顱腦損傷英文版

“Boy,doIhaveanExcedrinheadache!!”

managingtheheadinjuredpatientLeaugeayWebreBS,CCEMT-P,NREMT-PScenarioWhiledescendingMtHoodinOregon,Bobtumbledheadoverheels,andcametoastopdanglingoffaprecipicebyhisTelemarkskiat11,000ft.OnarrivaltheskipatrolparamedicsBob’sbreathingwassonorousandshallow,andhehadaGCSof3-4.Theonlyobviousinjuriesweretohishead.HisBPwas87/55,HR100andRR16

Howshouldtheparamedicstreatthispatient?Shouldhebeintubated?Shouldhebefluidresuscitated?Commonmajortrauma4millionpeopleexperienceheadtraumaannuallySevereheadinjuryismostfrequentcauseoftraumadeathGSWtocranium:75-80%mortalityAtRiskpopulationMales15-24InfantsYoungChildrenElderlyIntroductiontoHead,Facial,

&NeckInjuriesTIMEISCRITICALIntracranialHemorrhageProgressingEdemaIncreasedICPCerebralHypoxiaPermanentDamageSeverityisdifficulttorecognizeSubtlesignsImprovedifferentialdiagnosisImprovessurvivabilityIntroductiontoHead,Facial,

&NeckInjuriesScalpStrongFlexiblemassofSkinFasciaMuscularTissueHighlyVascularHairprovidesInsulationStructuresBeneathGaleaAponeuroticaBetweenscalpandskullFibrousconnectivesheathSubaponeurotica(Areolar)TissuePermitsvenousbloodflowfromtheduralsinusestothevenousvesselsofscalpEmissaryVeins:PotentialrouteforInfectionAnatomy&Physiology

oftheHeadParietalSutureLineFrontalTemporalOrbitsMaxillaeMandibleTemporalMandibularJointOcciptalNasalBonesZygomaticArchSphenoidForamenMagnum(HoleinBase)CraniumBrainOccupies80%ofcraniumComprisedof3MajorStructuresCerebrumCerebellumBrainstemHighmetabolicrateReceives15%ofcardiacoutputConsumes20%ofbody’soxygenRequiresconstantcirculationIFBloodsupplystopsUnconsciouswithin10secondsDeathin4-6minutesAnatomy&Physiology

oftheHeadCerebralPerfusionPressurePressurewithincranium(ICP)resistsbloodflowandgoodperfusiontotheCNSPressureusuallylessthan10mmHgMeanArterialPressure(MAP)Mustbeatleast50mmHgtoensureadequateperfusionMAP=DBP+1/3PulsePressureCerebralPerfusionPressure(CPP)PressuremovingbloodthroughthecraniumCPP=MAP-ICPAnatomy&Physiology

oftheHeadCalculatingMAP(meanarterialpressure)DBP+1/3PPPP(pulsepressure)=SBP-DBPSBP+2(DBP)3CalculatingCPP(cerebralperfusionpressure)MAP–ICPICPnormally<10Anatomy&Physiology

oftheHeadCerebralPerfusionPressureAutoregulationChangesinICPresultincompensationIncreasedICP=IncreasedBPThiscausesICPtorisehigherandBPtoriseBraininjuryanddeathbecomeimminentExpandingmassinsidecranialvaultDisplacesCSFIfpressureincreases,braintissueisdisplacedAnatomy&Physiology

oftheHeadFaceMusclesMChewingmusclesMPosteriorpalateandpharynxMFaceMusclesMSightSOpticIIPupilConst,Rectus&ObliquesMOculomotorIIIOpthalmic(FH),Maxillary(cheek)Mandible(chin)STrigeminalVLateralrectusmuscleMAbducensVITastetoposteriortongueSVagusXTongueMHypoglossalXIITrapezius&Sternocleido.MusclesMAccessoryXIHearingbalanceSAcousticVIIISuperiorObliquesMTrochlearIVTongueSFacialVIIPosteriorpharynx,tastetoanteriortongueSGlossopharyn-

gealIXSmellSOlfactoryIInnervationFNameCNTypesofTraumaSofttissueSkullfracturePrimarybraininjuriesSecondarybraininjuriesThepatientpresentedtotheemergencydepartmentwiththegolfcubinhishead,whichwasremovedintheoperatingroomLateralskullx-rayofapatientwhopresentedwithasevereintracranialinjuryproducedbyagolfclubScalpInjuryContusionsLacerationsAvulsionsSignificantHemorrhageALWAYSReconsiderMOIforsevereunderlyingproblemsBrainInjuryAsdefinedbytheNationalHeadInjuryFoundation“atraumaticinsulttothebraincapableofproducingphysical,intellectual,emotional,socialandvocationalchanges.”ClassificationDirectPrimaryinjurycausedbyforcesoftraumaIndirectSecondaryinjurycausedbyfactorsresultingfromtheprimaryinjuryDirectBrainInjuryTypesCoupInjuryatsiteofimpactContrecoupInjuryonoppositesidefromimpactIntracranialPerfusionReviewCranialvolumefixed80%=Cerebrum,cerebellum&brainstem12%=Bloodvessels&blood8%=CSFIncreaseinsizeofonecomponentdiminishessizeofanotherInabilitytoadjust=increasedICPIntracranialPerfusionCompensatingforPressureCompressvenousbloodvesselsReductioninfreeCSFPushedintospinalcordDecompensatingforPressureIncreaseinICPRiseinsystemicBPtoperfusebrainFurtherincreaseofICPDangerouscycleICPBPIntracranialPressureRoleofCarbonDioxideIncreaseofCO2inCSFCerebralVasodilationEncouragebloodflowReducehypercarbiaReducehypoxiaContributestoICPCausesclassicHyperventilation&HypertensionReducedlevelsofCO2inCSFCerebralvasoconstrictionResultsincerebralanoxiaFactorsAffectingICPVasculatureConstrictionCerebralEdemaSystolicBloodPressureLowBP=PoorCerebralPerfusionHighBP=IncreasedICPCarbonDioxideReducedrespiratoryefficiencyIncreasedpressureCompressesbraintissueAgainst&aroundFalxCerebriTentoriumCerebelliHerniatesbrainstemCompromisesbloodsupplySigns&SymptomsUpperBrainstemVomitingAlteredmentalstatusPupillarydilationMedullaOblongataRespiratoryCardiovascularBloodPressuredisturbancesPressure&StructuralDisplacementAlteredMentalStatusAlteredorientationAlterationinpersonalityAmnesiaRetrogradeAntegradeCushing’sReflexIncreasedBPBradycardiaErraticrespirationsSigns&Symptoms

ofBrainInjuryVomitingWithoutnauseaProjectileBodytemperaturechangesChangesinpupilreactivityDecorticateposturingPathophysiologyofChangesFrontalLobeInjuryAlterationsinpersonalityOccipitalLobeInjuryVisualdisturbancesCorticalDisruptionReducementalstatusorAmnesiaRetrogradeUnabletorecalleventsbeforeinjuryAntegradeUnabletorecalleventsaftertrauma“RepetitiveQuestioning”FocalDeficitsHemiplegia,WeaknessorSeizuresSigns&Symptoms

ofBrainInjuryUpperBrainstemCompressionIncreasingbloodpressureReflexbradycardiaVagusnervestimulationCheyne-StokesrespirationsPupilsbecomesmallandreactiveDecorticateposturingNeuralpathwaydisruptionSigns&SymptomsofBrainInjury

PhysiologicalChangesMiddleBrainstemCompressionWideningpulsepressureIncreasingbradycardiaCNSHyperventilationDeepandRapidBilateralpupilsluggishnessorinactivityDecerebrateposturingSigns&SymptomsofBrainInjury

PhysiologicalChangesLowerBrainstemInjuryPupilsdilatedandunreactiveAtaxicrespirationsErraticwithnopatternIrregularanderraticpulserateECGChangesHypotensionLossofresponsetopainfulstimuliSigns&SymptomsofBrainInjury

PhysiologicalChangesDifferentpathologythanolderpatientsSkullcandistortduetoanteriorandposteriorfontanellesBulgingSlowsprogressionofincreasingICPIntracranialhemorrhagecontributestohypovolemiaDecreasedbloodvolumeinped’sGeneralManagementAvoidhyperextensionofheadTonguepushessoftpalletclosedVentilatethroughmouthandnoseSigns&SymptomsofBrainInjury

PediatricHeadTraumaSigns&SymptomsofBrainInjury

GlasgowComaScalePhysiologicalIssuesIndicatepressureonCN-II,CN-III,CN-IV,&CN-VICN-III(OculomotorNerve)Pressureonnervecauseseyestobesluggish,thendilated,andfinallyfixedReducedperipheralbloodflowPupilSize&ReactivityReducedPupillaryResponsivenessDepressantdrugsorCerebralHypoxiaFixed&DilatedExtremeHypoxiaSigns&SymptomsofBrainInjury

EyeSignsSkullFracturesTheskullwillnotfracturewithoutextremeforceClosed/openlineardepressedcomminutedbasilarimpaledobjectCranialInjuryTraumamustbeextremetofractureLinearDepressedOpenImpaledObjectBasalSkullUnprotectedSpacesweaken

structureRelatively

easiertofractureCranialInjuryBasalSkullFractureSignsBattle’sSignsRetroauricularEcchymosisAssociatedwithfractureof

auditorycanalandlower

areasofskullRaccoonEyesBilateralPeriorbital

EcchymosisAssociatedwithorbital

fracturesCranialInjuryBasilarSkullFractureMaytearduraPermitCSFtodrainthroughanexternalpassagewayMaymediateriseofICPEvaluatefor“Target”or“Halo”signBasilarSkullFractureCribiformplatefractureBattle’ssignPeriorbitalecchymosisCSFleakagePrimaryBrainInjuryResultsfromdirecttraumaFocalDiffuseDirectBrainInjuryCategoriesFocalOccurataspecificlocationinbrainDifferentialsCerebralContusionIntracranialHemorrhageEpiduralhematomaSubduralhematomaIntracerebralHemorrhageSubarachnoidHemorrhageDiffuseConcussionModerateDiffuseAxonalInjurySevereDiffuseAxonalInjuryFocalContusionsIntracerebralhematomaSubduralhematomaSubarachnoidhematomaEpiduralhematomaContusionsLOCwithresultantcellulardamage“bruising”TemporalinjuryoftenpresentswithrepetitivequestioningAyoungmalearrivedintheemergencydepartmentafterexperiencingagunshotwoundtothebrain.Theentrancewasontheleftoccipitalregion.ACTscanshowstheskullfractureandalargeunderlyingcerebralcontusion.Thepatientwastakentotheoperatingroomfordebridementofthewoundandskullfracture,withrepairoftheduramaterFocalBrainInjuryCerebralContusionBlunttraumatolocalbraintissueCapillarybleedingintobraintissueCommonwithbluntheadtraumaConfusionNeurologicdeficitPersonalitychangesVisionchangesSpeechchangesResultsfromCoup-contrecoupinjuryEpiduralHematomaLocatedbetweenskullandduramaterUsuallyinvolvesarterialbleeding-middlemeningealarterySharplydefinededgesonCTUsuallynounderlyingbraininjuryClassicalpresentationis“l(fā)ucidinterval”MayquicklyevolveintoherniationLucidIntervaltransientLOCfollowedbyalucidperiodwherepatientisneurologicallyintactfollowedbyasecondaryonsetofHAanddecreasingLOCEpiduralHematomaBleedingbetweenduramaterandskullInvolvesarteriesMiddlemeningealarterymostcommonRapidbleeding&reductionofoxygentotissuesHerniatesbraintowardforamenmagnumFocalBrainInjury

IntracranialHemorrhageCTscanofanacuteleft-sidedepiduralhematoma.Notethetypicalconvexorlens-shapedappearance.Thehematomatakesthisshapeasthedurastripsfromtheundersurfaceofthecranium,limitedbythesuturelines.Amidline

shiftoftheventricularsystemexists.SubduralHematomaLocatedbetweentheduramaterandpiamaterAllvenousbleeds,usuallypresentwithslowonsetIndistinctonCTUnderlyingbraininjuryMaynotpresentwithSxforhoursordaysSubduralHematomaBleedingwithinmeningesBeneathduramater&withinsubarachnoidspaceAbovepiamaterSlowbleedingSuperiorsagitalsinusSignsprogressoverseveraldaysSlowdeteriorationofmentationFocalBrainInjury

IntracranialHemorrhageAcutesubduralhematoma:notethebright(white)imagepropertiesofthebloodonthisnoncontrastcranialCTscan.Notealsothemidlineshift.Subacutesubduralhematoma:thecrescent-shapedclotislesswhitethanonCTscanofacutesubduralhematoma

IntracerebralHemorrhageRupturebloodvesselwithinthebrainPresentationsimilartostrokesymptomsSignsandsymptomsworsenovertimeFocalBrainInjury

IntracranialHemorrhageIntracerebralHematoma LocatedinthebrainparenchymaDifficulttodistinguishfromcontusionIntracranialhemorrhage.CTscanofrightfrontalintracerebralhemorrhagecomplicatingthrombolysisofanischemicstroke.SubarachnoidHemorrhageMaynotpresentwithphysicalfindingsHAstiffnecknuchalrigidityBloodinCSFBrainCTscanshowssubtlefindingofbloodattheareaofthecircleofWillisconsistentwithacutesubarachnoidhemorrhage.DiffuseBrainInjuryDuetostretchingforcesplacedonaxonsPathologydistributedthroughoutbrainTypesConcussionModerateDiffuseAxonalInjurySevereDiffuseAxonalInjuryConcussionTransientLOCUsuallycompleterecoveryMildformofdiffuseinjuryOftenpresentswithabriefperiodofconfusionPtmayexhibitretrogradeorposttraumaticamnesiaDiffuseAxonalInjuryRapid,profound,prolongedunconsciousnessOftenleadstoincreasedICPMildtomoderateformofDiffuseAxonalInjury(DAI)NervedysfunctionwithoutanatomicdamageTransientepisodeofConfusion,Disorientation,EventamnesiaSuspectifpatienthasamomentarylossofconsciousnessManagementFrequentreassessmentofmentationABC’sDiffuseBrainInjury

Concussion“ClassicConcussion”SamemechanismasconcussionAdditional:MinutebruisingofbraintissueUnconsciousnessIfcerebralcortexandRASinvolvedMayexistwithabasilarskullfractureSigns&SymptomsUnconsciousnessorPersistentconfusionLossofconcentration,disorientationRetrograde&AntegradeamnesiaVisualandsensorydisturbancesMoodorPersonalitychangesDiffuseBrainInjury

ModerateDiffuseAxonalInjuryBrainstemInjurySignificantmechanicaldisruptionofaxonsCerebralhemispheresandbrainstemHighmortalityrateSigns&SymptomsProlongedunconsciousnessCushing’sreflexDecorticateorDecerebrateposturingDiffuseBrainInjury

SevereDiffuseAxonalInjuryPathwayofDeteriorationCranialinsultTissueedemaIncreasingICPCompressionofarteriesDecreasedcerebralbloodflowDecreasedO2withcellulardeathEdemaaroundnecrotictissueCon’tIncreasingICPwithcompressionofbrainstemandrespiratorycenterAccumulationofCO2resultinginvasodilationIncreasingbloodvolumefurtherincreasingICPDeathAnyswellingorbleedingdecreasesthecirculatingbloodvolumeandcerebralbloodflowDecreasedcerebralbloodflowresultsinhypoxiaandCO2risesHypercarbiadilatescerebralbloodvesselscausingincreasingBPAttemptstoperfusebrainresultinginincreasedICPHerniationDepressionof3rdcranialnerveresultsinpupillarydilation-aniscoriaLateralparesisCushing’striadDecorticateposturingDecerebrateposturingDecorticatePosturingResultsfromlesionsofinternalcapsules,basalganglia,thalamusorcerebralhemisphereInterruptscorticospinalpathwaysPresentswithflexedarmsandextendedlowerextremitiesDecerebratePosturingResultsfrominjurytomidbrainandponsIndicativeofbrainstemdysfunctionPresentswithextendedupperextremitiesandpronationExtendedlowerextremitiesUsuallyindicativeofgraverinjuryCushing’sReflexLatesignofincreasingICPBradycardiaWideningpulsepressure/increasingBPChangesinrespiratorypatternsRespiratoryPatternsMaybeindicativeofinjurylocationinthebrainCheyne-StokesCentralNeurogenichyperventilationApneusticClusterbreathingAtaxicbreathingCheyne-StokesRespirationsPeriodicbreathinginwhichdepthofeachbreathincreasestopeakthendecreasestoaperiodofapneaHyperpneicstageusuallylastslongerthanapneicphaseBilaterallesionsincerebralhemispheresCentralNeurogenicRespirationsSustainedregular,rapidanddeepbreathingMidbrainandupperponsinjuryApneusticRespirationsBreathingwithalongpauseatfullinspirationorfullexpirationRespiratoryfunctionpresentatbrainstemlevelonlyClusterBreathingGaspingbreathswithirregularpausesLesionhighmedullaorlowponsAtaxicBreathingTotallyirregularconsistingofbothdeepandshallowbreathsassociatedwithirregularpausesConsistentwithmedullainjurysincetheinspiratoryandexpiratorycentersarelocatedhereGlascowComaScaleWidelyusedtomeasureseverityofinjuryinapatientandprognosisUsebestpossibleresponseMostpredictivesubsequenttoresuscitationGCSEyeopening1-4Verbalresponse1-5Motorresponse1-6TraumaScoreRespiratoryrateBloodpressureMaybeincorporatedintotheGCSSecondaryBrainInjuryHYPOXIAHYPOTENSION

AnemiaHyperglycemiaHypoglycemiaHyperthermiaIntracranialmassSignificanceSurvivingtheinitialinjuryisasmallpartofthebattleforthetraumaticbraininjuredpersonSecondaryinjurymayhaveagreaterinfluenceoverthefinaloutcomethantheprimaryinjuryTwomostcommonhypoxiaandhypotensionandmaybeasdevastatingastheprimaryinjuryHypotensionSinglemostprognosticfactorAsingleepisodeofdecreasedBPhasbeencorrelatedwithpooreroutcomeBrainrequiresbloodflowforperfusionKeepBP>90systolicCPP=MAP-ICPMostimportanttokeepMAP=/>70HypotensioninthefaceofcerebraledemaresultsindecreasedCPP(cerebralperfusionpressure)MAP(2)DBP+SBP

3Normal(70-100)HypoxiaDefinedasSpO2<90%LeadstocelldamageandresultantswellingCloselyfollowshypotensionininfluenceRSIfasterandmorereliableLessthan8intubateTreatmentProvideadequateventilationProvideadequatefluidresuscitationContinuallymonitorVSHOB@30degreesandheadmidlineConsidermannitolandhyperventilationifherniationimminentProphylacticseizuremedicationisnotindicatedVentilationRSIandventilateataratetomaintainEtCo2between35-45mmHgLidocaine1mg/kgpriortoanyintubationattemptHyperventilationHasbecomeverycontroversialrecentlyandisnolongerautomaticallyrecommendedMayexacerbatebraininjuryinallbuttheherniatingpatientReceptorsrespondtoincreasedO2withvasoconstrictionInjuredtissueisnolongerperfusedResultsinincreasededemaandnecrosisFluidResuscitationInitiateIVinfusiontomaintainSBP=/>90PreferablyMap>70mmHGFluidofchoiceLRorNSGlucosecausesfluidtobepulledintocellsresultingincerebraledemaMonitorContinuouslymonitorVSforSxofrisingICPChangesinbreathingpatternsIncreasingBPDecreasingHRUnequalpupilsPosturingPositionElevatedHOBMidlineheadplacementAssistswithvenousdrainagefromtheheadwhichdecreasesICPHyperthermiaCausesanincreaseinICPandshouldberegulatedHeadinjuredpatientsoftensufferfromincreasedbodytemperaturesandshouldbemonitoredAcetaminophenandothercoolingtechniquesmaybeusedDonotinducehypothermiawhichmayleadtoshiveringwhichresultsinincreasedICPSeizuresIntheeventofseizurestreatmentshouldbeinitiatedimmediatelyduetoresultanthypoxiaandincreasedICPTreatmentmayincludetheuseofValiumandCerebyxValiumdoesnotterminateabnormalelectricaldischargeasfosphenytoindoesPatientsmayneedtobeinaninducedbarbituratecomaTreatmentinHerniationHyperventilatetoEtCo2ofno<30mmHgMannitol-osmoticdiureticwhichmaybeusefulindecreasingICP1-1.5mg/kgLasixisaloopdiureticandnotusefulPurposeistokeepthepatientalivefordefinitivetreatmentsurgicalevacuationdrainplacedMedications:OxygenPrimary1stlinedrugAdministerhighflowHyperventilationiscontraindicatedReducescirculatingCO2levelsNRB:15LPMBVM:12-20timesperminuteKeepSaO2>95%Medications:DiureticsMannitol(osmotrol)MOALargeglucosemoleculeDoesnotleavebloodstreamOsmoticDiureticEffectiveindrawingfluidfrombrainContraindicationHypovolemia&HypotensionCHFDose1gm/kgCAUTIONFormscrystalsatlowtemperaturesReconstitutewithrewarming&gentleagitationUSEIN-LINEfilter&PREFLUSHlineMedications:DiureticsFurosemide(Lasix)MOALoopDiureticInhibitsreabsorptionofNa+inKidneysIncreasedsecretionofwaterandelectrolytesNa+,Cl–,Mg++,Ca++.Venousdilation&ReducescardiacpreloadMaybegivenincombinationwithMannitolNoteffectiveinreducingcerebraledemaContraindicationPregnancy:fetalabnormalitiesDoseSlowIVPorIMover1-2minutes0.5-1mg/kg:Commonly40or80mgMedications:ParalyticsSuccinylcholine(Anectine)MOADepolarizingMedicationCausesFasciculationsOnset&DurationOnset:30-60secondsDuration:2-3minutesPrecautionParalyzesALLmusclesincludingthoseofrespirationIncreasesintraocculareyepressureContraindicationPenetratingeyeinjury&DigitalisDose1-1.5mg/kgIVConsideradministrationofdefasiculatingdoseofparalyticUsewithlidocaine1mg/kginheadinjuredpatientsMedications:ParalyticsPancuronium(Pavulon)MOANon-depolarizingagentDoesnotaffectLOCOnset&DurationOnset:3-5minDuration:30-60minDoseMustpremedwithsedative0.04-0.1mg/kgVecuronium(Norcuron)MOANon-depolarizingagentDoesnotaffectLOCOnset&DurationOnset:<1minDuration:25-40minDoseConsiderpremedwithsedative0.08-0.1mg/kgMedications:SedativesDiazepam(Valium)MOABenzodiazepineAnti-anxietyMusclerelaxantOnset&DurationOnset:1-15minDuration:15-60minDose5-10mgMidazolam(Versed)MOABenzodiazepine3-4xpotentthanvaliumDoseSLOWIVP1mg/min1-2.5mgtitratedMedications:SedativeMorphineMOAOpiumalkaloidAnalgesicSedationAnti-anxietyReducesvascularvolume&cardiacpreloadIncreasesvenouscapacitance