脊髓损伤(SCI)课件

脊髓损伤（SCI）钟鸣Leadingcauses&Locationof

SpinalcordinjuryMotorvehicleaccidents(47%)Falls(21%)Sports(14%)Actofviolence(14%)LocationofSCI:cervical(53%),thoracic(35%),lumbarandsacral(10%)PatternsofspinalcordinjuryCompletesyndromesNomotororsensoryfunctionIncompletesyndromesBrown-SequardSyndromeCentralCordSyndromeAnteriorCordSyndromeAutonomicdysreflexiaSpinalcordlesionaboveT6Hypertensionandincreasedsympatheticoutflow,flushing,sweatingabovedermatomeduringincreasedvisceralinput(bladderover-distension,urination,rectaldistension,surgery,UTI)RiskofheartfailureandstrokeBladderneckcontractionduringvoidingCardiovascularComplicationsinSpinalCordInjurySpinalcordinjurycanresultinsignificantcompromiseofcardiovascularcontrol

duetoanimpairedautonomicnervoussystem

andskeletalmuscleparalysisAcuteCardiovascularComplicationsfromtheNSCID2005SpinalCordandAutonomicNervousSystemAnatomyEvolutionofthecontrolofthecardiovascularsystemCourseofEventsImmediatelyafterSCIoccurs,bloodpressurerisesduetoreleaseofnorepinephrinefromtheadrenalglandsandbyapressorresponsefrommechanicaldisruptionofvasoactiveneuronsandtractsinthespinalcord.Thisisfollowedbyaperiodofspinalshock(decreasedcorticalspinalandsympatheticactivityandunopposedvagaltone).

Overtimereflexesandspasticity

returnduetocompensatorychangesoccurinthevascularbeds,skeletalmuscle,andrennin-angiotensinaldosteronesystem.

Hypotension

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

Cardiacarrhythmias

TheANSmodulatescardiacelectrophysiologyandautonomicdysfunctioncanleadtoventriculararrhythmias.BradycardiaTachycardiaBradycardiaUnopposedVagalStimulationseenwithSCIaboveT1Bradycardia100%ofpatientswithmotorcompletecervicalinjuriesdevelopbradycardia,68%arehypotensive,35%requirepressors16%haveprimarycardiacarrest.35-71%developbradycardiawithmotorincompletecervicalinjuriesandfewhavehypotensionorrequirepressors.Patientsinthisgrouprarelyhaveprimarycardiacarrest.13-35%havebradycardiawiththoracolumbarinjuries.Thisproblemusuallyresolvesoverthefirst2-6weeksafterSCI.

BradycardiaItisoftenprecipitatedbytrachealorrectalstimulation(eg,duringsuctioningorbowelprogram)andhypoxia.Atropinemaybeneeded,andtemporary(sometimespermanent)cardiacpacemakershavebeenused.Thisproblemusuallyresolvesoverthefirst2-6weeksafterSCI.TachycardiaPSVTSinusetachycardiaAtrialFlutterAtrialFibrillationAutonomicDysreflexia

Autonomicdysreflexia(AD)istheimbalanceofexcessivereflexsympatheticdischargeoccurringinpatientswithspinalcordinjury(SCI)abovethesplanchnicsympatheticoutflow(T5-T6)duetonociceptiveinput..SignsandSymptomsofADHeadacheNasalstuffynessFacialflushIncreasedspasticityElevatedbloodpressureSeizureStrokePoikylothermiaPoikylothermia:PatientswithlesionsaboveT6arepoikilothermicandcannotregulatetheirbodytemperature.ThelackofvasoconstrictorsandabilityshiftbloodflowtowarmorcoolthebodyTheinabilitytosweatbelowthelevelofthelesion.TreatmentofPoikylothermiaAvoidexcessivewarmorcoolenvironmentsDressappropriatelyAddorremoveblanketsWearahatifitiscoolWaterspraybottleifitiswarmIntravenousfluidsshouldbewarmed.Deepveinthrombosis(DVT)Overallincidencewithoutprophylaxisisestimatedtobe40%basedonmeta-analysisofDVTinpatientswithacuteSCI.PowellM,KirshblumS,O'ConnorKC.ArchPhysMedRehabil.1999Sep;80(9):1044-6BloodFlowDeepVenousThrombosisSwellingFeverofunknownoriginIncreasedspasticityandADClinicallyapparentDVToccursinapproximately15%to50%.DVTcanleadtopulmonaryembolism(5-10%)anddeath.DVTTreatmentAnticoagulationwithLovenox,Heparin,andorcoumadinIfclinicallycontraindicatedplacevenacavalfilterContinueactivityandcompressiongarmentsDVT/PEPreventionGuidelinesAllpatientswillbeonLovenoxorHeparintopreventbloodclot:Non-complicatedspinalcordinjury(noco-morbidity)willhave8weeksoftreatmentComplicatedspinalcordinjury(havingatleastoneco-morbidity)willhave12weeksoftreatmentStandardofcaretopreventDVT:AnticoagulationTherapyattherapeuticdoses(Lovenox30mgSQBIDorHeparin5000unitsSQBID/TID),SCD’swhileinbed,andTedhoseand/orAceWrapswhenoutofbed.PearlsDVToccursin40-90%ofpatientsdependingonthedegreeofprophylaxis.Riskfactorsdeclinein8-12weeks.ProximalprogressionofDVTandpulmonaryembolismoccurin20-50%.HistoricalyclinicalfactorsbelievedtobeassociatedwithDVTincludemotorcompleteinjuries,paraplegia,andmalegender.InarecentstudybyPowelletal,therewasnostatisticaldifferenceinincidenceofDVTbetweenmotorcompleteversusmotorincompleteinjuries,tetraplegicversusparaplegic,ortraumaticversusnontraumaticcauses.Thus,allSCIpatientsareatriskofdevelopingaDVT.PowellM,KirshblumS,O'ConnorKC.ArchPMedRehabil.1999Sep;80(9):1044-6PulmonaryEmbolismVenacavalFilterCoronaryHeartDiseaseCoronaryHeartDiseaseisthoughttoincreaseafterSCIdueto:physicalinactivityobesityhyperlip