脊髓損傷SCI課件

脊髓損傷（SCI）1編輯版pptLeadingcauses&Locationof

SpinalcordinjuryMotorvehicleaccidents(47%)Falls(21%)Sports(14%)Actofviolence(14%)LocationofSCI:cervical(53%),thoracic(35%),lumbarandsacral(10%)2編輯版pptPatternsofspinalcordinjuryCompletesyndromesNomotororsensoryfunctionIncompletesyndromesBrown-SequardSyndromeCentralCordSyndromeAnteriorCordSyndrome3編輯版pptEffectscont.Cervical:AboveC4:VentillatorC5-C7:Littlehand/armcontrolThoracic:Paraplegic:wrist/handokT1-T8:PoortorsocontrolT9-T12:Bettertorsocontrol4編輯版pptAutonomicdysreflexiaSpinalcordlesionaboveT6Hypertensionandincreasedsympatheticoutflow,flushing,sweatingabovedermatomeduringincreasedvisceralinput(bladderover-distension,urination,rectaldistension,surgery,UTI)RiskofheartfailureandstrokeBladderneckcontractionduringvoiding5編輯版pptCardiovascularComplicationsinSpinalCordInjury6編輯版pptSpinalcordinjurycanresultinsignificantcompromiseofcardiovascularcontrol

duetoanimpairedautonomicnervoussystem

andskeletalmuscleparalysis7編輯版pptAcuteCardiovascularComplicationsfromtheNSCID20058編輯版pptChronicCardiovascularComplicationsfromtheNSCID20059編輯版pptSpinalCordandAutonomicNervousSystemAnatomy10編輯版pptCardiovascularAnatomy11編輯版pptEvolutionofthecontrolofthecardiovascularsystemCourseofEventsImmediatelyafterSCIoccurs,bloodpressurerisesduetoreleaseofnorepinephrinefromtheadrenalglandsandbyapressorresponsefrommechanicaldisruptionofvasoactiveneuronsandtractsinthespinalcord.Thisisfollowedbyaperiodofspinalshock(decreasedcorticalspinalandsympatheticactivityandunopposedvagaltone).

Overtimereflexesandspasticity

returnduetocompensatorychangesoccurinthevascularbeds,skeletalmuscle,andrennin-angiotensinaldosteronesystem.12編輯版pptShort-andlong-termconsequences.HypotensionCardiacarrhythmiasAutonomicdysreflexiaPoikylothermiaDeepveinthrombosisCoronaryheartdiseaseExerciseresponse13編輯版ppt

Hypotension

DecreasedcompensatoryvasoconstrictionVenouspooling(skeletalmuscleandsplanchnicregions),venouspoolingintheextravasculartissueslowerextremities(legswelling)reducedvenousbloodreturnresultinginreducedstrokevolume,andbloodpressure.Hypotension,andespeciallyorthostasis,usuallyimproveswithindaystoweeksascompensatorychangesoccurinthevascularbeds,skeletalmuscle,andrennin-angiotensinaldosteronesystem.14編輯版pptHypotensionManagementLegelevation,AbdBinder,Acewraps,TedHose,TiltinspaceW/C,Tilttable,EasystandSalttablets.Pseudoephedrine(ActifedandPseudofed)Fludrocortisone(Florinef)Midodrine(ProAmitine)Desmopressin(DDAVP)ErythropoietinOctreotide15編輯版ppt

Cardiacarrhythmias

TheANSmodulatescardiacelectrophysiologyandautonomicdysfunctioncanleadtoventriculararrhythmias.BradycardiaTachycardia16編輯版pptBradycardiaUnopposedVagalStimulationseenwithSCIaboveT117編輯版pptBradycardia100%ofpatientswithmotorcompletecervicalinjuriesdevelopbradycardia,68%arehypotensive,35%requirepressors16%haveprimarycardiacarrest.35-71%developbradycardiawithmotorincompletecervicalinjuriesandfewhavehypotensionorrequirepressors.Patientsinthisgrouprarelyhaveprimarycardiacarrest.13-35%havebradycardiawiththoracolumbarinjuries.Thisproblemusuallyresolvesoverthefirst2-6weeksafterSCI.

18編輯版pptBradycardia

duetounopposedvagalstimulation19編輯版pptBradycardiaItisoftenprecipitatedbytrachealorrectalstimulation(eg,duringsuctioningorbowelprogram)andhypoxia.Atropinemaybeneeded,andtemporary(sometimespermanent)cardiacpacemakershavebeenused.Thisproblemusuallyresolvesoverthefirst2-6weeksafterSCI.20編輯版pptTachycardiaPSVTSinusetachycardiaAtrialFlutterAtrialFibrillation21編輯版ppt

Autonomicdysreflexia

DuetolossofsupraspinalcontrolofhyperreflexicSympatheticNervousSystemactivity,causedbynoxiousstimulibelowthelevelofinjuryinindividualswithSCI.Thiscanleadtodangerouslyhighbloodpressuresthatcanresultincerebralhemorrhage.22編輯版pptAutonomicDysreflexia

Autonomicdysreflexia(AD)istheimbalanceofexcessivereflexsympatheticdischargeoccurringinpatientswithspinalcordinjury(SCI)abovethesplanchnicsympatheticoutflow(T5-T6)duetonociceptiveinput..23編輯版pptSignsandSymptomsofADHeadacheNasalstuffynessFacialflushIncreasedspasticityElevatedbloodpressureSeizureStroke24編輯版pptTreatmentofADSitupChecktheBloodPressureApplyNitropasteSeekoutthecause90%ofthetimeitisrelatedtothebladdersoreplacethefoleyBowel,skin,fracture,DVT,Infection,ingrowntoenail,legbagstrap25編輯版pptPoikylothermiaPoikylothermia:PatientswithlesionsaboveT6arepoikilothermicandcannotregulatetheirbodytemperature.ThelackofvasoconstrictorsandabilityshiftbloodflowtowarmorcoolthebodyTheinabilitytosweatbelowthelevelofthelesion.26編輯版pptTreatmentofPoikylothermiaAvoidexcessivewarmorcoolenvironmentsDressappropriatelyAddorremoveblanketsWearahatifitiscoolWaterspraybottleifitiswarmIntravenousfluidsshouldbewarmed.27編輯版pptDeepveinthrombosis(DVT)Overallincidencewithoutprophylaxisisestimatedtobe40%basedonmeta-analysisofDVTinpatientswithacuteSCI.PowellM,KirshblumS,O'ConnorKC.ArchPhysMedRehabil.1999Sep;80(9):1044-6BloodFlow28編輯版pptDVT:PathophysiologyPredisposingriskfactorsforthedevelopmentofDVTfollowingSCIcanbeclassifiedwiththeVirchowtriadVenousstasisresultsfromlossofpumpingfunctionprovidedbycontractingmuscles.Hypercoagulability

canoccurasaresultofstimulationofthrombogenicfactorsfollowinginjury,withresultantincreaseinplateletaggregationandadhesion(reducedfibrinolyticactivityalongwithhigherlevelsofvonWillebrandfactorantigenandFactorVIII-relatedantigenandresultinginhyperactiveplateletaggregationIntimalinjurymayresultdirectlyfromthereleaseofvasoactiveamineswithtraumaorsurgery,orindirectlyfromexternalpressureontheparalyzedleg.

29編輯版pptDeepVenousThrombosisSwellingFeverofunknownoriginIncreasedspasticityandADClinicallyapparentDVToccursinapproximately15%to50%.DVTcanleadtopulmonaryembolism(5-10%)anddeath.30編輯版pptDVTTreatmentAnticoagulationwithLovenox,Heparin,andorcoumadinIfclinicallycontraindicatedplacevenacavalfilterContinueactivityandcompressiongarments31編輯版pptDVT/PEPreventionGuidelinesAllpatientswillbeonLovenoxorHeparintopreventbloodclot:Non-complicatedspinalcordinjury(noco-morbidity)willhave8weeksoftreatmentComplicatedspinalcordinjury(havingatleastoneco-morbidity)willhave12weeksoftreatmentStandardofcaretopreventDVT:AnticoagulationTherapyattherapeuticdoses(Lovenox30mgSQBIDorHeparin5000unitsSQBID/TID),SCD’swhileinbed,andTedhoseand/orAceWrapswhenoutofbed.32編輯版pptPearlsDVToccursin40-90%ofpatientsdependingonthedegreeofprophylaxis.Riskfactorsdeclinein8-12weeks.ProximalprogressionofDVTandpulmonaryembolismoccurin20-50%.HistoricalyclinicalfactorsbelievedtobeassociatedwithDVTincludemotorcompleteinjuries,paraplegia,andmalegender.InarecentstudybyPowelletal,therewasnostatisticaldifferenceinincidenceofDVTbetweenmotorcompleteversusmotorincompleteinjuries,tetraplegicversusparaplegic,ortraumaticversusnontraumaticcauses.Thus,allSCIpatientsareatriskofdevelopingaDVT.PowellM,KirshblumS,O'ConnorKC.ArchPMedRehabil.1999Sep;80(9):1044-633編輯版pptPulmon