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Firstedition 2003 Reprinted 2005 ISBN07506 22636 British Library Cataloguingin PublicationData Acatalogue record forthisbookisavailablefrom theBritishLibrary Library ofCongress Cataloguingin PublicationData Acataloguerecord forthisbookisavailablefrom the Libraryof Congress Note Medicalknowledgeisconstantly changing. Asnew information becomes available,changesintreatment, procedures, equipmentand the liseofdrugsbecomenecessary.Theeditors, contributorand the publishershavetaken caretoensure thattheinformationgivenin this text isaccurate and up to date. However, readersarestronglyadvised toconfirm that the information,especiallywithregardto drug usage, complies with the latestlegislationandstandardsofpractice. TIle Publisher yoursourcetorhook", BLSBVIBR journalsandnll.ltimedlu intheheatth.fi(if.~ncHC:; www.elsevierheolth.com Working together to grow libraries in developing countries www.clsevier.com I www.bookaid.org I www.sabre.org The publisher's policyis\0use JIIIMlI'manullCluJwd Transferredtodigitalprinting2006 fromlu","lnlIblelorelll I PrintedandboundbyCPIAntonyRowe.Eastbourne Contributors Editors Judith DavidsonBAppSc(OT)MAppSc(Ergon) OccupationalTherapist, RosemaryProsser Prince ofWalesHospital, CHTMSc(Hand&UpperLimb)PGDSport5c&ExBAppSc(Phty) Randwick,Sydney,Australia Director, SydneyHandTherapy& RehabilitationCentre; VictoriaFramptonMCSPSRP ConsultantHandTherapist, HandTherapist, Private Practitioner,Canterbury; StLuke'sHospitalHandUnit, HandTherapyAdvisorto EastKent Hospitals Sydney,Australia Trust,Kent,UK WBruceConollyAMFRCSFRACSFACS KarenGinnPhDBScGradDip(Manips) Associate ProfessorofHandSurgery, SeniorLecturer, UniversityofNewSouthWales; SchoolofBiomedicalSciences(Anatomy), ClinicalAssociate Professor, UniversityofSydney, DeparhnentofSurgery, Lidcombe, Sydney,Australia UniversityofSydney; StaffSurgeon,SydneyHospitalHandUnit; ClaudiaRGschwindMDFRACSFMH(Switzerland) Director, Hand& MicrosurgeryUnit, OverseasHandSurgery& Rehabilitation Projects, RoyalNorthShorePrivateHospital, StLuke'sandSydneyHospitalHandUnits, Sydney,Australia Sydney,Australia TImothyJHerbertFRCSFRACS EmeritusConsultant, Contributors SydneyandStLuke'sHospitalHand Units, Jill AllenGradDip(Phty) Sydney,Australia Physiotherapist,Principal,PrivatePractice (Specialising in theShoulder1991-2001), Jeffery HughesMBBSFRACS(Ortho)FAOrthA Chatswood,Sydney,Australia OrthopaedicSurgeon,PrivatePractice, Chatswood,Sydney,Australia CraigAllinghamBAppSc(Phty)GDSport5c CertMens'Health Elaine juzlGDPhysMCSP Sports Physiotherapist;Director,Physiocare; ClinicalSpecialist in HandTherapy, AdjuctSenior Lecturer, Wellington Hospital; SchoolofPhysiotherapyandExerciseScience, Partner, GriffithUniversity, NESHandTherapyTraining; Queensland,Australia London,UK vIII CONTRIBUTORS SandraKay MClinSc(Hand&UpperLimb)BAppSc(Phty) Lisa NewellBAppSc(Phty) HandPhysiotherapist, PrivatePractitioner, Physiotherapy Department, NorthShorePrivateHospital, RoyalAdelaideHospital, StLeonards,Sydney,Australia Australia MarkMJPerkoMBBSFRACS Paul LaStayo PhDPTCHT OrthopaedicSurgeon, AssistantProfessor, NorthSydneyOrthopaedic& DepartmentofPhysical Therapy, Sports Medicine Centre, NorthernArizonaUniversity, Sydney,Australia Flagstaff,AZ,USA MichaelJSandowBMBSFRACS AnnetteLeveridgeDipCOTSROT HeadofService,HandandUpperLimbService, PrivatePractitioner, DepartmentofOrthopaedicSurgery and Trauma, OccupationalTherapySpecialist, RoyalAdelaideHospital, HandTherapyand Bums; Australia previouslyHeadofOccupationalTherapyService, MountVernonHospital,UK PeterScougallMBBSFRACS(Ortho)FAOrthA ConsultantHand& WristSurgeon, AmeliaLucas MHlthSc(OrthoManips) SydneyandStLuke'sHospitalHand Units, Practice Principal,Cabramatta,Sydney; Sydney,Australia previouslySeniorAcademicAssociate, CSU/AAOMTpost-graduateMastersDegree, DavidH SonnabendMDBSc(Med)FRACS CharlesSturtUniversity, ProfessorofOrthopaedicandTraumaticSurgery, WaggaWagga,Australia UniversityofSydneyand RoyalNorthShore Hospital, Jenny McConnellMBiomedEngGradDip(Manips) Sydney,Australia BAppSc(Phty) Physiotherapist,PrivatePractice, AnneWajon CHTMAppSc(Phty)BAppSc(Phty) Mosman, Sydney,Australia Director,HandTherapyatHornsby, Hornsby, Australia DeirdreMcGheeBAppSc(Phty)DipTCM(China)MATMS Physiotherapist,PrivatePractice; Lecturer, DouglassWheenMBBSFRACS Director,StLuke'sHospitalHand Unit; UniversityofWollongong, ConsultantHand Surgeon, Wollongong, Australia SydneyHospitalHandUnit, Sydney,Australia James AMasson MBBS(Hons)FRACS Director, SydneyHospitalHandUnit, MaureenWilliamsAUABA Sydney,Australia Physiotherapist,NorthShore PrivateSuites, StLeonards,Sydney,Australia BryceMMeadsBHBMBChBFRACS(Orth) ConsultantHandSurgeon, JudithWiltonMSPGDHlthScBAppSc(OT) SydneyandStLuke'sHospitalHandUnits, Director,HandRehabilitationSpecialists, Sydney,Australia WestPerth,WesternAustralia,Australia Preface Theoutcomeforany patientwithadisorderofthe Although there have been great advances hand or upper extremity depends on the mutual in surgery, e.g. tissue transplantation based on understandingand cooperationofthe three main microsurgerytechniques,and greatimprovements parties concerned: the patient, the surgeon and inmany handtherapytechniques, thebasicprinci the therapist. ples of hand surgery and hand therapy remain: The surgeon must know the indications and thorough assessment/examination, accurate diag rationale for, and results of surgery, as well as nosisand appropriatetreatmentofeachindividual both the physiotherapy and occupational ther patientand theirproblem. apy aspects of hand therapy. The therapist, like Manyyearsago,theeditorswere invitedtopro wise, must know the indications and rationale duce a text on the rehabilitation of the hand and for,and results ofhand therapy,as well as those upperlimbthatwouldbeapplicable intheclinical ofsurgical treatments. The patientmusthave an situation.This resultingbook is forsurgeons and understandingofhis orherpathologyandhis or therapists at all levels of experience and training her role in its management, along with the roles whomightbe treatingpatients with adisorder of ofthe surgeonand therapist. their handorupperlimb. RP,WBC,2003 Acknowledgements Wewouldliketoexpressourthanksto:DrBarbara supportovermany yearsgoes to all members of Grunseit, Director of Clinical Services, StLuke's St Luke's and Sydney Hospital Hand Units and HospitalComplexand the Board ofthathospital Sydney HandTherapyandRehabilitation Centre. for making available the Hand Unit office staff; We would like to convey our appreciation to Pam Morris, St Luke's Hospital Hand Unit ourcontributingauthors, all ofwhom are recog secretary for her assistance in the preparationof nised by theircolleagues as experts in their par the manuscript,handlingofcorrespondenceand ticularfield. proofreading;andMrDavidRobinson,StLuke's Finally, we thank Caroline Makepeace, who Hospital Hand Unit Medical Photographer, for initiated the project, and Zoe Youd,Heidi Allen, producingmanyofthe photographsand coordi David Burin and Derek Robertson who have nating the illustrations. Appreciation for their helpedbringthis booktofruition. RP,WBC,2003 1 CHAPTERCONTENTS A. Woundandtissue healing 1 Woundhealing 1 Introduction Factorsaffectingwoundhealing 3 Abnormalscars 4 B. Therapyprinciples andmodalities 5 Treatmentofthepatient 5 Treatmentrationale 6 Assessment 7 A. WOUND ANDTISSUE HEALING James AMasson WOUND HEALING Wound healingisa complex continuumofphys iological, biochemical, cellular, molecular and immunological responses to tissue injury, regu lated by growth factors and cytokines released fromthewounditself(Fig.1.1).Theaimofwound healing is to restore structural and functional integrity to the damaged tissues. Traditionally, wound healing has been divided into three phases- theinflammatoryphase,theproliferative phaseandthe remodellingphase' (Fig.1.2). Inflammatory phase Theinflammatoryphasecommencesuponinjury and lasts for approximately 72 hours. The first eventin tissue injury is disruption ofblood ves sels, followed by a brief period of vasoconstric tion andplateletdegranulation. This initiatesthe clotting cascade, ending in the production of a fibrinclot.Activated plateletsalsoinitiatetheplas minogen,complementandkinin cascades, result ing in vasodilatation and increased small vessel permeability, giving rise to tissue oedema. The activated plateletproducesmany growth factors whichare chemotacticand mitogenic forinflam matorycells,suchasneutrophilsandmonocytes, the latter transforming into macrophages.v' The increased vessel permeability allows these 2 INTRODUCTION neutrophils and monocytes to pass out between the first6hoursand reach apeakat 24-48 hours. theendothelialcellsby aprocessofdiapedesis. Wound healingcan stillprogressnormally in the In the initial stages of healing, the inflamma absence ofneutrophils.Macrophagesfirstappear tory cellseliminatebacteriaanddebrisbyphago 48 hours after injury and remain in the wound cytosis. Neutrophils arrive in the wound within until healing is complete. The macrophages are also responsible for recruiting the mesenchymal cells,whichsignalthetransitiontotheproliferative phase.Theyarethemostimportantcellsinampli fyingandsustainingthewoundhealingprocess.' T lymphocytes appear around the fifth day and play a part in the regulation of macrophage activities. They also secrete lymphokines, which affect endothelial cell behaviour and fibroblast recruitmentandproliferation." Proliferative (fibroblastic) phase The next phase of wound healing, also known as the granulation phase, commences 3-4 days aftertheinitialinjuryandlastsapproximately2-4 weeks.Themacrophages,whichappearedduring the initial inflammatoryphase,continuetomove intothewound.Theysecretecytokinesand growth factors which attract fibroblasts and new blood vessels. The fibroblasts lay down a loose matrix Figure1.1 Overview ofhealing.(Reproduced withkind of fibronectin, hyaluronic acid and collagen into permission fromHuntTK:Basicprinciples ofwoundhealing. JTrauma30(12Suppl):S124, 1990.) which the blood vessels grow.This composite of Figure1.2 Generaltimeframeofthewound healingprocess.(Reproduced fromHomDB:Thewoundhealingresponsetograftedtissue.Otolaryngol Clin North Am27:14, 1994.) WOUNDANDTISSUEHEALING 3 fibroblasts, macrophages and new capillaries is knownas 'granulationtissue'. Within hours of injury, epithelial cells at the periphery of the wound and in residual dermal epithelialappendagesrestoreepidermalcontinu ity through the processesofmobilisation,migra tion, mitosis and cellular differentiation. During mobilisation,thecellsimmediatelyadjacenttothe wound edge enlarge, flatten, detach from neigh bouringcellsand flowawayfromthem.Migration continues until cells touch one another, produ cingcontactinhibition.Epithelialmitosis actually begins within hours of injury, but intensifies Days Weeks Months during the proliferative phase. Fixed basal cells away from the wound edge multiply to replace FIgure1.3 Thethreephases ofwound healing, showing thephasesofrepairandthegainintensile strength in the migrating cells, and the cells that have eachperiod.(Reproduced withpermission fromBoscheinen migratedalsomultiply.Oncethewoundhasbeen MorrinJ,ConollyWB:Thehand:fundamentals oftherapy. bridgedbyacompletelayerofepithelialcells,the Oxford:Butterworth-Heinemann,2000.) cells differentiate from basal cells through the various stages of differentiated keratinocytes to number of myofibroblasts within the wound? produceastratumcorneum. Wound contractioncan be used to advantage by thesurgeonand therapist,e.g.infingertip wounds or the open palm technique in Dupuytren's con Remodelling (maturation) phase tracture. The final resultofthe healing process is During the final phase ofwound healing, which a mature scar, which may take up to 18months begins about 3 weeks after the injury and lasts from the time ofthe initial injury.The increase in for several months, the extracellular matrix is wound tensile strength that takes place during reorganised.Bothcollagensynthesisanddegrad the fibroblastic phasecorresponds tothe increas ation are increased, so there isno netincrease in ing levels of collagen within the wound.f The collagencontent.Thetypeillcollagenwhichwas tensile strength of a wound never reaches the secretedinitiallyisgraduallyreplacedby mature pre-injury state, and probably plateaus at about type Icollagen, whichishighlycross-linked and 80% of normal at approximately 60 days after reoriented in response to mechanical stress. injury" (Fig.1.3). There is an overall reduction in cell numbers (fibroblasts and macrophages) and a decrease in FACTORS AFFECTING WOUND tissue vascularity. HEALING Wound contraction is an active, essential part of the repair process which begins around the Therearemanyfactorswhichcanhave anadverse fifthdayandlasts for2weeks. Aspecialisedtype affect on wound healing. Only those of clinical offibroblastwithinthewound,themyofibroblast, relevance to the hand surgeon and therapist will providesthecontractileforce,"Themyofibroblast be discussed here. differs fromthe normalfibroblastinhavingsome ultrastructuralsimilaritiestosmoothmusclecells. Oxygen Myofibroblasts are present throughout the wound, not just at the periphery, so that the Various steps in the wound healing process are entire granulating surface of the wound acts as particularly oxygen-sensitive: namely, collagen a contractile organ. There isa direct relationship synthesis, angiogenesis and epithelialisation.!" between the rate of wound contraction and the Therefore,thecommonestreason that woundsfail 4 INTRODUCTION to heal is an inadequate tissue oxygen tension. glycosylated and competes with oxygen. In the This may resultfrom insufficientdebridementof initialinflammatoryphase,the whitecellsofdia atraumaticwound,leavingnecrotictissuebehind; betics have a decreased ability to phagocytose unsatisfactory vascularity of tissues; tightsutur and killbacteria.P ing or postoperative swelling,producingwound tension; wound infection, which may compete ABNORMAL SCARS for the availableoxygen; or anaemia,withinsuf ficient haemoglobin to transfer the available Whenexcessive accumulationofcollagenoccurs oxygen. from increased collagen synthesis or decreased collagenbreakdownduringthe proliferativeand Infection remodelling phases of wound healing, a hyper trophicscar or keloid mayresult." Infection decreasestheoxygenlevelinthe tissues Hypertrophic scars are limited to the confines and increases the breakdown of collagen. Italso oftheinitialinjury,whereaskeloidsextendbeyond impairsangiogenesisandepithelialisation.l' theoriginalwound.Hypertrophicscarsare much more common than keloids. In fact, the hand is quite a privileged site in terms of occurrence of Age true keloids. Hypertrophic scars are not infre Withincreasingage,the phasesofwoundhealing quently seen in the palmar skin, whereas true take longer,andthe rate ofcellularmultiplication keloidsrarelyare.Thesamecannotbesaid forthe isslower. Tissues ofelderlypatients are also less dorsumof the hand or the volarand dorsal fore resistanttoischaemia. arm skin, especially in predisposed individuals, i.e. young dark-skinned or Asian individuals. Keloids seem to be hormone-sensitive, often Smoking worsening during pregnancy and resolving followingmenopause. Nicotine causes sympathetically induced vaso constriction, producinglocalised tissue ischaemia, and decreased oxygen delivery. Smoke also Management contains carbon monoxide, which binds with haemoglobin to form carboxyhaemoglobin. The Surgery is rarely indicated in the management oxygen molecules then have to compete for free of hypertrophic scars or keloids. Unless the haemoglobinmoleculesfor transport. abnormalscar followed adefinedcomplication e.g. wound infection, haematoma, dehiscence further attempts at surgical correction will often Steroids only worsen the situation. Therefore, all non Steroids arrest the inflammatory process. They surgical modalities should be exhausted before inhibit wound macrophages and interfere with surgery is considered. Many modalities have collagen formation, angiogenesis and wound been used experimentally and clinically. Once contraction.12 again, onlythose ofclinicalrelevancein the hand patientwill bediscussed. Diabetes mellitus Pressure Patients with diabetes mellitus have decreased oxygen delivery to the tissues due to stiff red Itisthoughtthatpressuredecreasestissue metab bloodcellsandincreasedbloodviscosity,making olism and increases collagen breakdown by it more difficult for the corpuscles to negotiate increasingthe activityofcollagenase.ISThecolla the capillaries. Their haemoglobin also becomes genaseenzymeisheat-sensitive, withits activity THERAPYPRINCIPLESANDMODALITIES 5 increasing lOOO-fold for every degreecentigrade siliconeoilwhichbleedsfrom the gel,orperhaps increase in temperature. Therefore, the local the occlusive effectofthe dressing.16,17 warming produced by a pressure garment may have its effect partially by this mechanism. Intraleslonal steroids However, as with all conservative measures, treatment should persist for at least 6 months Intralesionalinjection of steroidspreventsexces and, inburnspatients,often forupto2years. sive collagendeposition, and allows collagenase to correct the imbalance in collagen metabolism. Injectionmaybecombinedwithexcision.Import Silicone gel ant side effects are local hypopigmentation The exact mechanism of action of silicone gel is (which can be quite distressing in dark-skinned not known.Itmayberelatedtosomeeffectofthe individuals),skin atrophyand telangiectasiae. REFERENCES 1.HowesEL,SooyJW,HarveySC:Healingofwoundsas 10. HuntTK,PaiMP:Theeffectofvariantambientoxygen determinedbytheir tensilestrength.JAMA92:42,1929. tensionsonwoundmetabolismandcollagen synthesis. 2.MartinP,Hopkinson-WoolleyJ,McCluskeyJ:Growth SurgGynecolObstet135:561,1972. factorsandcutaneouswoundrepair.ProgGrowthFactor 11. RobsonMC,StenbergBD,HeggersJP:Wound healing Res4:25,1992. alterationscausedbyinfection.ClinPlastSurg 3.MoulinV:Growthfactors inskinwoundhealing. Europ 17(3):485,1990. JCellBio168:1,1995. 12.StephensFO,DunphyJE,HuntTK:Effectofdelayed 4.Clark RAetal:Roleofmacrophagesinwoundhealing. administrationofcorticosteroidsonwoundcontraction. SurgForum27:16,1976. AnnSurg173:214,1971. 5.PetersonJMetal:SignificanceofTlymphocytesin 13. MorainWD,Colen LB:Wound healingindiabetes woundhealing. Surgery102:300,1987. mellitus. ClinPlastSurg 17(3):493,1990. 6.GabbianiG,RyanGB,MajnoG:Presenceofmodified 14.CohenII<etal:Collagensynthesisinhumankeloid and fibroblasts ingranulationtissue,andpossible rolein hypertrophicscar.Surg Forum22:448,1971. woundcontraction.Experientia27:549,1970. 15.ThomasOWetal:Thepathogenesisofhypertrophic/ 7.RudolphR:Locationoftheforceofwoundcontraction. keloidscarring. IntJOral MaxillofacSurg 23:232,1994. SurgGynecol Obstet148:547,1979. 16.QuinnKJ:Siliconegelinscartreatment.Burns13:533, 8.MaddenJW,PeacockEE:Studieson thebiologyof 1987. collagen duringwoundhealing.III.Dynamicmetabolism 17.SawadaY,SoneK:Hydrationandocclusion treatment ofscarcollagenand remodelingofdermalwounds. forhypertrophicscarsandkeloids. BrJPlastSurg AnnSurg 174:511,1971. 45:599,1992. 9.Levenson SMetal:Thehealingofratskin wounds. AnnSurg 161:293,1965. techniques, anunderstandingofthepatient'sabil B. THERAPY PRINCIPLES AND ity and motivation to participate in the therapy MODALITIES programme,andhavingthe appropriate therapy skills,materialsandequipmentavailable. Rosemary Prosser TREATMENT OFTHE PATIENT Hand therapy, occupationaltherapyandphysio therapy require a knowledge of science and an Itis essential to understand the impact of upper appreciation of humanity. One needs a logical limb dysfunction on each patient's ability to scientificbasis in order to problem solve and set work, play sport, perform hobbies or general appropriate treatment goals. Developing treat activities ofdaily living (ADL).Aseach patientis ment strategies requires a knowledge ofvarious an individual, the response will be different and