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

GhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourse

Lecture Objectives   EpidemiologyofHeadInjury  Definition  Pathophysiology  MechanismsofInjury  ClinicalFeatures  EvaluationoftheHeadInjuredPatient  ManagementofHeadInjury  SequelaeofHeadInjury


Epidemiology   UnitedStates•  1.4millionannualincidentsofTBI

  50,000diefromTBI  235,000arehospitalized  1.1millionaretreatedandreleasedfromED

•  PeakIncidence=15-24yearsold(50%)  Smallerpeaksinelderlyandchildren  Children–typicallyresultofchildabuse

•  Highcosttosocietyintermsoflostproductivityandmoneyrequiredtocareforpatientsinlongtermfacilities

  Ghana•  EpidemiologyofHeadInjuryUnknown•  RTAaresignificantproblemandcauseofmortality

GhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourseGhanaEmergencyMedicineCollaborativeAdvancedEmergencyTraumaCourse

Epidemiology   EtiologyofHeadInjury(U.S.)


Falls28%

MotorVehicleTraffic20%Struckby/against

19%

Assault11%

PedalCycle(NonMotorVehicle)

3%

OtherTransport2%

Suicide1%

Other7%

Unknown9%


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


http://commons.wikimedia.org/wiki/File:Trepan1b.gif


Definition   TraumaticBrainInjury•  SpectrumofIntracranialInjury•  Resultsfrom:

  DirectForces=ObjectStrikingorpenetratingcranium  IndirectForces=Acceleration/DecelerationorRotationalMechanism

•  TraumaticBrainInjuryScale  GlasgowComaScale=30minutesafterheadinjury•  Mild=14-15,Moderate=9-13,Severe<9•  DynamicScale•  Over25differentscalesavailable


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


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.”


Normal Cerebral Autoregulation   Brainisasemisolidorganthatoccupies80%ifcranialvault•  20%ofthebody’soxygensupply•  15%ofcardiacoutput

  CranialVault=Fixedinsizebyouterrigidskull•  Containsbraintissue,bloodvesselsandCSF

  Monroe-KelliDoctrine•  Definestherelationshipbetweenthevolumesofthethreecompartments•  TheexpansionofonecompartmentMUSTbeaccompaniedbyacompensatoryreductioninthevolumesoftheothercompartmentstomaintainastableintracranialpressure(ICP)


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


Pathophysiology   TraumaticBrainInjury•  PrimaryBrainInjury

  TypesofPrimaryBrainTissueInjury  CellularInjuryMechanisms

•  SecondaryBrainInjury  SystemicInsults  IntracranialInsults

•  MechanismsofTraumaticBrainInjury  SkullFractures  Extra-axialFluidCollections  IntraparenchymalHemorrhage  SubarachnoidHemorrhage


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


PatrickJ.Lynch;illustrator;C.CarlJaffe;MD;cardiologist(Wikipedia)


Primary Brain Injury – Cellular Level


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


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


Secondary Brain Injury   OtherSystemicInsults•  Seizures•  ElectrolyteAbnormalities•  Coagulopathy•  Infection•  Hyperthermia•  Iatrogenic(Under-resuscitation)

  IntracranialInsults•  IntracranialHypertension•  Extra-axialLesions•  CerebralEdema(Peaksat24-48hrspostinjury)


Mechanisms of Injury   MechanismsofInjury•  Mediatorsof1oand2oInjury

  SkullFractures  Extra-axialLesions•  EpiduralHematoma•  SubduralHematoma

  IntraparenchymalHemorrhage  SubarachnoidHemorrhage


Skull Fractures   SkullFracture=HighDegreeofEnergy  Classification:•  Location•  Patternoffracture•  Openvs.Closed

  Locationmayindicateunderlyinginjury•  Depressedskullfracture=Oftentearunderlyingduraltissue•  Fractureoverpteryion=MiddleMeningealArtery=EDH•  Fractureoverduralsinus=SubduralHematoma

  Presenceofskullfractureincreasesriskofintracranialbleeding174timescomparedtopatientswithoutaskullfracture


Extra-axial Fluid Collections   EpiduralHematoma•  MiddleMeningealArtery(36%)•  HeadInjuryw/LOC+LucidIntervalfollowedbydeterioration

  Classicpresentation=47%ofcases•  LenticularShapeonCT

  SubduralHematoma•  InjurytoBridgingVeins•  Bloodaccumulationbetweenduramaterandpiaarachinoidmater

•  Increasedriskinelderlyandalcoholicsduetodecreasedbrainvolume

•  Hyperdensecrescentshapedlesion


http://www.unipa.it/~sparacia/rimg/caso1.jpg

Wikipedia


Intracerebral Hemorrhage   IntraparenchymalHemorrhage  SubarachnoidHemorrhage•  Disruptionofsubarachnoidvessels•  Commoninmoderatetoseverebraininjury•  Worseprognosis

  Twiceaslikelyasotherheadinjuredpatientstosufferfromdeath,persistentvegetativestateorseveredisability


Imagesfromhttp://www.radiology.co.uk/srs-x/tutors/cttrauma/tutor2.htm


Clinical Features   TraumaticBrainInjury•  Spectrumofclinicalpresentations•  HallmarkSymptoms

  Confusionandamnesiaw/orw/oLOC•  Severebraininjuryoftencharacterizedbydecreasedmentalstatusandpresenceofneurologicaldeficits•  Patientsmayalsodeterioratefrommildtosevereheadinjuryduringcourseofevaluation


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


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


Clinical Features   GlasgowComaScale


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


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


Clinical Features   MildHeadInjury•  Signsandsymptoms(early/late)


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


Clinical Features   GradingscaleformildheadinjurywithGCS=between14-15andconcussionsyndrome•  DevelopedbyColoradoMedicalSocietyandAmericanAcademyofNeurology•  CompositeGradingSystem

  Grade1–Anyheadinjurywithtransientconfusion,noLOCandsymptomsthatlastlessthan15minutes

  Grade2–Transientconfusion,noLOC,symptomsthatlastlongerthan15minutes

  Grade3–AllheadinjurywithLOC


Clinical Features   Moderate•  GCS=9-13•  Clinicalpresentationvarieswidely•  10%ofpatients•  SpecializedSubset=“TalkandDieSyndrome”

  Initially,talkativeandwithoutsignificantsignsofexternalinjury  Within48hoursofinjury,rapidlydeteriorate  EpiduralHematomaiscausein78-80%ofcases  Patientswith“talkanddiesyndrome”whopresentwithaGCS>9butwhodeterioratehavebeenshowntohaveaworseoutcomethanpatientswhopresentwithsevereTBIatoutset•  ?DelayedDiagnosis


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


Evaluation of the Head Injured Patient   SidelineEvaluation•  HeadInjurymaynotberecognizedbyaninjuredplayerornon-medicalpersonnel•  MultipleStandardizedtoolsforevaluationofheadinjuredsportsplayer  StandardizedAssessmentofConcussion(SAC)  SportConcussionAssessmentTool(SCAT)

  E.D.Evaluation•  NeurologicalExam•  Imaging


Neuroimaging   SkullRadiography  CTScan(GoldStandard)  MagneticResonanceImaging(MRI)  ExperimentalModalitiesforNeuroimaging•  FunctionalMRI(fMRI)•  PETScanning•  SPECTScanning•  MagneticSourceImaging(MSI)


Neuroimaging   SkullRadiography•  PriortoCT,Skullradiographyusedastriagetool•  Canevaluatefor

  Skullfractures  Pneumocephalus  Bloodinsinus  Penetratingforeignbody

•  Patientswithabnormalfindingsareatincreasedriskofintracranialfindings•  However,stillmissesalargenumberofpatientswithnormalskullfilmsbutextensiveinjury•  LimitedutilityatveryruralsiteswithoutaccesstoCTimaging


Neuroimaging   ComputedTomography(CTScan)•  Imagingmodalityofchoice•  Especiallygoodatidentifyingskullfracture,extra-axialfluidcollectionandhemorrhagiccontusion•  CTimaginghasincreasedinUnitedStates120%from1990to2000•  Highutilizationhasledtoclinicaldecisionrulestoidentifyappropriatepatientsrequiringevaluation  NewOrleansCriteria  CanadianHeadCTRule


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


Mild Head Injury Management   Management•  Symptomatictreatmentandpreventionofsecondaryinjury•  Appropriatemanagementdependsonassessmentofriskofneurologicaldecompensationandriskfactorsforintracranialhematoma•  Riskfactorsforintracranialhematoma

  Coagulopathy,Drug/AlcoholIntoxication,Previousneurosurgicalprocedures,Pre-traumaepilepsyorolderage(>60y/o)

•  Lowriskfeatures•  Allpatientswithmildtraumaticbraininjuryshouldbeobservedfor24hoursafterthatinjury(eitherinpatientoroutpatient).


Mild Head Injury Management   AdmissionCriteria•  HospitalAdmissionisrequiredforallpatientsathigherriskforcomplicationsincluding:

  GCS<15  AbnormalCTScan  SeizureActivity  AbnormalBleedingParameters(Anticoagulationorbleedingdiathesis)  Unabletobeobservedathome

  DischargeCriteria•  Lowriskpatientscanbedischargedhomewithoralandwrittendischargeinstructions

•  Patientscanbedischargedif:  GCS=15  Normalneurologicalexam  NormalHeadCT  Nopredispositionforbleeding


Mild Head Injury Management   DischargeInstructions•  Appropriatefollow-upinstructionsshouldbeprovidedbothverballyandwritteninstructions.

•  Noneedtoawakenpatientq2hours•  PatientswhoreturntoEDduetopersistentsymptomsshouldundergocarefulrepeatneurologicalevaluationbutlittledatasupportsrepeatCTScanning

  ReturntoPlayGuidelines•  Patientsshouldreturntosportingactivitiesinastep-wisefashionthatemphasizesphysicalandcognitiverest

•  Patientsshouldnotreturntosportingeventsiftheyarestillsymptomatic•  Therearemanycommonlyusedtoolsforassessingaplayersabilitytoreturntosportingevents.


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


Mod/Severe Head Injury Management   GeneralPrinciples•  AllmoderateandsevereheadinjuredpatientsshouldundergoCTimaging

•  Stabilizationandpreventionofsecondaryinsultsismainstayoftreatment  AirwayManagement•  Preventionofhypoxiaandhypoventilationkeytopreventingsecondaryinsults

•  PatientswithGCS<9,shouldhaveendotrachealairwayplaced•  RapidSequenceIntubationispreferredmethodofintubation•  NasotrachealIntubationcontraindicatedduetotendancyforICPtoincrease2/2cough/gag

•  LidocaineforpreventionofincreasedICPhasnotbeenshowntohaveabenefit

•  Specialattentionshouldbepaidtomaintainingcervicalspinalimmobilization


  HemodynamicAssessment•  Hypotension(SBP<90)shouldbeaggressivelytreatedassignificantcauseofworseoutcome•  Rarely,hypotensionisduetoheadinjuryitselfandothertraumaticinjuriesshouldbeinvestigated•  Treatmentofhypotensionisdirectedatmaintenanceofcerebralperfusion  Hypotonicfluidsarecontraindicated  Typicallyisotonicfluidsareused(NS)


Mod/Severe Head Injury Management


  Sedatives,AnalgesiaandNeuromuscularBlockade•  Agitationiscommonfindingandmayresultfrompain,deliriumordifficultieswithoxygenationandventilation

•  MinimizingagitationshouldbegoaltolimitincreasesinICPorinabilitiestooxygenateandventilate

•  Typically,shortactingopiatesandbenzodiazepinesareutilizedtodecreaseagitation

•  Longtermsedationshouldbeaccompaniedbysedationholidaystoevaluateneurologicalexam(Diprovan,Midazolam)

•  BarbituratesarenottypicallyusedintheemergencydepartmentbutdohavealimitedroleinlongtermmanagementofpatientswithincreasedICPwhorequiresedationandhavefailedothermedicalandsurgicaltreatmentsforincreasedICP.

•  NeuromuscularblockadeisindicatedforairwaycontrolwithRSIbutlongactingblockingagentsshouldbeavoidedbecausetheylimitserialexaminations




  SeizureProphylaxis•  Post-traumaticseizures=Seizuresoccurringinlessthan7dayspost-injury•  Riskfactors=GCS<10,CerebralContusion,DepressedSkullFracture,EDH,SDH,Intracerebralbleeding,Penetratingheadinjuryorseizureactivitywithin24hoursofinjury•  BrainInjuryFoundationrecommendsanti-epilepticmedicationsbeadministeredtohighriskpatientsforfirst7dayspost-injury•  Acutemanagementofseizureactivityismanagedwithbenzodiazepinesandothertypicalanti-epilepticagents•  Noprovenbenefittoadministrationofanti-epilepticmedsafter7daystodecreasingpost-traumaticepilepsy




  OperativeManagement•  Indications

  Penetratinginjuriesorbluntinjurieswithbreachofthecalvarium/skull

  Presenceofexpandingintracranialhematoma•  EpiduralHematoma

  Ifvolume>30cm3orifcomatose(GCS<9)•  SubduralHematoma

  Ifsize>10mmonCTorif5mmshiftregardlessofGCSscore

  DecompressionifGCSdecreasesby2pointsfromtimeofinjurytohospitalarrival

  ICP>20mmHGorifptwithfixed,dilatedpupils Malignantcerebraledema




  OperativeManagement•  DecompressiveCraniotomy

  SalvageoperationusedtomanageincreasingICP  Removalofpartofskullandunderlyingdura  DecreasesICP,improvescerebralperfusion,preventsischemia

  Servestolimitsecondaryinsults  Literaturedividedontruebenefit




Intracranial Monitoring   IntracranialMonitoring•  Developedin1960’sforclosemonitoringofICPinintubatedpatients•  Indications

  SevereTBIwithGCS<9  IntubatedpatientswithmoderateorsevereheadinjurywithsignificantintracranialfindingsonCT

  MethodsofMonitoring•  ExternalVentricularDrain

  Blindplacementofcatheterthroughbrainparenchymaintolateralventriclewithtransducertomeasurepressure

  CanalsodrainexcessCSFinhighICPpatients•  SubduralBoltCatheter

  Technicallyeasierthanventriculostomy  Monitoringboltplacedbeneaththeduraintothesubarachnoidspace  Doesn’tallowforCSFdrainage

•  FiberopticCatheter  SimilartoaSubduralboltbutprovidesmoreaccuratereadings


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


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


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



Questions?

Dkscully(flickr)


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author(s): patrick carter, daniel wachter, rockefeller

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