllre 2009;29(3):494-8.

See a demonstration of the original low-Dye technique augmented with reverse sixes an d calcaneal slings

6. Pohl MB, Buckley IG. Changes in foot and shank

anchored to the lower leg.

coupling due to alterations in foot strike pattern duri n g running. C/in Biomech (Bristol, Avon) 2008;23(3):

III

RECOMM END ED WEBSITES

Barton

C/. Bonanno D, Mcnz HB. Development and

334-4I. 7. Mann RA, Baxter DE, Lutter LD. Running symposium.

evaluation of a tool for the assessment of footwear characteristics: www,ncbLnlm.nih.gov/pmc!articles/

Foot Ankle 1981;r{4):I90-224. 8. Williams KR. Biomechanics of runnin g. Exerc Sport Sci

PMC.z678 ro8/?too!.,pubmed

m

Rev 1985;ln89-441. 9· Ferber R, Davis 1M, Williams DS , 3rd. Gender

RECOMMENDED READING

differences in lower extremity mechanics during

Barton q, Bonanno D, Menz HB. Development and evaluation of a tool for the assessment of footwear

running. clill BiomeciJ (Bristol , Avon) 2003;18{4):3S0-7. IO. Riley PO, DellaCroce U, Kerrigan DC. Effect of age on

characteristics. J Foot Allkle Res 2oo9;23{2):IO.

lower extremity joint moment contributions to gait

Kaufman KR, Brodine SK, Shaffer RA, Johnson CW, Cullison TR, The effect of foot structure and range of motion on musculoskeletal overuse injuries. Am J

Sports Med 1999:27(S):585- 93. Lang LM, Volpe RG, Wernick

J. Static biome, ')

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 fruit~ 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

~ I.

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

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

from simulated learn post exercise.] Sci Med Sport

REFERENCES

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

10.

144

l8. Ivy JL, Goforth HW Jr, Damon 8M et aL Early

water immersion on repeated cycling performance and

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

and cumulative fatigue in competitive basketball.

Coingestion of protein with carbohydrate during

] Sports Sci 2008;26(n):lI35-4S.

recovery from endurance exercise stiumulates muscle

Ingram J, Dawson B, Goodman C et a1. Effect of

protein synthesis in humans.] Appl Physio12009;106:

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 physi~ 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.

William Osler

When a patient presents with an overuse injury, \~!''l ('.... an accurate pathological diagnosis must be I~~ ~ supplemented by assessment of the etiologic factors l!i\f':) h 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.

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:

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

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, espe~ 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 Add straight leg raise

Shoulder abducted to 110° 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

4·

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

iii L

2001;29:300 -3.

5·

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

6.

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

2.

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

3.

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

156

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 con~ 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). Avoiding re-injury is important, as re-injury can account for the greatest time lost from sporting activity. If early active mobilization is begun immediately after a moderate soft tissue injury. a larger connective tissue scar can develop.8 In contrast. immobilization appears to provide the new granulation tissue with greater tensile strength to withstand the forces created by generated muscle forces.>·8 Complete immobilization is primarily required for acute fractures. Certain stress fractures (e.g. tarsal navicular fractures) also require immobilization. Occasionally in severe soft tissue injuries, it may be helpful to immobilize the injured area for up to 48 hours to limit pain and swelling. Immobilization can be obtained through the use of rigid braces, air splints, taping. thermoplastic materials or, most commonly, with the use of a plaster cast. Despite the poor strength of plaster cast compared to the more rigid fiberglass cast, the low cost and supreme molding properties keep plaster cast clinically popular.') Plaster casts have the disadvantages of being relatively heavy, prone to damage, and not waterresistant. For undisplaced fractures and immobilization of soft tissue injuries, fiberglass casts are preferred. Fiberglass casting material is light, strong, and waterproof. A waterproof underwrap is available that enables the athlete to bathe without the need to protect the cast. This allows those with lower limb casts to exercise in water to maintain fitness.

Treatments used f o r musculoske l etal co n dit i o ns

Protected mobilization Mobilization has num erous tissue benefits.,G One way to achieve early, but safe, mobilization is by "protected mobilization." This term refers to the use of protective taping or bracing to prevent movement in a direction that would cause excessive stress on an injured structure. For example, a hinged knee brace prevents valgus strain in a second degree medial collateral ligament injury. Non-injured structures are allowed to move (L e. the knee joint continues to function), and this feature distinguishes protected mobilization from complete immobilization. This allows enough movement to prevent stiffness, maintain muscle strength, and improve the nourishme nt of the articular cartilage, while still protecting the damaged ligament. After the short initial immobilization period, the mobilization of the injured skeletal muscle should be started gradually (I. e. within the limits of pain) as soon as possible. Early mobilization induces more rapid and intensive capillary ingrowth into the injured area, better regeneration of muscle fibers, and more parallel orientation of the regenerating myofibers in comparison to immobilization.S. 8. JO

Continuous passive motion Continuous passive motion is currently a part of patient rehabilitation regimens after a variety of orthopedic surgical procedures. It can enhance the joint healing process, and has shown to stimu· late chondrocyte PRG4 me tabolism in laboratory shIdies.'1

athletes u sed some form of medicati on during the Atlanta and Sydney Olympics respective ly. 1 8. :o. ~f The most frequently u sed therapeutic dmgs included nonsteroidal an ti-inflammatory drugs (NSAIDs), respiratory drugs, and various analgesics. This section discusses a range of therapeutic drugs includi ng analgesics, NSAJDs, corticosteroids. nitric oxide, and antidepressants. Various methods of drug delivery, including iontophoresis , cortico· steroid, and anesthetic injections, as well as thera· pies such as sclerosing therapy and prolotherapy, are discussed. Interventions for articular cartilage and osteoarthritis including hyaluronic acid therapy, glucosamine sulfate, and chondroitin sulfate use are also discussed.

Analgesics The RICE approach, mentioned above, can provide nonpharmaceutical pain relief in the acute phase of some sporting injuries. Although the RICE approach is important in the early stage of tissue healing. it may not always provide adequate pain relief. Analgesic drugs are often then considered. The term "anal· gesicn translates from the Greek an (without) and algos (pain). Therefore an analgesic is used to relieve pain or achi eve an algesia. Analgesics are used in the acute phase immediately after injury to reduce pain. Subsequent use depends on the degree and duration of pain. Pain reduction during rehabilitation may facilitate move· ment. Aspirin (ASA). paracetamol (acetaminophen), and codeine are the most commonly used analgesics, either singly or in combination.

Therapeutic drugs The sports medical team plays an important role in preparing and maintaining an athlete at peak performance. Every attempt is made to promote both the health and the performance of a player. Therapeutic drugs can help accelerate rehabilitation, and as a result can allow a quicker rehIrn to sport post injury. In addition, therapeutic drugs can allow a player to continue their sport while injuries are healing, which is especially relevant at a professional level of sport. Recent studies have investi gated the use of thera· peutic drugs and nutritional supplements by athletes during sporting competition s. IS-~~ These shldies have shown an average use of 1.7 supplements per athlete and 0.8 medications per athlete during competition in track and field event s, and 0.63 medications per player per m atch among international soccer players.J8.2o.21 Additionally, 61% and 54% of Canadian

Aspirin At low dosages (2S0- JOO mg). aspirin (or acetylsalicylic acid (ASA]) h as an analgesic and antipyretic effect. At higher dosages aspirin also has an antiinflammatory effect. but these dosages are associ· ated with a significan t incidence of adverse effects, particularly of the gastrointestinal system. We advise against the use of aspirin in acute injuries because it inhibits platelet aggregation and, thus, may increase bleeding associated with the injury.

Paracetamol Paracetamol (acetaminophen) has an analgesic and antipyretic effect but has no influence on the inflam· matory process and no effect on blood clotting, and is ineffective in inten se pain;>' 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 system.~) ' --'-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. ~choll P, Fedderm ann N, Junge A et aL The use and abuse of painkillers in international soccer. Am J Sports Med 20°9:37(2):260-;.

22. Tscholl P, Junge A, Dvorak J.111e lise of medication and nutritional supplements during FJFA World Cups 2002

and 2006. Br J Sports Mrd 2.008;42725-30.

23. Bertolini A, Ferrari A, Oltani A et al. Paracetamol: new vistas of an old drug. e NS Dnlg Rev 2006;12{3- 4}: 25 0 -75. 24. Dani M, Guindon J, Lambert C et al. 111e local

antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors. Eur] P/UJnIJUCOI2007;S73(1-3):214-15· 2). Toms L, Derry 5, Moore AR e t al. Single dose oral

paracetamol (acetaminophen) with codeine for postoperative pain in adults. each Data Syst ReI' 2009:1. 26. Derman EW. Pain management in sports medicine:

Sports M,d 2007;28 (II):909-15. 35.

Paolorri JA, Milne C. Orchard J el al. Non·ste roidal anli-inflammatory drugs in sports medicine: gUidelines for practical but sensible use. Br] Sports Mcd

2009:43(11):863- 5· 36. Radi Z, Khan N. Effects ofcyclooxygenase inhibition

on bone. tendon, and ligament healing. IlIjlmll Res

200S:S4{9Hs8-66. 37. Rahusen FTG. Weinhold PS, Almekinders l C. Nonsteroidal anti·inAammalory drugs and acetaminophen in the treatment of an acute muscle injury. Am J Sporls Med 2004:32(8):1856- 9. 38. Derman E. Schwellnus M. Pain management in sports

medicine: use and abuse of anti·anflammatory and other agents. Stll Afii can Fam Pmc 2010;S2{i):29- 32. 39. Warden SJ. Prophylactic misuse and recommended use

of non-steroidal anti-inflammatory drugs by athletes.

Br] SporlS Mtd 2009;43 (8 ):548~9. 40. Zi ltene r JL, Leal 5, Fournier PE. Non·ste roidal anti·

inflammatory drugs for athletes: an update. A)!/} Phys

Rellab Med 20 10;S3(4):2.78-88. 41. Kroenke K, Krebs EE, Bair MJ. Pharmacotherapy of

use and abuse of anti-inflammatory and other age nts.

chronic pain: a synthesis of recommendations from

Slh African Fam Pmc 20 IO:p{t):27-32.

systematic reviews. Gell Hosp Psych 20°9;31(3):206-1 9.

27. Stanos SP. Topical agents for the managem en t

of musculoskeletal pain .] Pail! SYIl1P Manage 20°7:33(3):34 2-55 . 28. Vriens

J, Nilius B, Vennekens R. Herbal compounds

and toxins modulating TRP channels. ClIrr Nellropliarll! 2008;6(1)79-9 6. 29. Mason L, Moore AR, Edwards IE et a1. Systematic

review of efficacy oftopica[ rubefacients containing salicylales for the treatment o f acute and chronic pain.

BM] 20°4:328(7446 ):9 5. 30. Mason L, Moore RA. De rry S et al. Systematic review of topical capsaicin for the treatment of chronic pain. BM] 2.0°4:328(7446):9 9 1. 3I. Li Wan. Po A. PI Practice checklist: Topical analgesicS.

Plianl1 J 1996. 32. Gorski T. Cadore EL, Pjnto 55 et al. Use of

Nonsteroidal anti·inflammatory drugs (NSA IOs) in triathletes: prevalence, level of awareness, and reasons for use. Br] Sports Med 2011; 4 5(2):85-9 0 . 33. \Vharam PC, Speedy DB . Noakes TO et a1. NSAID use increases the risk of developing hyponatremia

42. Smith C. Timing of NSAID treatment afte r muscle

injury or training. eME :W08;26(7):3SD-S. 43. Alaranta A. Alaranta H, Helenius I. Use of prescription

drugs in athleles. Sports Med 2008;38 (6):449-63. 44. De Carli A. Volpi P. Pelosini I etal. New therapeutic

approaches for management of sport-induced muscle strains. Adl' Tiler 20°9;2 6(12):1°72-8345. Dietzel D. Hedlund E. Injections and relurn to play.

ell" Pain

HUldac/te Rep 20°5:9( 1):11- 16.

46 . Tokisk JM . Powell ET. Schlegel TF el al. Ketorolac

use in the National Football league. PIi'ls Sp0risltled 2ooz;30{ 9):19- 25·

47. Marnelt LJ. The caXIB experience: a look in the rearview mirror. All)! Rw Pharmacol Toxicol 2oo9;49{1): 26S-9°· 48. Mason 1, Moore RA. Edward JE et '11. Topical NSAIDs

fo r chronic musculoskeletal pain: systemic review and meta·analysis. BMC MllsCllloskdet Disord 2004;5:28. 49. Hyldahl RD. Keadle" Rouzier PA et al. Effects of

ibuprofen lopical gel on muscle soreness. Med Sci Sparls Exerc 2.0!O;42(3):614- 2.r.

203

SO. Bogduk N. A narrative review of intra·articular corticosteroid injections for low back pain. Pain Med 2ooS;6(4):287-96 . SI. Scott A, Khan KM. Corticosteroids: short·term gain for long· term pain? Lancet 2010;376(9754):1714-15. S2. Scutt N, RolfC, Scutt A. Glucocorticoids inhibit tenocyte proliferation and tendon progenitor cell recruitment.] Orlh Res 2006;24(2):173-82. 53. Wong MW, Tang YY, Lee SK et al. Effect of dexamethasone on cultured human tenocytes and its reversibility by platelet-derived growth factor.] Bone

Joint Surg AJJ1 200r85-A{IO):I914-20. 54. Brukner P, Nicol A. Use of oral corticosteroids in sports medicine. Cllrr Sports Med Rep 2oo4;p81-3, 55. Gebhard KL, Maibach HI. Relationship between

Am] Sports Med 2008;36(6):n60-3. 64. Paoloni fA, Murrell GA, Burch RM et aL Randomised, double-blind. placebo-controlled clinical trial of a new topical glyceryJ trinitrate patch for chronic lateral epicondylosis. Br] Sports Mea 2009:43(4):299-3°2. 65. Cumpston M, Johnston RV, Wengier L et al. Topical glyceryl trinitrate for rotator cuff disease. Cocll Delta Sysl Rev 2oo9(3):CDo06355,

66. McCallum SD, Paoloni JA, Murrell GA. Five-year prospective comparison study of topical glyceryl trinitrate treatment of chronic lateral epicondylosis at the elbow. Br] Sports Med 2011:45(5):416-20, 67. Paoloni JA, Murrel GA. Three-year followup study of topical glyceryl trinitrate treatment of chronic

systemic corticosteroids and osteonecrosis. Am] Clin

noninsertional Achilles tendinopathy. Foo~ Allkle lilt

Dmnato! 2001;2(6):377-88.

2007:2.8{ro):ro64-8.

56. Gurney AB, Wascher DC. Absorption of

68. Alfredson H, 6hberg L, Zeisig E et al. Treatment of

dexamethasone sodium phosphate in human

midportion Achilles tendinosis: similar clinical results

connective tissue using iontophoresis. Am] Sports

with US and CD·guided surgery outside the tendon

Med 2008;36(4)753-9.

and sclerosing polidocanol injections. Kllee Surg Sports

57. Hamann H, Hodges M, Evans B. Effectiveness of iontophoresis of anti-inflammatory medications in the

Tmum Artl! 2007;15(12):1504-9. 69. Ceulen RPM, Bullens-Goessens YIJM. Pi-Van

treatment of common musculoskeletal inflammatory

De Venne SJA et aL Outcomes and side effects of

conditions: a systematic review. Phys Tiler Rev

duplex-guided sclerotherapy in the treatment of great

2006:11(3):190-4·

saphenous veins with r% versus 3% polidocanol foam:

58. Bolin DJ_ Transdermal approaches to pain in sports injury management. CUrr Sports Med Rep 2003;2:

30 3-0 9. 59. Osborne HR, Allison GT. Treatment of plantar fasciitis by Low Dye taping and iontophoresis: short term results

results of a randomized controlled trial with I-year follow-up. Dermatol Surg 20°7:33(3):2.76-81. 70. Rabago 0, Slattengren A, Zgierska A. Prolotherapy in primary care practice. Primary Care 2010:37 (1):65-8o. 71. Cusi M, Saunders J, Hungerford B et al. The use of

of a double blinded, randomised. placebo controlled

prolotherapy in the sacroiliac joint. Br] Sports Med

clinical trial of dexamethasone and acetic add, Br]

2010A4(2):IOO-4·

Sports Med 2006;40(6):S45- 9. 60. Paoloni fA Appleyard RC, Nelson J et al. Topical nitric oxide application in the treatment of chronic extensor tendinosis at the elbow: A randomized. double-blinded, placebo-controlled clinical trial. Am] Sports Med 2003;31(G):915-20. 6r. Paoloni JA, Appleyard RC. Nelson J et al. Topical glyceryl trinitrate treatment of chronic noninsertional achilles tendinopathy. A randomized. doubleblind, placebo-controlled trial.] Bone Joint Surg Am 2004;86 (5):9 16- 22.. 62. Paoloni lA, Appleyard RC, Nelson J et al. Topical glyceryl trinitrate application in the treatment of chronic supraspinatus tendinopathy: a randomized,

72. choi H . McCartney M, Best TM. Treatment of osteitis pubis and osteomyelitis of the pubic symphysis in athletes: a systematic review. Br] Sports Med 2on:45(I):57- 6 473. Rabago D. Best TM, Zgierska AE et al. A systematiC review of four injection therapies for lateral epicondylosis: prolotherapy, polidocanol, whole blood and platelet-rich plasma, Br] Sports Med 2009A3(7):471-SI. 74. Yelland MJ, Sweeting KR, Lyftogt JA et aL Prolotherapy injections and eccentric loading exercises for painful Achilles tendinosis: a randomised triaL Br] Sports Med 2.011;45(5):421- 8. 75. Wandel S f P, funi P, Tendal B et al. Effects of

double-blinded, placebo-controlled clinical triaL Am]

glucosamine. chondroitin, or placebo in patients with

Sports Med 2005:33(6):806-13.

osteoarthritis of hip or knee: network meta-analysis,

63. Kane TPC, Ismail M, Calder JDF. Topical glyceryl

204

trinitrate and noninsertional achilles tendinopathy.

EM] 201O{Sep 16):341:C4675.

Tre at m en t s us ed fo r m u s c u loske let al co n ditio ns 76. Bellamy N, Campbell

r. Robinson V et al.

91. Hogan Q, Dotso n R, Erickson S et al. Local anesthetic myotoxicily. a case and re view. AIl(st/lesio/ogy

Viscosupplemenlation for the treatment of

osteoarthritis orlhe knee. Coclmllle Dataoose Syst Rev 2005; 18(2):CDo0 5J2L

1994;80(4):94 2 -7. 92. James P, Barbour T, Stone 1. The match day use of ultrasound during professional football fina ls matches.

77. Mei-Dan 0, Klsh B, Shaba! S, M ct a1. Treatment of

BrJ Sports Med 2010;44(16):U49-P,

osteoarthritis of the ankle by intra-articular injections of hyaluronic acid: a prospective s tud y. ] Am Podinlr Med

93- Porozov S, Cahalon L. Weiser M e t al. Inhibition of 11·1 13 and TNF·(l secretion from resting and activa ted

Assoc 2010:100(2):93-100.

human immunocytes by the homeopathic medication

78. Migliore A. Granata M. Intra-articular me of hyaluronic

Traumeel S. elin Drv II11n1 2oo4:n(2}:143-9.

acid in the treatment of osteoarthritis. Clill Inl er Aging

9 4. Orizola AJ. Vargas F. The efficacy of Traum eel S versus

2008 :3(2):3 6 5-9_

dic10fenac and placebo ointment in tendinous pain in

79. Agganval A, Sempowski JP. Hyaluronic acid injections

elite athletes: a random ised con trolled trial. Med Sci

for knee osteoarthritis. Syste matic review of the

Sports Exerc 2oo7:39(,):s79.

literatu re. Can f'am Physician 2004;50:249-56. 80. Anandacoomarasamy A, March L. Current evidence fOT

95. Drake MT Clarke BL. Kh osla S. Bisphosphonates: mechanism of action and role in clinical practice.

osteoarthritis treatments. T111:r Adv MIlSc Dis

Mayo C/in Proc 2008:83(9):1032-45,

2010;2 11):17- 28. 8 1. Arrich

J. Piribauer

F, Mad P et al. Intra-articular

96. McNichoJl OM , Heaney LG, 111C safety o f bisphosphonate u se in pre-menopausal women on

hyaluronic acid for the treatmen t of osteoarthritis of the

corticosteroids. CIIIT Dmg 5afzolo ;5(2) :18z-7.

knee: sys tematic review and meta-analysis. Ca ll Mrd

Assoc] 2005:172(8):1039- 4 3.

97. Black OM, Kelly MP . Cenant HK et 01.1. Bisphosphonates and fractures of the

82. Conrozier T. Vignon E. Is there evidence to support

subtroch anteric or diaphyseal femur. N EnglJ Med

the indusion of viscos upplementation in the treatment paradigm fo r patients with hip osteoarth ritis? eli)! Exp RheulHalo!2ooS;23(5):7 11- 16.

2010;362: l761-71. 98. Milgrom C, Finestone A. Novack V e t al. The effect of prophylactic treatment with risedronate on stress

83. La GH, LaValley M. McAlindon T et a1. Intra·articular

fracture incidence among infantry recruits. Bolte

hyaluro nic acid in treatment of knee osteoarthritis: a m eta ·analysis. ]AMA 2003;29°(23):3115- 21.

20°4;35:4 18 -24. 99. Stewart GW, Brunet ME. Manning MR et a l. Treatment

84. Qvislgaard E. Christensen R, Torp-Pederse n S et

of stress fractures in a thletes with in travenous

al. Intra.·articular treatmen t of hip osteoarthritis: a randomized trial of hyaluronic acid, corticos teroid. and iso tonic saline . O5leo Cart 2006;14(2):163-7 0. 8S. Moulin DE. System atic drug treatment for chronic muscu loskeletal pain. c/in] Pa ill 200l;ITS86- 93. 86_ O'Malley PC. Balden E, Tomkins G et 01.1. Treatment of fibromyaJgia with antidepressants, a m eta-analysis. ] Gm rllt Med 2000;15{9 ):6 59-66. 87. Tofferi JK Jackson

JJ. O'Malley PC . Treatment of

pamidronate, Clill] SpOrl Med 200S ;15{2):92- 4, TO O,

Connell DA. Ali KE . Ahmad M et al. Ultrosoundguided autologou s blood injectio n for tennis elbow,

Skeltwl RadioI2006;3S(6):371-7. 101. Edwards SG. Calandruccio JH, Autologous blood injections for refractory lateral epicondylitis,] Halld

511rg Alii 2003;28 (2):272-8. 102. Ehrenfest DMD . Rasmussen L, Albrcktsson T. C lassification of platelet concentrates: from pu re

fi bro myalgia with cydobenzaprine: a m e ta·analysis.

platelet-rich plasma (P-P RP) to leucocyte· and platelet·

Aliliritis Rheum 20°4;51(1):9-1 3.

rich fibrin (L-PRF). TWlds Biotcclino/ 2oo9;27{3):

88. Goldenberg DL. Pharmacological treatment of fibromya\gia and other chronic musculoskeletal pain.

1;8-67. 103. de Mos M. van der Windt AE, Jahr H et al. Can

Best Prad Res eli" RJu!umatoi2007:2IU):499-5U.

platelet-rich plasma e nhance tendon repair? A cell

89, Orch ard J. Be nefits and risks of u sing local anaestheic

culture snldy, Am j Spo rt s Med 2008:36(6):1 17 1-8.

for pain relief to allow early return to play in professional football. Br] Sports Mal 2002;3 6:209 - 13. 90. Zink W Graf 8M. Local anaesthetic myotoxicity. Rrg

Allestl, Pain Med 2oo4;29:3H-40.

104. Sanchez M, Ani tl.1a E. Azofra J et 01.1. Comparison of surgically repaired Achilles tendon tears using platelet· rich fibrin matrices. Am] Sport Med 2007:35 (2): 245-5 1•

205

105. Schepull T. Kvist J, Norrman H et a1. Autologous

of therapeutic ultrasound use by physical therapists

achilles tendon ruptures: A randomized single-blind

who are orthopaedic certified specialists. Phys T1ur

study. Am] Sports Med 20n;39(1):38-47. lO6_ Kon E, Filardo G, Oe\cogliano M et al. Platelet-rich

plasma: new clinical application. A pilot study for the treatment of jumper's knee. Injury 20°9:4°: 59 8- 60 3. I07. Filardo G, Kon E, Della Villa S et al. Use of plateletrich plasma for the treatment of refractory jumper's knee. Jnt OrtllOP 2010 Aug;34{G)909-I,. 108. Gaweda K, Tarczynska M, Kryzanowski W. Treatment of achilles tendinopathy with platelet-rich plasma.

lilt] Sports Mal 20IO;3 I(8):S77-83I09. Randelli P$, Arrigoni p. Cabitza Pet al. Autologous platelet rich plasma for arthroscopic rotator cuff repair. A pilot study. Dis ReiJab 2008;30:1584-9. lIO.

Mishra. A Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am J

Sports Med 2006;34:1774-8. III. Peerbooms JC, Sluimer J, Bruijn OJ et al. Positive effect of an autologous platelet concentrate in lateral epicondylitis in a double-blind randomized controlled trial. Am J Sports Med 2010;38(2):255-62. 1I2. Herrera E, Sandoval MC, Camargo OM et a1. Motor and sensory nerve conduction are affected differently by ice pack. ice massage, and cold water immersion.

Phys T1Uf 2010;9°(4):581-91. n3. Tolbert TA. Binkley HM. Treatment and prevention of shin splints. Strength Condit J 2009;31(S):69-72. 114. HingWA, White SG. Bouaaphone A et at. Contrast therapy-A systematic review. Phys T11er Sport 2008;9(3):148- 6 1. tI5. Brancaccio P, Maffulli N, Limongelli FM. Creatine kinase monitoring in sport medicine. Br Med Bull 20°7:81-2 (I) :.2,0 9-3 0. n6. Chmura J, Nazar K. Parallel changes in the onset of blood lactate accumulation (OBLA) and threshold of psychomotor performance deterioration during incremental exercise after training in athletes. Inti J

PsyciJophysio/2010;7P87-90. 117. Chipchase 1S, Trinkle D. Therapeutic ultrasound: clinician usage and perception of efficacy. Hmlg Kong

PhysioJ 2oo3;21(1):,-14. II8. Ferrari CB, Andrade MAB, Adamowski Je et al. Evaluation of therapeutic ultrasound equipments performance. Ultrasonics 2010:5°(7):7°4-9. II9. Watson T. Ultrasound in contemporary physiotherapy practice. UltrasOllics 2008;48(4):321-9.

206

120. Wong RA, Schumann B, Townsend R et al. A survey

platelets have no effect on the healing of human

2007;87(8j:986-94· 121. Mitragotri S. Innovation: Healing sound: the use of ultrasound in drug delivery and other therapeutic applications. Nature Rev Drug Disc 2005:4(3):255-60. 122. Aytar A. Tuzun EH, Eker L et al. Effectiveness of low-dose pulsed ultrasound for treatment of delayedonset muscle soreness: a double-blind randomized controlled trial. Isokille Ex Sci 2008;16(4):239-47. 123. Pounder NM, Harrison AJ. Low intensity pulsed ultrasound for fracture healing: a review of the clinical evidence and the associated biological mechanism of action. Ultrasonics 2008;48(4):330---S. 124. Warden SJ. A new direction for ultrasound therapy in sports medicine. Sports Med 2oo3:33{2):95-I07. 125. Warden 5J, McKeeken 1M. Ultrasound usage and dosage in sports physiotherapy. Ultrasound Med BioI 2002;28(8) :1°75-80. 126. Jones I. Johnson MI. Transcutaneous electrical nerve stimulation. COlltill Edllc Allaesth Crit Care Pain 2oo9;9{4):I30-S· 127. Khadilkar A. Milne S, Brosseau 1. Transcutaneous electrical nerve stimulation (TENS) for chronic lowback pain. Coch Data Syst Rev 2005(3):C0003008. 128. Nnoaham KE, Kumbang J. Transcutaneous electrical nerve stimulation (TENS) for chronic pain Cach Data

Syst Rev 2008{3):CDo03222. 129. Scudds R/, Scudds RA, Baxter GO et al. Transcutaneous electrical nerve stimulation for the treatment of pain in physiotherapy practices in Hong Kong and the United Kingdom- a survey of usage and perceived effectiveness compared with other pain relieving modalities. HOllg Kong Physio J 2oo9:27(1):II-20. 130. Khadilkar A, Odebiyi DO, Brosseau Let al. Transcutaneous electrical nerve stimulation (TENS) versus placebo for chronic low-back pain (review).

Coch Data Syst Rev 2008(4):C0003008. 131. Bjordal/M, Johnson MJ. Ljunggreen AE. Transcutaneous electrical nerve stimulation (TENS) can reduce postoperative analgesic consumption. A meta-analysis with assessment of optimal treatment parameters for postoperative pain. fur J Pain 2°°3;7(2):181-88. 132. Bjordal JM, Couppe C, Chow RT et al. A systematic review oflow level laser therapy with location-specific doses for pain from chronic joint disorders. AilS J

Physio 2°°3;49:107-16.

Trea tm e n ts used fo r mus culos ke le tal cond i tions

133. Bjordal 1M, Johnson M. Iversen V et a1. Low-level

144. Eccles NK. A critical review or randomized controlled

laser therapy in acute pain: a systematic review of

trials of static magnets for pain relier. J Altern Comp

possible mechanisms of action and clinical effects in

Med 2005;1I(3):495-509.

randomized placebo-controlled trials. PJlOtollwd Laser SlIrg 2006;24(2):237-47_ 1}4- Bjordal JM , Lopes-Martins RAB. Iversen VV.

A randomised, placebo controlled trial of low level laser therapy for activated Achilles tendinitis with

145. Mikesky AE, Hayden MW. Effect of static magnetic therapy on recovery rrom delayed onset muscle soreness. Pliys 11ler Sport 2005;6(4): 188- 94. 146_ Pittler M H . Brown EM. Ernst E_ Static magnets for reducing pain: systematic review and meta-analysis of

microdiaiysis measuremen t of peritendinous

randomized trials. Can Med Assoc J 2007:177(7):

prostaglandin E2 concentrations. Br J Sports Mui

73 6 -4 2 .

2oo6AO(I):7G-8o.

147. McKay IC, Prato FS. Thomas AW. A literature review:

135. Chow RT, Bamsley L. Systematic review of the

the effects or magnetic field exposure on blood

literature oflow-levellaser therapy (lUI) in the

flow and blood vessels in the microvasculature.

management of neck pain. Lnsers Slug Med 20 °5:37:46 -;2.

136. World Association crLaser Therapy (WALl). Standards for the design and conduct of systematic reviews with low-level Jaser therapy ror musculoskeletal pain aud disorders. Photonted Laser

Surg 200 6;24(6)759- 60. 137. Lopes-Martins RAS. Albertini Ret al. Steroid receptor

antagonist mifepristo ne inhibits the anti·inflamma tory effects of pholoradiation. P11OlomM umr Surg 006;24(2):197- 20 1.

138. Bjordal JM , Lopes-Martins RAB, Joensen J et al. A systematic review with procedural assessments and meta-analysis of low level laser therapy in lateral elbow tendinopathy (tennis elbow). BMC Musculoskdet Disord 2008;975· 139. Leal Junior E, Lopes·Martins R, Baroni 8 et al. Effect 0[830 urn low-level laser therapy applied before high-intensity exercises on skeletal muscle recovery in athletes. Lasers Med Sci 2009;24(6):857-63_ 140. Stergioulas A, Stergioula M, Aarskog R et a1. Effects of

low-level laser therapy and eccentric exercises in the treatment of recreational athletes with chronic Achilles tendinopathy. Am J Sports Med 2008;36(5):881-7. 141. AI-Mandeel MM . Watson T. The thermal and

nonthermal effects orhigh and low doses of pulsed

Bioe/ecJrontaglletics 2007:28(2):81-98. 148. Laakso L. Lutter F. Youn g C. Static magnets - what are they and whal do they do? Rev Bras Fisiotu 200 9;13(1):10-2.3. 149. Markov M. Magnetic field therapy. a review. Electromag

Bioi Mcd 2007:2.6:1- 23.

150. Reeser IC. Smith DT. Fischer V et al. Slatic magnetic fields nejthe r prevent nor diminish symptoms and signs of delayed onset muscle soreness. Arch Phys Med

Rehab 2005;86(3):565-70. 151. Aktas I. Akgun K, Cakmak B. Therapeu tic effect of pulsed electromagnetic field in conservative trea tment of subacromial impingement syndrome. CUll

Rheumatol2007:26:1234-39· 152.. Zorzi C, DalrOca C. Cadossi Ret a1. Effects or pulsed electromagnetic fields on patients' recovery after arthroscopic surgery: prospective, randomized and double-blind study. Kllee Slirg Sports Traumatol Art!J 2007:15(7):830-4 .

153. Rompe JD, MaffulIi N. Repetitive shock wave therapy for lateral elbow tendinopathy (tennis elbow): a systematic and qualitative analysis. Br Med Bull 2007;83(1):355- 78 . 154. Schmitz C, DePace R. Pain relief by extracorporeal shockwave therapy: an update on the curre nt understanding. Ural Res 20°9;37(4):231- 4. 155. van Leeuwen MT. Zwetver J, van den Akker-Scheek I.

short wave therapy (PS\VT). Physiother Res lilt

Extracorporeal shockwave therapy for patellar

20ro;IS(4):199-2II .

tendinopathy: a review of the literature. Br J Sports Mcd

142. Jan M-H. Chai H·M, Wang C·L et al. Effects of repetitive shortwave diathermy for reducing

20°9:43(3):163-8. 156. Rompe 10, CacchioA, Furia JP e t al. Low-energy

synovitis in patients with knee osteoarthritis: an

extracorporeal shock wave therapy as a treatment

ultrasonographic study. Phys Ther 2006;8G{2):2.36- 44.

for medial tibial s tress syndrome_Alii J Sports Med

143. Colbert AP. Wahbeh H . Harling N etal. Static magnetic field therapy. a critical review of treatment parameters. eCAM 2009 :6(2):133-9.

2010;38:125-32.. 157· Vavken P, Holinka

J, Rompe JD et al. Focused

extracorporeal shock wave therapy in calcirying

207

Fu n d ame nt a l p r i n ci p l es

tendinitis of tile shoulde r: a meta-analysis. Sports

Heald. : A MultidiscipliJlClry Approach 20°9;1(2):137-44_ 158. Buchbinder R, Creen S, Youd J M et al. Shock wave

treatment of chronic pain. Clill J Pain 2001 ;17:S70-6. 173. Ernst E. Canter PH. A systema tic review of systematic

therapy for late ral elbow pain (review). each Data Syst

reviews of s pinal manipulation. J R Sex: Med

Rev 2oo5(4):CDo o3524.

2006:99(4):19 2- 6.

'5 9- Thomson C. Crawford F, Murray G.1be effectiveness of extra corporeal shock wave therapy for plantar heel

174. Wa lser RF, Meserve BB, BoucherTR.111e effectiveness of thoracic spine manipulation for

pain: a systematic review and meta-analysis. BMC

the management of musculoskeletal conditions: a

Muse Dis 2005;6(1):19.

systema tic review and meta·analysis of randomized

160. Zimmermann R, Cumpanas A, Midea F et al. Extracorporeal sh ock wave therapy for the treatment of

clinical trials. J Man MClllip nlt:r 2009 ;17(4):237-46. 175. Graham N, Gross A, Goldsmith C. Mechanical h"action

chronic pelvic pain syndrome in males: a randomised.

for mechanical neck disorders: a systematic review.

double·blind. placebo-con trolled s tudy. Eur Urol

J Rehab Med 2006;38(3):145-52. 176. Clarke lMA. van Tulder MP, Blomberg SMDP etal.

20°9;56:418--24. 161. Cyriax

J. TexrboClk oforllzopaedic medicine. 6th edn.

London: Bailliere Tindall , 1975. 162, Kalte nborn F. Mallllal lllerapv ofllle extrernily j oints.

Traction for low back pain with or without sciatica: an updated system atic review within the fram ework of the cochra ne collaboration. Spille 2006:3 1(14): 159 1-9. 177. Gay RE, Brault

Oslo, Bokhandel, 1975. 163. Maitland GO. Vertebralmanipulatioll. 5th ed. london: Butterworths, 1986.

IS.

Evidence-inform ed management

of chronic low back pain with traction therapy. Spille J 2008:8(1):2)4- 42.

164. McKenzie R. 11le lumbar spille: mcchanical diagllosis

alld tlierapy. Waikane: Spinal Publications, 1981. 165. Bronfort G, Haas M. Evans R et a1. Evidence.informed

178. Graham N, Gross A, Goldsmilh C e t al. Mechanical traction for neck pain with or without radiculopathy.

Cex:h Da ta Syst Rev (J) 2008:3:CDo06408.

management of chronic low back pain with spinal

179. Macario A. Pergolizzi JV. Systematic literature review

manipulation and mobilization. Spille J 2007;8(1):

of spinal deco mpression via motorized traction

21 3- 2 5.

for chronic discogenic low back pain. Pain Pmct

166. Sra n MM . To treat or not to treat: new evidence for the effectiveness of manual therapy. Br J Sports Med

2006 ;6 (3):17 1- 8. 180. Gerwin R, Shan non S, Hong C-Z et al. Interrater reliability in myofascial trigger point examination.

2004;38:521- 5. 167. Vernon H, Humphreys K, Hagino C. Chronic

Pain 1997;69:65-73'

mechanical neck pain in adults treated by m anual

181. Lucas KR. Polus BI . Rich PA. latent myofascial

therapy: a system atic review of change scores in

trigger points: their effects on muscle activa tion

randomized clinical trials. J Ma nip Pilysiol71lCr

and movement efficiency. J Bodywork Move Ther

2° °7;3°(3):215- 27. 168. Hoving JL, Koes BW, de Vel HC e l aI. Manuallhera py, physical the ra py. or continued care by genera)

20°4;8(3):160-6. 182. Selkow N, GrindslaErT, Cross K et al. Short-tenn effect of muscle e nergy techn ique on pain in individuals

practitioner fo r patients vt ith neck pain. Ann Intern

with non-specific lumbopelvic pain: a pilot study.

Med. 2002;136:7 13-22.

J Ma'i Mallip 11ler 2009;17(I):EI4-I8.

169. lull GP, Trott P, Polter HP et al. A randomized con trolled trial of exercise and manipulative therapy for cervicogenic headache. Spine 2002;27(17):1835- 43. 170. Aure OF, Hoel Nilsen

J, Vasseljen O. Manual

therapy

and exercise the rapy in patients with chronic low back pain: a randomized, controlled trial with I-year follow·up. Spine 200p.8(6):;25-31. 17J. Cleland lA, Childs MID, McRae M et a1. Immediate effects of thoracic man ipula tion in patients w ith neck pain: a randomized clinical trial. Mallllal11l1:r 2°°5;1°(2): 127- 35.

208

172. Mior S. Manipulatio n and mobilization in the

[8J. Chaitow L. Muscle energy Jc:cliniqlUs: advanced soft tissue techniques. 3rd ed. Elsevier Health Sciences, 2006. 184. Burns DK. Wells MR. Gross range of motion in the cervical spine: the effects of osteopathic muscle energy technique in asymptomatic subjects. J Am Osteopath Assoc 2006:J06 (3):137-42.

185. Smith M. Fryer G. A comparison of two muscle energy techniques for increasing flexibility of the hamstring muscle group. J BodYlVork Mov TIler 2008:12(4):312-17. 186. Wilson E. Payton 0 , Donegan -Shoaff... Dec K_ Muscle ene q~'Y

tec.hnique in patients with acute lower back

Tr eatments used for muscul oske l e t a l condition s pain: a pilot clinical trial. J. Ort/IOp Sports Pliys Ther

20°3;33:5°2-12.. 187_ Ellis RF, Hing WA. Neural mobilization: a systematic

review of randomized controlled trials with an

analysis oflherapeutic efficacy. J Man Manip Th er 2008;16(1):8--22. 188. Madsen MV, Gotzsche PC. Hrobjartsson A.

Acupuncture treatment for pain: systematic review of randomised clinicallrials w ith acupunchtre, placebo acupuncture. and no acupuncture groups. BM] 2009;

33 8:a311 5189_ Ernst E. Acupuncture: What does the most reliable evidence tell us? J Pain Symp Man 20 °9;37 (4):7°9-14. 190. Manheimer E, Wieland S, Kimbrough E et al. Evidence from the Coch rane Collaboration for traditional

201. Tough EA, White AR, Cummings TM et al. Acupuncture and dry n eedling in the management of myofascial trigger point pain: a systematic review and meta-analysis of randomised controlled trials. Eur j

Pain 20°9;13(1):3-10. 202. Gatvey TA, Marks MR. Wiesel Sw. A p rospective, randomised, double-blind evaluation of triggerpoint injection therapy for low·back pain. Spinc 19 89; 14:9 62- 4. 203. H ong C. lidocaine injection versus dry needling to myofascial trigger point: the importance of the local twi tc.h response. Am j Phys Med Rehab

'9 94:73141'256- 26 3 204. Furlan AD, van Tulder M, Cherkin 0 et a1. Acupuncture and d ry-needling for low back pain: an

Chinese medicine therapies. J Altan Comp Med

updated systema tic review within the frame work of

20 °9;15(9):1001- 14-

th e Cochrane collab oration. Spine :W05;30(8 ):

191. Sun 0 -1, Zhang y, Chen 0-1. Research progress in sports fati gue prevented and treated by acupuncture_

j AcuPJlnc 1ilina Sci 2009:7(2):123- 28_ 192. Sun Y, Gan TJ, Dubose JW et al. Acupuncture and related techniques for postoperative pain: a systematic review of randomized controlled trials. Br j Anae-st1l. 2008;101 (2) :151-60. 193. White A, Foster NE , Cummings M et a1. Acupuncture treatment for chronic knee pain: a systematic review.

Rlzeumatology 2007:46 (3):384-9 0 194. Yuan JP, Purepong NM , Ke rr DP P et ai. Effectiveness of acupuncture for low back pain: a systematic review.

Spillt 2008;33(23):E887-900. 195. Dh illon SM. The acute effect of acupuncture on 20-km cycling performance. eli" j Sport Med 2008;[8 (1):

76- 80. 196. Itoh K, ami H , Kitako ji H . Effects oftender point acupuncture on delayed onset muscle soreness (Da MS) - a pragmatic trial. Chill Med 2008:3(1): 14 . 197. l..ewit K. TIle needle effect in the relief of musculoskeletal pain. Pain 1979;6:83. 198. Simons DC. Clinical and etiological u p d ate of

944- 6 3205. Hsieh Y.LP, Kao MJ. Kuan TS et al. Dry needling to a key m yofascial trigge r point may reduce the irritability of satellite MTrPs. Am J Phys Med Rehab

2007;8615)'397-403206. Huguenin L, Brukner PO, McCrory P et a1. Effect of dry needling of gluteal muscles on straighlleg raise: a randomiscd, placebo controlled, do uble blind trial.

Br J Sports

Mw 2005;39(2):84-9°'

207. D'agostino·Dias M, Fon tes B, Poggetti RS e t al. H yper bark oxygen therapy: types of in jury and number of sessions - a review of 1506 cases. Ull dcrsea

Hyperb Mcd 2008;35(1):53- 60. 208. Mortensen CR. Hyperbaric oxyge n therapy. Cllrf AMes

enl Care 2008;19 :333-7. 209. BOl,omeo eN. Ryan

JL, Marcheno

PA et al.

H yperbaric oxygen therapy for acute ankle sprains. Am j Sports Med 1997;2S{S):619 - 25'

210. Staples

JR, Clem en t DB , Taunton IEet al. Effects

of hyperbaric oxygen on a h uman model ofinjury.

Am j Sports Mcd 1999;27(5):600-5. 211 . Kawada S. Fukaya K, Ohtani M et al. Effects of

myofascial pain from trigger points. J Muse Pail!

pre·exposure to hyperbaric hyperoxia on high-

1996~(I):93-I22 .

intensity exe rcise performan ce, j Strellgth Cond Res

199. Simons DC . Domme rholt J. Myofascial pain syndrome-trigger points. J Musc Pain 2007;15(1):

63- 79200. Huguenin LK. Myofascial trigger points: the curren t evidence. PJt}lS TIler Sport 20°4:5(1):2-12.

2008;22(lj :GG- 74 212. Rozenek R, Fobel BF, Banks

Ie et aI.

Does hyperbaric

oxygen exposure affect h igh-intensity, s hortduration exercise performance? J Strtllgth CO/ld Res 2007;2 1(4):1037-41.

209

Cha pter 14

• Annika Sorellstam:s 500 daily sit-ups are !a.lnous. EJ Clair, Junior Editor Pacific Nortltwest Golf Magazine In recent years, an understanding of the concept of core stability has changed the way in which we rehabilitate our patients. This book uses the term "core stability" but there are many other interchangeable terms (Table '4.I). The musculoskeletal core of the body includes the spine, hips and pelvis, proximal lower limb, and abdominal structures. We use the term "stability" rather than "strength" because strength is just one component of the dynamic stability required. Dynamic stabilization refers to the ability to utilize strength and endurance and motor control in a functional manner through all planes of motion and action despite changes in the centre of gravity, ' A comprehensive strengthening or facilitation of these core muscles has been advocated as a preventive, rehabilitative. and perform anceenhancing program [or variou s lumbar spine and musculoskeletal injuries. The stability of the lumbopelvic region is crucial, to provide a foundation for limb movement, to support loads. and to protect the spine.1 Nearly 30 years ago, PanjabP described an innovative model of s pinal stabilization that s till serves as an appropriate model of

understanding core stability today. The model incor· porates a passive subsystem, an active subsystem. and a neural control system (Fig. ]4.]). The passive subsystem consists of bony and ligamentous structures of the spine. While passive com· ponents of the system are integral components of spinal stability. on their own they are unable to bear much of a compressive 10adH and offer most restraint toward the end of range. Thus the active subsystem is vital to allow for support of the body m1.0) and lateral musculature.-I The single-legged squat exercise (Fig. 14.7) is also used as an indicator oflumbopelvic-hip stability. TIle single-legged squat is functional, requires control of the body over a single weight-bearing lower limb, and is frequently used clinically to assess hip and trunk muscular coordination and/or control. Ultrasound imaging is also used as an assessment technique.

Decreasing spi nal and pelvic viscosity

Figure 14.7 Sing le-legged squat exercise

Spinal exercises should not be done in the first hour after awakening due to the increased hydrostatic pressures in the disk during that timeY TIle cat/camel (Fig. I4-8 overleaf) and the pelvic translation exercises are ways to achieve spinal segment and pelvic accessory motion prior to starting more aggressive exercises. As well, improving hip range of motion can help dissipate forces from the lumbar spine. A short aerobic program may also be implemented to serve as a warm-up. Fast walking appears to cause less torque on the lower back than slow walking); 215

Fundamental principles feedback. There is some evidence that the use ofultrasound to both guide treahnent and assess outcome has been successful in monitoring multifidus)) and transversus abdominis function lG with positive clinical outcomes in patients with chronic low back pain. Accurate feedback is critical for skill learning, and feedback with ultrasound imaging may increase the quality of training, particularly for the group of patients who find it difficult to activate these muscles. Several studies using ultrasound imaging in the training of muscle control in patients with low back pain have reported positive outcomes}' However, whether the outcome with inclusion of ultrasound was improved above that which could be achieved without ultrasound feedback has not been established_

Stabilization exercises

Figure 14.8 Cat/camel exercise

Use of biofeedback and real-time ultrasound in retraining core control Pressure biofeedback units are used to help facili· tate the activation of the multifidi and transversus abdominis. 6 Verbal cues may also be useful to facilitate muscle activation. For example, abdominal "hollowing" is performed by transversus abdominis activation; abdominal "bracing" is performed by cocontraction of many muscles including the transversus abdominis, external obliques, and internal obliques. However, most of these isolation exercises of the transversus abdominis are in non-functional positions. When the trained muscle is "awakened," exercise training should quickly shift to functional positions and activities. The lise of real-time ultrasound imaging has become increasingly popular as a means of assessing muscle size and activity during the rehabilitation process. Most emphasis has been on the assessment of muscle size and muscle activation in the transversus abdominis and multifidus muscles. These measures have been shown to be valid.Y1 Ultrasound imaging may improve treahnent from two perspectives-as a measure of muscle dysfunction and outcome, and as a tool for provision of 216

Stabilization exercises can be progressed from a beginning level to more advanced levels. There are many different programs published; however, the general principles are common to all. Initially the motor skill (e.g. activation of transversus abdominis and multifidus) must be learned, but ultimately the activation must become automatic without conscious effort when performing the patient's sporting activity. Rehabilitation of these muscles takes place in three distinct stages: 1. formal motor skill training 2. functional progression 3. sport-specific training.

Most clinicians agree that a motor relearning approach, especially teaching patients to activate their deep stabilizing muscles (transversus abdominis and multifidus), is the first stage of the program_ Richardson et al. 6 advocate a segmental stabilization approach focusing on the co-contraction of transversus abdominis and multifidus, and also stressing the importance of the pelvic floor musculature. The most significant motor skill that is linked to the stability of these two muscles is the action of abdominal "drawing iri' (Fig. '4.9). The aim is for the patient to use the correct muscles in response to the command "draw in your abdominal wall without moving your spine or pelvis and hold for 10 seconds while breathing normally." The four-point kneeling position (Fig. '4.10) is the best position to teach the patient the action. Ask the patient to take a relaxed breath in and out and

Core stab i li ty

Figure 14.9 Diagrammatic representation of the muscle contraction of "drawing in" of the abdominal wall w ith an isometric contraction of the lumbar multifidus

Figure 14.10 The four-point kneeling position then draw the abdomen up toward the spine without taking a breath. The contraction must be performed in a slow and controlled manner. At the same time. the patient contracts the pelvic floor and slightly anteriorly rotates the pelvis to activate the multifidi. Assessment of optimal recruitment of these muscles can be done through palpation or with the use of biofeedback or ultrasound imaging. Once the contraction has been achieved. the patient should commence breathing in a slow and controlled manner, holding the contraction for 10 seconds. Once the action is understood by the patient, the formal test is conducted with the patient lying prone and using a pressure biofeedback unit. The patient lies prone with anns by their side, and the pressure biofeedback unit is placed under the abdomen, with

the navel in the center and the distal edge of the pad in line with the right and left anterior superior iliac spines. The pressure pad is inflated to 70 mmHg and allowed to stabilize. The patient is again instructed to breathe in and out and then, without breathing in, to slowly draw in the abdomen so that it lifts up off the pad, keeping the spinal position steady. Once the contraction has been ach ieved, the patient should commence normal relaxed breathing. The contraction is held for 10 seconds and the procedure repeated up to 10 times. A successful performance of the test reduces the pressure by 6-10 mmHg. This pressure change indicates that the patient is able to contract the transversus abdominis into its shortened range independently of the other abdominal muscles. Once the abdominal drawing-in technique is successfully learned in the prone position, the patient is encouraged to continue the exercise while in the sitting and standing positions. Richardson et al.6 describe this process of segmental stabilization as a three-stage exercise model-Stage I, local segmental control; Stage 2, closed-chain segmental control; Stage 3. open-chain segmental control (Fi g 14.11 overleaf), which forms the building blocks for the developmen t of joint pro· tection medlanisms. Others have a different approach to the drawingin exercise. McGill advocates bracing of the spine:' which activates all the abdominal musculature and extensors at once. TIlis is usually performed with the patient in a standing position, by simultaneously contracting the abdominal musculahtre and the extensors. Bracing activates all three layers of the abdominal musculature. not just the transversus abdomi nis. Once the patient has learned to stabilize the lumbopelvic region with the above isometric exercises to create a functional muscle corset, he or she can progress towards dynamic stabilization. McGill advocates early incorporation of his "big threen exercises into the program:1 These are outlined below: 1. Curl-ups for the rectus abdominis (Fig. 14.12 overleaf). The rectus abdominis is most active during the initial elevation of the head, neck, and shoulders. The lumbar spine should stay in neutral. The exercise ca n be advanced by asking the patient to raise the elbows a coupl e of centimeters. 2. Side bridge exercises for the obliques, quadratus lumborum, and transversus abdominis (Fig. 14.13 overleaf). Abdominal bracing is also required.

217

p rin cip les

Open-chain

segmental control

Closed-chain

segmental control

Figure 14.11 The segmental stabilization model for the prevention and treatment of low back pain FROM RICHARDSON"

The exercise can be advanced initially by placing

the free arm along the side of the torso, and subsequently by straightening the legs. 3. Bird dog exercise (Fig. 14.14). Leg and arm

extensions in a hands- knees position, eventually leading to the "bird dog" exercise for the back extensors. Figure 14.13 Side bridges (a) In the beginning, position the patient on the side supported by the elbow and hip. The free hand is placed on the opposite shoulder pulling it down

Figu re 14.12 Curl-ups. Patient lies supine with the hands supporting the lumbar region. Do not flatten the back to the floor. One leg is bent with the knee flexed to 90°, Do not flex the cervical spine. Leave the elbows on

the floor while elevating the head and shoulders a short distance off the floor

218

(b) The torso is straightened until the body is supported on the elbow and feet

Co r e st a b il ity Table 14.3 Stabilization and abdominal program described by Saal J1 Finding neutral posi tion Sitting stabilization Prone gluteal squeezes Supi ne pelvic bracing PelViC bridging progression Quadruped Kneeling stabilization Wall slide quadriceps strengthening Figure 14.14 Bird dog exercise. The bird dog

pos ition is with hands und er the shoulders and knees directly under the hips. Initially. simply lift one hand or knee a couple of centimeters off the floor. The

patient can progress to raising the opposite hand and knee simultaneously, then raising one arm or leg

at a time and then raising the opposite arm and leg simultaneously, as shown

Other frequently used exercises include the clam (Fig. ' 4-'5 ) and the bridge (Fig. '4.,6). It is important to avoid incorrect techniques (Fig. 14.I6c). Many clinicians base their progressive exercises on Saal and Saal's seminal dynamic lumbar stabiliza· tion efficacy study (Table r+3 )." Sahrmann also describes a series of progressive lower abdominal muscle exercises (Table 14.4 overleaf). '7

Figure 14.15 Clam

Position transition with postural control Curl-ups Dead bugs Diagonal curl-ups Straight leg lowering

Functiona l progression The initial bas ic strengthening exercises described above are initiated on the ground. The exercises must progress to pos itions of function, from a stable ground environment to a progressively less stable environment, and movements must increase in compl exi ty.~i In other words , the sportsperson must progress from muscle activation and strengthening to a program of dynamic stabilization.

(b) Supine bridging with leg extension

Figure 14.16 Bridging (a) Supine bridging

(e) Incorrect bridging technique

219

Fu ndam e n tal p rinciples Table 14.4 Sahrmann's lower abdominal exercise

progression 17 Position

Exercise

Base position

Supine with knee bent and feet on floor; spine stabilized with "navel to spine" cue

Level 0.3

Base position with one foot lifted

Level 0.4

Base position with one knee held to chest and other foot lifted

Level 0.5

Base position with one knee held lightly to chest and other foot lifted

LevellA

Knee to chest (>900. of hip flexion) held actively and other foot lifted

Level 1B

Knee to chest (at 90° of hip flexion) held actively and other foot lifted

Level 2

Knee to chest (at 90" of hip flexion) held actively and other foot lifted and slid on

Level 3

Knee to chest (at 90" of hip flexion) held actively and other foot lifted and slid not on ground

Level 4

Bilateral heel slides

LevelS

Bilateral leg lifts to 90~

ground

Several important principles must be applied to exercise progression. These include dynamic exercises, multiplanar exercises, balance, proprioception, power exercises (plyometrics), sport specificity, and motor programming. When the sportsperson has first mastered proper activation and control of the lumbopelvic region, he or she should progress from a stable surface to a labile surface. Eventually, external input can be added to cha11enge the athlete even more (Fig. 1+17). Secondly, exercises must be performed in all planes. While sagittal (sit-ups, lunges) and frontal plane (side-walking, side bridges) exercises are popular, the transverse/rotational plane is frequently neglected. Thirdly, proprioceptive training should be incorporated (Fig. 14.18). Balance-board or dura-disk training improves proprioception in a11 the joints, tendons, and muscles, not just those at the ankle. Plyometrics should also be incorporated (Fig. 14.19) as jumping exercises require a strong and stable core. Advancement to a physioball (Fig. 1+20 on page 222) can be done at this stage (Table 1+5 on page 22)).

Figure 14.17 Progression from Single-leg squat on the floor to a single-leg squat on a dura disk

220

Core stabi lit y

Figure 14.19 Plyometric exercises. These exercises

Figure 14.18 Proprioceptive training using a balance

should be multi planar and upgraded to include labile

board tal Balance board with both legs

surfaces

(b) Balance board on single leg

(b) Explosive movement

tal Preparing for take·off

22 1

Fundamental princ i p les

,

f- '"-l" ,

Figure 14.19 (cont.) (e) Maintaining good core control

Figure 14.20 Useofphysioball (a) Leg lift seated on ball

(b) Bird dog or superman on ball

(d) Absorbing forces on landing with knee flexion and activation of deep abdominal muscles

222

(e) Push-ups

Core sta bi lity Core strengthening for sports Core training programs for sports are widely used by strengthening and conditioning coaches at the col· legiate and professional levels. An example of Vern Gambetta's program is provided in Table I4.6)9 Different fitness programs incorpora te various aspects of COfe strengthening and may be a useful way to maintain compliance in many individuals (Table 14-7). Tabl e 14 .6 Advanced core program used by Vern

Gambetta 39 Figure 14.20 (cont.) (d) Bridging on ball

Body weight and gravitationalloading - push-ups, pUll-Ups, rope climbs Body blade exercises Medicine ball exercises-throwing and catching Dumbbell exercises [n diagonal patterns Stretch cord exercises Balance training with labile surfaces Squats Lunges

Tabl e 14.7 Fitness programs utilizing core strengthening principles

(e) Plant on the ball, moving hips forward

Pilates Yoga (some forms) Tai-chi Feldenkrais Somatics Matrix dumbbell program

Efficacy of core strengthening exercise

(f ) Hamstring pull in

Core strengthening programs have not been well researched for clinical outcomes. Studies are hampered by the lack of consensus on what constitutes a core strengthening program. For example, some srudies describe remedial neuromuscular retraining, some describe sport-specific training, and others describe functional education. No randomized controlled trial (ReT) has been conducted on the efficacy of core strengthening. Most studies are prospective, uncontrolled case series.

Tabl e 14.5 Physioball exercises for the core Abdominal crunch Balancing exercise while seated Superman prone exercise

Modified push-up

Pelvic bridging

Prevention of injury and performance improvement In 2001, Nadler et aI. attempted to evaluate the occurrence of low back pain before and after incorp. oration of a core strengthening program. Z) The core strengthening program included sit-ups, pelvic tilts,

223

squats, lunges, leg presses, dead lifts, hang cleans, and Roman chair exercises. Although the incidence of low back pain decreased by 47% in male athletes, this was not statistically significant. In female athletes, the overall incidence of low back pain slightly increased despite core conditioning. This negative result may have been due to the use of some unsafe exercises (e.g. Roman chair extensor training).(>,40 In addition, the exercises chosen for this study included only frontal and sagittal plane movements, which may have affected the results. Future studies incorporating exercises in the transverse plane may help to solve the issue surrounding core strengthening exer' cise and low back pain. A study com paring core stability measures between male and female sportspeople and their incidence of lower extremity injury found that reduced isometric hip abductor and external rotation strength were predictors of injury. From this, the authors claimed that "core stability has an important role in injury prevention."4! While the findings of this study may be important, core stability was not measured. 4 " Another study found a rehabilitation program consisting of progressive agility and trunk stabilization exercises was more effective than a program emphasizing isolated hamstring stretching and strengthening, in promoting return to sports and preventing injury recurrence in sportspeople suffering an acute hamstring strain.';l

Treahnent aflaw back pain The first study conducted of a core stability program was an uncontrolled prospective trial of "dynamic lumbar stabilization" for patients with lumbar disk herniations creating radiculopathy)8 The impact of therapeutic exercise alone was difficult to ascertain in this study, due to other non-operative interventions being offered, such as medication, epidural steroid injections, and back school. The exercise training program was well outlined and consisted of a flexibility program, joint mobilization of the hip and the thoracolumbar spinal segments, a stabilization and abdominal program (see Table 14-3), gym program,

224

and aerobic activity. Successful outcomes were achieved in 50 of 52 (96%) individuals. The described dynamic lumbar stabilization program resembles the current concept of a core stability program without the higher level sport-specific core training. Several other authors have since described similar programs.4-1- .j, More recently, Tsao and Hodges 36 have shown that delayed activity of transversus abdominis in individuals with low back pain can be changed (and maintained after 6 months) with training.

Effectiveness in sports injuries To date, the only studies to have shown a positive benefit of core stability training in the management of sporting injuries are Sherry and Best's study43 on the treatment of hamstring strains, and a study by Holmich et a1. 46 on the rehabilitation of sportspeople with chronic groin pain which incorporated some stability training into its program. However, a number of other sporting pathologies theoretically would benefit from this mode of training. These include stress fractures of the pars interarticularis of the lumbar spine, a common injury among cricket fast bowlers and other sports that involve repetitive hyperextension and rotation. The positive results from O'Su11ivan et a1.'s study4i in non-sporting patients with spondylolysis would suggest that core stability training may be effective in this condition. Lumbar instability seen commonly in gymnasts is another condition for which theoretically a core stability program may be helpful. Many physiotherapists now incorporate an element of core stability training in the rehabilitation of a wide variety oflower limb injuries.

Conclusion The concept of core stability has a theoretical basis in the treatment and prevention of various musculoskeletal conditions. However, other than studies in the treatment of low back pain, research is severely lacking. With the advancement in knowledge of motor learning theories and anatomy, core stability programs appear to be on the cusp of innovative new research.

Co re stab i li ty

IrlI

for rehabilitation. Med Sci Sport s Exert 200f;33( 11)

R EC O M ME N DED READ I NG

,88 9- 98.

Akuthota V, Nadlet S. Core strengthening. Arch Phys Med

12.

RelHlbil2oo4; 85: 586--92. Bliss LS. Teeple P. Core stability: the centerpiece of any training program. ClIrr SpoTt s Med Rep 2005; 4: 179--83. Bogduk N. Clil1icai anatomy of/he lumbar spine £Il/{i sncmm. 3rd edn. New York: Churchill Uvingstone, '997. McG ill S. Lolli back disorders: r:videllce-based prevelllioll and

rehabilitation. Champaign, ll: l-!uman Kmetics,

2004 .

Z7 6 }-9·

iml'uirl11wt syndromes. 5t Louis: Mosby. 2002.

I.

Ir

Sci Rev 2001;29(1):z6- 31.

1- 2.

16. Cowan SM. Schache A. Brukner P et a!. Delayed o nset of tr;msversus abdominus in long-standing groin pain.

R EE E RENCES

Med Sci Sports Exerc 2004;36(12):2040-S ·

Hodges PW. Richardson CA. Inefficient muscular

17. Sahrmann S. Diagnosis alia treatment oJlJlov£ment

stabilizatio n of the lumbar spine associated with low

impllinlleut syndromes. St Louis: Mosby. 2002.

18. Lyons K, Perry J, Cronley JK et al. Timing and

hack pain. Spinc. 1996;21(22):2640-50. 2. Panjabi MM . 11le stabiliZing system of the sp ine. Part

I.

Function. dysfunction. adaptation and enhancement,

j Spinal Disord 1992;5{S):383--9.

relative intensity of hip extensor and abductor muscle action during level and stair ambulalioll. Pliys TIIi:r 198 }:6}( 10 ):1597-605 .

}. Lucas DB Bresler B. Stability oJlhe ligamentous spille.

19. Beckman SM, Buchanan TS. Ankle inversion injury

San Francisco: Biomechanics Laboratory. University of

and hypermobility-effect on hip and ankle muscle

California. 1961-

electromyography onset latency. Arell PJIYS Med ReJlab

4. McGill S. Low back disorders: evidellce-based prevention

(lnd rehabilitiatiol1. Champaign, II: Human Kinetics, 2002. muscle activity to assure stability of the lu mbar spine.

1 l:1ectroll1yogr Kil1esio/20 0P}3S3-9·

JA.

Therapeu tic exercise Jor spinal segmclllol stabilization illloL/.! back

6. Richardson CA, Hodges PW, Hides

1995-;J6(Jz):U38 -43· 20. Cowan SM, Crossley KM, BenneIl KL Altered hip and trunk m uscle function in individuals with

5. McCill SM , Gre nier S, Kavcic N et al. Co-ordination of

paill-sciclilijic basis and dilliro l f1/'proaclT. 2nd edn. Edinburgh: Churchill Livingstone, 20°4. 7. Bergmark A. Stability of the lumbar spine: a shldy in mechanical engineering. Acta Ortll Scand, 1989:230 ($upP):20- 4· 8. Panjabi MM, Clinical Instability and low back pain.

j Electromyogr KillesioI2003:13(4):371-9. J, De Rosa C. Mtchallicallow back paill: perspectives in follctiollalallatomy. 2nd edn.

9. Porterfiled

Philadelphia: WB Saunders. 1998. 10. Akuthota V. Nadlet S. Core strengthening. Arch Phys

Med Ri!lwb 20°4;85:586-92.. II.

recovery is not automatic after resolution of acute. first.episode low back pai n. Spine 1996:21(23):

IS. McGill S, Low back stability: from formal description to issues for performance and rehabilitation. Exerc Sport

Sheny M, Best T. Heiderscheit B. The core: where are we

(I

The pos terior layer of the thoracolumbar fascia. Its function in load transfe r from the spine to legs. Spine 14. Hides lA, Richardson CA, Jul1 GA. Multifidus muscle

Sahrmann S. Diagnosis and treatment ofmoLlt:lI1ellJ

and where are we going? C/ill j Sport Mt d 20°5:

347· 13. Vleeming A, pool-G oudzwaard AL. Stoeckart R et al.

199PO(71'7SJ-8.

2002.

Richardson C, Jull G, Hodges P et a1. Therapeutic n:crcisefor spillal segmelllai stabilization ill low back pain. 2nd cdn. Edinburgh: Churchill Livings to ne.

Solomonow M. Introduction to surface electromyography. j Electromyogr KillesioI1998;8tS):

pa tellofe moral pain. Br j Sp«>0''.''''''''''. ,om. poO . . . ,h/>uId,...."" "",, th.dlO~ • .,.....", 0..,,,,.,

...

• ~yoo .ro "'''''' '"' P '''' "'''''_''''' to

",," ,doclOtt .. )'Oo''~p,.,, 'h .I;o''

" ., fo.you," "".,,''''''''

1t '''''''''''l h ~«11)'"1'''''0''''''''' "O

Return to play during the subsequent week Whether or not to allow the concussed patient to return to training and then competition is one of the most difficult decisions the sports physician must make. In minor cases of concussion, where all symptoms resolve quickly and there is no amnesia, no sign of cortical dysfunction, nor evidence of impairment of short-term memory or information processing, the player may be allowed to return once recovered. Neuropsychological testing may be used to confirm

278

full recovery. A player permitted to return to play should be closely observed for any signs of impaired function. A multifaceted clinical approach is used to manage players in the week following injury. In practical terms, this involves five sequential steps: 1. a period of cognitive and physical rest to facilitate recovery 2. monitoring for recovery of post~concussion symptoms and signs 3. the use of neuropsychological tests to estimate recovery of cognitive function 4. a graduated return to activity with monitoring for recurrence of symptoms 5. a final medical clearance before resuming full contact training and/or playing. Period of cognitive and physical rest to facilitate recovery Early rest is important to allow recovery following a concussive injury. Physical activity, physiological stress (e.g. altitude and flying) , and cognitive loads (e.g. srudying, video games, or computer work) can all worsen symptoms and possibly delay recovery following concussion. Players should be advised to rest from these activities in the early stages after a concussive injury, especially while symptomatic (see "Concussion injury advice," p. 4 of SCAT2). Similarly, the use of alcohol, narcotic analgesics, anti-inflammatory medication, or sedatives can exacerbate symptoms following head trauma, delay recovery, or mask deterioration; these should also be avoided. Specific advice should also be given on avoidance of activities that place the individual at risk of further injury (e.g. driving). The cornerstone of concussion management is physical and cognitive rest until symptoms resolve, and then a graded program of exertion prior to medical clearance and return to play. The recovery and outcome of concussion may be modified by a number of factors that may require more sophisticated management strategies. The Zurich consensus panel agreed that a range of "modifying" factors may influence the investigation and management of concussion and, in some cases, may predict the potential for prolonged or persistent symptoms. These modifiers would also be important to consider in a detailed concussion history and are outlined in Table 17.2. When these modifying influences are present, simple RTP advice may be inappropriate. It may be wise to consider additional investigations including

Table 17.2 Factors that influence whether investigation or more sophisticated management (e.g. referral to a physician with expertise in concussion management) is indicated Factors

Modifier

Symptoms

Number Duration (> 10 days) Severity

Signs

Prolonged LOC (> 1min) Amnesia

Sequelae

Concussive convulsions

Temporal

Frequency-repeated concussions over time Timing-injuries close together in time "Recency"-recent concussion arTB1

Threshold

Repeated concussions occurring with progressively less impact force or slower recovery after each successive concussion

Age

Child and adolescent «18 years old)

Co- and premorbidities

Migraine Depression or other mental health disorders Attention deficit hyperactivity disorder (ADHD)

Learning disabilities Sleep disorders Medication

Psychoactive drugs Anticoagulants

Behavior

Dangerous style of play

Sport

High-risk activity Contact and collision sport High sporting level

formal neuropsychological testing, balance assessment, and neuroimaging. It is envisioned that athletes with such modifying features would be managed in a multidisciplinary manner coordinated by a physician with specific expertise in the management of concussive injury. Monitoring for recovery of post-concussion symptoms and signs The symptoms of concussion are dynamic and evolve over time. It is important that players who are suspected of having a concussion be monitored over time to assess for delayed symptom onset. Monitoring of

post-concussion symptoms and signs can be facilitated by the use of the SCAT2. Use of neuropsychological tests to estimate recovery of cognitive function Cognitive deficits associated with concussion are typically subtle and may exist in a number of domains. Common deficits that follow concussion in sport include reduced attention and ability to process information, slowed reaction times, and impaired memory. The use of neuropsychological tests in the management of concussion overcomes the reliance on subjective symptoms, which are known to be poorly recognized and variably reported, and allows detection of cognitive deficits, which have been observed to outlast symptoms in many cases of concussion. There are a number oflevels of complexity of cognitive testing, including: formal neuropsychological testing screening computerized cognitive test batteries basic paper-and~pencil evaluation (i.e. SCAT2).

Formal neuropsychological testing remains the clinical best practice standard for the assessment of cognitive function. 14 Formal testing is logistically impractical for routine use following concussive injuries, but is recommended in any case where there is uncertainty about recovelY, or in difficult cases (e.g. prolonged recovery). Screening computerized cognitive tests provide a practical alternative for the assessment of cognitive recovery. Ideally, the tests should be compared to the individual's own pre-injury baseline. A number of screening computerized cognitive test batteries have been validated for use following concussion in sport and are readily available. These include test platforms such as CogS tate Sport (www.cogstate.com/go/ sport), ImPACT (www.impacttest.com). Headminder (www.headminder.com). and the US military tool Automated Neuropsychological Assessment Metrics (ANAM) (www.armymedicine.army.mil/prr/anam. htm!). Screening computerized cognitive tests are strongly encouraged in the routine management of concussion in sports with a high risk of head injury (e.g. football codes). Computerized tests provide a quick, valid, and reliable measure of cognitive recovery following a concussive injury. Furthermore, routine use of computerized screening tes ts in 279

the pre·season facilitates screening of players for cognitive deterioration over time. Basic paper·and.pencil cognitive tests (e.g. SCAT2, Fig. 17.2) are the quickest and s implest of the cognitive screening tests; however, they are the leas t sensitive to subtle cognit ive changes that accom· pany concussion} In cases where the concussion has resulted in brief symptoms and clinically the pl ayer has recovered well, basic paper-and-pencil cognitive tests can be used to provide an estimate of cognitive func tion. The use of a basic paper-and-pencil evaluation should be combined with a conservative RTP approach. and careful monitoring of symptoms as the player progresses through a graduated RTP program. Overall, it is important to rem ember that neuropsychological testing is only one component of assessment, and therefore should not be the sale basis of management decis ions. Neuropsychological testin g does not replace the need for a full hi story, and clinical and neurological examination. Graduated return to activity Followi ng a concussive inj ury. players should be returned to play in a graduated fas hion once clinical features have resolved and cognitive function returned to baseline. When considering RTP, the ath lete should be off all medications at the time of considering commencement of the rehabilitation phase or at the fina l medical assessmen t. Overall, a more conservative approach (i.e. longer time to return to sport) should be used in cases where there Ta ble

is any uncertainty about the player's recovery "if in doubt, sit them out." In accordance with current consensus guidelines, there is no mandatOIY period of tim e that a player must be withheld from play following a concussion. However, at minimu m, a player must be symptom. free at rest and wi th exertion, and have returned to baseline level of cognitive performance. The Zurich consensus statement' recommends a stepwise graduated RTP protocol (Table 17.)). If a player remains asymptomatic for 24 hours at level I , they may progress to level 2. They are allowed to advance provided that they remain asymptomatic. Using this protocol, an athlete should take approxima tely a week before re turn ing to normal game play. If an y symptoms surface during the progression, players should drop back to the previous level in which they were asymptomatic for a further 24 hours attempting to progress. A final medical clearance before resuming full contact training and/or playing A player who has suffered from a concussive injury must not be allowed to return to play before havi ng a medical clearance. In every case, the decision regarding the timing of return to train ing should be made by a medical doctor with experience in concussive injuries. This assessment is multidimensional and based on evidence of resolutio n of the athlete's symptoms, physical signs, and cognitive deficit. Ideally, cancussed players should be exam ined by an experienced medical practitioner with the decision about return

17.3 Graduated return-ta-play protocol Functional exercise at each stage of

Rehabilitation stage

rehabilitation

Objective at each stage

1. No activity

Complete physical and cognitive rest

Recovery

2. light aerobic exercise

Walking. swimming. or stationary cycling

Increase heart rate

keeping intensity

0

4

2

Total number of symptoms IM""rnum "",,,101. 22) Symptom severity score (Add.oJ KOI~ "" lllbl~. "",..mum POSSIble 12 x 6. 132) Do Ih~ 5)'fl1pl0mS get WOlse WIth phyS-!{al activity? Do the symptoms get wo~e wrth mental actiVity?

4

6

6

5

6 6 6

5

, ,

6

N N

Overall rating II you know the alhlete wel l pllor 10 the InJury. how CI/ferent IS the Q/lJI Consen\U, meellng on COf1CU'S'O.n In Sport Meld .n lUllcM . SWiller la nd .n November 1008 Th~ full deta ll l of tMe ,onf~ re",e outcome, ol nd the authors of the mol ~re pub ~,shed In !lnt.sh JournJI cf Sporti Me d'One. 2009. vo lume 43. supp le ment 1 T~" outcome p~p e r WIUa lso br \lmu l tJneous l ~ (o·publ,\.he d In the May lOW I Slue~ o f Cll nl'JI JournJl 01 SPOTts MediCIne. Ph~S lcal MedICln .. & Rchabl!1101IOn. Jou rnal 01 Athlel'" Tr. ,n.n g. Journ al of Clin-cal NeurO.ci(.'II(e. JournJI of Scoenct' & Medoc .ne In Spon. Neu rosu rgery. Se 2001. 11 176·181

•McC,." M . RJndolph C. Kelly J 5tandolrd .z('d Al.ses>m""'l at COn(,,'I.on Manual lcr J drl''' n IW ~t IO". ,coring and Interpret. l.en W.,eon,.n. USA

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SCATl SPORT CONCUSSION ASS £SMENT TO OL 2 I PAGE 2

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Orientation score

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Best verbal response (V) No v€ rb al response IncomprehenS ib le so unds Inappropriate word~ Con lused Onente(

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left

5 correct 'et r l,lIOnl ,n < 4 "',end . .. 1

Standardized Assessment af Concussion (SAC)

Tan d e m stance: -NoW stand h~/-to- toe with your non-dominant foot in bock. Your weight should be evenly distributed aerou both feet. Ag ain. you should tty to m aintain stability for 20 seconds with your hilnds on your hips and your eyes closed. I wl/l be counting the number o f times you move auf of this position. If you stlJmble out of this POSilion, open your e)'t's and return to the start position and continue ba lancing. I will start timing when you are set and hiJve closed your eyes."

C. e ....r.. ell I~

wa, tested

Scor ,ng

I'- Coordination score

(b)S ing le leg stance: -If you were toklc/( II ball, which foo t would you use7 [Thrs ~.... II be til!' dominan t foot] Now srand all your non·dominant foot. The dominant leg should b", h",ld in approximately 30 degrees of hip fleKion and 45 degret1s of knee fleKion. Again, you should try to rniJintaln stability for 21J sewnds with your hands on your hips and your eyes dOlif!d. I will bE' co unting the numb!!r of tim es you move out of this position. If you ~tumble out of this posit,'on, open your eyes and return to the start position and con tinue balancing. I will start timing when you are set and have closed your eyes. (e)

i

0130

Scoring d a ta from the SCAT2 or SAC should not be used as a s ta nd alone method to diagnose concuss ion, measu re recovery or make decisions about a n at hlete'S readiness to ret urn to competition after concussion,

SCAT2 51'01lT CONCUSSION

AS5 £~MENT

Figure 17.2 (cont.) Sport Concussion Assessment Tool (SCAT)

TOO L 2

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285

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Athlete Information Any 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 )

Correct

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 tendon .~ 8 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 faclors:~" 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 dis~ 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 predominantly in young or middle~aged males engaged in strength activities (e.g. weightlifting). Partial ruptures are more painful than complete rup~ tures, due to mechanical irritation of the remaining intact tendon. Early surgical repair of complete rup~ 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 com~ 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

•

\~~~

H~

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 patien~ s 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.

~ I.

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

REFERENCES

Sports Phys Ther 2004;34(12):77o-80.

Clarke AW. Ahmad M. Curtis M eta!. Lateral Elbow Tendinopathy. Am J Sports Med 2oro;38(6}:1209-14.

2.

decreased motor performance of arms in patients

,+

model oflateraI epicondylalgia. Br j Sports

du Toit C, Stieler M, Saunders Ret aL Diagnostic accuracy of power Doppler ultrasound in patients with

chronic tennis elbow. Br J Sports Med 2oo8;42{n):

87 2 - 6.

patients with lateral epicondylalgia: a pilot clinical trial.

} Man Manip Ther 2005;13(3):143-51.

,6. Smidt N, Lewis M, van der Windt D et a1. Lateral epicondylitis in general practice: course and prognostic

4· Milz S, Tischer T, Buettner A et a1. Molecular composition and pathology of entheses on the medial and lateral epicondyles of the humerus: a structural basis for epicondylitis. Ann Rheum Dis

2004;63(9):I0I5-21. 5· Coonrad RW, Hooper WR. Tennis elbow-its course, natural history, conservative and surgical management.

} Bone Joint Surg Am I973;55(6):Il77-82.

Mea

2°°9;43(4):25 2- 8. Cleland JA, Flynn TW, Palmer JA. Incorporation of '5· manual therapy directed at the cervicothoracic spine in

3· Fairbank SM, Corlett Rf. The role of the extensor digitorum communis muscle in lateral epicondylitis.

J Hand Surg Br 2002;278(5):4°5-9.

Coombes BK, Bisset L, Vicenzino B. A new integrative

indicators of outcome.} Rheumalolzo06;33(1O):

20 53-20 59. '7· Pienimaki T, Karinen P, Kemila T et al. Long-term follow-up of conservatively treated chronic tennis elbow patients. A prospective and retrospective analysis.

Scand} Rthabil Med 1998;3°(3):159-66. ,8. Coombes B, Bisset L, Connelly L et al. Optimising

6. NiIschl RP, Pettrone FA. Tennis elbow. the surgical treatment oflateral epicondylitis. j Bone joint Surg Am

corticosteroid injection for lateral epicondylalgia

I979;6I(6):832-5). 7· Kraushaar BS, NiIschl RP. Tendinosis of the elbow (tennis elbow) - Clinical features and findings of

randomised control trial with placebo comparison.

histological, immunohistochemical, and electron

with the addition of physiotherapy: a protocol for a

BMC Mlisculoskelet Disord 2009;10(1):76. '9· Pienimaki IT, Tarvainen TK. Siira PT et al. Progressive strengthening and stretching exercises and ultrasound for chronic lateral epicondylitis. Physiotller

microscopy studies.} Bone Joint Surg Am 1999;81(2):

259-'7 8. 8. Alfredson H, Ohberg L, Forsgren S. Is vasculo-

20.

neural ingrowth the cause of pain in chronic Achilles

regime including eccentric training for lateral humeral

tendinosis? An investigation using ultrasonography

epicondylalgia. Scand} Med Sci Sports 2001;n(6):

328 -34-

and colour Doppler, immunohistochemistry. and diagnostic injections. Knee Surg Sports Traumatol

2L

meta-analysis oflow level laser therapy in lateral elbow

9· Regan W, Wold LE, Coonrad R et al. Microscopic

tendinopathy (tennis elbow). BMC Musculoskelet Disord

histopathology of chronic refractory lateral epicondylitis. Am} Sports Med 1992;20(6)746-9.

w. Bisset LM, Russell T. Bradley S et al. Bilateral sensorimotor abnormalities in unilateral lateral

Bjordal JM, Lopes-Martins RAB, foensen J et a1. A systematic review with procedural assessments and

Arthrosc 200pl(5):334-8.

410

199 6;82(9):5 22-3°' Svemlov B, Adolfsson L Non-operative treatment

...

2008;9:75· Staples MP, Forbes A, Ptasznik R et al. A randomized controlled trial of extracorporeal shock wave therapy

El bow and ar m pa in for lateral epicondylitis (tennis elbow).] Rheumalol 2008;3 5(I0): 2038-46. 23. Olesterton LS . van der Windt DA . Sim J et al. Transcutaneous electrical nerve stimulation for the

35. Scot! A. Khan KM. Corticosteroids: short·term gain for long-term pain? Lallcel: 376 (9754):17'4- 5' 36. Coombes BK. Bisset L. Vicenzino B. Efficacy and safety of corticosteroid injections and other injections

management of tennis elbow. a pragmatic randomized

for management of tendinopathy: a sys tematic

controlled trial: the TATE trial (ISRCTN 87t410841-

review of randomised controlled trials. Lancet

BMC Muswloskelet Disord 2009;10:156.

24. Bjordal JM , Johnson MI . Ljunggreen AE.

2010:37 6 (9754):175 1- 67. 37. Bisset L. Smidt N. van der Windt DA et al.

Transcutaneous eLectriol nerve stimulation (TENS)

Conservative treatments for tennis elbow-do

can reduce postoperative analgesic consumption.

subgroups of patients respond differently?

A meta·analysis with assessment of optimal treatment parameters for postoperative pain. EL,r] Pain 20°3;'7(2):181-8. 25. van der Windt DA, van der Heijden GJ, van den Berg SG et al. Ultrasound therapy for musculoskeletal disorders: a systematic review. Pain 1999;81(3):257-7I. 26. Oeken 0, Kahraman Y, Ayhan F et ai. The short-term efficacy ofla ser, brace. and u ltrasound treatment in lateral epicondylitis: A prospective, randomized. controlled triaL] Hand Vier 2008;21(t):63-8. 27. Vicenzino

n, Hing W. Rivett D et al. Mobilisatiol1lVith

movement: the art and tile sciellce. Sydney: Churchill livingstone.20n . 28. Bisset L. Beller E, lull G et aL Mobilisation wilh

Rheumatology 20°7;46(10):1601-5. }8. Munell GA. Using nitric oxide to treat tendinopathy. Br ] Spor.s Med 2°°7:41(4):.227-31.

39. Paolon i lA. Murrell GA. Burch Ret al. Randomised, double blind, placebo controlled, multiccntre doseranging clinical trial of a new topical glyccryl trinitrate patch for chronic lateral epicondylosis. Br] Sports Med 2009~3:399-302.

40. Espandar R. Heidari P. Rasouli MR et al. Use of anatomic measurement to guide injection of botulinum toxin for the management of chronic lateral epicondylitis: a randomized controlled trial. CMA] 2010;182(8)768- 73. 41. Vicenzino B. Coombes Bit A single botulinum toxin

movement and exercise. corticosteroid in jection. or

injection at a precise anatomic point on the forearm

wait and see for tennis elbow: randomised trial. BM]

reduces pain at rest, compared to placebo injection in

2006;333(7575)'939-4'· 29. Vicenzino B. Cleland fA. Bisset L Joint manipulation in the management of lateral epicondylalgia: a clinical commentary. j Man Ma nip TIler 2007;IS{I):5o-6. }o. Stasinopoulos D. Stasinopoulos L Comparison of effects of Cyriax physiotherapy, a supervised exercise programme and polari.:zed polychromatic non·coheren t light (Bioptron light) for the treatment of lateral epicondylitis. Clilt Relwbil2006;20(1): IZ- 23.

3I- Verhaar l A. Walenkamp G, van Mameren H et al. Local corticosteroid injection versus cyriax·type physiotherapy for tennis elbow.] Bone joillt Surg 1996;78B(I):128- 32. 32. Bisset L. Paungmali A, Vicenzino B et al. A systematic review and meta·analysis of clinical trials on physical interventions for lateral epicondylalgia. Br j Sports Med 2005;39(7):411-22. 33. Ng G. The effects offoreann brace tension on neuromuscular performance in subjects with lateral humeral epicondylosis: a review. lilt Sportwed] 2005:6(2):124-29. 34· Vicen2ino B. Brooksbank J, Minto J et a1. Initial effects of elbow taping on pain-free grip s trength and pressure pain threshold. j Ort/IOp Sports Phys TIler 2°°3;33(7):4°0- 7·

pa tients with chronic refractory lateral epicondylitis.

Evid Based Med 2010:15(5):149-5°. 42. Peerbooms l C. Sluimer I, Bruijn OIJ et al. Positive effect of an autologous platelet concentrate in lateral epicondylitis in a double· blind randomized controlled trial. A m] Sports Med 2010;38(2):255- 62. 43. Kazemi M, Azma K. Tavana Bet al. Autologous blood versus corticosteroid loca l injection in the short·term treatment oflateral elbow tendinopathy: a r:mdomized clinical trial of efficacy. Am] Phys Med Rellabil 2010;89(8):660-7 44. Rabago D, Best T, Zgierska A et al. A systematic review of four injed ion therapies for lateral epicondylosis: prolotherapy, polidocanol. whole blood and platelet rich plasma. Br] Sports Mtd 2009 Jul;4}(7):471-81. 45. Mishra A, Pavelko T. Treatment of chronic elbow tendinosis with buffered platelet-rich plasma. Am]

Sports Mui 2006;34(lI):1774- 8. 46. Karkhanis S. Frost A, MaffulIi N. Operative management of tennis elbow: a quan titative review.

Br Mtd BuIl2008;88(t}:171-88. 47. Ciccotti MC, Schwartz MA, Ciccot!i MG. Diagnosis and treahnent of medial epicondylitis of the elbow.

eli/! Sports Med 2004;23(4):693--7°5.

411

48. Park GY. Lee SM. Lee MY. Diagn ostic value of ultrasonography fo r clinical medial epicondylitis.

Arch Pill's Med Rehabi/2008;89(4):738--42. 49· King J. Brelsford HJ, Tullos HS. Analysis of the pitching arm of the professional baseball pitcher.

eli" Ortllop Relat Res. 1969;67: u 6-23. 50. Frostick SP, Mohammad M, Ritchie DA. Sport injuries of the elbow. Br] Sports Med 1999;33(5):301-1I. 51. Jacobson fA, Jebson PfL, Jeffers AW et a!. Ulnar nerve dislocation and snapping triceps syndrome: diagnosis with dynamic sonography- report of three cases.

Radiology 2001;220(3):601-5. 52. Richard MJ, Messmer C, Wray WH et a1. Management of subluxating ulnar nerve at the elbow. Orthopedics 53. Appelboam A. Reuben AD. Benger fR et al. Elbow extension lest to rule out elbow fracture: muLticentre. prospective validation and observational study of diagnostic accuracy in adulls and children. BM]

Incidence an d risk factors for the deveLopment of radiographic arthrosis after traumatic elbow injuries.

J Halld 511rg Am 2010;35(12):1976-80. 57. O'Driscoll SW. Morrey BF. Korinek S et at. Elbow subluxation and dislocation. Clill Ortltop Rei Res 1992(280):r86-97· 58. Ross G. McDevitt ER. Chronister R et al. Treatment of simple elbow dislocation using an immediate motion protocol. Am J Sports Med 1999;27(3):308-11. 59. Verrall GM. Return to Australian rules football after acute elbow dislocation: a report of three cases and

IC.

245- 50 . 60. Konjengbam M. Elangbam,. Radial nerve in the radial runnel: anatomic s ites of entrapment neuropathy_

Clin Allat 2004;17(1):21-5. 61. Sarhadi NS. Korday SN, Bainbridge LC. Radial mnnel

2008;Dec 9:337:a2428. Elbow fractures-treating to

avoid complications. Phys Sportsmed 1995;23(4): 39-5 0 . 55. Ellerin BE, Helfet D, Parikh S et al. Current therapy in the management of h eterotopk ossification of

412

Rehabil 1999;78(3):259-71. 56. Guitton TG , Zurakowski D, van Dijk NC et aL.

review of the literature.] Sci Med Sport 200I:4(.2):

2010;33(9):672 .

54. Shapiro MS. Wang

the elbow: a review with case studies. Alii j Pill'S Med

syndrome: diagnosis and management. J Halld Surg 199 8 ;.23(5): 617- 19. 62. Lee IC. Malara FA. Wood T et a1. MRI of stress reaction of the dis tal humerus in elite tennis players. Am J

Roelllgel101.2o06; r87(4):90 1-4·

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..., ., . •

~:

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

(b l 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 IJ!I~ 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 (computer~related, 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 pick~up 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-

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

~ '0"" months forthe scaphoid and lunate to separate ~IjV~ 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 fractures.~ 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

fr~;. If a scaphoid fracture is susp ecte d cli nically butthe

~

7~ 'V ">

'brry

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 frachtres~the 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

uncomplicated

Conservative

SD

Total

4.2

21

7.9

TOTAL (95% (I)

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

Heterogeneity: Tau ~ = 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 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 cross~sectional 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 are more likely to occur in pre~season training. S9 It 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 adductor~related 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 reduc~ 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 inser~ 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 adductor~ 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 training. (,~ 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:43 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. ~ RIj

MRI can help identify injury location, contribute to

,..- ~C'"n determ ining the likely prognosis, and help predict ~ 'b"" recurrence for certain inju ries. This is a major new 7fJ'(?

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.

In the large majority of hamstring strains, the £~;; injured muscle is biceps femoris (reported as ~ '0'" 76- 87%).5Semimembranosus injury is uncommon; )(j'rj".) semitendinosus inj ury is rare. 'i'RA ('

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

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.

injury.~'

Type I acute hamstring strain: sprinting-related

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).'" !Q.~! The injury location can be determined both by maximal pain palpation and by

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. 1 ~. Il\. 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

-"'" 80 60

=c.-

proximal muscle belly

proximal

.q ~

_ c ~:~ ~

I -£ 40

'0

lendon junction

.t

20

0 4h~-r----r--------'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 pre~injury flexibility levels

>0"" .<

proximal",

-0-

Dancers

-0- Sprinters 0 4h---r----r-------~ proximal

proximal muscle tendon junction

10 21 Time after injury (days)

42

belly

dislal muscle tendon junction

distal

,

(b) Knee flexion strength in the injured leg expressed as a percentage ofthe uninjured leg in the sprinters (n = 18) and dancers (n :::: 15) showing markedly increased reduction in strength in the sprinters' injuries (type I)

belly

dislaltendon

(b) Type II injuries (the stretching type) are typically located close to the ischial tuberosity and involve the proximal free tendon of semimembranosus 16

sprinting,2J.. Z.j a time in the stride cycle where they are highly activated as they work eccentrically to decelerate the swinging tibia and control knee extension21 in preparation for foot strike.

602

2

Patients who present with type I acute hamstring strain typically complain of sudden onset of pain in the hamstring region that usually stops them. On examination, careful palpation and testing usually locates the injury in the long head of biceps femoris, often the proximal muscle-tendon junction. '4· '7 If imaging is deemed necessary (e.g. if presence of type I acute hamstring strain is unclear on clinical grounds), MRI (Fig. 31.7) is the recommended imaging modality because it is non-invasive and of high resolution. The only disadvantage may be its cost. MRI can be helpful in accurately identifying

Po st erio r thig h pai n

10

20

30

40

50

60

70

80

Time to return to pre-injury level (weeks)

{el Relative number of su bjects in each group plotted against the corresponding time, in weeks, to return to pre-injury level of performance (n = 18 for the sprinters type I, n = 13 for the dancers type II) demonstrating the prol onged rehabilitation time for type 11 injuries

the loca tion of the injury (semimembranosus versus biceps femoris long head versus semitendinosus; distal versus proximal) and the type of tissue involved (muscle fiber, tendon, muscle-tendon junction) rather than relyin g on palpation. Both the size 5· 16. '7 and location'('· 17 of the lesion on MRI can be used to help predict prognosis. MRI

can also be useful for determining the likelihood of recurrence (i.e. larger lesions tend to be as sociated with greater risk of recurrence).;6. }.'J MRI should always be done when a total rupture is s uspected.

Type II acute hamstring strain: stretch-related (dancers) Type II acute ham string strains more commonly occur in sports tha t necessitate large amplitude movements and ballistic limb actions, such as ballet

Figure 31.7 MRI showing type I hamstring inj ury

dancing and gymnastics. The common m echanism of injury in these instances is an excessive stretch into hip flexio n. In contrast to type I injuries, the stretching type injuries typically are located close to the ischial tuberosity and involve the proximal free tendon of semimembranosus.!G. .u This can be shown on MR I (Fig ) [.8). Although type II hamstring strains can cause a less dramatic acute limitation than type I strains, their rehabilitation period is often longer than that of type I strains/e It is important to directly inform the sportsperson that the rehabilitation is likely to be prolon ged. Unrealistically optimistic information only reinforces the disappointment and fru stration of the injured sportsperson. The sportsperson can often do quite demanding rehabilitation training early on, as long as pain·provoking exercises are avoided. Passive stretching and heavy·load exercises seem to aggravate the stre tch type of hamstring injuries by increasing pain.

Management of hamstring injuries Factors related to the prognosis of hamstring injuries are shown in th e box overlea£ There is very little scientific evidence on which to base the management of hamstring injuries. According to a recent systematic review, Ie only three randomized controlled trials have evalua ted the efficacy of a particular intervention for the rehabilitation of acute hamstring stra ins." -n Consequently, much of th e approach described below is on the basis of clinical experience. The management of acute hamstring strains is summarized in Table 31.3 overleaf.

Figure 31.8 MRI shows the site of the type II injury close to the ischial tuberosity

603

Re gi o na l p r o b l e ms Table 3 1.3 Management of hamstring injury First 4 8 hours The following factors have been shown to be associated

RICE (rest, ice, compression, elevation)

with increased length of time to return to play (RTP):

Early pain-free muscle contractions (Fig. 31.9)

Time (days) to walk at normal pace pain-free has been shown to be significantly associated with RTP time (>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

Quadriceps

- Iliopsoas Neural mobilizing (Fig. 31.11 on page 607) 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 n~ver 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 ~ R~-:: 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) Single~leg 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 ~Il('.-' In summary, there is limited scientific evidence to support the use of any medication in the 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 stra i n. 4 t" I~ 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 strains. ~ HI 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 side~ 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. ~s 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 extension . ~O 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· ~I 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 reJationships.)~ 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.

~ R~-:. l~

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

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)

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

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." ~·l~ 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

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

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

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.

(b) Maximal hip flexion

614

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

/flJ-~1-.. ~

71J\{?

'0'"

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 indi~ 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 high~risk 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 three~foId) 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 exer~ cises (Fig. J'.'4e on page 609) followed by a weekly seasonal program. There was also an approximate 2.5~fold 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 ham~ 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 per~ 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 values. ?~ 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 set~up 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 -+-

gluteus mediu s

X'

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. 50% prevalence) that could be repaired, but scientific data to support this is lacking. The decision is also influenced by the demands placed on the knee. A young sports person who wishes to return to a pivoting sport (such as football or basketball) is more likely to need an AC L reconstruction than a sportsperson who is prepared to confine activity to those sports that do not involve a large amount of twisting, turning, and pivoting. However, some patients in the form er category do perform well two years after rehabilitation alone. 26 It is likely that repeated episodes of "giving waf increase the risk of developing knee osteoarthritis , but there is no scientific evidence to support that an ACL reconstruction redu ces the incidence of future osteoarthritis. A recent report did not reveal any differences in the frequency of osteoarthritis between surgically reconstructed and non-surgically treated patients IO years after ACL inj ury.~9 Another important factor to assess is the likelihood of the patient adhering to a comprehensive. timeconsuming rehabilitation progra m. If the patient indicates a lack of willingness to unde rtake appropriate rehabili tation, treatment may not be successful. It is also important that the result of an ACL reconstruction is dependent on a successful postopera tive rehabilitation. Other factors to consider are the cost of surgery and rehabilitation, and the amount of time off work. Surgery is recommended for sportspeople wishing to participate in a high-speed sport with constant change of direction and pivoting. Rehabilitation without surgery has, however, been shown to be a velY good alternative also for this patient category,

649

and could be increasingly used as the first treatment of choice. As with other conditions, a trial of non-surgical management does not rule out the possibility oflater surgery when indicated.

Surgical treatment There are numerous surgical techniques used in the treahnent of ACL injuries. As ACL tears are usually in-substance tears and therefore not suitable for primary repair, reconstruction of the ACL is the surgical treatment of choice. Numerous methods of ACL reconstruction have been described. ACL reconstructions are performed "alihroscopically aided" through small incisions. Arthroscopic surgery utilizes small incisions to help visualize the inside of the joint and facilitate runnel placement of the ACL graft. Depending on the type of graft. inci· sions to harvest the graft and secure runnel access for graft fixation are made as well. Patient information about what happens during ACL reconstruction surgery is provided in the box. This is also available as a downloadable PDF file at 'NWw.clinicalsportsmedicine.com.

Type of graft The aim of an ACL reconstruction is to replace the torn ACL with a graft that reproduces the normal kinetic functions of the ligament. In most cases, an autogenous graft, taken from around the knee joint, is used. Autograft

The most common grafts used are the bone-patellar tendon-bone (BTE) autograft involving the central third of the patellar tendon, and a four-strand hamstring (semitendinosus +/- gracilis tendons) graft using the ipsilateral limb. Other autograft choices include the quadriceps tendon, and autograft:s from the contralateral limb. Graft choice depends on a number of factors, including surgeon competency, and his or her familiarity with the various techniques. Among orthopedic surgeons, there is considerable debate on graft choice-in particular patellar tendon versus hamstring tendon. A systematic review published in 2004 showed no difference between the two techniques as assessed by failure rate, knee range of motion, isokinetic strength, and arthrometer testing of knee laxity)O Each case should be considered on its merits, taking into account some of the differences in

650

potential postoperative issues. For example, after patellar tendon ACL reconstruction, pain with kneeling is common with up to 50% of patients reporting such pain. Patients who have a hamstring graft ACL reconstruction have decreased end-range knee flexion power. The incisions used for hamstring grafts are smaller and more cosmetic. Potential problems need to be addressed in the rehabilitation program and for that reason we advocate rehabilitation regimens with different emphases for the two types of surgery. Allograft Other graft options include allografts (the transplantation ofcadaver tissue such as ligaments or tendons). Allografts are associated with a low risk of infection, including viral transmission (HIV and hepatitis q, despite careful screening and processing; however, they have been used successfully for many years and are associated with decreased morbidity, and patients return to their daily activities more quickly. It has been suggested that allografts may also be associated with earlier rerum to sport; however, there is little evidence to support this theory.2. 4 The incorporation of allograft tissue appears to take at least as long as autograft tissue and arguably longer; therefore, many consider delaying the rerum to full sporting activities for eight to nine months. Recently published literature suggests a higher failure rate with the use of allografts in young active patients returning early to high-demand sporting activities.'1 The reason for this higher failure rate is unclear. It could be due to graft material properties (sterilization processes used, graft donor age, storage of the graft). Allograft surgery may be more often associated with ill-advised earlier return to sport by the sportsperson because of a faster perceived physiological recovery, when the graft is not biologically ready to be loaded and stressed during sporting activities. Further research in this area is necessary.

When should surgery be performed The timing of ACL reconstruction after an acute injury has come under review. Traditionally, and with very little evidence in support, ACL reconstructions were performed as soon as practical after the injury. However, there is evidence that delaying the surgery may decrease the postoperative risk of arthrofibrosis {see below)Y Initial reports suggested three weeks

Acute knee i nj u ri es

.-

W_.h~..!

happens --d l!,.':i ng

reconstructive

The surgical reconstruction technique of an ACL tear

involves harvesting the tendon (patellar or hamstring,

notch on the femur at which the graft is at a fixed tension throughout the range of knee movement.

Fig. 32.10a) through a small incision, and threading

Once the graft attachment areas have been delin-

the tendon through tunnels drilled in the bones. The

eated and prepared, the graft is fixed by one of a

most crucial part of the operation is the points of entry

variety of different methods. These methods include

of the tibial and femoral tunnels, and then the fixation

interference screw fixation (Fig. 32.1 ~b), staples, or the

of the graft.

tying of sutures around fixation posts. The better the

The tibial attachment should be in the center of the

quality of graft fixation, the more rehabilitation can be

previous anterior (ruciate attachment (at the level of

advanced in the first weeks after surgery. Improvement in the quality of graft fixation is a major reason for

the inner margin of the anterior portion of the lateral meniscus), The femoral attachment is to the so-called isometric point. This is a position in the intercondylar

advancement of rehabilitation in the first weeks after ACL surgery, as it is the weakest link in the first six to eight weeks after ACL reconstruction surgery.

bonepatellar tendon-

bone

OR

(b) Replacing the ruptured ACL with the graft tendon tissue; interference screw shown

semitendinosus & gracilis tendons quadruple bundle

Figure 32.10 The key steps in the process of ACL reconstruction (a) Harvesting graft tissue for the patellar tendon (top panel) or semimembranosus and gracilis tendon (Uhamstring graftU) ACL reconstruction

(e) After surgery-the knee with the new graft or "neoligament" in place

651

as the appropriate delay in surgery, but now focus is more on the condition of the knee, rather than the actual time. The injured knee should have little or no swelling, have near full range of motion, and the patient should have a normal gait. More important than a specific timing is, however, the actual need to perform a reconstruction. Since it was recently shown that several ACL-injured sportspeople perfonned equally well after rehabilitation alone as did those treated with ACL reconstruction, the timing of surgery needs to be carefully considered. The option of delaying surgery until it has been proven to be needed is evidence-based and should increasingly be used in the clinical setting. A recent studyll studied preoperative factors for knee function two years after reconstructive surgery of the ACL in the hope of finding predictive factors of who does well after ACL reconstruction. Results showed preoperative quadriceps muscle weakness and meniscus injuries have significant negative consequences for the mid-term (two-year) functional outcome after ACL reconstruction. The authors suggested that ACL reconstruction not be performed before quadriceps muscle strength of the injured limb is at least 80% that of the uninjured limb. n

Combined injuries Injuries of the ACL rarely occur in isolation; most ACL injuries occur in combination with other injuries. The presence and extent of associated injuries may affect the way in which the ACL injury is managed. Associated injury to the MeL (grades II-lII) poses a particular problem due to the tendency to develop stiffness after this injury. Most orthopedic surgeons initially treat the MCl injury in a knee brace for a period of 4- 6 weeks, during which time the sportsperson undertakes a comprehensive rehabilitation program (Table )2.8). This allows for early healing of the ligament injury and any potential capsular injury, reducing the risk of chronic valgus instability.

Rehabilitation after ACL injury Traditionally, most rehabilitation principles have been evaluated as postoperative rehabilitation protocols due to the frequent use of ACL reconstruction as the treatment of choice. Recently, however, rehabilitation alone, performed according to a protocol similar to that used postoperatively, has been shown to provide similar two·year outcomes to the combination of ACL reconstruction plus rehabilitation. 46

652

Thus, rehabilitation may be performed in a similar setting regardless of whether additional reconstructive surgery is performed or not. Rehabilitation after ACL injury has changed dramatically in recent years, resulting in greatly accelerated rehabilitation programs}" The major change over the past few years is the incorporation of a core stability program, along with increased emphasis on proprioceptive and balance exercises. These exercises have been used in successful ACL prevention programs (Fig. 32.6). Despite the widespread acceptance of these elements into rehabilitation programs, the two randomized trials have not shown convincing evidence of their efficacy. IS. ,6 The rehabilitation program is shown in Table 32.8. The time frames in the table are a guideline only and must be adjusted depending on the progress of the individual patient. It is essential to rehabilitate each patient individually, taking into consideration the extent of damage to the knee (e.g. articular cartilage damage), the patient's adherence to the exercise program, the amount of knee stiffness (which varies considerably between patients), and the eventual functional aims of tlle patient (e.g. daily activities, high-level sport). The patient must be taught to monitor the signs and symptoms around the knee following each workout. Ice may need to be applied if pain, inflammation, or swelling is present. The timing of return to sport depends on several different factors, including the nature of the sport, the therapist's and coach's opinions, and the confidence of the patient. Most surgeons consider that ACL graft maturation takes up to six months, and most advocate a sixmonth return to sport as an initial guideline. Beyond this temporal guideline, functional testing should be used to help assess readiness to return to sport. Functional tests include agility tests, the standing vertical jump and the "Heiden hop." The patient performs the "Heiden hop" by jumping as far as possible using the uninjured leg, landing on the injured leg. Sportspeople with good function are able to land solid with a single hop, to "stick it." Those with functional disability step further or take anotller small hop. Another way of testing function is by incorporating sport-specific drills. Isokinetic testing may be used to evaluate muscle strength. Quadriceps and hamstring strength should approximate those of the uninjured leg. In the light of all these factors and the varying progress of different

Table 32.8 Rehabilitation (ollow ing ACL reconstruction (see Figs 32.5 and 32.6) Time post

Physiotherapy

Phase

Goal of phase

surgery

treatment

Prehabilitation

No/minimal swelling

N/A

(preoperative rehabilitation)

Restore fuJI ROM, particularly

activity

Cryotherapy

Dependent on ability of patient

Wa lking

Electrotherapy

In early stages, follow the exercise program

Compression

extension General 4+15 lower limb

Manual therapy

strength or better Patient education-anatomy, surgical procedu re,

Functional/ sport-related Exercise program

from phase' and progress to phase 2

If patient has high level of function, start w ith

Gait re-ed ucation

exercise program from phase 2 and progress

Exercise modification

weights and repetitions as appropriate

Bike riding Swimming (light kick and no breaststroke)

and supervision

rehabilitation commitment, and goal setting Phase'

PWB-fWB

Cryotherapy

Gentle flexion ROM

Elimina te swelling

0-2 weeks

Electrotherapy

Extension ROM to 0"

0-100" ROM

Compression

QuadricepsNMO setting

4+/5 quadriceps strength 515 hamstring strength

Manual therapy

Supported (bilateral) ca lf raises

Gait re-education

Hip abduction and extension

Patient education

Hamstring pulleys/rubbers

Nil

Gait drills Phase 2

Cryotherapy

ROM drills

Walking

Full knee hyperextension

Electrotherapy

QuadricepsNMO setting

Exercise bike

Knee flexio n to 1300 +

Compression

Mini squats and lunges Leg press (doub le-leg, then single-leg)

No swelling

2-12 weeks

Full squat

Manual therapy

Good balance and control

Gait re-education

Step-ups

Unrestricted walking

Exercise modification

Bridges (double-leg, then single-leg) Hip abduction and extension with rubber tubing Single- leg calf raises Gait re-education drills Ba lance and proprioceptive dri lls (si ng le-leg)

continues

'"w "Ymptomatic patellofemoral malalignment. Am] Sports

Med 1995;zG{5):703-9. 19. Sanchis-Alfonso

patellofemoral pain syndrome. Am j Sports Med 2oo9;37(n):2IOS-16. 30. Messier SP. Davis SE. Curl WW et al. Etiologic factors associated with patellofemoral pain in runners. Med Sci

Sports Exerc 199I;23(9):1008--t5. 3t. Myer GO, Ford KR, Barber Foss KD et al.l1lC incidence and potential pathomechanics of patellofemoral pain in female athletes. eli/! Biomech 201O;ZS{7):700-7. 3z. Witvrouw E. Bellemans J, Lysens Ret al. Intrinsic risk £'lctorS for the development of patellar tendinitis in an athletic population. Am] Sports Med 200r:29(2): r90-5· 33. Watson

q, Propps M. Galt W et al. Reliability of

McConnell's classification of patellar orientation in

v, Rose116-Sastre E.

symptomatic and asymptomatic subjects. ] Orthop

Immunohistochemical analysis for neural markers of the lateral retinaculum in patients with isolated symptomatic patellofemoral malalignment. Am] Sporis

Med zooo;z8(5)725-3f. 20. Witonski 0, Wqgrowska-Danielewicz M. Distribution of substance-P nerve fibers in the knee joint in patients with anterior knee pain syndrome. A preliminary report. Kl1ee Surg Sports Traumatol Arthro5c

'999:7(3):'77-83. ZI. Duri ZAA, Aichroth PM. Dowd G. TIle fat pad. Am J

Knec SlIrg r996;9(2):SS-66. 22. Tsirbas A. Paterson RS, Keene GCR. Fat pad impingement: a missed cause of patellofemoral pain?

AustJ Sci Med Sport 1990;December:z4-26. 23. Fulkerson JP. Disorders oftke patellofemoraljoil1t. 3rd edn. Baltimore: Williams & Wilkins, 1997. 24. Matthews LS. Sonstegard DA, Henke JA.load bearing characteristics of the patella-femoral joint. Acta Orthop

Sports Phys Ther 1999:29(7):386-93. 34. McConnell J. Reliability of McConnelrs classification of patellar orientation in symptomatic and asymptomatic subjects - invited commentary. j Ort/lOp Sports Phys

71ltr 1999:29(7):388-91. 35. Van Tiggelen 0, Cowan S, Coorevits P et al. Delayed vastus medialis obliquus to vastus lateralis onset timing contributes to the development of patellofemoral pain in previously healthy men. Am J Sports Med 2009; 37{6): 10 99-1oS· 36. Ireland ML, Wilson JD, Ballantyne BT et aL Hip strength in females with and without patellofemoral pain. ] Orthop Sports Phys TIm' 200nr67I-6.

37. Tyler TF. Nicholas SJ, Mullaney MJ et al.lbe role of hip muscle function in the treatment of patellofemoral pain syndrome. Am] Sports Med 2006:34(4):630-6. 38. Cowan SM, Bennen KL. Hodges PW. lberapeutic patellar taping changes the timing ofvasti muscle

Seand 1977:4S{s):srr-16. 2S. Powers CM. 111e influence of altered lower-extremity kinematics on patellofemoral joint dysfunction: a theoretical perspective. ] Orthop Sports Pliys 71ler

activation in people with patellofemoral pain syndrome. Clinj Sport Mal 2002;12:339-47. 39. Ng GYF, Cheng JMF. The effects of patellar taping on pain and neuromuscular performance in subjects

2oo3;33{rr):639-46. 26. Grelsamer RP, Weinstein CH. Applied biomechanics of the patella. Cli'l Ort/lOp Rel Res 2001;389:9-1427. Dye SF. Vaupel GL. The pathophysiology of

with patellofemoral pain syndrome. Clin Rehabil 2002;16(8):821-7· 40. Salsich GB, Brechter JH, Farwell D etaL The effects

patellofemoral pain. Sports Med Arthrosc Rev 1994;2:

of patellar taping on knee kinetics. kinematics, and

203-10.

vastus lateralis muscle activity during stuir ambulation

28. Barton

CJ, levinger P, Menz H B et aL

Kinematic

gait characteristics associated with patellofemoral pain syndrome: a systematic review. Gait Postllre 2009:30(4}:40s-r6. 29. Boling MC, Padua DA Marshall SW et al. A prospective investigation ofbiomechanical risk factors for

in individuals with patellofemoral pain. J Orthop Sports

Phys 71ler 2002;32:3-10. 41. Wilson T, Carter N, 1110mas G. A multicenter, singlemasked study of medial, neutral. and lateral patellar taping in individuals with patellofemoral pain. j Orthop

Sports Phys 71ur 2003;33:437-48.

711

Regiona l prob l ems

42. Christou EA. Patellar taping increases vastus medialis oblique activity in the presence of patellofemoral pain.

J Elcctromyogr Kinesiolzo04;I4(4):495-So+ 43. Aminaka N, Gribble P. A systematic review of the

56. Vicenzino B, Collins N, Cleland Jet aL A clinical prediction rule for identifying patients \\,1th

effects of therapeutic taping on patellofemoral pain

patellofemoral pain who are likely to benefit from foot

syndrome. J Alhl Train 20°5;4°(4):341-51.

Olthoses: a preliminary determination. Br] Sports Mrd

44. GilleaId W. McConnell J. Parsons D. The effect of patellar taping on the onset of vastus medialis obJiquus and vas Ius lateralis muscle activity in persons with

patcllofemoral pain. Phys T/Jer 1998;78(1):25- 32. 45. Cowan SM, Hodges PW, Crossley KM et a1. Patellar taping does not change the amplitude of

zOlO;44(12):862-6. 57. Vicenzino B, Foot orthotics in the treatment of lower limb conditions: a musculoskeletal physiotherapy perspective. Mcm TIler 2004;9(4):J85-96.

58. Barton q, Menz HB, Crossley KM. Clinical predictors of foot orthoses efficacy in individuals with

clectromyographic activity of the vasti in a stair

patellofemoral pain. Med Sci Sports Exert ZOIIA3(9):

stepping task. Br J Spans Med 2006;4°(1):30-4.

1603-IO.

46. Cerny K. Vastus medialis oblique/vastus lateralis

59. Collins NJ, Bisset LM, Crossley KM, et aL Efficacy

muscle activity ratios for selected exercises in persons

of non·surgical interventions for anterior knee pain:

with and without patellofemoral pain syndrome. Pliys

systematic review and meta·analysis of randomised

Ther I99S;7S(8):672-83. 47. Powers CM, Landel R, Sosnick T et ai. The effects

trials. Sports Med in press (2012).

60, Gecha SR, Torg JS. Clinical prognosticators for

of patellar taping on stride characteristics and joint

the efficacy of retinacular release surgery to treat

motion in subjects with patellofemoral pain.] Ort/lOp

patellofemoraI pain. Gin Orthop Rei Res 1990;253:

Sports Pllys Ther 1997:26(6):286~91. 48. Powers CM, Ward SR. Chan L-O et al. we effect of

20 3- 8.

61. SchOttle PB. Fucentese SF. Romero J. Clinical and

bracing on patella alignment and patellofemoral joint

radiological outcome of medial patcllofemoralligamcnt

contact area. Med Sci Sports Exerc 2OO4:36(7):1226-p.

reconstruction with a semitendinosus autograft for

49. Powers CM. Ward SR, Chen Y et a1. we effect of bracing on patellofemoral joint stress during free and fast walking. Am] Sports Med 20°4;32(1):224-31. 50. Lun VMY, Wiley Preston J. Meeuwisse WH et a1. Effectiveness of patellar bracing for treatment of

patella instability. Knee SlIrg Sports Traumatol Artllrosc

2005:13(7):516-2I. 62, Blazina ME, Kerlan RK, Jobe FW etal./umper's knee.

art/lOp clill North Am t973;4(3):665- 78. 63. Khan KM. Bonar F, Desmond PM etal. Patellar

patellofemoraI pain syndrome. Clin] Sport Med

tendinosis (jumper's knee): findings at histopathologic

2ooPS(4):z35-40 .

examination, US. and MR imaging. Radiology

SI. Crossley K, Bennell K, Green S et al. Physical therapy for patellofemoral pain. A randomized. double-

1996 ;ZOO(3):821-7· 64. Maffulli N, Khan KM, Puddu G, Overuse tendon

blinded, placebo controlled study, Am] Sports Med

conditions. Time to change a confusing terminology.

2002;3 0 (6):857-6 5.

Arlhroscopy 1998:14:84°-3.

52. Collins N, Crossley K, Beller E et a\. Foot orthoses and physioth~rapy in the treatment of patellofemoral pain syndrome: randomised clinical trial. BM]

2008;337=aI 735, proximal, distal, and local factors. An international research retreat. J Ort)lOp Sports Phys Ther

20IO;4 0 (3):AI-48. 54. Noehren B, Scholz

65, Khan KM, Cook JL, Bonar F et al. Histopathology of common tendinopathies: update and implications for clinical management. Sports Med 1999;27:393-408.

66. Maffulli N. Binfield PM, Leach WJ et al. Surgical

53. Davis IS. Powers C. Patellofemoral pain syndrome:

r, Davis L we effect of real-time

management of tendinopathy of the main body of the patellar tendon in athletes. elin] Sport Med

1999:9(2):5 8 - 62 . 67. Visentini PJ. Khan KM. Cook JL et aI, The VISA score: an index of severity of symptoms in patients with

gait retraining on hip kinematics, pain and function in

jumper's knee (patellar tendinosis). J Sci Med Sport

subjects with patellofemoral pain syndrome. BrJ Sports

1998:1(1):zz-8.

Med zon;45(9):691-6. ;;. Franettovich M, Chapman A Blanch P et al. Continual use of augmented low-Dye taping increases arch height

712

in standing but does not influence neuromotor control of gait. Gait Posture: 20l0:31{z):z47-50.

68, Khan KM, Maffulli N. Coleman BD et ai. Patellar tendinopathy: some aspects of basic science and clinical management. Br J Sports Med 1998;32:346-55.

A nt e r i o r k n ee

69. Cook

Jt.. Khan KM , Kiss ZS e t al. Prospective imaging

training in asymptoma tic soccer players wi th

eli te junior baske tball players. ) Ultrasollud Med

ultrasonographic abnormalities in achilles and patellar

2000;19(7):473-9· 70. Richards DP , Ajemian SV, Wiley fP et a1. Knee joint dynamics predict patellar tendi nitis in elite volleyball players. Am J Sports Med 1996;24(:,) :676-83. 71. Cook fl, Khan KM , Kiss ZS et at. Patella r te ndinopathy in junior basketball players: a con trolled clinical and ultrasonographic study of 268 patellar tendons in players aged 14-18 years. Scalld J Med Sci Sports 2000;10(4):216-20. strategies of athletes with an asymptomatic patellar te ndon abnormality. Med Sci Sports Exerc

2olO:42(n ):2072-8o.

eccentric traini ng on jumper's knee in vollcyball players during the competitive season. elill J Sport

M~d

200 5: 15(4):227- 34. 83. Wilson J, Sevier T. Helrst R ct a1. Comparison of rehabilitation methods in the treatment of patellar tendinitis.) Sport ReJwbil2000;9:304-14. infra patellar tendinitis: a combina tion of modalities and transverse fric tion m assage versus iontophoresis.

) Sport RelltlbiI 1994:P35-45. 85. Cook J L, Purdam CR. Is tendon pathology a

73. Malliaras P, Cook JL, Kent P. Reduced ankle dorsiRexion range may increase the risk of patellar tendon injury among volleyball players. J Sci Med Sport 2006;9(4):3 04-9. 74. Jensen K, Di Fabio RP. Evaluation of eccentric exercise in treatment of patella r tendini tis. PIIYS TIler

continuum? A pathology model to explain the clinical presentation ofload·induced tendinopathy. Br) Sports

Med 20 09:43(6):409- r6 . 86. Alfredson H, Ohberg L Neovascularizatioll in chronic painful patellar tendinosis-promising results after sclerosing neovessels outside the tendon c.halle nge the need fo r surgery. Knee Surg Sports TraU lllatol Art/trose

1989 :69(3):211-16. 75. Cannell

tendons. Alii j Sports Med 2008:36(3):45T- 60. 82. Visnes H , Hoksrud A, Cook Jet al. No effect of

84. Pellecchia GL, Hamel H, Behnke P. Treatment of

72. Edwards S, Steele JR , McGhee DE et a1. Landing

LJ , Taunton I E, Clement DB et a1.

A randomised clinical trial of the efficacy of drop squats

20°5: 13(2):74-80 . 87. Hoksrud A, Ohberg l, Alfredson H et al.

or leg extension/ leg curl exercises to treat clinicallr

Ultrasound·guided sclerosis of neovesscls in painful

diagnosed jumper's knee in athletes: pilot study. Br)

chronic patellar tendi nopathy. Am J Sports Med

2006:34(11):173 8-46.

Sports Med 200 1;35:60-4. 76. Purdam CR, Cook IL Ho pper OM et al. Descriminative

n.

81. Fredberg U, Bolvig l, Andersen NT. Prophylactic

study of asymptom a tic patellar tendinopathy in

88. Fredberg U, Bolvig L, Pfeiffer-Jensen M et al.

ability of functional loading tests for adolesccnt

Ultrasonography as a tool for diagnosis. guidance of

jumper's knee. Pllys TIler Sport 2003:4:3-9 .

local s teroid in jection and, together with pressure

Young MA, Cook IL, Purdam C R et a\. Eccentric decline

algometry, monitoring of the treatment of athletes

squat protocol offers superior results at

12

months

compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. Br J Sports Med 20 ° 5:39(2):1 02.-5.

78. Bahr R, Fossan n, loken Set al. Surgical treatment compared with eccentric training for patellar tendinopathy (jumper's knee). A random ized, controlled trial. ) BOlle joillt Surg Am 2006;88(8):

168 9- 9 8. 79. StasinopouJos D, Stasinopoulos I. Comparison of effects of exercisc programme. pulsed ultrasound and transverse fr iction in the treatment of chronic patellar tendinopathy. Ciill Relltlbii2004;18(4):347-P.

80. Kongsgaard M, Kovan en V, Aagaard Pet al. Corticosteroid in jections, eccentric decline squat training and heavy slow resistance training in patcllar

with chronic jumper's knee and Achilles tendi niti s: a randomized, double-blind, placebo·controlled s tudy.

Scand J RlteWlIato!2004;33(2):94-101. 89. Elardo G, Kon E, Della Villa S et 31. Use of platele t-rich plasma for the treatment of refractory jumper's knee. Inl Orthop 20 10;34(6):9°9-15.

90. Bahr R. Fossan B, loken S, et al. Surgica l treatment compared with eccentric training for patellar tendinopathy (Jumper's Knee). A randomized, controlled trial. J Bone )oillt Surg Am 2006 ;88 (8): 168 9-9 8 . 91. Coleman BD , Khan KM, Kiss ZS e t al. Open and arthroscopic patellar tenotomy for chronic patellar tendinopathy: a retrospective outcome stud y. Alii J

Sports Med 2000;28(2):193-90. 92, WiUberg L. Sunding K, Ghberg L,. et a\. Treatment of

tendinopathy. Sca/ld) Mui Sci Sports 2009;19(6):

Jumper's knee: promising short-term results in a pilot

79°-802.

study using a new arthroscopic approach based on

713

imaging findings. Knee Sllrg Sports Tralln1(llo/ Artllrosc zo07;15(5):676-8r. 93. Kaeding CC, Pedroza AD, Powers Be. Surgical treatment of chronic patellar tendinosis: a systematic review. Gin Ort!Jop Rei Res zo07:455=10z-6 94. Coleman BD, Khan KM, MafFulii N et al. Studies of surgical outcome after patella tendinopathy: clinical significance of methodological deficiencies and guidelines for future studies. Scand] Med Sci Sports ZOOO;IO:Z-II. 95.

Saddik 0, McNally EG, Richardson M. MRI of Hoffa's

fat pad. Skelet Radio/zo04;33(8):433- 44. 96. Ducher G. Cook I, Spurrier 0 et al. Ultrasound imaging of the patellar tendon attachment to the tibia during puberty: a 12-month follow-up in tennis

103. lbomee R. A comprehensive treatment approach for patellofemoral pain syndrome in young women.

Physical Therapy 1997;77(12):1690--17°3. 104. van Linschoten R, van Middelkoop M, Berger MY, et al. Supervised exercise therapy versus usual care for patellofemoral pain syndrome: an open label randomised controlled trial. EM] Z009:339:b4074. 105. Witvrouw E, Danneels L, Van Tiggelen 0, et al. Open versus closed kinetic chain exercises in patellofemoral pain: a s-year prospective randomized study. Am]

Sports Med 2004;3z(5):JJ22-30. J06. Witvrouw E, Lysens R, Bellemans

J, et al. Open versus

closed kinetic chain exercises for patellofemoral pain-A prospective, randomized study. Am] Sports

players. scalld J Med Sci Sports 20IO;zo(I):e35-40.

Med zooo;z8(5):687-94. 107. van den Dolder PA, Roberts DL Six sessions

97. Warden SI. Kiss ZS. Malara FA, et al. Comparative

of manual therapy increase knee Aexion and

accuracy of magnetic resonance imaging and

improve activity in people with anterior knee pain:

ultrasonography in confirming clinically diagnosed

a randomised controlled trial. Aust] PltvsiotiJer

patellar tendinopathy. Am] Sports Mal 20°7;35(3):

2006:52(4):261-4· JOS. Jensen R, Gothesen 0, Liseth K, et al. Acupuncture

4 2 7-3 6 . 98. Collins N, Crossley K, Beller E. et al. Foot orthoses and physiotherapy in the treatment of patellofemoral pain syndrome: randomised clinical trial. EM] 2008;337:aI 735· 99. Eng JJ, Pierrynowski MR. Evaluation of soft foot orthotics in the treatment of patellofem oral pain syndrome. Phys TIler 1993;73(2):62-8; discussion 68-7°· 100. Nakagawa TH, Muniz TB. Baldon Rde M, et al. lbc effect of additional strengthening of hip abductor and lateral rotator muscles in patellofemoral pain syndrome: a randomized controlled pilot study. Clin

Rehabil2008:2Z(I2): IO SI-60. lOr. Herrington L, AI-Sherhi A. A controlled trial of weight-bearing versus non-weight·bearing exercises for patellofemoral pain.] Ort}lOp Sports Phys Ther 2°°7;37(4) :155- 60 . 102. Song CY, Lin YF, Wei TC, et al. Surplus value of hip adduction in leg·press exercise in patients with patellofemoral pain syndrome: a randomized controlled trial. Physical Therapy 2009;89(5):4°9-18.

71 4

treatment of patellofemoral pain syndrome.] Aitem

Complement Med 1999:5(6):521-7. J09. Noehren B. Scholz I. Davis I. The effect of real·time gait retraining on hip kinematics, pain and function in subjects with patellofemoral pain syndrome. Br] Sports Med 20n;45(9):691-6 lIO. Australian Acute Musculoskeletal Pain Guidelines Group. Evidence-based management ofacute Inllswloskelelal pain. Brisbane: Australian Academic Press Pty. Ltd., 2003. III. Mason M. Keays SL, Newcombe PA. lbe effect of taping, quadriceps strengthening and stretching prescribed separately or combined on patellofemoral pain. Physiother Res Int zOll;r6(2):109-I9. llZ. Stakes NO. Myburgh C. Brantingham]W et al. A prospective randomized clinical trial to determine efficacy of combind spinal manipulation and patella mobilization compared to patella mobilization alone in the conservative management of patellofemoral pain syndrome.] Am Chiroprac Assoc 2006;43(7): II-8.

I retired becaLlse I had a knee inj",y, my cmtilage was wearing out, it was pail1fid al1d J could,,'t put in the fOLlr/tours of practice each day that I needed to. Guy Forget, fo rmer French professional tenn is player Although acute knee injuries and anterior knee pain are very common presentations in sports medicine practice, patients presenting with lateral, medial, or posterior knee pain ca n also provide challenges to the practitioner.

Lateral knee pai n Pain about the lateral knee (Fig. 3+1) is a frequent

problem, especially among distance runners and

abnormalities can precipitate ITBFS. PateUofemoral syndrome (Chapter 33) may also present as lateral knee pain. In the older active person, degeneration of the lateral meniscus or lateral compartmen t osteoarthritis shou ld be considered. The biceps fe moris tendon m ay cause pa in as it passes posterolaterally to the knee and inserts into the head of the fibula; this occurs in sprinters and footballers. Injuries of the superior tibiofibular joint

cyclists. The most common cause oflateral knee pain is iliotibial band friction syndrome (lTBFS) which is an overuse injury. Traini ng errors and biom echanical biceps femoris

vastus lateralis

(/ong headJ

biceps femori s

- -lIlc+'ri

(short head)

semimembranosus lateral collateral ligament & bursa

iliotibia l band

patella

Il'if'iilfill

plantariS biceps fem oris bursa

patellar tendon

soleus

Figure 34.1 latera l aspect of the knee (a) Su rface anatomy

(b) Anatomy of lateral aspect of the knee

7 15

may cause lateral knee pain. Lateral knee pain may be referred from the lumbar spine. The causes and differential diagnoses oflateral knee pain are shown in Table 3+1.

Clinical approach As with acute knee injuries (Chapter 32) history and physical examination are the key to an accurate diagnosis.

the lower leg may indicate common peroneal nerve entrapment.

Examination Full assessment of the ligaments of the knee (Chapter 32) should be included in the examination. Biomechanical examination should also be performed.

EvwJ

History

A detailed knee examination can be seen in the Clinical Sports Medicine masterclasses atwww. c1inicalsportsmedicine.com

A history of overuse suggest ITBFS or biceps femoris tendinopathy. If there is a history of excessive downhill running or running on an uneven surface, ITBFS may be implicated. If the pain occurs with sprinting or kicking activities, biceps femoris tendinopathy is more likely. Lateral knee pain following knee or ankle injury may indicate the superior tibiofibular joint or lateral meniscus as the site of injury. The pain associated with biceps femoris tendin· opathy flares up on initial activity and then starts to settle with warming up; it usually recurs following cessation of activity or the next day. When left untreated, pain persists during exercise and the athlete may not be able to continue with sporting activity. Iliotibial band (ITE) pain usually does not settle with ongoing activity and can be associated with local swelling. Pain on sudden twisting or a history of giving way or locking may indicate degenerative lateral meniscus problems. Pain associated with excessive lateral pressure syndrome increases with activity. In active individuals who are over 50 years old, lateral compartment osteoarthritis should be considered. The presence of back pain may suggest referred pain from the lumbar spine. Associated neurological symptoms such as weakness and paresthesia in

1. Observation

(al (bl (cl (dl

standing walking supine side-lying

2. Active movements (a) knee flexion (b)

knee extension

(c)

repeated knee flexion (0-30°) (Fig. 34.2a)

(d)

tibial rotation

3. Passive movements (a) knee flexion/extension

(bl tibial rotation (Fig. 34.2bl (c)

superior tibiofibular joint (i) accessory glides (Fig. 34.2c)

(d)

muscle stretches

(II ITB (Ober's testl (Fig. 34.2dl (ij) quadriceps (iii) hamstring 4. Resisted movements (a) knee flexion (Fig. 34.2e) (b)

tibial rotation

5. Functional movements

(al

hopping

(b)

squat/single-leg squat

(cl

jumping

Table 34.1 Causes of lateral knee pain Common

Less common

Not to be missed

Iliotibial band friction syndrome

Patellofemoral syndrome

Common peroneal nerve injury

Lateral meniscus abnormality Minor tear

Osteoarthritis of the lateral compartment of the knee

Perthes'disease

Degenerative change

Excessive lateral pressure syndrome

Cyst

Biceps femoris tendinopathy Superior tibiofibular joint sprain Synovitis of the knee joint Referred pain •

716

Lumbar spine Neuromechanical sensitivity

Slipped capital femoral epiphysis

Lat e r a l, med i a l, and poste ri or knee pain 6. Palpation (al lateral femoral epicondyle (Fig. 34.2f overleaf) (b) lateral joint line

(el

lateral retinaculum

(d) lateral border of patella (el superior tibiofibular joint (0 biceps femoris tendon (g) gluteus medius

7. Special tests (al

full knee examination (Chapter 32) (i) effusion (Fig. 34.29 overleaf)

(b)

neurodynamic tests

(ii)

(el

(d)

McMurray's test (Fig. 34.2h overleaf)

(i)

prone knee bend

(ij)

slump (Fig, 34.2i overleaf)

lumbar spine (Chapter 26)

biomechanical assessment (Chapter 8) (Fig. 34.2j on page 719)

(e) Passive movements-accessory anteroposterior glide to superior tibiofibular joint

Figure 34.2 Examination of the patient with lateral knee pain

(al Active movements- repeated flexion from 00 to 30°, This may reproduce the patient's pain if ITBFS is

the cause. It can be performed in a side-lying position (illustrated), standing or as a squat

(b) Passive movements-tibial rotation This is performed in knee flexion to assess superior tibiofibular joint movement

(d) Passive movement-ITB stretch This is performed in a side-lying position with the hip in neutral rotation and knee flexion. The hip is extended and then adducted.lf the ITB is tight, knee extension will occur with adduction (Ober's test)

(e) Resisted movement-knee nexion Concentric or eccentric contractions may reproduce the pain of biceps femoris tendinopathy

717

(h) Special tests-McMurray's test The knee is flexed and, at various stages of flexion, internal and external rotation of the tibia are performed. The presence of pain and a palpable "clunk" are a positive McMurray's test and are consistent with meniscal injury. If there is no "clunk" but the patient's pain is reproduced, then the meniscus may be damaged or there may be patellofemoral joint abnormality (f) Palpation - lateral femoral epicondyle

(9) Special test-knee effusion Manually drain the medial subpatellar pouch by stroking the fluid in a superior direction. (1) Then "milk"the fluid back into the knee from above (2) while observing the pouch for reaccumulating fluid (i ) Special tests-slump test

Investigations Although the majority of younger patients with lateral knee pain do not require investigations, MR imaging can be useful in cases of persistent lateral knee pain when a degenerative lateral meniscus is suspected. It is also indicated if there is a clinical suspicion of lateral compartment osteoarthritis. X-ray has poor sensitivity for osteoarthritis. When imaging is not readily available, a diagnostic local anesthetic 71 8

injection can be used to differentiate local soft tissue pain (e.g. ITBFS) from intra-articular or referred pain.

Iliotibial band friction syndrome Iliotibial band friction syndrome (ITBFS) is an overuse injury presenting as lateral knee pain that is exacerbated by sporting activity. It is commonly seen in runners, cyclists, military recruits, and endurance

La t era l , m ed i a l, an d p oster ior kn ee p ai n

ITB ----,---';-

fibers fat pad

--/-I--If\,,-J\1

biceps femori s

tendon lateral collateral

lateral

meniscus Gerdy's tubercle

ligament

Figure 34.3 Anatomy of the iliotibial band insertion (j) Special tests-biomechanical assessment Full lower limb biomechanical assessment should be performed while standing, walking, and lying.

VL == VASTUS l ATERAlIS; RF ;; RECTUS FEMORIS; ITB '" ILIOTIBIAL BAND FROM FRANKLIN-MILLER A. ET At. CL/NICAL SPORTSA NATOMY. MELBOURNE: MCGRAW-HILL, 2010; P. 269

Abnormal pelvic movements (e.g. excessive lateral eilt) should be noted

athietes.'-4 Incidence rates in running range from 1.6% to 12% and 1% to 5.5% in military populations.'

In cycling, ITBFS accounts for 15% to 24% of overuse injuries,l

Anatomy Traditionally ITBFS was considered to be the result of friction, between the ITS and the underlying lateral epicondyle of the femur. This friction was thought to contribute to local inflam mation and irritation of an anatomical bursa lying between the tendon and the

lateral epicondyle) However. recent studies do not support the presence of an anatomical bursa around the lateral femoral epico ndyle .~·.j Instead of a bursa, it has been proposed that a richly innervated and vascularized layer of fa t and connective tissue separates the ITB from the lateral femoral epicondyle, and this could be the likely source of pain seen in ITB FS . ~· " The ITB itself is not a discrete band bu t a lat eral thickening of the circumferential fascia

lata that envelops the whole thigh like a stocking (Fig. 34.3).'·'· '111e fTB inserts along the length of the femur down the linea aspera via the lateral in termuscular sep tum. u ,,, Proximally, the tensor fascia lata mu scle inserts into the ITB, as does a substantial portion of the gluteus m aximus m uscle. Distally, the ITS crosses the lateral femoral epicondyle and is connected to that epicondyle by strong fibrous bands. The ITB continues, acting like a lateral ligament, from the lateral fem oral epicondyle to insert onto the patella and Gerdy's tubercle on the tibia (Fig. 34.)). The ITB can also pro ject onto the fibula. This anatomical orientation of the lTB demonstrates the close relationship between the ITS and the knee and hip complex and its role in lateral stability. Movement of the ITB around the lateral femoral epicondyle is restricted by its strong fibrous band attachm en ts . However, altering tension of the fascia lata and hip mu sculature can result in compressive forces around the lateral femoral epicondyle.~' "

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Therefore pain may result with compressive loads rather than being due to transverse frictional forces.

ITB biomechanics The lTB plays a role in stability around the hip with its role in hip joint centering through its tension~ ing effect. In hip adduction and flexion, an increase in pressure around the greater trochanter has been reported.' This pressure is further increased by knee flexion. The same pressure is reduced in hip abduc~ tion, and knee extension. This role is supported by surgical studies that have shown that ITB lengthen~ ing can lead to favorable outcomes in trochanteric bursitis presentations. It was originally thought that ITBFS was associ~ ated with repetitive knee flexion and extension move~ ment. However, a biomechanical study found no significant difference in sagittal knee movements between an ITBFS population and matched controls.> This suggests other planes of motion may be more relevant. For example, an increase in tibial internal rotation can augment compressive forces around the lateral femoral epicondyle by moving the ITB's distal attachment to the tibia more medially.6 Tibial internal rotation may result from poor prox~ imal control (increased hip adduction/internal rota~ tion), genu valgus, and/or poor rear foot mechanics. An increase in hip adduction, especially during the loading phase of running, increases the eccentric demand on the hip abductors.(i Runners with ITBFS can have significant weakness of their hip abductors in the affected limb'; and decreased ability of the hip abductors to eccentrically control abduction. x There is also often weakness in knee Bexion and knee extension, with decreased braking forces.'! Weakness and fatigue can result in increased compressive forces around the lateral femoral epicondyle and therefore lead to lTBFS. Neural feedback from the richly innervated fat and connective tissue between the ITB and lateral femoral epicondyle may result in decreased tension in the hip abductors to reduce these compressive loads. ~ This can lead to hip muscle imbalances and altered biomechanics. I

running, or cambered courses are often aggravating factors. On examination, tenderness is elicited over the lateral femoral epicondyle 2-3 em (-I in.) above the lateral joint line (Fig. 34-2f). Crepitus and local swelling may also be felt. Repeated flexion/extension of the knee may reproduce the patienfs symptoms. Obers test (Fig. 34-2d) often reveals lTB tightness and may produce a burning sensation. Tightness may be secondary to shortening of the tensor fascia lata and/or gluteus maximus muscles proximally, or excessive development of the vastus lateralis, placing increased tensile load on the ITB. Imaging is not usually required to confirm the diagnosis of ITBFS. Both ultrasound and MRI can show thickening of the ITB over the lateral femoral condyle and often a fluid collection deep to the ITB at the same site.IO

Treatment Treatment of ITBFS should address not only local symptoms, but also foot and especially hip biomechanics for more favorable long~term results. Although pathology is felt distally, treatment should be focused proximally. Local treatment includes ice and electrotherapy appliedtotheareaaroundthelateralfemoralepicondyle. Nonsteroidal anti~inBammatory drugs (NSAIDs) may be helpful in the initial stages. Corticosteroid injec~ lion (Fig. 34.4) has traditionally been used to inject the "bursa." The inconsistent results from these injections can be attributed to a misunderstanding of the pathology. Corticosteroid injection can be helpful in reducing pain and this facilitates the patient undertaking rehabilitation exercises.

Clinical features Clinically, a sportsperson with ITBFS typically complains of an ache over the lateral aspect of the knee which is aggravated by running or cycling. The pain often develops at about the same distance/time during activity. Longer training sessions, downhill 720

Figure 34.4 Corticosteroid injection if used, is aimed deep to the ITB tendon-between it and the underlying lateral femoral epicondyle

Soft tissue treatment to the proximal ITB (Figs 3+sa, b), dry needling (Fig. 3+Sc) and self massage with a foam roll (Fig. 3+sd) all help to reduce muscle tension and tone in the ITB. Stretching (Fig. 34.6 overleaf) is routinely proposed as a treatment for lTBFS. However, because the ITB inserts into the entire length of the fe mur via the lateral intermu scular septum, stretching exercises may have a li mited effect on th e ITB itself. Stretching may have so me effect on reducing the tension in the tensor fascia lata. 2 . 4 Stretchin g of the gluteus maximus muscle may prove more beneficial because ofits close relationship to the ITB. Tightness of the gluteal muscles and tensor fascia lata are commonly associated with ITBFS. The presence of trigger points in the tensor fascia lata, gluteus minimus, and gluteus medius may contribute to lTBFS. Gluteal trigger point dry needling (Fig. 34.se

overleaf) and ischemic pressure can reduce the tension and relieve local pressure around the lateral femoral epicondyle. Strengthening of the hip external rotators (Fig. 34.7a overleaf) and abductors (Fig. 34.7b overleaf) is an importa nt component of the treatment to correct the underlying weakness and fatigability of these muscles. Surgery to release the ITB may be indicated if conservative man agement fails. Me thod s used include excision of a triangular area of the ITB from the area overlying the lateral condyle when the knee is in a 30° position," transec tion of the posterior halfof the width of the ITB over the lateral condyle,'" Z-lengthening of the iliotibial band,'j and distal detachment and multiple puncture. '4

Figure 34.5 Treating tight myofascial structures (a) Sustained myofascial tension to the proximallTB

(e) Dry needling to ITB trigger points

(b) Ischemic pressure to the body of the ITB

(d) Foam roll self-massage to the ITS

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(e)

Dry needling to gluteal trigger points

Figu re 34.7 Strengthening exercises forthe external hip rotators and abductors (a) Exercise involves the patient standing on one leg and slowly performing a squat maintaining pelvic stability

(b) Hip abduction in side-lying

Lateral meniscus abnormality The lateral meniscus is more circular than the medial

Figure 34.6 ITB stretch-the ITB on the left side is being stretched. The symptomatic leg is extended and adducted across the uninvolved leg. The patient exhales and slowly flexes the trunk laterally to the opposite side until a stretch is felt on the side of the hip

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one, which is more C·shaped (Fig. )2.) on page 6J4). The lateral meniscus is loosely connected to the lateral joint capsule and, to some degree, communicates with the posterior cruciate ligament. Acute meniscal injuries are discussed in Chapter 32. A discoid (disk-shaped) lateral meniscus is an anatomical abnormality reported in children. A

Lat eral , m ed i a l, an d po ste r ior kn ee pain discoid meniscus can present as chronic "snapping knee syndrome," can be asymptomatic, and may be an incidental finding on MRI later on in life.'s What risk is associated with this abnormality, especially in active adolescent and adult populations, remains unclear. Wh en sym ptomatic (i.e. painful, presence of

joint effusion, symptoms of clicking and locking), it is often associated with a meniscal tear, which is then treated arthroscopically.')

In children and early adolescents, di agnosing meniscal injury can be difficult because of vague subjective findings and difficulty in localizing pain. ,G This

can result in delayed diagnoses and increase chron· icity. Meniscal injury in children is more common than previously thought, and is under-diagnosed.l(j Tenderness along the lateral joi nt line with associated joint effusion and a positive McMurray's test is indicative of meniscal injury. X-ray can rule out differential diagnoses such as osteochondritis dissecans, and osteochondral and tibial pla teau fractures. ls . 16 MRI is useful , but can be associated with false positivesY; Treatment is based on the athlete's age, duration of symptoms, area of meniscal pathology (vascular areas compared with non -vascular) and number of associated injuries (such as cruciate ligament tear). In adults degeneration of the lateral m eniscus ca n also present as a gradual onset of lateral knee pain, and is often associated with quadriceps muscle atrophy.

If a runner presents complaining of lateral knee pain that comes on after 20 minutes of running and (' ~1.. is aggravated by funn ing up hills, the practitioner ~ 0"" shou ld not automatica lly assume that the ~tJ'.(? patient has ITBFS- the proble m may relate to a degenerative meniscu5. ~ R~

Careful physical examination should help distinguish the lateral meniscal degeneration from ITBFS conditions. A lateral meniscus injury is often tender along the joint line, 2-3 em below the site of tenderness in ITBFS (at the lateral femoral epicondyle). McMurray's test in full flexion (Fig. 34.2h) should also help to dis-

tinguish the conditions, as it should be positive when a meniscal injury is present and negative in cases of ITBFS.

A degenerative meniscus ca n present as a painful or non-painful lump at the lateral joint line. TI1is is not an JIB bursa. If there is doubt as to the correct diagnosis, MRI is the investigation of choice.

Osteoarthritis of the lateral compartment of the knee Lateral knee pain can also be caused by degeneration of the lateral tibial plateau; this can be associated with meniscal injury, knee malaHgnment (e.g. valgus malalignment), and obesity.'7. '11 Early in the disease. the patient may give a hi story ofincreasing knee pain with activity and stiffness after a period of rest. As the disease progresses, the patient may start to experience pain at night that may disturb sleep, and morning stiffness. usually lasting less than half an hour. In the early stages, examination may only reveal a small effusion. A useful investigation is a weight-bearing plain X-ray. This has greater sensitivity than views taken with the patient supine. Initial treatment of osteoarthritis includes symptomatic relief with analgesia and NSAIDs if required, modification of activity, and exercise prescription, together with weight loss if indica ted. In tra-articular hyaluronic aci d supplements (viscosu pplements) have a similar efficacy to NSAIDs. and the patien t does not have to take tablets daily. I'.p o Functional motor control assessment foc using on load di stribution such as single-leg squat, stair negotiation and gai t, can iden tify biomechanical contributing facto rs. Early identification of th ese factors may delay or even prevent further degeneration. Patients with severe clinical symptoms may require unicompartmental-" or, eventually, total knee replacement.

Excessive lateral pressure syndrome Excessive lateral pressure syndrome (lateral patellar compression syndrome) occurs when there is excessive pressure on the lateral patelIofemoral joint resulting from a tight lateral retinaculum. The lateral retinaculum is not one distinct anatomical structure. but is composed of three layers. There is a deep fascia layer (not attached to the patella). an in termediate layer (composed of the ITB and the quadriceps aponeurosis and their attachments to the patella), and the deepest layer is the joint capsul e.~;' Therefore an increase in pressure around the lateral retinaculum will affect the joint capsule, the patellofemoral joint, the ITB. and the quadriceps muscles. This can lead to bone strain on the lateral patella, inflammation of the lateral retinaculum, and ITBFS. Eventually the increased bone strain on the lateral patella may lead to development of a vertical stress fracture or even separation of the lateral patellar 723

fragment. This must be differentiated radiologically from a congenital bipartite patella. The separated fragment is in the superolateral aspect of the patella. MRI has been used to image this condition:'-l Initial treatment of excessive lateral pressure syndrome consists of patellofemoral mobilization and soft tissue therapy to the lateral retinaculum. Taping techniques rarely help. Surgical lateral retinacular release or even removal of the lateral patellar fragment is occasionally required.~4

Biceps femoris tendinopathy Biceps femoris tendinopathy occurs with excessive acceleration and deceleration activities, and is often associated with running and cycling. As with most tendinopathies, it does not initially restrict sporting activity and therefore has a high risk of chronicity when not recognised early. Pain is described around the posterolateral knee and often settles after activity. Morning stiffness post exercise is often reported. The pain can be produced with resisted flexion, especially with eccentric contractions (Fig. 34-2e) and on palpation of the tendon as it inserts onto the fibula. It is often associated with tightness of the hamstring and gluteal muscles. Stiffness of the lumbar spine and poor core stability may contribute to hamstring tightness. Both MRI and ultrasound examination may help confirm the diagnosis. Treatment is based on the general principles of the treatment of tendinopathy-load modification, soft tissue therapy (Fig. 34-8), and strengthening, especially eccentric strengthening of the hamstrings (Fig. 34-9), Strengthening ofthe hip muscles, specifically the gluteus maximus, may also prove useful.~5 In rare cases, failed conservative measures mean surgical approaches may be considered. Surgical approaches include stripping of the paratenon, removal of degenerative tissue, and other repair techniques for torn tendons. ~()

Figure 34.8 Soft tissue therapy in the treatment of biceps femoris tendinopathy.lschemic pressure at the musculotendinous junction (shown) and muscle belly can be effective

Figure 34.9 Eccentric strengthening exercises in the treatment of biceps femoriS tendinopathy. Drop~and~ catch is performed in prone positions (Chapter 31). This may be progressed to include hip flexion (Le. patient lying over the end of the bed)

Superior tibiofibular joint injury The superior tibiofibular joint comprises the articulation between the lateral condyle of the tibia and the fibular head. The joint capsule is strengthened by superior anterior and posterior ligaments.2.7. 2.8 The superior tibiofibular joint plays a role in tibiofemoral joint stability through its surrounding anatomical structures, which include the lateral collateral ligament, arcuate ligament, popliteofibular ligament, biceps femoris tendon, and popliteus muscle.,8 The 724

superior tibiofibular joint externally rotates during ankle dorsiflexion and is thought to dissipate torsional stresses from the ankle.~R When injured, the superior tibiofibular joint can affect knee and ankle function and can be a source oflateral knee pain. Superior tibiofibular joint injUlY may result from direct trauma resulting in subluxation or dislocation of the fibula. The superior tibiofibular joint can also be sprained during twisting injuries. The mechanism

Latera l, m e d ia l, a n d pos t erio r knee p ai n of injury is often described as a combination of rotation and knee flexion (e.g. pivoting, cutting) and has been reported in sports such as mgby, soccer, skiing and the various forms of martial arts. '1 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 implicated. ~7 The incidence of medial tibial sb-ess syndrome has been reported to be between 4% and 35% in military personnel and sportspeople. ~('·~'

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. ~3 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

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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 promising. ~7. 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

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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 syndrome.4~ 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.

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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

recommended: ~

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.

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 \" R,., surgical fi xation of unstable tibia l fractures, with r ~~ intramedullary nailing. This allows sportspeop le ~ b..... earlierweight·bearing, and earlier conditioning

}~'3 months

im provement

(peritendonous injection, NSAIDs, or physiorherapy)

diameter Platelet-rich plasma injection (PRP) + eccen tric exercise (EE) vs. placebo injection

deVos et aI., 20 10 40

+

eccentric exercise AirHeel bracing 'M+ eccentric exercise (EE) vs. eccentric

Knobloch et aI., 2008'1

exercise

VISA-A,selfassessments

6, 12, and 24 weeks

n = 54 (26/281 9 competitive spo rts,

(treatment success

37 recreational sports,

over the standard EE

and return to sport (likert Scale)

8 sedentary

rehabilitation program

Foot and Ankle

12 weeks

n = 97 (63/ 341 34 ru nners, 8 soccer, 17

Outcome Score (FADS) and pain

other ball sports, 38 no t specl/ied

(Visual Analog Sca le

[VASil Night splint (NS) vs. eccentric exercise (EE) vs. night splin t + eccentric exercise

Roos et al.,

200419

The PRP inj ection showed The injection was guided by no significant benefi t ultrasound imaging

Foot and Ankle Omcome Score (FAOS), physical

6 weeks, 3, 6, and

n = 4S (22/ 231 29 active in sports

12 months

activity level (Likert

Although microcirculation was greatly better using the AirHeel"· Brace, no

No supervision for the

."

eccentric exercise program Brace was worn all day, regardless of sports

=>

participatio n (not worn

-;r

found over EE alone

sleeping)

'" » ...,

EE alone was observed to result in the best shortterm and long-term

worst outcome both

EE was not supervised but a quality check was performed at 1 week from baseline Night spli nts were custom formed for each patient and only worn at night

short- and long-term Running/jumping (R/J) (Achilles loading ) + eccentric exercise vs. eccentric exercise

VISA-A-S, pain (Visual Silbernagel et al., 2007 J6 Analog Scale [VAS])

6 weeks, 3,6, and 12 mont hs

n = 38120/ 181 Based on the Physical

'-J

'"

No significant differences were found between

Activity Score

R/J+EEvs.EEat

(1 [sedenta ry),

12 months

6 (extremely active)): mean = 4.45; range

'"=>

clinica l advantages were

outcomes EE + NS resulted in the

Scale)

EE was unsupervised

EE program followed based on Silbernagel's Ueccentric overload training" Runni ng/jumping exercises restricted by a pain model

= 1-6

continues

~

-;r

'" ~

"'" '"

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 4o 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 high~jump 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 ~

7lJ'i ~

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 tibia~ 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 X~ray. 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.

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.

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

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 m alleolar s tress fra cture secondary to ch ronic ankle

1995 ;29:9- 14. 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 -E~'--;;=

talonavicular joint

'EJ~"",,~lumbricals

& 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,9 A retrospective case study found no difference in terms of pain, function, or abnormality on CT between surgical management and conservative management after two years. 40

(Fig·4°·91}6.,8 Often, patients with a stress fracture of the navicu· lar present after a long period of pain Of after a period of weight·bearing rest. All patients, even if they have been unsuccessfully treated with prolonged weightbearing rest or short-term cast immobilization, should undergo cast immobilization for a six week period. This method of treatment is associated with an 80% successful return·to·sport rateJ.6 and may be successful even in longstanding cases. Some clinicians advocate surgical treatment with the insertion of a screw where there is significant separation of the fracture (Fig. 4o.8c). In cases of delayed or non·union, surgical internal fixation

854

Post·cast rehabilitation and prevention of recurrence Following removal of the cast, it is essential to mobilize the stiff ankle, and subtalar and midtarsal joints. The calf muscles require soft tissue therapy and exercise to regain strength. These must be done before resuming running. Activity must be begun gradually, slowly building up to full training over a period of six weeks. Predisposing factors to navicular stress fractures may include tarsal coalition, excessive pronation, and restricted dorsiflexion of the ankle. These factors need to be corrected before resuming activity.

Extensor tendinopathy

Treatment

The extensor (dorsiflexor) muscles of the foot com· prise the tibialis anterior, extensor halluds longus and brevis, as well as extensor digitorum longus and brevis. The insertions in the foot and actions of the extensor muscles are shown in Table 40.3Tibialis anterior tendinopathy is the most common tendinopathy occurring in the extensor muscles of the fo ot. Tendinopathies of the exten sor hallucis longus and brevis and extensor digi torum longus and brevis mu scl es are rare.

Popular clinical treatment involves relative rest and soft tissue therapy to the extensor muscles. Extensor muscle s trengthening is advocated as is the case with other tendinopathies. The underlying precipitating cause n eeds to be addressed. This may include mobilization of the first ray, and tarsometatarsal and midtarsal joints, if the first MTP joint and midfoot is stiff. A change of lacing pattern or placing adhesive foam to the underside of the tongue of the shoe will help if compression by the shoelaces is the cause. Modification of running technique may be required. Rarely. footwear will need to be replaced.

Causes The tibialis anterior muscle resists plantarflexion and eversion of the foot at heel s trike and its tendon is therefore susceptible to overuse injury. Tendinopathy may be related to extensor muscle weakness or, alter· natively, it may occur secondary to a recent increase in the training load or compression by excessively tight shoelaces. Stiffness of the first MTP joint and midfoot joints may contribute.

Clinical features Generally after a period of overuse, the patient with extensor tendinopathy complains of an aching dorsal aspect of the midfoot. Examination may reveal tenderness, often with mild swelling, at the insertion of the tibialis anterior tendon at the base of the first metatarsal and the cuneiform. Resisted dorsiflexion and eccentric inversion may elicit pain. Functional assessment m ay reveal excessive heel strike or over-striding during running. Both ultrasound and MRI may reveal swelling of the tendon at its insertion and exclude the presence of a degenerative teaT.

Midtarsal joint sprains The midtarsal joint (Chopart's joint) consists of the talonavicular and calcaneocuboid joints. Other joints in the midtarsal area are th e n aviculocuneiform, cuboid cuneiform, and intercuneiform joints. Injuries to the midtarsal joints are most commonly seen in gymnasts, jumpers, and footbailers. Individual ligamentous sprains to the m idta rsal joints are uncommon; they usually affect the dorsal calcaneocuboi d or the bifurcate liga m ent (comprising the ca1caneonavicular and ca lcaneocuboid ligament).

Dorsal calcaneocuboid ligament injury Patients present with pain in the lateral midfoot following an inversion injury. Examination reveals localized tenderness and swelling at the dorsolateral aspect of the calcaneocuboid joint. Stress inversion of the foot eli cits pain. X-ray is required to exclude fracture. MRI may confirm the diagnosis.

Table 40 .3 Extensor muscles, their insertions at the foot, and their actions

Muscle

Insertion in foot

Action

TIbialis anterior

Medial cuneiform and base of 1st metatarsal

Dorsiflexes foot at ankle Inverts foot at subtalar and transverse tarsal joints Maintains medial longitudinal arch

Extensor digitorum longus

Extensor expansion of lateral four toes

Extensor haJJucis longus

Base of distal phalanx of big toe

Extends toes and dorsi flexes foot Extends big toe DorsifJexes foot Inverts foot at subtalar and transverse tarsal joints

Extensor digitorum brevis

long extenso r tendons to second, third, and fourth toes

Extends toes

Extensor hallucis brevis

Proximal phalanx of big toe

Extends big toe

855

Taping may provide additional support and help relieve pain. Orthoses may be required. Following a joint sprain, joint inflammation occasionally develops. This generally responds well to NSAIDs but, if it persists, the patient may benefit from a corticosteroid injection into one of the midtarsal joints.

1st metatarsal

Bifurcate ligament injuries Injury to the bifurcate ligament (comprising the calcaneonavicular and calcaneocuboid ligament) may be associated with fractures of the anterior process of the calcaneus and may occur secondary to violent dorsiflexion, forceful plantarfiexion, and inversion injuries. Patients present with lateral midfoot pain and swelling. usually fonowing an anlde sprain or injury. Examination reveals local tenderness and occasionally swelling overlying the ligament. with pain elicited at the site with simultaneous forefoot supination and plantar flexion. X.rays are required to assess for a frachlre of the anterior process of the calcaneus. If a fracture is present. a CT scan may be required for further assessment. An MRI scan can be used to confirm the joint/ligament sprain. Treatment is similar to the dorsal calcaneocuboid sprain mentioned above. If there is a non-displaced or mildly displaced fracture of the anterior process of the calcaneum, four weeks' immobilization is required. If the fracture is displaced, surgery is required.

~-4~q.,.

transverse ligaments

Lisfranc ligament medial cuneiform navicular l~o!!";'::::':.J Figure 40.10 Ligamentous attachments of the Lisfranc joint articulation

grade I-sprain

\1 ~ -

~~

lm~: ~ Usfranc ligament sprain-no d iastasis

Lisfranc joint injuries The eponymous Lisfranc joint refers to the tarsometatarsal joints-the bases of the five metatarsals with their corresponding three cuneiforms and cuboid (Fig. 40.10). Injuries to these joints are given this eponym after Jacques Lisfranc, a surgeon in Napoleon's army. who described an operation for amputation through the tarsometatarsal joint. The spectrum of injuries of the Lisfranc joint complex ranges from partial sprains with no displacement, to complete tears with separation (diastasis) of the first and second metatarsal bones and. depending on the severity. different patterns of tarsal and metatarsal displacement (Fig. 40.II). Although Lisfranc joint injuries ("midfoot sprains") are not common in the general population, they are the second most common foot injury in sportspeople. They generally occur as a consequence of a low-velocity indirect

856

Lisfranc ligament rupture 1-5 mm diastaSIS

Lisfranc ligament rupture >5 mm diastasis Figure 40.11 Lisfrancjoint injury classification system

force, in contrast to the general popUlation, where they occur as a consequence of a high-velocity force. Lisfranc joint fracture-dislocation is rare in sport, but, because of its disastrous consequences

if untreated , the diagnosis must be considered in all cases of "mid foot sprain" in the sportsperson.

capsule may rupture and the metatarsal may displace dorsally. Thus, a fractu re at the plantar base of a metatarsal can be a clue to a subtle Lisfranc joint injury.

Causes There are two main mechanisms of injury: Direct-t his injury is relatively uncommon and occurs as a si mple crush injury to the tarsometatarsal joint region . There is no specific pattern of damage or distinctive appearance with a direct injury. Indirect-this mech ani sm is more common a nd generally occurs secondary to a longitu dina l force sustained while the foot is plantarflexed and slig htly rotated. There are three commo n injury situations: longitudinal compression (Fig. 40.12). a backward fal l with the foot entrapped, and a fall o n the pa int of the toes.41

The extent of the damage depends on the severity of the injury-in milder injuries, the weak dorsal tarsome tatarsal ligaments are ruphlred; with more severe injuries, there may also be fractures of the plantar aspect of the metatarsal base, or the planta r

Clinical features A patient with Lisfranc joint injury may complain of midfoot pain and difficulty weight-bearing, following an acute injury by the mechanisms described above. Pain is classically aggravated by forefoot weightbearing-the patient is unable to fun on the toes and feels pain on the push-off phase of running and sometimes during walking and on calf raises. Often the presentation may be delayed, and the pa tien t presents with ongoing midfoot pain and swelling, aggrava ted by running. ~Jl ('..... Midfoot pain that persists fo r more than five days

~~ 7&\(,>0

post-injury should raise suspicion of a lisfranej oint injury.

Examina tion reveals: tenderness wi th o r without swelling on the dorsal midfoot. often with associated bruising in this region pain with combined eversion and abduction of the forefo ot whi le the calcaneus is held still.

Neurovascular examination is mand atory as the dorsalis pedis artery can be compromised in the initial injury or by subsequent swelling of the fOOt.~'

Investigations

Figure 40.12 Mechan ism of injury to lisfranc jointlongitudinal compress ion

Plain X-rays while weight-bearin g are recommended. Diastasis between the first and second metatarsal bases of greater than 2 mm (0.1 in.) (Fig. 40.13a overleaf) suggests a Lisfranc joint inj ury, although in patients with a metatarsus adductus a 3 mm (0.15 in.) separation may be normal. In such cases, it is essential to take comparative weight-bearing X-rays of the non-injured side. as a difference in diastasis of greater than I mm (0.05 in.) between the t\.....o sides is considered diagnostic. Other radiological signs that may indicate an injury to the Lisfranc joint include a "fleck sign," which appears as a fleck fracture near the base of the second metatarsal or medial cuneiform or, in the lateral view, either dorsal displacement of the metatarsal bases relative to the tarsus or flattening of the medial longihldinal arch. However, a dislocation may reduce spontaneously, and the foot may appear normal on plain X-rays despite the presence of severe soft tissue disruption.

857

It'R4('

MRI sca ns are sensitive in detecting tears of the

,~~;:, lisfranc ligament when plain X-rays ap pear normal, ~ 0'" and shou ld be performed if there is a possib le '1(J' 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 \~!:'lC'--, hyperthermia during the first weeks of their ~ ~ pregnancy. Moderate exercise in normal 71i'V~"O 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.

Hemodynamically significant heart disease 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 Unevaluated maternal cardiac arrhythmia

Advantages of exercise during pregnancy

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

\'.!.,'l ('......

recreational physical activity during pregnancy

)1J"v~o

for gestational diabetes compared with inactive

~ f:

Absolute contraindications

have approximately 50% reduction in the risk 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 introduced and self~paced in low-impact aerobic

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. _ M,d Sci Sports Exerc 1978:1o(3):2]&-22.

Br j N Ull' 20°5:93(5):731-9. 14. Wya tt KM, Dimm ock PW. O'Brien PM . Selective

serotonin reuptake inhibitors for premenstrual

26. Naltiv A, Puffer )C, Green GA. Lifes tyles and health risks of collc-giate athletes: a multi-center study. CUll J

SIJort M,d 1997:7(4) :262-72.

931

~

-

r'

r

l

27. Kaiserauer S. Snyder AC, Sleeper M et aL Nutritional.

physiological. and menstrual status of distance runners. Med Sci Sports Exerc I989;21(2):120-5. 28. Chan fL, Mantzoros CS. Role ofleptin in energy·

deprivation states: normal human physiology and clinical implications for hypothalamic amenorrhoea and anorexia nervosa. Lallcet 2005:366(9479):74-85. 29. De Souza MJ. Williams NL Beyond hypoestrogenism in amenorrheic athletes: energy deficiency as a contributing factor for bone loss. Curr Sports Med Rep 20°5:4(1):3 8 -44. 30. Cann CE, Martin MC, Genant HK et a1. Decreased

prevalence of amenorrhea and oligomenorrhea.] Bone Miner Res 1995:10(1):26-35. 41. Nattiv A, Loucks AB, Manore MM et aI. American

College of Sports Medicine position stand. The female athlete triad. Med Sci Sports Exerc zo07;3 9(10): I867-8z . 4z. Torstveit MK, Sundgot·Borgen

J. Tbe female athlete

triad exists in both elite athletes and controls. Med Sci Sports Exerc zo05:37(9):1449-59. 43. Myerson M, Gulin B. Warren MP et a1. Total body

bone densilY in amenorrheic runners. Obstet Gynecol

'99 2 ;79(6):973-8.

spinal mineral·content in amenorrheic women. ]AMA

4+ Hetland ML, Haarbo J, Christiansen C et a!. Running

1984;25 1(5):6z6-9· 31. Drinkwater BL, Nilson K. Chesnut CH 3rd et a1. Bone

unaffected, except in amenorrheic women. Am J Med

mineral content of amenorrheic and eumenorrheic athletes. N Engl] Med 1984;3 II:277-8 1. 32. wnnell SL, Stager JM , Blue PW et a1. Bone mineral

content and menstrual regularity in female runners.

Med Sci Sports Exerc 1984;16(4):343-8. 33. Marcus R, Cann C. Madvig P et a1. Menstrual function and bone mass in elite women distance runners. Endocrine and metabolic features. Alii. Illtern Med 1985:102(2):158- 63. 3+ Rutherford OM. Spine and total body bone mineral

density in amenorrheic endurance athletes.] Appl PhysiolI993;74(6):2904-8. 35. Micklesfield LK, Lambert EY. Fataar AB et a1.

Bone mineral density in mature, premenopausal ultramarathon runners. Med Sci Sports Exerc

'995'27(;),688-9 6 . 36. Tomten SE, Fa1ch A, Birkeland KI et at Bone mineral

density and menstrual irregularities. A comparative study on cortical and trabecular bone shUctures in nmners with alleged normal eating behavior. Int]

Sports Med 1998;19(2):92- 7. 37. Pettersson U, StaInacke BM, AhU:nius GM et a1. Low

bone mass density at multiple skeletal sites, including the appendicular skeleton in amenorrheic runners.

CalcifTissuc lnt t999;64(Z):II7-25. 38. To WW. Wong MW. Lam IV. Bone mineral density differences bet

71J'i~

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 par~ 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 train~ 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 p eopl e~they 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 u sed 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 the Lifestyle In terventions and

REFERENCES

Independence for Elders Pilot (LIFE-P) study. ] Gerontol

Nelson ME, Rejeski Wj . Blair SN et aL Physical activity and public health in olde r adults: recommendation from the American College of Sports Medicine and

the American Heart Association. Meri Sci Sports Exerc 2007;39(8):143:;-45.

2. Gill TM . DiPietro L. Krumholz HM. Role of exercise

s tress testing and safety monitoring for older persons

starting an exercise program. JAMA 2000 ;284(3):

34 2 -9. 3. Galloway MT, 10kl P. Aging successfully: the importance of physical activity in maintaining health and function. ] Am AUld Orthop 511rg 2000:8(1):37- 44. 4. Timi ras P, ed. Pltysi%gicallmsis ofaging alld geriCltrics. 3rd ed. Boca Raton, FL:

eRe Press. 2003.

5. Christmas C, Andersen RA. Exercise and older patients: guidelines for the clinician. JAm Ceriatr Soc 2000:4 8 (3):3 18- 24. 6_ Daley MJ, Spinks WL Exercise. mobility and aging.

Sports Med 2000 ;29 (1 ):1- 12. 7. Rowe JW. Kahn RL. Successful aging. Geront%gist 1997:37(4):433-4°. 8. Sun Q, Hu FB, Groc.lslein F. Invited commentaryphysical activity benefits various aspects of healthy aging: comment on "PhysiGlI activity at midlife and health-related quality of life in older men." Archllltern Med 201O;I7o(13):tt72-3.

A Bioi Sci Med Sci 2006;6I(Il):U57-65. IS.

Rejeski WJ. Marsh Ai'. Ch melo E et al. TIle Lifestyle Interventions and Independ ence fo r Elders Pilot (LIFE-P): 2·year follow-u p_J Geronlol A 8iol Sci Med Sci 2009;64(4):46z-7·

16. America n College of Sports Medicine. Position stand: the recomm ended quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitne ss in healthy adults. Mt'd Sci Sports Exerc

199 0 ;22(2):26 5- 74_ 17. Ades PA. Coello CEo Effects o f exercise and cardiac rehabilitatio n on cardiovascular ou tcomes. Med Clill

Nortll Alii 2000;84 (1):251-65, x- xi. 18. Jolliffe

IA. Rees K, Taylor RS et al. Exercise-ba sed

rehabili tation for coronary heart disease. Cochrane

Database S)'st Rev 2001(1):CDoor800. 19. Booth F\V. Gordon SE. Carlson

CJ

et al. Waging war on

modern chronic diseases: primary prevention through exercise biology. J Appl Physiol 2000:88(2)774-87. 20. Lacasse Y. Goldstein R. Lasserson 11 ct al. Pulmonary rchabilitation for chronic obstructive pulmonary disease. Cochrane Databast' Sy5t Rev 2006(4): CDo03793· 21. Nylen ES, Kokkinos p. Myers J et a1. Prognostic effect of exercise capacity on mortali ty in older adu lts with

9. Newman AB, Arnold AM , Naydeck BL et al. HSuccess ful

diabetes mellitus. ] Am Genatr Soc; 58(10):1850-4.

aging"; effect of subclinical cardiovascula r disease. Arcll

22. Messier SP. Royer TO, Craven TE et al. Long· te rm

IlIlern Med 200p63(19):23 J5-22_ 10. Meisner BA, Dogra S. Logan AJ ct al. Do or ded ine~ Comparing the elTects of physical inactivity on biopsychosocial components of successful aging. I I.

Trial (FAST). JAm Ceriatr Soc 2000;48(2):131-8. 2}. von Stengel S. Kemmler W, Kalender WA e t al.

] Health PsychoI2oJo;rs(s):G88-96 .

Differential effects of strength versus power training

Leveille SG, Guralnik JM. Ferrucci Let a1. Aging

on bone minera l density in postmenopausal

successfully until dea th in old age: opportunities

women: a 2·year longihdinal study. BrJ SpOl1S Med

for increasing active li fe expectancy. Am J Epidemiol

2007;41( 10):649- 55; discussion 655.

1999;149(7):654-6 4. 12. Simonsick EM, Guralnik 1M. Volpato S et al. Just

24. Tolomio S. Ermolao A. Trava in G et a l. Short· te rm adapted physical activity program im proves bone

get ou t the door! Importance of walking outside the

quality in os teopenic/os teoporotic postmenopausal

home for maintaining mobility. findings from the

women. ] P/lys Act Hea lth 200 8;5(6):844-53.

women's h ealth and aging s tudy. ] Am Gerialr Soc

25. Sherrin g ton C. Whi tney JC. Lord SR et al. Effective

2oo5:S3(2) :198- 2°3. I}.

exercise a nd its effect o n balance in older. osteoarthri tic adults: results from the Fitness, Arthritis, aud Seniors

Keysor

JJ. Does late-life physical activity or exercise

prevent o r minimize disablement? A critical review of th e scientific evide nce. Am] Prev Med 2003;2) (3 SuppI2j:r29 - }6. J4. Pahor M. Blair SN, Espeland M et a1. Effects of a physical activity intervention on measures of physical

exercise for the prevention of falls: a systematic review and m e ta·analysis. JAm Geriatr Soc 200&:56( 12): 2234- 43· 26. Reid KJ, Baro n KG. Lu 8 ct al. Aerobic excrcise improves sclf.rep0l1ed sleep and q uality ofHre in older adults with insomnia. Sleep Med 2oro;1I(9 ):

934-4 0 .

941

Spec i a l groups of partic ip an t s

27. Li F. Fisher KJ. Harmer P et al. Tai chi and self·rated q uality of sleep and daytim e sleepiness in older adults: a randomized controlled trial. jAm Celiolr Soc

20°4:52.(6):892-9°0. 28. Uu-Ambrose T. Donaldson MG. Exercise and cog nition in o lder adults: is there a role

fOf

resistance training

programmes ? BrJ Sports Med 2Oo9:43{lj:25-7. 29. Kramer AF, CoJcombe 51. McAuley E et al. Fitness, aging and neurocognitive function. Ne.llrobjol Agillg 20°5:26 SUppl1 : 12 4- 7· 30. Colcombe $, Kramer AP. Fitness effects on the cognitive function of older adults: a meta-analytic study.

Psychol Sci 20°3;14(2):125-3°. 31. Blankevoort CG, van Heuvelen MJ, Boersma F et al.

111

daily li fe activity to reduce fa lls in olde r

adults. Aust OCCIiP n ,,!r j 20l0; 57(1):4 2-50.

36. Stiggelbout M. Popkema DY, Ho pman-Rock M et al. Once a week is not e nough: effeds of a widely implemented group based exercise programm e for older adults: a randomised controlled trial. ) Epirlem iol CO IIZIIIU/lity Health 2004;58(2):83- 8. 37. Williams B, Poulter NR. Brown MJ et a1. Guidelines

for management of hypertension : report of the fourt h workin g patty oflhe British Hypertension Socie ty, 2oo4-BI-lS IV] HU11l Hypertens 2oo4:r8(3):

139-8 5. 38. RosendorIT C, Black HR , Cannon CP et al. Treatment ofhyperten siol1 in the prevention and management

Review of c!Teets of physical activity a ll strength.

of ischemic heart disea se: a scientific statement

balance. mobility and ADL performance in elderly

from the Am erican Heart Association Council for

subjects with dementia. Demellt Gerilltr Cog" Disord

High Blood Pressure Research and the Councils o n

2010;3°(5):39 2-4°2.

Clinical Card iology and Epidemio logy and Preven tion.

32. Singh NA. Stavrinos T M, Scarbek Y et al. A randomized control led trial of high verslls low intensity weight

eirell/otion 2007;115(21):276 1-88. 39. Mason 1M, Dickinson HO, Nicolson DJ e t aL TIle

training versus general pract itioner care fo r clinical

d iabetogenic potential of thiazide-type diuretic

depress ion in older adults. J Geronlol A BioI Sci Med Sci

and beta-blocker combinations in patients with

2005:60(6):768-76. 33. Salminen M, [soaho R, Vahlberg T et al. Effects

hypertensio n. ) Hyper/ens 20°5:23(10):1777-81. 40. Thomas S, Macki ntosh S, Halbert r. Does the 'Otago

of a health advocacy, counselling, and activation

exercise programme' reduce mortality and fall s in older

programme on depress ive symptoms in older

adul ts? A systematic review and meta-analysis. Age

co ro nary heart disease patients. Il1t J Ceriatr Psyclliall1' 2005;20 (6 ):55.2-8. 34. Campbell AJ. Assertive screening: health checks prior

Agr:ing 2010 :3 9 (6):681-7. 4!. Davis IC, Robertson MC, Ashe MC e t al. Does a homebased s trength and balance programme in people aged

to exercise programmes in older people. Br J Sports Med

~80

20 °9:43(1):,.

fa ll s? A sys tematic review of economic evaluations

15. Clem son L, Singh MF. Bundy A et al. li FE Pilot Study: A randomised trial of balance and strength training

942

embedded

years provide the best value for money to prevent

o r falls preven tion in terventions. a,.] SPOIts Med 20 10 ;44: 80-89.

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, u1ti~ 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 Year

M ilitary

N

Weeks

Gender

Incidence

Rate per 100/year

1982

US Army

767

8

Fema le

42%

252

1982

US Army

3437

8

Male

23%

138

1994

South African Army

1261

9

Male

31%

179

1995

US Navy

4415

9

Fema le

22%

127

1995

US Navy

9500

9

Male

11%

63

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

Australian

Norwegian

New Zealand

Cause

US infantry 8

medical evacuations ll

recruit5 ~

recruits 12

recruits 4

Training-related

47%

19-21%

19.2%

Falls/jumps

1B%

Motor vehicle-related

12-16%

Runn ing

36.6%

Obstacle cou rse

14.6%

Basic training

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 lit e ra ture. ~·6. 9 . 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 result of training-related injuries_~ Australian studies 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 The standard principles of strength training need to be adapted according to the disability. The wheelchair user may be unable to stabilize the trunk to perform the action; however, the equipment can be adapted to allow the exercise to take place. Although there has been concern that sports people with cerebral palsy may suffer increased muscle tone from strength training, there is little evidence for this. The standard principles of biomechanics also need to be re-examined where, for example, stroke technique in swimming, symmetry of running/7 or javelin throwing techniques must be re-evaluated in the light of the disability. Efforts can be made to improve streamlining in the water or to improve range of motion in a joint, for example. but normal models of "correct technique" may have to be re-evaluated. 967

Winter sports and common injuries Winter sports exist in a variety of disciplines for people with disabilities, and participation can include the competitive Paralympic level (Table 46.1). The alpine events cater for the visually impaired, spinally injured, or the limb-deficient sportsperson. Guide skiers are used for the visually impaired and a sitting monoski is used for paraplegic sports people. Standing sportspeople are at risk of the usual skiing injuries (e.g. head injury or anterior cruei· ate ligament rupture). In the sitting classes, small outriggers are used with a ski on the end to control the ski, so forceful impact landing on the outrigger can cause wrist fracture or shoulder injury. The cross-country events are associated with overuse injuries, and the sit-skier may suffer shoulder and elbow problems. Biathlon (skiing and shooting) can be performed by the visually impaired using a sighting mechanism that utilizes an audible signal with increasing tone as the competitor points toward the center of the target. Sledge hockey is an adapted form of ice hockey. Competitors sit on the sledge and skate by pushing two sticks, which are also used to strike the puck. A variety of disability groups participate in this sport as there are only minimal disability entry criteria. Injuries occur by direct contact between players, use of the stick (intentionally or accidentally), or by being hit by the puck. Sports people with spinal cord injury-induced low bone mass are susceptible to fracture in this sport. Wheelchair curling was introduced to the Paralympic Winter Games in Torino in 2006 and caused few injuries.

Anti-doping issues The IOC is a signatory to the Worl d Anti-Doping Code (WADA) (Chapter 66). The list of prohibited substances is the same for Paralympic athletes as for able-bodied athletes. Because of the nature of athletes' disabilities, it is more likely that they may need to take medications on the prohibited list to manage medical conditions. To do this, they must complete a therapeutic use exemption (TUE) application process that is outlined in Chapter 66. A successful application has to meet the same criteria as for able-bodied athletes: 1. that the athlete would experience a Significant impairment to health if the prohibited substance or method was to be withheld in the course of treating an acute or chronic medical condition

968

2. that the therapeutic use of the prohibited substance would not produce additional enhancement of performance other than that which might be anticipated by a return to a state of normal health 3. that there are no reasonable therapeutic alternatives to the use of the prohibited substance or method 4. that the necessity for the use of the prohibited substance or method is not as a consequence of prior non-therapeutic use of the prohibited substance.

There are some differences to the sample collection process which vary according to the disability. Sportspeople who use intermittent catheterization are permitted to use their own catheter to collect the urine sample. For sportspeople who use a condom and leg bag drainage system, the contents of the leg bag must first be emptied, and a fresh sample of urine collected. This is to avoid the potential for inserting a "clean" sample of urine into the leg bag prior to competition. Sportspeople who are visually impaired receive help to complete forms and are supervised by their own observer in the sample collection process. The sportsperson's representative observes the Doping Control Officer during the sample collection process to ensure that there is no tampering of the sample during the collection process. Sportspeople with an intellectual disability need to be accompanied by a representative who understands the process. Disability sport does not appear to be rife with abuse of prohibited substances. However, as in ablebodied sport, power lifting has been tainted by anabolic steroid use. Understandably, there have been claims of inadvertent use of diuretics or beta blockers to treat hypertension. It is challenging for sportspeople to be aware of the anti-doping restrictions on medication used to manage their medical conditions; this population requires particularly skilled sports medicine care.

Travel with teams Although Chapter 64 is devoted to travel with teams, sportspeople with disability have specific needs. Firstly, the simple logistics of boarding a team of wheelchair users on and off an aircraft takes additional time and may require lifting and handling. Toileting on board aircraft using a small-wheeled aisle chair is difficult and is likely to decrease the fluid intake of wheelchair users, leading to dehydration. Transportation at the destination needs to

Th e at h le t e w it h a di sab ili ty be accessible. The team clinician should aim to be familiar with the accessibility of toilets, rooms, and sports facilities in advance. Prolonged sitting without the use of the normal pressure cushion may result in pressure areas on the skin. Sportspeop\e should try to take pressure-

relieving mea sures during th e journey an d check pressure areas on arrival. The risk of deep vein thrombosis exists for all long-haul passengers. Dependent edema can be a particular problem among individuals who do not have the capacity to use the active muscle pump. Compression stockings can be appropriate.

969

Specia l groups of participants

~ 1.

insulin sensitivity in early rehabilitation of spinal cord

REEERENCES Booth FW. Gordon SE, Carlson

CJ et at Waging war on

modern chronic diseases: primary prevention through exercise biology. ] App/ Physiolzooo;88(z):774- 87. 2. Groah SL. Nash MS, Ward EA etaJ. Cardiometabolic risk in community-dwelling persons with chronic spinal cord injury. } CardiaplIIIll Rdwbil Prell 2ou;3I(zj :

73-80 . 3. Schmid A, Schmidt-Trucksass A, Huonker M et al. Catecholamines response of high performance wheelchair athletes at rest and during exercise with autonomic dysreAexia. Int J Sports Med 2001;22(1):2-7. {. Dela F. Mohr T, Jensen eM et al. Cardiovascular control during exercise: insights from spinal cord·injured

humans. Circulation 2oopo7(I6):ZI27- 33.

5. Hopman MT, Houtman S, Groothuis JT et al. lbe effect of varied fractional inspired oxygen on arm exercise performance in spinal cord injury and ablebodied persons. Arch Phys Med Rdwbil2004;8S(2}: 319-2 3. 6. Jacobs PL, Nash MS. Exercise recommendations for individuals with spinal cord injury. Sports Med 2004:34(11):727-51. 7. Nash MS. Exercise as a health-promoting activity

cooling strategies on thermore6,ulatory responses of tetraplegic athletes during repeated intermittent exercise in the heat. J Appl PII}'sioI2005;g8(6):21OI-7·

I6. Webborn AD. 'Boosting' perfonnance in disability sport BrJ Sports Med 1999:33(2)74- 5. I7- Klenck C. Gebke K. Practical management: common medical problems in disabled athletes. Cli" J Sport Med 2007;17:55- 60. 18. Garcia ME. Esc!arin De RU2 A. Management of urinary tract infection in patients with spinal cord injuries .

Clilt Microbial Infect 2003;9:780-5. Ig. Agarwal S, Triolo RJ, Kobetic Ret a1. Long·term user perceptions of an implanted neuroprosthesis for exercise. standing, and transfers after spinal cord injury. J Reliabi! Res Dev 2°°3;4°(3):241- 52. 20. Burkett B. Is daily walking when living in the Paralympic village different to the typical home environment? Br J Sports Mer/20IO;44:S33-6 21. Klenck C, Gebke K. Practical management: common m edical problems in disabled ath letes. ClinJ Sport Mt:d

2005;29 (2) :87- 103. ra6.

2007;17(1):55- 60.

individuals with spinal cord injury. J NtlIrol Phys Ther 200P9(2}:104- 6 . 9. Wheeler GO, Andrews B. Lederer R et al. Functional electric stimulation-assisted rowing: increasing cardiovascular fitness through functional electric stimulation rowing training in persons with spinal cord injury. Arch Phys Med Rehabil2002;83(8):I093-9. 10. Halliday SE. Zavatsky AB, Hase K. Can functional

22. Malanga GA. Athletes with disabilies. Emedicillt: 2005. Available at: www.emedicine.com 23. Tasiemski T, Bergstrom E, Savic G et a1. Sports, recreation and employment following spinal cord injury-a pilot study. Spinal Cord 2000 :38(3):173- 84. 24. Bhambhani Y. Physiology of wheelchair racing in athletes with spinal cord injury. Sports Med 2002; P(I):23-5I. 25. van der Woude LH. Bouten C. Veeger HE et al.

electric stimulation-assisted rowing reproduce a

Aerobic work capacity in elite wheelchair athletes:

race-winning rowing stroke? Arch Phys Med Relwbil

a cross-sectional analysis. Am J Phys Med Rehabil

2004:8S(8}: 126S-72.

2002:81{4):261- 7 L

Shields RK. Dudley-Javoroski 5, Law lAo Electrically

26. Vanderthommen M, Franc.aux M, Colinet C et al.

induced muscle contractions influence bone density

A m u ltistage field test of wheelchair users for

decline after spinal cord injury. Spine 2006;31(5):548-53.

evaluation of fitness and prediction of peak oxygen

12. Giangregorio LM, Craven BC, Webber CEo Musculoskeletal ch anges in women with spinal cord injury: a twin study. ] Clin Densitom 2oo5;8(3}:347-5L 13. de Groot PC, Hjeltnes N, Hei jboer AC et al. Effect of training intensity on physical capacity. lipid profile and

970

Games. Atlanta. BrJ T1Jer Relwbil 1996;3:429-36. 15. Webborn N, Price Mi, Castle PC et al. Effects of two

following spinal cord injury. J Neurol Phys Ther 8. Myslinski MJ. Evidence·based exercise prescription for

II.

injured individuals. Spinal Cord 20°3:41(12):673-9 . 14. Webborn AD. Heat-related p roblems for the Paralympic

consumption. J Rehabil Res Dev 2002;39(6):685-92. 27. Burkett B, Smeathers J, Barker T. Walking and running inter-limb asymmetry for Paralympic trans-femoral amputees: a biomechanical analysis. Prost/let Grthot lilt 20°3:27(1):3 6 -47.

Part 0

FOltune f avors the prepared mind. This chapter addresses emergencies-the life- or limb-threatening situations that require more advanced medical knowledge, skills, and equipment. As with many elements of sport and exercise medi~ cine (Chapter 2) these situations are best managed using a team approach (if possible). Because athletes and their accompanying clinical teams travel widely both nationally and internationally, not all athlete emergency care occurs near high-level definitive services. We were aware of this when writing this chapter.

Because emergencies are infrequent, itis tempting not to prepare and practice for such events because of all the other pressing demands on clinicians' time. Unfortunately, life- and limb-threatening con· ditions require immediate and expert care. Are you and your clinical team well prepared and rehearsed in the skills, knowledge, and equipment required? Clinicians with the responsibility of caring for athletes a t any level should undertake a recognized and accredited medical emergency care course.

Louis Pasteur

Although there are skills and procedures described in this chapter that are legally resh'icted to medical practitioners, the chapter is also relevant for physiotherapists. The physiotherapist performs a vital role in the management of sporting emergencies either as the team leader or team member. As a member of an emergency team, the physiotherapist assists the physician in preparing for an emergency situation, and in the overall immediate management of the patient with a life- or limb-threatening condition. If the physiotherapist is the emergency team leader, he or she has the responsibility for preparing for and managing the emergency situation.

Emergency care principles When an emergency occurs, the onus is on the most senior clinician present to perform a rapid assessment of the situation and the patient and initiate life- and/or limb-saving management. Leadership and team roles must be clearly defined and outlined well in advance, and the skills related to each role rehearsed as a team. The sequence of events for emergency care is outlined in the box below.

The role of the physiotherapist in emergency care Most sporting situations take place in the absence of a physician trained in the management of sporting emergencies. Thus, the responsibility of preparing for, and managing, an emergency may fall to other clinicians such as the physiotherapist or athletic trainer. All clinicians must be aware of the limits of their practice, as determined by their national eredentialing organization. Those responsible for sporting teams or athletes are strongly encouraged to gain further training in emergency care.

972

1. Preparation 2, Triage

3. Primary survey 4. Resuscitate and stabilize S. Focused history

6. Secondary survey 7. Continuous reassessment 8. Definitive care

Me d ical eme rgencies i n the sporting context

Preparation The two components of preparation are: pre-situation preparation situation preparation.

Pre-situation preparation The clinical team must prepare and rehearse its approach to possible emergencies. A clinical team responsible for motor sports will have different emergency priorities and preparation than a team responsible for swimmers. Similarly, preparation is very different for a clinical team managing athletes in a major capital city with ready access to Pre-hospital Emergency Medical Services {PH EMS) such as a well-developed and professionally run ambulance service and nearby major medical facilities, compared with the clinical team taking care of sportspeople in a rural area (see also Chapter 63, "Providing team care," and Chapter 6+ "Traveling with a team"). Pre-situation preparation comprises: emergency medical knowledge emergency medical skills emergency medical equipment/adjuncts clinical team rehearsal ensuring your clinical team, sportspeople, and officials are aware of emergency response procedures, exit points, and assembly points at the venues where they train and participate.

Situation preparation When the emergency occurs, the clinical team leader should: survey the scene oversee universal precautions organize the clinical team.

Surveying the scene requires ensuring your and your clinical team's safety as an absolute priority. Establish that the environment is safe for you and the team to enter before proceeding. The biggest risk is for the medical team to rush into a situation without surveying the scene first, thereby compromising the safety of all concerned. Universal precautions are for the safety of the clinical team---cIinical team safety must remain a priority. As an absolute minimum each team member should be issued with and wear gloves, goggles or glasses, and protective footwear. Depending on the sport and situation, more extensive protective gear

may be necessary, this must be determined in the pre-situation phase. Organizing the clinical team requires confirming roles previously assigned as well as which members will be responsible for which pieces of medical equipment to be brought to the scene.

Triage Triage is the sorting of patients based on their need for treatment and the resources available. For this chapter we assume the clinical team will be confronted with either a single-casualty emergency or a multiple-casualty emergency where the number of casualties and the severity oftheir injuries do not overwhelm the clinical team or the resources available. Even where there are multiple casualties, the triage priorities remain: Airway, Breathing, Circulation and Disability. The topic of sporting event disasters preparedness-events with mass casualties-is outside the scope of this chapter. At the time of triage, the clinical team leader may wish to delegate the role of notifying the Pre~~;; hospital Emergency Medical Services (PHEMS) (a lso ~ 0"" widely kn own as ambulance service or emergency 7H "J":. medical service (EMS)) of the situation. It is always better to notify early rather than late. "Rile

Primary survey TIle primary survey is when life-threatening conditions are identified and treated simultaneously. Although the primary survey (Fig. 47.1 overleaf) is divided into system priorities for teaching purposes, in reality several life-threatening issues may be identified and treated at the same time. There are subsequent "surveys" to the primary survey, although this chapter only focuses on the "primary" and "second· ary" surveys as these are the times to identify and treat life-threatening conditions (primary survey) as well as limb-threatening conditions (secondary survey). The primary survey (Fig. 47.1) is somewhat different from how a physician would usually assess and treat a patient. In the primary survey, compromise or life threat is rapidly identified and treated. Parts of the patient history are often deferred until after the primary survey is complete, and when examinations are performed they are very specific and focused. In the pre-hospital setting very few medical investigations are performed, with the exception of obtaining vital signs, oxygen saturation, and electrocardiograph (ECGjEKG).

973

Primary survey

Airway with cervical spine protection

Circulation with hemorrhage control

Disability

Exposure and environment

I

I

Oxygen, assume cervical spine injury

Perform a Glasgow Coma Scale (which gives a baseline)

Appropriate and adequate exposure; maintain body temperature

Breathing

Oxygenate and ventilate

Assess organ perfusion and STOP any bleeding

Figure 47.1 The primary survey At the time of the primary survey, the patient is positioned to facilitate assessment and treatment. In most situations, the supine position best allows the clinical team to assess, observe, and treat the patient with minimal movement and delay. The key priorities for each system in the primary survey are as follows (these are expanded later in this chapter): A. Airway and cervical spine control: 1. The first priority in any emergency situation is to establish a patent airway. 2. In any emergency that has resulted from trauma or has involved an event in which the patient may have sustained a spinal injury, ensure cervical spine stabilization at the time of establishing airway patency. 3. At this time, high-flow oxygen may be administered to the patient. In the critically ill or injured patient, in the acute stages, assume that there is no absolute contraindication to the administration of oxygen. B. Breathing and ventilation: 1. Airway patency does not ensure adequate ventilation. 2. Once the airway is patent and the cervical spine stabilized, assess the patient's breathing to determine if it is adequate or if conditions exist which may compromise breathing. 3. The aim is that the patient will be breathing effectively alone (active ventilationj.lf the patient is unable to breathe, the clinical team should ventilate the patient (passive ventilation).

974

C. Circulation and hemorrhage control:

1.

In patients who have sustained trauma and demonstrate signs and symptoms of shock, assume that the cause of shock is hypovolemia. Bleeding is a major cause of preventable death following trauma. Thus any external bleeding must be immediately controlled by direct and firm pressure. 2. The shocked state in the patient who has not been involved in trauma is likely to be as a result of marked peripheral vasodilation, pump failure, and/or inadequate heart rate. 3. In the primary survey, both traumatic shock and atraumatic shock are treated similarly. 4. Don't underestimate the importance of splinting fractures as part of hemorrhage control. Significant blood loss can occur internally especially at femoral fracture sites. Early and appropriate fracture immobilization may be indicated during this phase of assessment. D. Disability: 1. This refers to neurological assessment and is usually performed toward the end of the primary survey. This important assessment provides (a) an early measure of neurological fun ction-essential as a baseline against which to compare change as time progresses (b) in the absence of head injury, an altered level of consciousness indicates cerebral hypoxia or hypo perfusion-this should

Medical emergen c ies i n t he sporting c o n te x t immediately alert the clinician to reassess Airway, Breathing, and Circulation.

2.

It is best assessed by performing a Glasgow Coma Scale (GCS) and pupillary size and response (see under the Disability section later in this chapter).

E. Exposure/ environment control: 1. One of the major pitfalls in emergency care is

not looking. Neve r assume that the injuries or compromise you initially see are all that is to be found.

2.

Adequate and appropriate exposure of the patient is essential. The privacy provided on a sporting field or arena is indeed limited and must be kept in mind by the clinical

team. Ensure as much patient privacy and confidentiality as is possible without compromising inspection of all body

3.

surfaces. Environment control is an aspect of care that is often neglected. One must remember that a critically ill or injured patient may lose the abi lity to thermoregulate, thereby becoming poikilothermic, adopting the surrounding temperature. The natural inclination is to "keep the patient warm" but the ideal plan is to "keep the patient normothermic:' Keep core temperature as close to 37"( (98.6 F) as possible. Note that your own comfort level may not be accurate or appropriate as a monitor of environmental condition.

be missed. Depending on the circumstances it may be appropriate to change the sequence of events between "focused history" and "secondary survey," thereby performing the secondary survey prior to or simultaneously with the focused history. Initially, at the time of the primary survey and resu scitation, history-taking may be very basic. Apply the A MIST acronym: A Ag e and sex of patient M Mechanism of injury or circumstances surrounding the event Injuries sustained or problems identified 5 Signs and Symptoms T Treatment given so far

This acronym is also useful when handing a patient over to PH EM S (ambulance, emergency care) or definitive medical care. Once the primary survey is compl ete and the patient stabilized, a more focused history may be performed. Apply the AMPLE acronym: A M P

Allergies Medications Pa st illnesses/Pregnancy

L E

La st oral intake (solids and liquids) Events/Environment related to the situation

Q

Resuscitate and stabil ize In the clinical setting, the resuscitation and stabilization of the patient are performed at th e same time in the primary survey. However, this phase is differentiated because an important aspect of emergency medical managem ent is the use of drugs~ and adjuncts. Adjuncts include intercostal catheters, intravenous catheters and fluids, pulse oximetry, and cardiac monitoring. Because legally a physician can use emergency drugs and medical adjuncts, the physician is an important member of the clinical team in an emergen cy.

Focused history The history allows the clinical team to identi fy injuries or potential for compromise that might otherwise Throughout this chapter all drug doses will assume an ad ult patient unless otherwise specified.

Secondary survey Depending on the distance of the emergency to defini tive care, the severity of the condition, and the response time of the PH EMS, a secondary survey may not be performed. The primary obj ective in emergency care is to prevent loss of life; then to identify and prevent potential compromise and limbthreatening conditions. It is only when the clinical team leader is satisfied that the pa tient is stable and that all aspects of the primary survey are complete a nd have been addressed that attention should move to the secondary survey. The secondary survey is a complete assessment of the patient-essentially a full system s review, with assessment of all body surfaces. A Glasgow Coma Scale should also be performed ifit has not been performed earlier. Also perform a log roll , so the back and spine may be more adequately assessed. It is during this sta ge tha t non- life-threa ten ing conditions are identified and treated. If at any time the pa tient's condition changes, the priority is to recommence the primary survey and reassess Airway. Breathing, Circulation, and Disability.

975

Management of medical p ro b l ems

ReaSSeSS1TIent

Basic life support

Reassessment is one ofthe most important aspects of emergency management. You must be continuously vigilant for changes in the patient's condition and have a very low threshold for reviewing and reassess· ing all components of the primary survey.

In most countries and regions it is a community and legal expectation that a person accepting the responsibility of clinical care for a sporting team or athletes is familial' and competent with performing basic life support. It is also an expectation that all physicians are familiar and competent with advanced life support techniques. This expectation is greater when the clinician is charged with the responsibility of care outside a hospital or clinic environment when the clinician is most likely to be the initial responder in an emergency situation. Each member of the clinical team should be familial', skilled, and practiced in basic life support techniques, such as those a recognized and accredited training provider may offer. An essential component of basic life support is the immediate management of a cardiac arrest and the effective performance of cardio-pulmonary resuscitation (CPR). A basic life support flowchart (Drs ABCD) is outlined in Figure 47.3; the chart is available through the Australian Resuscitation Council (www.resus. org.au}). Details of basic life support are not within

I'R 4

If at any time the patient's condition chang es, the

!I'JJ-~;' patient is moved, or you are feeli ng overwhelmed ~

7lJ>J'l,

0""

by the situation, recomme nce the pri mary survey sta rting with reassessment of the airway.

It is important not to consider emergency care as a linear progression. The continuum of care should be considered as a continuous cycle of assessment and reassessment (Fig. 47.2).

Definitive care Most patients who require out-oE-hospital emergency care will require transfer to definitive medical care. In many situations this is done by a well-coordinated PHEMS; in most countries this is a highly skilled and professional paramedic ambulance selvice. In all situations, but particularly in rural and remote sporting locations, an important responsibility of the clinical team leader is to be familiar with the medical resources, facilities, availability, and skills of the PHEMS and the distance these are from the sporting venue and athlete accommodation. (This responsibility also applies with home events.)

Basic Life Support D.

•

~

••

The primary survey in detail In this section we discuss basic life support, then each component of the primaty survey. We also outline how to assess and manage each system and we discuss the use of appropriate primary survey adjuncts. At the end of each section we discuss how to identify and manage some common clinical emergency scenarios.

r D

\ B reathing

isability

/

C irCUlation Figure 47.2

976

The cycle of emergency management

([}l'lnlin!!lJOl C:;PR ,gntil re§PQnsiven~§l? l'lr. nl'lrmai breathinll returh -,,.,, Figure 47 ,3

Basic life support flow chart

FROM AUSTRALIAN RESUSCITATIO N COUNCIL, WWW.RESUS.ORG.AU

Med ica l emergenc ies the scope of this chapter. Each member of the clinical team should recertifY in basic life support skills annually.' A very important skill for clinical team members to be confident and competent with, especially the physician, is performing bag-valve-mask (BVM) ventilation. The mask is held onto the face using the jaw thrust technique (Fig. 47.4). When positioning and holding the mask it is important to remember that the concept is to bring the patient's face into the mask rather than forcing the mask onto the patient's face. The latter causes unnecessary operator finge r fatigue and has the potential of flexing the patient's head, thereby risking an occluded airway. Once the mask is positioned, the operator is able to perform either mouth-ta-mask ventilation or BVM ventilation with supplemental oxygen (if available). For the inexperienced operator, BYM ven tilation is best performed by two operators, one securing the mask to the patient's face and the other compressing the bag finnly.

Airway with cervical spine control The first priority in any emergency is to establish a patent airway. The quickest way to identify the patency of the airway is to ask the patient their name and how they are. This Io-second assessment provides the clinical tea m with four valuable pieces of information: the patency of the airway if the patient is unable to answer it may Imply unconsciousness or an occluded airway presence of stridor or noises coming from the airway suggests a degree of obstruction

Fig ure 47.4 Applying a face mask using the jaw thrust technique. Bring the patient's face into the mask

the effectiveness and ease of breathing the hemodynamic status of the patient, as adequate cerebral perfusion is required to respond the neurological status of the patient. If the patient is maintaining his or her own airway, aU that is required is constan t monitoring of its patency. In many instances ailway patency is relatively easy to achieve using basic ailVlay techniques. which are discussed below (pp. 978- 82). Oxygen is one of the most va luable drugs used in the emergency situation. Along with establishing and maintaining a patent ailVlay. the patient should have oxygen administered (if it is available). I n most initial situations, oxygen should be admini stered in high concentrations although oxygen delivery devices providing lesser concentrations may be more appropriate to maintain optimal oxygen saturation. Initially, oxygen delivelY is best achieved using a nonrebreather [ace mask aiming for an oxygen saturation of at least 94-98% in patients without a history oflung disease.;: With any critically ill or injured person, it is safe to assume that there are no absolute contraindications to the administration of oxygen. Apply the mask as soon as possible and initially set the oxygen flow rate to 15 L per minute. Titrate the flow against the patient's oxygen saturation (aiming for at least 94- 98%).

Cervical spine management In any patient who has sustained significant trauma, an associated cervical sp ine injury or potential injury should be considered to be presen t. Thus, maintaining cervical spine control is an essential aspect of care. Each member of the clinical team mu st be competent at both sizing and fitting a cervical collar. Cervical collars are available in both fixed and adjustable collar sizes. The adjustable semi-rigid collars are most appropriate in the sporting context as they are compact and negate the need to carry mUltiple collars of various sizes (Fig. 47.5a overleaf). Adjusting the collar to the correct size is imperative; this is demonstrated in Figure 47.sb-e overleaf. Initially the cervical spine is held stable by one member of the clinical team (Fig. 47.5f overlea f), the head and spine should remain in line, with the head in the neutral position. Then slide the correctly sized collar behind the patient's neck, position it correctly, and secure it quite firmly to prevent excessive movement (Fig. 47.5g-j on page 979). It is important to remember that a cervical collar does not "immobilize" 977

Manage m e n t of m e d i ca l pr o b l e ms

Figure 47.5 Cervical spine management

(a) Laerdel style adjustable semi-rigid cervical collar (d) Release locking lug and adjust collar so red marker (Fig. 47.5e) aligns with the correct measured hole

(b) Sizing a cervical collar using fingers as a guide

(e) Red marker positi oned at sizing hole

(e) Use this predetermined distance to measure from

the blue plastic edge to nearest hole

the cervical spine; it merely assists in stabilization and helps remind the patient and the clinical team to assume spinal injury and manage accordingly.

Airway management technique adjuncts How the patient is positioned and where the clinician stands are important initial steps. In most situations the patient is positioned supine and the clinician is either at the top or to the side of the patient's head.

978

(f) In-line stabilization of the cervical spine

The priority in airway management is to maintain patency. Another priority in airway managemen t (although less important than ensuring the patency of the airway) is protecting the airway and preventing the passage of blood or vomitus.

Medica l emergencies in the sporting cont ex t

(g) Positioning and securing of cervical collar-step 1

(i) Positioning and securing of cervical collar-step 3

(h) Positioning and securing of cervical collar-step 2 L-~'"

Maintaining a patent airway can be achieved using one or a combination of several techniques. Inspect the mouth and upper airway for obstruction (teeth, blood, vomitus, a mouth guard). Remove any

obstruction using gloved fingers, long forceps, and/or suction. Once foreign matter has been removed from the airway. the next possible obstruction is the tongue and soft tissues at the back of the throat. To address this poss ibility use the "jaw lift" or "pistol grip' (Fig. 47.6 overleaf). This is achieved by grasping the lower jaw of the patient finnly and, while keeping the fingers clear of the throat, moving the jaw anteriorly so as to lift the tongue from the back of the throat. This is usually combined with

j

(j) Positioning and securing of cervical collar- step 4

head tilt which is obtained by tilting the head, not the neck, back. A more effective technique is "jaw thrust" (Fig. 47.7 overleaf) . This technique is performed by placing tile fou rth and fifth fingers behind the angles of the jaw and moving the entire mandible anteriorly. This subluxes the jaw anteriorly and moves the tongue well d ear of the back of the throa t. Oropharyngeal airway

A useful adjunct for maintaining airway patency is the oropharyngeal airway (Fig. 47.8a overleaf). This curved piece of hollow plastic is placed into the airway

979

p ro b l e m s

Figure 47.6 Jaw lift to clear the tongue from the back of the throat

and sits posterior to the tongue. It provides passage for air to flow. The lumen of an oropharyngeal airway is relatively narrow and the tube remains mobile in the airway and unsecured, so airway patency cannot be assumed. Frequent reassessment is essenti al. Inserting the correct size of oropharyngeal airway is essential so as not to obstruct the airway. To size an oropharangeal airway, align the airway to the outside of the patient's mouth, so that the flange sits just anterior to the front tee th and the tail curves around the angle of the iaw (Fig. 47.8b). To insert the airway use some lubricant or water on the tube. Wid, d,e patienfs mouth held slightly opened, insert the tube so the distal part of the tube, or its tail, is pointing toward the patient's nose (Fig. 47.9a). It is then passed over the tongue and

Figure 47.7 Jaw thrust-a more effective technique than the jaw lift (al Lateral view Figure 47.8 (a) Oropharyngeal airways

(b) Anterior view (b ) Sizing the oropharyngeal airway

980

M edi c al em e r ge nc ies i n th e sp or ti ng co ntext when the tail of the tube is at the back of the patienfs throat. it is rotated 180 0 to rest in the posterior pharynx. The flange should sit anterior to the fro nt tee th so as the reinforced bite area of the tube sits between the front teeth (Fig. 47.9b).

Endotracheal tube Although patency is the fi rst priority, providi ng the patient with both a paten t and a protected airway is ideal. This can be achieved with a cuffed tube in the trachea-an endotrach ea l tube (ETT). The technique requires skill and training that must be practiced on a regular basis (as there is the potential for substantial risks in inexperienced operators' hands). Inserting an E1T is made significantly more difficult when attempted in an uncontrolled environment such as in the middle of a sporti ng field. It also requires the use of other instruments- such as a laryngoscope, which is costly and requires skill to use. Endotracheal intubation should only be performed by practi tioners

skilled and practiced in the technique. The technique of E1T insertion is beyond the scope of this book. ~4(',.."

~~

Airway patency is the priority.

llJ"J ";'b

Laryngeal mask airway

A laryn geal mask airway (LMA) (Fig. 47.1 0 ) con· sists of an inflatable mask and a conn ecting tube. It is inserted into the pharynx. The use of a laryngeal mask airway (LMA) requires skills and training that are within the scope of many physicians. Insertion of the LM A may be simplified as a three-step process (Fig. 47. II overleaf). The LMA, once inserted and the cuff inflated, provides for a patent airway and offers partial airway protection. The patien t may be ventilated through the LMA using the same technique as that used with an

ETT. Essential airway adjuncts ~~

Non-rebreather mask initially connected to high-flow oxygen Cervical co llar- sized correctly and positioned securely

Potentially Iife·threatening airway problems Three potentially fata l airway problems require vigilance-choking, anaphylaxis. and inabili ty to clear the airway.

Fig ure 47.9 (al Inserting the oropharyngeal airway tn an adult (with the tail pointing toward the nose)

Choking-airway blockage A common cause of partial or complete airway blockage is a foreign body. If the airway cannot be cleared by the procedures outlined above. then follow the

- -----

(b) Final position of oropharyngeal airway (after rotating 180°)

---

Figure 47.10 Laryngeal mask airway (lMA)

981

Management of medica l p r oblems

algorithm on choking as outlined by the Australian Resuscitation Council (Fig. 47.12). Anaphylaxis Anaphylaxis can occur at any time in response to allergens to which the person has been previously sensitized (e.g. bee sting. peanuts). Ideally, the clinician should be aware of any adverse, allergic, or anaphylactic reactions which a sports person has pre-

viously experienced. Plan appropriate management to prevent it occurring again. Signs and symptoms of anaphylaxis are outlined in the box below.

1

Anaphylaxis is likely when all of the fo ll owing are present: There is Iife·threatening airway, breathin g, or circu lation compromise. There are skin and/or mucosal changes (although these may be subtle). These features are of sudden onset and the progression is rapid.

The immediate management of anaphylaxis is:! Follow an emergency management plan that has been previously developed for the patient. Remove any residual traces of the causative substance if possible (e.g. the bee's stinger). Administer oxygen, titrated to maintain saturation of at least 94%. Give adrenaline (intramuscular) 0.3-0.5 mg IMl injection for adult 0.01 mg/kg 1M injection for child - Repeat every three to five minutes if there is inadequate response

1

Figu re 47.11 Inserting a laryngeal mask airway in three

stages

982

Anaphylaxis, although also a shock state, may cause significant airway compromise. Signs and symptoms of anaphylaxis may include: wheezing stridor flushed, red, andlor itchy skin hives swelling of the throat, tongue, andlor lips tachycardia extreme anxiety collapse followed by unconsciousness if not immediately treated.

Me d ica l emergencies in the sport in g co nt ex t

AUSTRALIAN RESUSCITATION COUNC IL

MANAGEMENT OF FOREIGN BODY AIRWAY OBSTRUCTION (CHOKING)

Severe airway obstruction

Mitd airway obstruction

I

Encourage coughing

Conscious

Unconscious

1

!

Continue to check casualty until recovery or deterioration

Call ambulance

Call ambulance

Commence CPR

Give up to 5 back blows

Call ambulance

If not effective Give up to 5 chest thrusts Figure 47.12 Flow chart for the management of foreign body airway obstruction FROM AUSTRALIAN RESUSCITATION COUNCil, ww w.re.us.org.au

-

The patient may have his or her own adrenaline

Admin ister both histamine Hl (e.g.loratadine) and

for self-administration which contains a

H2 receptor antagonists (e.g. ranitidine), preferably

predetermined dose (Epipen).

by the intravenous route, if the drug is able to be

Give inhaled sa lbutamol if there is eVidence of

administered this way, or orally.

bronchospasm (e.g. wheeze). Obtain an intravenous access if possible. Fluid resuscitation jf there is hemodynamic

Give hydrocortisone 4 mg/kg IV six-hourly followed by prednisone 1 mg/kg up to a maximum of 50 mg orally daily for four days.

compromise.

983

Oxygen and adrenaline are the first drugs to be administered during anaphylaxis. Note that the adrenaline is administered 1M I-intramuscular injection. Intravenous access is not immediately required. As adrenaline will only work for a certain period, corticosteroid (hydrocortisone) administration should be commenced early. TIle dose of adrenalin should be repeated if there is ongoing compromise. As anaphylaxis is a serious medical event, any patient who has experienced it must be educated appropriately, given strict instructions to always avoid the offending substance, have a well understood and regularly reviewed management plan, and have close medical follow-up after the event. Any patient who has experienced anaphylaxis should be assessed in a hospital emergency department after the event, even if initially managed successfully.

Significant facial swelling, facial trauma, or inability to clear a complete airway obstruction Inability to clear a complete airway obstruction is a rare event, but potentially fatal. All initial interventions, as previously outlined, should be attempted firs t. If all attempts are unsuccessful and airway obstruction cannot be relieved, a needle cricothyroido tomy should be performed. This, although only temporizing, is a life-saving procedure. It is a relatively easy technique to perform, alth ough the physician must be rehearsed in both identifying anatomicallandmarks and also the technique of needle insertion, and it should only be performed by those who are trained and legally qualified. TIle purpose of this procedure is to oxygenate the patient who is attempting to breathe for him or herself on a short-term (usually no longer than 30- 40 minutes) basis, until a more definitive airway can be achieved. The administration of oxygen must be provided by jet insufflation as outlined below. See box below for issues relating to cricothyroido tomy.

Emergency cricothyroidot~ml Equipment to prepare for needle cricothyroidotomy A 12G or 14G standard intravenous cannula, the lower the gauge the less airflow resistance AS mL or 10 mL syringe Standard oxygen therapy tubing A skin preparation solution or swabs Oxygen supply, although the delivery of expired air via the cannula may be performed if oxygen is unavailable A 3-way tap

Anatomical landmarks and technique for performing needle cricothyroidotomy Palpate the thyroid cartilage and thyroid notch (Adam's apple).

Slide your fingers inferiorly until you are in the space between the thyroid and cricoid cartilages; this is the cricothyroid membrane. With the region of the cricothyroid membrane identified (Fig. 47.13a), stabilize the trachea firmly with your thumb, second, and third fingers. If time permits, clean the overlying skin.

984

Assemble

the

cannula

onto

the

syringe

(Fig.47.13b).

Insert the cannula into the center of the cricothyroid membrane (Fig. 47.13a) and angle the cannula 45° in the caudal direction while aspirating the syringe. Aspiration of air identifies entry into the trachea; at this point insert the cannula several millimeters further. Withdraw the syringe and stylet and at the same time advance the cannula sheath into the trachea. Secure the cannula sheath and connect the 3-way tap with the oxygen tubing attached, ensuring all three ports of the tap are open (Fig. 47,13c). While holding the cannula sheath and 3-way tap securely with one hand, with the thumb of the other hand occlude the third port of the tap for one second to allow for oxygen flow into the trachea (Fig. 47.13d); release your thumb for four seconds to allow for expiration (Fig. 47.13e). Remember this is a temporary life-saving measure; urgent defrnitive medical Care must be arranged.

Med i ca l eme r gencies in the spor t ing co n text

Cricothyroid membrane

Figure 47.13 Emergency cricothyroidotomy (a) Cricothyroid membrane-position for needle cricothyroidotomy

(d) Ensure all three po rts are open and co nnected as

(b) Large-bore cannula attached to a syringe in preparation for a needle cricothyroidotomy

shown and the oxygen turned on. Occlude t he port open to the atmosphere w ith your thumb for one

second to deliver oxygen to the patient

{el Once the cannula sheath is inserted and secured

in the trachea, attach the three~way tap with oxygen

{el Release the t humb over the port for four seconds

tubing

to allow for exhalation

985

problems Breathing and ventilation Breathing assessment and adjullcts are shown in the box below. 1<

•

~

"~ Breath'mg assessment and adjuncts > . .'

Stethoscope Pulse oximetry if ava ilable

Once the ai rway is patent and secured, assess the

patient's breathing and ventilation (note that performing auscultatio n and percussio n at a noisy sporting venue

ca n be difficult): 1. Inspecti on (a) While positioned at the head of the patient with

th e patient's chest exposed, inspect for: ii) rate, effort, and symmetry of breathing (iiJ the presence of wounds or bruising to the chest or neck, which may suggest significant

underlying airway or lung damage (iii ) evide nce of distended neck veins suggesting a tension pneumothorax or cardiac

tamponade. 2. Palpation (a) With the patient's head in the neutral position, palpate trachea to ensure it is midline. Deviation of the t rachea may suggest a tension

pneumothorax. (b) Palpate t he face, neck, and chest for evidence of s ubcutaneous emphysema suggesting a pneumothorax. (c) Pa lpate the anterior chest to check for symmetry a nd d egree of expansion. 3. Ausc ultation (a) Using the stethoscope auscultate t he chest at the apices, in th e axillae, and towards the bases, noti ng: (i) equality of air e ntry (ii) degree of presence of breath sounds. Decreased breath sou nds may suggest a p neumo thorax or hemothorax, whereas completely absent breath sounds may suggest a tension pneumothorax (ii i) any added sound s such as wheezes. 4. Percussion (a) Perc uss all accessible reg ions of the chest, because much information is gained from the "fe el" of the percussion as with the sound. (b) Du ll ness to percussion may suggest a hemotho rax, especially if it is identined toward the lu ng bases or toward the posterior aspect in t he su pine patie nt.

986

If there is no compromise to breathing or ventilation, move to the next stage of assessment, always having a low threshold for reassessment.

Potentially life-threatening breathing and ventilation problems Potentially life-threatening breathing and ventilation problems include pneumothorax and acute severe asthma. Pneumothorax- the presence of air within the pleural space--can become rapidly life-threatening_ A pneumothorax can be closed (simple or tension) or open. Simple pneumothorax 'i'R4('

C-~-::.

'~

'0[;; Rib fractures are a common cause of pneumothorax.

IHV-::'

In most cases a simple pneumothorax can be managed by the administration of oxygen until definitive medical care is reached. Occasionally a spontaneous pneumothorax can become life-threatening if it develops into a tension pneumothorax. Open pneumothorax An open pneumothorax results from a penetrating chest wound where the pleural space communicates directly with the outside. This situation is best managed by applying plastic wrap over the wound and taping the wrap on three sides only so as to produce a one-way Rutter-valve effect. As the patient exhales, air from the pleural space is forced out under the wrap, and when the patient inhales, the plastic wrap is sucked onto the wound, thereby preventing air entering the pleural space. Tension pneumothorax A tension pneumothorax is an emergency. It may develop rapidly or gradually. If untreated, a tension pneumothorax is generally fatal. Tension pneumothoracies are made worse by active ventilation of the patient; occasionally they are the result of active ventilation. Keep this uppermost in your mind if you need to ventilate a patient. Signs and symptoms of a tension pneumothorax are shown in the box opposite.

Tension pneumothorax management Management of a tension pneumothorax requires a needle thoracentesis to relieve the tension immediately (see box opposite). This, however, does not treat the resultant simple pneumothorax. A needle thorocentesis should only be performed by those appropriately trained and licenced_

Me d ica l emergencies i n the sport i ng contex t Acute severe asthma

Tachypnea Patient anxiety and distress Distended neck veins (if not hypovolemi c)

Tachycard ia Low oxygen satura tion (althoug h high-flow oxygen may mask this to some extent)

Tracheal deviation to the opposire side ofthe pneumothorax, although th is may be a late sign Absent breath sound s on

As outlined in Chapter 50. the cl inician must be aware of all sportspeople under his or her care who have a diagnosi s of asthma. Know the medications prescribed and the asthma action plan for the sportspersol1. This chapter focuses on management of a severe asthma attack. The signs and symptoms of severe asthma arc outlined in the box below. Signs and symptoms , of s vere astnma

same side as the

pneumothorax

Marked dyspnea

Hyperresonance on the same side as t he

tnability to speak or only speak in single words

pneumothorax

Developing exhaustion

Cyanosis may be a late sig n If being passively ventilated, the patient may become

The chest may be "silent" to auscultation (this is an

progressively more difficult to ventila te

ominous sign)

----,~"I

Use of respiratory accessory mu scles

..

Steps for a needle tho.!..~~ e-nt~sli's Identify t he appropriate anatomical landmarks (Fig. 47 .14a) on the side with the suspected tension.

used and inserted its full length into the lower

Th e site where the needle should be in serted is

half of this space

the intersection of the mid ~ clavicular line and the

bundle which funs inferior to each rib. A standard

second intercostal space. (This is best found by pal-

intravenous cannula may be too short and not enter

A 12G or 14G long intravenous cannula may be

so as to avoid

t he neurovascular

pating for the angle of Louis, wh ich is w here the

the pleural space; su bsequent ly a longer and more

manubrium joins the body of the sternum. Slide

specific cannula may be req uired (Fig. 47. 14b).

your finger parallel with this joint toward the side

Remove the stylet and leave the ca nnula sheath

ofthe sus pected tension; you will meet t he second rib where it articulates with the sternu m. Go just

open to the atmosphere.

below this rib and this is the second intercostal space.) MI(I·cI;,vl(ulllar line

~ Angle Of LOulS~

"8 ::!

1

~

2nd rib -------~--

~

m

;;; ~ ~

~ Figure 47.14 (a) Anatomical landmarks fo r needle

(b) Th e cannula designed for needle thoracentesis is on t he left (blue) compared with a sta ndard 14G

thoracen tesis

intravenous cann ula (o range)

987

Management of severe asthma

The management of severe asthma is as follows: Unless contraindicated, the patient should be positioned sitting up. Commence high-flow oxygen via a non-rebreather mask. If a nebulizer mask and oxygen supply are available, commence -

salbutamols mg diluted with 3 mL of normal sa line

If there is no response to the initial dose, repeat immediately, then every 15-30 minutes or give continuously depending on patient response ipratropium bromide 500 micrograms

-

2-to

4-hou rl y:~-6

If a nebulizer mask or oxygen supply are not available, use the following metered dose inhalers , via a large volume spacer ·8 - salbutamol100 m icrograms 4 to 10 inhalations repeated as necessary ipratroplum bromide 500 micrograms 2- to 4-hourly.4-6

-

Give prednisone 50 mg orally

OR hydrocortisone 100 mg IV.s Start inhaled corti costeroids as soon as possible.

Circulation and hemorrhage control If the cause of circulatory compromise or life threat is bleeding, it must be stopped. The most effective means of controlling external hemorrhage is by direct pressure to and elevation of the bleeding site.

Signs and symptoms of blood loss Signs and symptoms of blood loss are listed in the box below.

The patient usually needs to have lost up to 25% of circulating blood volume before a substantial drop in systolic blood pressure is noted. This is particuJarly so in a supine patient and a very fit athlete (Fig, 47.15).

Sites of blood loss Some sites of hemorrhage are easy to address, while others are impossible to manage outside an operating room. Possible sites of blood loss and what to do are shown in Table 47.1.

Circulation management principles The priorities must always be Airway, Breathing, and then Circulation. The only exception to this is life-threa tening external hemorrhage likely to result in rapid exsanguination, such as from a carotid or femoral artery. In that case, initiate hemorrhage control immediately. The basic principles of hemorrhage control have been outlined above. As part of the circulatory management, insert two large-bore intravenous cannulae (14G or IGG), The ideal position for these is in large veins in or around the cubital fossae but any venous access is acceptable. If the patient is exhibiting features of shock (see box below left), immediately infuse a bolus of crystalloid solution, either compound sodium lactate or sodium chloride (0.9%) (normal saline) at a dose of 20 mL/kg. Carefully monitor the patienfs response. Ifblood loss continues or there is inadequate or only transient response to the fluid. repeat the bolus once or twice and continue to call for urgent assistance. For patients who have ongoing and uncontrolled hemorrhage it is safer to maintain a systolic blood pressure of around 90 mm Hg (rather than higher 200

-0- Systolic BP ---tr- Diastolic BP

V RAe

,~ ~ Hypotens ion is not an early reliable sign of

~

?fJ'·)1 The guidelines concede that many affected athletes may not fall victim to SCD in the event of continued participation in high-dynam ic and highintensity sporting disciplines; however, the aim is to identify/ca pture/ensure the safety of all individuals with preventable premature deaths. Idiopathic Jeft ventricular hypertrophy Idiopathic left ventricular hypertrophy is a term used to describe increased left ventricular mass of greater than 500 mg in the absence of myocyte disarray (the histological hallmark of HCM).' Most deaths from idiopathic LVH are described in sportspeople of African/Afro-Caribbean origin.'· 2. ~ It is unclear whether idiopathic LVH is a variant of HeM or whether it rep resents a situation whereby co nfounding genetic variables in black athletes result in the well-recognized exaggerated hypertrophic response,P which itself may become pathologic and predispose to arrhythmias. Conversely, the increased left ventricular mass identified in the athlete may represent a benign innocent bystander where the true cause of death from a potential ion channel disorder or accessory pathway has not been identified. Arrhythmogenic right ventricular cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC) is the commonest cause of SCD in young sportspeople in Italy. 2 ' . 2~ It is a familial disorder that is inherited as an autosomal dominant trait and is caused by mutations in genes encoding several cardiac desmosomal pro teins. The diso rder predomi~ nantly affects the right ventric1e,ll although left ventricular involvement is also recognized l4 in isolation and co-existent with right ventricular involvement in advanced cases. It is characterized histologically by progressive loss of myocardial cells with subsequent fibra-fatty replacement. The condition manifests with arrhythmias of right ventricular origin and morphological changes affecting the right ventricle.

1001

Most deaths in athletes occur during sport, particularly soccer, and predominantly affect males. It is postulated that under conditions of mechanical stress, the inherent weakness of cell--cell junctions due to abnormal desmosomal proteins results in myocyte detachment and predisposes the athlete to fatal ventricular arrhythmias and SCD. The myocardium is subsequently repaired by fibro-fatty replacement, which forms further substrate for ventricular arrhythmias and subsequent right heart failure»' j6 Most athletes are asymptomatic and SCD is usually the first presentation, although a small number present with palpitation, dizziness, and exertional syncope.~!

The prevalence of ARVC in the general popUlation is between I in 1000 and I in 5°00;;1 however, the prevalence of ARVC in sports people is unknown. There is some evidence that intensive ultra-endurance exercise may promote changes within the right ventricle that are identical to ARVC, indicating that ARVC might be acquired through intensive exercise in a small proportion of athletes."l7-4 The diagnosis of ARVC usually requires a combination of clinical suspicion from personal symptoms or family history together with a plethora of electrocardiographic and imaging studies. These include 12-1ead ECG/EKG, signal averaging where indicated, 24-hour Holter monitoring, exercise ECG/ EKG, echocardiography with contrast to improve endocardial definition, and cardiac magnetic resonance.4~ The diagnosis of ARVC can be difficult to make, especially in the concealed form of the disease, when the ECGjEKG may exhibit very subtle changes that overlap with electrical manifestations of athletic training and cardiacimaging tests appear norma1. 4J Although the right ventricle is amenable to endocardial biopsy, histological diagnosis of ARVC is rarely possible and is potentially dangerous for several reasons-the disease is patchy, characteristically affects the thinnest portions of the right ventricle (notably the right ventricular inflow and outflow tract), and transmural tissue sampling is required for definitive diagnosis. Phenotypic manifestations of ARVC on the 12-lead ECG/EKG include T-wave inversions and prolonged QRS duration in right ventricular leads (VI-V3), epsilon waves (delayed repolarization), and ventricular extrasystoles of right ventricular origin (manifest with left bundle branch block morphology) (Fig. 48.4). Holter monitoring and exercise testing are useful for identifying sustained or non-sustained

ventricular arrhythmias with left bundle branch block morphology (Fig. 48.5). Echocardiography reveals thinning of the akinetic and dyskinetic segments affecting the right ventricle or overt right ventricular dilatation and hypokinesia, but may be normal in the early phases of the disease. The sensitivity of echocardiographic diagnosis is improved with contrast agents. Cardiac magnetic resonance imaging (cardiac MRI) may be more sensitive than echocardiography for the diagnosis of ARVC provided it is performed by an experienced operator. 4l ~4 ('.. . . The diagnosis of ARVC in an athlete is an indication for disqualification from all competitive sports other I&'o. 3' However. gentle exerci se for up to 30 m inutes per day (moderately brisk walk or gentle cyc1 ing) may offer prognostic benefit. Pharmacological therapies in the form of ACE inhibitors and beta blockers are advised in all sportspeople with DCM.

Disorders of the coronary arteries and aorta Congenital coronary artery anomalies

Congenital coronary artery anomali es (CCAA) are reported as a cause of SCD in 12- 33% of athletes wh o have SCD. I-C. A main coronary artery originating from the opposite sinus of Valsalva is the most common anomaly associated with seD in athletes (Fig. 48.6) and is present in approximately 1% of the general population. 4H6 Anomalous origin of the left: coronary artery from the right sinus of Valsalva is less prevalent in the general population (0.2%) but is more serious than origin of the right coronary artery from the left sinus ofValsalva. 47 Mechanisms of seD associated with ceMs include myocardial ischemia precipitated by exercise due to impaired coronary blood flow because of an abnormal ostium of the anomalous vessel. compression of the anomalous artery as it courses between the pulmonary artery and ascending aor ta. or. possibly. coronary spasm triggered by endothelial dys· fun ction. In the ma jority of cases SCD is the first presentation, although some athletes may experience exertional chest pain associated with pre-syncope or syncope:IS Diagnosis of CCAA from a resting ECG/EKG. transthoracic echocardiography, and even exercise stress testing is notoriously difficult; most cases do not exhibit inducible myocardial ischemia during exercise stress testing even at high workloads. CT coronary angiography or magnetic resonance angiography IFig. 49.1 on page 1028) are the imaging modal· ities of choice when clinical suspicion is raised. 49 Recommendations state that athletes with anomalous coronary origins are disqualified from all competitive sports; however, participation three months

Figure 48.6 Origins of both main coronary arteries arising from the sa me sinus ofVaisalval6

1003

after surgical correction is permitted in cases without prior myocardial infarction, left ventricular dysfunction, or ventricular tachycardia during maximal exertion)O, }J Premature coronary artery disease

Premature coronary artery disease accounts for 3-4% of all SCDs in young sportspeople in large series from the US and Italy;,-6 however, it has been reported more commonly in Japan, Australia, and the UK.4 The disorder is a common manifestation of familial hypercholesterolemia, which has a prevalence of I in 500. Sudden death is almost always the first presentation in young athletes. Prodromal symptoms of myocardial ischemia may be absent; however, peripheral stigmata of hypercholesterolemia including xanthelasma, corneal arcus, palmer, and eruptive xanthomata are common and their presence should raise the suspicion ofthe disorder (Fig. 48.7). Marfan syndrome

Marfan syndrome is a collagen disorder caused by mutations in the gene encoding fibrillin. It is inherited as an autosomal dominant trait and has a prevalence of I in 5000. The condition is characterized by skeletal, cardiac, and ocular abnormalities (Fig. 48.8). Cystic medial necrosis in the tuna media of the aorta results in aortic dilatation and rupture or aortic dissection. The disorder accounts for approximately 3% of all exercise-related SCDs in young sportspeople. Affected patients are excessively tall and, by virtue of this trait, usually excel in basketball or volleyball. Exercise-related increases in aortic pressure may expedite aortic root dilatation, dissection, and rupture causing instantaneous death during sport. 50 \' R,tJ

f~-i..1... ~

1!;J't/"':.

'0'"

Participation in sporting discipli nes where isometric stress is a significant component is prohib ited (e.g. powerlifting, wrestling, judo, sprinting, rowing, and canoeing).sl

In the past, beta blockers were considered to retard progressive aortic dilatation, but recent analyses have cast doubt on this claimY Preliminary studies with angiotensin receptor blockers (losartan) hold great promise in preventing aortic complications in Marfan syndrome. 53 Annual aortic surveillance is recommended and prophylactic aortic root replacement should be considered when the aortic root diameter exceeds 50 mm. Marfan syndrome is discussed further in Chapter 49.

1004

Figure 48 .7 Peripheral stigmata of premature coronary artery disease (a) Eruptive xanthomata

(b )

Xanthelasma

Premature corneal arcus in a patient with familial hypercholesterolemia

(c)

Sudde n cardiac deat h in sport

I

.A.lI .

reported where MVP was the only abnormality identified in the literature and only three occurred during physical exertion.s~ Because of the relatively high frequency of MVP in the general population, it is not known whether the identification ofMVP in a victim of SCD is causal or coincidental.

,

.,.

Figure 48.8 Features of Marfan syndrome (al High-a rched palate

(b)

Arachnodactyly

The current gu idelines state that an ath lete with MVP is at low risk of SCO un less there is a history of ~-~ ~ syncope or documented ventricular arrhythmias, ~ c'" fam ily history of premature SCO, disablin g and } (i v ~ protracted chest pain durin g sport, or associated mode rate to severe mitra l regurgitation. ~ R,ol("

Athletes with MVP as part of the spectrum of Marfan syndrome or coexistent long QT are precluded from participating in strenuous physical exertionY Aortic stenosis Aortic stenosis due to a congenital bicuspid aortic valve is a rare but recognized cause of SCD in young athletes which can be identified through basic screening efforts involving cardiovascular physical examination. Individuals with mild aortic stenosis may compete in sporting disciplines of low to moderate dynamic intensity or static sports if there are no symptoms and arrhythmias, and ifleftventricular function is normal at rest and during an exercise echocardiogramY

SCD due to congenital or genetic abnormalities predisposing to primary electrical disorders of the heart up to 4% of athletes who die suddenly have no identifiable cause at postmortem examina tion. ~4('.A This phenomenon-autopsy negative sudde n unexplained death- is referred to as sudden adult }&'1".J. death syndrome.!6

~c~

Ie) Lens dislocation in Marfan syndrome

Valvular heart disease Mitral valve prolapse Mitral valve prolapse (MVP) is probably the commonest congenital valvular disorder; it affects 3-5% of the general population. Most individuals are asym ptomatic, but in rare instances the condition is associated with ventrirular tachycardia. 54 The exact mechanism for ventricular tachycardia is unknown.

Fewer than roo cases of sudden death have been

Experience from studies in first-degree relatives of victims of sudden adult death syndrome indicates that a proportion of these deaths are attributable to inherited ion channelopathies. Fatal tachyarrhythmias due to undiagnosed accessory pathways comprise other potential causes (Table 48.3).

Congenital long QT syndromes The congenital long QT syndromes (LQTS) are inherited as autosomal dominant or recessive traits and characterized by abnormalities in cardiac sodium or potassium ion channels. Abnormal shifts in electrical currents result in membrane instability during

1005

Management of medica l problems cardiac repolarization and predispose to polymorphic ventricular tachycardia and ventricular fibrillation. There are currently 12 different identified loci accounting for the disorder; these are termed LQTS-I-LQTS-I2 respectively. LQTS-I (potassium ion channel), LQTS-2 (potassium ion channel), and LQTS-3 (sodium ion channel) account for approximately 95% of all known cases of the disorder.}] Adrenergic surges provoke ventricular arrhythmias, particularly in individuals with the LQTS-I genotype.,8 Many deaths in sport occur in young females during swimming and are attributed to the adrenergic surge associated with diving suddenly into cold water. Affected sportspeopJe may present with palpitations, dizziness, and unheralded syncope secondary to polymorphic ventricular tachycardia. The latter may be associated with brief myoclonic movements, resulting in a misdiagnosis of epilepsy in recurrent cases. Long QT syndrome is usually diagnosed on a resting ECGjEKG, which reveals a long QT interval (Fig. 48.9C) in approximately 60% of cases (QTc >440 ms in males and QTc >460 ms in females).

Exercise testing is recommended in all patients with suspected LQTS and often exhibits paradoxical prolongation of the QT interval in LQTS-r and occasionally LQTS-2.5 9 Holter monitoring is also recommended to evaluate the possibility of associated episodes of polymorphic ventricular tachycardia.5 s The prevalence of congenital LQTS in the general population is approximately I in 2500)1 However, based on the findings from screening programs in athletes, a long QT interval is identified in 0.42% of elite athletes. 60 TIle low death rate from sudden adult death syndrome in athletes in the context of a relatively high prevalence of long QT observed in this group suggests that the vast number of athletes with a slightly prolonged QT interval probably do not harbor gene mutations for LQTS. However, calculating the QTc accurately in this group is difficult because of profound bradycardia, sinus arrhythmia, slightly wide QRS complexes, and prominent U waves associated with athletic training. In the absence of symptoms or a family history of LQTS or premature SeD, clear diagnosis of

Figure 48.9 ECG/EKG changes in common structural and electrical cardiac abnormalities associated with sudden cardiac death Panel A HCM-Ieft ventricular hypertrophy associated with left axis deviation, 5T-segment depression in leads I and aVL, and deep T-wave inversion in leads I, aVL, V5 and V6 Panel B ARVC-inverted T waves in V1-V4 Panel C LQT5- a prolonged OT interval of >500 msec Panel D Brugada syndrome- incomplete right bundle branch block and caved 5T-segment elevation in several leads but most marked in leadsVl-V3

1006

?:~':

-

~-

Sudden cardiac death in sport the disorder can occur only in athletes with a QTc >500 msec, or in athletes with a shorter QT interval in the presence of exercise-related paradoxical QT prolongation, the demonstration of polymorphic ventricular tachycardia, or the identification of a long QT interval in a first-degree relative. Go Genetic testing is recommended in all cases as it may facilitate clinical management; however. the diagnostic yield from genetic analysis is only 70%. Athletes diagnosed with LQTS are recommended to avoid all sports associated with adrenergic surges. 61 All affected individuals should be treated with a beta blocker unless contraindicated. High-risk individuals include those with a QTc >500 msec, unheralded syncope, and LQTS-2 and LQTS-J genotypes."

Wolff-Parkins on-White syndrome (WPW) Wolff-Parkinson-White syndrome (WPW) is characterized by the presence of an accessory conduction pathway between the atria and ventricles with a predilection to re-entrant supraventricular tachyarrhythmias, which may degenerate to ventricular fibrillation. It is a rare cause of SeD in sportspeopIe. The prevalence of \VPW syndrome is I in 750 persons. The risk of seD in WPW syndrome is believed to be approximately 0.4%. Mos t deaths occur in athletes with previous symptoms of palpitation, dizziness. or syncope. The accessory pathway can be identified by the presence of a delta wave and a short PR interval on the 12-lead ECG/EKG (Fig_ 48_10). Electrophysiological studies to assess the refractory period of the pathway are essential to gauge the risk of atrial fibrillation with high ventricular rates.

:.-..::. :::-

...'IlT'_u," --::::,.. I=-~

Figure 48.10 Short PR interval and slurred upstroke to the QRS complex (delta wave) in Wolff-Parkinson-White syndrome

I ,

C!" a}l?te f 48

Radiofrequency ablation is the definitive treatment in athletes with high-risk pathways wh o wish to continue to participate in competitive sporty· 6, Return to sport after successful ablation is possible after three months.

Brugada syndrome Brugada syndrome (BrS) is an autosomal dominant sodium ion channelopathywith an incidence reported between I in 2000 and I in 5000.61 The condition is characterized by a partial right bundle branch block pattern with associated coved ST-segment elevation (Fig. 48.9 panel D) and a propensity to fatal ventricular arrhythmias. Affected individuals may pres ent with unheralded syncope or SCD. Mixed phenotypic expressions of the disease, ranging from distinct repolarization abnorm alities to subclinical cardiac conduction defects. also occur. Most deaths from Brugada syndrome occur at slow heart rates with deaths typically occurring during sleep, and theoretically, the condition should not preclude high-intensity sport. 64 However, chronic intensive exercise promotes increased cardiac vagal tone with subsequent resting bradycardia. Furthermore, prolonged exercise is associated with high core temperatures of >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 35 years old) , risk factors for coronary ar telY atherosclerosis such as hypertension, diabetes, hyperlipidemia. tobacco use, and a family history of premature atherosclerotic disease should be investigated.

Clinical approach to symptoms associated with cardiac conditions In this section we outline the clinical approach to five common "cardiovascular" sym ptoms (syncope/ near-syncope. unexplained seizure activity. exertiona l 1025

chest pain, palpitations, and excessive fatigue! dyspnea) and the red flag of family history of early sudden cardiac death (Table 49.2).

Syncope/near-syncope Syncope is common in young individuals, including sports people. The lifetime prevalence of syncope approaches 40-50 %.~r .u In a review of 474 athletes with a history of syncope Of near-syncope detected during pre-participation screening, 33% whose syncope occurred during exercise were found to have structural cardiac di sease known to be capable of causing sudden cardiac death. zl The diagnostic workup of exertional syncope is usually performed in consultation with a cardiologist and should include ECGj EKG (electrocardiogram),

echocardiogram, stress ECG! EKG , and possibly advanced cardiac imaging (such as MRI or Cl) to rule out rare structural abnormalities (such as ARVC and CCAAs) that are associated with syncope. If all these studies are normal. prolonged m oni toring with an external ambulatory monitor should be considered. A small percentage of individuals may even require an implantable loop monitor. The specific cardiac causes of syncope and near-syncope are discussed below.

Neurogenic syncope (vasovagal syncope) In the young the most common underlying di sorder of syncope or near-syncope is neurocardiogenic syncope, also known as vasovagal syncope. Z4 Neurocardiogenic syncope is more common in the

Tab le 49.2 Associated disorders and recommended evaluation in sportspeople w ith cardiovascular symptom s Symptom

Potential card iac disorders

Evaluation and test ing to consider

Syncope/near-syncope

Cardiomyopathy (HCM, ARVC, lVNC)

ECG/ EKG. echocardiography, consider cardiac MRt to evaluate cardiac morphology

during exercise

and presence of delayed gadolinium enhancement that indicates myocardial fibrosis Congenital coronary artery anomalies (CCAA)

Echocardiography, consider cardiac CT or MRI if coronary artery origins not well Visualized

Ion channel disorder (LQTS, CPVT, SQTS,

ECG/EKG, stress ECG/EKG, ambulatory

Brugada syndrome)

monitoring

Critical aortic stenosis

Echocardiography

Unexplained seizure

Ion channel disorders, cardiomyopathy, and

ECGJEKG, echocardiography, stress ECG/EKG,

activity

all potential causes ofsCO

cardiac MRI, consider EEG if not performed

Exertional chest pain

Coronary artery atherosclerosis

ECG/EKG. stress ECGlEKG

Congenital coronary artery anomalies (CCAA)

Echocardiography. consider cardiac CT or MRI

Cardiomyopathy

ECG/EKG. echocardiography, consider cardiac

if coronary artery origins not well Visualized

MRI Critical aortic stenosis Palpitations

Excessive dyspneal fati9ue during exertion

Echocardiography

Supraventricular tachyarrhythmias, ventricular ECG/EKG, echocardiography, stress ECG/EKG, arrhythmias, premature atrial and ventricular

ambulatory monitoring, consultation with

contractions, sinus tachycardia

electrophysiologist

Cardiomyopathy, myocarditis

ECG/EKG, echocardiography, stress ECG/EKG, consider pulmonary function testing

ARVC = arrhythmogenlc right ventricular cardiomyopathy; CPVT = catecholamlnergic polymorphic ventricular tachycardia; ECGJEKG = electrocardiogram; EEG = electroencephalogram; HeM = hypertrophic cardiomyopathy; lQTS = long QT syndrome; lVNC = left ventricular noncompoetion (outside the scope of this book); SCO = sudden cardiac death; sQTs = short QT synd rome

1026

Manag i ng cardiovascular symptoms in spo rt speople young than in the old, and children plagued by this syndrome tend to grow out of it by age 30- 40 yea rs.

Neurocardiogenic syncope is often triggered by certain events such as fear, pain, excitement, venepuncture, or prolonged standing. It nearly always occurs while the patient is standing. It is unusual for this type of syncope to occur with sitting and nearly im possible for it to occu r while lying down . Premon itory symptoms are common and include lightheadedness. dizzin ess, flushing, nausea, tunnel vision. and profuse sweating. The individual typically

slumps to the ground and is not completely uncon· scious and, therefore. is usually able to avoid injury. Once the individual is on the ground. blood flow is restored to the brain, so typically the syncope episodes are short-lived. Howeve r, following the episode individuals often have a prolonged period of nausea a nd fati gue, and occasionally individuals may feel ill until they have had some sleep.

Exertional syncope Exertional synco pe is always a concern. Exertional syncope can occur because of outflow obstruction (e.g. in HCM or aortic ste nosis) or a rrhythmias. Exercise typically triggers arrhythmias in individuals with ARVC. HCM, CPVT, a nd LQTS (conditions that are outlined in Chapter 48). The syncope associated wi th exertional outflow obstruction is during peak exercise with a brief period oflightheadedness followed by syncope. Syncope caused by arrhythmic disorders often occurs during exertion (not post-exertion) with abrupt loss of consciousness or only a very brief period of lightheadedness prior to the syncope. Secondary injury is common as individuals are unconscious before they hit the ground a nd, therefore, cannot protect their h ead. Syncope due to a ventricular arrhythmia (such as ventricular tachycardia or ventricular fibrill ation) is a life-threatening event. I n some cases, the ventricular arrhythmia self-tenninates and th e individual rega ins co nsciousness, usually withi n seconds of collapse. Prolonged syncope should be treated as a sudden cardiac arrest (Chapter 48),

~Il ('...,. Exertional syncope is frequently due to a cardiac cause and should be thoroughly investigated. ] !f'0.5 seconds regardless of symptoms or fa mily history distinguishes individuals most at risk for sudden cardiac death. II

Echocardiography and associated tests for structural disease (cardiac CT, MRI) Echocardiography remain s the standard to evaluate for structural cardiac disease such as hypertrophic cardiomyopathy. The diagnosis is suggested by pathologic, asymmetric left ventricular wall thickening (>16 mm) usually involving the intraventricular septum, a non·dilated left ventricle, and impaired diastolic function. In cases where the diagnosis of hypertrophic cardiomyopathy is uncertain (i.e. borderline left ventricularventricu lar wall thickness

of 1)-15 mm), cardiac MRI (Fig. 4 9. 1) can provide accurate estimations of left ventricularventricular morphology and evaluate for delayed gadolinium enhancement from myocardial fibrosis/scar which would support a diagnosi s of hypertrophic cardiomyopathy. Alternatively. repeat echocardiography after 4- 6 weeks of decondition ing may resolve hypertrophy related to the athlete's heart and help distinguish p,thologic hypertrophy from physiologic ,daptations. Cardiac MRI also may be helpful in sportspeopie with marked T-wave inversion in the inferior and latera l leads on ECGjEKG to rule out apical-variant hypertrophic cardiomyopathy that may not be easily identified by echocardiography. Echocardiogram, cardiac MRI, or computed tomography (IT) may demonstrate right ventricular dila· tation and wall thinning, reduced right ventricular ejection fraction, foca l right ventricu lar wall motion abnormalities, or right ventricular aneurysms suggestive of ARVC. Fibro-fatty infilt"tion of the right ventricle consistent with a diagnosis of ARVC is best seen on cardiac MRJ. In evaluation of the coronary artery origins, transthoracic echocardiography can reliably identify the coronary ostia in about 95% of patients. Advanced cardiac imaging such as CT angiography, cardiac MRI, or coronary angiography may be needed in some cases to detect anomalous origins and can also identify other coronary anomalies such as an acute angled take~off, intra myocardial course, and hypoplastic coronary arteries.

Genetic testing when there is a family history of early sudden cardiac death Many of the diseases that put a patient at risk of sudden cardiac death have a genetic origin. Thus, a family history of sudden cardiac death, especially if the relative died when they were younger than 50 years, should heighten awareness about th e potential for an inheritable cardiac disease. Most of the cardiac disea ses that cause sudden cardiac death are autosomal dominant; thus, only one paren t need be affected. These diseases, including hypertrophic cardiomyopathy. ARVC. Brugada syndrome, cpvr and LQTS, can be diagnosed with genetic testing. although the exact role of genetic testing in sportspeople remains to be determined. In hypertrophic cardiomyopathy, approximately 65% of the individuals have an identified gene mutation, and a small percentage have multiple muta tions.

1033

Table 49.4 ECG/EKG interpretation in sportspeople-abnorma[ findings

Any abnormal finding is considered training-unrelated and suggests the possibility of underlying pathologic cardiac disease, requiring further diagnostic work-up. Abnormal ECG/ EKG find ing

Definition

T-wave inversion l")

> 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 )~'i""

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. etiology of sudden death in NCAA athletes. elin J Sport Med 2010;20(2):136,

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

2°°9;43(9):7°8-15. 15. Hevia AC, Fernandez MM, Palacio JM et aL ECG as a 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 In addition to the above complicatfons associated with regular use of beta-2 agonists, salmeterol has the additional problem of a reduction in the acute bronchoprotection against exercjse~induced bronchospasm.47 leukotriene antagonists Leukotrienes are potent bronchoconstrictors that also act to stimulate bronchial secretion of mucus and

1048

increase venopermeability, leading to airway edema. They are present in the airways of asthmatics but not normal subjects. Leukotriene antagonists (montelukast, zafirlukast) given orally prior to exercise attenuate the bronchoconstrictor and inflammatory response that would otherwise occur in response to the exercise.~ll One study showed that montelukasts provided superior protection compared with inhaled salmeterol (a long-acting beta-2 agonist).49 Inhaled corticosteroids Inhaled corticosteroids improve asthma symptoms by reducing airway inflammation and bronchial hyperreactivity. They do not have an immediate bronchodilator effect and are not effective if used as prophylaxis just prior to exercise. The main role of corticosteroids is that of a maintenance therapy to help control asthma, but in doing so they also act to reduce bronchial responsiveness to exercise, thereby reducing the propensity for exercise~induced bron~ chospasm. They are often used on a regular basis, with sodium cromoglycate (cromolyn) or nedocromil sodium given prior to exercise. Inhaled corticosteroids have been shown to reduce the incidence and severity of exerciseinduced bronchospasm,s°' 5! The main adverse effects are oral candidiasis and dysphonia, both of which can be reduced by rinsing the mouth following administration.47 Theophylline The role of theophylline in the management of asthma has changed profoundly over recent years, as research into the inflammatory etiology ofasthma has led to the development of medications aimed to minimize this inflammation. Theophylline should not be used as intermittent prophylaxis for exercise-induced bronchospasm as it is not a potent bronchodilator. In addition, the intermittent use increases the likelihood of adverse effects such as headaches, nausea, vomiting, tachycardia, and central nervous system stimulation. The use of theophylline is, therefore, now limited to those with moderate-severe chronic asthma not controlled by main-line anti-asthmatic medications.

Other agents Recent studies have suggested that fish oil, P diets low in sodium,Sl and diets high in vitamin C'A may all playa protective role in the development of exerciseinduced bronchospasm.

Resp i r at o ry sy m pt oms du r i n g exe r cise Treatment model It is important to note that some drugs used to treat

asthma are banned by the WADA (Chapter 66). In athletes subject to drug-testing procedures, clinicians are urged to check curre nt banned drug listings. A treatment model for those athletes with exercise-

induced bronchospasm is shown in Table 50.7. In athletes who are prone to developing exercise· induced bronchospasm, the regular use of medication prior to exercise is advised.

Conditions that may mimic exerci seinduced bronchospasm Vocal cord dysfunction Vocal cord dysftmction is a psychogenic disorder of breathing, resulting in exercise-induced breathing difficulties. During normal breathing the true vocal cords abduct during inspiration and expiration; however, during vocal cord dysfunction , the true vocal cords adduct inappropriately during inspi· ration. resulting in airflow obstruction. Less com· monly, severe narrowing of the vocal cords may occur during expiration. The condition commonly occurs in 20- to 40 -yearold women, although it may also occur in men and adolescents. Although in some situations it is related to an underlying psychiatric illness, such as generalized anxiety, depression, post-traumatic stress disorder, or a history of sexual abuse, in many cases there is no underlying psychological condition. Clinical features The classic symptoms of vocal cord dysfunction commonly occur during exercise and resolve within five minutes of cessation, They consist of a marked throat tightness or choking, in conjunction with severe dyspnea and an inspiratory stridor-the hallmark feature of vocal cord dysfunction, The symptoms are variable and not necessarily reproducible when exercising under identical conditions, Both acute or Tabl e SO.7 Pharmacological treatment

prophylactic treatment with inhaled beta-z agonists is ineffective, The symptoms may be worse during times of stress or moderate-to-severe lethargy, Vocal cord dysfunction should be considered in all sportspeople complaining of exercise-induced dyspnea, especially when either a diagnos is of exercise-induced bronchospasm has been excluded or, alternatively, made but the athlete has failed to respond to appropriate treatment. The features of vocal cord dysfunction are shown in Table 50.8 overleaf. Investigations The diagnosis is often one of exclusion, An appro· priate bronchial provocation challenge test should be performed, preferably an EVH d,aHenge test, to exclude underlying exercise-induced bronchospasm. Ideally, reproduction of the symptoms during an exercise challenge or. in some situations, participation in normal competition is required as it is essential for the treati ng physician to witness the sportsperson when experiencing the symptoms. Typically the sportsperson struggles to breathe, with rapid shallow breaths and a loud inspiratory stridor; the sportsperson often leans forward. complaining of severe tightness of the throat. Spirometry should be performed at the time of symptoms, when a flattening or truncation of the inspiratory limb of the flow-volume loop is usually seen,ss However, in some cases, spirometry m ay miss the diagnosis.s6 ~-'l('.... In a patient with loud inspiratory stridor but with a

~ ~ )/iV? ~

normal EVH, the diagnosis of vocal cord dysfunction should be considered, especia lly in a young female.

Direct laryngoscopy is required to exclude other causes of upper airway obstruction such as vocal cord paralysis, glottic or tracheal stenosis, laryngeal polyps, and other laryngeal abnormalities. Although difficult, it is essential to perform direct laryngoscopy

of exerCise-induced bronchospasm

Severity

Pre-exercise treatment

Mild

Sodium cromoglycate (cromolyn)/nedocromil

Short-acting beta-2

sodium

agonist

Moderate

Severe

Regular treatment

Symptom treatment

Short-acting beta·2

Sodium cromoglycate {cromolyn)/nedocromil

low-dose inhaled

sodium

corticosteroids

agonist

Sodium cromoglycate (cromolyn) and/or

Higher dose inhaled

Short-acting beta-2

nedocromil sodium

corticosteroids

agonist

1049

Tab le 50.8 Comparative features of exercise-induced bronchoconstriction, vocal cord dysfunction, and

exercise~

induced hyperventilation Exercise-induced Feature

bronchospasm

During or after exercise

Worse in first 12 minutes following cessation of exercise

Reproducibility under

Vocal chord dysfunction

Hyperventilation

Worse during exercise

Worse during exercise

Resolves within 5 minutes

Resolves within 5 minutes

of cessation

of cessation

Reproducible

Often not reproducible

Often not reproducible

controlled situations Classic symptoms

Chest tightness

Throat tightness/choking

Throat tightness

Dyspnea

Dyspnea

Dyspnea

Cough

Inspiratory stridor

Expiratory wheeze Site of tightness

Chest

Throat

Throat

Bronchial provocation

Abnormal

Normal

Normal

May be abnormal at rest

Normal at rest; abnormal

Normal at all times

challenge tests Spirometry

during episode Laryngoscopy

Normal

Effect ofbeta-2 agonists

Prophylactic-prevents episode

Abnormal

Normal

Prophylactic-nil effect

Prophylactic-nil effect

Therapeutic- nil effect

Therapeutic-nil effect

Absent

Absent

Thera peutic-resolves symptoms Symptoms outside exercise

May be present

while the acute symptoms are present to visualize laryngeal closure.

treatment, nearly all sportspeople who have vocal cord dysfunction should be able to exercise and compete unimpeded. 51:(

Treatment

Treatment revolves around speech and relaxation therapy. It is essential that the speech therapist has experience with patients with vocal cord dysfunction. The focus of speech therapy is on respiratory control and diaphragmatic breathing patterns. As the sportsperson gains control over breathing patterns, he or she may realize a sense of control of this condition and reduce the emotional stress associated with dyspnea. Consultation with a psychologist is recommended to help the sportsperson to recognize and come to terms with stress. It is also important for the psychologist to assess for, and manage, any other underlying psychological condition. Speech therapy, alone or in combination with other treahuent interventions, has proven to be suc· cessful in reducing or eliminating the paroxysms of wheezing, stridor, and dyspneaY With appropriate

1050

Exercise-induced hyperventilation Exercise-induced hyperventilation is a common condition occurring in both sportspeople with underlying exercise-induced bronchospasm and also those without. Often during intense exercise the sportsperson loses control of his or her breathing, resulting in rapid shallow breaths-the abdominal muscles are not used. The patient typically presents with shortness of breath and throat tightness occurring while exercising, and resolving immediately with rest. The features of exercise· induced hyperventilation are shown in Table 50.8. Bronchial provocation challenge tests, preferably a eucapnic voluntary hyperpnea challenge test, should be performed to exclude underlying exercise-induced bronchospasm. In those with known exercise-induced bronchospasm not responding to treatment the challenge test should be performed

Resp ira t o r y symptoms during exe rcise while the sports person is on medication to confirm adequate control. An exercise chalIenge test should be performed to allow the treating physician to assess the sportsperson while he or she is experiencing the symptoms. Laryngoscopy is required to exclude vocal cord dysfunction. Treatment involves educating the sports person to breathe. especially during times of stress or intense exercise. Consultation with a psychologist with experience in this area is essential. Training is required and appro priate exercises are given. Concentration on the use of abdominal muscles during breathing is required. Principles similar to the Butyeko m ethod of breathing may be used.

Sinus-related symptoms Sinusitis is a common disorder in both sports people and non-sports people. While acute infections are eas ily diagnosed. chronic sinusitis may be far more subtle in its presentation. The paranasal sinuses are air-filled spaces within the skull that commu nicate with the nose. Most commonly, the maxillary sinus is affected. Clinical features of acute sinusitis may include facial pain. headadle, too thache. post.nasal drip, cough, rhinorrhea , nasal obs truction, pyrexia, and epistaxis. It is importa nt to establish whether these symptoms are evidence of infective sinusitis or, alternatively, inflammation that is causing pain in the absence of infectio n. Inflammatory sinus pain may accompany acute exacerbations of rhiniti s and is often short-lived. Features of chronic sinusitis are vague facial pain, post-nasal drip, cough , nasal obstruction, dental pain, malaise, and halitosis. General and local factors may predispose toward sinusitis. General factors include diabetes. immune deficiency, mucus abnormalities, and disturbances in cilia func tion. Specific or local factors that may predispose sporlspeople to this condition include anatomical deform ities, polyps, foreign bodies, dental infections. cigarette smoking, barotraumas, and local tumors. Failure to respond to therapy or recurrent episodes should prompt the search for a complicating condition (e.g. fracture. tumor, or other abnormality).

Inves tigations When investigating these patients, assessment may be difficult due to the degree of edema. This may obscure the relevant abnorm ality. Full examination some times must be delayed until treatment has

been effective. The use of plain X.rays should he interpreted with ca ution since up to I em (0.5 in.) of mucoid thickening may he regarded as normaL In children, a number of developmental changes also make radiolog ical interpretation almost impossible. Useful find ings that may be seen on plai n X-ray include the presence of a fluid level and/ or opacification of a si nus. \' R4 ('

ltii-~~ CT scan is the investigation of choice in sinus· related

~

0"'"

~&\J'"

conditions.

In the patient with infective sinusitis, microbiological culture of nasal pus may be useful; however, the presence of normal bacterial flora makes interpretation difficult. Approximately 50% of infections are due to Hemophilus injluenzae or Streptococcus pneumoniae but there are a variety of other organisms that may playa role, including Branhamella catarrhalis (most common orga nism in children) and other mixed oral anaerobes.

Man agemen t of sinusitis TIle principles of management of si nusitis are: 1. appropriate antibiotic therapy 2. the establishment of sinus drainage through the release of obstruction and the stimulation of mucus fiow

3. the control of any predisposing factors. The antibiotic of fi rst choice is amoxicillin. ei ther alone or in combination with davulanic acid. Penicillin'allergic patients should use cefador. cotrimoxazole, or doxycycline. If a dental infection is the primary source, then anaerobic cover should be added (e.g. metronidazole). Systemicall y adminis te red decongesta nts. including pseudoephedrine, are of some value in the treatment of acute sinusitis. However, a topical decongestan t is more effective and will have fewer systemic adverse effects. Antihistamines usually slow mucociliary function but may have a role, especially if sinusitis is the result of nasal allergy. The use of topical s teroids is widely advocated in the acute situation but there is often a latent period before these are effective. TIle maintenance of hydration in the treatment of these patients is critical. There m ay well be a role for surgery in either the acute or chronic condition where there is an

105 1

anatomical deformity, polyps, or a failure to respond to medical treatment.

Other exercise-related conditions Exercise-induced anaphylaxis Approximately 500 cases of exercise-induced anaphylaxis have been reported, mostly occurring in sportspeople.'9' 60 Numerous attacks may occur before the diagnosis is correctly made. The condition is characterized by a sensation of warmth, pruritis, cutaneous erythema, angioedema, urticaria (greater than I em [0.5 in.] diameter), upper respiratory tract obstruction, and, occasionally, vascular collapse. It is considered a distinct entity from other exertion-related phenomena. Risk factors include: previous atopic history (50%) family atopic history (67%) food ingestion (e.g. shellfish, celery, nuts, alcohol) weather conditions (e.g. heat, high humidity) drug ingestion (e.g. aspirin [ASA], NSA1Ds). The management of this condition involves: 1. prevention through modification of the exercise

program to; (a) decrease intensity (b) avoid exercise during warm and humid days (c) stop exercise at the earliest sign of itching (d) avoid meals 4 hours before exercise 2. drugs/therapy (a) antihistamines (b) cromoglycate (cromolyn) (c) adrenalin (epinephrine)-should have an injection available (d) pre-treatment does not prevent onset.

1052

Cholinergic urticaria Cholinergic urticaria is an exaggerated cholinergic response to rapid elevation of the core body temperature through a mechanism such as exercise (most commonly), hot showers, fever, or anxiety.G! It is characterized by generalized flushing, tan urticarial rash, and pruritus. Generally, the urticarial papules appear first within IO minutes of starting exercise on the neck or upper thorax and spread to the limbs. 62 Systemic reactions such as syncope, abdominal pain, and wheezing are rare. Cholinergic symptoms such as lacrimation, salivation, and diarrhea may be observed. Recovery usually occurs spontane· ously in 2-4 hours provided there are no systemic symptoms. 61 Antihistamines are generally used in treatment (e.g. hydroxyzine, 250 mg/day or cyproheptadine, 4 rug/day).

Exercise-induced an gioedema Angioedema is a non-itchy swelling occurring in the deep dennis and subcutaneous tissue. Although angioedema can affect any body region, it tends to involve the face and oral region. Occasional visceral manifestations occur. Attacks may be life-threatening if the airway is involved. Frank asthmatic attacks rarely occur in the setting of exercise-induced angioedema. G3 Prevention may be achieved with modification of the exercise program and/or the use of antihistamines (e.g. diphenhydramine). The selective histamine Hz -receptor blockers (e.g. cimetidine) have been used in the treatment of this condition.

DlI

RECOMMEND ED READING

Anderson SD. Indirect challenge tests: aiTWay

5. Fitch KD. Management of allergic Olympic athletes.

j AI/erg)' Clill Immuliol 1984;73:722-7. 6. Corrigan B. Kazlaukas R. Medication use in athletes

hyperresponsiveness in asthma: its m easurement and

clinical significance. Chest

2010;138(2

selected for doping control at the Sydney Olympics

SUppl):2SS-30S .

Carlsen KH, Anderson SO , Bjermer Let al Exercise-induced

(2000) . ClinJ Sport Med 2oop3:33-40' 7. Voy RO. The

asthma, respiratory and anergic disorder s in elite athletes: epidemiology, mech anisms and d iagnosis: part 1 of the report from the Joint Task Force of the

Exerc 1986;18(3):328- 3°.

8. Weiler 1M. Layton T, Hunt M. Asthma in United States

European Res piratory Society (ERS) and the European

Olympic athletes who participated in the 1996 summer

Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA2LEN. Allergy 2oo8;G3(4}:

games. ] Allergy Clilt Immunol 199 8;102(5):722-6. 9. Weiler JM. Ryan EI 3rd. Asthma in United States

387- 4 0 }Carlsen KH . Anderson S D. Bjenner Let a1 Exercise-induced

Olympic athletes who participated in the 1998 Olympic winter games. J Allergy Clin IlI1l11uno1

asthma, respiratory and allergic disorders in elite athletes: epidemiology. mechanisms and diagnosis:

2000;10 6(2):267- 7 1. 10.

rewarming. The second reaction sequence in exercise-

European Respiratory Society (ERS) and the European

induced asthma. j elin Invest 1992:90:699-704.

Academy of Aller gy and Clinical Immunology (EAACI) 49 2 -5°5. Cockcroft DW. Direct challenge tests: Airway hyperresponsiveness in asthma: its measurement and ciinical significance. Chest 2010 AUg;138(2 Suppl):

II.

I8S- 24S elite athlete: summary of the International Olympic

19 84;73: 66 0-5. 12. Godfrey S, Bar-Yishay E. Exercise-induced asthma revisited. Respir Med 1993:87:331-44. 13- Argyros GI, Philli ps YY, Rayburn DB e t al. Water loss without heat Hux in exercise-induced bronchospasm.

Am Rev Respir Dis 199P47:1419-24. 14 . Schmidt A, Bundgaard A. Exercise·induced asthma

Committee's consensus conference. Lausanne,

after inhalation of aerosols with different osmolarities.

Switzerland. January 22-24. 2008. J Allergy Clill

1"ltIl!lnm 2008;122(2):254- 60 Holzer K, Brukner P, Douglass

J. Evidence-based

management of exercise-induced asthma. Curr Sports

Med Rep 2002;1:86-92. Millward DT, Tanner LG . Brown MA. Treatment options fo r the management of exercise-induced asthma and bronchoconstriction. Phys Sportsmed 2010; 38{4):74-8o.

Eur J Respir Dis SllppI I986;I43:,7- 61. I).

Anderson SD, Smith CM. Osmotic challenges in the assessment of bronchial hyperresponsiveness. Am Rev

Respir Dis 1991;143:543-6. 16. Burge PS, Harries MG. Lam WK et al. Occupational asthma due to forma ldehyde. Thorax 1985:4°:255-60. 17. Godfrey S. Exercise-induced asthm a. In: Barnes PI , Gruns tein MM. Leff AR et aI., eds. Asthma. Philadelphia: Lippincott-Raven, 199]:1105-20.

REFERE N CES

18. Boulet L-P, Turcotte H, Laprise C. Compara tive degree

National Institutes of Health. Practical guidefor Ihe

an d type of sensitisation to common indoor and

diagnosis ami management ojasllmla. Be thesda. M D:

outdoor aUergens in subjects with allergic rbinitis

NIH Publication. 1997. 2.

Anderson SO. Is there a unifying hypothesis fo r exercise-induced asthma? ] Allergy Clin Iml11ullol

Fitch KO . Sue·Chu M, Anderson SO et al. Asthma and the

I.

Gilbert lA. McFadden ER. Airway cooling and

part II of the report from the Joint Task Force of the

in cooperation with GA2lEN. Allergy 2008; 63(5):

II

us Olympic committee experience with

exercise-induced bronchospasm , 1984. Med Sci Sports

Institute of Medidne. Clearing Ihe air: (istJlIlla and

and/or asthma. Cli,! Exp Allergy 1997;27:52-9. 19. Helenius IJ, Tikkanen HO, Haahtela T. Association

iudoor air exposure. Washington, DC: National Academy

between type of training and risk of as thma in elite

of Press. 2000.

athletes. Thorax 1997:52:157- 60.

3. Anderson SD. Exercise-induced asthma. In: Midd leton E, Reed C, Ellis E e t aI., eds. Allergy: principles

and practice.. 4th ed. St Louis: CV Mosby, 1993=1343-67. 4. Anderson S. Exercise·induced asthma. In: Carlsen K-H, Ibsen T, eds. Exerciu-indl4ced asthma and sports ilt aslhma. Copenhagen: Munksgaard Press, 1999:11-17.

20. Holzer K, Anderson SD. Douglass

I. Exercise in elite

summer athletes: challenges fo r diagIlosis. j Allergy

CUll Illtlllullolzo02;nO(3):374- 8o. 21 . Warner 10. Bronchial hyperresponsiveness. atopy, airway inflanunation and asUuna. Pedialr Allergy

IllllllllnoI 1998;9:56- 60.

1053

2.2.. Langdeau fB, Boulet LP. Prevalence and mechanisms of development of asthma and airway hyperresponsiveness in athletes. Sports Med 2.001;3 1 (8):601-16. 2.3. Drohnic F. Freixa A. Casan P et aL Assessment of chlorine exposure in swimmers during training. Med 2+ 25.

26.

27.

Sci Sports Exerc 1996;28(2):27r-4. Anderson SO, Silverman M. Konig P eta1. Exerciseinduced asthma. A review. Br J Dis Chest 1975;69:1-39. Rundell KW, 1m f, Mayers LB et al. Self-reported symptoms and exercise-induced asthma in the elite athlete. Med Sci Sports Exerc 2001;33(2):2.08-13. Holzer K, Douglass f, Anderson SO. Methacholine has a low sensitivity to identify elite athletes with a positive response to eucapnic voluntary hyperpnea and should not be used to exclude potential exercise-induced bronchoconstriction. Respirology 2.002:7(SUPpl.):A28_ Anderson SO. Exercise-induced asthma. In: Kay AB. ed. Allergy and allergic diseases. Oxford: Blackwell Scientific

Publications. 1997;692--711. 28. Anderson SO. Argyros GJ, Magnussen H et al. Provocation by eucapnic voluntary hyperpnoea to identifY exercise induced bronchoconstriction. Br J

37. de Bisschop C, Guenard H, Desnot P et al. Reduction of exercise-induced asthma in children by short. repeated warm ups. Br J Sports Med 1999;3J:IOO- 4. 38. Schnall RP, Landau LI. Protective effects of repeated short sprints in exercise-induced asthma. Tlwmx J980;35:828-32. 39. McKenzie DC, McLuckie SL, Stirling DR. The protective effects of continuous and interval exercise in athletes with exercise-induced asthma. Mrd Sci Sports

Exerc 1994:26(8):951- 6. 40. Edmunds A, Tooley M. Godfrey S. The refractory period after exercise-induced asthma: its duration and relation to the severity of exercise_ Am Rev Respir Dis

1978 ;IIT 247-54· 41. Anderson SO. Exercise-induced asthma: stimulus, mechanism, and management. In: Barnes PJ, Rodger I, Thomson NC. eds. Asthma: basic mechanisms and clinical

management. London: Academic Press, 1988:5°3-22. 42. Speelberg s, VerhoeffNPLG, van den Berg NJ et al. Nedocromil sodium inhibits the early and late asthmatic response to exercise. Ellr Rcspir J 1992.;5:43 0-7. 43. Spooner C, Rowe BI-I, Saunders LD. Nedocromil sodium in the treatment of exercise-induced asthma:

Sports Med 2001;35:344-7. 29. Holzer K, Anderson SO. Chan H-K et al. Mannitol

a meta-analysis. Eur Respir J 2000;16(1):30-7.

as a chaUenge test to identify exercise-induced

44. Spooner CH. Saunders LD, Rowe BH. Nedocromil

bronchoconstriction in elite athletes. Ant J Respir erit

Care Med 2003;167(4):534-47. 30. Anderson SO, Brannan J. Spring J et al. A new method for bronchial-provocation testing in asthmatic subjects using a dry powder of mannitol. Ant J Respir Crit Care

Mw 1997;156:758-65. 31. Mahler DA. Exercise-induced asthma. Med Sci Sports Exmise 1993;25(5):554-6L 32. Nisar M, Spence DPS, West 0 et al. A mask to modify inspired air temperature and humidity and its effect on exercise induced asthma. Thorax 1992.;47446-5°33. Shturman-Ellstein R, Zeballos RJ, Buckley 1M et aL The beneficial effect of nasal breathing on exerciseinduced bronchoconstriction. Am Rev Respir Dis 1978;118:65- 73. 34. Fitch KD. Blitvich JD. Morton AR. TI1e effect of running training on exercise-induced asthma. Ann

Allergy Asthma ImlHtmol 1986;7:90- 435. Welsh L, Kemp JG. Roberts RG_ Effects of physical conditioning on children and adolescents with asthma.

Sports Med 2005;35(2):127-4I. 36. Ram FS, Robinson SM, Black PN. Effects of physical training in asthma: a systematic review. Br J Sparts Med 2000;34(3):162-7·

1054

sodium for preventing exercise·induced bronchoconstriction (Cochrane review). Cochrane

Database Syst Rev 2002:I:CDoon83_ 45. Bhagat R, Kalfa S, Swystun A. Rapid onset of tolerance to the bronchoprotective effect of salmeterol. Chest 1995;108:12 35-9' 46. Ferrari M, Balestreri F, Baratieri S et al. Evidence of the rapid protective effect of formo terol dry-powder inhalation against exercise-induced bronchospasm in athletes with asthma. Clin lnvest Med 2000;67:510-I3. 47. Rupp NT. Diagnosis and management of exerciseinduced asthma. Phys Sportsl1ud 1996;24(1):77- 87. 48. Makker HK. Lau LC. Thomson HW et al. The protective effect of inhaled leukotriene 0 4 receptor antagonist ICI 204,219 against exercise-induced asthma. Am Rev

Respir Dis 199P47:1413-18. 49. Ferrari M, Segattini C. Zanon R et al. Comparison of the protective effect of salmeterol against exerciseinduced bronchospasm when given immediately before a cydoergometric test. Respiration 2.002;69(6):509- 12. 50. Henriksen fM. Dahl R. Effects of inhaled budesonide alone and in combination with low·dose terlmtaHne in children with exercise-induced asthma. Am Rev Respir

Dis 198p28:993- 7'

Respira t o r y symptoms du ri ng exercise 51. Waalkans H f, van Essen-Zandvliet EE . Gerritsen J el al. 11te effect of an inhaled corticosteroid (budesonide) on exercise-induced asthma in children. Eur R~spir J

1993: 6 :6 52 - 6 . 52. Mickleborough TD, Lindley MR. ]one scu AA e l al. Pro led ive efTcct o ffi sh o il supplemen tation o n exercise· induced bronchocol15triction in asth ma. Clust

2006;129(1):39-49_ 53. Mickleoorough TD. Salt intake, asth ma, and exerciseinduced bronchoconstriction: a review. Pilys Spar/silled 2 01O;3 8{1):II8-3 1.

54. Tecklenburg SL. Mickleborough TD, Fly AD et al.

Ascorbic acid supplementation attenuates ('xerciscinduced b ronchoconstriction in patients with asthma.

Resp Mal 2007:101(8): 1770-8. 55. Newman KB, Mason III UG. Sch malin g KB. Clinical features of vocal cord dysfunction. Am] Rcspir Crit Care

Med 199PP{4 Pt 1):1382-6. 56. Morris MJ , Deal L, Bean DR et al. Vocal cord

dysfunction in patients with exertional dyspnea. Chest

1999:116{6):1676-82. 57. Sullivan M D, Heywood 8M, Beukelman DR. A treatment for vocal cord dysfunction in female athletes; an outcome study. Laryngoscope 200I:IlI(IO):1751- 5. 58. Newshaun KR, Claben OK , MiUer DJ et ai, Paradoxical

vocal cord dysfunction management in athletes. j AtllI Tra in 200 2:37:325- 8.

59. Castells Me, H oran RS, Sheffer AL Exercise induced anaphylaxis. CIiIl Rev Allergy 111111111/1011 999:17:4 13-24.

60, CasteUs Me, Horan RS. Sheffer AL Exercise induced anaphylaxis. Curr Allergy Astlmla Rep 2003:P5-2!. 6I. Vokheck CW, Li J1. Exercise-induced urticaria and ana phylaxis. Mayo CUll Prot 1997:72(2):140--'7.

62. Sweeney 1M . Dexte r WW. Cholinergic urticaria in a jogger. ruling ou t exercise-induced anaphylaxis. Phys SPOl't51J1i!d 2oo3:31{6}:32-6. 63. Leung AKC, Hedge HR. Exercise-induced angiodema and asthma. Am j Sports Med 1989 ;17(3);442- 3.

1055

fit ' 997 dLiring the Hawaiian Ironman I pLished my body to the limit. I was vomiting, had diarrhea and stomach cramps, bLit TjLlst had to fin ish the race. JLlst 50 metres FOIn the finish line I coUapsed. ShOlt lyaft fl', I had to have surge/y to remove one third oInty lmge bowel, as it had died. Chris Legh, quoted from www.coolrunning.com.au/general/ 2oo3 / 2oo3eoI3·shtmI

The gut is not an athletic organ. During exercise, blood is directed away from the splanchnic vessels and to the exercising muscles. The gut therefore becomes relatively ischemic, and it is this which causes the majority of gastrointestinal symptoms during exercise. These symptoms may be divided into those relating to the upper gut and those relat· ing to the lower gut (Table 5I.I). Bleeding is another important clinical presentation, as discussed below. Physiological changes that alter gastrointestinal function during exercise include reduced blood flow to the abdominal viscera, gastrointestinal hormonal changes. and alterations to gastric emptying rates and intestinal motility. Also. vigorous diaphragm atic m ovements. abdominal con tractions. and intestinal jarring can all cause abdominal symptoms.' Although the inc idence of gastrointesti nal symptoms is increased with exercise, the presence of symptom s in a sportsperson should not

automatically be assumed to be solely related to exercise. Sportspeople as well as non-sports people suffer from common conditions. such as hiatus hernia and peptic u1ceration, inflammatory bowel disease, polyps, and cancer. Physical activity confers a 25% reduction in colon cancer risk.:t Clinical judgment is required to appreciate when these conditions must be considered in the sportsperson with gastrointes tinal symptoms. A summary of the management of common gastrointestinal symptoms is shown in Table 51.2.

Tab le 51 .2 Treatment of common gastrointesti nal problems

Symptoms

Treatment

Heartburn,

Avoid solid foods prior to exercise

reflux,

Antacid medication

epi gastric pain

Histam ine H2 -receptor antagonist

Ta bl e 5 1.1 Gastrointestinal symptoms associated with exercise

Gastrointestinal

Upper gastrointestinal tract

Lower gastrointestinal tract

Heartburn

Cramping

Reflux

Urge to defecate

Nausea

Diarrhea

Vomiting

Rectal bleeding

Bloating

Flatulence

Epigast ric pain

1056

(rarely necessary)

bleedin g

Ensure adequate hydration Reduce jarring (e.g. food, shoes, soft surfaces)

AbdomInal "stitch

ff

Runner's diarrhea

Reassurance Avoid pre-exercise meal Reduce fiber content of food 24 hours prior to run Antidiarrheal medication (e.g. loperamide)

Gastrointestinal symptoms during exercise

Uppe r gastrointestinal symptoms Heartburn, reflux, nausea, vomiting, and upper abdominal pain are the most common upper gastrointestinal tract symptoms related to exercise. Gastroesophageal reflux is a common complaint among sportspeople and can even cause asthma-like symptoms.> 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. Distinguishing between chest pain due to gastroesophageal reflux or esophageal muscular ~-~~ spasm, and chest pain due to chest wall or cardiac ~ 0'"" causes can be difficult. Any sportsperson presenting II:J"$'>, with chest pain on exertion must be thoroughly assessed to exclude cardiac causes. ? R4('

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 associ~ 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 ('

,IA-~~ Acute diarrhea is usually due to an infective ca use

~ '0"'" 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 57).' ~ 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 it~pl e m en ted 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

~:'l('..... Reserve NSA IDuse fo r those injury problems where a significant inflammation is prese nt {e.g. joint !(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 'symp~qms lien exercising-advice for sportspe~'p le _ 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. hjgh~fiber foods prior to competition. Only take anti~inflammatory 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 pre~race 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

1061

mRECOMMENDED

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 ~nefits 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.

~ I.

R EF E RE NCE S

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-ang io 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. ~.4('..... Rhabdomyolysis is a potentially fatal condition, and

,~ ~ requires hospital admission for dose observation J(j'of":. b

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 en t 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-

~

)'~nl~

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_

8. Bernard

RECO MMEND E D R E ADING

Rayner B, Schwellnus M P. Exercise and the kidney. rn:

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.

98-1°3· 9. Batt M. Nephrology in sportspeople. In: Fields K.

Poortmans JR. Exercise and renal function. Sp{))1S Mal

19 84;1: 125-53

Br J Urol

and return 10 play. ellrr Sports M,d Rep 2009;8(2) :

GuidelineLaftec Kidney_Transpianl.as px

II

haematuria.~

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 F~tStrati ng. 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 rela~ 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

--, 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

Cha~~r j 53

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 com~ 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

_I

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: i ~port ~>~>t 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 com ~ 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

'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

4 hours), including ultramarathons, equipment for measuring the serum sodium concentration must be available so that potentially lethal exercise-induced hyponatremia (EAH) can be diagnosed expeditiously. Intravenous therapy should only be considered after a serum

Table 58.1 Guidel1nes for determining the severity of the collapsed sportperson's condition

Severe Immediate assessment Conscious

Unconscious or altered mental state

Alert

Confused, disoriented, aggressive

Rectal temperature: 40°C (104°F)

Systolic blood pressure: > 100 mmHg

Systolic blood pressure: 148 mEq/L) Body weight loss: > 10% Body weight gain: >2%

1134

Exe rcis e in t he heat sodium concentration greater than 135 mmoljL (>13 5 mEqjL) has been measured. It is no longer defensible not to measure the serum sodium concentration in a sportsperson admitted to a medical tent after a sporting event of four or more hours and in whom there is evidence of some alteration in the level of consciousness. 16

~.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 overload.~--S· '~-40 Sports people with EAHE and serum sodium concentrations below 129 mmol/L (129 mEq/L) are ove~ 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.

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.

Etiology of EAH and EAHE The 1985 seminal paper describing the first cases of exercise·as50ciated hyponatremia concluded, on /lIi-~~ the basis ofthe history, the clinical findings, and the ~ b'" estimated sodium and water balance during exercise 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% H R"",~

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: ACSM~ Guidelines (or exercise testing ond prescription;9 ACSM~ 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

Aerobic (e.g. large-muscle activities such as walking, swimming, cycling, rowing,

3- 5 days/week

Intensity

Time

11 - 16/ 20 RPE

Limited by symptoms

150-300 mins/week Emphasize duration over intensity

60- 80% lRM

8- 12 reps/day

6O- 80% HR~.

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 prescription;~ 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

fi tness. physical activity. and fu nctional limita tio n

Bouchard C, Blair SN, Haskell WL. eds. Physical activity alld

in adults aged 4 0 and o lder_ M,d Sci Sports Excrc 199 8 ;3°(9):1430-5.

health. 2nd 00. Human Kinetics 20lt. Thompson WR, ed. ACSM's Guidelinesfor exercise Jesting

and prescription. 8 th ed. Philadelphia PA: Lippincott Williams & Wilkins, 20[0.

J. Nieman D, eds. ACSM's

Myers

Resollrcesjor dillical

exercise physiology: muscu/oskdetal, neuromuscular, ncoplastic. immunologic, alld IICtntl t% gic conditions. 2nd ed. Philadelphia PA: Lippincott Williams &

20IC

clinical

practice guidelines for the diagnosis and managem ent

Blair SN. Physical inactivity. the bigge st public health

Mea 2oo9:43 (1}:

1- 2. 2. Sallis R. Developing healthcare systems to support exercise: exercise as the fifth vital sign. Br J Sports Med 2011;45(6):473-4' 3. World Health Organization . Global recommendations on physical activity for health . Switzerland: World Health Organization, 2010.

14. Evenson KR, Stevens J, Cai J et a1. The effect of

Physical activity ill t/le prevelJtion and treatment ofdisease (in Swedish). 2008. Health USP. National physical activity plan.

ameliorate the health hazards of obesity? Br) Sports

Mcd 2009;43(1):49-51. 16. Ruiz JR, Sui X, Lobelo F et al. Muscular strength and adiposity as pred ictors of adulthood cancer mortality in men. Cancer Epidemiol Biomarkers Prey 2009;18(5):

'468-76. 17. Ruiz J R. Sui X. Lobelo F e t a!. Association between muscular st ren gth and mortality in me n: prospective cohort stud y. BM) 2008;33T '439.

18. Donnelly JE. Smith B. Jacobsen OJ e t al. The role of

4- FYSS llle Swedish National Institute of Public Health.

exercise for weight loss and maintenance. Best Pmct Res

Clin Gastrocllttro/ 2004;18(6):lO09-29. 19. Durstine IL, Moore GE. Painter PL et aI., cds. ACSM's

WW1V.

pliysicalm:tivil ypltUl .orgfhealtJlcare.pllp. 2010. 6. Patrick K. Pratt M . Sallis RE. The healthcare secto r's

us national physical activity plan. j

Pltys Act

HUl lth 2009;6(Supp12):S2II- 19. 7. US Department of Health and Human Services. Physical activity guidelines for Americans. wWlv.ltealth.

govjpaguidelillcsj.2008. 8. Tremblay MS . Warburton DE. Janssen I et a!. New Canadian physical activity guidelines. AppI PllysioI Nlllr

Metab 2011 ;36 (1):36- 46; 47-58. 9. Thompson WR. ed. ACSM's Guidelines forcxercise

testing and prescription. 8th 00. Philadelphia PA: Lippincott Williams & Wilkins, 20IO.

2006;6I(n): I1 57- 6 5·

15. Lee DC. Sui X. Bla ir SN . Does physical activity

REE ERENCES

role in the

interventio ns and independence for elders pilot

2003:35(2):270-7.

m

s.

Effects of a physical activi ty intervention o n measures of physical perform ance: results of the lifestyle

mortality in women and men. M,d Sci Sports Excrc

2010;182(17):1864- 73.

problem of the 21St century. Br J Sports

4 12- 16 . 13. LIFE Study Inves tigators. Pahor M, Blair SN et al.

cardiorespiratory fitness and obesity on cancer

of osteoporosis in Canada: summary. CMAJ

1.

Brill PA, Macera CA, Davis DR et 3 1. Muscular s trength and physica l fun ction. Med Sci Sports Excrc 2000;32:

(UFE·P) study.) Gerontal A Bioi Sci Me.d Sci M,d Sci

Wilkins, 2010.

Papaioannou A, Morin S, Cheung AM et a1.

12.

Exercise mallagelf1U1t for persons with chrollic diseases and disabilities. 3rd ed: Hu man Kinetics, zo09. 20. Donne lly JE. Blai r SN. Jakicic 1M et al. American College of Sports Medicine position stand. Appropriate physical activity interven tion strategies for weight loss and preven tion of weight regain for adults.

Mea Sci

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:

11 71

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

capacity and body composition as predictors of

society for heart and lung transplantation. Circulation

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

2oo4;27(1):83-8. 39. Church TS, LaMonte

Mf.

Barlow CE et a1.

Cardiorespiratory fitness and body mass index as

Association committee on exercise, rehabilitation, and

predictors of cardiovascular disease mortality among

prevention. Circlilation 2oop07:I2IO- 6.

men with diabetes. Arch Illtem Med 2oop65{18):

26. Heart Failure Society of America (HFSA). 2010 comprehensive heart failure practice guideline. J Card Fail20IO:r6:el-194· 27. Whelton SP, Chin A, Xin X et al. Effect of aerobic exercise on blood pressure: a meta-analysis of randomized, controlled trials. An/t lltt Med 2002;13 6 (7) :493-5 03· 28. Carvalho J, Marques E, Ascensao A et al.

2114- 20. 40. American Diabetes Association: Standards of medical care in diabetes-2oo7. Diabetes Care 20°7:30 Suppl I: S4-41. 41. Johansen KL. Exercise and chronic kidney disease: current recommendations. Sporls Med 2005;35(6):

48 5-99. 42. McNeely ML, Peddle

CJ. Parliament M et al. Cancer

Multicomponent exercise program improves blood lipid

rehabilitation: recommendations for integrating

profile and antioxidant capacity in older women. Arclt

exercise programming in the clinical practice setting.

Gerontol Gerialr 2010;51{1):1-5. 29. Kelly RB. Diet and exercise in the management of hyperlipidemia. Am Fam Phys 20IO;81(9):I097-102. 30. Wilund KR. Feeney LA, Tomayko EJ et a1. Effects of endurance exercise training on markers of cholesterol absorption and synthesis. Physiol Res 2009;58(4): 545-52· 31. Fletcher E, Berra K, Ades P et al. Managing abnormal blood lipids: a collaborative approach. Circulation 2005 ;112 (20): 3184- 209. 32. O'Donnell DE, Aaron S, Bourbeau J et aI. Canadian ThoraciC Society recommendations for management of chronic obstructive pulmonary disease-2oo7 update.

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

EpidemioI2006;16:197-,:w 5. 44. Bicego D. Brown K, Ruddick M et al. Effects of exercise on quality of life in women living with breast cancer. a systematic review. Breast J 2° °9:15(1):45-51. 45. Holmes MD. Chen wy, Feskallich 0 et a1. Physical activity and survival after breast cancer diagnosis.

JAMA 2005;293{20):2479-86. 46. Meyerhardt JA. Giovannucci EL. Holmes MD et aI. Physical activity and survival after colorectal cancer diagnosis. J Clil1 OncoI2006;24{22):3527-34· 47. Meyerhardt JA, Heseltine 0, Niedzwiecki 0 et al.

histories ilt cardiopulmollary physical therapy. Thorofare,

Impact of physical activity on cancer recurrence and

NJ: SLACK Incorporated. 2004.

survival in patients with stage III colon cancer: findings

34. Niti L, Donner C. Wouters E et al. American Thoracic Society/European Respiratory Society Statement on pulmonary rehabilitation. Am J Respir Crit Care Med 2006;173(12):139 0-413.

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 nonspe 2 mins ./ x Slump neural test x ./ SIJ pain positive tests ./ x SIJ ASlR & SIJ closure ./ x

............................ cm ............................ cm ./ x ./ x x ./ ./ x ,/ x

General observation ...................................................................................................................................................................................... General palpation ..........................................................................................................................................................................................

Inner core TA/multifidus/ pelvic floor-activation with RTUS Inner core-most effective cues

Functional testing 3 x hop for distance Single-leg hop for height Multi-hop test (no ofba/ance corrections)

Quality of movement testing Single-leg deep squats (comment on quality) Single-leg "running man"x 5 (comment on quality) Dynamic lunges (comment on quality) Hip/pelvis dissociation exercises (comment on quality) Jump landing posture- varus knee position (comment on quality)

11 94

............................ cm ............................ cm

............................ cm ............................ cm

Screen i ng the el i te sportsperson

ECG/EKG should be mandatory in pre~participation screening of sportspeople. In the same journal issue, Drezner and Corrado agreed that the pool of scientific evidence supports the efficacy and cost~effectiveness of ECG/EKG screening for sportspeople. 6 They also acknowledge that in most countries there are still feasibility issues and practical concerns regarding false· positive results, cost-effectiveness, physician infrastructure, and healthcare resources for large-scale implementation of EeG/EKG screening. These issues should

be addressed through physician education and use of contemporary standards for EeG/EKG interpretation in young sportspeople. A particular emphasis must be in distinguishing physiologic cardiac adaptations from underlying pathology to minimize false-positive results (Chapter 49, Tables 49-4b-c)!' Similarly, a British Medical Journal head-to-head debate highlighted divergent opinions among NO eminent sports medicine groups on the value of ECG/EKG in preventing sudden cardiac death." 8 A number of sporting bodies now require an ECG/EKG to be performed prior to participation. For the 2010 FIFA World Cup, both ECG/EKG and echocardiograph were mandatory. The questions relating to cardiovascular problems in our questionnaire are adapted from those recommended by the American Heart Association (see box below).4

.

-

I

I

•

I

I

•

Have you ever passed out, become dizzy, or had chest pain during or after exercise? Has anyone in the family died suddenly and unexpectedly before the age of SO? Have you ever had a heart abnormality or murmur diagnosed by a doctor? Have you ever had an abnormal heart rate, palpitations, or irregular heartbeats? Have you had high blood pressure or high cholesterol? Has a physician ever denied or restricted your participation in sport because of heart problems? Have any of your relatives ever had cardiomyopathy, Marfan syndrome, long QT syndrome, or a significant heart arrhythmia? Adapted from those recommended by the American Heart Association 4

Medical health Generally, fit, young sportspeople have very little occasion to visit a physician. Some of the sportspeople will not have been to see a physician for many years and may not have a regular general practitioner, especially if their sporting prowess has resulted in them moving from their hometown. The examining physician should not assume that basic medical procedures such as auscultation of the heart and blood pressure measurement have ever been performed on the sportsperson. The screening questionnaire necessarily focuses on the more common conditions affecting young sportspeople. Asthma and exercise-induced asthma have a significant prevalence of both under- and over-diagnosis, as well as under- and over-treahuent. The efficacy of different methods of screening'! for the presence of asthma and exercise-induced asthma are described in Chapter 50. The standard questions in our protocol are: Do you have asthma, chest tightness, wheezing, or coughing spells during or after exercise? Have you been tested in an accredited laboratory? Obviously, many items could be included in a health questionnaire in an attempt to detect some abnormality. Apart from the cardiovascular and respiratory questions mentioned above, we include the following questions in our questionnaire: Do you have a history of concussion, fits, or faints? Do you have any history of loss of consciousness or head injury requiring time off training/playing? Any problems with your vision? Do you require glasses or contact lenses? Do you have any problems with your bowels such as constipation, diarrhea, GI upset? Do you have any problems with passing urine, or urine infections? Do you have any history of recurrent infections? Do you have any recent loss of appetite or weight loss? Do you have any recurrent ear, nose, throat, or sinus problems? Do you have any skin problems-eczema, psoriasis, dermatitis? Do you have any chronic illnesses or see a physician regularly for a medical problem? Do you take prescribed medication or supplements? Do you have any allergies? Have you ever been a smoker? If so, when and how much?

11 95

Practica l spo rt s med ic i ne What is your weekly alcohol intake? Does anyone in your family have any of the following medical problems-heart disease, stroke, hypertension, cancer, blood disease, vascular problems, DVT, arthritis, chronic joint or muscle problems, diabetes, allergies, asthma, hormonal problems (e.g. thyroid)? Have you ever had an infection that has required treatment in hospital? Have you had infections while overseas? Have you ever had a blood transfusion? Have you had hepatitis? Have you ever had surgery or required hospitalization?

In our clinical experience, the incidence of mild depression among high-level sports people is quite significant. The medical screening presents an opportunity for the sports person to discuss their depression. If the sportsperson complains of excessive fatigue, depression should be considered among other possible causes of the fatigue: Have you, or a close relative, ever suffered from depression? Have you ever suffered from excessive fatigue or overtraining?

Menstrual abnormalities are commonly associated with intense athletic activity in females and may lead to significant bone loss resulting in stress fractures and osteoporosis. Therefore, it is important to include questions designed to detect abnormal menstruation in the questionnaire: Have you started your periods? _ __

If so, what age _ _ _ _ _ __ Date of your last gynecological examination/PAP smear? _ _ I _ _ I _ _ Have you ever missed your period for more than 6 months? Does your menstruation affect your performance?

The screening also presents an opportunity to check the vaccination status of the sportsperson: Vaccinations (please put dates if you have had any of the following): - Tetanus - Rubella (German measles) - Influenza

- Typhoid -

1196

Hepatitis A Hepatitis B

-

Yellow fever Chickenpox Meningitis C Polio

Hepatitis A and B may be in a combination vaccine, usually a series of three injections over 6 months. Measles, mumps, and rubella is a combination vaccine, part of the usual childhood series.

Baseline data collection In certain sports, particularly at the elite level, regular monitoring of hematological and biochemical parameters is performed to detect early evidence of deficiencies. An example is the monitoring of serum ferritin levels in female endurance sportspeople. Table 62.1 on pages II98-1200 lists the possible blood and biochemical tests that can be performed in a comprehensive screening of a professional sportsperson. Blood and biochemical tests that may be included in the medical screening of a sports person are: FBC/U+E LFTITFT Glucose Clotting lipids Vit B1/folate Iron/ferritin RBC Mg/zinc Calcium/phosphate/vit 0 UriC acid

ESR/CRP Sickle cell/thalassemia Creatine kinase

Hep AlBIC HIV Urine dipstick Blood group.

In contact sports such as footban, team physicians are increasingly using neuropsychological testing to monitor recovery from concussion (Chapter 17). A team physician might wish to perform baseline testing before the season to use as a comparison in the recovery process.

Musculoskeleta l screening A full injury history should be taken and any deficits remaining post-injury should be fuHyassessed with a view to designing a rehabilitation program to restore full function. This is important as athletes

Screening th e e l ite sportsperson

will often resume athletic participation following a significant injury and yet stilI have considerable limitations in strength, range of movement, proprioception, etc. Thequestionnaire asks the sportsperson to describe the nature and date of any previous injury and list any residual problems. They are asked to describe the nature, date, and symptoms of any current injury.

Which tests? Every musculoskeletal screening should be individually developed to address the specific risks involved in each sport or each sports person. Before deciding whether to include any specific tests to your screening, you must consider what you are trying to achieve with each test. There are multiple reasons for wanting do musculoskeletal screening. These are: to prevent injury to establish a clinical baseline to establish a functional baseline to achieve a holistic picture of the sportsperson. The box below shows information about these reasons.

Prevent injury There is limited evidence to support anyone musculoskeletal screening protocol in terms of preventing injury. There is, however, reasonably good evidence to support a number of different individual tests that may highlight risk of injury and this is the primary goal of screening. It is achieved by finding any physical deficits that may pre-dispose a sports person to injury and then implementing appropriate rehabilitation programs to correct them. For a test to be included on this basis, there should be evidence to show that it is reliable, valid, and predictive of injury. A clinical baseline Having a "normative" value on a test when a sportsperson is fully fit makes a subsequent test far more relevant when the player is re-examined after any injury. The second test results can be seen in context of that particular sportsperson and how he or she presents when uninjured. For a test to be included on this basis, there should be evidence to show that it is both reliable and valid.

When planning a musculoskeletal screening one should start with a spreadsheet that clearly outlines which tests are to be included and why (some tests may fit into more than one categOlY). Ideally this would be supported by references to the supporting literature. See Table 62.1 overleaf for an example of this process-a musculoskeletal screening tool for footballers, where the primary concern is the lower limb.

Imaging As a result of the musculoskeletal history and examination, imaging may be appropriate to help determine the current state of a region (e.g. knee) that has been previously injured. As part of "pre-signing" medicals in high-level sports, the team doctor may deem it appropriate to perform MRI of all vulnerable joints, both to detect any abnormality and to use as a baseline in case of future injury. This is obviously an expensive exercise.

In jury prevention There is limited research evidence showing associations between the presence of certain risk factors and

A functional baseline It is often difficulttodecidewhen a sportsperson who is going through the injury rehabilitation process should be allowed to return to play. Reliable information from functional tests taken when that sports person was uninjured gives a good baseline for comparison and may help you in clearing the person to return to play. For a test to be included on this basis, there only needs to be evidence to show that it is likely to be reliable. A holistic picture of the sportsperson There are many tests that you may consider worthwhile to gain a full insight into an individual player. These may include tests that involve making judgments on the "quality of movement;' on the "feel" of a test, or simply clinical tests that have not yet been proven reliable or involve significant levels of subjective observations. These tests may be included in your screening as part of a holistic approach. However it must be recognized that without any proof of reliability or validity, their results must be taken as part of a general holistic appraisal and not as reliable measures for comparison.

1197

Table 62.1 Musculoskeletal screening tests Football pre-season screening Possibly predicts injury

Clinical baseline measure

Functional baseline measure

Holistic picture

Personal details Age

Games played in past 3 seasons

• • •

Regular strappings Orthotics

• • •

Dominant foot Position Detailed past history of injury Feet and ankles Foot Posture Index

•

Ankle dorsiflexion lunge

*

,

Calf endurance (repeated raises) Achilles palpation Anterolateral drawer Inversion stress test Ankle plantarflexion range

•

Star excursion balance test Posterior impingement sign Midfootfbifurcate ligament test Syndesmosis test (foot external rotation + ankle dorsiflexion) General observation

•

General palpation Knees Effusion-brush/swipe test Passive knee ROM

• •

Patellar apprehension test ACl laxity (Lachman's) PCl laxity (Posterior drawer)

• ,

lCl laxity (DO and 30°)

,

Joint line tenderness

•

Waddle walk (deep f1exion/ rotation/FWB)

•

General observation

• ,

General palpation

1198

Screen in g t he e l ite spor t sperson Football pre -seaso n scree ning Possibly predicts injury

Clinical baseline

Functional

measure

baseline measure

Holistic picture

Hamstrings Isokinetic testing

•

Hamstring le ngth- active knee extension

•

90/90 Hip flexion strength - with dynamometer

•

Sing le-leg hamstring bridges

•

General observation

General palpation

Quad riceps Isokinetic testing

•

General observation

•

Genera l palpation

Hips and groins

Adductor squeeze power- with

•

•

•

•

dynamometer at 45° knee flexion

Hip internal rotation- sitting off

bed Hip external rotation-sitting off

bed Thomas test

•

Hip flexion impingement sign

FABER's sign

Adductor length- bent knee fall out

Anterior hip capsu le tightness Genera l observation

•

General palpation Lumbar spine/sacroiliac joint Flexion (Schober's)

Extension (Schober's) Quadrant pain provocation testing Back m usc le e ndurance - Biering~

•

• • • •

Sorensen Slump neurodynamic test 5U pa in posit ive tests

• •

51) ASLR +/- SIJ closure General observation

• continues

1199

Pr actica l spo rts medicine Table 62.1 Musculoskeletal screening tests continued

Football pre-season screen ing Possibly predicts injury

Clinical baseline measure

Functional baseline measure

Holistic pictu re

•

General pa lpation

Inner core

•

Transvere abdominus/multifidus/ pelvic floor-activation with realtime ultrasound Inner core-most effective cues

Functional testing

•

3 x hop for distance Single-leg hop for height

• •

Multiple hop test Bridging hold test

Quality of movement testing Single-leg deep squats Single leg "running man x 1O"-actlve Trendelenburgs 1,4

decline squat single-leg - active

Trendelenburgs

•

Dynamic lunges Hip/pelvis dissociation exercises

•

Jump landing posture-varus knee control

DF =dorsiflexion; ER;::: external rotation; IR;::: internal rotation; ROM = range of movement; SIJ =sacroiliac joint; FABER"" flex ion abduction external rotation; ASlR "" active straight leg raise; RTUS = real-time ultrasound; ACl = anterior cruciate ligament; pel posterior cruciate ligament; MCl medial collateral ligament; lCl = lateral collateral ligament; FWB = full weight bear

=

=

particular injuries. One example of an association is the presence of menstrual abnormalities or an eating disorder leading to the development of stress fractures. Clinical experience suggests other possible relationships. The medical screening process is an opportunity to identify potentially correctable risk factors and implement measures designed to reduce that risk. It is also an opportunity to ensure that appropriate equipment (such as helmets, mouth guards, and shin pads) is used in relevant sports by asking questions such as: Do you wear orthoses? Do you wear any protective equipment when playing your sport?

1200

Performance screening The screening process is an opportunity to assess areas that may not necessarily have an impact on health but may affect performance. 111ere are components of both the medical and musculoskeletal screening that will highlight deficiencies that may directly affect performance. From the medical screen, issues are nutrition, psychology, and biomechanics. A brief assessment of these areas may suggest a problem that can then be followed up by an appropriate expert. Sports in which competitors have to be under a specified weight (e.g. wrestling, boxing) or where being thin is thought to have some aes thetic (gymnastics) or performance (distance running) advantage provide an additional risk to consider during

Screen i ng the e l ite sports pe rson medical screening. Athletes in these sports may be at an increased risk of unhealthy ea ting habits or the development of an eating disorder. If you are wary of this, common questions that should be included are: Do you have problems making weight for your

sport? Do you follow any specia l diet (e.g. vegetarian,

weight loss)? Have you ever had a nutritional deficiency

diagnosed (e.g. iron, vitamin 8 11 )? From the musculoskeletal screen issues such as decreased muscle strength, joint range. poor joint stability, or poor performance on functional testing may all highlight areas that contribute to suboptimal performance. Any issue that could be suspected of contributing to decreased performance should be discussed in detail among the sports science and medicine teams to achieve the appropriate multidiSCiplinary solutions. The final part of screening to optimize performance m ay also require the input of sports scientists and/or coaches. There are likely to be simple, reli able, sport-specific tests that can be done on players in pre-season to identify weak areas. Team clinicians and coaches can then develop specific programs to address those weaknesses and improve athletic performance. These programs need to be developed in a sport- and athlete-specific way.

Advantages and disadvantages of screening Professional relationship with th e sports person The medical screening process on entry into a professional team or institute program gives an opportunity for the team physician to commence his or her professional relationship with the sportsperson. It enables the physician to become fully aware of the person's past history and gives an insight into the person. The sportsperson is given the opportunity to list on the form any iss ues that he or she would like to discuss with the physician.

Education The medical screening presents an opportunity for the physician to educate the sportsperson on ma ny issues, such as inju ry prevention (stretching, warm-up), immediate inj u ry management (RICE),

nutrition, appropriate equi pment. the use of medications and supplements, and vacci nation s.

Problems Th.ere are a number of problems inherent in the medical screenin g program. There is no uniformity of protocols. Some are very long (up to 40 pages of questionnaire, with fu ll muscle and joint examinations) and are therefore time-consuming for both sportsperson and physician, resu lting in compliance issues. In som e cases multiple screenings are performed by different organizations on the same person. For example, an elite 18-year-old basketballer in Australia may have screenings as part of his professional team , his state or national institu te of sport, the national basketball team, an d the Australian Olympic team. All will probably be slightly different and this represents a waste of time and resources. Ano ther issue is that of follow-up. Often an extensive screening is performed with various recommendations emanating from it. Unfortunately there is frequently no mechanism [or follow-up. We recommend that the examining physician or Chief Medical Officer ICMO) folIows up with tile sportsperson eith er by telephone or in person approximately six weeks after the screening to ensure that the recommended actions have taken place. Who has access to the data from the screening? The spor tsperson? The team or organization? The examining physician? The information obtained from medical screening is bound by the same confidentiality restrictions as any medical in formation. Certai nly, the sportsperson has the right to the information. How the information is presented to the sportsperson is another area of controversy. SportspeopJe who are traveling constantly (e.g. tennis players or golfers on in ternational ci rcui ts) should have the screenin g information in their possession at all times so that the treating practitioner can be made aware of any problems. One suggestion is that traveling sportspeople have a "medical passport" (hard copy and CD-ROM ) containing all relevant information. The confidential medical information obtained at the screening should not be distributed to the team or institute administration. It should be held by the CMO of the organization and forwarded to relevant m edical and paramedical practitioners only as necessary and appropriate for the optimal management of the athlete, and only with the ath lete's consent (see also Chapter 67)120 1

Practica l sports medicine

I§J

RECOMMENDED READING

3·

BestTM. The preparticipation evaluation: an oppommity for change and consensus.

Clil~ J

arrhythmias, long QT syndrome. arrhythmogenic right

Sport Med

ventricular cardiomyopathy/dysplasia, and Bmgada

2004;14(3):r07-8. Bmkner PO, White S. Shawdon A et aL Screening of athletes-the Australian experience. Clin J Sport Med

syndrome.] Electrocardiol 2000;33(SUpplj:I-IO. 4·

200 4;14(3):145-52.

after implementation of a pre-participation screening program. ]AMA 2006;296(13):1593-601.

5·

participation examination? Clill] Sport Med 2011;21;

common lower extremity musculoskeletal screening

6.

Cardiovascular pre-participation screening of young

pre-participation examination? Clill] Sport Med 20U;21(1):18-24· 7·

8.

of the Working Group of Cardiac Rehabilitation and Exercise Physiology and the Working Group of Myocardial and Pericardial Diseases of the European Society of Cardiology. Eur Heart] 2oo5;26(5}:SI6-24. 2.

Maron BJ. Hypertrophic cardiomyopathy. Pllys

Sportsmed 2002;30(t):19-24.

1202

Pelliccia A. Corrado D. Can electrocardiographic screening prevent sudden death in athletes? Yes. BM]

proposal for a common European protocol. Consensus Statement of the Study Group of Sport Cardiology

13-17. Drezner J, Corrado D, Is there evidence for recommending electrocardiogram as part of the

IjJ REFERENCES ,. Corrado D, Pelliccia A, Bjornstad HH et al. competitive athletes for prevention of sudden death:

Borjessoll B, Dellborg M. Is there evidence for mandating electrocardiogram as part of the pre-

Gabbe B1, Bennell KL, Wajswelner H et aL Reliability of tests. Phys I1u:r Sport 20°4:5:9°-7.

Corrado 0, Basso C, Pavei A et al. Trends in sudden cardiovascular death in young competitive athletes

2°°4;14(3): 16 9-77. Fallon KE. Utility of hematological and iron-related screening in elite athletes. Clill J Sport Med

Marcus FI, Electrocardiographic features ofillherited diseases that predispose to the development of cardiac

2010:34 1 :49 230 Bahr R. Can electrocardiographic screening prevent sudden death in athletes? No. BM].2010;34I:'1919.

9·

Holzer K. Brukner PD. Screening of athletes for exercise-induced asthma. Clin] Sport Med 2004:14(3):134- 8.

r 63

Contra ry to popular belief, there most celiai nil' is an "I" in "tea 1'11 . " It is the same "l" that appears three times j.n "respol1 sibility. ,. Amber Harding One of the most challenging yet enjoyable aspects of sports medicine is involvement in team care. Working with a team provides opportunities to: belong to a team and share in its successes and failures

work closely with athletes on a regu lar basis implement preventive strateg ies manage acute injuries from the time of injury

closely monitor the progress of injuries learn and develop decision-making skills in a competitive environment work closely with other clinicians and disciplines

and thereby develop your own skills (e.g. massage, nutrition advice)

liaise closely with coaching and fitness staff better understand the demands of the particular sport understand the psychological pressures on the players fully appreciate the importance of team dynamics.

Many of the skills gained in the team environment can be incorporated into everyday practice.

The off-field team The size and make-up of the medical support team often depends on the size of the sporting team, the standard of competition, and financial considerations. Frequently, the support team will consist of just one individual. who may be either a physiotherapist. physician. massage therapist, or trainer. Specialists from various branches of medicine can contribute to the sports and exercise medicine team. !- J A solo clinician should develop a network of supporting

colleagues who can assist where additional specialized management is indicated. Support teams for professional sports often consist of representatives of different health disciplines. Whoever is responsible for assembling such a team must ensure that all the individuals have high professional standards and work well collectively.4 The ethical issues facing professional teams' clinicians are different from those of volunteer clinicians' (see also Chapter 67).'-' If possible, the professional sporting team should have access to the services of a sports physician, physiotherapist, massage therapist, podiatrist, dietitian, psychologist, orthopedic surgeon. and sports trainer as well as the coaching and fitness staff. Clearly defining roles may help avoid conflict. Ideally, one member of this team should be the leader and take ultimate responsibility for difficult managemen t decision s and the smooth running of the group.

Coaching and fitness staff Clinicians caring for a team have multiple responsibilities. Although their primary responsibility is to the sports people, they also have responsibilities to the coach, the team management, and fellow support staff. Thus, the medical team should liaise closely with the coaching and fitness staff for the sportspeople's benefit. Fitness staff should be included in the regular sports and exercise medicine team meetings to maintain a coord inated approach. This enables the clinicians and fitness staff to have input into injury prevention training programs (Chapter 9)· It is particularly important that medical and fitness staff collaborale closely in injury rehabilitation so 1203

that a player's post-injury rehabilitation transfers seamlessly from the physiotherapist/athletic trainer's care to that of the conditioning coach. Unfortunately, cases have arisen where the player receives conflicting instructions from "competing" members of the rehabilitation team!

Pre-season assessment As team sports have a distinct playing season, all players should be reviewed at the end of a season to plan appropriate individual treatment and offseason rehabilitation. Arrangements for how this will be monitored by the sports clinician should also be made. Similarly, there should be full assessment of all team members at the beginning of pre-season training. New recruits should be evaluated as soon as possible. The pre-season assessment consists of a comprehensive history and examination. The purpose of this assessment is to look for evidence of medical illness and evaluate musculoskeletal conditions. Further tests may be performed if necessary. The assessment is described further in Chapters 61 and 62 and is often carried out in conjunction with a fitness assessment.

Educate team members- health literacy Worldng with a team provides an ideal opportunity to educate sportspeople and coaches. Pre-season assessment provides one opportunity. Other teaching moments arise during follow-up consultations or treatments and in regular brieftalks given to the team by the sports medicine practitioners. Experienced team clinicians have found that relevant topics of education include: injury prevention strategies (e.g. appropriate warm-up, stretching, strength programs, protective equipment) the importance of players reporting injuries early the importance of the first 24 hours in acute injury management a request that the players report any other treatment being received for their injuries nutritional advice advice regarding permitted and banned medications-team members should be told that it is essential that they do not take any medication without checking first with the medical staff.?

1204

In many cases the most important education for athletes in sports that are subject to drug lr~~ testing is advice regarding permitted and banned ~ '0'" medications-team members should be told that 7fJ '3 time zone) for a stay longer than five days, circadian adaptation is desirable.'7. 18 Prefli ght adjustment to travel may speed up adapta tio n.~ o 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

'i'R 4

Ath letes shou ld spend time outdoors, rather than

c

~....... -::. indoors, during the sun light hou rs particularly

"''0""n on arrival at the destination. Natural light resets

I

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circadian rhythm.

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CI ~ 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.

----------------

I I I I

Ambu lance Red zone

I I I

...

I I I I

I I I I

Triage area I I I I I ____________

Main entrance

---- --- -

,,'

,

r - ..... - - - - -. I I I

--

Admission area

.. _--_ .. -

I I I

---- -.- - - - - --- - - -

, -- _... ,

I

f'_ ' _~~-

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r""""""""""""""""" I

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I I I I

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I I I

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I I

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t

-..0- "'- '"

Toilets

I

._----------

I

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)

J. Unsatisfactory progress • reassess • change zone • discharge to hospital

J.

Green zone non-severe

~

Discharge area • record time out offacility • check medical card filled out satisfactorily • record discharge and diagnosis on computer

+--

----+

Red zone severe

Within each zone • · • •

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 'Im' ara"tho~~~~l;Irse with 1000 competitors

Pens and paper for record collection Laptop computer for data entry Athletic trainer's kit

Stretchers (S) Blankets (5) 10 cm (4 in.) and 15 cm (7.5 in .) elastic bandages (6 each)

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, dru g~taking 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

so: NonMapproved substances 1

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

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 in~competition 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)

Anemia secondary to chronic renal disease

Increased endurance

Increased blood viscosity

Human growth hormone (hGH)

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

Myocardial infarction

~

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

~

"0

o

~

inflammatory Severe asthma

Enhancement of oxygen transfer

Blood doping

Nil

Some evidence of performance

~

~

enhancement Improves endurance

3 Transfusion reaction Increased blood viscosity

Artificial oxygen ca rriers (hemoglobin

Provide rapid blood

oxygen carriers, perfluorocarbon

volume expansion

emissions)

following acute blood loss

AAS = anabolic androgenic steroids

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,

~4(',.A While the incidence of AAS use is highest in elite athletes, there is a disturbingly high incidence 7lJV? '0 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 AAS.~ 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

I~ ~ 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),'')' ~o and benign and malignant hepatic tumors. 1 Following the lifting of the ban . the use of pseudoephedrine wa s monitored by WADA and its incidence in testing samples increased dramatically especially among cyclists. While only 0 .2 % of specimens measured between 20 0 1 and 2003 yielded pseudoephedrine 1evels greater than 25 mg/mL. 3.9% of all samples analyzed in 2007/2008 were found to contain more than the formerly exi sting threshold value. 'O) These data sugges t that the misuse of the stimulating agent pseudoephedrine was rather limited as long as the substance was prohibited and that lifting the ban resulted in a much more frequent use aiming for performance enhancement. Consequently. a new threshold value for urinary pseudoephedrine of 150 mg/mL becoming effective in January 2010.

Cocaine Cocai ne is more a community drug prob1em than a drug for performance enhancement. It emerged in the I960 s to become a major health problem. Recently, th e introduction of "crack," a purer form of cocaine, ha s increased the risks associated with its use. Cocaine has a minimal performance-enhancing effect because of the bri ef duration of its action. Decreased fatigue ha s been noticed and cocaine u se causes increased activi ty and talkativeness. The main feeling produced by cocaine is one of euphoria and a sense of wellbeing. The mood elevation appears similar to th at produced by amphetamines but is far more transient. The feeling of euphoria is usually followed soon after by a feeling of dysphoria and craving. This may be overcome by another dose of cocaine. Tachyphylaxis (rapid decrease in the response to a drug due to previous exposure to that drug) occurs following repeated use. The positive effects on athletic performance are minimal. and may be associated with heightened arousal and increased alertness with low doses. Detrimental effects on performance are reported more frequently and include impaired hand-eye coordination, distorted sense of time, and inappropriate aggression. The adverse effects of cocaine are numerous and include:

1250

serio us cardiovascular problems, such as myocardial infarction, cardiac arrhythmia cerebral hemorrhage convu lsion s similar behaviora l changes as occur with the use of amphetamines (page 1248).

The normal clinical use of cocaine is restricted to its use as a topical anesthetic agent in eye and n ose surgery but it cannot be used in sport as a topical anesth etic. Its u se is illegal in most countries and possession of cocaine can carry heavy penalties.

Modafinil In the 20 0 3 World Track and Field Championships, Kelli White was di squalified after her victories in th e 100 m and 200 m sprints when she tested positive for the presence of modafinil. which she claimed she was taking for the treatment ofnarcolepsy. At the time modafinil was not specifically listed on the prohibited list, but th e International Association of Athletics Federations IIAAF) considered that modafinil fell under the category "a nd related substances" for stimu lants and recommended that she be stripped of her m edals. Modafinil is not a classic psychos timulant and it is not clear if it is a performance-enhancing agent. IO "" Those who are prescribed modafinil in the treatment of narcolepsy should apply for a TUE, which requires the diagnosis of narcolepsy to be confir med by on e of the accepted methods le.g, sleep studies in an accredited institution).

Narcotics Na rcotics prohibited in competition are listed in the

box below. Narcotics are derivatives of the opium poppy and include morphine, pethidine. and diamorphine (heroin). They are commonly used in the management of moderate-to-severe pain. In addition to their analgesic effect, narcotics m ay cause: mood disturbances drowsiness

The following narcotics are prohibited in competitionbuprenorphlne, dextromoramide. diamorphine (heroin), fentanyl and its derivatives, hydromorphone, methadone. morphine, oxycodone, oxymorphone. pentazocine. pethidine.

Dr u gs and t he athlete mental clouding constipation nausea

vom iting.

In high doses they may cause: respiratory depression hypotension muscle rigidity addiction

significant withdrawal effects.

Narcotics have no ergogenic effect but have the potential to mask pain and permit athletes to compete with musculoskeletal injuries. For this reason, they are included on the list of prohibited substances. Codeine, dextromethorphan, dextropropoxyphene, dihydrocodeine. diphenoxylate. ethylmorphine. pholcodine, propoxyphene, and tramadol are permitted.

Cannabinoids Cannabinoids that are prohibited in competition are listed in the box below. The products of the cannabis plant such as marijuana. hashish. hash oil. sensernilla , and others are considered to be the most popular illicit drug in the world. The most important compound contained in the plant is the cannabinoids, in which the substance delta-9-tetrahydrocannabinol (THC) is the most significant compound because of its psycho· active properties. The ra te of absorption ofTHC by the lungs is very high. Maximal blood concentrations are obtained after 3- 8 minutes; the onset of action on the central nervous system is observed in approximately 20 minutes. and the peak effect in 2-4 hours. Duration of action for psychoactive effects is 4-6 hours. For occasional users cannabinoid metabolites can be detected in urine up to five to seven days after the exposure. In chronic users it may be detected for as long as 30 days after the last exposure. Since 1989, cannabis has been included on the list of dmgs subject to certain restriction s. A concentration in the urine of carboxy-THe greater

than IS ng/mL has been used to allow for the pos· sible effect of passive smoking. In the 1998 Nagano Winter Olympics, snowboarder Ross Rebagliati tested positive for cannabinoids. was suspended. and was subsequently reinstated. Cannabinoids have a negative effect on sports performance through impairment of psychomotor skills. altered perception of time, and impaired concentration. They may also have a negative effect on exercise performance.'Qj The well-recognized "amotivational" syndrome associated with long-term marijuana use may be particularly damaging to a sporting career.

Glucocorticosteroids All glucocorticosteroids are prohibited in competition (see box). Glucocorticosteroids (Ges) exert many beneficial actions in exercising humans. Glucocorticosteroids increase the availability of metabolic substrates for energy needs of muscles (increased lipolysis and plasma free fatty acids [FFAJ. increased glycogen synthesis) and maintain normal vascular integrity and responsiveness during exercise. In addition. glucocorticosteroids prevent an overreaction of the immune system as a result of exercise· induced muscle damage (immunosuppressive and anti·inflamma tory effects). Cortisol also prepares the organism for the next bout of exercise. explaining why. when an acute bout of endurance·exerci se is stopped. cortisol levels may return to pre·exercise values with a delay hours post·exercise).,06 These physiologic properties of glucocorticosteroids suggest tha t they could enhance performance, and this explains why they are in such widespread use in the s porting world. Indeed. the expected effects of the use and abuse of glucocorticosteroids are numerous-neurostimulatory effects at cerebral glucocorticosteroid receptors could attenuate central impressions of fatigue , and anti-inAammatory and analgesic effects could inhibit sensations of muscle pain on effort and raise the fatigue threshold. The metabolic effects of these compounds consolo idate glycogen reserves in muscle tissue and accel· erate lipolysis and glycolysis mechanisms induced

«2

58: Cannabinoids1 59: Glucocorticosteroids' Natural (e.g. cannabis, hashish, marijuana) or synthetic de lta 9-tetrahydrocannabinol (THe) and

All glucocorticosteroids are prohibited in competition

cannabimimetics (e.g. "Spice" [containing JWH018,

when administered by oral, intravenous, intramuscular,

JWH0731, HU-210l are prohibited.

or rectal routes.

125 1

Practical sp o r ts med i cine

by catecholamines and growth hormone, thereby leading to more efficient use of energy sources by the muscles in the course of exercise. IOG Research reveals inconsistencies regarding the ergogenic effect of glucocorticosteroid administrations in humans. These inconsistencies may be attributed to: the glucocorticosteroid administration dosage,

route, and mode (acute or short term)

Substances prohibited in particular sports in-competition Alcohol The prohibitions relating to alcohol and competitive sport are shown in the box below. Alcohol generally has a negative effect on sports performance, impairing reaction time, hand-eye coordination, accuracy, balance, gross motor skills. and strength. 109

the type, duration, and intensity (submaximal, maximal) of exercise tested the participants (highly trained or professional versus recreationally trained)

.

..

Alcohol (ethanol) is prohibited in-competition only, in

the differences in diet, such as whether or not

the following sports. Detection will be conducted by

experiments are food-controlled and whether or not

analysis of breath and/or blood. The doping violation

subjects fasted

threshold (hematological values) is 0.1 a gIL.

glucocorticosteroid intake coupled or not with intensive training. H)6

a1. '07

Arlettaz et found that after short-term prednisolone (a glucocorticosteroid) administration (60 mg for 7 days) there was a significant improvement of performance (154% compared with placebo) measured by time to exhaustion at 70% to 75% VO "max in healthy, recreationally trained men. To determine if the effects of glucocorticoster. oid treabnent could be extrapolated to elite athletes. Collomp et a1.!08 investigated the influence of shortterm prednisolone administration (60 mg for 7 days) combined with standardized training (2 hours per day) on performance measured by time to exhaustion at 70% to 75% YO "max. Compared with the placebo condition, strenuous training associated with the glucocorticosteroid treahnent resulted in a marked improvement in endurance performance (average increase of about 80% compared with an average increase of 54% in their previous study without training). The health risks of using glucocorticosteroids are well characterized. Long-tenn glucocorticosteroid use may lead to complications, notably on bone tissue (osteoporosis), metabolism (insulin resistance), and the cardiovascular system (hypertension and atherosclerosis). While the inclusion of corticosteroids on the WADA Prohibited List is controversial, there would appear to be sufficient evidence of performance enhancement and health risk to justify their presence. Some'oG would argue that systemic use of gIucocorticosteroids should be prohibited at all times (in and out of competition) and not just in-competition as in the current WADA legislation.! 1252

Aeronautic (FA!) Archery (FGITA, IPC) Automobile (FIA) Karate (WKF)

Motorcycl ing (FIM)

Ninepin and tenpin bowling (FlO)

Powerboating (UIM).

Beta blockers TIle prohibitions relating to beta blockers and com· petitive sport are shown in the box opposite. Beta blockers are drugs commonly used in the treahnent of hypertension, angina, arrhythmia. migraine, anxiety. and tremor; they are also used following myocardial infarction. Their anxiolytic and anti-tremor effects resulted in their use in the sports of shooting and archery where steadiness of hand and arm is important. Beta blockers do not show any other positive effect on performance; in fact, they may have negative effects on both anaerobic and aerobic endurance. Adverse effects may include fatigue, depression, nighhnares, bronchospasm, and sexual dysfunction. Alternative treatments to beta blockers are available for most clinical conditions they are indicated for.

Therapeutic use of a prohibited substance (therapeutic use exemption) Athletes may have illnesses or conditions that require them to take particular medications. If the medication an athlete is required to take to treat an illness or condition happens to fan under the Prohibited Ust, a therapeutic use exemption (TUE) may give

Drugs and t h e ath lete

Unless otherwise specified, beta blockers are prohibited, in competition only, in the following sports: Aeronautic (FAil Archery (FGITA, IPe) (also prohibited out of

competition) Automobile (FIA)

Billiards and snooker (WeBS) Bobsleigh and skeleton (FIST) Boules (CMSB) Bridge (FMB) Curling (WCF) Darts (WDF)

Golf(IGF) Motorcycling (FIM) Modern pentathlon (UIPM) (for disciplines involving shooting) Ninepin and tenpin bowling (FIQJ

Powerboating (UIM) Sailing (ISAF) (for match race helms only)

Shooting (ISSE fPC) (also prohibited out of competition) Skiing/snowboarding (F1S) in ski jumping, freestyle

aerials/halfpipe and snowboard halfpipe/big air Wrestling (FILA).

Beta blockers include, but are not limited to, the fotlowing-acebutolol, alprenolol, atenolol, betaxolol, bisoprolol, bunolol, carteolol, carvedilol, celiprolol, esmolol, labetaloL levobunolol, metipranolol, metoprolol, nadolol, oxyprenolol, pindolol, propranolol, sotalol, timoloL

that athlete the authorization to take the needed medicine. The criteria necessary to be fulfilled to grant "therapeutic use" are all three of:

athletes with documented medical conditions can request a TUE, and have such a request appropriately dealt with by a panel of independent physicians called a Therapeutic Use Exemption Committee (TUEC). Those athletes wishing to take a prohibited substance can begin treatment only after receiving the authorization notice from the relevant organization. TUEs are granted for a specific medication with a defined dosage and specific length of time.

Permitted substances Drug groups permitted by WADA are listed in the box below.

Recently deleted drugs As mentioned above. a number of drugs have been removed from the prohibited list over the past few years and are now being monitored by WADA to detect possible patterns of misuse. TIle most controversial omission is caffeine.

Caffeine Caffeine is the most commonly used drug in the world. It occurs naturally in more than 60 plants and is contained in coffee, tea, chocolate, cola, and various beverages. Until 2004, caffeine was on the prohibited list with urine levels above 12 pg/mL deemed illegal. This was thought to be the equivalent of six to eight cups of coffee. A typical cup of brewed coffee contains about 100 mg of caffeine, the same amount as an Australian No-Doz tablet. (A US No-Doz tablet contains 200 mg of caffeine.) For many years athletes in various sports have been using caffeine in doses below the banned level. A list of the amounts

.. . .

the athlete would experience significant health

Antibiotics Antidepressants

problems without taking the prohibited substance

Antidiarrheals

or method

Antihistamines

", ,

..

.

the therapeutic use of the substance would not

Antihypertensives (excluding beta blockers)

produce significant enhancement of performance

Antinauseants

there is no reasonable therapeutic alternative to

Aspirin (ASA), paracetamol (acetaminophen), codeine,

the use of the otherwise prohibited substance or method.

WADA has issued an International Standard for the granting of TUEs. The standard states that all international federations and national anti-doping organizations must have a process in place whereby

dextropropoxyphene Eye medications Nonsteroidal anti-inflammatory drugs (NSAIDs) Oral contraceptives Skin creams and ointments Sleeping tablets

1253

of caffeine contained in various foods and drinks is shown in Table 66.3. There is clear evidence that caffeine is an ergogenic aid for a variety of sports, although studies involving elite athletes and field sihtations are lacking. Further research is needed to define the range of caffeine protocols and sports activities that show evidence of performance enhancement, as well as the benefits or harm to other issues underpinning recovery after exercise or preparation for an event.HO Newer evidence suggests, at least in endur· ance sports, that the maximal benefits of caffeine are seen at small to moderate caffeine doses (2- 3 mg.kg- l ), which are well within the normal daily caffeine intakes of the general population. This makes the recent decision to remove caffeine from the list of prohibited substances in sports a pragmatic choice. To date, there is little evidence that this change has increased the use or misuse of caffeine by athletes, at least within the levels of elite and sub·elite sport, where anti·doping codes apply. Caffeine use may also enhance the performance of sport in recreational ath· letes, but it is inappropriate and unnecessary for use by young adults.lIO

Non-intentional doping in sports When athletes test positive for a banned substance, they frequently deny the claim and allege circumstances other than intentional doping. Typical defenses include that their drink had been spiked, Tab le 66 .3 Caffeine contained in various foods and drinks Caffeine

passive inhalation of drug smoke, or inadvertent taking of a nutritional supplement or food that contained a prohibited substance. Studies have shown that it is possible that an individual could produce detectable levels of canna· binoids in urine samples only after extremely severe conditions of passive exposure to marijuana smoke. Similarly, only individuals exposed to passive cocaine smoke under extremely harsh condi tions would show cocaine metabolites in a urine sample. Research has indicated that both poppy seedcontaining food Ill and herbal cocoa teaJ\~· II) can produce levels of morphine and cocaine metabolites above the allowed limit. Studies have also shown that it is possible to yield illegal positive results for anabolic agents after consumption of meat originating from animals treated with anabolic agents."~ A number of studies have shown that there is a significant number of "nutritional supplements" that contain substances other than those described on the label, and that a number of these are prohibited substances such as pro·hormones or anabolic steroids. 1I5 The IOC has reported that 1+8% of some 650 products sampled contained levels of banned substances sufficient to result in a positive urine sample. None of the substances carried warnings or product information on the contents. IIG Athletes should be wary of ingesting these supplements. Biotransformation products of permitted sub· stances can also cause an athlete to test positive. One example is the permitted analgesic codeine, which is metabolized to morphine at levels above the threshold.

Food or drink

Serve

content (mg)

Instant coffee

Drug t est ing

250 ml

60

Brewed coffee

250ml

80-100

Tea

250 ml

30

Hot chocolate

250 mL

5-10

Chocolate

60 g bar

50

Coca-Cola

375 ml can

50

Drug testing has become commonplace in both amateur and professional sport. The clinician providing services to the team or individual must be famil· iar with the list of prohibited substances and the drug testing procedure itself. The athlete is entitled to have a representative present to confirm that the correct testing procedures have taken place. Often the representative is the team clinician.

(variable)

Red Bull energy drink

250 ml can

80

Venergy drink

250 ml can

50

lift Plus

250 mL can

36

Black Stallion

250 mL can

80

1254

Testing procedure Selection An athlete can be selected for a drug test at any time (including while injured and/or postoperatively).

Dr ugs and the athlete

Notification An athlete can be notified of their selection for a drug test by a drug control official either: in person (at any time, in or out of competition) by telephone (out of competition) by written notice (out of competition).

The criteria for deciding which athlete is tested vary from event to event. At some competitions, placegetters are tested; at others, competitors are selected randomly; while at other times. certain events may be targeted for testing.

Presenting for a drug test TIle drug control official records the athlete's details on a notification form, which is then signed by the athlete. A copy is kept by the athlete for his/her records. In the presence of the chaperone. the athlete may. receive necessary medical attention attend a victory ceremony fulfill media commitments compete in further events warm~down

eat or drink (at his/her own risk)-during competition events sealed drinks are provided and it is recommended that athletes only consume these nuids until after the testing is completed.

Sample collection The athlete is required to provide a urine sample in the direct view of a drug control official who is the same gender as the athlete. The athlete's representative is not permitted to observe the actual collection of the sample, only the testing procedures and paperwork. A minimum of 90 mL of urine is required for a competition test and 60 mL for an out-o:kompetition test. If there is insufficient sample, the initial sample will be sealed with a temporary seal and additional urine sample(s) will be collected and mixed with the original sample until there is sufficient. Following the collection of the sample, the athlete will return to the doping control area, where a second doping control official will be present, as well as the athlete's representative (if there is one), to complete the sealing of the sample and paperwork. The athlete will be asked to select a sample collection kit, which consists of two bottles (labeled

"/'\' and "B" with identifying numbers) housed in a sealed polystyrene outer case. It is important that the athlete, and his or her representative, checks that the kits are sealed correctly, that the bottles are clean, and that the lids are suitable.

Splitting, sealing, and labeling of the sample The athlete will be asked to pour a measured amount of urine into both the A and B bottles, leaving a small amount behind for the drug control official to test the specific gravity. The athlete will seal the bottles with the self-sealing, one-use only lids provided. The sample code number of the kit will be identified and recorded on the drug testing form.

Checking the concentration of sample The drug control official will check the specific gravity of the sample. If the urine has a specific gravity of less than 1.005, a further specimen is required.

Final paperwork At this stage, the competitor provides the medical declaration. The medical declaration is eXh'emely important. The competitor is asked to list all medications taken in the previous week, including over-thecounter medications, prescription drugs, and other substances taken by mouth, injection, inhalation, or suppository. This list should include all vitamins, amino acids, and other supplements. It is vitally important that this list be completed accurately as all substances taken in that period are likely to show up in the laboratory test. The competitor, his or her representative, and the drug control officer then check an the written information and, if satisfied, sign the drug testing form. The competitor is given a copy of the form. The sealed samples and the section of paperwork that does not disclose the athlete's name are then sent in a sealed bag to an accredited laboratory where the sample is analyzed using gas chromatography and mass spectrometry. Initially only the A sample is analyzed. If the laboratory finds a possible positive test result in the sample in the A bottle, it informs the drug testing agency, which then informs the competitor that a possible positive test result has been recorded. The competi. tor, or a representative, is then entitled to be present at the unsealing and testing of the B sample. If the B sample also proves positive, the relevant sporting organizations are informed. It is the responsibility

1255

Pract i cal sports medici n e of the relevant sporting organization to determine what penalty/sanctions are to be applied following a report of a positive test result. The testing agency does not determine the penalty to apply. WADA has designated penalties to which most sporting bodies now adhere.

The role of the team clinician The team clinician has an extremely important role to play in the prevention and management of doping problems. The primary role of the team clinician should be education of team members. TIlis should involve regular briefings. especially prior to the season. Topics covered should include: the Prohibited List (available at < http://www.wadaama.org/en/World-Anti-Doping-Program/Sportsand~Antj - Doping-OrganizationsjJnternational -

5 ta nda rd sIP ro h ib ited- List!> ) 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

mJ I.

REEERENCES

16. Thiblin I , Lindqui st 0 , Rais

WADA . www,wada-am a,org/en / World-A nti-Doping-

Program/ Spol1s-and-Anti-Doping.Organizat ions!

J Forensic Sci 2000;45=1 6 - 23_ 17. Rich J D, Dicki n son SP , FeUer A et al. T he infectious

In ternational-S tandards/ P rohibi ted· Li$t, 2 0 11 . 2. Harlgen s F, Kuipers H . Effects of androgen ic-an abolic

s teroids in athletes. Sports M uf 2004:34(8):513- 54. 3- Yesalis I I I C E, Herrick RT. Buckley W E et al. Sel f·

complications of anabolic-androgenic steroid injection.

lilt J Sports Med 1999 :20:56 3- 6 . 18. Ishak KG , Zimmerman HJ. Hepa totoxic e ffects of th e an abolic/androgen ic steroids. $'111 Liver Dis 1987:7(3):

reported w;e of anabolic-androge nic ste ro ids by elile power lifters. Phys SportsfIl cd 1988; rG{I2) :gl-B.

230-6.

19. Bagheri SA, Boyer IL Peliosis hepati s associ ated with

4. Lindstrom M, Nilsson AL, Katzman PL e t a1. Use of

a ndrogenic-an abolic s teroid therapy. A severe form of

anabolic-androgenic steroids among body buildcrsfrequency and attitudes. J In /em Mrd 1990;227:407-lI , 5- Buckley W E. Ycsalis C E, Friedl KE ct al. Estimated

prevalence of anabolic-androgenic steroid use among

male high school seniors. JAMA 198 8;260: ]44 1-5. 6. Corbin CB, Feyrer-Melk SA. Phelp s C et al. Anabolic s tero ids: a stud y of h igh school ath letes. Ptd Extrc Sci 1994 ;6:149-58.

Ca basso A_ Peliosis hepatis in a young ad u lt bodybuilder. M, d Sci Sports Exerc 1994:26 (1) :2-4.

21. Creagh T M, Ru bin A, Evans

DJ.

Hepatic tumours

in du ced by ana bolic steroids in an athlete. J elin PClth 19 8 8:4 1 :44 1-3. 22. Klava A, Su per P. Ald rid ge M el al. Body builde r's Jive r. 2] . Cohen L1 , Hartford CG , Rogers GG . Li popro tein (a) and

androgenic steroids by Can ad ian students. eli))] Sport

ch olesterol in body builders using anabolic androgenic

Mtd 199 6:6:9-14.

stero ids. Med Sci Sports Exerc 1996;28{z) :176---9 .

8 . Terney R, Mcla in LG. The use of anabolic s te roids in h igh school s tudents. Am] Dis C/,ild J9 90;14 4:99-103. 9 . Thiblin I, Peterssoll A. Pharm acoepidemio!ogy of anaboli c a ndrogenic steroids: a review. Fund eli"

Phcl1'Il1acoI2004;19:27- 44 ·

I T.

he patic inju ry. Au n lll tem M,d 1971;8 !:610-1 8. 20.

J R Soc Med 1994:87:4 ]- 44.

7. Melia P, Pipe A, Greenberg L The use of ana bolic-

10.

J. Caus(, and m anner of

dea th amon g lIsers of anabolic androgen ic ste roids .

Yesalis C E, Bahrke MS. Ana bolic-androgenic

24. Eben bich ler CF , Sturm W, Ganzer H et al. Flowmed iated emlo theliu m-depcude nl vasodilata tion is impaired in male body b uilders takin g anabolicandrogenic steroids. Atherosclerosis 200 1:158:

4 83- 9 0 . 25 . Kuipers H , Wijnen

fA. Hartgens F et al. InAuence of

ste roids a nd related substan ces. Curr Sports Mt cl Rep

ana bolic s te roid s on body compos ition, blood pressure,

2002; 4 :2 4 6 -)2.

lipid profi le . and liver [unctio ns in body builders . lilt J

Bhasin S, Storer T W, Berman N et al. The effects of suprapbysiologic doses of testos terone on muscle size

Sports Med 1991 ;12:413-18. 26. Ach ar S, Rostamian A, Narayan SM . Cardiac and

and stren gth in n orm al men . N Eng/ ] Mea 1996 :335:

me tabolic effects o f anabolic-androge nic steroid abuse

1- 7·

on lipids, blood pressure, le ft ven tricu lar d imensions .

12. Forbes G B, Porta CR . He rr BE e t al. Sequence o f changes in body composition induced b y testos teronE' and reversal of changes a fter drug is stopped . JAMA 199 2 ;26 7: 397-9.

and rh ythm. A m J Cardio! 201O:1O6 (6 ):893-90l. 27. Melchert RB, Welder AA. Cardiova scu lar effects of androgenic-an abolic s teroids. Med Sci Sports Exerc

199 P7{9}:T252-62.

13. Gio rgi A, Weath erby RP, Mur phy pw. Muscu lar st re llgth , body com position , and health respon ses to

28. Hartgens F, Kuipers H. Body composition , ca rd iovascu lar risk facto rs a nd liver function in lon g-

th e u se of testosterone en an thate: a do u b le blind study.

le rm androgen ic-anabolic steroids usmg body builders

J Sci

three m onths after drug withdrawal. lilt J Sports Med

Mt:d Sport 19 99;2:341- 55.

I4- Sinha· J-1jkim I, Artaza

J, Woodhou se L et aL

Testosterone-ind uced in crease in muscle size in healthy young me n is associated with mu scle fib e r h ypertrop hy. Alii J P/l ysiol Endocrillol Mt:lab 200 2:283:EI54-64,

15 . Parssinen M, Ku jala U, Vartiainen E e t a1. Increa sed

19 9 6 ;IT4 2 9-33· 29. Riebe D, Fernhall B, Tho mpson PD. The blood pressure response to exercise in anabolic steroid use rs .

Med Sci Sports Exerc 199 2:24(6 ):633- 7. 30. Ferenchick GS, Adelman S. Myocardial infarction

prematu re mortali ty of competitive power lifters

associated with an abolic steroid use in a p reviously

su sp ected to h ave u sed an aoolic agents. bll J Sports Mrd

health y 37-year-old weigh t lifter. Am H eart J

2000 :21:225-7·

199 2:124(2):5°7-8.

1257

Prac t ical sports medicine

) 1.

}2.

Sullivan ML. Martinez CM . Gellnis Petal. The cardiac

Effects of anabolic precursors on semm testosterone

1998:41:1-1,.

concentrations and adaptations to resistance training ill

Mochizuki RM. Richter KJ. Cardiomyopathy and cerebrovascula r accident associa ted with anabolicandrogenic steroid use. Pllys SportsUled 1988;18(II):

10 9- 14. 33. 8aggish At. Weiner RB, Kanayama G et al. Long·teml anabolk·androgenic steroid use is associated with left ventricular dysfunction. Cire Heart FaiI2oro;3(4):472-6.

34. Kiraly CL. Androgenic·a nabolic steroid effects on serum and skin surface lipids, on red cells, and on liver enzym es. lilt} Sports Mcd 1988;9:249-52. 35· Walker J. Auams 13. Cutaneous Manifestations of anabolic-androgenic steroid use in athle tes. lilt} D"lIIato/2009:48(lo):1044-8. 36. Bahrke MS, Yesalis III CEo Wright IE. Psychological

young me n. l"t} Sport Nutr fixerc Me/ab 2001;10: 34 0 - 59. 49. We lle S. foze fowicz R, Stat! M. Failure of dehydroepiandrosterone to influence energy and protein metabolism in humans.} Cli" Eudocrillol Me/au 1990;71:1259-64.

50. Kazlauskas R. Designer s teroids. Handb Exp PllIlrmacol 2010:195: 1 55-8 5.

5'- Van Eenoo P, Delbeke FT. Metabolism and excretion of anabolic steroids in doping control-new steroids and new insights.) Steroid Biocllem Mol Biolzoo6;lol: 161-78.

;2. Caitlin DH. Sekera MH. Ahrens BH et a1. Tetrahydrogestrinone discovery, synthesis , and

and behavioural effects of endogenous testosterone

detection in urine Rapid

levels and anabolic·androgenic steroids among males.

2004 :18:1245-9.

Sporls Med '99°;10(5): 3°3-3737. Trenton AI, Cu rrie r GW. Behavior Manifestations of anaboHc ste ro id use. CNS Dmgs 20°5:19(7):571-95.

38. Cooper CJ, Noakes T, Dunne T et al. A high prevalence of personality traits in chronic users of anabolicandrogenic steroid users. Br} Sports Med 1996;3°: 24 6-5 0 . 39. Midgley SJ. Hea ther N, Davies }B. Levels of aggression among a group of anabolic-androgenic steroid users.

Med Sci Law 2001;41:3°9-14. 40. Lubell A. Does steroid abuse cause-or excuse--violence? P/lys Sportsmed 1989:17(2):176-85. 41. Kashkin KB, Kleber H D. Hooked on hormones? An anabolic steroid addiction h}'pOthesis. )AMA

1989:262 (22.):3166-70. 42. larow I P, Lipshultz LI . Ambolic steroid-induced hypogonadotro pic hypogonadism. Am} Sports Med 1990 :18 (4):4 2 9 -}1. 43. Tan RS. Vasudevan D. Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse. Fertil SteriI200p9:203-5. 44. Friedl KE. Yesalis CEo Self-treatment of gynecomastia in bodybuilders who use anabolic steroids. Phys Sport5lllai

19 8 9: 17(3):67- 79. 4;' Rogol AD, Yesalis CE 3rd. Anabolic-androgenic steroids

Callilll i/ ll

Mass Sputrom

53. Malvey TC. Armsey TO. Tet rahydrogestrinone: the d iscovery of a designer steroid. Curr Sports Med Rep 2005:4:227- 30. 54. Death AK. McGrath KCY, Kazlauskas R et al. Tetrahydrogestrinone is a potent androgen and progestin.) Cli" Endocrinol Metab 2°°4;8 9:2498-500.

55. Prather 10, Brown DE. North P et a1. Clenbuterol: a subs titute for anabolic steroids? Med Sci Sport,; Exerc I99P7(8):I II8- 2I. 56. Scott

r. Phillips GC. Erythropoietin in sports: a

new look at an old problem.

CHIT

Sports Med Rep

2005:4:224- 6. 57. Audran M, Gareau R. Mate