外科学教学课件：Traumatic Brain Injury

TraumaticBrainInjuryIntracranialHypertensionHistoricalPerspectiveAlexanderMonro1783describedcranialvaultasnonexpandableandbrainasnoncompressiblesoinflowandoutflowbloodmustbeequalKellibloodvolumeremainsconstantCushingincorporatedtheCSFintoequation1926EventuallywhatwenowknowasMonro-KellidoctrineIntactskullsumofbrain,blood&CSFisconstantCerebralSpinalFluidChoroidplexus>70%productionTransependymalmovementfluidfrombraintoventriclesrestAveragevolumeCSFinchildis90cc(150ccinadult)Makeabout500cc/dRateproductionremainsfairlyconstantw/increaseICPitisabsorptionthatchangesCerebralbloodflowMorbidityrelatedtoICPiseffectonCBFCPP=MAP-ICPorCPP=MAP-CVPOptimalCPPextrapolatedfromadultsInintactbrainthereisauto-regulationCerebralvesselsdilateinresponsetolowsystemicbloodpressureandconstrictinresponsetohigherpressuresCerebralEdemaVasogenicIncreasedcapillarypermeabilitydisruptionBBBTumors/abscesses/hemorrhage/trauma/infectionCytotoxicSwellingoftheneuronsInterstitialFlowoftransependymalfluidisimpairedHydrostaticEdemaECFduetoacutehypertensionIntracranialpressuremeasurementNormalI.C.P.50-200mm.water(10mmHg)IncreasedICP16-20mmHg21–40mmHg>40mmHgMeasurement1.L.P:withthepatientonhisside,theL.P.needleisconnectedtoamanometer.Thismethodisnotaccurate,cannotbeusedformonitoringandcanbedangerous.2.Ventricularcannulation:Itismoreaccurate,canbeusedforlongperiods,butmaybecomplicatedbyinfection.3.Subduralsensor,ExtraduralsensorEffectsofincreasedICP1.Decreaseinrespiratoryrate.2.Bradycardia.3.Cardiacarrhythmias.4.Pupillaryconstriction,followedbyunilateralpupillarydilatation5.Increaseinpulsepressure.6.Increaseinarterialbloodpressure.CerebralbloodflowWhenICPincreases,cerebralbloodflowremainsconstantbyautoregulation.theefficiencyofthiscompensationdependsontherateofexpansionofthelesion,it'snatureandsite.Andalsoonthecomplianceoftheintracranialcontents.CBFisincreasedinresponsetoraisedICP,bycerebralvasodilatation,Howeverthiscausesincreaseincerebralbloodvolumeandproducesfurtherbrainswelling.Whenmaximalvasodilatationoccurs,furtherincreaseinICPcausesreductionincerebralBF.Clinicalsigns1.Headache:Istypicallymaximalinthemorningandisrelievedbyvomiting.Itiscausedbydistortion,stretchingorinvasionofpainsensitivestructuressuchasthebridgingveins,basalandmeningealarteries.2.Vomiting:Usuallyassociatesheadacheandtypicallyoccurswithoutnausea.3.Papilledema:ThisisthemostreliablesignofraisedICP.Brainherniation1.Cingulateherniation:compresstheinternalcerebralveinandtheanteriorcerebralartery.2.Centraltranstentorialherniation: *Compressionofthe3rd.Nerve------->Dilatedpupils. *Compressionofthepost.cerebralart.---->Hemianopia.Totalblindness. *Compressionorischemiaofthebrainstem.->Decerebration.Coma. *Distortionofthebrainstem--------->Hemorrhages.3.Upressionofthemid-brain,3rdnerveandthepost.cerebralart.4.Tonsilarherniation:Occurswhenthecerebellartonsils,herniatethroughtheforamenmagnum,resultingincompressionofmedulla,Decerebration,coma,cardiovascularandrespiratoryabnormalities(apnea).TraumaticBrainInjuryTraumaticbraininjuryLeadingcauseofdeathanddisabilityofyouthMortalityrate:50%ofsevereTBINeurosurgeonsplayimportantroleintreatingTBIpatientsEvidencebasedguidelinesforprehospital,surgical,medicalmanagementhaveemergedTraumaticBraininjuryDefinitionsofTraumaticBrainInjuryspecifythefollowing:Thereisaninjurytothebraincausedbyanexternalforce.Theinjuryisnotcausedbyadegenerativeorcongenitalcondition.Thereisadiminishedoralteredstateofconsciousness.NeurologicalorneurobehavioraldysfunctionresultsfromtheinjuryDirectinjuryIndirectInjuryHeadInjury,Headtrauma,Neurotrauma,TBI,Crainocerebralinjury,WhatcanbeinjuredScalpandSkullDura,brain,vessel,craino-nerve,cerebralspinalfluidLeadingCausesofTBIFalls

28%Motorvehiclecrashes

20%Beinghit/collidingwithanobject

19%Assaults

11%Others

12%GlasglowComaScaleEyeOpeningBestVerbalBestMotorSpontaneous4Oriented5ObeysCommand6ToVoice3Confused4Localizes5ToPain2Inappropriate3Withdraws4None1Incomprehensible2Flexion3None1Extension2None1MildTBIGlascowComaScalescore13-15ModerateTBIGlascowComaScalescore9-12SevereTBIGlascowComaScalescore8orlessClinicalFeaturesInHeadTrauma

ScalpInjuriesSkullFracturesDepressedSkullFracturesBasilarSkullFracturesVascularInjuriesPenetratingHeadInjuryIntracranialHemorrhageEpiduralHematomaSubduralHematomaSubarachnoidHemorrhageIntracerebralHemorrhageScalpInjuriesMostarelacerationSimpleLinear/StellateEDRxExtensive,Degloving/AvulsionRepairOverlyingDepressedSkull#,InfectionsRepair+ElevationOf#HematomasSkullFracturesOpenClosedLinear(3/4)Comminuted(multiplebranches)<3yrleptomeningealcyst,cephalomalacia,DepressedBasilarDepressedSkullFractureFromfocalblowClosedRx,forcosmeticreasons<skullthickness-noelevationOpen/frontalsinusintracranialwallelevateand+frontalsinusirrigationBasilarSkullFractureBasilarskullfracturesAssociatedwithhigh-energytraumaUsuallyoccurfollowingdiffuseimpacttotheheadSignsincludeCSFdrainagefromtheears,raccooneyes,andBattle’ssignRhinorrheaOtorrheaPathophysiologyofBrainInjuryBrainInjuryPrimarySecondary1.Delayedcelldeath2.Intracranialhypertensionandmasslesion3.Ischemiasystemichypoxia,hypercarbiaandhypotensionPrimaryBrainInjuriesItoccuratthetimeoforiginalinsultDirectdamagedonetobrainparenchymaandassociatedwithvascularinjuriesBraintissuecanbelacerated,puncturedorbruisedbybrokenbonesorforeignbodiesDamageisalreadydoneIrreversibleDamagecontrol(debridement)SecondaryBrainInjuryDamagethatoccursaftertheinitialinsult(ongoinginjuryprocesses)Expandingmasslesions,swellingEndresultisincreasedintracranialpressure(ICP)and/orherniationDiagnosisandtreatmentstargetminimizingtheeffectsoftheseindirectinsultsBrainInjuries–BrainConcussionUsuallycausedbybluntinjuries.InjuriespatientshowstransientalterationinneurologicfunctionMildinjuryusuallywithnodetectablebraindamage.Mayhavebrieflossofconsciousness.Shortmemorylossarecommon.CerebralContusion

Abraincontusionisdefinedbycelldeathaccompaniedbyhemorrhage(leakageofblood)ThesoftbraintissueisvulnerabletocontusioninheadtraumaThecontusionoftenoccursatasitedistantfromthepointofimpactDiffuseAxonalInjury

HallmarkofseveretraumaticbraininjuryDifferentialmovementofadjacentregionsofbrainduringaccelerationanddeceleration.DAIismajorcauseofprolongedCOMAafterTBI,probablyduetodisruptionofascendingreticularconnectionstocortex.TheshornAxonsretractandareevidenthistologicallyasRETRACTIONBALLS.LocatedpredominantlyinCORPUSCALLOSUMPERIVENTRICULARWHITEMATTERBASALGANGLIABRAINSTEMDiffuseAxonalInjury

Occursinupto1/2oftraumaticbraininjuriesIsadiffuseformofinjury,meaningthatdamageoccursoveramorewidespreadareathaninfocalbraininjuryDiffuseAxonalInjury

DiffuseAxonalInjuryIsoneofthemajorcausesofunconsciousnessandpersistentvegetativestateafterheadtrauma.Over90%ofpatientswithsevereDAIneverregainingconsciousness(thosethatdowakeupoftenremainsignificantlyimpaired)DiffuseAxonalInjuryAmicroscopicviewofaxonaldegenerationBrainInjuries–hematomaIsacollectionofbloodwithintissue.Hematomainsidethecraniumisnamedaccordingtoitslocation:Subduralhematoma:bloodcollectionbetweenbrainandduraEpiduralhematoma:bloodcollectionbetweenduraandtheskullSubarachnoidHemorrhageIntracerebralhematoma:bloodcollectionwithinthebrainEpiduralHematomas(EDH)Peakincidencein2nddecadeSource:meningealvessel,duralvenoussinus,veinfromskullfracturesymptomLucidinterval(33%),nonspecificConfusion,lethargy,agitation,focalneurologicaldeficits.SubduralHematomaCausehighvelocityimpact/assault/childabuse/fallfromsignificantheight.Associatedwithcerebralcontusions+DAISourcecorticalbridgingveins/Duralvenoussinuses.50%areunconsciousimmediately.FocaldeficitscommonHemiparesis–50%Pupillaryabnormality-28-78%Seizures–6-22%SubduralHematomasBloodbeneaththedura,overlyingthebrainandarachnoid,resultingfromtearstobridgingvesselsCrescentshapeddensitythatmayrunlengthofskullVerycommonintheelderlyScalpHematomaDuraBrainSubarachnoidHemorrhageTraumaisleadingcause.AcutefromdisruptionofperforatingvesselsaroundcircleofWillisinbasalcisternDelayedfromrupturedpseudoaneurysm.Rxmaintainintravascularvoltopreventischemiafromvasospasm.Mortality39%{nationaltraumaticcomadatabank}IntracranialHematomaFocalareasofhemorrhagewithintheparenchymaCT-hyperdense/mixedRx-small-nonoperative.Resolvein2-3weeksLarge-Surgicaldrainage.RepeatCTinsmallbleedsafter12-24hriswarrantedtofindlargehematoma.PenetratingHeadInjury

Rx.SurgicalDebridementofentryandexitwoundsRemoveaccessiblebulletandboneControlhemorrhageRepairDurallacerations+closureofwounds.NOATTEMPTTOREMOVEBULLETORBONEBEYONDENTRYANDEXITWOUNDS.Fallonsharpobjectswiththinskullandopenforaminaecouldpredisposefortheseinjuries.EntrywounddebridedandFBremovedwithindrivenbonefragments.PeriandpostopABXProphylacticanticonvulsantsHighermortalitywhenLowGCSonpresentation(3-4)hemispheric/brainsteminjury/IntraventriculartrackingHemodynamicinstability/apnea/bothUncontrolledICP.ERCareofSkullFracturesandBrainInjuriesAssumespineinjuryMonitorconsciouspatientforchangesinbreathingApplyrigidcollar,immobilizetheneckandspineAdministerhighconcentrationoxygenControlbleedingKeeppatientatrestTalktoconsciouspatient(emotionalsupport)DressandbandageopenwoundsMangethepatientforshockBepreparedforvomitingMonitorvitalsignseveryfiveminutesDiagnosis

NeuorologicalevaluationGeneralstatusandpreexistedconditionsCTisdiagnosticHeadinjuryManagementManagementGoalsEstablishdiagnosisAssurebrainmetabolism&preventsecondarybraininjuryConsultNeurosurgenearlyorearlytransferMildTBI-ClinicalManagementManagementofMildheadinjuryNormalCT:BroughtbacktoERifneed(Head-injurywarningdischarge instructions)2. Nocompanion==>AdmissionorobserveatERAbnormalCT:AdmissionSevereTBI-ClinicalManagementMonitorintracranialpressure(invasively)andintervenetolowerICPwhennecessaryElevateheadofbedMedicationstodecreaseswellingDecreasebrainactivitytoreduceblooddeliveryandswelling-->“medicallyinducedcoma”HypothermiaSurgicalDecompressionwhenriskforherniationishighSeizureprophylaxisSeizuresoccurinupto20%ofsevereTBIpatients,with~50%occurringwithinfirst24hoursOtherprioritiesAdequatenutrition,correctionofelectrolyteabnormalities,strictcontrolofbloodsugar,stricttemperatureregulationStandarddecompressivecranioectomyIntracranialHypertensionPathophysiologyICPmonitoringandcontrolarethecornerstonesofTBImanagementNormalICPAdults<10mmHgChildren3-7mmHgInfants1.5-6mmHgWhentotreat?Adults>20Children>15Infants>10MangementofICPGoaltomaintainCPPbyReducingICP,and/orIncreasingMAP{hyper/normovolumiaprefferedasopposedoldschoolHypovol}BriefperiodsofhypotensioncandoublethemortalityratesCPPshouldbematchwithcerebralmetabolicdemandtoavoidhypoperfusion/hypeeperfusion.HyperdynamictherapyTomaintainCPPofabout>70,byincreasingMAP{CPP=MAP-ICP}IVF-crystalloid/colloidPRBCiflowHCT(<30%)Pressorsasneeded(Dopa,Dobu,Phenylephri)ifautoregulationisintact?incresCPPvasoconstrictionconstantCBFlessvolumereductioninICP.IncreasingCPPbyreducingICPSedationandpaincontrolFentanyl/midazolamdripEtomidateininitialphaseQuietenvir+minexternstimuliPharmacologicalparalysisifneededIncreaseinPneumonia+sepsisIV/ETlidocaine(ET>IV)Duringintubation,beforeETsuctioning,ETmanipulationElevationofheadendby20-30degRedvenouspressICPCancauseorthostaticchangesfallCPPreboundICPriseExcessivePEEP,tightcervicalcollar,neckflexion/rotationCanriseICPBladderdistentionriseContindrainageOccultseizuresunexplainedriseProphylacticAnticonvulsantsFeverriseRx+hypothermia.SpecificmeasurestoreduceICPHyperventilationRapid&effectiveresponse.RedPaco2/incrpHvasoconstrictonRedCBFDisadvantagespaco2<30torrredCBFtoischemiclevelRegionalvariationinautoreghyperventilationinducedreversevascularstealCurrentrecommenda