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Physical Agents in Rehabilitation From Researchto Practice
Physlcal Agents ln Rehabllltatlon From Research to Practice Second Edition
Stichelle H. Cameron, PT, OCS l:est Lecturer l:aCuate Program of PhysicalTherapy j,.:ruel Merritt College I i
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SAUNDERS An Imynntof Elsevrcr 11830WesthneIndustrralDnve St Lours,Mrssoun63146 JnnO
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PHYSICAT ACENTS IN REHABILITAIION FROM RESEARCH TO PRACTICE Copyright @ 2003, Elsevier. AII rights resenzed.
0.7216-9378-4
No part of thrs pubhcatron may be reproduced or transmrtted rn any form or by any means, electroruc or mecharucal, mcludng photocopyrng, recordmg, or any nformailon storage and retneval system, wrthout permrsslon m wntmg from the pubhsher Permrssronsmay be sought drrectly from Elsevrer's Health ScrencesRrghts Department rn Phrladelphra, You may USA phone. (+ l)215-238-7869, fax. 1+ l)215-238-2239, emul:
[email protected]. also complete your request on-lme vta the Elsevrer Screncehomepage (http:/iwww.elsevrer com), by selectrng 'Customer Support' and then'Obtarmng Permrssrons'.
NOTICE Rehabrhtatron ls an ever-changrng field Standard safety precautlons must be followed, but as new research and clrrucal expenence broaden our knowledge, changes m treatment and drug therapy may become necessary or appropnate. Readersare advrsed to check the most current product mformahon provrded by the manufacturer of each drug to be admrmstered to verfiy the recommended dose, the method and durauon of admmrstratlon, and contrarndrcauons It rs the responsrbrlrty of the hcensed prescnber, relyrng on expenence and knowledge of the patlent, to determrne dosagesand the best treatment for each rndrvrdual patlent. Nerther the Pubhsher nor the author assumes any habrlrty for any mlury and/or damage to persons or properq/ ansrng from thrs pubhcatron.
Prevrous edrtron copyrtghted 1,999 Acqus fironsEdrtor'Manon Waldman DevelopmentalEdttors Sue Bredenstemer,Maqory Fraser PublrchmgSerwcesManage r' John Rogers ProlectManagar- Kathleen L Teal Deugner"Kathr Gosche CoverArt Kathr Gosche Pnnted m the Umted States of Amenca Lastdrgrtrstheprmtnumber'9
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tothememoryof Thisboobis dedicated myhusbandanddearest friend Cameron John rnetoaim high encouraging for I Vutmymindto. methatI coulddo whatever andteaching
Michelle H. Cameron, PT, OCS, is the owner of Health Potentials, a health education and consulting company. Sheis a physical therapist clinician, a teacher, researcher, and author, and now also a full-time medical student at the Universiry of California, San Francisco. She wrote the first edition and the currenr edition of this book, PhysicalAgents in Rehabilrtatrcn: FromResearch toPractice,published by Saunders.In addrtion, her research on phonophoresis is published in PhysicalTheraVy,the Journal of the Amerrcan Physical Therapy Association, and in ClinicalManagementmag-
vl11
azine, and earned her the California APTA Clinician ResearchAward. Michelle has also written and edited numerous articles on electrical strmulation, ultrasound and phonophoresis, and wound management, and wrote the section on ultrasound in Saunders'Manual for Physical TheraVy Practice.Michelle's discussions of ultrasound, electrical sumulation, thermal agents, biofeedback, and wound management bring together current researchand practice to provide the decisionmaking and hands-on tools that support optimal care within today's health care envirorunenr.
Acknowledg*ents First and foremost, I want to thank the readers and purchasersof the first edition of thrs book. Wrthout l"ou, there wouldn't be a second editron. In particular, I would like to thank those readerswho took the time to contact me with their comments, thoughts, and suggestionsabout what worked for them and what didn't. And, special thanks are due Dr. Marjorie -ltoore for her review and input on Frgures 3-4 duough 3-7 inthe chapter on pain. Thank you also to my friends, famtly, and col,eagues.Your ongoing support, encouragement, and patience has kept me h.ppy and relatrvely sane :,hroughthis endeavor and the rest of my hfe. I would also like to give specialthanks to: Andrew Allen, publishing director at Elsevier Science,for his consistent support throughout this nroject; As well as Marion Waldman, executive editor; Sue 3redensteiner, developmental editor; and Marjory
Fraser,ancillary and website developer and editor, for therr ongomg support. The contrrbuting authors to the first edition, including David Selkowitz, as well as those who have been part of both editions, and Sara Shapiro who is new to the team; Sara,for her persistenceand dedication with a job that turned out to be much more than she bargained for; Juhe Pryde, Diane Allen, and Gail Widener, who updated their respective chapters thoroughly and promptly; and Linda Monroe for keeping this text in line with the APTA Cuide to PhysrcalTheraprstPractice,second edition, and keeping my neck healthy through my hours at the computer. MichelleH. Cameron
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Lontrtbutors Diane D. Allen, MS, PT Adj unct Assistant Professor SamuelMerritt College FhysicalTherapist T:nterimHealth Care SanJose,California ChaVter(: ToneAbnormalrties
Linda G. Monroe, MPT, OCS PhysicalTherapist PnvatePractice and Guide to Physical ChaVter5: MotionRestictions TherapistPractice(secondeditioncontent) Suzana Otafro-Lata, MS SiomedicalEngineer 3ostonScientificCorp/Symbiosis 1"[iami,Florida Radiation(firstedrtion) Chayter'12:Electrornagnetic
Diana Perez,BSc,P! MSc lart-time Faculry& CourseCoordinator Faculryof Medicine Schoolof Physicaland OccupationalTherapy l-l.cGillUniversity l"tontreal,Quebec
julie A. Pryde, MS, PA-C, PT, OCS, SCS, ATC, CSCS AdjunctAssistantProfessor SamuelMerritt College Oakland,California PhysicianAssistant Muir OrthopaedicSpecialists Walnut Creek,California and Tissue ReVair Chayter2: Inflammation
Sara Shapiro, MPH, PT AssistantClinicalProfessor Universiryof CaliforniaSanFrancisco GraduateProgramin PhysicalTherapy SanFrancisco,California Owner Apex Wellness& PhysicalTherapy Chayter8: ElectricalCurrents
Gail L. Widerter, PhD, PT AssociateProfessor SamuelMerritt College Oakland, California Chayter4: ToneAbnormaliues
ihysical Therapist l"Ledi -Club Physiother apyand Me dicalWellness Center Radiation(firstedition) Chayter'12:Electromagnetic
xl
Pref^ceto theSecond Edition -:: rvriting the first editron of this book I tned to meet = need that I beheved exrsted-the need for a book -r the use of physical agents in rehabilitatron that -:...ered the breadth and depth of this material in a ::adly accessible and easy to understand manner. - rut together a text that leads the reader from the iasic scientificand physiological prrnciplesunderlying :::e applicatlon of physical agents,to the researcheval:.rng their clinical use, and thence, to the practrcal :.--arlsof selectrngand applyrng each specrficphysrcal :.-nt to optrmize patlent outcome. The enthusrasm ",,,:iewhich the first edition of this book was received, -:-:^udrng complimentary comments, adoption by :-;rly educational programs, and purchase by many :5cians, shows that the need was there and I met it. Given how well the first edition of this book was :r:eived, I was Ieery to make too many changes for --:-:ssecond edition. I have done my best to keep all :::. positive aspectsof the first editron whrle updatrng ::-. in-formatronin all chapters. In addition, the con-.:rs and language of the second editron of the -1-:erican Physical Therapy Associailon's Curde to :;:."sical Therapst Pracficeand the principles of evr:=::ce-basedmedicme have been incorporated rnto *-:s new edition, and a few areashave been clarified ::::nproved in other ways. Updates include consideri: rr1of the most recent researchin all areas,with par:::,ar attention to meta-analyses and systematlc ::l-iews of the literature. Over 50 new illustrauons :,:'"-e been added to clarrfy and update content. In : iirion, all aspects of the text, includrng the case ::;dies, have been modified to be conslstentwrth the -:":'-{eto Phyncal TherapistPractrce,second edrtion.* 1:-e order of the chapters has been changed and, the -1= Preferred Physrcal Theraprst Pracfice PatternsSM are copy:;:-:2002 Amencan PhysrcalTherapy Assocratronand are taken :-i:- rrhe Gwde to Physrcal TheraprstPractue (Gurde to Physrcal T:-::aprst Practrce,2"d Ed. Pht,s Ther 200I,81,9-744) All rrghts :r:,=:-.'ed. Preferred Physrcal Theraprst Practrce PatternsSM rs a :l j.:nark of the Amencan Physrcal Therapy Assocratron
origrnal chapter on traction and compressionhas been drvrded mto two separatechapters,in order to reflect patterns of clmrcal practice rather than the physical propertres of drfferent physical agents.The electrical currents chapter has also been rewritten to make its sfyle, content and level of detail more similar to that of the other chaptersin section rwo of the book. This chapter has been shghtly simplified and shortened while strll thoroughly covering all aspectsof the applicatron of electncal currents rn rehabilitation. In additron to updating this book, there is now comparuon Evolve Online Learning Resources,which is available onlne at hW :/ / evolve.elsevier.com/Cameron The Student ResourceCenter provides a Study Guide with many boards-type multiple-choice questions to help students learn and assess their knowledge. Instructors' resourcesare available to instructors who adopt thrs book. The Instructors' Resource Center rncludes suggestlonsfor laboratory activities, means to assessand document student competence in the selection and application of physical agents, and an electronic image collection of most of the figures in the text. Images in the collection can be copied into PowerPoint presentatlons. The Preface to the First Edition states that this book was intended primarily for physical therapy students and physical therapists although I believed that rt would also meet the needs of physical therapist asslstants,occupauonal therapists, chiropractors and physrcrans,and students m these fields learning about the use of physrcal agents. Since the first edition was releasedrt has come to my attention that many others, including athletic trainers, occupationai therapy assistants,osteopaths,veterinariansand animal trainers also find this book to be a useful tool in their practice. I hope that this new edition continues to meet a wide range of professionals'needs for a readily accessrble, ciear, and thorough text on the appiication of physrcal agentsin rehabilitauon. Michelle H. Cameron xl11
Pref^ceto theFirstEdition Teachingclassesand courseson physical agents,I was =equently asked by ^y students,"ls there a book you '.".'ouldrecommend that covers all this information?" ,rd I would respond, "One of these days I'll write :re.' So, when the phone rang and the person on the :--her end of the line said, "l'm calling from the pub''sher W.B. Saunders.Will you write a new textbook :n physical agents for us?" I immediately said "Yes, ;ue.'Then came the shock, the work, the excite::rent, and now, here, a few years and a few life events "-z.er, that book. is dthough there are other texts on physical agents,I ielieve none cover the information with the same breadth and depth as this one. After reading this book -:-e readerwill be familiar with all the physical agents ':sed by rehabilitation clinicians, including thermal =:ients, water, mechanical agents, and electrical ;gents. The reader will also understand the rypes of :aient problems that can be treated effectively with and the physical properties and phys::-,rz5l.u1agents ::iogical effects of physical agents. Additionally, the :eader will be able to apply this knowledge to select physical agents and treatment parame":propriate ::rs and to use safe and effective application tech::ques in order to optimize patient outcome. The :zader will also have a thorough understanding of -"4-:]yusing physical agents benefits patients, the rypes :: benefits that can be achieved by such interven:ons, and the mechanisms by which such interven:ons produce their effects. This book provides rehabilitation students and ::acticing clinicians with a thorough understanding =:d firm basis for applying physical agents in rehabili-jon. Aithough intended primarily for physical therand physical therapists,this publication ":y'srudents : so meets the needs of physical therapist assistants, : ;c,upationaltherapists,chiropractorsand physicians, =d students in these fields learning about the use of ::lvsical agents.The book is structured to be used by
students as a course text with outlines and objectives at the beginning of each chapter, lists that summarize content throughout the text, and chapter reviews; however, it can certainly be used by practicing clinicians as a reference. There is an accompanying instructor's manual and a study guide available to further facilitate the teaching and learning of the presented information. This book is divided into three sections.The first includes chapters about the physiological processes most commonly affected by the application of physical agents, the second includes chapters about the specific different rypes of physical agents and their application, and the third includes chapters about integrating the application of physical agents with other treatment proceduresand provides suggestions for future research on the application of physical agents in rehabilitation. In Section'l , the reader learns about tissue inflammation and healing, pain, tone abnormalities, and motlon restrictions. This information is presented first so that the information gained from assessment of a patient's presentingproblems can be used in making decisions regarding the selection and application of physical agents. In Section2, rhe readerleams about the specificphysical agentsand their recolrunended clinical uses.Details of contraindicationsand precautionsand specific guidelines for clinical application are presented in consistendy formatted passages that are immediately recognizable and make the material easy to understand and review. The physical and physiological bases for the application of physical agentsare describedfirst, followed by an examination of the researchon the effects of physicai agents,in order to provide a basisfor the recommended clinical application guidelines. This section includes chapters on thermal agents, hydrotherapy, traction and compression, ultrasound, electromagnetic fields and electrial currents.
xvr
Preface to the First Edition
Chapter 6, onthermal agents,describesthe mechanisms and effects of decreasing or increasing tissue temperature and the clinical application of both cooling and heating agents. Chapter 7, onhydrotherapy, describesthe basisfor the therapeutic application of water and provides guidelines for using water to cleanseopen wounds or as an environment for exercise.Chapter B covers the application of mechanical force in the forms of traction and compression;the section on traction focuses on the application of mechanical traction to the spine, while the section focuses on the use of compression for controlling edema. Chapter 10, on electromagnetic agents, describesthe electromagnetic spectrum and the physical agents, including ultraviolet, lasers, and diatherml, that apply electromagnetic radiation to achieve therapeutic effects. Chapter 1.t, on electrical currents, describesthe rypes of electrical currents used in rehabilitation and their application to produce muscle contractions, modulate pain, promote tissue healing, and facilitate transdermal drug penetration. All chapters in Sectionsl and 2 include clmical case studies that illustrate the presented material within the context of patient care and demonstrate the clini-
cal decision-making processesused in selectionof the optimal physrcal agentsand treatment parameters. Section3 integrates the information from the prior rwo sections. Chapter t2 discusses how physical agents may be used in conjunction with each other and with other rypes of interventions. A discussion of how physical agents may be used within the context of different health care delivery systems is also provided in this chapter. The final chapter explains why further research on the use of physical agents in rehabilitation is needed to validate and enable the progress of clinical practice and includes suggestions to direct such research. This is the book on physical agents that I and my students have been looking for. The logical and consistent format of each chapter makes the presented information readily accessible,and the depth of information, complete referencing, and illustratrve case studies facilitate the reader's understanding of how physical agents may be applied safely and effectively to enhance patient rehabilitation. Michelle H. Cameron
Contents z T0 PHYSICAL AGENTS, 1 INTR0DUCTION Definitronsand Examplesof PhysicalAgents,z of PhysicalAgents,z Categories History of the Useof PhysicalAgentsin Medicineand Rehabilitation,+ The Roleof Rehabilitationin PatientCare.s The Roleof PhysicalAgentsin Rehabilitation.o Effectsof PhysicalAgents,z GeneralContraindrcations andPrecautrons for the useof PhysicalAgents,ro ChapterReview,ro
Z: 4 TONE ABNORMALITIES, Dtane D. Allen and (]ail L. Widener Muscle Tone Deftned, za Terminology for Tone Abnormalities, zo Measuring Muscle Tone, 77 The Anatomical Basesof Muscle Tone and Muscle Activation, So Abnormal Muscle Tone and It's Consequences,qj Clinical Case Studies, to+ Chapter Review, ro7
lor RESTRICTI0NS, 5 MOT|ON hnda C. tUlonroe
ONE PATHOLOGY ANDPATIENT SECTION PROBLEMS ,s ANDTISSUE REPAIR, 2 INFLAMMATI0N JuheA. Pryde InflamationPhase(Days1-Q, rs ProliferationPhase(Days3-20),z+ Maturation Phase(Duy 9 On),zo ChronicInflammation,30 FactorsAffectingthe HealingProcess,sz Healingof SpecificMusculoskeletal Tissues,s+ ClinicalCaseStudy,sz ChapterReview,.tZ
+r 3 PAIN, Types of Patn,+z Mechanisms of Pain Reception and Transmission, +5 Pain Modulation and Control, sz Measuring Pain,5zt Pain Management Approaches, 57 Clinical Case Studies,rs Chapter Review, 6;
Introduction. t t z Types of Motion, rrz Patternsof Motion Restriction, 445 TissuesThat Can Restrict Motion, 4'tj PathologiesThat Can CauseMotion Restrictions,,t,tb Assessmentof Motion Restrictions,I tq Treatment Approaches for Motion Restrictions, 't23 The Role of Physical Agents in the Treatment of Motion Restrictions. I 26 Clinical Case Studies, rz7 Chapter Review, rz8
AGENTS TWO THEPHYSICAL SEGTION ISS ANDHEAT, AGENTS: GOLD 6 THERMAL Physical Principles of Thermal Energy, ts+ SpecificHeat, t s4 Modesof HeatTransfer,t s+ erapy, 437 Cold-Cryoth Effectsof Cold.rsa xvrl
Contents
xvlll
z,a CURRENTS, ELECTRICAL
Uses of Cryotherapy, 441 Contraindications and Precautionsfor Cryotherapy, 144 Contraindications for the Application of Cryotherapy, t44 Precautionsfor the Application of Cryotherapy,'t4b Adverse Effectsof Cryothercpy, 44b Application Techniques, r47 Documentation, t55 Clinical CaseStudies,rlt
Heat-Thermother rsa Effectsof.Heat,
SaraShadro
Introduction and History, zzo Terminol ogy for Electrical Currents, 220 Effectsof ElectrrcalCurrents, 227 Clinical Applications of Eiectrrcal Currents, zso ElectricalCurrent in ClinicalPracttce,zsz C ontraindications fo r Electri cal Stimulation, zs7 Precautionsfor ElectricalStimulati on, 238 Documentation, 250 ClrnrcalCase Studies,zsr Chapter keview, zs+
apy,', sa
Uses of SuperfictalHeat, rbz Contraindications and Precautionsfor Thermotherapy, rbz Contraindications for the Use of Thermotherapy, rbs Precautionsfor the Use of Thermothercpy, rb+ Adverse Effectsof Thermotherapy, r66 Application Techniques, t 68 Other Means of Applying Therm otherupy, 't77 DocumentatLon, 't77 Clinical Case Studies,rzz
zar HYDROTHERAPY, PhysicalPropertresof Water,262 PhysiologicalEffectsof Hydrotherapy, zos Uses of Hydrptherapy, zzo Contraindications and Precautionsfor Hydrothe rapy, 278 Contraindications for Local Immersion Forms of Hydrotherapy, zza Precautionsfor Local lmmersion Forms of Hydrotherapy, 27q Contramdrcauons for Full Body Immersion Hydrothe rapy, 280 Precautionsfor Full Body Immerston Hydrotherapy, 284 Precautionsfor Full Body Immersion in Hot or V"ry Warm Water, zrz Precautionsfor Nonimmersion Hydrotherapy, 283 Adverse Effectsof Hydrotherapy, zrs Application Techn iques, z8+ Documentation, 2q5 Safery IssuesRegardingHydrothe rapy, Including Infection Control and Pool Safery,zot Clinical Case Studies,zqs Chapter Review, "toz
Choosing Between Cryotherapy and Thermotherapy, r8o ChapterReview,rBc
rar ULTRASOUNDn History,rso Terminology, t87 Generation of Ultrasound, rg3 Effectsof Ultrasound, rg3 Thermal Effects, rqs Nontherm al Effects, r qs Clinical Applications of Ultrasound, tsb Contramdications and Precautionsfor Ultrasound,zo+ Contraindications for the Use of Ultrasound, zoq Precautionsfor the Application of Ultrasound,zob Adverse Effectsof Ultrasound. zoz Applrcatron Technrque,207 Documentation, 2to Clinical Case Studtes,zr r Chapter Review, zr4
:O; 1 0 TRACTION, Effectsof SprnalTraction, .lo8 Clinical Indications for the Use of Spinal Traction, s to Contraindications and Precautionsfor Spina1 Traction, srz Contraindlcatlons for the Use of Traction, ;2.;
,l::ll:' :lll:i:t: illill
xix
CONTENTS
for the Useof Traction,s,t4 Precautions AdverseEffectsof SpinalTraction,sr7 srs ApplicationTechniques, Documentation.ss+ ClinicalCaseStudies,-tst ChapterReview,ssl
s+o 1 1 COMPRESSION, Effectsof ExtemalCompression,s42 Clinicallndicationsfor the Useof External Compression,3+3 for External Contraindicationsand Precautrons s+9 Compression, Contraindicationsfor the Useof Intermittent or CompressionPumps,s+o Sequential Precautionsfor the Useof Intermittent or CompressionPumps,.t5r Sequential 35.r AdverseEffetsof ExternalCompression, ApplicationTechniques,3t 3 Documentation,3b2 ClinicalCaseStudies,soz ChapterReview,s66
',2 ELECTROMAGNETIC soo RADIAT\0N, -llrchelleIL Cameron.Dtana Perez.and Suzana Otafio-Lata
Physical Properties of Electromagnetic Radia tiorr, szt Physiological Effects of Electromagnetic Radi atiorr, szs PhysicalProperties of Ultraviolet Radiation,sz.r Effectsof UltravioletRadiatron,374 ClinicalIndicationsfor the Useof Ultraviolet Radiation,szt Contraindicationsfor the Useof Ultraviolet Radiation,szz Precautions for the Useof Ultraviolet Radiation,szz AdverseEffectsof UltravioletRadiation.sza ApplicationTechniqves,s7q Documentation,382 SelectingaWLamp,ssz ClinicalCaseStudy,saz PhysicalProperties of Lasers,38.3 Effectsof Cold Lasers,s8t ClinicalIndicationsforthe Useof Cold Lasers.s8b
Contraindlcatronsand Precautionsfor Lasers,:8z Contramdrcationsfor the Use of Lasers,.188 Precauuonsfor the Use of Lasers,.taz PhysicaiPropertiesof Diathermy-Thermal and Nonthermal, .lB8 Typ.r of Diathermy ApplLcators,38q Effectsof Diathermy, 3q2 Clinical Indrcations for the Use of Diathermy,3q3 Contraindications and Precautionsfor Diathermy,395 Contramdrcauons for All Forms of Diathermy,3go Contrandications for Thermal-Level Diathermy, iqb Contraindications for Nonthermal Pulsed ShorwvaveDiathermy, 3q7 Precautionsfor A11Forms of Diathermy, 3q8 Precauilonsfor Nonthermal PulsedShorwvave Diathermy, jgg Adverse Effectsof Diathermy, 3qq Applicatron Techn Lques,i qq Documentatton, 402 Selectrnga Diathermy Devic e, 403 Clinical Case Studtes,/to+ Chapter kevtew, +ob
THREEINTEGRATING SECTION AND AGENTS INTOPRESENT PHYSIGAL PRACTICE FUTURE AGENTS INTO PHYSICAL 13 INTEGRATING PATIENT CARE,+,s Attributes to be Consrderedin the Selectionof Physical Agents,+rb Usrng Physical Agents in Combinatron with Each Other or with Other Interventions, +zo Using Physical Agents within Different Health Care Delivery Systems,+27 Chmcal CaseStudres,+za Chapter Revtew,+.17
RESEARCH AND FORFUTURE 14 DIREGTIONS APPLICATI0N, ++, Why Further Researchon the Physical Agents in Rehabilitation Is Needed, ++z
Contents
Areasfor FutureResearchon Physical Agents,++z of Future MethodologicalCharacteristics Researchon PhysicalAgents,++6 Conclusion,4i3 ChapterReview,+5s
APPENDICES Terms, Used A Glossary of Commonly +ss Abbreviations and B Commonly Used Acronyms, +oo C Unils,+ot
Introductionto Ph icalA7ents :,'i l
SUMMARY
OF
IIVFO RMATlOA/
Definitions and Examplesof PhysicalAgents Categoriesof PhysicalAgents History of the Use of PhysicalAgentsin Medicine and Rehabilitation The Role of Rehabilitationin Patient Care
COVERED
The Role of PhysicalAgents in Rehabilitation Effectsof PhysicalAgents GeneralContraindicationsand Precautionsfor the Use of PhysicalAgents Chapter Review t, ,
,.,.,
OB]ECTIVES UVoncomVletion of this chayter,thereaderwill beable to:
t . Describe, categorize, and compare the types of
5 . Identify the physiologic effects of physical
physical agents used in rehabilitation. 2 . Summarize the history of the clinical application of physical agents. 3 . Explain the role of rehabilitation in patient care. 4 . Explain the role of physical agents in rehabilitation.
agents. 6 . Outline the general contraindications and precautions for the use of physical agents.
'l o Introduction
This book is intended primarily as a course text for those learning to use physical agentsin rehabilitation. It was written both to meet the needs of studenrs learning about the theory and practice of applying physical agents and to assistpracricing rehabilitation professionalsin reviewing and updating their knowledge about the use of physical agents. This book describes the effects of physrcal agents, gives guidelines on when and how physical agents can be most effectively and safely appiied, and describes the outcomes that can be expected from integrating physical agents wrthm a program of rehabilitation. The theory underlying the application of each agent and the researchconcerning its effects are covered to provide a rationale for the treatment recommendations. Information is also provided on the physiologlc processesnfluenced by physical agents in general,and regardingthe specific effects produced by specific agents.After reading this book, rhe reader will be able to integrate the ideal physical agenr(s)and treatment parameters within a complete program of rehabilitation care to promore optimal patient outc om e. This book uses a framework for describing the clinical use of physical agenrs based on rhe Gwde to PhysrcalTherapstPracilce,2ndedttion (herein nored as the Guide).1However, this book presentsmore specific, research-basedinformation regarding the theaU, rationale, assessment process, and treatment parametersfor the applicarion of physical agentsthan provided by the Guide. It is important ro note that the Guide is based on descriptions of preferred practice patterns for selected patient diagnostic groups. These practice patterns are not prescriptive, nor are they based on a review of available research evidence. Following this introductory chapter, the book rs divided into three secrions.The first section covers the different rypes of musculoskeletaland neuromuscuiar problems that may be addressed by the use of physical agents. The second section describes the physical properties, physiologic effecrs, and application techniques for the different rypes of physical agents available.The third secrion integrates information from the first wvo and summarizes how different rypes of problems may be influenced by different physical agenrs, how rreatments with physical agents may be integrated into a patienr's compiete plan of care, and how physical agenrsmay be applied under different health care delivery
to Physical Agents
systems.The final chapter discussesdirectionsfor future researchon the useof physrcalagentsin rehabilitation.A glossaryof termsand abbreviations used in describingand documentingthe apphcationof physicalagentsrs provrdedin Appendx A on pages 456-459.
DEFINITIONS ANDEXAMPLES OFPHYSICAL AGENTS Physicalagentsare various forms and means of applying of energy and materials to parienrs. Physical agents include heat, cold, water, pressure, sound, electromagnetrcradratron,and electncalcurrents.The term Vhysicalagentcan be used to describethe general rype of energy,such as electromagnetic radiation or sound; a specific range within the generaltype, such as ultraviolet radiation or ultrasound and the actual means of applying the energy, such as an ultravioiet lamp or an ultrasound transducer.The rerms Vhysical modality and modality are also frequently used in place of the term yhysical agent and are used interchangeably in this book, with variation for ease of reading.
CATEGORIES OFPHYSICAL AGENTS Physical agents are most readlly categorized as thermal, mechanical,or electromagnenc (Table 1-1). Thermal agents include deep-heatingagents,superficial heating agents, and superficial cooling agents. Mechanical agents include traction, compresston, water, and sound. Electromagnetic agents include electromagneticfields and electricalcurrents.
Thermal Agents Thermal agents transfer energy to a patient to produce an increase or decreasein tissue temperature. Different thermal agents produce the greatestchange in temperature in different rypes and areas of tissue. For example, a hot pack producesthe greatesttemperature increasein superficial tissueswith hrgh thermal conductiviry in the area directly below rt. In contrast, an ultrasound produces the most heat in tissues with high ultrasound absorption coefficlents, such as tendon and bone. It produces this effect up to a depth of 5 cm but only in a small area, approximately twice that of the effective radiating area of the transducer.
4 o INTRODUCTION TO PHYSICAL ACENTS
Thermal
Deep-heatmg agents Superficral heatrng agents Cooling agents
Drathermy Hot pack Ice pack
Mechanical
Tracuon Compressron Water Sound
Mechamcal tracuon Elastrcbandage Whrrlpool Ultrasound
Electromagnertc
Electromagnetlc fields Electrrc currents
TENS
Thermal agents that increase tissue temperature are most commonly appliedwhen increasing of circulation, metabolic rate, and soft tissue extensibiliry or the decrease of pain ire expected to promote the goals of treatment. Thermal agents that decreasetissue temperature are most commonly applied when decreasing circulation, metabolic rate, or pain is expected to promote the treatment goals. A full discussion of the principles underlying the processesof heat transfer, the methods of heat transfer used in rehabilitation, and the effects, indications, and contraindications for applying superficial heating and cooling agents is provided in Chapter 6. The principles and practice of applying deep heating agents are discussedin ChapterT inthe section on thermal applicarions of ultrasound and in Chapter 1,2inthe section on diathermy. Ultrasound is a form of sound that cannot be heard by humans becauseof its high frequency. It is defined as sound with a frequency of greater than 20,000 qgcles/second. Ultrasound a mechanical form of enerry composed of alternatingwaves of compression a.rrdrarefaction. Ultrasound is used as a physical agent :n rehabilitation to produce both thermal and nonthernal effects. Thermal effects, including increased deep and superficial tissue temperature, are produced by :ontinuous ultrasound waves of a sufficient intensiry while nonthermal mechanical effects, including caviadon, microstreaming, and acoustic streaming, are ?roduced by both continuous and pulsed ultrasound. l-hermal-level ultrasound is used for the same pur:oses as other thermal agents when deep tissue is rvolved. These purposes include increasing circula-
Ultravrolet
tion, metabohc rate, and soft tissue extensibiliry and decreasing pain. Ultrasound is applied in a pulsed manner to optlmlze the nonthermal effects and facilitate tissue healing or promote transdermal drug penetration. Further information on the theory and practice of applying ultrasound can be found in Chapter 7.
Agents Mechanical Mechamcal agents apply mechanical force to increaseor decreasepressurein or on the body. Water provides resistanceto increaselocal pressure,hydrostatic pressure to increase circumferential pressure, and buoyancy to decreasepressureon weight-bearing structures. Traction decreasesthe pressure berween structures, and compression increases the Pressure between structures. Water can be applied by immersion or nonimmersion techmques.The therapeutic application of water is known as hydrotherafy. Immersion in water produces pressure around the immersed area, provides buoyancy, and, if there rs a difference in temperature between the area and the water, transfers heat to or from the area.Movement of the water produces local pressure,which can be used as resistancefor exercise when an areais immersed and for cieansingor debriding openwounds with orwithout immersion. Further information on the theory and practice of hydrotherapy is provided in Chapter 9. Tracilon is most commonly used to alleviate pressure on structures, such as nerves or joints that produce pain or other sensory changes or that become inflamed when compressed.Tractron application can
4 c Introduction
normalize sensationand prevent or reduce damage or inflammation of compressed structures. The pressure-relievingeffects of traction may be temporcry or permanent, depending on the nature of the underlying pathology and the force, duration, and means of traction application used. Further information on the theory and practice of applying traction is provided in Chapter 10. Compression is used to counteract tluid pressure and control or reverse edema. The force, duration, and means of application of compression can be varied to control the magnitude of the effect and to accommodate different patient needs. Further information on the theory and practice of applying compressionis provided in Chapter 1,1,.
neticAgents Electromag Electromagneti c agents apply electro magnetrc energy in the form of electromagneticradiation or an electrical current. Variation of the frequency and intensity of electromagnetic radiation changes its effects and depth of penetration. For example, ultraviolet radiation, which has a frequency of 7.5 x 1914so 1915 cycles/second,produces erythema and tanning of the skin but does not produce heat, whereas infrared radiation, which has a frequency of 1011 to L014 cycles/second,produces heat only in superficial tissues. Continuous shorrwave diathertrtl, which has a frequency of 10 million to 100 million cycles/second, produces heat in both superficial and deep tissues. When shortwave diathermy is pulsed to provide a low average intensity of energy,it does not produce heat; however, the electromagneticenergy is thought to modify cell membrane permeabiliry and cell function by nonthermal mechanisms and thus acts to control pain and edema. Further information on the theory and practice of applying electromagnetic radiation is provided in Chapter 12. The effects and clinical applications of electrical currents vary according to the waveform, intensiry duration, and direction of the current flow and according to the rype of tissue to which the current is applied. Electrical currents of sufficient intensiry and duration can depolarize nerves, causing sensory or motor responsesthat may be used to control pain or increase muscle strength and control. Electrical currents with an appropriate direction of flow can attract or repel chargedparticlesand alter cell membrane permeabiliry to control the formation of edema, promote
to Physical Agents
tissue healing, and facilitate transdermal drug penetration. Further information on the theory and practice of electrical current application is provided in Chapter B.
AGENTS HISTORY OFTHEUSEOFPHYSICAL ANDREHABILITATION INMEDICINE Physical agents have been a component of medical and rehabilitation treatment for many centuries and are used acrossa wide variery of cultures. For example, the remains of origrnal bath houses with steam rooms and pools of hot and cold water that can still be seen in many major cities of the ancient Romans and Greeks provide evidencethat these cultures used heat and water to maintain health and treat various musculoskeletal and respiratory problems.2 The health benefits of soaking and exercising in hot water regained populariry many centuries later with the advent of health spas in Europe in the late 19th century in areas of natural hot springs. Today, the pracr tices of soaking and exercising in water continue to be popular throughout the world becausethey provide resistance, thereby allowing the development of strength, endurance, and buoyancy, and reducing weight bearing on compression-sensitivej oints. Other examples of the historic use of physical agents include the use of torpedo fish, in approxrmately 400 n.c., to apply electric shocks to the head and feet to treat headachesand arthritis, and the use of amber in the 17th century to generate static electriciry for the treatment of skin diseases,inflammation, and hemorrhage.3 There are also reports from rhe LTth century of charged gold leaf being used to prevent scarringfrom smallpox lesions.a Before the widespread availabiliry of antibiotics and effective analgesic and antiinflammatory drugs, physical agents were commonly used to treat infection, pain, and inflammation. Examples of such applications include the use of sunlight for the treatment of tuberculosis, bone and joint diseases,and dermatologic disorders and infections, and the use of warm Epsom salt baths for the treatment of sore or swollen limbs. Although physical agentshave been used for their therapeutic benefits throughout history over time, new uses, applications, and agents have been developed, and certain other agents and applications have fallen out of favor. New uses of physical agents have developed as a result of increased understanding of
I o INTRODUCTION TO PHYSICAL AGENTS
the biologic processesunderlying disease, dysfunction, and recovery, and in response to the availability of advancedtechnology. For example, the use of transcutaneous electrical nerve stimulation (TENS) for the treatment of pain was developed based on the gate control theory of pain modulation, as proposed by Melzack and Wall. In contrast, the various modes of TENS application now available are primarily the result of the recent development of electrical current generators that allow fine control of the frequency, intensiry, and pulse duration of the applied electrical current. The use or specific application of a physical agent falling out of favor, usually occurs because the treatment is ineffective or because other, more effective ffeatments are developed. For example, infrared lamps were commonly used to treat open wounds because the superficialheat they provide can dry out the wound bed; however, these lamps are no longer used for this appiication because of the knowledge that wounds heal more rapidly when kept moist.5,6 During the early years of the 20th century sunlight was used to treat tuberculosis; however, since the advent of antibiotics, which are generally effective in eliminatnng bacterial infections, physical agents are now rarely used to treat tuberculosis or other infectious diseases.A number of physical agentshave waned in populariry becausethey are cumbersome,have excessive associatedrisks, or interfere with other aspectsof ffeatment. For example, the use of diathermy as a Ceep-heatingagent was very popular 20 to 30 years ago, but becausethe machines are large and awkward :o move around, can easily burn patients if not used appropriately, and the electromagnetic fields can nterfere with the functioning of computer-controlled equipmentnearby, diathermy is rarely currently used -l the United States. This book focuses on the physical agents most :ommonly used in the United States today. Physical sgents that are not commonly of current use in the ',-nited Statesbut were popular in the recent past, and iose that are popular abroad or are expectedto come back into favor as new delivery systems and applica:ons are developed, are covered more briefly. Also -:rcludedin this book is some discussionof modalities being used abroad that are awaiting :urently :nproval by the Food and Drug Administration (FDA) :er clinical use in the United States.The populariry of :arricular physical agentsand applications is basedon :eir history of clinical use and, in most cases,
research data supporting their efftcacy; however, in some cases,their clinical application has continued despite the lack or limitations of supporting evidence. In most cases,more researchis necessaryto elucidate the ideal treatment and patient characteristics for optimal resultsand the precisenature of the outcomes to be expectedfrom the application of physical agents in rehabilitation.
THEROLE OFREHABILITATION PATIENT IN CARE Rehabilitation is a goal-oriented treatment process designed to maximize independence in individuals who have compromised function as a result of underlying pathologic processes and secondary impairments. Rehabilitation generally addressesthe sequelae of pathology rather than the pathology itself. A number of classification schemes exist to categorrze the sequelae of pathology. In 1980 the Wodd Health Orgaruzation (\MHO) published the first classification scheme known as the International Classification of Impairments, Disabilities and Handicaps (ICIDH).7-eThir scheme, based primarily on the work of Wood, classifies the sequelae of pathology as impairments, disabilities, and handicaps.10,11 Shordy thereafter, Nagi developed a model that classified the sequelae of pathology as impairments, functional limitations, and disabilities.12In L993, the National Center for Medical Rehabilitation Research(NCMRR) published a classificationscheme der:ed from a combination of the Nagi model and the original ICIDH mode1.13Most recently, in2001, WHO further revised their classification scheme in their International Classification of Functioning, Disabiliry and Health (ICIDH-2) scheme.la The models of disability and the language used have been revised over time to reflect and creare changesin perceptions of people with disabilities and to meet the needs of different groups of individuals. The original models were intended to differentiate disease and pathology from the limitations they produced. These models were developed primarily for use by rehabilitation professionals. The new expandedmodels have a more positive perspectiveon the changes resulting from pathology and diseaseand are intended for use by a wide range of people, including communiry, national, and global institutions that create policy and allocate resourcesfor persons with
5
4 o Introduction
disabilities. Specifically,the NCMRR model added a category of societallimitations to the functional problems associatedwith disabiliry and it abandoned the previous linear modeling approach to reflect the frequently nonsequential nature of the relationships bewveen categories.The ICIDH-2 has tried to change the perspective of disabiliry from the negative focus of "consequencesof disease"used in the 1980 model to a more positive focus on "components of health." Thus, while the first ICIDH used categoriesof impairments, disabilities, and handicaps to describe sequelae of pathology, ICIDH-2 uses categories of health conditions, body functions, activities, and participation to focus on abilities rather than on restrictions and limitations. This book usesa scheme consistentwith the terminology and framework of the Cuide to Physical TherapistPractice,2nd edition, which is based on the work of Nagi (Fig. 1-1), to evaluate clinical findings and determine a plan of care for the casestudies presented.l
Pathology Diseaseor injury
Functional limitation Restrictionsin the ability to performcomponents of daily life
Disability Inabilityto performtypical activitiesof daily living
Figure1-1, Ciassificationof the sequelaeof pathology. (Data from American Physicai Therapy Association: Cuide to PhysicalTheraqstPractice,ed 2, Alexandria,VA, 200I, The Associatron.)
to Physical Agents
According to the Nagi scheme, the sequelae of pathology are classified as impairments, functional limitations, or disabilities.T,r2Pathologyrefers to the alteration of anatomy or physiology due to diseaseor injury. Lumbar disc herniation and joint inflammation are examples of pathology. are defined as alterations in Impairments anatomic, physiologic, or psychologic structures or functions as the result of some underlying patholagy.7'rzAn impairment is a measure at the organ or organ system level and is equivalent to a sign or an objective measure. For exampie, decreased cervic mobiliry diminished deep tendon reflexes, and absent sensation are all impairments. Impairments may lead to functional limitations or disabilities. A functional limitation, as defined by the Nagi model, is a restriction in the abiliry to perform an acdviry in an efficient, typically expected, or competent manner. Examples of this classification include an inabiliry to lift more than 20lbs or a limitation in sitting tolerance. The Nagi model, then, defines a disabiliry as the inabiliry to perform activities requiredfor self-care,home, work, or community roles. Examples of disabiliry according to the Nagi model are the inabiliry to lift one's child or to walk to the bathroom at home. While medical treatment is genenlly'directed at the underlying pathology or disease, rehabilitation focuses primarily on reversing or minimizing the associated impairments, functional limitations, and disabilities. Essentially, rehabilitation professionals must assessand set goals not only at the level of impairment, such as pain, decreasedrange of motion, or hypertonicity, but also at the level of functional limitation. These goals should include the patient's goals, such as being abie to get out of bed, ride a bicycle, work, or compete in a marathon.
AGENTS THEROLE OFPHYSICAL INREHABILITATION Physical agents are tools to be used, when appropriate, as components of rehabiiitation. The American Physical Therapy Association's (APTA) position statement concerning the exclusive use of physical agents, published in 1995, states that "Without documentation which justifies the necessiryof the exclusive use of physical agents/modalities, the use of physical agents/modalities, in the absenceof other skilled therapeutic or educational intervention, should not be
,I o INTRODUCTION TO PHYSICAL AGENTS
considered physical therapy.'1s This is a clear statement that the APTA believes that the use of physical agents alone does not generally constitute physical therapy, and that, in most cases, physical agents should be applied in conjuncrion with orher inrerventions. The skilled application of physical agents that constitutes a component of physic altherapy involves the integration of the appropriate intervention(s), which may include the application of a physical agent or agentsor the education of the patienr in such application, into the complete program of a patient,s care to facilitate progress toward the functional goals of ffeatment. The aim of this text is to give clinicians a berter understanding of the theory and appropriate applica:ion of physical agents.Therefore the examples, documentation, and clinical casestudies described focus rn the physrcal agent being discussed.Inclusion of all eossible goals and interventions for a given impair:rrent or iimitation is beyond the scope of this book. Physical agents have direct effects primarily at the -evel of impairment. These effects can then promote -:nprovements at the levels of functional limitation disability. Physical agents are used primarily to "nd :educe or eliminate soft tissue inflammation or circu-atory dysfunction, increase the healing rate for soft ::ssue in1ury, modulate pain, modify tone, increase :onnective tissue extensibiliry and length, remodel --:artissue,or treat skin conditions. For example, ther=al agents can be used to increase circulation and ,:celerate the metabolic rate to acceieratehealing, :::d electrical currents can be used to stimulate sen:1ry nerves to control pain or to stimulate motor :-irves to produce muscle contractions. Physical agents are frequently used in conjunction ',-:fi, or in preparation for, other interventions such as --:-erapeuticexercise, functional training, or manual :-cbrhzation to increase the efficacy of these inter=rtions. For example, a hot pack may be applied :=:ore stretching to increase the extensibiliry of the :::erficial soft tissuesand thus promote a more effec:'.'e and safe increase in soft tissue length when the ,:etching force is applied. r,Vhen considering rhe application of a physical .:ent, one should begin the examination by checking : -r physician's referral, if one is required, for a diag--:;is of the patient's condition and any precautionsto :. observed.The examination should include but nor := jmited to the patient's medical history; subjective : : rplaints; review of systems, tests and meisures;
functional status; and disabilities. The examination findings are then evaluated and, when possible, quantified. Following this analysis, a plan of care is established including anticipated goals. Given an understanding of the effects of different physical agents, the clinician can assesswhether treatment using a physical agent may help the patient progress toward the anticipated goals. The clinician can then determine the treatment plan, including the ideal physical agent(s) and treatment parameters if indicated. The treatment plan is modified, as appropriate, when the patient's outcome is assessed.The sequence of examination, evaluation, and intervention is followed in the casesrudiesin Section 2 of this book. Goals and interventions in this text prim afiIy refer to treatment of impairment with the physical agent(s)being discussed.
EFFECTS OFPHYSICAL AGENTS Modiff inflammation and healing Relieve pain Alter collagen extensibility Modiff muscle tone The application of physical agents primarily resulrs in modification of tissue inflammation and healing, relief of pain, alteration of collagen extensibiliry or modification of muscle tone. A brief review of these processesfollows; more complete discussions of these processes are provided in Chapters 2 through 5.
Inflammation andHealing When tissue is damagedby trauma or disease,it usually responds in a similar and predictable way. The first phase of recovery after damage has occurred is inflammation. This is followed by the proliferative phase of healing, which is completed during rhe maturation phase. Modification of inflammation and tissue healing can result in acceleratedpatient progress toward more active participation in rehabilitation and can expedite achievement of the therapy goals. Faster tissue repair can also reduce the risk and severiry of the adverse effects of prolonged inflammation, pain, and disuse. Thermal agents generally modify inflammation and healing by changing the rate of circulation and the
4 o Introduction
rate of chemical reactions. Mechanical agents control motion and alter fluid flo*, and electromagnetic agents alter cell function, particularly membrane permeability and transport. When selected and applied appropriately, physical agents can acceleratethe completion and resolution of the phasesof tissue healing, stimulate necessaryprocessesto resume if they have stopped, accelerate recoveryj and improve the final patient outcome. Physical agents can also minimize the risk of adverse effects from delayed or incomplete healing. However, if selected or applied inappropriately, physical agents may prolong inflammarion, increasethe severity ofassociatedsymptoms, prevent or delay healing, and increase the probabiliry of adverse consequencesand a poor outcome. A brief review of the processesof inflammation and healing and the factors that influence rheir progression follows; a more complete discussion of these processes is provided in Chapter2. During the inflammatory phase of healing, which generally lasts for I to 6 days, the ceils necessary for removing debris and limiting bleeding enrer the rraumatized area. This phase is characterized by heat, swelling, pain, redness, and loss of function. The more quickly this phase is completed and resolved, the more quickly healing can proceed and the lower the probabiliry of joint destruction, excessive pain, swelling, weakness, immobilization, and loss of function. Physical agents generally assist during the inflammatory phase by reducing circulation, reducing pain, reducing enzyme activiry rate, controlling motion, and promoting progression to the proliferative phase of healing. During the proliferative phase, which generally starts within the first 3 days after injury and lasts for approximately 20 days, collagen is deposited in the dama ged areato replace tissue that was destroyed by the trauma; in addition, if necessary myofibroblasts contract to accelerate closure, and epithelial cells migrate to resurface the wound. Physical agents generally assist during the proliferative phase of healing by increasing circulation, increasing errzyme acdviry rate, promoting coliagen deposition, and promoting progression to the remodeling phase of healing. During the maturation phase, which usually srarrs approximately 9 days after the initial injury and can last for up to 2 years, both deposition and resorption of collagen occur. The new tissue remodels itself to resemble the original tissue as closely as possible to
to Physical Agents
best serve its original function. During this phase, the healing tissue changes both in shape and structure to allow for optimal functional recovery.The shape conforms more closely to the original tissue, often decreasingin size from the proliferative phase, and the structure becomes more organized; thus, greater strength is achieved with no change in tissue mass. Physical agents generally assist during the remodeling phase of healing by altering the balance of collagen deposition and resorption and improving the alignment of the new collagen fibers.
PainControl Pain is an unpleasant sensory and emotionai experience associatedwith or describedin terms of actual or potential tissue damage.16-18puitr usually protects individuals by preventing them from performing activities that would cause tissue damage; however, it may also interfere with normal activities and thus result in functional limitation and disability. For example, pain frequently interferes with an individual's ability to sleep,work, or exercise.Relieving pain can allow patients to participate more fuliy in normal activities of daily living and may acceleratethe initiation of an active rehabilitation program, thereby limiting the adverseconsequencesof disuseand ailowing more rapid progress toward the patient's functional goals. Pain may be due to an underlying pathology, such as joint inflammation or pressure on a nerve that is in the processof resolution, or by a pathology, such as a malignancy, that is not expected to fully resolve. In either circumstance,relieving pain may facilitate resolution of the functional limitations and disabiliry that result from the underlying pathology and can therefore assist the patient. The use of pain-relieving interventions, including physical agents, may be continued as long as pain persists and should be discontinued when the pain resolves. Physical agents can control pain by modi Aing pain transmission or perception or by changing the underlying process causing the sensation. Physical agents may act by modulating transmission at the spinal cord level, changing the rate of nerve conduction, or altering the central or peripheral release of neurotransmitters. Physical agents can change the processesthat causepain by modifying tissue inflammation and healing, altering coliagen extensibility, or modifying muscle tone. The processesof pain per-
4 o INTRODUCTION TO PHYSICAL AGENTS
;eption and pain control are explained in greater Cetailin Chapter 3.
Extensibility Collagen Collagen is the main supportive protein of skin, tenCon, bone cartlTage,and connective tissue.19Tissues -hat contain collagen can become shortened as a :esult of being immobilized in a shortened position or -ceing moved only through a limited range of motion. :-mmobilization may be the result of disuse as a result rf debilitation or peripheral or central neural injury, or :nay be due to the application of an external device such as a cast, brace, or external fixator. Movement nay be limited by internai derangement, pain, weak:tess,or poor posture or may be due to the application rf an external device. Soft tissue shortening may ;ause impairment of restricted joint range of motion, shortened muscles,tendons, or joint capsules. To return soft tissue to its normal functional -ength, thereby allowing fuli rnotion without damagng other structures, the collagen must be stretched. Coliagen can be stretched most effectively and safely 'vhen it is most extensible. Since the extensibiliw oF ;ollagen is temperature dependent, increasing in :esponse to increased temperature, thermal agents are frequently applied before soft tissue stretching to cptimize the stretching process20-24(Frg. I-2). The processesunderlying the development and treatment cf motion restrictions are discussed in detail in Chapter 5.
f o ?h z UJ F
x
UJ
z
ul (5 J J
o () TEMPERATURE Figure1-2. Changesin collagenextensibiliqyin response ro changesin temperature.
9
Muscle Tone Muscle tone is the underlying tension that servesas a background for contraction in a muscle.2s Muscle tone is affected by both neural and biomechanical [actors and can vary in responseto a pathology, expected demand, pain, and position.26Abnormal muscle tone is usually the direct result of nerve pathology or is a secondary sequela of pain due to injury of other tissues."' Central neryous system injury, as may occur with head trauma or a stroke, can result in increased or decreased skeletal muscle tone in the affected area, whereas peripheral motor nerve injury as may occur with nerve compression,traction, or sectioning, can decrease skeletal muscle tone in the aFFected area. For example, a patient who has had a stroke may have increased tone in the flexor muscles of the upper extremiry and the extensor muscies of the lower extremity on the same side, whereas a patient who has had a compression injury to the radial nerve as it passesthrough the radial groove in the arm may have decreased tone in the wrist and finger extensors. Pain may cause an increase or decreasein muscle tone. Muscle tone may be increased in the muscles surrounding a painful injured area in order to splint the area and limit motion, or tone in a painFul area may be decreasedas a result of inhibition. Although protective splinting may prevent further injury as a result of excessive activiry, if prolonged it can also impair circulation, retarding or preventing healing. Decreasedmuscle tone as a result of pain-as occursr for example, with the reflexive hypotonicity of the knee extensors-that causes buckling of the knee, when knee extension is painful, can limit activity and thus result in functional iimitation. Physical agents can alter muscle tone either directly, by altering nerve conduction or sensitivity or by altering the biomechanical properties of muscle, or indirecdy, by reducing pain or the underlying problem causing pain. Normalizing muscle tone will generally reduce Functionallimitations and disabiliry allowing the individuai to improve the performance of functional and therapeutic activities. Attempting to normalize muscle tone may also promote better outcomes from passive treatment techniques such as passive mobilization or positioning. The processes underlying changesin muscle tone are discussedfully in Chapter 4.
10
4 e Introduction to Physical Agents
tion to such tissue.Somephysicalagentsaccelerate the growth or metastasisoFmalignanttissue.These effectsarethoughtto resultfrom increasedcirculation or alteredcellularfunction. Care must also be taken when consideringtreatingany areaof the body that Pregnanry currendy has or previously had cancercelis, since Malignanry malignanttissuecan metastasizeand may therefore Pacemaker be oresentin areaswhere it hasnot yet beendetected. Impaired sensation ih" ,rr" of physicalagentsis generallycontraindiImpaired mentation catedwhen rfreenergyof the agentcanreacha pacemakerbecausethe energyproducedby someof these agentsmay alter the functioning of the pacemaker and thus dangerousiychangethe patient'sheartrate. Restrictionson the use of particulartreatmentinterImpairedsensationand mentationare contraindior freventions are categorizedas contraindications Contraindicationsare conditionsthat render cationsor precautionsfor the use of many physical cautions. a particularform of treatmentimproper or undesir- agentsbecausethe end limit for the applicationof theseagentsis the patienl'sreport of how the treatable,while precautionsare conditionsunder which ment feels. For example,for most thermal agents, be applied should of treatment form a particular the patient'sreport of the sensationof heat being absolute The terms limitations.6 special care or with comfortableor painful is used as a guide to limit be can relative contraindications and contraindications the intensity oFthe treatment.If the patient cannot and precautions, place of contraindications used in feelheat or pain due to impairedsensation,or cannot respectively. report this sensationaccurateiyand consistentlydue and preAlthough the specificcontraindications cautions for the application of particular physical to impaired mentation or other factors affecting agentsvary,a numberof conditionsare contraindica- the ability to communicate,the applicationof the tions or precautionsfor the use of most physical treatmentwould not be safe and is thereforecontraindicated. agents.Thereforecautionshouldbe usedwhen conand precautions,includSpecificcontraindications sideringapplicationof a physicalagentto a patient and featuresto assess patient ask the to ing questions with any of theseconditions.In patientswith such of eachphysicalagent, the application before before conditions,the nature of the reslriction,the nalure this book in eachoFthe 2 of in Section are provided and distribution of the physiologic eFfectsof the types of physical different the chaptersconcerning physicalagent,and the distributionof the energyproagents. The ducedby the physicalagentmust be considered. conditionsfor which treatmentwith most physical or requirecautionarc prcg agentsarecontraindicated REVIEW CHAPTER nancy, malignancy,the presenceof a pacemaker, Physicalagentsarevariousforms of energyandmateimpairedsensation,and impairedmentation. rials and their means of applicationas applied to Pregnancyis generallya contraindicationor prepatients.Physicalagentsinclude heat, cold, water, caution for the application of a physical agent if radiation,and elecpressure,sound,electromagnetic the energy produced by the agent or the physiologic effectsof the agentmay reachthe fetus.These trical currents.These agentscan be categorizedas restrictionsapply becausethe influencesof these thermal, mechanical,or electromagnetic'Physical types of energyon fetal developmentare usually agentshave been used for many centuriesand by many culturesand continue to be used today as a not known and because Fetai development is adversely affected by many influences,some oF comoonentof rehabilitation. Rehabilitationfocuseson the treatment oF the which aresubtle. sequelaeof pathology,includingimpairments,funcor precautionfor Malignancyis a contraj.ndication tional limitations,and disabilities.Physicalagentsare the applicationof physicalagentsif the energyproincludedin rehabilitationcareprimarily to afFectthe ducedby the agentor the physiologiceffectsoFthe agentmay reachmalignanttissueor alterthe circuia- impairments dftecrly, thereby reducing functional
CONTRAINDICATIONS GENERAL FORTHEUSE ANDPRECAUTIONS AGENTS OFPHYSICAL
4 I INTRODUCTION TO PHYSICAL AGENTS
limitation and disability. The use oFphysical agents is generally integrated into a program of patient treatment that includes other interventions to optimize the benefit and outcome. When appropriately selectedand applied, physical agents can promote the resolution of inflammation, acceleratetissue healing, relievepain, increasesoft tissue extensi.bllity, and/or modify muscle tone. Most physical agents should not be applied when the energy provided by the agent or the physiologic effects produced can reach a fetus, malignant tissue, or a pacemaker. In addition, physical agents that use the patient's report as a guide for dosage or intensity should not be applied to patients with impaired sensation or mentation.
l1
11. WagstaffS: The use of the InternationalClassification of Impairments,Disabilitiesand Handicapsin rehabilitation, Physiotherayy 68:548-553,1.982. 12. Nagi S: Disability conceptsrevisited.In Pope AM, Tarlov AR, eds:Disabilityin America:Towarda National Agendafor Prevention, Washington,DC, 1,991,, National AcademyPress, 13. National Institutes of Health: ResearchPlan for the Irlailonal Center for Medical RehabilitarionResearch, Bethesda, I\AD,1993,The Institutes. 14. World Health Organization International Classification of FunctioningDkability and Heahh (ICIDH-2), Geneva, 200l, The Organization. 15. American Physical Therapy Association: Positionon exclusiue useof Vhysicalagentsmodalities, Alexandria,VA 1995,Houseof Delegates ReferenceCommrttee,25-95. 16. Sweet WH: Pain: In lield J, Magoun HW, and Hall WE: Handbook of Physiology, Section I, References Neurophysiology, vol. 1, WashingtonDC,1959,Amer 1. American Physical Therapy Association: Guide to PhysiolSoc,pp. 459-506. PhysicalTheraVistPractice,ed 2, .Alexandria,YA, 2001,, 17. BonicaJJ:Pain:What is sciencedoing about rt?Pain The Association. 2:12-15,1975. 2. JohnsonEW: Back to water (or hydrotherapy),J Bacb 18. Merskey H, ed: Classification of chronic pain: Musculosbel Med 4(4):ix,1.994. Descriptionof chronicpain syndromesand definition 3. BakerLL, McNeal DR, BentonLA, et al: Neuromuscular of pain terms,Pain 13(SupplS):s1,, L986. ElectricalStimulation:A PracticalCuide, ed 3, Downey, 1,9. Dorland'slllustrared MedicalDictionaryed2g,PhiadeIphia, CA, 1,993, LosAmigosResearch & EducationInsrirute. 2000,WB Saunders. -1.RobersonWS: Digby'sreceipts,Ann Med HistT(3):216, 20. Lentell,G, Hetherington Eagan et al: The useof ther! J 1925. mal agentsto influencethe effectiveness of low load proJ. Hyland DB, Kirkland VJ: Infrared therapy for skin longed stretch,J Orthoy SVortPhys Ther 16(5):200-207, ulcers,AmJ Nurs80(10): 1800-1801,1980. 1.992. 5. CummingsJ:Role of light in wound healing.In Kloth L, 21,.WarrenC, LehmannJ,Koblanskii: Elongationof rat tail McCullochJM,IeedarJA,eds: rWo und H ealing:Alternativ es tendon:Effectof load and temperature, ArchPhysMed -474, 484,1.97 inManagement, Philadelphia,1990,FADavis. Rehabil 52:465 1.. -. Melvin JL, Nagi SZ: Factorsin behavioralresponse 23. Warren C, LehmannJ, KoblanskiJ: Heat and stretch to impairments, Arch Phys Metl Rehabil 51.:532-537, procedures:An evaluation using rat tarl tendon, Arch 1,970. PhysMed Rehabil 57:122-126,1976. :. SchenkmanM, Buder RB: A model for muitisystem 24. CerstenJW: Effect of ultrasoundon tendon extensibilevaluation,interpretatioq and treatment of individuals rty,AmJPhysMed34:362-369,1955. with neurologic dysfunction,Phys Ther 69(7):538-547, 25. LehmannJ, MasockA, WarrenC et al: Effectof thera1989. peutictemperatureson tendon extensibility,ArchPhys ;. World Health Organization International Classification of M ed Rehab il 5 I :481-487,I970. Imyairments, DisabilitiesandHandicaVs (ICIDH), Geneva, 26. KeshnerEA: Reevaluatingthe theoreticalmodel under1980,The Organization. iying the neurodevelopmental theory: A literature - -,. Wood PHN: The languageof disablement:A glossary review,PhysTher6I:L035-I040,1981. relatingto diseaseand its consequences, Int RehabMed 27. Brooks VB: Motor control: How postureand move2:86-92,1.980. mentsaregoverned,PhysTher63:664-673,1983.
:€-*'
Pathologyand Patient Problems
Inflammation and ssueReVair JulieA. Pryde,MS, PA-C,PT,OCS,SCS,ATC,CSCS SUM,T,IARY O1 lNFOR -nflammation Phase(Days 1-Q lroliferation Phase(Days 3-20) -\laturation Phase(Day 9 on) lhronic Inflammation
WATlOIV
COVERED
Iactors Affecting the Healing Process Healing of SpecificMusculoskeletalTissues Clinical CaseStudy Chapter Review
OBJECTIVES Uponcomyletionof this chaVtet,the readerwill beable to: Define inflammation and identify its possible causes. Identify the five cardinalsignsof inflammation and tfeir causes. List the phasesof tissueinflammation and repair and their relative time ftames. Describethe four responsesof the inflammatory phase. Discussedemaand its qualitative variability. Describethe four processesthat occur in the oroliferation phaseof healing.
7 . Differentiate between the different types of collagenand their rolesin tissuerepair. 8. Describethe differencesbetween the cellular fesponsesin acute and chronic inflammation. 9. Identify local and systemicfactorsthat can affect tissuehealing. 10. Discusshow different types of musculoskeletal tissueheal. 11. List the physical agentsthat can affect or modify tissuehealing.
13
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Trauma or injury to vascularizedtissueresultsin a coordinated,complexJand dynarnic seriesof events collectively refered to as inflammatiotland re7air. Although there are variationsbenveenthe responses of different tissue t)?es, overall the processesare remarkably similar The sequelaedepend on the sourceand site of injury, the stateof local homeostasis, and whether the injury is acute or chronic.The ultimate goal of inflammation and repair is to restore function by eliminating the pathologicalor physical insult,replacingthe damagedor destroyedtissue,and promoting regenerationof noImal tissuestructure. Rehabilitation professionalstreat a variety of inflammatory conditionsresultingftom trauma, surgical procedures,or problematic healing.The clinicianwho is calledupon to managesuchinjuriesneeds to understandthe physiology of inflammation and healingand how it canbe modified. The cliniciancan enhancehealing by the appropriate application of various physical agentsJtherapeutic exercises,or manual techniques.The foundation for a successful rehabilitation program requiresan understandingof biomechanics,the phasesof tissuehealing,and the effects of immobilization and therapeuticinterventions on the healingprocess. Common Causesof Inflammation Soft tissue trasma (spfains, stfains, and contusions) Fractures Foreign bodies (sutures) Autoirnmune diseases (rheurnatoid arthritis) Microbial agents (bacteria) Chemical agents (acid, alkafi) Thermal agents fturns or frostbite) Irradiation (fV or radiation)
This chapterwill provide readerswith information about the processes involvedin inflammationand tissue repair so they can understand how physical agentsmay be used to modify these processesand rmprovepatrentoutcome. The processof inflammationand repairconsistsof three phases:inflammation,proliferation,and maturation. The inflammation phasepreparesthe wound for heaiing;the proliferationphaserebuildsthe damaged structuresand strengthensthe wound; and the marurationphasemodifiesthe scar ussueinto it' matureform (Fig.2-1).The durationof eachphase variesto some degree,and the phasesgenerallyover-
Figure2-1. Flow diagram of the normal phasesof inflam-^-r^-
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-^-^:-
One o PATHOLOGY AND PATIENTPROBLE\4S
Iap. Thus the timetables for the various phasesof healing provided in this chapter are only general guidelines,not precisedefinitions(Fig.2-2).
(DAYS 1-6) PHASE INFLAMMATION Inflammation, from *re Latrn inllamel meaning "to seton fire," beginswhen the normal physiologyof tissue is alteredby diseaseot trauma.l This immediate protectiveresponseattemptsto destroy,dilute, or isolate the cellsor agentsthat may be at fault. It is a norprerequisiteto healing.Ifthere is no nal andnecessary inflammation,healingcannotoccur.Inflammationcan aisobe harmful, particularlywhen it is directedat the '.vrong tissue or is overly exuberant.Ior example, :nappropriatelydirectedinflammatory reactionsthat '-rnderlieautoimmune diseasessuch as rheumatoid :nhritis can causeexcessivescarrinq,which can be
ul
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10 15 20 25 30 35 40 45 s0DAYSFROM TIMEOFINJURY
s
: gure2-2. Time line of the phasesof inflammation and .,1air.
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15
disfiguring and limit joint mobility. Although the inflammatory process follows the same sequence regardlessof the causeof injury somecausestesultin or prolongationof certalnevents. exaggeration CorneliusCelsusfirst describedthe inflammatory phasenearly2000yearsagoasbeingcharacterizedby the four cardinal signsof calor,rubor,tumor,anddolor (Latin terms for heat, redness,swelling, and pain). Functiolaesa(lossof function) was later addedto this list by Virchow, bringingthe numberof cardinalsigns of inflammationto five (Table2-1). An increasein blood in a given area, known as hyyeremia, accountsprimarily for the increasedtemand rednessin the area of acute inflammaperature tion. The onset of hyperemiaat the beginningof the inflammatory responseis conffolled by neurogenic and chemicalmediators.2Localswelling resultsfrom increasedpermeabiliryand vasodilatationof the local blood vesselsand infiltration of fluid into the interstitial spacesof the injured area.Pain resultsftom the pressureof the swelling and from irritation of painsensitivestructuresby chemicalsreleasedfrom damagedcells.2Both pain and swellingmay result in loss of function. There is somedisagreementin the literatureabout the duration of the inflammationphase.Someinvestigatorsstatethat it is relativelyshort,lastingfor less than 4 days,3'aand othersbelieveit may last for up to This discrepancymay be the resultof indi6 days.5,6 vidual and injury-specificvariationor the overlapping natureof phasesof inflammationand tissuehealing. The inflammatory phase involves a complex sequence of interactive and overlapping events includingvascular,cellular,hemostatic,and immune processes. Humoral and neuralmediatorsact to control the inflammatorv phase.
Z-t Cu.airralSignsof Inflammation Sign (Bnglish)
Sign (Latin)
Heat
Calar
Increasedvascularity
Redness
Rubar
lncreasedvasculariry
Swelling
Tumor
Blockageof lymphatic drainage
Pain
Dolor
Physrcalpressureand/or chemical iIIitation of pain-sensitivestructures
Lossof function
Functiolaesa
Painand swelling
l6
2 . Inllamnratiou nnd fi,,ue kfnir
Vascular Response Alterations in the anatomy and function of the microvasculature, inciuding the capillaries, post-
capiliary venules and lymphatic vessels,are among the earliest responsesin the inflammatory phase.T Trauma.such as a lacerarion.sprain.or contusion physicallydisruptsthesestructuresand may produce bleeding,fluid loss,cell injury and exposureof tissues to foreign matedal,including bacteria.The damaged vesselsrespondrapidiy with transientconstdctionin an attempt to minimize blood loss. This response, which is mediatedby norepinephrine,generailylasts for 5 to 10 minutesbut can be prolongedin the small vesselsby serotonin releasedfrom mast cells and platelets. Followingthe transientvasoconstrictionof iniured vessels,the noninjured vesselsnear the injured areadilate.Capillarypermeabilityis also increased by injury of the capillary walls and in responseto chemicalsreleasedfrom injured tissues(Fig.2,3). The vasodilation and increase in capillary permeability are initiated by histamine, Hageman f a c t o r . b r a d y k i n i n .p r o s r a g l a n d i n a s .n d c o m p l e ment fractions.Vasodilationand increasedcapil lary permeabilitylast for up to t hour after tissue damage.
Histamine is released by mast cells, platelets, and basophils at the injury site.dHistamine causesvasodilation and increased vascular permeability in venules, which contributes to local edema (swelling) formation. Histamine also attracts leukocytes to the damagedtissuearea.9Histamine is activefor approximately t hour after tissue injury10 (Iig. 2-4). Separation of endothelialcell junctionscreates gapsallowing leukocyte to escape
Erythrocytes
lvlarginationof leukocytes on endothelialsudace Figure2-3. Vascular responseto wound healing.
I VasoactiveMediators . Histamine . Serotonin . Bradykinin . Anaphylatoxins . Leukotrienes/ Prostaglandins . PlateletActivating Faclors{PAF)
Chemolactic Factors . FormylatedPeptides . LymPhokines . Monoklnes
Activation ol Plateletsand CoagulationSystem
tt Thfombus Formatron
FlecruitrnenV of Stimulation Inflammatory Cells
vasoaclrve Mediators tl
v
Pe-rea5rlity
IncreasedVascular Pemeability Acute lnflammation . PMNS . Platelets
Chfonic lnflammalion . Macrophages . Lymphocytes . PlasmaCells
Fiqure 2-4. Mediatorsofthe inflammatoryresponse.
One . PATHOLOCY AND PATIENT PROBLEMS
Hagemanfactor (also known as dotring faaor Xll), an enzyme found in the blood, is activated by contact with the negatively charged surfaces of the endothelial lining of vesselsthat are exposed when vesselsare damaged.The role of Hagemanfactor is wvofold. First,it activatesthe coagulationsystem to stop local bleeding. Second, it causes vasoconstrictionand increasedvascularoermeabiliw by actlvatingother plasmaproreins.lt conuert"plasminogen to plasmin and prekallikrein to kallikrein, and it activates the altemative complement Dathw a y r l ( F i 82. - 5 ) . Plasmin augmentsvascularpermeability in botlL the skin and lungs by inducing breakdown of fibrin and by cleavingcomponentsof the complementsystem. Plasminalso activatesHageman factor, which initiatesthe cascadethat generatesbradykinin. Plasmakallikrein attractsneutrophils and cleaves kininogen to generateseveralkinins suchasbradykinin. The ability of a chemical to attuactcells is known as cheffiotaxis. Kinins, suchas bradykinin,are biolog! cally active peptides that are potent inflammatory substancesderived lrom plasma. Kinins function similarly to histamine,causinga marked increasein permeability of the microcirculation.They are most prevalentin the early phasesof inflammation, after
Figure2-5. Hageman factor activation and inflammatory tr p.li, f^r
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they ge rapidly destroyedby tissueproteases
oI Ktnlnases.'"
Prostaglandins(PCEs)are producedby nearly all cellsin the body and are releasedin responseto any damageto the cell membrane.Two prostaglandins affectthe inflammatory phase:PGEl and PGEr.PGE, increases vascuJar permeabilityby anragonizing vasoconstdction,and PCE2atffactsleukocytesand synergizes the effects of other inflammatory mediators such as bradykinin. Proinflammatoryprostaglandins are alsothought to be responsiblefor sensitizingpain receptors.In the early stagesof the healingresponse, prostaglandinsmay regulatethe repair process;they are also responsiblefor the later stagesof inflammation.13 Steroids and nonsteroidalantiinflammatory drugs inhibit prostaglandinsynthesis.Ior example, acetyisalicylic acid (aspirin) and acetaminophen (Tylenol@)disrupt the production of prostaglandins but act at different points in their synthesis.Since prostaglandinsare responsiblefor febrilestates,these medicationsareeffectivein reducinsfever. The anaphylatoxins C3a.C4a.andC5aareimportant products of the complement system. These complement fractions causeincreasedvascularpermeabilify andinducemastce11 and basophildegranultaion, causinga further releaseof histamineand thus potentiatinga further increasein vascularpermeabiliqt QabIe2-2). Aside from the chemically mediated vascular changes, changes in physical attraction betlveen blood vesselwalls also alter blood flow. Durins the initial vasoconstriction. rhe opposingwalls oF the small vesselsbecomeapproximated,causingthe lining of the blood vesselsto stick together Under normal physiologicconditions,the cellmembranesof the inflammatory cells and the basement membranes have mutually repulsivenegative chargesjhowever, after injury this repulsiondecreases and the polarity may actuallybe reversed.This resultsin a decreasein the repulsionberween the circulatinginflammatory cellsandthe vesselwalls andcontributesto the adherenceof inflammatory cellsto the blood vessellinings. As blood flow slows resultins from vasoconstriction of the postcapillaryvenulesandincreasedpermeabiliry of the microvasculature,an increasein the cellularconcentrationoccursin the vessels,resulting in increasedviscosiry In the normal physiological state, the cellular componentsof blood within the microvasculatureare confined to a central axial column,and the blood in conractwith the vesselwall
18
2 . Inflauuntion
2-2 Mediators of the Inflammatorv Response Response
Mediators
Vasodilation
Histamine Prostaglandins Serotonin
Increasedvascular permeabihty
Bradykinin C3a,C5a PAF Histamine Serotonin Prostaglandins
Chemotaxrs
Histamrne Monokines Kallikrein Lymphokines
Fever
Prostaglandins
Pain
Prostaglandins Hagemanfactor Bradykinin
is relativelycelf free plasma.Very early in the inflammatory response,neutrophilsin the circulatingblood begin migrating to the injured area.The sequenceof eventsin the journey of these cells from inside the blood vesselto the tissueoutsidethe blood vesselis known as extavasation. The neutrophils,which are a type of leukocyte(white blood cell),breakaway from t}te centralcellularcolumn of blood and start to ro11 along the blood vessellining (the endothelium)and adhere.They line the walls of the vesselsin a process known as margination. Within t hour, the endothelial lining of the vesselscan be completelycoveredwith leukocytes.As thesecellsaccumulate,they lay down in Iayersin a processknown as yavemetting,Certain mediatorscontrol the adherenceof leukocytesto the endothelium, either enhancing or inhibiting this process. for example, fibronectin, a glycoprotein presentin plasmaand basementmembranes,has an important role in the modulation of cellular adherence to vessel walls. After injury to the vessels, increasedamountsof fibronectinare depositedat the injury site. The adherenceof the leukocytesto the endotheliumor vascularbasementmembraneis critical for the recruitmentof leukocytesto the site of the injury.
nnd Ti<
After margination occurs, leukocytes begin to squeezethrough the vesselwalls in a processknown The leukocytesinsert their pseudopods asdiayedesis. junctions into the betweenthe endothelialcells,crawl *rrough the widened junctions, and assumea position betlveen the endothelium and the basement membrane.Then, attracted by chemotacticagents, *rey escapeto reachthe interstitium.This processof leukocytemigration from the blood vesselsinto the perivasculartissuesis known asezgrationFlg.2-C1. Edema is an accumulation of fluid within the extravascularspaceand interstitial tissues.Edemais the result of increasedcapillaryhydrostaticpressure, increasedinterstitial osmotic pressure,and an overwhelmed lymphatic systemthat is unableto accommodate this substantialincreasein fluid and plasma proteins.Edemaformation and control are discussed in detail in Chapter 11.The clinicalmanifestationof edemais swelling. The fluid that first forms edemadurins inflammation has very few cells and very litcle piotein. This fluid is known astransudate. Transudateis madeup of predominandydissolvedelectrolytesand water and has a specificgravity of lessthan 1.0.As the permeability of the vesselsincreases,more cellsand lower molecular weight plasma proteins cross the vessel wall, making the extravascular fluid more viscousand cloudy. This cloudy fluid, known as exudate,has a specificgravity of greaterthan 1.0.lt is alsocharactertzed 6y a high content of lipids and cellular debris. Exudateis often observedearly in the acute inflammatory processand forms in responseto suchminor injuriesasblistersand sunburns. The loss of protein-rich fluid from the plasma reducesthe osmotic pressurewithin the vesselsand increasesthe osmotic pressureof the interstitial fluids.which. in turn. increasesthe outflow of fluid from the vessels,resultingin an accumulationof more fluid in the interstitial tissue.When the exudate'sconcentration of leukocytesincreases,it is known as prs or supFurative exudate.Pus consistsof polymorphonuclear neutrophils, liquefied digestion products of underlyingtissue,fluid exudate,and very often bacteria if an infection is present.When localizedsuppurative exudateoccurswithin a solid tissue,it resultsin an abscess, a localizedcollectionof pusburiedin a tissue,organ,or confined space.Pyogenicbacteriaproduceabscesses. Fourmechanismsare responsiblefor the increased vascularpermeabilityseenin inflammation.The first
One . PATHOLOCY AND PATIENT PROBLEX'IS
19
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Chemoanractant
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:erris. nor ma tnd fluom .uid to!
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Sour"" o, ,nru,, Figure2-6. Illustration of leukocytic events in inflammation: margination, adhesion, diapedesis,and emigration in responseto a chemoattractantemanatingfrom the sourceof the iniury
and predominantmechanismis endothelialcell conraction, which leadsto a widening ofthe intercellular iunctions or gaps. This mechanism affects venules ',vhilesparingcapillariesand arterioles.It is controlled by chemicalmediators and is relatively shortJived, lastingfor only 15to 30 minutes.laThe secondmech anismis a resultof direct endothelialinjury and is an immediate, sustainedresponsepotentially affecting all levelsof the microcirculation.This effect is often seenin severeburnsor lytic bacterialinfections,andis often associatedwith plateletadhesionand thromboendothesis or clot formation. Leukocyte-dependent iralinjury is the third mechanism.Leukocytesbind to lhe area of injury and releasevarious chemicalsand enzvmes that damase the endothelium and thus
increasepermeability.The final mechanismis leakage by regeneratingcapillariesthat lack a differentiated endothelium and therefore do not have tight gaps. This may accountfor the edemacharacteristicof later healinginflammatror.(Frg.2-7).
Response Hemostatic The hemostaticresponseto injury controlsthe blood losswhen vesselsare damagedor ruptured.Platelets, the first cellsat the siteofthe injury enterthe areaand bind to the exposedcollagen,releasingfibrin to stimulate clotting. Plateletsalso releasea regulatoryprotein known as Vlareletderivedgrowthfaaor (PDCF), which is chemotacticand mitogenic to fibroblasts
20
2 . Inflammation and TissueRepair
MECHANISM OF LEAKAGE ANDDISTRIBUTION
Endothelial contraction . venules
Directinjury . all microvessels
Leukocyte-dependant . mostlyvenules .lungcapillaries
Regeneraling endothelium . capillaries . olhervessels
Arteriolar dilatation
Openingof capillary beds
Venular dilatation I
Increased bloodtlow B Figure2-7. A, Illustration of four mechanismsof increasedvascularpermeability in inflammation. B, Vascularchanges associatedwith acute inflammation
and may alsobe chemotacticto macrophages, monocytes,andneutrophils.lsThus plateletsplay a role not only in hemostasisbut also contdbute to the control of fibrin deposition, fibroblast proliferation, and angiogenesis.
When fibrir and fibronectin enter the injured area they form cross-linkswith the collagento createa fibrin lattice.This tenuousstructur€providesa temoorary plug in the blood and lymph vessels,limiting local bleedingand fluid drainage.The lattice sealsoff
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Ore . PATHOLOCY AND PATIENTPROBLEMS
damagedvesselsand confinesthe inflammatory reaction to the areaimmediately surroundingthe injury The damaged,pluggedvesselsdo not reopenuntil later in the heaiingprocess.The fibrin latticeservesas the wound's only sourceof tensilestrengthduringthe inflammatoryphaseof healing.l6
Response Cellular Circulatingblood is composedof specializedcells suspendedin a fluid known as ylasma.These cells include erythrocytes (red blood cells), leukocytes (white blood cells),and piatelets.Redblood cellsplay a minor role in the inflammatory process,although they may migrateinto the tissuespacesif the inflammatory reactionis intense.The primary role of the red blood cells,oxygentransport,is carriedout within the confinesof the vessels.Art inflammatory exudatethat containsblood usually indicatessevereinjury to the microvasculature. The accumulationof blood in a tis sueor organis refeffed to asa hematama; bloody fluid that is present in a joint is called a hemarthrosis. Hematomas in muscle can cause pain and limit m o r i o no r f u n c t i o nr:h e yc a na l s oi n c r e a ssec a r i s s u e formation. A critical function of inflammation is to deliver leukocytesto the area of iniury via *re circulatory system.Leukocytesare classifiedaccordingto their structure into polymorphonucleocytes(PMNs) and mononuclearcells. PMNs have nuciei with several lobes and contain cytoplasmic granules.They are Furthercategorized,by their preferencefor specific histological stains, as neutrophils, basophils, and eosinophiis.Monocytes are larger than PMNs and have a singlenucleus.ln the inflammatory process, leukocytes play the important role of clearing the injured site of debris and microorganismsto set the stagefor tissuerepair(Fig.2-8). Migration of leukocytes into the area of injury occurswithin hours of the in1ury.Eachleukocyte is specialized and has a specificpurpose.Someleukocytes aIe more prominent in early inflammation, whereas others become more impoftant during the later stages.Initially the number of leukocytes at rhe injurysiteis proporrional to theirconcenrration in the circulatingblood (Table2-3). Sinceneutrophils have the highest concentration in the blood, they predominatein the early phasesof inflammation. Chemotacticagentsreleasedby other cells,suchas mast cellsand platelets,attractleuko-
CONNECTIVE TISSUE I\,IATRIX
27
VESSELS
CONNECTIVE TISSUE CELLS
A
Basement
@
membranel Collagentype lV Laminin Fibronectin Proteoglycans Entaclin
Mastcell
n
rioroorast Itl
Elasticfibers
V
td'.\
rg
Collagen fibers
l\,4acrophage
d\+d Proteoglycans
-----,--J
Basophil Figure2-8. Intravascular cells, colnective tissue matdx, and cellsinvolved in the inflammatory response.
$ g
2-3 Cot ."ntration of Leukocytes in Adult Human Blood Typ"
Concentration
Poly morphonuclear Cells Neutrophils Eosinophils Basophils
62.0./. 23% 0.4./.
Mononucleat Cells Monocytes Lymphocytes
5.3./. 30.0%
cytes at the time of injury. Neutrophils rid the injury site of bacteria and debris by phagocytosis. When lysed, the lysosomes of the neutrophils release proteolytic enzymes (proteases)and colwhich begin the lagenolyticenzymes(collagenases),
22
2 c lttllatttttntion
debridementprocess.Neutrophils remain at the site of the injury for only 24 houri, after which time they disintegrate.However, they help to perpetuatethe inflammatory response by releasing chemotactic agentsto attractother leukocytesinto the area. Basophils release histamine after injury and contribute to early increasedvascularpermeability. Eosinophilsmay be involvedin phagocytosisto some degree. Ior 24 to 48 hoursafteran acurernjury.monocytes predominate. Monocytes make up bewveen 4o/o and 8% of the total white blood cell count. The predominanceof thesecellsat this staseof inflammation is thoughr to resuk in parr from rheir longer lite span.Ly'rnphocytessupply antibodiesto mediatethe body's immune response.They are prevalent in chronicinflammatory conditions. Macrophage Products Proteases Elastase Collagenase Plasminogen activator Chemotactic factors fot other leukogztes Complement components of the alternative and classical pathways Coagulation factors Growth-promoting factors for fibroblasts and blood vessels Cl'"tokines Arachidonic acid metabolites Monocytes are converted into macrophages when they migrate from the capillaries into the tissue spaces. The macrophage is considered the most important celi in the inflarnmatory phase and is essen-
nnd Tisstc Reyair
tial for wound healing.Macrophagesare important becausethey produce a wide range of chemicals. They play a major role in phagocytosisby producing enzymes such as collagenase(Fig. 2-9). These enzymesfacilitatethe removal of necrotictissueand bacteria.Macrophagesalso produce factors that are chemotacticfor other leukocytes. Macrophagesalsoprobablyplay a role in localizing the inflammatory processand attractingfibroblaststo the injuredareaby releasingchemotacticfactorssuch as fibronectin. Macrophages chemically influence the number of fibroblastic repak cells activated; therefore,in the absenceof macrophages,fewer, less mature fibroblastsmigrateto the injuredsite. Platelet derived growth factor (PDGI) releasedby platelets during clotting is also releasedby macrophagesand canactivatefibroblasts.In the later stagesof fibroplasia,macrophagesmay also enhancecollagendeposition by causingfibroblaststo adhereto fibrin. As macrophages ingest microorganisms, they excreteproductsof digestionsuchashydrogenperoxide, ascorbic acid, and lactic acid.17Hydrogen peroxideassistsin the control of anaerobicmicrobial growth. The other two products signal the extent of the damagein the area, and their concentration is interyreted by the body as a need for more macrophagesin the area.l8This, in turn, causes increasedproduction of by-products, which then resuitsin an increasedmacrophagepopulation and a more intenseand prolongedinflammatoryresponse. Macrophagesare most effectivewhen oxygen is presentin the injured tissues.However,they can toleratelow oxygen conditions,as is apparentby their presencein chronic inflammatory states.Adequate oxygentensionin the injuredareais alsonecessaryto minimizethe riskof infecrion.I issueoxygentension
Macrophage
Figure2-9. Diagrammatic repres€ntationof the processof phagocl,tosis.
Oqe . PATHOLOCY AND PATIENT PROBLEMS
nt t-
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dependson the concentrationof atmosphericoxygen available for breathing, the amount of oxygen absorbedby the respiratoryand circulatorysystems, and the volume of blood availablefor tlansDortation. as well as rhe stare of the tissues.Local topical application of oxygen to an injured area does not influencetissueoxygen tension as much as the level of oxygenbrought to the injured areaby the circuiating blo6d.le-2t
lmmune Response The immune responseis mediated by cellular and humoral factors. The roles of lyrnphocytes and phagocyticleukocytesin the immune responsewere discussedpreviously.The other mechanisminvolved in the immune responseis the complementsystem which is an important sourceof vasoactivemediators. The complementsystemis one of the most important plasmaprotein systemsof inflammation as its components participate in virtually every inflammatory
ClassicalPathway Activated by immune complexes of antibodies withantigens
23
response.The complementsystem can be activated by antigen-antibodycomplexesand by bacteria,foreignmaterial,and other cellularproducts. The complementsystem is a seriesof enzymatic plasma proteins that is activated by two different pathways, the classical and the alternative.22 Activation of the first componentof either pathway of the cascaderesults in the sequentialenzymatic activationof the downstreamcomponentsof the cascade(Fig.2-10).The end product of the cascade,by either pathway, is a complex of C6, C7, C8, and C9, which form the membraneattack complex (MAC). The MAC creates pores in plasma membranes, *rereby allowing water and ions into the cell. This causesloss of membraneintegrity and cell lysis. The subcomponents generated earlier in the cascade also have important functions. Activation of components C1-C5 produces subunits that enhance inflammationby making bacteriamore susceptibleto phagocytosis(known asopsonization), attractingleukocytes by chemotaxisand acting as anaphylatoxins.
AlternativePathway Activated by cell surfaces
ActivatesClr+C1s
Ite
to on
ActivatesC6, C7, C8, C9 to form membraneattack complex (MAC)
Figure2-10. Overview of the complement system- classicaland alternativeactivation pathways.
24
2 . ltrflarnrnatiortntt/1 li.,ttc Rcfatr
Anaphylatoxinsinducemastcellandbasophildegranu- the classical pathway, C1, C2, and C4 are not lation, causing the release of histamine, platelet involved in the alternativepathway. activatingfactot and leukotrienes.Thesefurther proln summary therearethreemajor consequences of mote increasedvascuiarpermeability. the inflammatory phase.Iirst, fibrin, fibronectin,and The classicalpathway of the complement cas- collagencross-linkto form a fibdn lattice that limits cade is activated by an antigen antibody complex blood loss and providesthe wound widr some initial interactingwith *re first componentof the complestrengdr.Then macrophagesbegin to remove damment cascade, C1.C1 consistsof threeproteins:C1q, aged tissue.finally, endothelialcells and fibroblasts C l r . a n d C l s . C i q b i n d s t o t h e a n t i g e n - a n t i b o d y are recruitedand stimulatedto divide. This sets the complex, resultingin a conformationalchange.Clr stagefor the proliferationphaseof healing(Table2-4). enzymaticallyactivatesC1s so that it can act on C4 and C2. C4 and C2 are cieavedro form C4bC2a,a (DAYS PR0LtFERATt0N PHASE 3-20) complex that acts as a C3 convertase.C3 is cleaved into C3b and C3a by the C3 convertase.C3b then The secondphaseof tissuehealingis known as the cleavesC5, producingC5aand C5b. C5b activatesthe yhase.Thisphasegenerallylastsfor up to Vroliferation production of the terminal products of the cascade, 20 daysand involvesboth epithelialcellsand connecc6-c9. tive tissues.lo Its purposeis to coverthe wound and The alternativepathway of the complementcas- impart strengthto the injury site. cadeis activatedby a variety of cellularand microbial Epithelial ceils form the covedng of mucous and productsand by foreign material.The binding of C3 serousmembranes,and the epidermis of the skin. with tlvo plasmaproteins,factorsB and D, catalyzes Comective tissueconsistsof fibroblasts,ground subthe conversionof C3 to C3bBbwhich functionsas a stance,and fibrous strandsand providesthe structure C3 convertasegeneratingadditional C3a and C3b in for other tissues.The structure,strength,and elastican amplificationstep.C3b then cleavesC5, resulting ity of conn€ctivetissuevariesdependingon the type in the formation of the MAC, C6-C9. In contrastto of tissueit comorises. Fourorocesses occursimultane-
p
,-O ,"--ary
of Eventsof the InflammatoryPhase
Response
Changes in the injured area
Vascular
Vasodilationfollowed by vasoconstnctionat the capillaries,postcaprllaryvenules,and lymphatics Vasodilationmediatedby chemicalmediators histamine,Hagemanfactor,bradykimn, prostaglandins, complementf ractions Slowingofblood flow Margination,pavementing,and ultimatelyemigrationof leukocytes Accumulationof fluid in the interstitialtissuesresultingin edema
Hemostatic
Retractronand sealingoff of blood vessels Plateletsform clotsandassistin burldingoffibrin lattice,which servesasthe wound's sourceoftensile strengthin the inflammatoryphase
Cellular
Delivery ofleukocytesto the areaof injury to rid the areaof bacteriaand debrisby phagocl,tosrs Monocytes,the precursorsof macrophages, areconsideredthe most important cellin the inflammatoryphase Macrophagesproducea numberofproducts essentralto the healingprocess
lmmune
Mediatedby both cellularand humoralfactors Activationof the complementsystemvia the alternativeand classicalpathwaysresultingin componentsthat increasevascuiarpermeability,stimulatephagocytosrs, and act aschemotactic stimuli for leukocytes
One . PATHOLOCY AND PATIENT PROBLEMS
they begin to align themselvesperpendicuincreases, lar to the capillaries. The fibroblastssynthesizeprocollagen,composed of three polypeptide chainscoiled and held together by weak electrostaticbondsinto a triple helix. These chains undergo cleavageby coilagenaseto form Epithelialization tropocollagen.Multiple tropocollagen chains then :oithelialization, *re reestablishmentof the epider- coil together to form collagen fibrils, which then make up collagenfilaments and ultimately combine ::ris,is initiated earlyin prolilerationwhen a wound is ..rperficial.often within a few hours of injury73 to form collagen fibers (Fig. 2-13). CrossJinking .\tLena wound is deep,epithelializationoccurslater, between collagenmoleculesprovides further tensile =:ter collagen production and neovascularization. strengthto the injuredarea. Tissue containing the newly formed capillaries, :oithelialization providesa protectivebarrierto pre-.ent fluid and electroly'telossand to decreasethe risk fibroblasts,andmyofibroblastsis refercedto asgranulation tissue.As the amount of granulation tissue :i infection.Healingof the wound surfaceby epithethereis a concurrentreductionin the sizeof -:alizationalone doesnot provide adequatestrength increases, the fibrin clot, allowing for the formation of a more 3 meet the mechanicaldemandsplacedon most tispennanentsupportstructure.Theseeventsare medi:ues. Suchstrengthis provided by the collagenproated by chemotacticfactorsthat stimulate increased :uced duringfibroplasia. During epithelialization,uninjured epithelial cells fibroblasticactivity and by fibronectinthat enhances misration and adhesionof the fibroblasts.The fibrob:om the margins of the injured area reproduceand tasasinitially produce a thin, weak-structuredcolla:rigrate over the injured area,coveringthe surfaceof --rewound and closingthe defect.It is hypothesized genwith no consistentorganizationknown asty7eIII Thrs period is the most tenuoustime during rat the stimulusfor this activity is the lossof contact collagen. the healingprocessdue to the limited tensilestrength :rhibition that occurswhen epithelial cells are norof the tissue. During the proliferation phase an =ally in contact with one another. The migrating :rithelial cells stay connectedto their parent cells, injured areahas the greatestamount of collagen,yet -:rerebypulling the intact epidermisover the wound its tensile strensth can be as low as 15% of that of normaltissue.2i :Cge. When epithelial cells from one edge meet Iibroblasts also produce hyaluronic acid, a glyrigrating cellsfrom the other edge,they stop moving :ue to contactinhibition (Iig. 2-11).Aithough clean, cosaminoglycan(CAC), which draws water into *re :.oproximatedwounds can be clinically resurfaced area,increasesthe amount of intracellularmatrix, and '.,.'ithin48 hours, larger open wounds take longer to facilitatescellularmigration. It is postulatedthat the compositionof this substanceis relatedto the num]t *ren takes severalweeks for this thin :esurface,24 thereby implyber and location of the cross-bridges, ,ayerto becomemultilayeredand to differentiateinto ing rhat the relationship benveenCAC and collagen =e variousstrataof normalepidermis(Frg.2-12). 17'28 dictatesthe scararchitecture. The formation of cross-1inksallows the newly Production Collagen formed tissueto tolerateearly,controlledmovement without disruption. However, infection, edema, or ibroblasts make collagen. Fibroblast growth, excessive stressonthe healingareamay resultin further takes place in connective tissue. :nown asfibroplasra. and additional depositionof collagen. hflammation :ibroblastsdevelopfrom undifferentiatedmesenchycollagen depositionwill result in excessive Excessive ral cells located around blood vesselsand in fat. that may lirnit the functional outcome. 1ey migrate to the injured areaalongfibrin strands, scarring By the seventhday afterinjury thereis a significant :r responseto chemotacticinfluences,and arepresent increasein the amount of collagen,causingthe tensile i.rroughoutthe injured area.25Adequatesuppliesof strength of the injured area to increasesteadily.By :>,ygen,ascorbicacid, and other cofactorssuch as day 12, the initial immature ty?e IIl collagenstartsto inc, iron, manganese,and copper are necessaryfor :broplasia to occur.26As the number of fibroblasts be replacedby type I collagen,a more mature and :us1y in the proliferation phase to achieve coales:ence and closureof the injured area:epithelializa:on, collagenproduction, wound contraction, and ::eovascularization.
e o t-
d rd o. )le c)e e-
25
26
2 o Itflannation
anl7'issra
Refair
With Injurybasal cells detach irom the basementmembrane.
ce s
The cells migratewhile holdingon to their 'parent'cellsand pulllhem into the center to close the wound. Contact Inhibition
when thetwosrdesmeet,movement ceases,
Basalcells differenliateand proliferate...
...1obecomemultilayered and restorethe epidermis.
Figure 2-11. Schematicdiagramof epithelialization.
strongerform.16,29,30 The ratio of type I to type III collagenincreases sreadilyfrom chispojnron.
Wound Contraction Wound contractionis the finai mechanismfor repairing an injured area.In contrast to epithelialization, which coversthe wound surface,contractionpullsthe edgesof the injured site toged-rer, in effect shrinking the defect.Successfulcontractionresultsin a smaller areato be repairedby scarformation. Contractionof the wound beghs approximately5 days after injury
and peaksafter about 2 weeks.31Myofibroblastsare the primary cel1sresponsiblefor wound contraction. Myofibroblasts,identified by Gabbianiet aI rn 1971, are derived from the same mesenchymaicells as fibroblasts.32 Myofibroblastsare similarto fibroblasts exceptthat they alsopossess the contractileproperties of smooth muscle.Myofibroblastsattachto the margins of the intact skin and pull the entire epithelial layerinward.The rateof contractionis proportionalto the number of myofibroblastsat and under the cell marginsandis inverselyproportionalto the latticecol lagenstructure.
Otc . PATHOLOCY AND PATIENTPROBLEMS
HEALINGBY PRIIVARYINTENTION
27
HEALINGBY SECONDARYINTENTION
24 hours
3 to 7 days
lvlitosis Granulationtissue lvlacrophage Fibroblast New capillary
Fibrous union Wound contraction
; ale rion.
)7r, iasts rties :rar_ :e1ial ral to :cell : col-
Figure2-l2 Diagrammatic comparison of healing by primary intention (left) and secondaryintention (right).
Accordins
rn
rhc
.'.t,''o
tr:mc
th"^^,
.h"
'.vound margin beneath the epidermis is the location :f myofibroblast action.33 A ring of myofibroblasts noves inward from the wound margin. Although :ontractile forces are initially equal, the shape of the
picture frame predictsdre resultantspeedof closure (Frg.2-14).Linear wounds with one narrow dimension contractrapidly;squareor rectangular wounds, wi*r no closeedges,progress at a moderatepace;and circularwounds contractmost slowly.34
28
2 . lrrflotnrnationnnd li..tc Rcynir
Collagen filament Collagen fibril
Primitive coUagen fiber Collagen fibers
Figure 2-13.Dragran-matic representalion of one uopocollagenunit joinirg wirh orhersro lorm collagentilamenrs and, ultimately, collagenfibers.
Figure2-14. Illustration of the picture frame theory of wouno contlactron.
If wound contraction is uncontrolled it can result in the formation of contractures. Contracrures are con ditions of fixed high resistance to passive stretch that may ^result from fibrosis of tissues surrounding a joint.35 Contractures may also result from adhesio'ns, muscle shortening, or tissue damage. Contractures are discussedin greaterdepth in Chapter 5.
Wounds that are rapidly closedwith sutureswith minimallossoltissueandminimalbacterialcontamination can heal without wound contraction.This is known a, healingbv yrimaryunionytimaryinrenrionor When thereis significantlossof tissueor frst ixtention. bacterialcontamhation,wound contractionis necessaryto closethe wound. Wound contractionis the feature that most clearly differentiatesprimary ftom secondaryhealing,alsoknown as healingby secondary intentioxor iadirectuniou.36 Later approximationof a wound's edgeswith suturesor the applicationof skin graftscan reducewound contractionand is krrown as healiugbydelayedyrimatyintention .37'38fo minimize contraction,graftsmust be appliedearlyil the inflammatory phase,beforethe processofcontractionbegins.39 As scartissuematures,it developspressureand tension-sensitivenerveendingsto protect the immature vascularsystem,which is weak and can bleed easilywith any insult. During the proliferationphase, the scaris red and swollen due to the increasein vascularity and fluid, the innervationof the healingsite, and the relativeimmatudty of the tissue.The tissue can easily be damagedand is tender to tension or pressure.
Neovascularization Neovascularization,the developmentof a new blood supply to the injured area, occurs as a result of angiogenesis, the growth of new blood vessels. Healing cannot occur without angiogenesis. These new vessels are needed to suppiy oxygen and nutrients to the injured and healing tissue. It is thought that macrophages signal the initiation of neovascularizatron. Angiogenesis can occur by three different mechanisms: generation of a new vascular network, anastomosts to preexisting vessels,or coupling of the vesselsin the injured area.4o Vesselsin the wound periphery develop small buds that grow into the wound area. These outgrowths eventually come in contact with and join other arterial or venular buds to form a capillary loop. These vesselsfill the injured area,giving it a pinkish to bright red hue. As the wound heals, many of these capillary loops ceaseto function and retract, giving the mature scar a more whitish appearance than the adjacent tissues. Initially the walls of these capillaries are thin, making them prone to injury Therefore immobilization at this stage may help to protect these vesseis and permit further regrowth, whereas excessiveearly
One . PATHOLOGY AND PATIENT PROBLEITIS
/ith
motion can causemicrohemorrhagingand increase 'he likelihood of infection.
29
p ,-s aou"*enTypes
JLS
,or 30r
:om :lary rfa skin nas ma39 and leed
SItC,
ssue nor
looo rgionew ts to that ^-L
f the buds wths artehese rioht
illary ature rt trstnm, tltza^ :ssels early
(DAY PHASE MATURATToN I0N) -\s dre transitionfrom the proliferationto the maturaion stageof healingis made,changesoccurinthe size, :orm, and strengthof the scartissue.The maturation rhaseis the longestphasein the healingprocess.It can rersist for over a year alter *re initial insult. During -Jristime the number of fibroblasts,macrophages, nyofibroblasts,and capillariesdecrease and the water :ontent of the tissue deciines.The scar becomes '.vhiterin appearanceas the collagenmaturesand the '.'ascularitydecreases. The ultimate goal of this phase :srestorationofthe prior functionof the injuredtissue. Severalfactors determine tl-terate of maturation :rrd the final physicalcharacteristics ofthe scar.These :rclude fiber odentation and the balanceof collasen .vnrhesis andlysis. Throughout the maturation phase, synthesis and lysrs of collagen occur in a balancedfashion. llormonal stimulation secondary to inflammation :ausesincreasedcollagendestructionby the enzyme ;ollagenase.Collagenaseis derived from polymor:nogranular leukocytes, the migrating epithelium, ai-rdthe granuiationbed. Collagenaseis ableto break -re strong crossJinkingbonds of the tropocollagen =olecule,causingit to becomesoluble.It is then .xcretedasa wasteby-product.Although collagenase :smost activein the actualareaofthe injury its effects :an alsobe noticed,to a lesserextent,in areasadja-enr to the injury site. Thus remodelrngoccurs --:rrough a processof collagenturnover. Collagen,a glycoprotein,providesthe extracellular :amework for all multicellularorganisms.Although :ore than 27 types of collagenhave been identified, re following discussionis limited to types I, Il, and -llr' f|able 2-5).AII collagenmoleculesaremadeup of -rree separatepolypeptide chains wrapped tighdy :ogetherin a triple left-handedhelix.Type I collagenis re primary collagenfound in bone,skin, and tendon, andis the predominantcollagenin maturescars.Type -l collagenis the major coliagenin cartilage.Type III :ollagenis found in the gastrointestinaltract, uterus, and blood vesselsin adults.It is also the first woe of :olJagen ro be deposited duringrhehealingproceis. During the maturationphase,the collagensynthe;ized and depositedis predominantlyrype I. The bal:nce between synthesisand lysis generallyslightly
Tw"
Distribution
Most abundantform ofcollagen:skn, bone,tendons,and most organs
II
Major cartilagecollagen,vitreoushumor
III
Abundantin blood vessels,rrterus,skin
IV
Ali basementmembranes Mrnor componentof most interstitial ussues
VI
Abundantin most interstitialtissues
VII
Dermal-epidermaljunctron
UII
Endothelium
x
Cartilage
X
Cartilage
favors synthesis.As type I collagenis strongerthan the rype III collagendepositedin the proliferation phase,tensile strengthincreasesfaster than mass.If the rate of collagenproduction is much greaterthan the rate of lysis, a keloid or hypeftrophic scar can result. Both keloids and hypertrophic scarsare the result of excessivecollagendepositiondue to inhibition of lysis. lt is believedthat this inhibition of lysis is due to a genetic defect. Keloids extend beyond the original boundaries of an injury and invade the suffounding tissue,whereas hypertrophic scars, although raised, remain within the margins of the original wound. The treatment of keloid scars through surgery medications,pressure,and iradia44 tion hasonly limited success.42 Collagen synthesis is oxygen dependent,while collagenlysis is not.asThus, when oxygenlevelsare low, the processof maturation is weighted toward lysis,resultingin a softer,lessbulky scar.Hypertrophic scarscan be managedclinicallywith prolongedpressure,which causesa decreasein oxygen,resultingin decreasedoverall collagensynthesiswhile maintaining the level of collagenlysis.37This is one of the basesfor the use of pressuregarmentsin the treatment of patientssufferingftom bums, and for the use of elastomerin the managementof scarsin hand therapy. Eventually,balanceis achievedwhen the scar bulk is flattenedto approximatenormal tissue.
30
2 . Inflannatiou
Collagensynthesisand lysis may last for up to 12 to 24 monthsafreran injury.The high rateof collagen turnover during this period can be viewed as both detrimentaland beneficial.As lonq as the scartissue appearsredderrhanthe surroundingtissue,rernodeling is sLilloccurring.AJthougha joint or rissuesrructure canIosemobiliry quickly duringthis stage,sucha Ioss can still be reversedthrough appropriateinterventron. The physical structure of the collagen fibers is largelyresponsible tor the finalfunctionof rheinlured area.Collagenin scartissueis always lessorganized than collagen in the surrounding tissue. SCarsare inelastic,so redundantfolds are necessaryto Demit mobiliryof the srruturesto which they areattached. To understandthis conceptbetter,onemay considera spring,which, aithoughmadeof an inelasticmaterial, has a spiraledform that, like the redundantfolds of a scar,allows it to expandand contract.If short, dense adhesions are formed, these will restrict motion becausethey cannotelongate. Two theorieshave been proposedto explain the orientation of the collagenfibers in scar tissue:tlre inductiontheory and the tensiontheory.Accordingto the induction theory the scarattemptsto mimic the charactedsticsof the tissue it is healins.46Thus a densetissueinducesa dense.highlycro"s-linledscar, whereasa more pliable tissueresultsin a loose,less cross-linkedscar.Densetissuetypes havea preferential status when multiple tissue types are in close proximity. Basedon this theory, surgeonsattempt to designrepair fields that separatedenseand soft tissues.If this is not possible,as in the caseof repaired tendonleft immobileover bone Fracrures, adhlsions and poorly gliding tendonscan result.In such cases, earlyconrrolledmovementmay be beneficial. According to the tension theory, the intemal and extemalstresses placedon the injuredareaduring the maturationphasedeterminethe final tissuestructure.aoMuscle tension, joint movementJsoft tissue loadingand unJoading. fascialgliding. temperarure changes,and mobilizatjon are alJ forces that are thought to affect collagensfiucture.Thus the length and mobility of cheinjuredareamay be modified-by the applicationof stressduringthe appropriatephases of healing.This theory has been supported by the work of Arem and Madden, which has shown *rat the two most important variablesresponsiblefor successful remodeirngare the phasei of the repair processin which mechanjcal forceswere introduced
and fi>:uc Rerair
and the natureof the appliedforces.aT Scarsneedlowload, long-duration stretch during the appropriate phasefor permanentchangesto occur Studieshaveshown *rat the applicationof tension duringhealingcausesan increasein censilestrength. and immobilization and stress deprivation reduce tensilestrengthand collagenstructure.The recovery curves for tissue experimentallyimmobilized For bet:ween2 and 4 weeks reveal that these processes cantakemonths to reverse,andreversalis oftennever complete. Eachphaseof the healingresponseis necessary and essentialto the subsequentphase.In the optimal scenario,inflammation is a necessarvaspectof the healingresponse and the [irst srept;ward recovery, seting rhe stagefor the ocherphasesof healing.It repeatedinsults or injury occur,however, a chronic inflammatory response may develop that can adverselyafFectthe outcomeof the healingprocess. Acute inflammatory processescan have one of four outcomes.Iirst, and most beneficial,is the complete resolutionand replacementof the injured tissue with like tissue.Second,and most common,is healing by scarformation.The third is the formation of an abscess.Fourth is the possibility of progressionto chronicinflammation.1o
CHRONIC INFLAMMATION Chronic inflammation is the simultaneousproqression of activeinflammation.tissuedestruccion,-and healing.Chronicinflammationcanarisein oneof two ways. The first follows acute inflammation and can be due to the persistenceof the injurious agent(such asa cumulativetrauma)or to someother interference with the normal healing process.The second is a resultof an immune responseto eitheran alteredhost tissueor a foreign material,such as an implant or a suture,or is t}le resultof an autoimmunediseasesuch asrheumatoidarthritis. The normal acute inflammatory processlasts for no morethan2 weeks.II ir continuesfor morechan4 weeks,it is known as subacute inflammation.3 Chronrc inflammationis inflammationthat lastsformonths or years. The primary cells presentduring chronic inflammation aremononuclearcellsincludinglymphocytes, macrophages, andmonocytes(Iig. 2-15).Occasionally eosinophilsare alsopresent.aB The progressionof the inflammatory responseto a chronicstateis a resultof
O e . PATHOLOGY AND PATIENT PROBLEMS
31
Characteristics / Functions
Leukocyte e
Associatedwith . chronic inflammation . phagocytosts
Lysosome
n IJ
e
ibrolyticpathways Regulatescoagulation/f
v
Regulateslymphocyteresponse
)t :S
Ivlonocytesare convertedto macrophageswhen they emigrate from capillanesinto the tissue spaces
:r
v ^l
a
IC
v' If ic
Associatedwith . chronicintlammation
=
immuneresponse Key cell in humoraland cell-mediated
tn
rf :l-
te
Lymphocyte
Ll'
Sparse endoplasmic reticulum
tn
ro
Associatedwilh . allergicreactions . parasiticinfectionsand associatedinflammatoryreactrcns
Granules
Modulatesmasi cell-mediatedreactions rS-
rd 1Q
Eosinophil
ch ce
Assocrated with . acuteinflammation . baclerialandforeignbodyphagocytosis
a )st :a
ch :OI
r4 ric OI
m1ly he oI
@
. Not phagocytic . Contarnshistamine,which causes increasedvascular permeabilfy
Basophil
Figute2-15, Cellular components of acute and chronic inflammation.
32
2 . Itflafltfiatiot
both immunologicand nonimmunologicfactors.The macrophageis an important sourceof inflammatory a n di m m u n o l o g im c e d i a c oa r sn di s a n i m p o r t a ncro m ponent in the regulationof their actions.The role of eosinophilsis much lessclear,althoughthey are often presentin chronic inflammatory conditions that are causedby allergicreactionsor parasiticinfection.4s Chronic inflammation also results in increased fibroblastproliferation,which in turn increasescollagen production and ultimately increasesscar tissue and adhesionformation. This may lead to a loss of function asthe delicatebalancebetweenootimal tensile strengthand mobility of tbe involvei tissuesis lost.
FACTORS AFFECTING THEHEALING PROCESS A number of factors, either local or systemic, can impact or modify the processesof inflammation and repav (Table 2-A1.Localfactors that can affect wound healing include the type, size, and location of the injury infection, blood supply, and external physical forces.
LocalFactors
awl Tissre Repair
Smallerwounds heal faster than larger wounds, and sursicalincisionsheal faster*ran wounds caused by blunl trauma.l6Softtissueinjuriesover bonestend to adhereto the bony surfaces,preventingcontraction and adequateoppositionof the edgesand delaying healing.l6 lnfection Infection in an injured area is the most problematic local factor that can affect healing.Among the complications of wound healing, S0'/" are due to local infection.ll Infections affect collagen metabolism, reducingcollagenproduction and increasinglysis.49 lnfectionoften preventsor delayshealingand encourgranulauon agesexcessive tissueformation.l6 Vascularsupply The healing of injuries largely dependson the availability of a sufficient vascular supply. Nutrition, oxygen tension, and the inflammatory responseall depend on the microcirculatory system to deliver rheir components.50Decreasedoxygen tension resultingfrom a compromisedblood supplycanresult in the inhibition of fibroblastmigration and collagen slmthesis,leadingto decreasedtensilestrengthof the injured area and increasedsusceptibility to infection.2o
Type, size,andlocation oftheiniury Injurieslocatedin well-vascularized tissue,suchas the scalp,heal fasterthan thosein poorlyvascular- Extefnalforces ized areas.16Injuries in areas of ischemia, such as those that may be caused by arterial obstruction or excessivepressure,heal more slowly.16
h p
2-6 FactorsInfluencing Healing Local
Systemic
Type, size,andlocationofinjury Ag" Infection
Infectionor disease
Vascularsupply
Metabolicstatus
Movement/excessive pressure
Nutrition
Temperaturedeviation
Hormones
Topicalmedications
Medication
Electromagnetic energy
Fever
Retainedforeignbody
Oxygen
The application of physical agents including thermal agents,electromagneticenergy,and mechanical forcesmay also influenceinflammation and healing. Cryotherapy (cold therapy), thermotherapy (heat), therapeutic ultrasound electromagnetic radiation, electricalcurrents,and mechanicaipressurehave all been used by rehabilitation professionalsin an attempt to modify the healingprocess.The impact of thesephysicalagentson tissuehealingis discussedin Section2 of this text, which describeseach type of physicalagent,its effects,and its clinicalapplications. Movement Early movement of a newly injured area may delay healing.Thereforeimmobilization may be usedto aid early healing and repair.However, sinceimmobiliry can result in adhesions and stiffness by altering collagencrossJinkingand elasticiry continuouspassive motion (CPM) with stricdy controlled parameters is often usedto remobilize and restorefunction safelv.)rThe use of CPM in coniunctionwi*r short-
One o PATHOLOGY AND PATIENT PROBLEMS
ied nd ac-
rtrc mcal i0, -19
ur-
-:] ofl,
all ver ion' iult 9€n Lhe
:erm immobilization, compared to immobilization alone, has been shown to achieve a better func:onal outcome in some studies; however, odrer srudieshave found differencesonly in early rangeof Ir has also been reponedrhar padents =ocion.5753 :iilizing CPM during the inflammatory phaseof soft :ssue healingafter anterior cruciateligament reconjrruction usesignificandylesspain-relievingnarcotics -,:ranpatientsnot usingcPMs4(Fig.2-10.
Factors Systemic Age -\ge is a factor to be consideredbecauseof variations :r healingbetween the pediatric,adult, and geriatric :opulations.In childhood,wound closure occurs :rore rapidly than in adulthood becausethe physio-rgical changesand cumulative sun exposure that -;cur wtth aging can reducethe healingrace.ss A :ecreasein the density and cross-linkingof collagen, '...'hichresultsin reducedtensile strength,decreased :-umbersof mast cells and fibroblasts,and a lower s- 1n" : rre oI epiLne]ializaLion. occursin the elderly.56 :oor organizationof cutaneous vesselsin olderpeo:le alsoadverselyaffectswound healing.
33
leading to a decrease in local blood flow. Neuropathies, which are alsocommon,canincrease the potential for trauma and decreasethe ability of softtissuelesionsto heal. Patientswho are immunocompromised,such as those with acquired immune deficiency syndrome (AIDS) or those taking immunosuppressivedrugs after organtransplantation,are more prone to wound infections becausethey have an inadequateinflammatory response.AIDS alsoaffectsmany other facets of the healing processthrough its impairment of phagocytosis,fibroblast function, and collagensynthesis.59 Problemsinvolving the circulatorysystem,including atherosclerosis, sicklecell disease,and hypertension, can also have an adverse effect on wound healing since inflammation and healing depend on the cardiovascularsystemfor the delivery of components to the local area of injury Decreasedoxygen tension resulting from a reducedblood supply can result in an inhibition of fibroblast migration and a decreasedcollagensynthesis,resulting in decreased tensilestrengthandmakingthe injuredareamore susceptibleto reinjury Wounds with a decreasedblood supplyarealsomore susceptibleto infection.20'60
tc-
IEI-
ical
LOn,
Disease --.' number of diseasescan affect wound healing ::ther direcdy or indirectly.Ior example,poorly con:ol1eddiabetesmellitus impairs collagensynthesis, r:r.creases the risk of infection due to a dampened and decreases -:rununeresponseJ phagocytosisdue to 58Peripheralvasirerations in leukocytetunction.S0 :.rlar compromiseis alsoprevalentin this population,
I AII an tof dLn rof )ns.
Figure2-16.CIM machine. (Courtesy Thera-l(netics Jompany, Cherry Hill, New Jersey.)
Medications Patientswith injuries or wounds often take medications with systemiceffectsthat alter tissuehealing. Forexample,antibioticscanpreventor fight off infection, which can help to speedhealing but may also havetoxic effectsthat inhibit healing. Corticosteroids,such as prednisoneand dexamethasone,block the inflammatory cascadeearly on by blocking the release of arachidonic acid.61 Corticosteroidshavebeenshown to impair all phases of healingby stabilizingcell membranesand inhibiting the production of prostaglandins.They also decreasethe margination,migration, and accumulation of monocytesat the siteof inflammation.62 They severelyinhibit wound contracture,decreasethe rate of epithelialization,and decreaseahetensilestrength of closed, healed wounds.6366 Corticosteroids that are administeredat the time of injury have a greaterimpact becausedecreasingthe inflammatory responseat this early stagedelayssubsequentphases of healingand increasesthe incidenceof infection. In comparisonwith corticosteroids,nonsteroidal antiinflammatory drugs (NSAIDs)such as ibuprofen are lesslikely to impair healing.They act later in the
34
2 . l la
tnaliol, oud Tis
inflammatory cascade,interruptingthe production of prostaqlandinsfrom arachidonic actd6r Fil 2-77). ih"y Jr. ttot thorrghtto adverselyaffectthe function NSAIDs can of fibroblastsor tissue macrophages.6T causevasoconstrictionand suppressthe intlammatory response,l2however, and some NSAIDs have been found to inhibit celi proliferationduring tendon healing.6B
Studieshave shown that a deficiency of specific nutrients may also affect healing. Vitamin A deficiencvcanretardepithelialization,the rateof collagen synthesis,and croisJinking.TlThiamine (vitamin B) collagenformation, and vitamin ieficiency decreases the tensilestrengthof healed B. deficiencydecreases Vitamin ti"ssue andreducesthe fibroblastnumber.72'73 C deficiency impairs collagensynthesisby fibroblasts, increasesthe capillary rupture potential, arld /a increasesthe susceptibilityof wounds to infection Many mineralsalsoplay an important role in healins. Insufficientzinc can decreasethe rate of epithelialization, reduce-ocollagensynthesis,and decrease tensilesuength.-5 Magnesiumdeficjencymay also causedecreasedcollagensynthesis,and copperinsutto a reduction ficiencymay altercrossJinking,leading in tensilestrength./a
Nutrition Nutrition can have a profound effect on healing tissues.Deficiencyof any o[ a number of important amino acids,vitamins, minerals,or water, as well as insufficient caloric intake, can result in delayed or impairedhealing.This is becausephysiologicalstress from the injury inducesa hypermetabolicstate.Thus if insufficient "fuel" is availablefor the processof inflammationand repair,healingis slowed. ln most cases,healing abnormalities are asso- HEALING OFSPECIFIC ciated with general protein-calorie malnutrition TISSUES MUSCULOSKELETAL rather than depletion of a single nutrient.69Such is The primary determinantsof the outcomeo[ any the casewith patientswith extensivebums who are injury are the type and extent of the injury the rege-nin a prolongedhypermetabolicstate A protein de[ieritive caoaciw of the tissuesinvolved, the vascular ciency can result in decreasedfibroblasticproliferaof damagelo tion, reduced proteoglycanand collagensynthesis, supplvof the iniuredsrte,andthe extent of princrples basic framework.lhe decreasedangiogenesis,and disrupted collagen the extracellulai howall tissues; remodeling./0Protein deficiency can also adversely inflammation and healing apply to which may lead to an increased ever, there is some tissue specificity to the healing affect phagocyto_sis, response.For example,the liver can regenerateeven riskoI infection.ou
Figure2-17, Comparison of the site in the inflammatory cascadeacted on by NSAIDs and steroids
Ore . PATHOLOCY AND PATIENT PROBLEMS
when over half of it is removed, while even a thin hactureline in cartilageis unlikely to heal.
Cartilage
r ) f
:I
Cartilagehas a limited ability to heal becauseit lacks lymphatics, blood vessels,and nerves.77However, ;artilage reactsdifferently when injured alone than -.vheninjured in conjunction with dre subchondral 'cone to which it is attached.Injuriesconfinedto the ;artilage do not form a clot or recruit neutrophilsor nacrophages,and the cells adjacent to the injury ,how a limited capacityto induce healing.This lim:red responsegenerallyfails to heal the defect, and -Jrese lesionsseldomresolve.Ts In injuries that involve both articular cartilage and subchondralbone, the vascularizationof the :ubchondralbone allows for the formation of fibrinibronectin gel, giving accessto the inflammatory -ells and permitting the formation of granulation :ssue. Differentiationofgranulationtissueinto chonCrocytescan begin within 2 weeks. Normafappearng cartilagecan be seenwithin 2 months after the njury However,this cartilagehasa low proteoglycan :ontent and is thereforepredisposedto degeneration :nd erosivechanges./Y
Tendons andLigaments Iendons and ligamentspassthrough similar stagesof realing.Inflammationoccursin the first 72 hours,and :o1lagensynthesis occurs within the first week. - ibroplasiaoccursfrom intrinsic sourcessuchasadja:ent cells,and from extrinsic sourcessuch as those :rought in via the circulatorysystem. The repair potential of tendon is somewhat con=oversial.Both intrinsic cells such as epitendonous :nd endotendonouscellsand extrinsicperitendonous rells pafticipate in tendon repair.The exact role of -Jresecellsand the final outcome dependon several :actors,including the type of tendon, the extent of iamage to the tendonsheath,the vascularsupply,and -he duration of immobilization. The first two stages rftendon healing,inflammationandproliferation,are similar to the healing phasesof other tissues.The -hird phase,scarmaturation,is unique to tendonsin -iat this tissuecan achievea state of repair closeto :egeneration. During the first 4 days following an injury, the with an infiltration of nllammatory phaseprogresses
35
both extrinsicand intrinsic cells.Many of thesecells developphagocyticcapabilities,while othersbecome fibroblastic.Collagensynthesisbecomesevident by days7 to 8, with fibroblastspredominatingat around day 14.Earlyin this stage,both cellsand collagenare oriented perpendicularto the tendon's long axis.80 This orientation changesat day 10, when new collagen fibersbeginto alignthemselvesparallelto the old longitudinalaxis of the tendon stumps.BlFor the following 2 months,thereis a gradualtransitionofalignment, through remodelingand reorientation,parallel to the lone axis. Ultimate maturation of the tissue dependson sufficientphysiologicalloading. If the synovial sheathis absentor uninjured, the relative contributions of the intrinsic and extrinsic cellsare balancedand adhesionsare minimal. If the synovial sheath is injured, the contributions of the extrirsic cellsoverwhelm the capacitiesof the intrinsic cellsand adhesionsarecommon. Factorsaffectingthe repairof tendonsare different from those associatedwith the repair of ligaments.s2 Studieshave shown that mobilization of tendonsby controlled forcesacceleratesand enhancesstrengthening of tendon repair, but mobilization by active contractionof the attachedmusclelessthan 3 weeks after repair generallyresultsin a poor outcome.]he poor resultsmay be a result of the fact that high tension can leadto ischemiaand tendon rupture.Recent studieshavefound no significantdifferencein tendon strengthwhen tendonsare exposedto controlledlow lt or high levelsof passiveforce after repair.8384 appearsthat mechanicalstressis neededto promote appropriate oientation of the collagen fibrils and remodelingof collageninto its mature form and to optimize strength,but the amount of tensionnecessary to promote the optimal clinical responseis not certaln."",""
Many variablesinfluencethe healing of ligamentous tissue,the most important of which are the rype of ligament,the sizeof the defect,and the amount of loadingappiied.For example,injudesto capsularand extracapsularligaments generallystimulate an adequate repair response,while injuries to intracapsular ligamentsoften do not. In the knee,the medial collateral ligament often heals without surgicalintervention, whereasthe anteriorcruciateligamentdoesnot. These differencesin healing may be due to the s)movial environment, the limited neovascularization, or the fibroblastmigrationfrom surroundingtissues.Treatments that stabilize the iniurv site and
36
2 c Inflannatiot
maintainthe appositionof the torn ligamentcanhelp *re ligamentheal in its optimal length and minimize scarring.However, mature ligamentousrepair tissue is still30% to 50oloweakerthan uninjuredligament.sT This does not usually clinically significantly impair joint function becausethe repairedtissue is usually larger than the uninjured ligament. Early, controlled loading of healingligamentscan also promote healing, althoughexcessiveloading may delay or disrupt the healingprocess.88,89
atdTissue Repait
Stages of Fractsre Healing 1. Impaction 2. Induction 3. Inflammation 4. Soft callus 5. Hard callgs 6. Remodeling
Young children have a more elastic bone structure that allows their bones to bend, accountingfor the greenstick-typefracturesseenin this population. Muscle Skeletal Induction is the stage when cells that possess Musclesmaybe injuredby blunttraumacausing a conosteogeniccapabilitiesare activated.lnduction is the tusion,byviolent contractionor excessive stretchcaus- least well-understood stage of bone healing. lt is ing a strain,or by muscle-wastingdiseases. Although thought that the cells may be activatedby oxygen skeletalmusclecellscannotproliferate,stemor reserve gradients,forces,bonemorphogenicproteins,or noncells,known as satellite rclls,can,under some circumcollagenousproteins. Although the timing of this stances, proliferateanddifferentiateto form new skele- processis not known exactly,it is thought to be initital musclecellsafterthe deathof adultmusclefibers.79 ated after the moment of impact.The durationof this Skeletalmuscleresenerationhas beendocumentedin stageis alsonot known, althoughthe influenceof the musclebiopsy tp.ii-".rr kom patientswith diseases induction forcesseemsto lessenwith time. Therefore such as musculardystrophy and poll'rnyositis;howoptimizing the early conditions for healing to miniever, skeletal muscle regenerationin humans after mize the potentialfor delayedunion or nonunionis traumahas not beendocumented.Followins a severe imperative. contusion.a calciFied hematoma.known is nyasiis Inflammationbeginsshordy after impact and lasts ossifcans, may develop.Myositis ossificansis rarefof until somefibrousunion at the fracturesiteoccurs.At lowing surgeryif hemostasisis controlled. the time ofthe fracture,thereis disruptionofthe blood supplyand formationof a fracturehematoma,aswell asa decrease in oxygentensionand pH. This environBone ment favors the growth of the early fibrous or cartilagiBone is a specializedtissuethat is able to heal itself nous callus.This callusforms more easilythan bone with like tissue.Bone can heal by two mechanisms: and helpsto stabilizethe fracturesite, decreasepain, primary or secondaryhealing.Primaryhealingoccurs andlessenthe likelihoodof a fat embolism.lt alsorapwith rigid internalfixation of the bone,while second- idly andefficiendyprovidesa scaffoldfor furthercircuary healingoccursin the absenceof suchfixation. latiorqandfor canilageandendostealboneproduction. Bone goes through a seriesof four histologically The amount of movement at the fracturesite infludistinct stagesin the healing process:inflammation, encesthe amount and quality of the callus. Small soft callus,hard callus,and bone remodeling.Some amounts of movement stimulate callus formation, investigatorsalsoincludethe stagesof impactionand while excessivemovement can disrupt callusformainductionbeforeinflammationin tltis scheme. tion andinhibit bony union. Impactionis the dissipationof the energytrom an The soft callus stage begins when the pain and insult. The impact of an insult is proportionalto the swelling subsideand lasts until the bony fragments energy applied to the bone and is inverselyproporare united by fibrous or cartilaginoustissue. This tional to the voiume of the bone. Thus a fracture is period is marked by a greatincreasein vasculariry more likely to occurif the forceis greatot the bone is ingrowth of capillariesinto the fractufe callus, and small. Energydissipatedby a bone is inverselyproincreasedcellproliferation.The tissueoxygentension portional to its modulus of elasticity.Therefore the remains low. but the oH returns to normal. The bone of a personsufferingfrom osteoporosis,which hematoma becomes organized with fibrous tissue has low elasticiry will sustaina fracturemore easily. cartilageand bone formation; however, no callus is
Orc t PATHOLOGY AND PATIENT PROBLEMS
37
) Clinical CaseStude a The following casestudy summarizesthe conceptsof inflammationand repairdiscussedin this chapter.Based on the scenariopresented,an evaluationof the clinical findingsand goalsoftreatment areproposed.
Case 4
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JPis a 16-year-oldhigh schoolstudent.Sheinjured her right anlle 1 week ago playing soccerand was treated conservativelywith crurches;rest, ice. compression. and elevation (NCE); and NSAIDs. She rcports some improvement,althoughsheis unableto play soccerdue to continued complaints of right lateral ankle pain. Her x-rayfilms showedno kacture,andherfamily physician diagnosed the injury as a grade II lateral ankle sprain. Shecomesto your clinic with an order to (evaluateand treat.' JPsustainedthis injury during a cutting motion while dribblinga soccerball. Shenoted an audiblepop, immediate pain and swelling,and an inabiliry to bearweight. Shereportsttrat herpainhas decreased in intensityftom 8/10 to 6/10 but that it incleaseswith weight bearing and with certain demonstrated movements. The objectiveexam revealsmoderatewarmth of dre skin of the anterolateralaspect of the right ankle. Moderateecchymosisand swellingare alsonoted,with a girth measurement of 34 cm on the right ankle compared with 30 cm on the left. Her range of motion is restrictedto 0 degreesdorsiflexion,30 degreesplantarflexion,10 degreesinversio4 and5 degreeseversion,
with pain noted especiallywi*r plantarflexion and inversion. She exhibits a decreasedstance phase on the right lower extremity. Pain and weakrressoccur on strengti tests of the peroneals,gastrocnemius,and soleusmuscles.JP also exhibits a marked decreasein proprioception,as evidencedby the single-legbalance test.Her anteriordrawertestis positive,and hertalar tilt rsne8at1ve. EVALUATION OF CLINICALFINDINGS The patient presentswith impairmentsof pairl loss of subtalarand talocmalmotioq decreased strengthof the evertomand plantarflexors,increasedgirth of the right ankle, and decreasedproprioceptionresultingin functional iimitation of ambulationand sportsactivitv. She performs home activities independently,without che useof adaptiveequipment. PREFERREDPRACTICEPATTERN Impaired joint Mobiliry, Motor Function, Muscle Performance,and Range of Motion AssociatedWith CoonectiveTissueDysfunction,(4D). PLAN OF CARE The goals of treatment at this time are to control the pain and edema,acceleratethe resolutionof the acute inflammatory phaseof h€aling,and speedthe recovery olJP'snormalrangeof motion, strength,proprioception, and function.
PhysicalTheraPistPracticePattemssMl4DjisCopyright2002AmericanPhysicalTherapy Associatron.All rights reserved. :'reFerred le n.
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visible radiographically.The callusis electronegative :elative to the rest of the bone during *ris period. Osteoclasts remove*re deadbonefrasments. The hard callusstagebeginswhei a sticky.hard ;allus coversthe endsof the fracture,and endswhen 1ew bone uniteswith the fragments.This period cor:espondsto d:)eperiodofclinical and radiologicalfracrure healing.The duration of this period dependson ;he fracture location and the patient's age, and can rangeftom 3 weeksto 4 mon*ts. The remodelingstagebeginswhen the fractureis 'coth clinicallyand radiologicallyhealed.It endswhen -,hebone has returned to its normal state and the catency of the medullary canal is restored. The ibrous bone is convened to lamellar bone, and the nedullary canalis revised.This processcan take severalmonths to severalyearsto complete.90
CHAPTER REVIEW The processesof inflammation and tissue repair involve a complex and dynamic seriesof events,the ultimate goal of which is the restorationof normal function. In these events the involved tissue progressesthrough three stages:inflammation,proliferation, and maturation. The inflammation phase involves interaction of hemostatic.vascular cellular. andimmuneresponses mediatedby a numberof neural and chemical factors.The proliferation phaseis characterizedby epithelialization,fibroplasia,wound contractior\ and neovascularization. The maturation phaseinvolvesbalancedcollagensynthesisand lysis to ultimately remodelthe injuredarea. This seriesof eventsfollows a similar timely and predictablecourse.If the normal healing processis interferedwith however, healingmay be delayedor
38
2 e ln[Iammaion
and Ti>sue Reyair
15. PierceCF,MustoeTA, SeniaRM et al: In vivo incisional wound healingaugmentedby PDCF and recombinant c-sis gene homodimeric proteins, / E^xyMed 167: 975,987,1988. 16. Maninez-HemandezA, Amenta PS:Basicconceptsin wound healing. In Leadbener \48, Buckwalter JA, lxflammatlo4ParkRidge, GordonSL,eds:Spons-lxduced IL, 1990,AmericanAcademyof OnhopaedicSurgeons. 17. Hardy M: The biology of scar formation, Phys Ther 69:1074-1024,1989. 18. RutherfordR" RossR: Plateletfactorsstimulatefibroblasts and smooth muscle celis quiescent in plasma serumto proliferate,J CellBlol69:196-203,1976. 19. Mathes S: Roundtablediscussion:probiem wounds, References PersyectPIasrrc Surg 2 :89-120, 1988 L. Stedmar'sMedrcalDrcnoxaryed 25, Baltimore, 1990, 20. Whimey JD, Heiner S, Mygrant BI et al: Tissue and Williams & Wilkins. wound healingeffectsof sholt duration postoperative 2. Price SA, Wilson LM: Pathophysiology: Cliwcal o*lgen therapy,Biol ResNursJan;2(3):206-215 ed 2, New York, 1982, Coxceptsol DiseaseProtesses, ,2001. 21. Davidson JD, Mustoe TA: Oxygen in wound healing: McCraw Hili. more than a nutrient, \1(/oundReValr Regen May3. KellettJ: Acute soft trssuenjunes a review of the hterature,Med St SVorts Ererc18:489-504,1986. Jun;9 Q):175- 177,2001,. 4. Galrett WE Jr,LohnesJ: Cellularand matrix responses 22. Bell.anttJA,ed: ImnunologyIII, ed 3, Piitadelphia,1985, WB Saunders. to mechanicalinjury at the myotendmousjunction. In 23. Werb A, Cordon S: Elastasesecretionby stimulated Ieadbetter\48, BuckwalterJA, Cordon SL,eds:Spons' macrophages, ItducedInflammauot,Park fudge, IL, 1990,American J ExyMed 142:361-377 , 1975 . 24. Madden JW: Wound healingrbiologic and clinical feaAcademyof OrthopaedicSurgeons. of tures.ln SabistonDC, ed: Davk-ChrktoyherTextbook 5. AndriacchiI SabrstonP, DeHavenK et a1:Ligament: Swgety,ed 1L, Philadelphia,1997,WB Saunders. Injury andrepair InWoo SL-l BuckwalterJA,eds:It4ury 25. Clark RA-F:Overview and general considerationsof and ReVaitof theMusculosleeletal Saftllsaes, Parkfudge, wound repair. In Clark MF, Henson PM, eds: Tle IL, 1988,AmericanAcademyof OrthopaedicSurgeons. Molecular atd Cellular Biology of \Y/oundRepak, New 6. CarrettWE Jr:Musclestraininjuries:Clinicaland basic York, 1988,PlenumPress. aspects, Med Se SponsExerc22:436443,1990. 26. Stotts NA, Wipke-Tevis D: Co"factors in impaired 7. FantoneJC,Ward PA:Inflammation.ln RubrnE, Farber 1996. wound healing,Ostony42(2):44-56, Pl'riladelphra, 1988,JBLippincott. lL, eds:Pathology, L Wrlkerson CB: lnflammauon ln corurectlvelisoue: 27. LevensonS:Practicalapplicationsof experimentalstudies rn the care of primary closedwounds, An J Surg andmanage ment.Athl Ttututkg20:298-301 etrolog'y , 1985. 104:273-282 9. ChristieAI: The tissueinjury cycleand new advances , 1962. toward its managementin openwounds, Athl Trafuing 28. Nemeth-CsokaM. KovacsayA: The effect o[ glycosaminoglycans(CAC) on the intramolecularbind26:274-277 , 1,991. ngs of collagen,ActaBiol30(4):303-308, 1,979. Pathologic 10. RobbrnsSL,KumarV CotranRSet al: Robbins 29. Lachman SM Soft TissueInjuries ut Spotts, St. Louis, BasisofDisease, ed5, Philadelphia,1994,WB Saunders. 1988,Mosby. 11. Fantone JC: Basic concepts in inflammation. In LeadbetterWB, BuckwalterJA, Gordon SL, eds:S7otls- 30. Hunt TK, Van Winkle W Jr: Wound healing. In HeppenstallR3, ed: FractureTreatment and Healing, lwlucedhflamnalox, Park tudge, IL, 1990, American Philadeiphia,1980,WB Saunders. Academyof OrthopaedicSurgeons. 31. Daly T: The repair phase of wound healing: 1.2.PeacockEE\!/oundRepaLr, ed3,Phlladelphia,1984,WB re-eprthehalization and contraction. In Kloth L, Saunders. in McCullochJ,Feederl, eds \X/ound Healing:Abernatives 13. SalterRB,SimmonsDF,Malcom BW et al: The biologiManagement, Phl.adelphia,1990,FA Davis. cal effectsof continuouspassivemotion on the healing oI modified of fu1lthrcknessdefectsin arhcularcartilage,J BaneJoint 32. Cabbiani C, Ryan G, Majeno Gr Presence fibroblastsin granulationtissueand their possiblerole Swg 62-A:1,2321251, 1980. in wound contractioo,Experiertia27:549-550,1971. 14. Majno G, PaladeCE: Studieson inflammauon.L The 33. Watts CT, Grillo HC, GrossJ: Studiesin wound heal effect of histamine and serotoninon vascularpermeing: II. fhe role ofgranulationtissuein contraction,Ar?l ability: an electronmrcroscoprcstudy,/ BnphysBiochem Surg l4B1,53- 1,60, 1,958. Cytolll57l,1961,.
chronic inflammation may result. Various local and systemic factors can influence the progression of inflammation and tissue repair, including physical agents utilized by clinicians to facilitate the healing process. The rehabilitation specialist must assessthe state of inflammation and repair to determine the appropriate agent to incorporate into the treatment plan for an optimal outcome. The reader is referred to the Evolve Website at http://evolve.elsevier.com/ Cameron for study questions pertinent to *Lis chapter.
One . PAIHOLOGY AND PATIENT PROBLEMS
-VcGrath MH, Simon RHr Wound geometry and the kinetics of *re wound contraction,PlastReconstr Surg 72:66-73,1983. Taber's Cyclopedic MedicalDicuonary, ed 75,Philadelphia, 1985,FADavis. Billngham RE, RussellPS:Studieson wound healing, with specialreferenceto the phenomenaofconftacture rn expe mental wounds in rabbit skin, Am Surg 144:961, . , 1,956 SawhneyCP,Monga HL: Wound contracturein rabbits and the effectiveness of skin graftsin preventingitJBlr PlastSurg23:318-321,1970. Stone PA, Madden JW: Biological factors affecting wound contraction,SurgFotuu 26:547-548,1975. RudolphR: Contractionand the control of contraction, VorldI Surg4:279-287,1980. Alvarez OM: Wound healing. In Fitzpatrick T, ed: in CeneralMedicite,ed 3, New York, 1986, Dermatology McCraw-Hill. EyreDR: The collagensof musculoskeletal 5oft tissues. In LeadbetterWB, Buckwalter JA, Cordon SL, eds: SVonsInduced lxflammatiott,Park Ridge, IL, 1990, AmericanAssociarion of Orthopaedic Surgeons. McPhersonJM, Piez KA: Collagenin dermal wound repair.In Clark RAI, HensonPM, eds:Ile Molecularaftd Cellular Biologyof \Yound Repai, New York, 1988, PlenumPress. Kosaka M, Kamrishi H: New concept of ballooncompression wear for the treaffnent of keloids and hypertrophic scars,PlastRecottstr SargOct;108(5): 1454-1,455 , 2001. Uppal RS,Khan U, KakarS et al: The effectsof a single doseof 5-fluorouracilon keloid scars:a clinicaltrial of timed wound irrigation after extralesionalexcision, PlastRecottstt Sutg Oct;108(5):12f8-1224, 2001.. Hunt TK, Van WinlleW: WoundHealing:NormalRepair - Fundamentals of \Yourd Managemettin Swgery,South Plaintield. NJ,1976,Chirurgecom, Inc. MaddenJ:Wound healing:the biologicalbasisof hand surgery,Clh PlastSutg3:3-11,1976. Arem AJ, Madden IW: Iffects of stress on healing wounds: I. Intermittent nonryclica\ tensi.on,J SurgRes 2 0 : 9 31 0 2 , 1 9 7 6 . Fantone JC: Basic concepts of inflammation. In LeadbetterWB, BuckwalterJA,Cordon SL,eds:SponslnducedInflammauon, Park fudge, IL, 1990, American Academyof OrthopaedicSurgeons. Irvin T: Collagenmetabolismin rnfectedcolonicanastomoses,SurgCyxecolObstet143:220-224, 1976. CanicoT, Mehrhof A, CohenI: Biologyofwound healng, SurgClinNonhAn 64:721-733,l9B4. Woo SL, GelbermanRM, Cobb NC et a1:The importanceof controlledpassivemobilization on flexor tendon healing: a biochemical study,Acta OnhoVScatd 52:61,5-622,1,981.
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52. CelbermanRH, Woo SL,LothringerK et al: lffects of early intemittent passiveimmobilization on healing canineflexor tendons,l HandSurgT:170-175, 1982. 53. Lau SK, Chiu KY Use of continuouspassivemohon after total knee arthroplasty,/ AnhtoylastyApr;16(3): 336-339, 2001. 54. McCar*ry M\ Yates CK, Anderson MA et al: The eff€cts of immediate continuous passivemotion on pain duringthe inflammatoryphaseof soft tissuehealcruciare IigamentreconsuucEion, ing followingancerior 1993. IOSPT 17(2\:96-101, 55. Thomas DR: Age-relatedchangesin wound healing, -620,2001. DrugsAging18(8):607 56. Holm-PetersonP,Viidik A: Tensilepropertlesand morphologyof healingwounds in young and old rats,Scand Surg6:24-35,!972. I PlastReconstr 57. van de Kerkhoff PCM, van BergenB, Spruijt K et al: Age-related changes in wound healing, Cln Lrerc 4, 1994. Dernatol1,9:369-37 58. Goodson W, Hunt T: Studies of wound healing in experimentaldiabetesmellitus,/ SurgRes22:22L227, 1997. 59. PetersonM, Barbul A, BreslinR et al: Significanceof T-lymphocytesin wound healing, Surgery2:300-305, 1987. 60. Cogia PP: The biology of wound healtLng,Ostomy 38(9):12-22, 1992. 61. LeadbetterWB: Corticosteroid injection therapy n sports injuries. ln Leadbetter SE, Buckwalter JA, GordonSL,eds:Spo*-lxducedl(lannation, Parkfudge, IL, 1990,AmericanAcademyof OrthopaedicSurgeons. 62. Behrens TW, Coodwin JS: Oral corticosteroids.ln Leadbetter\48, BuckwalterJA,Gordon SL,eds:SportsIxducedlaflannation, Park fudge, IL, 1990, American Academyof OrthopaedicSurgeons. 63. EhlrichH, Hunt T: The effectof cortisoneand anabolic steroidson the tensilestrengthof healingwounds,A tl Sutg 170:203-206 , 1969. 64. BakerB, Whitaker W: Interfercncewith wound healing by the local ac on of adrenocorticalsterolds. 46.544-551, Eudoctixology 1950. 65. Howes E, Plotz C, Blunt J et al: Retardationof wound healingby cortisone, Surgery 28:177-1,81,,1,950. 66. StephensF, Dunphy J, Hunt T; The effect of delayed administration of corticosteroidson wound contracture,Ann Surg173:214-218 , 1971. 67. Abramson SB:Nonsteroidalanti-inflammatorydrugs: mechanismsof action and therapeuticconsiderations. In LeadbetterWB, Buckwalter JA, Cordon SL, eds: SVons-lxduced lnflammatlox,Park fudge, IL, 1990, AmericanAcademyof OrthopaedicSurgeons. 68. fuley CP,Cox M, HarrallRL et al: Inhibition of tendon cell proliferatronand matrix glycosaminoglycansynthesis by non-steroidal anti-inflammatory drugs in vitro,J HandSurg[Brl]rn;26(3):224-228, 2001.
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2 . Iaflamnation and TissueRepair
69. Albina JENutrition in wound heaLng,/Parnter E4teul
-376, 1,994. Nutr18(4):367 70. PollackS:Wound healing:a revtew.III. Nutritional factors affectrngwound healing,J Dernatol Sutg Onco! 1,979. 5:615-619, 7 1 . FreimanM, SerfterE, Connerton C: Vttamin A defiSutg,Forutt21t81-82,1'970. cienry andsurgicals:rress, 72. AlverezOM, GrlbreathRL:Thramrneinfluenceon collagen during granulation of skin wounds, J Surg Res 32:24-31, 1982. 73. GrenierJF,AprahamianM, Cenot C et al: Pantothenic acid (vitamin Br) effioency on wound healing, Acta . VtaminolEnzymol4:81-85, 1'982 74. Pollack S: Systemicdrugs and nutritional aspectsof wound healing,C/laDernatol2:68-80,7984. 75. Sandstead HH, HenriksenLK, GreferJLet al:Zinc nutri' ture in the elderly rn relauonto taste acuiry immune response,and wound healng, An J Cln Natr 36(Suppl 1982. 5):1046-1059, 76. Maitra AK, Dorani B: Roleof zinc m post-injurywound 1992. heahtg,Arch EmergMed Jut;9(2):122-124, 77. AthanasrouKA, ShahAR, HernandezRJet al; Basicsci' ence of arttcular cartilage repatr, Clin Spons Med Ap420(2):223-247,2001. 7 8 . GelbermanR, GoldbergY An K-N et al: Tendon ln Woo SL-l Buckwalter JA, eds: It4ury and Repar of Soft Tssues, Park fudge, IL, 1988, Musculosheletal AmericanAcademyof OrthopaedicSurgeons. 79. CaplanA, CarlsonB, FaulknerJet al: Skeletalmuscle.In Woo SL-Y Buckwalter JA, eds ltlury and Repai of Soft Tissues,Park fudge, IL, 1988, Musculosheletal AmericanAcademyof OrthopaedicSurgeons.
80. Strickland JW: Flexor tendon injuries, Otthoy Ret 15(10):21, 1986.
8 1 .LmdsayWK: Cellularbrologyof flexor tendonhealing ln Hunter JM, SchnerderLH, Mackin EJ, eds Tendon Sutgeryof theHand,St Louis, 1987,Mosby. AkesonWH, FrankCB,Amiel D et a1:Lrgamentbrology and biomechanics. In Frnnerman G, ed: Ameticax Symyostuwor Syons Surgeon's Acadenyof Onhoyaedrc M eddne, SrLours,1985,Mo sby. 83. KetchumLD: Primarytendonhealing:a revie:w, J Haxd 1977. Surg,2:428'435, 84. Goldfarb CA, Harwood F,Silva MJ et al: The effect of vanatlons rn applied rehab rtation force on collagen concentration and maturation at t}le intrasynovial flexor tendon repair slte, J Hatd Sutg lA,:tt] Sep;26(5):B4 I -846, 2001. 85. PeacockEE Jr: Brologicalprinciples in the healing of long tendons,Srrg Cln NonhAn 45:46L-476,1965 86. Potenza AD: Tendon healng wthin the flexor digital sheathin the dog,J Boxelont Sutg44A:49-64, 1,962. 87. FrankC, Woo SL-l Amiel D et al:Medial collateralligarn rabbits, ment healing:a multrdrscrplnaryassessment Med 1L.379'389,1983 AnJ Spons BB. FronekJ,FrankC, Amiel D et aLThe effectsof intermittent passlvemotron (lPM) in the healingof medial collateralligaments,Ir4 nsOrthoVResSocS:31,1983. 89. Long M, Frank C, SchacharN et al: The effects of motion on normal and healingirgaments , TMnsOfthol ResSocT:43,1982. 90. McKibben B: The brology of fracturehealing in long bones,J BoneI ont Surg(Bk) 60:150'162, 1978.
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S U A4A/A I R Y O F 1 , ^ / FO R M A T I O N C O V E R E D Typesof Pain -Mechanismsof PainReceptionand Transmission PainModulation and Control -\4easuringPain
PainManagementApproaches Clinical CaseStudies Chapter Review
rof
ong
OB]ECTIVES ofthis chayter,thereaderwill beableto: Uponcompletion L Differentiate acute,chronic, and referredpain.
2 . Discussthe peripheraland central mechanisms of nociception and pain transmission. Appraisecurrent theories ofpain control. 1 . Selectand apply appropriatemethods and tools to quantify and quali$r pain.
5. Compareand contrastvarious medical and usedto concrolpain. physicaltherapies 6. Evaluatethe use of physicalagentsfor ^^-+-^lt:-^
-^t-
4l
42
3 . Paitr
Painis an experiencebasedon a complex interaction of physical and psychologicalprocesses.it has beendefinedasan unpleasantsensoryand emotional experienceassociatedwith actual or potential tissue damageor describedin terms of suchdamage.l-3Pain usuallyservesas a warning to protect the body from damage and thus, although unpleasant,serves an essentialfunction in survival.aIt is important to realize that pain is not just the activationof receptorsof but also d:re noxious stimuli, known as nociceytion, sensoryexperiencesassociatedwith such activation, as well as the suffering and alterationsin behavior with suchactivation. associated Pain is the most common symPtom prompting patientsto seekmedical attention and is also a predominant D,mptom leadingpatientsto receiverehabilitation.s Many patients with musculoskeletalor neurologicalimpairmentspresentwith compiaintsof pain,andmostof theseindividualsconsiderpaincontroi or relieFto be the primary goalof treatment.oPain may also contribute to physicalimpaiment and disability, limiting participation in home, work, and recreationalactivities./The pain complaintsencountered 6y rehabilitation professionalsare generally relatedto inflammation of musculoskeletalor neurologicalstructurescausedby injury trauma,or degenerativedisease.Thesestructurescan be sourcesof of peripheral the responsiveness painandcanincrease pain recepto$to other painful stimuli.B-10 The goalsof pain treatmentinclude resolvingthe underlying pathology causingthe pain, when possible; modifying *re patient'sperceptionof the discomfort; and maximizing function within the limitations imposed by the source of pain, whether or not the sourceof pain can be modified. The final goal of treatment is resolution of the underlying condition. However,evenwhen the sourceof paincanbe modified by treatment,for example,in the caseof strucrural malalignmentbecauseof poor posrure or imbalancedmusclelength,or when the pain is caused by a self-limiting condition such as inflammation after an acutesoft tissueiniury it is beneficialto control pain during recovery so that the patient can participatemore fully in a rehabilitationprogram to correct the underlying deficit. When the pain is causedby a conditionthat cannotbe direcdymodified, suchasphantomlimb painor rheumatoidar*rritis,pain controlmay facilitateincreasedparticipationin a rehabilitation program, increasedpatient function, and decreased disabiliry
TYPES OFPAIN Pain can be categorizedaccordingto its duration or Acutepain is generor referred. sor:rceasacute,chronic, allv definedaspain oflessthan 6 mon*rs'duration for which an underlying pathology can be identified.ll Acute pain is felt in responseto actualor Potentialtissue damagethat resolveswhen tissuedamageor the threat of damagepasses.Chronic pain,alsoknown as persistentpain, persistsbeyond the normal time for tissue healing.l0Chronic pain conditions are generally the result of activation of dysfunctionalneurological or psychological responsesthat cause the individual to continueto experiencethe sensationof pain evenwhen no damagingor threateningstimulus is present.Referredpain is the experienceof pain in oneareawhen the actualor potentialtissuedamageis in anotherarea.Krowing whether a patient'spain is acute,chronic,or referredwill help the cliniciandeterthat may be conmine the mechanismsandprocesses tributing to the sensationand facilitate selectionof the most appropriateinterventionto controlor relieve this sFnptom.
AcutePain Acute pain consistsof a complex combination of unpleasantsensoryperceptual,and emotionalexpedences with associated autonomic, psychological, emotional, and behavioral reactions that occur in responseto a noxious stimulus provoked by acute Acute pain is generallyviewed injury or disease.l2'13 as biologically meaningful,useful, and timelimited. Acute pain is mediated through rapidly conducting pathways and is associatedwith increasesin muscle rone,heart rate. blood pressure.skin conductance, and other manifestationsof increasedsympathetic nervoussystemactivity.l4The intensity and location of the pain are usually relatedto the degreeof tissue inflarnmation.damage.or destructionin the areain which the pain is felt. Acute pain is generallywelllocalizedand defined,althoughits degreeof localization vades to some extent with the type of tissue involved. Pain sensationsfrom the skin are localized wirh grear accuracy.whereasmuscle pain is [requentlymorediffuse.l5l6 Acutepain lastsas longas the noxious stimulation persists.Acute pain servesa protective function foilowing an injury by Limiting activity to preventfunher damageandpromotetissue healingand recovery;however,it may alsoadversely
Ore . PATHOLOGY AND PATIENTPROBLEMS
,iect an individual's quality of life and impair the ,:,iry to function. Treatment of acute pain resulting from muscu:,.<eletalinjury generallyattemptsto facilitatereso,:on ofthe underlyingdisorder,reduceinflammation, .:-: modify the transmissionof pain from the periph::. ro the centralnervoussystem.
Pain - hronic
e ,f 5
n t5
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rf te
of rial. in Ite 'ed ed. cie rce. ?ttc 10n sue iin 'eLlisue zed iegas .ring SSUC
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-,:onic pain starts as acute pain. Most authors and ::anizations define chronic pain as pain that does -:: :esolvein the usualtime it takesfor the disorder :: :eal or that continuesbeyond the durationof nox: -s stimulation.lT However, some authors and :::anizations use time-based definitions, defining : :rnic pain asany pain lastinglongerthan 3 months The useof time-based definitionsis : i months.18'19 - : recommendedbecausethey do not take into .:-:trunt the variablecourseand duration of different :.=ologies and thereforedo not differentiatelong:.::: pain causedby chronic or progressivediseases : :athological states,such as rheumatoid arthritis, ftom painthat persists -:':er, or neuralentrapments, Chronic pain generpathology has resolved. the :'-:: stimuliareno longer ,-. :ontinuesevenatternoxious : :--'.'eandwhen thereis no longerany tissuedamage : -rreatof tissuedamage,whereaspain from a long::= disorderis generallyassociatedwith a long-term - rous stimulus.It has beenestimatedthat approxi-::ely one third of the American population has . -.::nic pain and 1,47ool the U.S. population suffers := chronicpain relatedto the joints andthe muscu: :ieletalsystem.20'21 with Jhronic persistentpain is generallyassociated -...;ical, psychological,and social dysfunction (see : - :.: . Patientswith chronicpain generallyhave been : - . :ically inactivefor a prolongedperiod,resultingin ;. of strength,skiil, and enduranceand thus progres: disability.They often dramatizetheir complaints, -,::ting that their pain is unbearableor incapacitattreatment,which - = andftequentlyreceiveexcessive , :-effective but can result in drug misuseor abuse -: progressivedependenceon others, including ':. -,i carepractitionersand family members.These including :::ents alsooften show signsof depression, : =,:r'edsleeponset and frequentawakening,altered The painbehavior , :--;rghabits,andsocialisolation.22 : -::epatientwith chronicpersistentpainmay be per-- ,tp..l hw Fin:nri:l o,in 23,24
43
Common Features of Patients with Ghronic Pain Have pain of several months' or years' duration. Have pair similar to the initial pain that is associatedwith a medical problem or injury. History of many treatment failures provided in great detail. Many medications tried, with a minimal to poor response. Continuous use of analgesics and tranquiJizets, despite patients' testimony that the medications offer no notable or long-lasting relief. Pain described as being unbearable and incapacitating. Strong belief that pain has an unidentified organic cause. Desire and willingness expressed to undergo "any treatrnent" for pain relief, Claim that everything will be fine if only the "doctor would treat my pain." Pain not relieved by any medical or surgical treaknent. Sqbstantial psychosocial changes present, especially depression, although patients vehemendy deny the label; they hequendy do admit to feeling frustated, angry, and iffitable, with disturbed sleep, altered moods, weight changes, decreased energy, decreased physical, social, recreational, and sexual activities, and increased family stresses and economic difEculties. From Cildenberg PL, DeVaul M: The ChrcnicPain Patient: andManagemeat, New York, 1985,Karger. Evaluatiotl
Chronic persistent pain may be the result of changesin sympatheticnervoussystem and adrenal activity, reducedproduction of endogenousopioids, or sensitizationof primary afferent and spinal cord neurons. Decreasedlevels of enkephalinsand increasednumbers and sensitivity of nociceptors have been observed in individuals with chronic pain.25These individuals frequendy have increased sensitivity to both noxious (hyperalgesia)and nonnoxious (allodynia)stimuli.26These changesin pain perceptionmay be the result of a processknown as wherebythe pathwind-uyor centralhyyersensitizatiaq ways that transmit pain continue to dischargeafter the discontinuationof intense or repeatedstimulation. Then, evena small additional stimulus exceeds Thus the threshold that is perceivedas painful.2T-3o for an individual with a painful condition that is severeor long-lasting,the noxious stimulation may
44
3 . Pait
resultin increasedpain receptoractivity and a consequentreducedtolerdnce for othernoxiousor nonloxious stimuli. Understanding of this sensitization mechanismhasled to increasedstudy and use of preemptive analgesiabeforeproceduresthat are known to be painful in an attempt to reducepostprocedural painandreducerecoverytime.31-33 Psychologicaland social factors have also been implicated in the etiology and maintenance of chronic pain.3aThe disturbedsleepassociatedwith depression may causemusculoskeletal pain,and the decreased activirymdy perpetuatepain by causing '2 weakness i".on'diiiorring. lndiuidualswiti "nd chronicpain alsofrequentlyadopt the dependentsick patient role and behaviors of the chronic invalid, which result in progressively reduced functional activiryto These behaviors may be unintentionally encouragedby the individual'sfamily members,who, i n a n . a t r e m p rh t oe l p a . c c u a l lpyr o m o t e* r e d e p e n d e n t
tissue include the pain associatedwith myocardial infarctionor anginacausedby cardiacischemiathat is felt in the upperchest,left shoulder,iaw and arm, and pain originating from the central portion of the diaphragmthat is frequently felt in the lateraltip of either shoulder.The gallbladderalsofrequendyrefers pain to the dght shoulderor the inferior angleof the right scapula,and the spleenrefers pain to the left shoulder It is proposedthat pain is refered in one of three ways: from a nerye to its area of innervation,from one area to another derived from the same dermatome, or from one area to another derived from the sameembryonicsegment,becausethe peripheral neuralpathways from thesedifferent areasconverge on the same or similar areasof the spinal cord and synapse with the same second-orderneurons to ascendthe spinalcord and reachthe centralcortex.39 For example,pain is referredfrom the diaphragmto role za the tip of the shoulder becauseboth of these areas Ideally,the developmentof chronicpain shouldbe initially developin the neck regionduring embryonic prevented by early identification of individuals at development, causing drem both to have efferent risk. Patientswith prolonged, severe,or very disinnervationfrom the phrenicnerveand afferentinnerabling acute pain are at increasedrisk of developing vation to the secondthroughfourth levelsof the cervichronic pain. Therefore, to reduce this risk, paincal spine.When pain that may be of eithervisceralor controlling interventions,such as physical agentsor musculoskeletalorigin convergeson the sameneuron medications,shouldbe appliedduring the acutestage in the spinal cord, it is usually interpreted to be of of an iniury and during the later recovery phases, musculoskeletalorigin. This may be becausemuscuw h e n .p a i ni ' s r i l lr h e r e s u l ro f p a i n r e c e p t oar c c i v a - loskeletal injuryandpainareso much morecommon tion.Jo S h o u l dc h r o n i cp a i nd e v e l o ps. u c c e s s ftur e l a t - that the brain "learns"that activity arrivingalongthat ment usually requires that all components of the pathway is associatedwith pain stimulusin a particudysfunction be addressed.Multidisciplinary treatIarmusculoskeletal area. ment programsbasedon a biopsychosocialmodel of Clinicians who treat neuromusculoskeletaldyspain have been specificallydevelopedto address functionmust be awareof the potentialfor pain referthese problems.a These treatment programs are ral and be familiar with common pain referral described beiowin the sectionon painmanagement. patternsto determinethe sourceof a patient'scomplaints and select appropriate treatment methods. Thereforewhen a patienrwith pain in a muscuReferred Pain loskeletalarea seekstreatment, the clinician should Referred pain is felt at a location distant from its first determineif the sourceof the pain is locatedin source. Pain may be referred ftom one joint to the areaof this sensation.Painof musculoskeletal orianother,from a peripheralnerve to a distal area of gin generallyvarieswith position or movementof the innervation.or from an internal organ to an area painful area,whereaspain causedby dysfunction in of musculoskeietal tissue.For example,hip joint other systemsgenerallyvaries with stresson those pathologyoccasionallyreferspain to the knee,particsystems.For example, shoulder pain that is aggraularly in children,and compressionofthe spinalnerue vated by raising the arm is likely to originatein the rootsat the L5 S1 level asthey exit throughthe spinal shoulder,whereas left shoulder pain that is aggraforamenmay causepain in the lateralleg becausethis vated by all forms of strenuousexercisemay be is the areaof sensoryinnervation.37.38 Common refercausedby a cardiaccondition.When assessing pain ral patternsfrom internal organsto musculoskeletal that is determinedto be of musculoskeletal origin, it is
Oqe . PATHOLOCY AND PATIENT qROBLEMS
:iso important to accurately determine the struc:.rre(s)at fauit to provide the most effective treat:rent. This can.be done by performing provocative :ests to reproduce the patient,s chief complaint. ?hysicalagentsmay effectivelyrelievereferrej pain; :.oweverthey shouldnot be usedas a ,ubstituti for :etermining the true sourceof the pain or for treatins := underlyingcause.They may be usedfor pain reliei '.';hilethe sourceofthe pain is beinginvestigated,dur_ :rg the recoveryprocess,and for conuollinq referred :arn where rhe underlyingcausecannorbe direcrly :eated.
MECHANISMS OFPAIN RECEPTION AND IRANSMISSION Specificity and pattern theories Pain receptors Peripheral nerve pathways Central pathways Sympathetically mediated pain The role ofsubstance P iain is generally felt in response to stimulation of :eripheral nociceptive structures. The stimulus is :ansmitted along peripheral nerves to the central ---ervoussystemJ from where it can reach the cortex .rd consciousness. The sensation of pain and the tdividual's response to the sensation are influenced .....a variety of factors, including the physiological ::echanisms of the pain receptoff, the anatomy of :ain transmitting structures, neurotransmitter levels, ::rd the motivation, behavior, and physiological -rd emotional state of the individual. Variations in ::ry of these factors can alter the individual,s :3rception of pain severity, type, location, and :lIatlon.
Specificity andPattern Theories Jver the years,varioustheoriesregardingthe nature :: peripheralpain receptionand transmissionhave ::en proposed.The primary early theorieswere the .:ecificity theory and the patterntheory Currentthe_ ::1es ntegrate componentsof both of these with :::orerecentfindings and obsewations.Accordingto -:respecificirytheory, as describedby Von lrey ind :-hers,the sensation of pain dependson the stimula_ - rn of specificnerveend,ings thar arespecialized for 42Thus a specrficrype :ch rype of sensarion.40 of
45
nerve fiber will always transmit the samesensation. no matrerhow intenselyor trequentlyir rssrimulared. According to *ris theory specific pain fibers are responsiblefor the transmissionof the sensationof pain (Iig. 3-1,.,1). Von lrey supportedthis theory with his identificationof freenerveendingswidely distributed in the skin that causeda sensationof pain when stimulated.He proposedthat thesefreenewe endinss were specificpain receptors.l2 Although rhe ,peJi_ ficity theory is consistentwith Von lrey,s findings,it has sincebeen found that the sensationof pain ioes not havethe preciseone-to-onerelationshipwith the type of receptorstimulatedthat would be predicted by-the specificitytheory The specificitytheory also failsto accountfor the fact that many qypesof siimuli are perceivedas painful and that pain can be modu_ Latedby input from the spinal cord or brarn.The limitations of the specificitytheory led to the devel_ opment of an alternativeexplanationof pain percep_ tion, the patterntheory According to the pattern theory the sensation . or pam re-sultsftom an appropriateintensity or fre_ quency of stimulation of receptorsthat also respond to other stimuli such as touch, pressure,or tem_ perature.'3Neural impulsesFromcheperipheryare combined and modified to summate in central nervous system structures,where the pain is then iocalizedand inrerprered. Accordingto rhe patrern theory and spatial summation of impulses _temporal along the pathways from the skin to the cerebral levels determinesthe individual,ssensationof pain (Iig. 3-1, B). This theory accountsfor the fact that a wide variety of stimuli cause the sensation of pain and also suggestsa role for centralinfluencebv pain summacion:however,ic [ar]sto considerthe roleo[ the idenLified specialized pain receprorsrruc_ tures and to account for affective or central pain modulation. theodesintegratecomponentsof the speci_ .. .Cuffent ficity theory and the pattem theory with other,more recent findings neuralanaLomyand Lhe ,regarding runcflonsot endogenous neurotransmiEters. currenf findings indicate that specific nerve endings called uociceprors respondro all painfulstimuli.anj specific nerve ryoes. small myelinatedA-delta tibers and unmyelinatedC fibers,transmitthe sensationof oain from these nerve endings to the spinal cord and thence,within specifictracts,to the brain.The quali$ of the pai,ndependson the type of tlssuefrom whicL the stimulusoriginatesand on which ofthe tvvonerve
46
3 . Ptritt
SPECIFICITY THEORY
Specialized heat receptor
PATTERNTHEORY
,il'il*l1ll-l l'il-11il*l{ll-l lil*l{1 |, Action potentials
-1,,,*1,*1,*1.*"1*l* Actionpotentjals
Figu]e3-1. Specificigz versuspattem theory of pain.A, Specificreceptorsfor eachrype of sensation.B, Patternof actionpotentialsresultingin sensation of pain. rypes transmitsthe pain; the intensiry of the pain is cles,and bareareasof axolemmathat are not covered relatedto the fidng rate of *re nerves.Painfrom cutaby Schwanncellprocesses.46 Nociceptors arepresent neous noxious stimulation is usuallv oerceived as in almostall typesof tissue.However,no nociceptors sharp.pricking.or tingling and is eisy to localize. are presentin the nucleuspulposusand the inner part 50 whereaspain from musculoskeletalstructuresis usuof the annulusfibrosusof the spinaldiscs.aT ally dull, hear,y,or achingand is harderto localize.aa Nociceptorscan be activatedby intense*rermal, Visceralpain has an aching quality similar to that of mechanical,or chemicalstimuli from exogenousor musculoskeletalpain but tends to refer superficially endogenoussources.Ior example,intensemechanirather than deeply.15Pain transmittedby C fibers is cal stimulation,suchas that causedby a brick falling usually dull, long-lasting,and aching,whereas pain on someonersfoot or a piece of broken bone comtransmittedby A-delta fibers is generallysharp.The pressinga nociceptor,will resultin nociceptoractivaintensity of the pain and the responsesto it are tion. Chemicalstimulation by exogenoussubstances thought to be more severewhen the relativeintensity suchas acid or bleach,or by endogenouslyproduced of nociceptive receptor stimulation is greater than substances suchasbradykinin,histamine,and arachithat of nonnociceptivereceptor stimulation, when donic acid, which are releasedas part of the inflamlevels of endogenousopioids are low, and with matory Iesponseto tissuedamage,can also activate certain vadations in *re individual's psychological nocic€ptors.Because thesechemicalmediatorsremain state.45 after the initial physical stimulus has passed,they generallycausepain to persist beyond the duration of the initial noxious stimulation. It is important PainReceptors to note that chemical mediators of inflammation Nociteytors are free, noncorpuscularperipheralnerve also sensitizenociceptors,reducing their activation endingsconsistingof a seriesof spindle-shaped, *rick thresholdto other stimuli.51,s2 This is the reason*rat, segments linked by thin segments to produce a clinically, many activities and stimuli to recendy injured areasare perceivedaspainful evenwhen they "string-of-beads"appearance.The beads and end :re nnt d:ma oino bulbs contain mitochondria,glycogenparticles,vesi-
Ote . PATHOLOGY AND PATIENT PROBLEMS
When nociceptors are activated, they releasea variery of neuropeptides from their peripheral terminals, including substanceP and a number of breakdown products of arachidonic acid such as prostaglandinsand leukotrienes.25 Nociceptorsalso convert the initial stimulus into electricalactivitv. in the form oI actionpotenrials. by a processknown as (Fig.3-2).It is thoughtrhat the released t'an,ductionzr neuropeptidesmay initiate or participatein transduction becausethey sensitizenociceptors.53 The action potentialsresultingfrom the processof transduction propagatefrom the nociceptorsalong afferentnerve pathwaystoward the spinalcord.
Peripheral NervePathways
47
C fibers,alsoknown asgroupIV afferexts, aresmall, unmyelinatednervefibersthat transmitactionpotentials quite slowly, at the rate of 1.0 to 4.0 meters/second.58They respondto noxiouslevelsof mechanical, thermal, and chemicalstimulation,causingpain that is generallydescribedas dull, throbbing, aching, or b:rgg^":d be reportedas tingling or rapry{."l= pingr"0o(Fig.3-3).The pain sensadons ffansmifted by these fibers have a slow onset after the initial painful stimulus, are longJasting,emotionally difficult for the individual to tolerate,and tend to be diffusely localized, particularly when the stimulus is intense.6l'62 They canbe accompaniedby autonomic responsessuch as sweating,increasedheart rate and blood pressure,or nausea.63 The pain associatedwith C-fiber activationcan be reducedby opiates,and this pain_rcliefis blockedby the opiate antagonistnalox-
Nociceptorsgive rise to two typesof first-orderafferent nervefibers,C fibersandA-deltafibers.The activone.oa ity in both rypes of fibers increasesin responseto A-delta fibers, alsoknown asgrouVIII afferexts,are peripheralnoxious stimulation,includingthat associ- also small-diameterfibers; however, they transmit atedwith acuteinflafirmationor muscleischemia.54-56 more rapidly than C fibers, at a rate of about 30 Eightypercentof afferentpain-transmittingfibersare meters/second,because they are myelinated.5S'65 C fibers,and the r ematnrng20%oare A-delta fibers.57 They are most sensitiveto high-intensitymechanical Cenerally,about 50% of the sensoryfibers in a cutastimulation,althoughthey canalsorespondto stimuneousnervehavenociceptivefunctions.45 lation by heat or cold and are capableof transmitting
Tissue
Mastcell 6---<4!)
Btood vesset ffi
/-\ =-'tfz\ Histamine (o o)*r( \-./
/,+
Substance P ,/
Leukotrienes
Arachidonicacid
\
Prostaglandins
Figule3-2. Pain transduction. (Modified with permission from lields HL, Levine JD: Pain-mechanisms and management fmedical p rogressl,WestJ Med 1.4I:347-357, 1984.)
3 . Pail
48
Stimuli
w
lvlechanical
0
il
Thermal
,n''
C fiber
Qltl) Chemical Stimuli
-
&t!
Yrxii
High intensity mechanical
Figure 3-3.Peripheral painpathways. nonnoxiousinformation.ooThe sensationsassociated with A-delta fiber activity are generallydescribedas sharp, stabbing, or pricking.asThe pain sensations transmitted by these fibers have a quick onset after the painful stimulus, last only for a short time, are generallylocalizedto the areafrom which the stimulus arose,and are not generallyassociatedwith emotional involvement.The pain associatedwith A-delta fiberactivationis generallynot blockedby opiates.6T Mechanicaltrauma usually activatesboth C and A-deltafibers.Takethe exampleof a brick landingon someone'sfoot. Almost immediately the individual feelsa sharpsensationof pain. The initial pain is followed by a deepachethat may last for severalhours or days.The initial sharp pain is transmittedby the A-deltafibersand is producedin responseto the highintensitymechanicalstimulationof the nociceptorsas a resultof the impact of the brick.The later,deepache is transmitted by the C fibers and is produced in responseto stimulationby chemicalmediatorsof inflammation releasedby the tissue after the initiai injury
either spinalcord.The C andA-deltafiberssynapse, direcdy or via interneurons,with second-orderneurons in the superficialdorsalhorn of the gray matter 7t SomeA-deltafibers (the substantiagelatinosa).58,68 penetratemore deeplyinto the dorsalhorn to terminate at the normal termination sites of A-beta afferents.The second-orderneuronsin the dorsalhorn are or T cells(Frg.3-4). known astransmission T cells make local connectionswithin the spinal cord,eitherwith efferentneuronsaspaft of spinalcord reflexesor with afferentneuronsthat oroiecttoward . o n L i n u eodr r e p e L i L iC v e- i i b e ra c t i v a L i o n t h ec o r t e xC can sensitizethe T cells,causingthem to fire more rapidly and to increasedreir receptorfield size, and input from other interneuronsoriginatingin the substantiagelatinosaof the spinalcord or from descending fibers originating in higher brain centers can inhibit T-ce1lactiviry72Inhibitory interneuronsin the substantia gelatinosaare activated by input from large-diameter,myelinated, low-threshold sensory neurons (primarily A-beta nerves) that respond to nonpainfu1stimuli.73,7a Theseinhibitory interneurons releasevarious neurotransmitters,including norepinephrine, serotonin, and enkephalins,to modulate rhe flow of t-heafferenrpainpar-hways.-sI hus t-he transmissioncellsreceiveexcitatoryinput from the C fibersand A-deltanociceptorafferentsand inhibitory
Thalamus C fiber (unmyelinated, slow;chronic parn)
Dorsal horn
Brainstem Spinothalamic tracts
Soutce of pain
@
Pathways Central
A-deltaliber (myelinated,last; acute pain)
The peripheral first-order C and A-delta afferents project from the periphery to the gray matter of the
Figure3-4. Ascendingneural pathway of pain via A-delta and C fibers.
Substantia gelatinosa
Fl :::
ai :tc :::l
O e . PATHOLOCYA^D PATIENTPROBLL\/IS
:.:tuf from large-diameter.nonnocicepror sensory ::rerenrs and- From fibers f rom hrgher ^d_"rTldi.ng. : - : r n c e n r e r s ' J( l ' i g .3 5 ) . T h e b a l a n c eo f t h e s ee x c r t a :,-ry and inhibitory inputs influences whether or not ---e individual feels pain and how severe the pain sen;:.rion is .73The inhibition of pain by inputs from non: rciceptor afferents is known as yain gatixg and rs :-scussed in greater detail below in dte section on : , i n m o d u l a t i o na n d c o n r r o lr h e o r i e ' . Transmission cell activation can also increasemus:-e spasm via a spinal cord reflex in which the trans-'-:ssioncell synapseswith anterior horn cells to cause :uscle contractions. The ongoing muscle contrac-rtrns can then cause accumulation of fluid and tissue ::itants. The contracting muscles may also directly :3come initiatorc of further nociceptive impulses by :.echanically compressing the nociceptors. In this .'.ay the combination of ongoing chemical and :echanical stimuli can set up a self-sustaining cycle : - pain causing muscle spasm, which then causes :-ore pain. This is known as the pain-syasm-yaincycle .ig. 3-6). Many interventions indirectly reduce pain, ..en after their direct analgesiceffect has passed, :ecause they reduce muscle spasms and thereby ::rerfere with this self-perpetuating cycle. Ascending second-order nerues carry stimuli ...'ithinthe spinal cord toward the higher brain centers - ig. 3-7). The second-order pathways that carry pain ::imuli are located primarily in the anterolateral , , p e c Lo f l h e c o r d . - 8T h i s a r e ao I t h e s p i n a lc o r d a J s o
49
Figure3-6. Pain-spasm-paincycle: nociceptor activation resultingin T cell activation stimulating an anterior hom cell to causea muscle fiber to contract,resulting in accumulation of fluid and tissue irritants and mechanical c o m p r e s . i oor Fr h er o c i c e p t o r a n idn c r e a s i rrgo c r c e p t o r acuvauon.
transmits information about temperature and touch. Most axons in the anterolateral system cross midline in the spinal cord to ascend contralaterally. Substantia '.cclceptive Information regarding pain is transmitted within the Cerebral gelatinosa :'deltaand C fibers cortex anterolateral cord via both the lateral spinothalamic {inhibitory tnlerneuron) tract and the larger anterospinothalamic tract to projI ...,/....... I ect to the thalamus. The lateral spinothalamic tract Thalamus projects direcdy to the medial area of the thalamus, whereas the anterospinothalamic tract separatesfrom the lateral spinothalamic tract in the brain stem to synapse with neurons in the reticular formation and the hypothalamic and limbic systems to then project to lateral, ventral, and caudal areas of the thalamus. The anterospinothalamic tract also relays information 'lonnociceptive to the periaqueductal gray matter, where there is a l.'betaandA-gammafibers large concentration of opiate recepto$, and is thought, : gure 3-5. Simple diagram showing the gate control thereby, to be associated with pain modulation. Impulses relayed via the lateral spinothalamic tract ::rechanismof pain modulation through the activation are involved in transmission of sharp pain and in :i A-delta and C-fiber input and gating/iniibition by locaiization of the painful stimulus, whereas those : lnnociceptor A-beta sensoryneruesand higher center :rput. sent via the anterospinothalamic tract are involved in
+
3 . Pail
of smooth and cardiacmusclesand with glandular Primary somatosensory secretion.This contrastswith most of the nervoussysconex
Thalamus
lnsula cortex
Hypothalamus
Midbrain
Reticular formation
Periaqueductal grey mater Lateralspinothalamic lract Anlerospinothalamic lracl
Nociceptor Spinal cord
Figure 3-7. Centralpainpathwaysfrom thespinallevelto the higherbraincenters. transmissionof more prolonged,achingpain and are thought to have stronger associationwith the disturbing emotionsthat accompanythe pain sensation. The second-orderneurons synapsein the thalamus with third-orderneuronsto projectto the cortex,from where the sensationof pain canreachconsciousness.
Sympathetic Nervous System Influences The sympathetic nervous system is a component of the autonomic nervous syslem.The autonomic nervous system consists of the sympathetic and parasympathetic svstems and is concerned with the activities
tem, which is concernedwith voluntary activationof the skeletalmusclesor with transmissionof sensory impulsesfrom the periphey'e,sO(Fig.3-8).The sympa*retic newous systemis consideredto be primarily involved in producingeffectstlLat preparethe body for "fight or flight," such as increasingheart rate and blood pressure,constdctingcutaneousblood vessels, and increasingsweating in the palms of the hands. Althoughit is normalfor the sympatheticneffous system to be activatedby acutepain or injury stimulation of the sympatheticnervoussystemefferentsdoesnot usuallycausepain.81HoweveEabnormalsy,rnpathetic activationrcausedby a hyperactiveresponseof the sympatheticnervoussystemto an acuteinjury or by a failure of its responseto subside,can increasepain signsandsymptomsof severityandcauseexaggerated vasomotoror sympatheric acrivirysuchas excessive sweating reactions.In patients with such signs and symptoms,pain relief can often be achievedby interruptingsympatheticnervoussystemactiviqyby chemical or surgicalmeans.B2-84 h addition, stimuli that evoke sympathetic discharges,such as the starde pain. reflexor emotionalevents,frequendyexacerbate sympaIt hascherefore beenproposedthat excessive thetic nervous system activation may increaseor maintainpain.Bo,79 Painthat is believedto involvesympa*reticnervous systemoveractivationhas a variety of names,including causalgia,reflex sympatheticdystrophy (RSD), shoulder-handsyndrome, posttraumaticdystrophy, Sudeck'satrophy, and sympatheticallymaintained pain.BsCurrently,the InternationalAssociationfor the Study of Pain(IASP)recommendsthe use of the term (CRPS).86 comylexregionalyainsyndrome CRPSinvolving tissuedamagewithout nervedamageis categorizedas tvoe I. and CRPSassociated with nerveinvolvementis caiegorizedastype IL86 CRPSgenerallyincludes the following signs and symptoms: severe pain that is out of proportion to the inciting injury or disease,hyperesthesia(excessive reaction to painful stimuli), and allodynia (the sensationof pain in responseto stimuli that are not usuallypainful).CRPSfrequendyalsoincludestrophic changessuch as skin atrophy and hyperhidrosis, edema,stiffness,increasedsweating,and decreased hair growth.86These symptoms generally result in decreased function and,if the syndromeis prolonged, sporryosteoporosis in the affectedarea.8Othersen-
o e.
PATHOLOCY AND PATIENTqROBLEI'\S
51
Eye
Superiorcervical gangron
Salivary granos
ch"d";;;h""'-'eyes,nose,mouth
r
J..",",
Svmoathetic cnatn
Parasympathetic nervoussystem Figure3-8. The autonomic nervous system.
sory vasomotot and skeletal motor abnormalities have also been associatedwith this syndrome.e8 CR.PScan occur in any areaof the body but is most common in the hand and, in suchcases,is frequently associatedwith ipsilateral restriction of shoulder motion. CRPS may develop as a consequenceof major or minor trauma,after visceraldiseaseor cen_ tral nervoussystem lesions,or without any known antecedentevent. The mechanismby which the sympatheticnerv_ ous systemaffectspain is not well understood;how_ ever,it may be the result of direct excitation of the nociceplor> by the sympathecic efferenrfibersor by the neurorransmifters releasedby rhe sympa*teric nerves.The normal activationof sympatheticactivity causedby pain may in some casesactivatethe affei_ ent C fibers,turther increasingpain,which couldthen
increase sympathetic activatioq creating a self_ zustaining vicious cycle. This cycle could amplify the sensationof pain and the signs of sympathetic activity, causingthem to^persistlong after an injury or diseasehas resolved./3 It has aiso b""n propos"i that faulty sympathetic effector mechaniims that cause inappropriate vasoconstriction,vasodilation, increasedcapillary permeabiliqz,or smooth muscle tone may indirectlycauseor exacerbatepain.45
p TheRoleofSubstance SubstanceP is a chemicalmediator that is thought to be involved in the transmissionof neuropathii and inflammatory pain. It is abundantin the centralnervous sy^s^tem and is found in approximately20% of C fibers.89It is alsoreleasedfrom'peripherainociceptors
3 . Pain
52
and has been detectedin inflammatory exudate.90-92 P release Substance has beenshown to excirepaintransmittingneuronsin the dorsalhorn of the spinal cord, and to be involved in nociceptiveprocessingat the spinal cord level.e3'9s Although less than 57o of the neurons in the dorsal horn expresssubstanceP receptors. the maioriryof pairr-transmirting neurons expressthese receptors.SubstanceP levels in the spinal cord increasein responseto induction of joint inflammation and in response to movement of inflamedjoints. Highly elevatedlevelsof substanceP have also been found in the cerebrospinalfluid of patients with persistentpain. SubstanceP receptor activationappearsto be invoived in the sensitization of pain-transmittingneuronsand in the development of hyperalgesia.95-98 Substance P release andreceptor to cissueinjury acLivation is thoughtro be a response andstress. A number of mechanismshave beenorooosedfor the action of substonceP on pain tiansmission. SubstanceP may facilitateexcitationof afferentpain fibers by activatingthe neurokinin-1receptorsin the spinal cord.99'100 When releasedinto the periphery substanceP increasesthe productionofthe inflammatory mediator prostaglandinE2 and the releaseof cytokines from macrophagesand neutrophils.l0l Both prostaglandins and cytokrnessensrtrze primary "Ff"r"^t.^.i.".t^'.
to explain pain control and modulation. These prooosed mechanisms attemDt to correlate what is lnown regardingpeople'seiperienceof pain with the structuresand physiologicalprocessesthought to be involved in pain transmission.Accordingto the gate control theory pain is modulated at the spinal cord level by inhibitory effects of nonnoxious afferent input. Accordingto the theory of endogenousopiates, pain is moduiatedat the peripheral,spinal cord, and corticallevelsby endogenousneurotransmitteffthat havethe sameeffectsasopiates.Psychologicalcentral control mechanismsare also thought to affect pain perceptionand control. Various physical, chemical, and psychological interventionshave beendevelopedbasedon the current understandingof the mechanismsunderlying painmodulation.Forexample,transcutaneous electrical nervestimuiationffENS) deviceswere developed basedon the gate control theory of pain modulation. AIso, the efficacy of a number of establishedtreatment aooroaches is now betterunderstoodbecause the unierlying mechanisms of pain control have becomeclearer.For example,it is now thought that themal agents,which havebeenusedto controlpain for centuries, may be effective for this purpose becausethey gate pain transmissionat the spinal cord.
t
{ l
;
i02
Treatmentsio control pain basedon the inhibition of substance P releaseor on the use of specificsubstanceP antagonistsare currentlybeingresearched.92 Opiates may in part exert an analgesiceffect by inhibiting *re releaseof substanceP from peripheral nervesl however, studies indicate that substanceP receptor-expressing neuronsare not the major site of actionof opiates.96'103
PAIN MOOULATION ANDCONTROL Gate control theory The endogenous opioid s;rstem
A number of observations make it apparent that pain transmission and perception are subject to inhibition and modification. for example, rubbing or shaking an area that hurts can relieve pain in that area, and stress can cause pain not to be felt at the time an injury occurs.Anumber of mechanismshave beenorooosed
Gate Control Theory The gate control theory of pain modulation was first According proporedby Melz.ck andWall in 1965.-3 to *Lis theory severityof the pain sensahonrs determined by the balanceof excitatory and inhibitory inDuts to the T cells in the spinal cord. These ce1ls receiveexcitatoryinput from a and A-delta nociceptor afferentsand inhibitory input, via the substantia gelatinosa,from large-diameter A-betanonnociceptor sensoryafferents.Increasedactivity of the nonnociceptorsensoryafferentscausespresynapticinhibition of the T cells,and thus effectively closesthe spinal the sensation sateto the cerebralcortexanddecreases ot parn(seefrg. 5-Jl. Many physical agents and rnterventrons are thoughtto controlpainin pan by activatingnonnociceptivesensorynerves,thereby inhibiting activation of pain transmissioncellsand closingthe gate to the For example,electrical transmissionof pain.1O4'tos stimulation,traction, compression,and massagecan ali activate low-threshold, large-diameter,nonnoci-
t
T
E
: I
One . PA|HOLOCY
AND PATIENT PROBLEMS
J5
:3Jtivesensorynervesandthereforemay inhibit pain by naloxone,an opiate antagonist.l13 Thesefindings :;rsmission by closingthe gateto paintransmission demonstratedthat these endogenouspeptides are '-.h"
Figule3-9. Indirect inhibition of pain by application of opiatesto opiate receptom.
54
3 . P/ritl
Electricalstimulation of areaswith hish levels of suchasrhePAGMandr-heraphenucleus, opiopeprins. hasbeenfound to stronglyinhibit the transmissionof pain messagesby some spinal dorsal horn neurons, therebycausinganalgesia.118,119 Electricalstimulation of theseareasof the brain can also relieveintractable pain in humans and increasethe amount of betaendorphinin their cerebrospinalfluid (CSI).120 Since these effects are reversedby the administrationof naloxone,they have beenattributedto *re releaseof opiopeptins.l2lThe concentrationof opiatereceptors and opiopeptinsin the limbic system,an areaof the brain largely associatedwith emotionalphenomena, also provides an explanation for the emotional responsesto pain, and for the euphoriaand relief of emotional stressthat is associatedwith use of morphine andthe releaseof opiopeptins.l22 The releaseof opiopeptinsis thought to play an important role in the modulation and control of pain during times of emotional stress. Levels of opiopeptinsin the brain and CSFbecomeelevated,and pain thresholdsincreasein both animalsand humans when stressis inducedexperimentallyby the anticipation of pain.r23'124 Experimentally,animals have been shown to expedencea diffuse analgesiawhen placed under stress.Humans demonstratea naloxone-sensitiveincreasein pain thresholdand a parallel depressionof the nociceptive flexion reflex when su6jectedto emotional s;ess.124,125 These findings indicatethat pain suppressionby stressis most likely causedby increasedopiopeptin levels at the spinal cord and highercentralnervoussystemcenters. The endogenousopiate system also provides an explanationfor the paradoxicalpain-relievingeffects of painful stimulationand acuouncture.Bearableleve1sof painful stimulation,suchastopicalpreparations that causethe sensationof burning,or noxiousTENS that causesthe sensationof pricking or burning,have been shown to reducethe intensity of less bearable preexistingpain in *re areaofapplicationand in other areas.125 Painful stimuli have also been shown to reduce the nociceptive flexion reflex of the lower limb.126Becausethese effectsof painful stimulation areblockedby naloxone,they arethought to be medi1 2 -1 2 8 aL e db y o p r o p e p t i in) .11 2 5 P a i nm a yb e r e l i e v e d becausethe applied painful stimulus causesneurons in the PACM regionsof the midbrain and thalamusto produceandrelease opiopeptins.l2s Placeboanalgesiais alsothought to be mediatedin paft by opiopeptins.This claim is supportedby the
observation that the opiate antagonist naloxone can reverse placebo analgesia and that placebos can also produce respiratory depression, a typical side effect of oPioids.l29'130
MEASURING PAIN Visual analog and numeric scales Comparison with a predeffned stimulus Semantic differential scales
To determine the most appropriatetreatment for a patient'spain and to assessthe efficacyof suchtreatment, it is helpful to assessthe natureand severiryof d:repatient'sexperienceof pain. Suchan assessment should attempt to ascertainthe causesand sourcesof pain, the intensity and duration of pain, and the degreeto which the pain resultsin disabilityor handicap.Variousmethodsand assessment toolshavebeen developedto quantifi/ and qualify both experimentally induced and clinical pain. These methods are basedon patientsrating their pain on a visual analog or numeric scale,comparingtheir presentpain with that experiencedin responseto a predefined,quantifiable pain stimulus, or selectingwords from a list to describetheir present expedenceof pain. Different tools providedifferentamountsand typesof information and requirediffering amountsof time and cognitive ability to complete.
Visual Analog andNumeric Scales Vsual analogandnumericscalesassess pain severiry by askingthe patient to indicatethe presentlevel of pain on a drawn line or to ratethe pain numericallyon a scaleof 1 to 10 or 1 to 100.131 With a visualanaloe scale.the patientmarksa positionon a horizonraloi verticalline, where one end of the line representsno pain and the other end representsthe most severe pain possibleor the most severepain the patient can imagine (Fig.3-10).With a numeric rating scale,0 is no pain and 10 or 100,dependingon the scaleused,is the mostseverepainpo'sibleor the mort qeverepain the patientcanimagine. Scalessimilarto the visualanalosor numericscales h a v eb e e nd e v e l o p e ldo r u s ew i t h i n d i v r d u a lws h o have difficulty using numeric or standard visual analogscales.lor example,childrenwho understand
Oqe . PATHOLOGY AND PATIENT PROBLEMS
Worstpain possible Pleaseplacaan X on thislineto indicat€ howsevereyourpainis now. Worstpain possible
f L
F .
f
tf
cc
Thesetypes of scalesare frequendyusedto assess the severiry of a patient's clinical pain because they are quick and easy to administer, are easily understood,and provide readily quantifiabledata.131 However, visual analog and numeric scalesprovide only a singlemeasureof the patient'spain complaint and fail to provide information about the patient's affectiveresponseto pain or the effect of the pain on his or her functionalactivity level.Also the reliability of visual analogand numeric rating vades between individuals and with the patient group examined, although the tr,vo scales have a high degree of agreementberween them.132These types of measures are most useful in the clinical setting when a quick estimate of a patient's perceivedprogressor change in symptoms over time, or ir responseto different activities or treatment interventions, is desired.
No pain
Figure3-10.Visual analogscalesfor rating pain severity.
witha Predefined Stimulus Gomparison
words or pictures but are too young to understand numericreDresentations of Daincan use a scalewith faceswith differentexpressions to representdifferent experiencesof pain, as shown in lig. 3-11.This type o[ scalecan also be used to assessoain in patients with limited comprehensionbecauseof linguage barriers or cognitive deficits. Pain scalesare also availablefor rating pain in very young children and infants. These are based on describingthe child's expressionand behavior[able 3-1).
Painquantificationmethodsthat involve comparison with a predefinedpainful stimulus are intended to provide a greaterdegree of intersubject reliabilit'y than visualanalogandnumericscales.Ior this rype of assessment, the individual comparesthe severity of his or her symptomswith the samepredefinedstimulus, causingtheir rating scalesto be more similar. Stimuli used for comparisoninclude the application of a toumiquet to the upper extremity to produce ischemiaand the applicationof electrical,thermal,or fingertip pressurestimuli.133,13a The toumiquet pain test is reported to correlatewell with pain assessMatching the ments using a visual analog scale.135
Which face shows how much hurt you have now?
/a\ /G\ /a\ \c/ a-Ar,;\ aA\ \7 !, 0 No hurt
1 Hurts littlebit
\r/
2 Hurts littlemore
\r/ \tY
3 Hurts evenmore
4 tlurls wholelot
5 Hurts worst
Figure3-11. Facescalefor rating pain severity in children age 3 years and older and others with limited numeric communication ability. The patient usesthis tool by pointing to eachface and using the brief word instructions under it to describepain intensiry from Wong DL, Peny SE,Hockenberry M} Matemal Child NursingCare,ed 2, St. Louis,2002, Mosby.)
56
p
3 . P/ril
f-t
*"orr"tal Infant Pain Scale(NIPS)Operational Definitions
Behaviorand score
Description
Facial Exqession 0 Relaxedmuscles 1 Cnmace
. Restfulface,neutralexpression . Tight facialmuscles,furrowedbrow, chin,jaw (negativefacialexpression n^<"
cty 0-Nocry I - Whimper 2 -Mgorouscry
-^,
'fh
".,1
h'^,-\
o Quiet, not crying o
Mild mnrnino
infPrmrrfPnr
. Loud screams,nsing,shrill,continuous(Note:Silentcry may be scoredif baby s ntubaced, a" evrdenced by obvrousmourh.lacialmovemenr.t
Breathing Patterns 0 - Relaxed 1 Changein breathrng
o Usualpatternfor thrsbaby o Indrawng. 'regular.tasterrhanusu"l.gaggrng. breachholding
Arrrrs 0 Relaxed/restraned 1 Flexed/extended
. No muscularrigidiry occasionalrandommovementsof arms . Tense,straightarms,rrgidor rapid extension,flexion
Legs 0 Relaxed/restrained 1 - Flexed/extended
. No muscularngidiry occasionalrandom1e8movement . Tense,straiShtlegs,rigid or rapid extension,flexion
Stateof Atorsal 0 - Sleeping/awake I Fussy
o Quret,peaceful, sJeeping, or alertandsettled o A1ert,resdess,and thrashing
NeonataiInfantParnScaleO 1989,Ch dren'sHosprtalof EasternOnrano.Usedwrth permrssron. Score0 = no parnhkely,maxlmum score7 = severeparnhkely.
intensity of clinical pain with electrical, thermal, or fingertip pressure stimuli has also been reported to correlate well with other measures of pain and has been reported ':r' to have a high degree of intrasubject reliability. lJ- gowever. I hese:ypes o[ pajn arressment tools also have a number of limitations. They require that the patient expefience clinical pain at the time at which the comparison stimulus is applied to make an accurate compadson. Also if a patient has severe pain, it may be both impractical and ethically unacceptable to induce a sufficiendy intense pain to provide a comparison with the clinical pain. For patients with pain that is different in quality from the pain of the expeimental stimulus; for example, burning or tingling rather d-ranthe ache of ischemic pain, a quantitative comparison may not be possible or meaningful. This type of pain measure also fails to
take into account, or report on, the emotional, behavioral, or motivational components of a patient's clinical condition. Thus although comparison pain measures may allow for a reliable gauge of some types of pain, particularly experimentally induced pain or clinical acute pain that is moderate or less severe, they are not well-suited for measuring clinical pain that is severe or chronic, or that has a quality different from that of the comparison stimulus.
Differenlial Semantic Scales Semantic differential scales consist of word lists and categories that represent various aspects of the patient's pain experience.The patient is asked to select, from these lists, words that best describe his or her present experienceof pain. These types of scales
One . PATHOLOGY AND PATIENTPROBLEMS
rre designedto collecta broad rangeof information :bout the patient's pain experienceand to provide ;uantifiable data for intra- and intersubiectcompar,,ons.The semanticdifterentialscaleincludedin rhe ,McGillpain questionnaire,or variationsof this scale, painl38-140 :re commonlyusedto assess Gig. 3-12). This scaleincludesdescriptorsof sensory affective, :nd evaluative aspects of the patient's pain and =roupsthe words into vadouscategorieswithin each rf these aspects.The categodesinclude temporal, ,.patial,pressure,and thermal to describethe sensory :spects of the pain; fear, anxret'4,and tension to jescribethe affectiveaspectsof the pain;and the cogitive experience ofthe painbasedonpastexpedence :nd learned behaviors to describe the evaluative .spectsof the pain. The patient circlesthe one word r eachof the applicablecategoriesthat bestdescribes :hepresentpain.13e,140 Semantic differential scales have a number of comparedwith other :dvantagesand disadvantages of pain measures. They allow assessment and rypes quantificationof various aspectsof the pain's scope, quality,and intensiry Counting the total number of '.vords chosen provides a quick gauge of the pain of pain severity severiryA more sensitiveassessment :an be obtained by adding the rank sums of all the '.vordschosento producea pair ratingindex (PRI).For sreaterspecificitywith regardto the mostproblematic area,an index for the three malor categoriesof the questionnairecan also be calculated.laO The primary of this scalearethat it is time-consuming 3isadvantages :o administer,and it requiresthe patient to have an ntact cognitivestateanda high levelof literacy.Civen -iese advantagesand limitations,the most appropriateusefor this type of scaleis when detailedinformaion about a patient's pain is needed,such as in a :hronic pain treatmentprogramor in clinicalresearch.
0therMeasures Other measuresor indicators of pain that may provide additionaluseful information about the individual's pain complaint and clinical condition include daily activiq/pain logs indicating which activities easeor aggravatethe pain, body diagramson which *re patient canindicatethe locationand natureof the pain (Iig.3-13), and open-ended,structuredinteru1"-r.141'1426physical examination that includes observationof posture and assessmentol strength, mobiliry sensation,endurance,responseto func-
J/
tional activity testing,and soft tissuetone and qualiry canalsoaddvaluableinformationto the evaluationof the severityand cause(s) of a patient'spain complaint. In selectingthe measuresto be used to assess pain, one should considerthe duration of the symptoms, the cognitive abilities of the patient, and the amount of time appropdateto assessthis aspect of the patient's compiaint. In many situations, a simple visual analogscalemay be sufficient to provide information regardinga progressivedecreasein pain as che parient recoversfrom an acute injury. However,in more complexor prolongedcases,more detailed measures such as semantic differential scalesor a combinationof severalmeasuresare more appropriate.
APPROACHES PAIN MANAGEMENT Pharmacological approaches Systemic aoalgesics Spinal analgesia Local injections to painful structrres Physical agents Multidisciplinary pain treatnent programs
Once the severity and nature of an individual's pain hasbeenevaluatedand, ideally,its sourceand nature determined,the goaiso[ treatmentinclude eliminating the cause of pain, controlling the nociceptor input, and reducing the degree of patient impairment. A wide rangeof pain managementapproaches may be used to help achievethese goals.These approachesare basedon our cuffent understanding of pain transmissionand control mechanisms,They may act by controlling inflammation, altering nociceptorsensitiviry increasingbinding to opiate receptors, modifying nerve conduction, modulating pain transmission at the spinal cord level, or altering higher-levelaspectsof pain perception.ln addition, some treatmentapproachesalso addressthe psychological and social aspects of pain. Different approachesare appropriate for different situations and clinical presentationsand are frequently most effectivewhen usedtogether The primary intervention used to alleviate pain is the administration of pharmacologicalagents. Although pharmacologicalagentsare often effective for this purpose, they can also produce a variety
3 . Paiq
58
Whaidoesyourpainteellike? Someof the words belowdescribeyour presentpain. Indicatewhich wordsdescribeit best. Leaveout any word group group-the onethatappliesbest thatis notsuitable.Useonlya singlewordin eachappropriate 1
2
'1Flickering 2 Quivering 3 Pulsing 4 Throbbing 5 Beating .6 Pounding
l Jumping 2 Flashing 3 Shooting
3 l Pricking 2 Boring 3 Drilling 4 Stabbling 5 Lancinating
4 1 Sharp 2 Cutting 3 Lacerating
5
6
7
8
'1Pinching 2 Pr€ssing 3 Gnawing 4 Cramping 5 Crushing
'! Tugging 2 Pulling 3 Wrenching
1 Hot 2 Burning 3 Scalding 4 Searing
l Tingling 2 ltchy 3 Smarting 4 Stinging
I
'10
11 l Tiring 2 Exhausting
l Sickening 2 Suffocating
14
15
16
1 Fearful 2 Frightful 3 Terrifying
1 Punishjng 2 Gruelling 3 Cruel 4 Vicious 5 Killing
1 Wretched 2 Blinding
17
18
19
1 Spreading 2 Radiating 3 Penetrating 4 Piercing
'1Tight 2 Numb 3 Drawing 4 Squeezing 5 Tearing
l Dull 2 Sore 3 Hurting 4 Aching 5 Heavy
1 Tender 2 Taut 3 Rasping 4 Splitting
I Cool 2 Cold 3 Freezing
1 Annoying 2 Troublesome 3 Miserable 4lntense 5 Unbearable 20 l Nagging 2 Nauseating 3 Agonizing 4 Dr€adful 5 Torturlng
Figure 3-12. Semantic differential scale from the McGill Pain Questionnaire. (Reprinted from Melzack R: The McGill Pain Questionnaire: major properties and scoring methods. In Pain, Amsterdam, 7975, Elsevter Science.)
ofadverseeffects.Thereforethe useofphysicalagents, which alsoeffectivelycontrolpainin many caseswhile producingfewer adverseeffects,may be more appropriate.Somepatients,particularlythose with persist-
ent pain,may needintegratedmultidisciplinarytreatment, which includespsychologicalaswell asphysiologicaltherapies,to achievepain relief or a retum to a morenormalfunctionalactivitylevel.
Ohe . PATHOLOCY AND PATIENT PROBLEITIS
59
Nonsteroid aI anti i nf Iam m atory dru gs NSAIDs have both analgesicand antiinflammatory properties and can therefore relieve pain from both inflammatory and noninflammatory sources. 4/7> shooringpain They inhibit peripheral pain and inflammation by inhibiting the conversion of arachidonic acid to prostaglandinsby cyclooxygenase;howeveq much X Sharppain lower doses and blood levels are required to NSAIDs reducepain than to reduceinflammation.143 been shown to reduce both spontaneous have Pleasemarkthetype and mechanicallyevoked activity in C and A-delta andlocationof your painon thesepictures fibers in acute and chronic models of joint inflammation. Evidencealso existsthat NSAIDSexert central analgesiceffects at the spinal cord and at the dtalamus.144-148 Front Back A.lthoughNSAIDs have excellentshort- to mediumFigure3-13. Body diagramsfor marking the location and term applicationfor the control of moderatelysevere nature ofpain. pain causedby musculoskeletaldisorders,particularly when the pain is associatedwi*r inflammation, sideeffectscanlimit their long-termuse.The primary long-term complicationof most NSAIDs is gastroinPharmacological Approaches testinal iritation and b1eeding.149,1s0 NSAIDs also cause decreased platelet aggregation and thus Pharmacologicalanalgesicagents control pain by modifying inflammatory mediatorsat the penphery, prolonged bleeding time. They can cause kidney damage, bone maffow suppression, rashes and alteringpain transmissionfrom the periphery to the anorexia,and decreasedrenal blood flow in dehycortex,or alteringthe centralperceptionof pain. The selection of a particular pharmacologicalanalgesic drared natienrs.lsll52 tlsins different NSAIDs togetherincreasesthe risk of sideeffects. agentdependson the causeof the pain, the length of The first NSAID was aspirin.Many other NSAIDs, time the individual is expectedto needthe agent,and the side effectsof the agent.Pharmacological agents such as ibuprofen (Motrin), naproxen sodium (Naprosyn,AJeve),and piroxicam (Feldene),are now may be administeredsystemicallyby mouth or injection, or locally by injection into sffucturessurround- availablebo*r over *re counter (OTC) and by preing the spinal cord or into painful or inflamed areas. scription. The principal advantagesof these newer NSAIDs over aspirin are that some have a longer These different routes of administrationallow conduration of action, allowing lessftequent dosingand centrationof the drug at different sitesof pain transbetter compliance,and some causefewer gastroinmission to optimize the control of symptoms with testinal side effects. However, for most patients, varyingdistributions. aspirin effectively relievespain at considerablyless expense,although with a slighdy higher risk of Systemicanalgesics gastrointestinalbleeding, than the newer NSAIDs. Administration of a systemicanalgesicis usuallythe Recendy, specific cyclooxygenaseq,?e 2 (COX?) primary me*rod of pain management.This type of inhibitor NSAIDs, such as celecoxib (Celebrex) treatmentis easyto administerand inexpensive,and can be an effective and appropdate pain-relieving and rofecoxib (Vioxx), have been developed.Prior NSAIDs inhibited both cyclooxygenasetypes 1 and interventionfor many patients.A wide rangeof analgesic medicationscan be systemicallyadministered 2. CyclooxygenaseLype 1, catalyzesthe production of prostaglandins associated with joint inflamorally or by other routes.Thesemedicationsinclude mation while cyclooxygenaseUtpe 2 catalyzes (NSAIDs), nonsteroidalantiinflammatorydrugs acetproduction tlte of prostaglandinsthat protect the aminophen,opiatesand opioids,andantidepressants.
fuIil,lo.n
60
3 t Pain
effects. They control pain that cannot be relieved by nonnarcotic agents and are most effective when the pain is dull and poorly Tocalized. The side effects of opiates, including nausea, vomiting, sedation, suppiession of cough, gastrointestinal mobility, and respiration, as well as their propensity to causephysicai iependence and depressionwith long-term use, limit their application for the long-term management of drugs. -,s.,rfoik"1eta1 pain. Respiratory depression also limits the dose that can be used even For short-term Acetaminophen administration. Tolerance causesdrug doses to mainAcetaminophen (Tylenol@) is an effective analgesic tain pain conlrol and to experience withdrawal, and for mild to moderately severe pain; however, unlike causesa consequent rebound increase in pain when an NSAID, it has no clinically significant antiinflamuse of the drug is decreased or discontinued after matory activity.lsa Taken in the same dosage as long-term use. Opiates are generally used clinically to aspirin, it has analgesic and - .antipyretic effects reliene postoperative pain or pain due to malignancy' comparable to those of aspirin.l5aAcetaminophen ts Unfortunately, concerns about tolerance and side administered primarily by the oral route, although effects frequently result in the administration of administration by suppository is effective for patients insufficient doses of these medications to patients who are unable to take medications by mouth. with severe pain, resulting in unnecessarilyhigh levAcetaminophen is useful Forpatients who cannot toiThe risk of psychological addiction els of pain.157,IsB erate NSAIDs because of gastric irritation or when or habituation should not prevent the appropriate use prolonged bleeding time causedby NSAIDs would be of opiate medications, particularly in the managea disadvantage.Prolonged use or large doses of acetament of terminal illness. minophen can causeliver damage;this risk is elevated Opiates can be delivered by mouth, intravenously, an occaalso are rashes Skin alcoholic. in the chronic 6 popular or by direct intraarticular iniection.159'160 sional side effect of this medication. particuiarly and effective means of administration, for hospitalized patients, is patient-controlled anaiOpiates a pump to Opiatesarenarcoticdrugsthat containopium,deriva- gesia (PCA). With PCA, patients use ielf-administer smali, rcpeated intravenous doses' dvesof opium,or any of severalsemisyntheticor synThe amount of medication delivered is limited by thetic drugs with opium-like activiqy. Morphine, preestablished dosing intervals and maximum doses hydromorphone, fentanyl, and meperidineare exama defined period. Pain control is more effective within appiicaclinical for used pies of opiatescommoniy eFfects are less common with this adverse and slightly have drugs tions. Although these opiate than with more convenadministration oF means opito all bind they differentmechanismso[ action, opiate administration tional,physician-controlled of them of all receptors,and the-effects
qut mucosa. Thus COX2 inhibitors have more speiific antiinflammatory effects and a lower risk of gastrointestinal irritation and bleeding. NSAIDs are primarily administered orally, although one, ketorolac fforadol@), is available for administration bv iniection.15311t" mode of administration does not aiter the analgesic or adverse effects of these
ate-specific methods.'"','"" are reversed by naloxone'1ssThe opiates differ and primarily in their potency, duration of action, restrictionof useasa resultof variationsin pharmaco- Antidepressants particularlythe tricyclicssuch as Antidepressants, dynamicsandpharmacokinetics' (Elavil@), have been found to be an amitryptiline It hasbeenproposedthat opialesprovideanalgesia of chronic pain treatcomponent adjunctive effective by mimicking the effectsof endorphinsand binding effective for this being doses with smaller ment, receptorsitesin the centralnervous to opiate-specific for the treatused typically those than application systlm.ls6'1heymay also relievepain by inhibiting these drugs o[ The efficacy depression.l63'164 of ment tire release of presynaptic neurotransmittersand to be thought pain is of chronic treatment the for inhibiting the activity of interneurons early in the and function, nerve on sleep, effects their to nociceptive pathways to reduce or block C-Fiber related with chronic patients that shown have Studies mood. inputsinto the dorsalhorn.116 pain who are also depressedreport much-higher levWhen givenin sufficientdoses,opiateswill control Lls of pain and show more pain-related behaviors even the most severeacutepain with tolerableside
One o PATHOLOGY AND PATIENT PROBLEMS
-j:an those who are not depressed.1'6s'1'66 Although it -i not certain if the higher 1evel of pain in such :arients is the cause or the product oF their depres::cn, the use of antidepressants in either situation ::ray prove beneficial. Spinalanalgesia :-ain relieFmay be achieved by the administration of irugs such as opiates, local anesthelics,and corlicos:eroids into the epidural or subarachnoid spaceof the ,rinal cord.167This route of administration provides ,nalgesia to the areas innervated by the segments of ::e cord receiving the drug and is therefore most =Jective when the pain has a spinal distribution, such .s a dermatomai distribution in a single limb. The :im.ary advantages of this route oF administration =:e that the ' ^ ^ - " .drus * D " . / | bvoasses the blood-brain barrier .:rd that high concentrations reach the spinal cord at :riate receptors at sites of nociceptive transmission, --:rusincreasing the analgesic effects while reducing :dverseside effects. Opiates administered spinally exert their effects by 'rimulating opiate receptors in the dorsai horn of -:'respinal cord.168When administered spinally, fatsoluble opiates have a rapid onset and a short dura=on of action, whereas water-soluble opiates have a slow onset and a more prolonged duration of .ction.169 Local anesthetics delivered spinally have --ne unique abilir,y to completely block nociceptive =ansmissionl however, with increasing concentra:on, these drugs also block sensory and then motor =ansmission, causing numbness and weakness.17o {igh dosesof these drugs can also causehypotension. These side effects of local anestheticslimit their appli;ation to the short-term control of pain and diagnostic rurposes. Catabolic corticosteroids, such as cortisone and dexamethasone, can be administered to the epidural or subarachnoid spaceto relieve pain due to nfiammation of the spinal nerve roots or surrounding strLlctures. These drugs inhibit the inflammatory :esponse to tissue injury; however, because of the side effects of repeatedor prolonged use, including fat and muscle wasting, osteoporosis, and symptoms of Cushing's syndrome, these drugs are not suitable for iong-term application.
Localinjection Local injection of a corticosteroid,opiate,or a local anestheticcan be particularlyeffectivefor relieving pain associatedwith local inflammation.ls9Such
67
injections can be administered into joints, bursae, trigger points, or around tendons and can be used for therapeutic purposes, to relieve pain, or for diagnostic purposes in identification of the structure(s) atfauh.l7l Although this type o[ treatment can be very effective, repeated local injections of corticosteroids are not recommended because they can cause tissue breakdown and deterioration. Local injections of corticosteroids directly after acute trauma are also not recommended because these drugs reduce the inflammatory response and may thus impair healing. Local injections of aneslhetics generally provide only short-term pain relief and are therefore used primarily during painFulprocedures or J:^^-^^+:^^11,, u r d S r r u ) L r L4 r r y .
PhysicalAgents Many physical agents effectively control or relieve pain. They are thought to exert these effects by moderatingthe releaseof inflammatory mediators, modulating pain at the spinal cord level, altering nerve conduction, or increasingendorphin levels. They may also indirectly rcducepain by decreasing the sensitivityof the musclespindlesystem,thereby reducingmuscle spasms,or by modifying vascular tone and the rate of blood flow, thereby reducing 4 lnaddition, physicalagents edemaor ischemia.172-17 may reducepain by helpingto resolvethe underlying causeof the painfulsensation. Different physical agentscontrol pain in different ways. For example, cryotherapy,the applicationof cold,controlsacutepain in partby reducingthe metabolic rate and thus reducing the production and reieaseof inflammatorymediatorssuchasserotonin, histamine,bradykinin, substanceP, and prostaglanThesechemicalscausepain direcdyby stimudins.17s iating nociceptors and indirectiy by impairing the local microcirculationand, in so doing, can damage tissueandimpair tissuerepair.Reducingthe releaseoF inflammatory mediatorscanthus direcdy reiievepain causedby acute inflammation and may indirectly limit pain by controllingedemaand ischemia.These short-termbenefitscan also optimize the rate o[ tissuehealingand recovery. Cry otherapy, thermotherapy, electrical stimulation, and traction, which provide thermal, mechanical, or other nonnociceptivesensory stimuli, are thought to alleviate pain in part by inhibiting pain transmissionat the spinalcord. Physicalagentsthat
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3 . Pain
act by this mechanismcan be usedfor the treatment 'needed,and so becomesmore independentof the of acuteand cfuonic pain becausethey do not gener- health care practitionerand pharmacologicalagents. ally produce significant adverse effects or adverse The application of such physical agents at home interactions with drugs, and they do not produce can be an effective component of the treatment physical dependencewith prolonged use. They are of both acute and chronic pain.177This type of selfalsoeffectiveand appropriatefor pain causedby contreatment can also assistin containins the costs of ditions that cannot be direcdy modified, such as medicalcare. pain causedby malignancyor a recentftacture,and Physical agents.usedeitheraloneor in conjunction for pain caused by peripheral nervous system with other interventions, such as pharmacological pathology, such as phantom limb pain and periphagents,manual therapy, or exercises,can also help eralneuropathy.lT6 remediatethe underlying causeof pain while conElectrical stimulation is also thought to control trolling *re pain itself. For example, cryotherapy pain in part by stimulatingthe releaseof opiopeptins applied to an acute iniury controls pain; however, at the spinalcord and at higherlevels.l2BStudieshave this treatment also controls inflammation, limiting shown that pain relief by certain types of electrical further tissue damage and pain. In this case, the stimulationis reversedby naloxone.128 use of NSAIDs, rest, elevation, and compression, Physicalagentshave many advantagesover other in conjunction with cryotherapy,could also prove pain-modifying interventions. They are associated beneficial, although it may make assessmentof with fewe5 andgenerallylesssevere,sideeffectsthan the benefits of any one of these rnterventlonsmore pharmacologicalagents. The adverse effects from difficult. The selectionof physical agentsand their using physical agentsto control pain are generally specificmechanismsof action and modesof applicalocalized to the area of application and are easily tion for controlling pain are discussedin detail in avoidedwith care in applying the treatrnent.When Section2 of this book regardingthe differenttypes of usedappropriately,attendingto all contraindications . h - . ; " , 1 " " " . r . and doserecommendations,the risk of further injury ftom the useof physicalagentsis minimal. For examMultidisciplinary PainTreatment Programs ple, an excessivelywarm hot pack may causea burn in the areaof application,but this risk can be miniOver the past 2 to 3 decades,multidisciplinary prorntzedby carefully monitoring the hot pack's tempergramshave beendevelopedspecificallyfor the treatature, using adequate insulation between the hot ment of chronic pain.a,178 Theseprogramsare based pack and the patient, not applyinghot packsto indion a biopsychosocialmodel of pain and attempt to vidualswith impaired sensationor an impaired abiladdressthe multiple facets of chronic pain with a ity to report pain, and by checkingwith the patient multidisciplinary coordinated program of care.4'179 for any sensationof excessiveheat. Patientsalso do These programs attempt to addressnot only the not developdependenceon physicalagents,although physical and physiological aspectsof the patients' they may wish to continue to use them even after pain but also the behavioral,cognitive-affective,and they are no longer effective because they enjoy environmental factors contributing to their sympthe sensation or attention associatedwith their toms by the useof medical,psychological,and physiapplication.Ior example,patientsmay wish to concal interventions.lBo,lBl tinue to be treatedwith ultrasoundeventhough they Psychologicalintervention is focusedon improvhave reacheda stageof recoverywhere they would ing the coping skills of patients and modi$ring benefit more from active exercise.Physicalagents their behavior,whereasphysicalactivitiesarefocused also do not generallycausea degreeof sedationthat on reversing the adverse effects of the sedentary would impair an individual'sabiliry to work or drive lifesryle adopted by most patients with chronic sarery. pain. Coping skills can be improved with relaxation Many physical agents have the additional training, activity pacing,distractiontechniques,cogadvantageof being readily used independendyby nitive restructuring, and problem solving.1B2,1B3 patientsto treat themselves.Ior example,a patient Behaviormodificationusingthe principlesof operant can be educatedto apply a pain-controllingagent, conditioning can also alter the patient's perception such as heat, cold, or electricalstimulation, when of and responseto pain.184Graded activation and
ex di
ac AI
le th m m be to
th m Ie n(
One . PATHOLOGY AND PATIENT PROBLEMS
::.:3rciseprograms,in which the patient iearns the ---:erenceberweenhurt and harm, can help patients .,.-:ih chronic pain retum to a more functional, ,:ive lifestyle.l8s The patients' family members ::: generally involved in these programs by -::rning appropriatecopingskillsfor *remselvesand -:e patient. Such involvement can assistthe family :embers to help individuals with chronic pain :-.cre effectively rather than reinforce pain-related ::haviors. In contrastwith traditional treatment approaches :--,acutepain,in which the goal of careis to eliminate =e sensation of pain, the goals of care in most =ultidisciplinarypain treaffnentprogramsalsoinclude ::rning to cope and function with pain that may r rt resolve,although frequently patientsalso report
63
a reduction in pain after completing these proGoals of treatment also generally grams.186'187 include decreasingdependenceon health care per sonnel and pain relieving medications,particularly h a b i t - f o r m r nogp i a r e so r o t h e rn a r c o L i cisn:c r e a s i n g physical activities; and retuming patients to their usual social roles. If necessarynarcoticmedications are replacedwith non-habit-forming drugs or with nonchemicalmodes of pain relief such as exercise or physical agents.aMany studies have shown that multidisciplinary pain treatment programs do result in increasedfunctional activity levels while reducing pain behaviors and the use of medical i n c e r v e n t i o ni ns p a r i e n t sw i t h c h r o n i cp a i n . 8 8l q l These programs have also been shown to be cost elfe ctrve.rBI,I 92194
) Clinical CaseStudies a The following casestudiessummadzethe conceptsof pain discussedin this chapterBasedon the scenariopresented,an evaluationofthe clinicalfindingsandgoalsof ft€atmentareproposed.This is followed by a discussion ofthe factorsto be consideredin treatmentselection.
Case'l M? is a 45-year-oldfemale who has been referredto physicaltherapywirh a diagnosisoflow backpain and a physician'sorderto evaluateand fteat.MP complainsof severecentral low back pain that is aggravatedby any movement, particularly forward bending. Shereports no radiation of pain or other symptoms into her extremities.Paindisturbsh€r sleep,and sheis unableto work at her usualsecretarialjob or perform her usualhousehold taskssuchasgroceryshoppingand cleaning.Shereports that the pain startedabout4 daysago,whenshe reached to pick up a suitcase,and hasgraduallydecreasedsince its initial onset ftom a severity of 8, on a scaleof 1 to 10,to a severity of 5 or 6. Her only curent treatment is 600 mg ibuprofe4 which she is taking 3 times a day. The obiective exam is significant for resuicted iumbar range of motion in all planes. Forward bending is restricted to approximately 207o of norma| backward bending is resfticted to approximately 50% of normal, and side bendingis resriccedro approximately30qoof nonnal in both directions. Palpablemuscleguardingand tendemess in the lower lumbar areaoccur when the patient is standing o! prone. All neurological testing, including straight
leg raise and lower exftemity sensation, strength, aad reflexesarewithin normalLirnics. OF CLINICALFINDINGS EVALUATION This patient seeksmedical treatment for the impainrlents o[ low back pain and restricted lurnbar range of motion. These impairments have resulted in difficulties with her nomal functionalactivitiesof sleeping,working, shopping, and cleaning. A.lthough further analysis may help identify the speciticsffucturescausingthis patient'spain, its rccentonsetrelatedto a specificevent usingthe painful areaand its gradualresoludonover tl.re last few days indicatethat her pain is acute and is the result of local musculoskeletalinjury and probable inFlammadon. PREFERREDPRACTICEPATTERN Impaired Joint Mobility, Motor lunction, Muscle ?erformance, Range of Motion, arrd Reflex Integrity AssociatedWith SpinalDisorders,(4I). PLANOF CARE The goalsof treatmentat this time includecontrolling pain to allow MP to sleep and return to other functional activities as soon as it is safe for her to do so. The anticipated goals of treatment would also include regaining normai lumbar rante of motion and, ideally, preventing a recurtence of the present svmDtoms, Continued
64
3. Pniu
) Clinical Case Stttdies-cottt'd ASSESSMENTREGARDINGSELECTIONOF THE OPTIMAL TREATMENT The optimal intervention would ideally address the acute s1'rnptomof pain and the underlying inflammation and, if possible,would help to resolveany underlying structural tissue damage or changes.Although a single ffeatxoentmay not be abie to addressall of theseissues, treafinentsthat addressasmany of theseissuesaspossib1eand that do not adverselyaffectthe patient'sprogress arerecommended. As is explainedingreaterdetailin Part 2 of this book, a number of physical agents, induding cryotherapyand electricalstimulation,may be used to control this patient's pain and reducethe probable acute inflammationof the lumbar structures,and lumbar traction may also help to relieve her pain while modifying the underlying spinal dysfuncrion.
Case 2 tj is a 45-year-oldfemalewho hasbeen referredfor therapy with a diagnosisof low back pain and an order to evaluate and treat, with a focus on developing a home program. TJ complains of stiffaess and generalaching of her lower backthat is aggravated by sittingformore than 30 minutes.she reportsoccasiorulradiationof pain into her left lateral leg but no other s;.rnptoms in her extremities. She states*rat the pain occasionallydisturbsher sleep,and she is unableto work at her usualsecretarial job becauseof her limited sitting tolerance.Shecanperform most ofher usualhouseholdtasks,suchasgrocery shopping and cleaning, although she ftequently receives help from her family. She reports that the pain started about 4 years ago,when she reachedto pick up a suitcase,and althoughit was initially severe,at a levelof 10 on a scaleof 1 to 10, and subsidedto somedegreeovel the first few weeks, it hasnot changedsignificandy in the past 2 to 3 years and is now usually at a level of 9 or greater Shehashad multiple diagnosticteststhat have not revealedany significaotanatomicalpathology,and she has received multipie treatments, including narcotic analgesicsand physicaltherapy consistingprimarily of hot packs,ultrasonography, andmassage, without significant benefit. Her only current treaftnent is 600 mg of ibuprofeq which sheis taking 3 times a day.The objective exam is significant for restricted lumbar range of motion in all planes.Forward bending is restrictedto approximately40% of normal, backward bending is restrictedto approximately50% of normal, and side bendingis resffictedto approximately507oof normalin both directions.?alpationrevealsstiffnessof the lumbar facetjoints at L3 throughL5 and tendemessin the lower lumbar area. All neurologicaltesting, including lower extremity sensation, strength, and reflexes are within
a
normal limits, although srraightleg raisingis limited to 40 degreesbilaterally by hamstring tightness and prone knee bending is limited to 100 degreesbilaterally by quadricepstighmess.T| is 5 leet 3 inchestall and reports her weight to be 180 pounds.She reportsthat she has gained 50 pounds sinceher initial back injury 4 years ago. EVALUATIONOF CLINICAL FINDINGS This patient seeksmedical ueatrnent for the impairments of low back pain and restricted lumbar range of motion. These impairments have resulted in difficulties widr her normal functional activities of sleeping, working, shopping, and cleaning. Although funher analysis may help identify the specificstructurescausingtJrispatient's pain, the long duration of the pain is well beyond t}re normal time neededfor a minor backinjury to resolve.The lack of changein her pain over the previous years and its lack of responseto multiple treatmentsindicatethat her pain may have a variety of contributory factors beyond local tissue damage, including deconditioning, psychological dysfunction,or socialproblems. PREFERREDPRACTICEPATTEFN Tmn:irarl
Pn
f/R\
PLAN OF CARE The proposed goals of treatrnent at this time may include controlling pain and regaining normal lumbar range of motion. However, the primary goals of treatment would be to retum fl to her maximal functional level and minirnize her dependenceon medicalpersonnel and further medical treatment. ASSESSMENTREGARDINGSELECTIONOF THE OPTIMAL TREATMENT The optimal intervention would ideally addressthe functional limitations causedby this patient's chronic pain and provide her widr independent means to manageher symptomswithout adverseconsequences. Thus the probablefocusof carewould be on teachingTJ coping skills and improving her physical condition, including strength and flexibiJity. The useof physical agentswouid probably be restricted to independent use for pain managementor asan adjunctto promoteprogressiontoward more functional goals-As is explained in greater detail in Section2 of this book, a number of physical agents, including cryotherapy, thermotherapy, and electrical stimulation,may be used by patientsindependentlyto conuol pain, while thermotherapy may also be used to help increasethe extensibiliry of soft tissuesto allow for more effective and rapid recovery of flexibiliry.
PreferedPhysicalTherapistPracticePaternssMl4Iand4Bl arecopynght2002AmericanPhysicalTherapy AIl rightsreserved. Association.
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CHAPTER REVIEW
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3. Merskey H, ed: Classificationof chronicpain: description of chronic pain syndromesand definition of pain terms,Parn(Suppl3)3(Suppl):S1, 1986. 4. Vasudevan SV, Llnch NT: Pain centers: organization and outcome, \YestJl\en $4F}532-535, t99t. 5. Vasudevan SV Rehabilitation of dre patient with chronic pain: is it cost effective?PainDigest2:99-L0L, 1992. 6. KazisLE,MeenanRI, AndersonJ:Painin the rheumatic diseases: investigationsof a key healt! statuscompo^er,t',Afthhk Rheum4(Suppl2):10-13,1983. 7. StrangP: Emotionaland socialaspectsof cancerpain, ActaOncol31(3):323-326 , 1992. 8. Stubble HG, Crubb BD: Afferent and spinal mechanismsof joint paiq Pah 55:5-54,1.993. 9. SlukaKA: Painmechanismsinvolved in musculoskeletai disorden,/ Onhop SVonPhys Ther24(4):240-254, 1,996. 10. Crigg B StubbleHC, SchmidtRI: Mechanicalsensitivity of group III and IV afferents from posterior articular nerve in normal and inflamed cat knee,J Newolhysiol 55635-643,7986. 11. BonicalJ: TheMaxagementof Pain, ed 2, Philadelphia, 1990,Lea& Iebiger 12. BonicalJ: Importanceof the problem.In Aronoff GM, ed: Evaluationand Treatmettof ChroxicPain, Baftinore, 1985,Urban & Schwarzenberg. 13. VasudevanSV Management of chronic pain: what have we achievedin the last 25 years?In Ghia JN, ed: The Muhidisciylinary Pain Cexter: Otgaxization and Petsoaxel Functions for Pait MaxagemetyBostoq 1988, Kluwer. 14. Melzack B" Dennis SC: Neurophysiologicalfoundations of pain. In StembachM, ed: ThePsychology of Pain,NewYork,1978, RavenPress. 15. KellgrenJH: Observationson referredpain arisingfrom muscle. Clin Sci3:175-190. 1938. 16. StaffPH: Clinicalconsiderationh referredmusclepain and tendemess-connectivetissuereactions,EutJ Appl Phvsiol57:369-372. 1988. 17. Black RC: Evaluationof the pain patrent,J Disabil 1,: 85-97,1990. 18. InternationalAssociationfor the Studyof ChronicPain, Sr.rbcommittee on Taxonomy:Classificationof Chronic Pain.Paiz(Suppl);3:SL-5225. 1986. 19. Crue BL, ed:
