author(s): patrick carter, daniel wachter, rockefeller
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Advanced Emergency Trauma Course
GhanaEmergencyMedicineCollaborativePatrickCarter,MD∙DanielWachter,MD∙RockefellerOteng,MD∙CarlSeger,MD
HeadInjury
Presenter:PatrickCarter,MD
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Lecture Objectives EpidemiologyofHeadInjury Definition Pathophysiology MechanismsofInjury ClinicalFeatures EvaluationoftheHeadInjuredPatient ManagementofHeadInjury SequelaeofHeadInjury
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Epidemiology UnitedStates• 1.4millionannualincidentsofTBI
50,000diefromTBI 235,000arehospitalized 1.1millionaretreatedandreleasedfromED
• PeakIncidence=15-24yearsold(50%) Smallerpeaksinelderlyandchildren Children–typicallyresultofchildabuse
• Highcosttosocietyintermsoflostproductivityandmoneyrequiredtocareforpatientsinlongtermfacilities
Ghana• EpidemiologyofHeadInjuryUnknown• RTAaresignificantproblemandcauseofmortality
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Epidemiology EtiologyofHeadInjury(U.S.)
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Falls28%
MotorVehicleTraffic20%Struckby/against
19%
Assault11%
PedalCycle(NonMotorVehicle)
3%
OtherTransport2%
Suicide1%
Other7%
Unknown9%
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Definition TraumaticBrainInjuryhaslongbeenrecognizedasaimportantmedicalentity• Hippocratesfirstcommentedonmechanismsofhead injury and first described trephination asmodalitytotreatheadinjury
• 16thcentury–FrenchmilitarysurgeonAmbrosePare introduced term commotio cerebri todescribemildheadinjurytobrain
• Traumatic Brain Injury first came into use in1996 after U.S. based Traumatic Brain InjuryActwhichestablished federal funding forstudyofbraininjury
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http://commons.wikimedia.org/wiki/File:Trepan1b.gif
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Definition TraumaticBrainInjury• SpectrumofIntracranialInjury• Resultsfrom:
DirectForces=ObjectStrikingorpenetratingcranium IndirectForces=Acceleration/DecelerationorRotationalMechanism
• TraumaticBrainInjuryScale GlasgowComaScale=30minutesafterheadinjury• Mild=14-15,Moderate=9-13,Severe<9• DynamicScale• Over25differentscalesavailable
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Definition Concussion• Concussionrepresentsasubsetofmildtraumaticbraininjury• DerivedfromLatinterm“Concutere”ortoshakeviolently• Historically,definedbythelossofconsciousness• 1965ConsensusDefinition=CongressofNeurologicalSurgeons
“ A clinical syndrome characterized by the immediatetransient post-traumatic impairment of neural functionsuch as alteration of consciousness, disturbance ofvisionorequilibriumduetobrainsteminvolvement”
Definitionrecognizedashasmanylimitations
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Concussion Definition American Academy of Neurology and the International Conference onConcussion inSportheld in2004createdamodifiedconsensusdefinitionof concussion as “ a complex pathophysiological process affecting thebrain,inducedbytraumaticbiomechanicalforcesthattypicallyincludes:• Concussionmaybecausedbyeitheradirectblow to thehead, face,neckorelsewhereonthebodywithan“impulsive”forcetransmittedtothehead
• Concussiontypicallyresultsintherapidonsetofshortlivedimpairmentofneurologicfunctionthatresolvesspontaneously
• Concussion may result in neuropathologic changes but the acuteclinicalsymptomslargelyrepresentafunctionaldisturbanceratherthanstructuralinjury
• Concussion results in a graded set of clinical syndromes thatmay ormay not involve loss of consciousness. Resolution of the clinical andcognitivesymptomstypicallyfollowsasequentialcourse.
• Concussion is typically associated with grossly normal structuralimagingstudies.”
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Normal Cerebral Autoregulation Brainisasemisolidorganthatoccupies80%ifcranialvault• 20%ofthebody’soxygensupply• 15%ofcardiacoutput
CranialVault=Fixedinsizebyouterrigidskull• Containsbraintissue,bloodvesselsandCSF
Monroe-KelliDoctrine• Definestherelationshipbetweenthevolumesofthethreecompartments• TheexpansionofonecompartmentMUSTbeaccompaniedbyacompensatoryreductioninthevolumesoftheothercompartmentstomaintainastableintracranialpressure(ICP)
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Normal Cerebral Autoregulation CPP=CBF=MAP–ICP CerebralAutoregulation• Protectivemechanismtomaintaina tightlycontrolledenvironment where fluctuations in systemic arterialpressure or ICP do not have a large impact oncerebralbloodflow• Maintainedbyintactbloodbrainbarrier,aspecializedsetofendothelialcellswithtightjunctions• Disruption of the blood brain barrier by traumaticinjurymayimpairnormalcerebralautoregulation
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Pathophysiology TraumaticBrainInjury• PrimaryBrainInjury
TypesofPrimaryBrainTissueInjury CellularInjuryMechanisms
• SecondaryBrainInjury SystemicInsults IntracranialInsults
• MechanismsofTraumaticBrainInjury SkullFractures Extra-axialFluidCollections IntraparenchymalHemorrhage SubarachnoidHemorrhage
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Primary Brain Injury PrimaryBrainInjury
• Directorindirectforcetobraintissue,resultingincellularinjury
TypesofPrimaryBrainInjury• CorticalBrainContusion
ShearStress2/2Coup/Contracoupinjury Focal injury at gray matter closest to the brainsurface generates localized brain edema anddisruptionofnormalneurologicalfunction
Sizeofcontusiondefinesextentofinjury• DiffuseAxonalInjury
RotationalMechanism–• Widespread shearing strain at deep cerebral whitematter that disrupts normal axonal organizationresulting in disruption of axonal fibers and myelinsheaths
Non-lateralizingneurologicaldeficits Generalizededemaoccursafterinjury,typicallywithin6hourswithoutanyfocallesiononCTimaging
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PatrickJ.Lynch;illustrator;C.CarlJaffe;MD;cardiologist(Wikipedia)
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Primary Brain Injury – Cellular Level
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PrimaryCellularInjury
“NeurotransmitterStorm”
MassiveDepolarizationofBrainCells
Glutamate
Calcium
NMDA Disruptionofnormalcellularprocesses:ProteinPhosphorylationMicrotubuleConstructionEnzymeProduction
MembraneandCytoskeletonBreakdown
CellDeath
OxygenFreeRadicalPathwayActivation
LipidPeroxidationCellMembraneDysfunction
CellLysis
NitricOxideSynthase
HighNitricOxideLevels
IntracellularSignalingProcesses
Secondary Brain Injury SecondaryBrainInjury• SystemicorIntracranialprocessesthatcontributestotheprimarybraininjurycycleandresultsingreatertissueinjury• Categorizedinto:
SystemicInsults IntracranialInsults
EmergencyDepartmentTreatment• Focusedonlimitingtheextentofsecondarybraininjury
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Secondary Brain Injury SystemicInsults• Hypoxia(PaO2<60mmHg)
MortalityofTBIptswithhypoxia=doubled 40%ofTBIEDpatientsexhibithypoxiaduringcourse
• Hypotension(SBP<90mmHg) Presentin33-35%ofTBIpatients Resultsfromhemorrhagicshock,cardiaccontusion,tensionpneumothorax,etc
Hypotension→↓CerebralPerfusion→↑CerebralIschemia→↑DoublesMortality
• Anemia2/2BloodLoss(↓OxygenCarryingCapacity)• Hypo/Hypercapnia
Hyperventilation→↓pCO2Levels→↑SerumpH→CerebralVasoconstriction→↓CerebralBloodFlow
Previouslywasamainstayoftreatmentandwillhelptobufferanexpandinghematomainshort-term,butwillultimatelydecreasecerebralperfusiontopenumbraregionandincreasetissuedeath
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Secondary Brain Injury OtherSystemicInsults• Seizures• ElectrolyteAbnormalities• Coagulopathy• Infection• Hyperthermia• Iatrogenic(Under-resuscitation)
IntracranialInsults• IntracranialHypertension• Extra-axialLesions• CerebralEdema(Peaksat24-48hrspostinjury)
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Mechanisms of Injury MechanismsofInjury• Mediatorsof1oand2oInjury
SkullFractures Extra-axialLesions• EpiduralHematoma• SubduralHematoma
IntraparenchymalHemorrhage SubarachnoidHemorrhage
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Skull Fractures SkullFracture=HighDegreeofEnergy Classification:• Location• Patternoffracture• Openvs.Closed
Locationmayindicateunderlyinginjury• Depressedskullfracture=Oftentearunderlyingduraltissue• Fractureoverpteryion=MiddleMeningealArtery=EDH• Fractureoverduralsinus=SubduralHematoma
Presenceofskullfractureincreasesriskofintracranialbleeding174timescomparedtopatientswithoutaskullfracture
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Extra-axial Fluid Collections EpiduralHematoma• MiddleMeningealArtery(36%)• HeadInjuryw/LOC+LucidIntervalfollowedbydeterioration
Classicpresentation=47%ofcases• LenticularShapeonCT
SubduralHematoma• InjurytoBridgingVeins• Bloodaccumulationbetweenduramaterandpiaarachinoidmater
• Increasedriskinelderlyandalcoholicsduetodecreasedbrainvolume
• Hyperdensecrescentshapedlesion
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http://www.unipa.it/~sparacia/rimg/caso1.jpg
Wikipedia
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Intracerebral Hemorrhage IntraparenchymalHemorrhage SubarachnoidHemorrhage• Disruptionofsubarachnoidvessels• Commoninmoderatetoseverebraininjury• Worseprognosis
Twiceaslikelyasotherheadinjuredpatientstosufferfromdeath,persistentvegetativestateorseveredisability
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Imagesfromhttp://www.radiology.co.uk/srs-x/tutors/cttrauma/tutor2.htm
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Clinical Features TraumaticBrainInjury• Spectrumofclinicalpresentations• HallmarkSymptoms
Confusionandamnesiaw/orw/oLOC• Severebraininjuryoftencharacterizedbydecreasedmentalstatusandpresenceofneurologicaldeficits• Patientsmayalsodeterioratefrommildtosevereheadinjuryduringcourseofevaluation
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Clinical Features Confusion
• Characterizedbythreecardinalfeatures Disturbanceofvigilanceandheighteneddistractibility Inabilitytomaintainacoherenttrainofthought Inabilitytocarryoutasequenceofgoaldirectedmovements
Amnesia• Maybeanterogradeorretrograde• Often characterized by repetitive questioning, inability to follow commands,inabilitytoretaininformationduringmedicalevaluation
• Amnesia will decrease slowly over time and small amount of memory deficitremains
• Nolossofbiographicaldata i.e.Name,etc.–typicallytheresultofhystericalrxnormalingering
• Durationdoescorrelatewithseverityandoutcomeofheadinjury LossofConsciousness
• Resultsfromrotationalforcesatthejunctionoftheuppermidbrainandthalamusthat results in disruption of reticular neuron function and inability to maintainalertness
• Presence of LOC is not a predictor of long term neuropsychiatric sequelae ofheadinjury
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Clinical Features GlasgowComaScale• DevelopedbyTeasdaleandJennettin1974• Originallydesignedformeasure6hoursafterinjurytoprovidelongtermprognosticinformationaboutmortalityanddisability
• Now,standardizedtomeasure30minafterinjuryandrepetitivemeasurementsthroughoutpatient’sstay
• Shouldbeperformedafteradequateresuscitationb/cscaleissensitivetohypotension,hypoxia,intoxicationandpharmacologicinterventions
• CurrentClassification GCS=14-15=MildHeadInjury GCS=9–13=ModerateHeadInjury GCS<9=SevereHeadInjury
• Bestprognosticindicatorofoutcome=CTScan
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Clinical Features GlasgowComaScale
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Glasgow Coma Scale (GCS) Eye Opening Opens spontaneously 4
Responds to verbal command 3 Responds to pain 2 No eye opening 1
Verbal Oriented 5 Disoriented 4 Inappropriate words 3 Incomprehensible speech 2 No verbal response 1
Motor Obeys commands 6 Localizes to pain 5 Withdraws to pain 4 Flexion to pain (Decorticate posturing) 3 Extension to pain (Decerebrate posturing) 2 No motor response 1
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Clinical Features NeurologicExam• PupillarySize+Reactivity
FixedDilatedPupil=IpsilateralIntracranialHematomaresultinginuncalherniation
BilateralFixed+Dilated=PoorBrainPerfusion,bilateraluncalherniationorseverehypoxia• Indicativeofverypoorneurologicaloutcome
• NeurologicalPosturing DecorticatePosturing=Upperextremityflexionwithlowerextremityextension
• CorticalInjuryabovethemidbrain DecerebratePosturing=Armextensionandinternalrotationwithwristflexion
• Indicativeofbrainsteminjury• VeryPoorpredictorofoutcome
• Full,CompleteNeurologicalExam Examineforsubtleneurologicaldeficits Lookforspecificinjurypatterns:
• Battle’ssign,CXFOtorrhea,CSFRhinorrhea,Hemotympanum,peri-orbitalEcchymosisisindicativeofskullfractureandisconcerningforunderlyingbraininjury
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Clinical Features MildHeadInjury• Signsandsymptoms(early/late)
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Signs and Symptoms of Head Injury Cognitive Somatic Affective
Confusion Anterograde amnesia Retrograde amnesia Loss of consciousness Disorientation Feeling “zoned out” Feeling “foggy” Vacant stare Inability to focus Delayed verbal/motor response Slurred or incoherent speech Excessive Drowsiness
Headache Fatigue Disequilibrium Dizziness Nausea/vomiting Visual disturbances Photophobia Phonophobia Difficulty sleeping Ringing of the ears
Emotional Lability Irritability Sadness
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Clinical Features GradingscaleformildheadinjurywithGCS=between14-15andconcussionsyndrome• DevelopedbyColoradoMedicalSocietyandAmericanAcademyofNeurology• CompositeGradingSystem
Grade1–Anyheadinjurywithtransientconfusion,noLOCandsymptomsthatlastlessthan15minutes
Grade2–Transientconfusion,noLOC,symptomsthatlastlongerthan15minutes
Grade3–AllheadinjurywithLOC
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Clinical Features Moderate• GCS=9-13• Clinicalpresentationvarieswidely• 10%ofpatients• SpecializedSubset=“TalkandDieSyndrome”
Initially,talkativeandwithoutsignificantsignsofexternalinjury Within48hoursofinjury,rapidlydeteriorate EpiduralHematomaiscausein78-80%ofcases Patientswith“talkanddiesyndrome”whopresentwithaGCS>9butwhodeterioratehavebeenshowntohaveaworseoutcomethanpatientswhopresentwithsevereTBIatoutset• ?DelayedDiagnosis
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Severe Head Injury GCS<9 10%ofpatientswithTBI Earlyaggressivetreatmentisrequiredwithairwaycontrol,resuscitation,admissiontoICUsetting
25%ofthispatientpopulationwillrequireneurosurgicalintervention Outcomeispoorwithmortalityashighas60% Examtypicallywithabnormalexam,oftenevidenceofexternaltrauma,abnormalpupillaryexamandneurologicaldeficits
Cushing’sTriad=Acuteentityseeninseverelyheadinjuredpatientswithsignificantincreasedintracranialpressureandimpendingherniation• Resultsfromischemiatohypothalamuswithpoorperfusiontothebrain,resultinginsympatheticstimulationofthehearttocorrectpoorperfusion.Thesympatheticstimulationresultsinhypertension,butcarotidbaroreceptorsrespondwithparasympatheticstimulationresultinginbradycardia
• Characterizedby: ProgressiveHypertension Bradycardia Irregularorimpairedrespiratorypattern
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Evaluation of the Head Injured Patient SidelineEvaluation• HeadInjurymaynotberecognizedbyaninjuredplayerornon-medicalpersonnel• MultipleStandardizedtoolsforevaluationofheadinjuredsportsplayer StandardizedAssessmentofConcussion(SAC) SportConcussionAssessmentTool(SCAT)
E.D.Evaluation• NeurologicalExam• Imaging
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Neuroimaging SkullRadiography CTScan(GoldStandard) MagneticResonanceImaging(MRI) ExperimentalModalitiesforNeuroimaging• FunctionalMRI(fMRI)• PETScanning• SPECTScanning• MagneticSourceImaging(MSI)
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Neuroimaging SkullRadiography• PriortoCT,Skullradiographyusedastriagetool• Canevaluatefor
Skullfractures Pneumocephalus Bloodinsinus Penetratingforeignbody
• Patientswithabnormalfindingsareatincreasedriskofintracranialfindings• However,stillmissesalargenumberofpatientswithnormalskullfilmsbutextensiveinjury• LimitedutilityatveryruralsiteswithoutaccesstoCTimaging
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Neuroimaging ComputedTomography(CTScan)• Imagingmodalityofchoice• Especiallygoodatidentifyingskullfracture,extra-axialfluidcollectionandhemorrhagiccontusion• CTimaginghasincreasedinUnitedStates120%from1990to2000• Highutilizationhasledtoclinicaldecisionrulestoidentifyappropriatepatientsrequiringevaluation NewOrleansCriteria CanadianHeadCTRule
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New Orleans Criteria CT imaging is required for patients with minor head injury with any one of the following findings. The Criteria only apply to patients who have a GCS of 15. 1. Headache 2. Vomiting 3. Age > 60 years 4. Drug or Alcohol Intoxication 5. Persistent anterograde amnesia 6. Visible trauma above the clavicle 7. Seizure Canadian CT Head Rule CT Imaging is only required for patients with minor head injury with any one of the following findings. The criteria apply to patients with minor head injury who present with GCS of 13-15 after witnessed LOC, amnesia or confusion. High Risk for Neurosurgical Intervention 1. GCS < 15 at two hours after injury 2. Suspected open or depressed skull fracture 3. Any sign of basilar skull fracture (Hemotympanum, Peri-orbital Eccymosis, Otorrhea or Rhinorrhea, Battle sign) 4. Two or more episodes of vomiting 5. Age > 65 years Medium risk for Brain Injury Detection by CT Imaging 1. Amnesia before impact of 30 or more minutes 2. Dangerous mechanism (E.g. Pedestrican vs. Motor vehicle, Ejection from motor vehicle or fall from an elevation of 3 or more feet or 5 stairs)
Neuroimaging HeadCTClinicalRules• NewOrleansCriteria
SensitivityandSpecificityofdetectingaclinicallysignificantCTfinding
Sensitivity=100% Specificity=24.5% EstimatedtodecreaseCTimagingby23%
• CanadianHeadCTRule SensitivityandSpecificityforneedforneurosurgicalinterventionandclinicallysignificantfindingonCTimaging
Sensitivity=100% Specificity=68% ProposedtoreduceCTscanningby46%
• BothdecisionruleshavesubsequentlybeenvalidatedGhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourseGhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourse
Management MildHeadInjury• AdmissionCriteria• DischargeCriteria• DischargeInstructions• ReturntoPlayGuidelines
ModerateandSevereHeadInjury• GeneralPrinciples• AirwayManagement• HemodynamicAssessment• SeizureProphylaxis• OperativeManagement• IntracranialMonitoring
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Mild Head Injury Management Management• Symptomatictreatmentandpreventionofsecondaryinjury• Appropriatemanagementdependsonassessmentofriskofneurologicaldecompensationandriskfactorsforintracranialhematoma• Riskfactorsforintracranialhematoma
Coagulopathy,Drug/AlcoholIntoxication,Previousneurosurgicalprocedures,Pre-traumaepilepsyorolderage(>60y/o)
• Lowriskfeatures• Allpatientswithmildtraumaticbraininjuryshouldbeobservedfor24hoursafterthatinjury(eitherinpatientoroutpatient).
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Mild Head Injury Management AdmissionCriteria• HospitalAdmissionisrequiredforallpatientsathigherriskforcomplicationsincluding:
GCS<15 AbnormalCTScan SeizureActivity AbnormalBleedingParameters(Anticoagulationorbleedingdiathesis) Unabletobeobservedathome
DischargeCriteria• Lowriskpatientscanbedischargedhomewithoralandwrittendischargeinstructions
• Patientscanbedischargedif: GCS=15 Normalneurologicalexam NormalHeadCT Nopredispositionforbleeding
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Mild Head Injury Management DischargeInstructions• Appropriatefollow-upinstructionsshouldbeprovidedbothverballyandwritteninstructions.
• Noneedtoawakenpatientq2hours• PatientswhoreturntoEDduetopersistentsymptomsshouldundergocarefulrepeatneurologicalevaluationbutlittledatasupportsrepeatCTScanning
ReturntoPlayGuidelines• Patientsshouldreturntosportingactivitiesinastep-wisefashionthatemphasizesphysicalandcognitiverest
• Patientsshouldnotreturntosportingeventsiftheyarestillsymptomatic• Therearemanycommonlyusedtoolsforassessingaplayersabilitytoreturntosportingevents.
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Warning Signs after Discharge Inability to awaken the patient Decreased/Altered mental status Severe or worsening headache Somnolence or confusion Restlessness, Unsteadiness Seizure activity Visual difficulties Change in behavior Vomiting, fever, neck stiffness Urinary or bowel incontinence Weakness or numbness
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Mod/Severe Head Injury Management GeneralPrinciples• AllmoderateandsevereheadinjuredpatientsshouldundergoCTimaging
• Stabilizationandpreventionofsecondaryinsultsismainstayoftreatment AirwayManagement• Preventionofhypoxiaandhypoventilationkeytopreventingsecondaryinsults
• PatientswithGCS<9,shouldhaveendotrachealairwayplaced• RapidSequenceIntubationispreferredmethodofintubation• NasotrachealIntubationcontraindicatedduetotendancyforICPtoincrease2/2cough/gag
• LidocaineforpreventionofincreasedICPhasnotbeenshowntohaveabenefit
• Specialattentionshouldbepaidtomaintainingcervicalspinalimmobilization
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HemodynamicAssessment• Hypotension(SBP<90)shouldbeaggressivelytreatedassignificantcauseofworseoutcome• Rarely,hypotensionisduetoheadinjuryitselfandothertraumaticinjuriesshouldbeinvestigated• Treatmentofhypotensionisdirectedatmaintenanceofcerebralperfusion Hypotonicfluidsarecontraindicated Typicallyisotonicfluidsareused(NS)
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Mod/Severe Head Injury Management
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Sedatives,AnalgesiaandNeuromuscularBlockade• Agitationiscommonfindingandmayresultfrompain,deliriumordifficultieswithoxygenationandventilation
• MinimizingagitationshouldbegoaltolimitincreasesinICPorinabilitiestooxygenateandventilate
• Typically,shortactingopiatesandbenzodiazepinesareutilizedtodecreaseagitation
• Longtermsedationshouldbeaccompaniedbysedationholidaystoevaluateneurologicalexam(Diprovan,Midazolam)
• BarbituratesarenottypicallyusedintheemergencydepartmentbutdohavealimitedroleinlongtermmanagementofpatientswithincreasedICPwhorequiresedationandhavefailedothermedicalandsurgicaltreatmentsforincreasedICP.
• NeuromuscularblockadeisindicatedforairwaycontrolwithRSIbutlongactingblockingagentsshouldbeavoidedbecausetheylimitserialexaminations
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Mod/Severe Head Injury Management
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SeizureProphylaxis• Post-traumaticseizures=Seizuresoccurringinlessthan7dayspost-injury• Riskfactors=GCS<10,CerebralContusion,DepressedSkullFracture,EDH,SDH,Intracerebralbleeding,Penetratingheadinjuryorseizureactivitywithin24hoursofinjury• BrainInjuryFoundationrecommendsanti-epilepticmedicationsbeadministeredtohighriskpatientsforfirst7dayspost-injury• Acutemanagementofseizureactivityismanagedwithbenzodiazepinesandothertypicalanti-epilepticagents• Noprovenbenefittoadministrationofanti-epilepticmedsafter7daystodecreasingpost-traumaticepilepsy
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Mod/Severe Head Injury Management
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OperativeManagement• Indications
Penetratinginjuriesorbluntinjurieswithbreachofthecalvarium/skull
Presenceofexpandingintracranialhematoma• EpiduralHematoma
Ifvolume>30cm3orifcomatose(GCS<9)• SubduralHematoma
Ifsize>10mmonCTorif5mmshiftregardlessofGCSscore
DecompressionifGCSdecreasesby2pointsfromtimeofinjurytohospitalarrival
ICP>20mmHGorifptwithfixed,dilatedpupils Malignantcerebraledema
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Mod/Severe Head Injury Management
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OperativeManagement• DecompressiveCraniotomy
SalvageoperationusedtomanageincreasingICP Removalofpartofskullandunderlyingdura DecreasesICP,improvescerebralperfusion,preventsischemia
Servestolimitsecondaryinsults Literaturedividedontruebenefit
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Mod/Severe Head Injury Management
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Intracranial Monitoring IntracranialMonitoring• Developedin1960’sforclosemonitoringofICPinintubatedpatients• Indications
SevereTBIwithGCS<9 IntubatedpatientswithmoderateorsevereheadinjurywithsignificantintracranialfindingsonCT
MethodsofMonitoring• ExternalVentricularDrain
Blindplacementofcatheterthroughbrainparenchymaintolateralventriclewithtransducertomeasurepressure
CanalsodrainexcessCSFinhighICPpatients• SubduralBoltCatheter
Technicallyeasierthanventriculostomy Monitoringboltplacedbeneaththeduraintothesubarachnoidspace Doesn’tallowforCSFdrainage
• FiberopticCatheter SimilartoaSubduralboltbutprovidesmoreaccuratereadings
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Increased Intracranial Pressure Mostfrequentcauseofdeathanddisabilityaftersevereheadinjury Identifiedinanypatientwithclinicalsignsofimpendingherniation,CushingtriadorrisingICPasidentifiedbyintracranialmonitoringtechniques
RecommendedICP<20mmHgwithCPP>60mmHg InitialFirstlinetreatmentofincreasedICP• HOB–30degrees
Subsequentfirstlinetreatmentmeasures• Shorttermhyperventilation• Osmoticdiureticadministration(i.e.Mannitol,Hypertonicsaline)
SecondLineTreatments• Highdosebarbiturates• Severehyperventilation• Mild/moderatehypothermia• Decompressivecraniotomy
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Emergency Burr Hole Trephination EmergencyBurrHoleTrephination
• Indication Patientw/TBIwithevidenceofrapiddeteriorationandsignsofimpendingtranstentorialherniationwithexpecteddelayinneurosurgicalmanagement
PerformedaftermedicalmanagementofincreasedICPhasfailed Ideally,hematomaislocalizedbyCTimagingbutcanbeperformedasblindprocedure• 85%ofthetimewillbeonthesamesideasthedilatedpupil
• Procedure Landmark=6cmanteriorandsuperiortothetragusoftheearoverthetempopareitalregion Verticalincisionismadethroughthescalp,subcutaneoustissueandtemporalismuscleuntilgaleaaponeuroticaisreached
Arotaryortwistdrillisthenusedtobreachtheinnertableofthecraniumandthesiteisexamined
EDHwillpresentasimmediateclotandbleedingbeforetheduraisreached SDHwillpresentasdarkbluishmassofbloodbeneaththebulgingdura InthecaseofaSDH,thedurawillneedtobeincisedwithascalpelandsubduralbloodwillneedtobesuctionedfromthesite
Ifnobloodisidentified,additionalholesaremadesuperiortotheinitialsiteandifbloodisstillnotidentified,thentheoppositesideisattempted
Allsitesshouldbecoveredwithasterilenon-occlusivedressingGhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourseGhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourse
Sequelae of Head Injury SecondImpactSyndrome• Rare,Controversialentity• Athletewhohassustainedamildconcussionwhosubsequentlysuffersasecondheadinjurybeforethesymptomsfromthefirsthaveresolved
• Patientssubsequentlydeveloprapiddiffusecerebraledema(within2min),increasedICPandeventualherniation,comaanddeath
• Thefirstheadinjuryispostulatedtocauseadisruptionofthenormalcerebralvascularautoregulationthatcausesincreasedcerebralbloodflow,makingthebrainvulnerabletothesecondimpact,whentherapidmalignantswellingoccurs
• Returntoplayguidelineshavebeendevelopedtopreventthistypeofsecondaryinjury
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Sequelae of Head Injury PostConcussiveSyndrome
• Constellationofsymptomsthatdevelopswithin4weeksoftheinjuryandmaypersistformonths(90%at1month,25%at1year)
• Treatmentiswithanalgesia,anti-depressentsandanti-emetics Post-traumaticEpilepsy
• Seizureactivity>7daysfromtraumaticinjury• Headtraumaiscauseoflongtermepilepsyin3%ofpatientswithepilepsy• Incidenceishighestinpatientswithcompoundskullfracture,intracranialhemorrhageorpresenceofearlyacutesymptomaticseizure(presenceofall3factorsincreasesriskby50-80%)
• Cannotbepreventedwithprophylacticuseofantiepileptics PersistentVegetativeState
• Rarecomplicationofsevereheadinjury,firstdescribedin1972byJennettandPlum
• Disruptionofcerebralcognitivefunctionwithsparingofbrainstemfunction• Noawarenessofthemselvesorenvironmentandcannotinteractwithothersbutwillmaintainnormalsleep-wakecycle
• Recoveryisrareifsymptomspersistfor>3months,norecoverydocumentedafter12monthsofsymptoms
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Questions?
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