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TintinallisEmergencyMedicine:AComprehensiveStudyGuide,8e>

Chapter257:HeadTrauma
DavidW.WrightLisaH.Merck

INTRODUCTIONANDEPIDEMIOLOGY
Traumaticbraininjuryisbrainfunctionimpairmentthatresultsfromexternalforce.1Theclinicalmanifestations
representabroadconstellationofsymptomsfrombriefconfusiontocoma,severedisability,and/ordeath.The
underlyingpathologyrangesfromtemporaryshiftsincellularionicconcentrationstopermanentstructural
damage.

Traumaticbraininjury(TBI)isclassifiedasmild,moderate,andseverebasedontheGlasgowComaScale
(GCS)score.Over80%ofTBIisdefinedasmild(GCS14to15)(mTBI)andisoftencalled"concussion."2
Thelabelofmild,however,isamisnomer.mTBImayleadtosignificant,debilitatingshortandlongterm
sequelae.ModerateTBI(GCS9to13)accountsforapproximately10%ofheadinjuries.Mortalityratesfor
patientswithisolatedmoderateTBIare<20%,butlongtermdisabilitycanbehigher.Overall,40%ofpatients
withmoderateTBIhaveanabnormalfindingonCTscan,and8%willrequireneurosurgicalintervention.In
severeTBI(GCS3to8),mortalityrateapproaches40%,withmostdeathsoccurringinthefirst48hoursafter
injury.Fewerthan10%ofpatientswithsevereTBIexperiencegoodrecovery.2,3

TheprevalenceofTBIistwiceashighinmalesasinfemales.Distributionofageatinjuryistrimodal,with
peaksat0to4years,15to24years,and>75yearsofage.Mortalityrateincreaseswithageattimeofinjury.4,5
Motorvehiclecollisionsaretheprimarycauseofbluntheadinjuryinyoungadultsandchildren,andfallsare
morecommonintheelderly.2TBIhasbeencalledthe"signatureinjury"oftheconflictsinIraqand
Afghanistan.6

PATHOPHYSIOLOGY
CEREBRALBLOODFLOW

Autoregulation,cerebralperfusionpressure(CPP),meanarterialpressure(MAP),andintracranialpressure
(ICP)areinterrelatedfactorsthataffectcerebralbloodflow(Table2571).Undernormalcircumstances,
autoregulationregulateslocalcerebralbloodflowtomaintainequilibriumbetweenoxygendeliveryand
metabolism.7Othersystemicfactors,suchashypertension,hypocarbia,andalkalosis,canaffectcerebralblood
flowbycausingvasoconstriction.

TABLE2571FactorsthatAffectCerebralBloodFlow
MAP=DBP+[(SBPDBP)/3]

CPP=MAPICP

Abbreviations:CPP=cerebralperfusionpressureDBP=diastolicbloodpressureICP=intracranialpressure
MAP=meanarterialpressureSBP=systolicbloodpressure.
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Undernormalsituations,autoregulationcanadjusttoCPPsfrom50to150mmHgtomaintainlocalcellular
AgeGroup IntracranialPressure(mmHg)
oxygendemandsandregionalcerebralbloodflow.Inbraininjury,autoregulationisoftenimpaired,soeven
modestdropsinbloodpressurecandecreasebrainperfusionandresultincellularhypoxia.ACPP<60mmHg
isconsideredthelowerlimitofautoregulationinhumans,belowwhichlocalcontrolofcerebralbloodflow
cannotbeadjustedtomaintainflowadequateforfunction.8Traumatichypotensionleadstoischemiawithinlow
flowregionsoftheinjuredbrain,soaggressivefluidresuscitationmayberequiredtopreventhypotensionand
secondarybraininjury.IntheabsenceofanICPmonitor,itisimportanttomaintainaMAPof80mmHg,
becauselowbloodpressureinthesettingofelevatedICPwillresultinalowCPPandbraininjury.

Thecraniumisanenclosedspacewithafixedvolume.Anychangestothevolumeoftheintracranialcontents
(suchasbleeding)affecttheICP,andanincreaseinICPcandecreasetheCPP.ICPisdeterminedbythevolume
ofthethreeintracranialcompartments:thebrainparenchyma(<1300mLintheadult),cerebrospinalfluid(100
to150mL),andintravascularblood(100to150mL).Whenonecompartmentexpands,thereisacompensatory
reductioninthevolumeofanother,and/orthebaselineICPwillincrease(Figure2571).ElevationsinICPare
lifethreateningandmayleadtoaphenomenonknownastheCushingreflex(hypertension,bradycardia,and
respiratoryirregularity).Hypertensionisanattempttomaintaincerebralperfusion.NormalvaluesforICPvary
withage(Table2572).

TABLE2572IntracranialPressurebyAgeGroup
AgeGroup IntracranialPressure(mmHg)
Adults <1015
Youngchildren 37
Infants 1.56.0

FIGURE2571.

Pressurevolumerelationshipinbraininjury.Normalcerebralbloodflowautoregulationcurveandtheabnormal
curvewithtraumaticbraininjury(TBI).Normalautoregulatorycontrol(blueline)maintainsarelatively
constantcerebralbloodflowoverabroadrangeofmeanarterialpressure(MAP).9Lossofautoregulation
resultsinamorelinearrelationshipbetweencerebralbloodflow(CBF)andMAP.Elevatedintracranialpressure
(ICP)candramaticallydecreaseCBFwhenautoregulationisimpaired(inflectionpointofredline).Increasesin
ICPmayresultinanetlossinCBF.

PRIMARYBRAININJURIES

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TheinitialinsultassociatedwithmoderateandsevereTBIimpartsmechanicalforcesthatproducehighlevelsof
directdamageandstraintothebrainparenchyma.Theprimaryinjuriesincludecontusions(bruisestobrain
parenchyma),hematomas(subdural,epidural,intraparenchymal,intraventricular,andsubarachnoid),diffuse
axonalinjury(stressordamagetoaxons),directcellulardamage(neurons,axons,andothersupportivecells),
lossofthebloodbrainbarrier,disruptionoftheneurochemicalhomeostasis,andlossoftheelectrochemical
function.

SECONDARYBRAININJURIES

Awaveofsecondarydamageisunleashedbytheimpactthatresultsinaseriesofdeleteriouscellularand
subcellularevents(alsoknownasthesecondaryneurotoxiccascade).10,11Thesecondaryneurotoxiccascade
causesongoingdamagetothebrainandultimatelyresultsinapoorerneurologicoutcomethanmighthave
occurredbasedontheoriginalmechanism.

Thesecondaryneurotoxiccascadeshouldnotbeconfusedwiththetermsecondaryinsults,atermusedinthe
clinicalliteraturetodescribeconditionsorcircumstances(e.g.,hypotension,hypoxemia,hyperglycemia)that
accelerateneurotoxicdamageandworsenlongtermoutcome.12,13Mediationofsecondaryinsultsreduces
morbidityandmortalityandisdiscussedinthetreatmentsection.

Thesecondaryneurotoxiccascadeisamassivereleaseofneurotransmitters,suchasglutamate,intothe
presynapticspace,withactivationofNmethylDaspartate,amino3hydroxy5methyl4isoxazolepropionic
acid,andotherreceptors.10Ionicshiftsactivatecytoplasmicandnuclearenzymes,inducemitochondrial
damage,andleadtocelldeathandnecrosis.10,14,15Proinflammatorycytokinesandotherenzymesarereleased
inanattempttocleanandrepairthedamage.Secondaryinjury,however,isindiscriminantandproduces
extensiveneuronalloss.Additionally,manysurvivablecellsundergoapoptosis,orprogrammedcelldeath,
duringsecondaryinjury.16Apoptosishasbeenreportedtooccurlongerthanayearafterinjury.16,17

BRAINEDEMA

BrainedemaresultsfromtwodistinctprocessesandcanbefatalinTBI.18Cellularswelling,orcytotoxic
edema,resultsfromlargeionicshiftsandthelossofcellularmembraneintegrityfrommitochondrialdamage
(lossofadenosinetriphosphate,ionpumpproductivity,andincreasedfreeradicalproduction).Extracellular
edemaresultsfromdirectdamageto,orthebreakdownof,thebloodbrainbarrier,ionicshifts,andalterationof
waterexchangemechanisms(e.g.,aquaporins).19,20Asintracellularandextracellularwatercontentrises,the
brainswellsandtheICPincreases,leadingtodirectcompressivetissuedamage,vascularcompressioninduced
ischemia,brainparenchymaherniation,andbraindeath.

BRAINHERNIATION

Therearefourmajorbrainherniationsyndromes:uncaltranstentorial,centraltranstentorial,cerebellotonsillar,
andupwardposteriorfossa.Themostcommonisuncalherniation,whichoccurswhentheuncusofthetemporal
lobeisdisplacedinferiorlythroughthemedialedgeofthetentorium.Thisisusuallycausedbyanexpanding
lesioninthetemporallobeorlateralmiddlefossa.Uncaltranstentorialherniationleadstocompressionof
parasympatheticfibersrunningwiththethirdcranial(oculomotor)nerve,causinganipsilateralfixedand
dilatedpupilduetounopposedsympathetictone.Furtherherniationcompressesthepyramidaltract,
whichresultsincontralateralmotorparalysis.Insomecases,thepupillarychangescanbecontralateral,
whereasthemotorchangesareipsilateral.

Centraltranstentorialherniationislesscommonandoccurswithmidlinelesions,suchaslesionsofthefrontalor
occipitallobes,orvertex.Themostprominentsymptomsarebilateralpinpointpupils,bilateralBabinski's
signs,andincreasedmuscletone.Fixedmidpointpupilsfollowalongwithprolongedhyperventilationand
decorticateposturing.
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Cerebellotonsillarherniationoccurswhenthecerebellartonsilsherniatethroughtheforamenmagnum.This
4ytoAdult Child<4y Infant
mayleadtopinpointpupils,flaccidparalysis,andsuddendeath.Upwardtranstentorialherniationresults
fromaposteriorfossalesionandleadstoaconjugatedownwardgazewithabsenceofverticaleyemovements
andpinpointpupils.

THEGLASGOWCOMASCALE

TBIseverityisclassifiedusingtheGCS(Table2573).Thescaleiscomposedofthreecomponents:eye
opening(1to4points),verbalresponse(1to5points),andmotorresponse(1to6points)(Table2573).The
sumofthesecomponentsdefinestheTBIseverityclassificationintosevere(GCSscoreof3to8),moderate
(GCSscoreof9to13),andmild(GCSscoreof14or15).Themotorscoreindependentlycorrelateswith
outcome,almostaswellasthefullscore.21

TABLE2573GlasgowComaScaleforAllAgeGroups
4ytoAdult Child<4y Infant
Eyeopening
4 Spontaneous Spontaneous Spontaneous
3 Tospeech Tospeech Tospeech
2 Topain Topain Topain
1 Noresponse Noresponse Noresponse
Verbalresponse
5 Alertandoriented Oriented,social,speaks,interacts Coos,babbles
Confusedspeech,disoriented,consolable,
4 Disorientedconversation Irritablecry
aware
3 Speakingbutnonsensical Inappropriatewords,inconsolable,unaware Criestopain
Moansorunintelligible Incomprehensible,agitated,restless,
2 Moanstopain
sounds unaware
1 Noresponse Noresponse Noresponse
Motorresponse
Normal,spontaneous
6 Followscommands Normal,spontaneousmovements
movements
5 Localizespain Localizespain Withdrawstotouch
4 Movesorwithdrawstopain Withdrawstopain Withdrawstopain
3 Decorticateflexion Decorticateflexion Decorticateflexion
2 Decerebrateextension Decerebrateextension Decerebrateextension
1 Noresponse Noresponse Noresponse
3

15

Note:Inintubatedpatients,theGlasgowComaScaleverbalcomponentisscoredasa1,andthetotalscoreis
markedwitha"T"(ortube)denotingintubation(e.g.,8T).

TheGCSisanobjectivemeasurementofclinicalstatus,correlateswithoutcome,isareliabletoolfor
interobservermeasurements,andiseffectiveformeasuringpatientrecoveryorresponsetotreatmentovertime.
However,thescalehasseverallimitations.Itmeasuresbehavioralresponses,nottheunderlying
pathophysiology.PatientswithsimilarGCSscoresmayhavedramaticallydifferentunderlyingstructuralinjuries
andrequiredifferentclinicalinterventions(Figure2572).Itisnotasusefulasasingleacutemeasureof
severityasitisasatooltomeasurediseaseprogressionovertime.TheGCSmayadditionallybeaffectedby

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drugs,alcohol,medications,paralytics,orocularinjuries.Finally,thescalelacksthegranularitynecessaryto
assessmTBI.

FIGURE2572.

EachoftheseCTimagesshowsadistincttraumainducedpathophysiologicabnormality,yetallpatientshada
GlasgowComaScalescoreof4.[ImageusedwithpermissionofAlisaGreen,MD,UniversityofCalifornia,
SanFrancisco.]

CLINICALFEATURES
Theresultsofhistory,examination,anddiagnosticimagingwillallowthedistinctionintotwocategoriesof
injury:moderateseverebraininjuryandmildbraininjury.Treatmentanddispositionarequitedifferentinthe
twocategoriesandaredetailedbelow.

HISTORY

Obtainanaccuratehistoryfromthepatient,witnesses,andEMScrewstogainimportantinsightintothe
mechanismofinjuryandoverallseverityofTBI(e.g.,heightoffall,impactsurfacecondition,damagesustained
tovehicle,airbagdeployment,seatbeltuse,historyofejectionfromthevehicle,orreportoffatalitiesatthe
scene).Premorbidmedicalhistory,medications(especiallyanticoagulants),druguse,and/oralcoholintoxication
arealsoimportantintheassessmentandtreatmentofacuteTBI.Initialclinicalfindingsandphysicalexamas
reportedbyEMSareanessentialcomponentoftriagingandmanagingTBI.Thepresenceofafocal
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neurologicdeficit,seizures,emesis,ordepressedlevelofconsciousnessincreasesconcernforunderlyingbrain
injury.

PHYSICALEXAMINATION

FollowAdvancedTraumaLifeSupportprinciplestoperformthetraumafocusedexamination,with
simultaneouslifesavingproceduresasneeded.Protectthecervicalspineduringevaluation,treatment,and
imaging.

ObtaintheGCS.Classifytheinjuryassevere(GCSscoreof3to8),moderate(GCSscoreof9to13),or
mild(GCSscoreof14or15).Ifemergencyintubationisnecessary,obtainapreintubationGCSand
recordthepatient'sbestscore.

Determinepupillaryresponse.22Inanunresponsivepatient,asinglefixedanddilatedpupilmayindicatean
intracranialhematomawithuncalherniationthatrequiresrapidsurgicaldecompression.Bilateralfixedand
dilatedpupilssuggestincreasedICPwithpoorbrainperfusion,bilateraluncalherniation,drugeffect(suchas
atropine),orseverehypoxia.Bilateralpinpointpupilssuggesteitheropiateexposureorcentralpontinelesion.

Alteredmotorfunctioncanindicatebrain,spinalcord,orperipheralnerveinjuries.Assessmovementinacoma
patientbyobservingthepatient'sreactiontonoxiousstimuli,suchaspressuretoanailbed.Decorticate
posturing(upperextremityflexionandlowerextremityextension)indicatessevereintracranialinjuryabovethe
levelofthemidbrain.Decerebrateposturing(armextensionandinternalrotationwithwristandfingerflexion
andinternalrotationandextensionofthelowerextremities)indicatesamorecaudalinjury.Forcompletely
unresponsivepatients,respiratorypatternandeyemovementscanprovideinformationregardingbrainstem
function.Remember,donotassessoculovestibular(coldcaloric)andoculocephalic(doll'seyes)responsesina
patientundercervicalspineprecautions.

IMAGING
Individuallyassesseachpatient'smechanismofinjury,history,comorbidities,andsignsandsymptoms
whendeterminingtheneedforCTimagingoftheheadandcervicalspine.

HeadCTisexquisitelysensitivetothepresenceofbloodandguidesEDmanagement.DonotdelayheadCT,
becauseexpandinghemorrhagiclesionsneedemergencyneurosurgicalintervention.Therefore,ifthepatientis
uncooperativeorcombative,intubationandsedationareoftenthebestoptionstoenablerapidCT
imaging.OthermeanstocontrolagitatedpatientswithTBIincludemidazolam(1to2milligramsIV)and
propofol(20milligramsevery10secondstodesiredeffect).

SeveraldecisionruleshavebeendevelopedtominimizeunnecessaryheadCTimaging.23,24,25,26,27The
guidelinesstrivetoidentifypatientswithsurgicalemergencies.Thesestudiesdonotspecificallyaddressthe
relationshipbetweenminorCTfindings(whichmayplacethepatientatriskforthedevelopmentofseizures),
thedurationofpostconcussivesymptoms,andprogressivechangesonCTduringthecourseofapatient's
evaluation.AdultswithmTBIandaGCSscoreof14or15willhaveanintracraniallesiononCTabout15%of
thetime,but<1%willrequireneurosurgicalintervention.28

TheprevalenceofcervicalfracturesincomatoseTBIpatientsisapproximately8%,andanestimated4%of
injuriesaremissedontheinitialassessmentofthetraumapatient.23Cervicalimagingisavitalcomponentinthe
careofthebraininjuredpatient.PerformCTimagingofthecervicalspineinpatientswithalteredmentalstatus
andwhowereinjuredbyamechanismthatincreasestheriskofcervicalspineinjury.CTissuperiortoplain
radiographyinpatientswithalteredmentalstatusandcanbeperformedatthesametimeastheheadCT.

TheNEXUSandCanadianCervicalSpineRulesarediscussedindetailinchapter258,"SpineTrauma."

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MRIcandetectsubtlelesionsmissedbyCTimagingandcanbetterdefinetheextentofcontusions.However,
NewOrleansCriteriaGCS15* CanadianCTHeadRuleGCS1315*
MRImaynotdetectsubtlelesions,cannotbeperformedifthepatientisunstable,andisnotalwaysavailable.

DECISIONRULESFORHEADCTIMAGINGINADULTS

Decisionrulescanguideclinicalpractice,buteachpatientmustbeassessedindividually,andnoneofthe
rulesdescribedbelowaddressshortorlongtermnonoperativesequelaeofTBI.Seechapter110,
"PediatricTrauma,"foradiscussionoftheroleofheadCTimaginginchildrenwithminorheadinjury.

ThetwomostcommonlyusedevidencebasedclinicaldecisionrulesforheadCTinadultsaretheNewOrleans
Criteria29andtheCanadianCTHeadRule.23Bothruleshavebeenvalidatedandare100%sensitivein
detectingpatientswhowillneedneurosurgicalintervention,buttheyhavelimitedspecificity(5%versus37%,
respectively).TheCanadianCTHeadRuleislesssensitive(83%)ifintracraniallesionisthedefinedendpoint.
Anegativefeatureofthesetwodecisionrulesisthatlossofconsciousnessoramnesiaisrequiredastheentry
point.Mostminorbraininjuryeventsdonotresultinlossofconsciousness,andlossofconsciousnessis
notthebestpredictorofintracranialpathology(Table2574).Donotapplytheserulestopatientstaking
anticoagulantsorantiplateletagents,ortochildren,becausethesevariableswerenotincludedinthe
validationstudies.

TABLE2574NewOrleansCriteriaandCanadianCTHeadRuleClinicalDecisionRules
NewOrleansCriteriaGCS15* CanadianCTHeadRuleGCS1315*
Headache GCS<15at2h
Vomiting Suspectedopenordepressedskullfracture
Age>60y Age65y
Intoxication Morethanoneepisodeofvomiting
Persistentantegradeamnesia Retrogradeamnesia>30min
Evidenceoftraumaabovetheclavicles Dangerousmechanism(fall>3ftorstruckaspedestrian)
Seizure Anysignofbasalskullfracture
IdentificationofpatientswhohaveanintracraniallesiononCT
100%sensitive,5%specific 83%sensitive,38%specific
Identificationofpatientswhowillneedneurosurgicalintervention
100%sensitive,5%specific 100%sensitive,37%specific

Abbreviation:GCS=GlasgowComaScale.

*PresenceofanyonefindingindicatesneedforCTscan.

TheNationalInstituteforClinicalExcellenceandtheNeurotraumatologyCommitteeoftheWorldFederationof
NeurosurgicalSocietieshaveevaluatedclinicalsignsandsymptomsassociatedwithTBIinadultsand
adolescentsandadults,respectively.27,30TheresultantdecisionrulesforheadCThavebeenappliedtolarge
datasetsandshowntoberelativelysensitive(NationalInstituteforClinicalExcellence:94%forneurosurgical
lesions,82%forintracraniallesionsNeurotraumatologyCommittee:100%forneurosurgicallesionsand
intracranialinjuries).Onestudyevaluated1101patientswithmTBIwhohadGCSscoresof14or15
approximately2%ofthesepatientswithoutlossofconsciousnesshadintracraniallesionsand0.6%required
surgery(ratessimilartopatientswithlossofconsciousness).

Oneofthemostimportantfindingsfromthesestudiesistherelativesignificanceofcertainelementsofthe
historyandphysicalexamination.Forexample,nauseaandvomitingafterconcussionhasanoddsratio
comparabletothatoflossofconsciousnessforapositiveCTfinding(Table2575).Importantly,thepredictive
valueofindividualclinicalsignsandsymptomsdiffersbetweenadultsandchildren(seechapter138,Head
InjuryinInfantsandChildren).
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TABLE2575OddsRatio(OR)forHeadCTandClinicalFeatures
Smitsetal30 Ibanezetal26 Fabbrietal27,70
Smitsetal30 Ibanezetal
OR(95%CI)
26
OR(95%CI) Fabbrietal
OR(95%CI)
27,70

OR(95%CI) OR(95%CI) OR(95%CI)

GlasgowComaScalescoreof14 2(13) 7(414) 19(1426)
Neurologicdeficits 2(13) 7(225) 19(1328)
Signsofbasilarskullfracture 14(822) 11(623) 10(616)
Lossofconsciousness 2(13) 7(411) 2(23)
Posttraumaticamnesia 1.7(12) 3(25) 8(612)
Headache 1.4(12) 3(26)*
Vomiting 3(24) 4(27) 5(38)
Posttraumaticseizure 3(110) 2(0.2517) 3(25)
Intoxication 1(0.62) 1(0.33)
Antithrombotics 2(14) 4(37) 8(39)
Age>65y 2(13) 2(13)
Dangerousmechanismofinjury 2(14) 3(24)

Abbreviation:CI=confidenceinterval.
*Forsevereheadache.

AsummaryoftheAmericanCollegeofEmergencyPhysiciansrecommendations28isgiveninTable2576.A
combinationofruleshelpsidentifypatientsatriskanddeterminethepossibleneedforaheadCT(Tables2574,
2575and2576).

TABLE2576CTScanningforAdultswithBrainInjury(AmericanCollegeofEmergencyPhysicians
Guidelines)
AdultswithaGlasgowComaScalescoreof<15atthetimeofevaluationshouldundergoCTimaging

Mildtraumaticbraininjurywithorwithoutlossofconsciousness:ifoneormoreofthefollowingispresent:

GlasgowComaScalescore<15

Focalneurologicfindings

Vomitingmorethantwotimes

Moderatetosevereheadache

Age>65y

Physicalsignsofbasilarskullfracture

Coagulopathy

Dangerousmechanismofinjury(e.g.,fall>4ft)

Mildtraumaticbraininjurywithlossofconsciousnessoramnesia:ifoneormoreofthefollowingispresent:

Drugoralcoholintoxication

Physicalevidenceabovetheclavicles

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Persistentamnesia
Treatment Comments
Posttraumaticseizures

TREATMENT
PREHOSPITALCARE

Earlyappropriatemanagementcanhaveaprofoundimpactonthepatient'sfinaloutcome.Forpatientswith
moderatetosevereheadinjury,providestabilizationandrapidtransporttoafacilitywithexperienceinthe
managementofbraininjury.Themostimportantprehospitalinterventionsareairwayandbloodpressure
management.Ifthepatientneedsprehospitalintubation,avoidhyperventilation(whichcausescerebral
vasoconstrictionandcannegativelyaffectoutcome),andusecapnometrytokeepPCO2at35to45mmHg.
Treathypotensionaggressively.Iftransporttimesareshort,donotgivemannitolorhypertonicsalinefor
elevatedICP.Guidelinesforprehospitalcareareavailableathttp://www.braintrauma.org.

EDTREATMENT

PrinciplesforEDcareofmoderate/severebraininjuryareprovidedathttp://www.braintrauma.organdare
discussedinthefollowingsection.Theprimarygoalsoftreatmentaretomaintaincerebralperfusionand
oxygenationbyoptimizingintravascularvolumeandventilationpreventsecondaryinjurybycorrecting
hypoxia,hypercapnia,hyperglycemia,hyperthermia,anemia,orhypoperfusionrecognizeandtreatelevated
ICParrangeforneurosurgicalinterventiontoevacuateintracranialmasslesionsandtreatotherlifethreatening
injuries.

Systolicbloodpressureof<90mmHgandhypoxemia(PaO2<60)areassociatedwitha150%increaseriskin
mortality.31

Observeforthesigns/symptomsofelevatedICP:changeinmentalstatus,pupillaryirregularities,focal
neurologicdeficits,decerebrateordecorticateposturing,orCTpathology.SomeCTsignsofintracranial
hypertensionareattenuationofthevisibilityofsulciandgyri,becausethebrainiscompressedagainsttheskull
compressedlateralventriclesandpoorgrey/whitematterdistinction.Papilledemamaynotbeevidentif
pressurerisesrapidly.SedationandanalgesiamaydecreasebaselineICPandpreventtransientrisesinICP
fromagitation,coughing,orgaggingfromtheendotrachealtube.Preventandcontrolseizureactivity.

Treathypotension,hypoxemia,hypercarbia,andhyperglycemia.Asingleoccurrenceofhypotensionand
hypoxiaafterbraininjuryisassociatedwitha150%increaseinmortality.22TBIisprogressive,soappropriate
earlymanagementwillhaveagreaterimpactonoutcomethantreatmentsinitiatedafterneuronalcelldeathand
thedevelopmentofsecondaryinjury,suchascerebraledema.Jointlydevelopandapplygoaldirectedprotocols
withemergencymedicine,trauma,neurosurgery,andintensivecareteams.Anexampleofearlygoaldirected
therapyisprovidedinTable2577.

TABLE2577ChecklistforEDTreatmentofBrainInjury
Treatment Comments
Cervicalspine Spinalprecautions
Maintainairway,intubateforGCS<8oras
Airway
needed
Oxygenation Oxygensaturation>90PCO2355 Noprophylactichyperventilation
andventilation

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Agent Treatment Comments Comments

SystolicBP>90mmHg,MAP80mmHggive Nopermissivehypotensionpressorsmay
BP NS,bloodproducts,ortransfuseasneeded berequirediffluidsnotsufficient
SerialGCSishelpfulinidentifying
GCSbeforeparalyticsifpossibletreatlife
ExamandGCS changekeepgoalof"brainresuscitation"
threateninginjuriesandactivebleeding
astoppriority
StatheadCT
andcervical IdentifymasslesionsandsignsofincreasedICP Protectcervicalspineuntilcleared
spineCT
CheckGCSforchangesandforsignsof Changeofmorethan2pointsshould
Repeatexam
impendingherniation/deterioration promptfurtherworkup
Checkglucose Treathypoglycemiaandhyperglycemia Hyperglycemiaisbadforthebrain
Control Aggressivecooling:Tylenol,cooling
Maintainbetween36Fand38.3F
temperature blanket,etc.
Seizure GiveantiepilepticdrugifGCS10,acuteseizure Phenytoin
prophylaxis withinjury,orabnormalheadCTscan (Dilantin)/fosphenytoin/levetiracetam
Consideraddinghypertonicsaline(3%
Identifyand Keepheadofthebedat30degreesensuregood
NaCl250mL/30min)forrefractory
treatelevated BP,ventilation,andtemperaturecontrolgive
elevationsinICPmonitorBPand
ICP,herniation mannitol1gram/kgIVbolusurgentNSconsult
electrolytes
Neurosurgery
ICPmonitoring,ventriculostomyforICP
referral/transfer ICPmonitoringandCSFdiversioninGCS
management,aggressivetieredapproachto
foradvanced 8
management,emergencysurgery
care

Abbreviations:BP=bloodpressureCSF=cerebrospinalfluidGCS=GlasgowComaScaleICP=intracranial
pressureMAP=meanarterialpressureNS=normalsaline.

AirwayandBreathing

Treatanyconditionthatcompromisesventilation(e.g.,alteredmentalstatus,facial/necktrauma,pneumothorax).
Patientswithsevereinjury(GCSscoreof8)requireintubation.Useshortactinginductionagentsthathave
limitedeffectonbloodpressureorICP(Table2578).Avoidnasotrachealintubationiffacialtraumaorbasilar
skullfractureisevidentorsuspected.Monitorbloodpressurethroughouttheprocedure.Preinductionagents
suchaslowdosesuccinylcholine,vecuronium,pancuronium,andlidocainedonotimproveoutcome,butcanbe
usedasadjunctsiftheydonotdelayairwaycontrol.32Maintaininlinecervicalspinestabilizationduring
intubation.

TABLE2578IntubationAgentsinBrainInjury
Agent Comments
Inductionagent
Maybeneuroprotectivemaylowerintracranialpressureadrenalsuppression
Etomidate,0.3milligram/kg unlikelywithsingleuse
IV
Rapidonsetandoffsetantiseizurepropertiescancausehypotensionif
Propofol13milligrams/kg inadequatefluidresuscitation
IV

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Agent Comments
Paralytics
Shortactingavoidinburns,extensivemuscleinjury,etc.
Succinylcholine11.5
milligrams/kgIV Shortacting,safeinhyperkalemia
Rocuronium,0.61.0
milligram/kgIV

MaintainoxygenationandusecapnometrytocontrolPCO2andavoidhyperventilation.Prolonged(>6hours)
hypocapniacausescerebralvasoconstrictionandworsenscerebralischemia.Keepoxygensaturation>90,
PaO2>60,andPCO2at35to45.

Circulation

Traumatichypotensionleadstoischemiawithinlowflowregionsoftheinjuredbrain.Ischemiaamplifiesthe
neurotoxiccascadeandincreasescerebraledema.Provideaggressivefluidresuscitationtopreventhypotension
andsecondarybraininjury.Maintainsystolicbloodpressureat>90mmHgandMAP>80mmHg.Ablood
pressurewithin"normal"rangemaybeinadequatetomaintainadequateflowandCPPifICPisincreased.
Permissivehypotensionworsensoutcomeinpatientswithbraininjury.

Isolatedheadinjuryrarelyproduceshypotension,exceptasapreterminalevent.Hypovolemicshockmaybe
seenwithpolytrauma,massivebloodlossfromscalplacerations,orinsmallchildrenfromsubgalealhematoma.
Iffluidandbloodresuscitationisnoteffective,usevasopressorstopreservecerebralperfusion.

PainandincreasedICPcancausehypertension.Treatpain,andassessforimpendingherniation(Cushing
reflex).Formanagement,seediscussionwithinthischapterunder"IncreasedIntracranialPressureManagement"
section.

Patient

PositioningRaisingtheheadofthebedmayimprovecerebralbloodflowbyloweringICP.However,the
interactionbetweenICP,MAP,andtissueoxygenationiscomplexandhighlyvariable.Responsetoposition
changedependsonmanyfactorssuchasdegreeofintactautoregulation,braincompliance,andindividual
patientvariability.Thereisstilluncertaintyastowhetherthisprocedureisbeneficial,butinthesettingof
suspectedelevatedICP,itiscurrentlyrecommendedasasimplemaneuvertoimprovecerebralbloodflow.One
mustensurethatthepatient'sbloodpressureismaintainedabovetheminimumrecommendedlevel(MAP80
mmHg),becauseelevationof30degreescandropthemeanpressurewithinthebrainbyupto10to15mmHg
andimproveCPP(rememberCPP=MAPICP,soloweringtheICPimprovesCPP,butloweringMAPinthe
settingofhypotensioncouldbecounterproductiveandlowerCPP).Elevatingtheheadofthebedto30degrees
canbesafelyaccomplishedevenwhenthespinehasnotbeencleared,aslongasneckmovementissecured.33

GlucoseControl

Hyperglycemiainthesettingofneurologicinjury(bothstrokeandTBI)isassociatedwithworseoutcome.Tight
hyperglycemiccontrolisrecommendedinpatientswithmoderatetosevereTBI.Insulindripsmayberequired
toachieveadequatecontrol(glucose100to180milligrams/dLor5.55to9.99mmol/L).

TemperatureControl

Elevatedtemperatureisassociatedwithanincreasedmetabolicdemandandexcessiveglutamaterelease.
ElevatedtemperatureelevatesICPandworsensoutcomeinmanyneurologiccriticalcareconditionsincluding
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TBI.Treatfeverwiththegoalofnormothermia.TheevidenceforhypothermiainTBIisnotsufficientto
GoalDirectedTherapySuggestedTargets
recommenditsuse.

SeizureTreatmentandProphylaxis

Seizuresafterheadinjurycanchangetheneurologicexamination,alteroxygendeliveryandcerebralbloodflow,
andincreaseICP.Prolongedseizurescanworsensecondaryinjury.TreatacuteseizureswithIVlorazepam,and
ifseizurescontinue,treatasforstatusepilepticus.Giveprophylacticphenytoin/phosphenytoiniftheGCSis
10,ifthepatienthasanabnormalheadCTscan,orifthepatienthashadanacuteseizureaftertheinjury.The
doseis18milligrams/kgIVat25milligrams/minute.Prophylacticanticonvulsantsreducetheoccurrenceof
posttraumaticseizureswithinthefirstweek.Phenytoin/phosphenytoinistheagentmoststudied.Levetiracetam
canbeused,buttherearelessdatasupportingitsuse.Steroidshavenorole.

CerebralHerniation

DevelopateamapproachtoICPmanagementbetweenemergencymedicine,neurosurgery,intensivecareunit,
andtraumateams.

Usepatienthistoryandphysicalexaminationtoidentifysignsandsymptomsofimpendingherniation.Indicators
ofrisingICPincludesevereheadache,visualchanges,numbness,focalweakness,nausea,vomiting,seizure,
changeinmentalstatus,lethargy,hypertension,coma,bradycardia,andagonalrespirations.Signsofimpending
transtentorialherniationincludeunilateralorbilateralpupillarydilation,hemiparesis,motorposturing,and/or
progressiveneurologicdeterioration.

MeasureneurologicdeteriorationbycomparingsequentialGCSscores.Inapatientwitharapidlydeteriorating
GCS,iftimepermits,obtainarepeatheadCTtoidentifyanexpandingintracranialhematoma.

Mannitoland/orhypertonicsalinecanlowerICP.MannitolisanosmoticagentthatcanreduceICPand
improvecerebralbloodflow,CPP,andbrainmetabolism.Mannitolisalsoafreeradicalscavenger.Itgenerally
hasaneffectwithin30minutes.Mannitolexpandsplasmavolumeandcanimproveoxygencarryingcapacity.
Administermannitolbyrepetitivebolus(0.25to1gram/kg),andnotbyconstantinfusion.Becausenodose
dependenteffectisseenwithmannitol,somecliniciansadvocatebeginningatthelowerrangeofthesuggested
dose.Mannitolresultsinanetintravascularvolumelossbecauseofitsdiureticeffect.Monitorthepatient'sinput
andoutput.Osmoticdiuresisisrelativelycontraindicatedinhemorrhageandhypotension.However,inthe
settingofacuteherniation,mannitolhasbeendemonstratedtoeffectivelyreducelifethreateningelevationsof
ICP.

Hypertonicsalinemaybeusedasanalternativetomannitolinthepatientwhoisnotadequatelyfluid
resuscitatedorhypotensive.TheBrainTraumaFoundationindicatesthatatthistime,datasupporttheprimary
useofmannitolfortheacutetreatmentofICP.MostEDshave3%NaCLavailablethedoseforadultsis250
mLover30minutes.Intensivecareunitsmaystock23.4%sodiumchloridesolutionthedoseforadultsis30
mLover30minutes.Monitorserumosmolalityandserumsodium.

Mannitolandhypertonicsalinemaybegivenseriallyandinconjunctionwithoneanother.

ADVANCEDTREATMENTOFBRAININJURY

Advancedtreatmentofbraininjuryrequiresinvasiveandclosemonitoring(Table2579).

TABLE2579GoalDirectedTherapyofBrainInjury
GoalDirectedTherapySuggestedTargets
Pulseoximetry90% CPP60mmHg Physiologicsodium135140mEq/L
SBP90mmHg ICP<20mmHg INR1.4
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GoalDirectedTherapySuggestedTargets
MAP80mmHg PbtO215mmHg Platelets75103/L
PaCO23545mmHg pH7.357.45 Hemoglobin8grams/dL
Temperature36.038.3C Glucose80180milligrams/dL

Abbreviations:CPP=cerebralperfusionpressureICP=intracranialpressureMAP=meanarterialpressure
PbtO2=braintissueoxygentensionmonitoringSBP=systolicbloodpressure.

CerebralPerfusionPressureManagement

IftheGCSis8,arrangeforplacementofanintracranialboltorextraventriculardrainwithmonitoring
capabilitiesassoonaspossibletomonitorICPandtodirecttreatment.MaintainCPPat55to60mmHgto
adequatelyperfusebraintissue.8IncreasingCPP>70mmHgmayresultininjurytootherorgans(e.g.,acute
respiratorydistresssyndromefromlungtissuetrauma).

ConsiderICPmonitoringforpatientswithanormaladmissionbrainCTscaniftwoormoreofthefollowing
criteriaaremet:ageover40years,unilateralorbilateralmotorposturing,andsystolicbloodpressure<90mm
Hg.Inaddition,provideICPmonitoringinpatientsundergoingemergencysurgery(e.g.,orthopedicrepair).
ManagementofCPPisessentialintraoperatively,wherethepatientwithelevatedICPmayexperiencelarge
shiftsincentralvolumestatusduetosurgicalbloodloss.

IncreasedIntracranialPressureManagement

AnICPof>20mmHgincreasesmorbidityandmortality.EarlyconsultationwithneurosurgeryfordirectICP
monitoring,cerebrospinalfluiddiversion,orsurgicalinterventionishighlyrecommendedinmoderateand
severeTBI.Incertaincircumstances,anICPmonitorwillbeplacedintheEDbyneurosurgerytohelpguide
medicalmanagementofICP,aswellasfordirectcerebrospinalfluiddiversiontolowerICP.

SPECIFICHEADINJURIES
SCALPLACERATIONS

Scalplacerationscanleadtomassivebloodloss,socontrolbleedingasrapidlyaspossible.Ifdirectpressureis
noteffective,locallyinfiltratelidocainewithepinephrineandclamporligatebleedingvessels.Beforeclosure,
carefullyexaminewoundstoidentifyforeignbodies,underlyingfractures,andgaleallacerations.Largegaleal
disruptionsshouldberepaired.Fordiscussionofrepairofscalplacerations,seechapter42,"FaceandScalp
Lacerations."

SKULLFRACTURES

PatientswhohaveoraresuspectedofhavingaskullfracturerequireaheadCTscan(seeTable2574).Skull
fracturesareusuallycategorizedbylocation(basilarversusskullconvexity),pattern(linear,depressed,or
comminuted),andwhethertheyareopenorclosed(Figures2573and2574).Alinearskullfracturewithan
overlyinglacerationisanopenfracture.Explorewoundsgentlytoavoiddrivingbonefragmentsintothebrain.

FIGURE2573.

LinearfractureseenonCT.Arrowindicatesskullfractureasterisksindicatenormalcranialsuturelines.[Image
usedwithpermissionofJosephPiatt,Jr.,MD,DivisionofNeurosurgery,A.I.duPontHospitalforChildren,

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Wilmington,DelawareDepartmentsofNeurologicalSurgeryandPediatrics,ThomasJeffersonUniversity,
Philadelphia,Pennsylvania.]

FIGURE2574.

Openskullfracturewithunderlyingcerebralcontusion.Thisinjurywassustainedfromafalloftwostories.
[ImageusedwithpermissionofJosephPiatt,Jr.,MD,DivisionofNeurosurgery,A.I.duPontHospitalfor
Children,Wilmington,DelawareDepartmentsofNeurologicalSurgeryandPediatrics,ThomasJefferson
University,Philadelphia,Pennsylvania.]

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Fracturesthatcrossthemiddlemeningealartery,amajorvenoussinus,orlinearoccipitalfractureshavehigh
intracerebralcomplicationrates.Patientswithskullfracturesthatareopenordepressed,involveasinus,orare
associatedwithpneumocephalusshouldbegivenantibiotics(vancomycin,1gramIV,andceftriaxone,2grams
IV).Askullfracturethatisdepressedbymorethanthethicknessoftheskullusuallyrequiresoperativerepair.

BASILARSKULLFRACTUREANDCEREBROSPINALFLUIDLEAKS

Thepresenceofabasilarskullfractureisasignificantriskfactorforintracranialinjury.Themostcommon
basilarskullfractureinvolvesthepetrousportionofthetemporalbone,theexternalauditorycanal,andthe
tympanicmembrane.Itisassociatedwithduraltearing,whichoftenleadstootorrheaorrhinorrhea.Basilarskull
fracturesmayoccuranywherealongtheskullbase,fromthecribriformplatethroughtheoccipitalcondyles.Do
notplaceanasogastrictubethroughthenaresifcribriformplatefractureissuspectedthiscanleadtodirect
intracranialinjury.Signsandsymptomsassociatedwithbasilarskullfracturesincludecerebrospinalfluid
leak,mastoidecchymosis(Battlesign),periorbitalecchymoses(raccooneyes),hemotympanum,vertigo,
decreasedhearingordeafness,andseventhnervepalsy.Periorbitalandmastoidecchymosesdevelop
graduallyoverhoursafteraninjuryandareoftenabsentintheED.Cerebrospinalfluidleaks(otorrheaor
rhinorrhea)aredifficulttodiagnosehowever,thepatientoftencomplainsofdischargeofclearfluidfromthe
noseorears.Fluidmaybecollectedandsentforanalysis(identificationoftransferrin).The2transferrin
isoformoftransferrinisfoundonlyincerebrospinalfluid,andnotinblood,mucus,ortears.

Patientswithacutecerebrospinalfluidleaksareatriskformeningitis.Antibioticprophylaxisisoften
recommendedtoreducetheincidenceofinfection.30Administrationofantibioticsshouldbedonein
consultationwiththeneurosurgeonwhowillbefollowingthepatient.Ifprophylacticantibioticsareinstituted,
thedrugsselectedshouldhavebroadcoveragewithgoodpenetrationintothemeninges,suchasceftriaxone,2
gramsIV,andvancomycin,1gramIV.Theheadofthepatient'sbedshouldbeelevatedto30degrees.Alumbar
drainisoftenplacedbytheneurosurgicalteam.Cerebrospinalfluidleaksmayrequirerepairbyaneurosurgeon
orotolaryngologist.

CEREBRALCONTUSIONANDINTRACEREBRALHEMORRHAGE

Contusionsmostcommonlyoccurinthesubfrontalcortex,inthefrontalandtemporallobes,and,occasionally,
intheoccipitallobes(Figure2575).Theyareoftenassociatedwithsubarachnoidhemorrhage.Contusionsmay
occuratthesiteoftheblunttraumaorontheoppositesideofthebrain,knownasacontrecoupinjury.

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FIGURE2575.

CTscandemonstratingdelayedintraparenchymalhemorrhagesfromatraumaticcontusion.[Imageusedwith
permissionofJackFountain,Jr.,MD,EmoryUniversityandGradyMemorialHospital.]

Intracerebralhemorrhagecanoccurdaysaftersignificantblunttrauma,oftenatthesiteofresolvingcontusions.
Thiscomplicationismorecommoninpatientswithcoagulopathy.CTscanfindingsimmediatelyafterinjury
maybenormal.ObtainserialCTsifanychangeinmentalstatusoccursinapatientwithcoagulopathyuntilthe
clotisstable.

SUBARACHNOIDHEMORRHAGE

Traumaticsubarachnoidhemorrhageresultsfromthedisruptionoftheparenchymaandsubarachnoidvessels
andpresentswithbloodinthecerebrospinalfluid(Figure2576).Patientswithisolatedtraumaticsubarachnoid
hemorrhagemaypresentwithheadache,photophobia,andmeningealsigns.Traumaticsubarachnoid
hemorrhageisthemostcommonCTabnormalityinpatientswithmoderatetosevereTBI.Patientswith
earlydevelopmentoftraumaticsubarachnoidhemorrhagehaveathreefoldhighermortalityriskthanthose
withouttraumaticsubarachnoidhemorrhage(42%versus14%,respectively).34Sometraumaticsubarachnoid

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hemorrhagescanbemissedonearlyCTscans.Generally,CTscansperformed6to8hoursafterinjuryare
sensitivefordetectingtraumaticsubarachnoidhemorrhage.

FIGURE2576.

CTscandemonstratingsubarachnoidhemorrhage.Arrow1indicatesprepontinecisternalblood,andarrow2
identifiesbloodintheambientcistern.[ImageusedwithpermissionofJackFountain,Jr.,MD,Emory
UniversityandGradyMemorialHospital.]

EPIDURALHEMATOMA

Anepiduralhematomaresultswhenbloodcollectsinthepotentialspacebetweentheskullandtheduramater
(Figure2577).Theanatomicrelationshipsofthebranchesofthemiddlemeningealarteryandthesequelaeof
fractureandlacerationofthearteryareshowninFigure2572.

FIGURE2577.

Epiduralhematoma.Notetheconvexshapeandfocallocation.[ImageusedwithpermissionofJackFountain,
Jr.,MD,EmoryUniversityandGradyMemorialHospital.]

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Blunttraumatothetemporalortemporoparietalareawithanassociatedskullfractureandmiddlemeningeal
arterialdisruptionistheprimarymechanismofinjury.Occasionally,traumatotheparietooccipitalregionorthe
posteriorfossacausestearsofthevenoussinuseswithepiduralhematomas.

Theclassichistoryofanepiduralhematomainvolvesasignificantbluntheadtraumawithlossofconsciousness
oralteredsensorium,followedbyalucidperiodandsubsequentrapidneurologicdemise.Thisclinical
presentationoccursinaminorityofcases.Traumaticblowstothethintemporalboneoverthelateralaspectof
theheadcarrythehighestrisk(e.g.,baseballorpoolstickinjury).Thediagnosisofanepiduralhematomais
basedonCTscanandphysicalexaminationfindings.TheCTappearanceofanepiduralhematomaisabiconvex
(footballshaped)mass,typicallyfoundinthetemporalregion.

Thehighpressurearterialbleedingofanepiduralhematomacanleadtoherniationwithinhoursafteraninjury.
Earlyrecognitionandevacuationreducesmorbidityandmortality.Underlyinginjuryofthebrainparenchymais
oftenabsentfullrecoverymaybeexpectedifthehematomaisevacuatedpriortoherniationorthedevelopment
ofneurologicdeficits.

SUBDURALHEMATOMA

Subduralhematomaiscausedbysuddenaccelerationdecelerationofbrainparenchymawithsubsequenttearing
ofthebridgingduralveins.Thisresultsinhematomaformationbetweentheduramaterandthearachnoid
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(Figures2578and2579).Subduralhematomatendstocollectmoreslowlythanepiduralhematomabecause
ofitsvenousorigin.However,subduralhematomaisoftenassociatedwithconcurrentbraininjuryand
underlyingparenchymaldamage.Brainswithextensiveatrophy,suchasintheelderlyorinchronic
alcoholics,aremoresusceptibletothedevelopmentofacutesubduralhematoma.Evenseeminglybenign
fallsfromstandingpositioncanresultinsubduralbleedingintheelderly.Children<2yearsoldarealsoat
increasedriskofsubduralhematoma.

FIGURE2578.

Smallsubduralhematomaintherightfrontotemporalregioninanadult.[ImageusedwithpermissionofJack
Fountain,Jr.,MD,EmoryUniversityandGradyMemorialHospital.]

FIGURE2579.

A.Bifrontalchronicsubduralhematomaextendingthroughtheanteriorfontanelleina1montholdchild.B.
Secondimageinthesamechildshowingbifrontalchronicsubduralhematoma,aswellassmall,acute
intraparenchymalhemorrhageintheposteriorfossa.

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Typeof Anatomic
CTFindings CommonCause ClassicSymptoms
Patient Location

Traditionally,subduralhematomashavebeenclassifiedasacute,subacute,orchronicdependingonthelengthof
timefromonsetandoccurrenceofactivehemorrhage.Acutesymptomsusuallydevelopwithin14daysofthe
injury.After2weeks,thetermchronicsubduralhematomaisused.Thereisnospecificclinicalsyndrome
associatedwithasubduralhematoma.Acutecasesusuallypresentimmediatelyafterseveretrauma,andoften
thepatientisunconscious.Intheelderlyorinalcoholics,chronicsubduralhematomasmayresultinvague
complaintsormentalstatuschanges.Often,thereisnorecallofinjury.OnCTscan,acutesubduralhematomas
arehyperdense(white),crescentshapedlesionsthatcrosssuturelines.Subacutesubduralhematomasare
isodenseandaremoredifficulttoidentify.CTscanningwithIVcontrastorMRIcanassistinidentifyinga
subacutesubduralhematoma.Achronicsubduralhematomaappearshypodense(dark)becausetheironinthe
bloodhasbeenmetabolized.

Thedefinitivetreatmentdependsonthetype,size,effectonunderlyingbrainparenchyma,andtheassociated
braininjury.Mortalityandtheneedforsurgicalrepairaregreaterforacuteandsubacutesubduralhematomas.
Chronicsubduralhematomascansometimesbemanagedwithoutsurgerydependingontheseverityofthe
symptoms.Table25710comparesintracranialinjuries.

TABLE25710ComparisonofIntracranialInjuries
Typeof Anatomic
CTFindings CommonCause ClassicSymptoms
Patient Location

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Typeof Anatomic
CTFindings CommonCause ClassicSymptoms
Patient Location
Young,rare Potential
Skullfracture ImmediateLOCwitha
inthe space Biconvex,
withtearofthe "lucid"periodpriorto
Epidural elderlyand between footballshaped
middlemeningeal deterioration(only
thoseage skulland hematoma
artery occursinabout20%)
<2y duramater
Acute:rapidLOC,
Morerisk lucidperiodpossible
Space Acceleration
inthe Crescentor
betweendura decelerationwith
Subdural elderlyand sickleshaped Chronic:alteredmental
materand tearingofthe
alcoholic hematoma stateandbehaviorwith
arachnoid bridgingveins
patients gradualdecreasein
consciousness
Bloodinthe Acceleration
Anyage Mild,moderate,or
basilarcisterns decelerationwith
groupafter severetraumaticbrain
Subarachnoid Subarachnoid andhemispheric tearingofthe
blunt injurywithmeningeal
sulciand subarachnoid
trauma signsandsymptoms
fissures vessels
Usually
Anyage Severeor
anterior Maybenormal
Contusion/intracerebral groupafter penetrating Symptomsrangefrom
temporalor initiallywith
hematoma blunt traumashaken normaltoLOC
posterior delayedbleed
trauma babysyndrome
frontallobe

Abbreviation:LOC=lossofconsciousness.

DIFFUSEAXONALINJURY

Diffuseaxonalinjuryisthedisruptionofaxonalfibersinthewhitematterandbrainstem.Shearingforcesonthe
neuronsgeneratedbysuddendecelerationcausediffuseaxonalinjury.Theconditionisseenafterblunttrauma,
suchasfromamotorvehiclecrash.Ininfants,shakenbabysyndromeisawelldescribedcause.35

Inseverediffuseaxonalinjury,edemacandeveloprapidly.Theunderlyinginjurycanresultindevastatingand
oftenirreversibleneurologicdeficits.ACTscanofapatientwithdiffuseaxonalinjurymayappearnormal,but
classicCTfindingsincludepunctuatehemorrhagicinjuryalongthegreywhitejunctionofthecerebralcortex
andwithinthedeepstructuresofthebrain(Figures25710and25711).Treatmentoptionsareverylimited,but
anattemptshouldbemadetopreventsecondarydamagebyreducingcerebraledemaandlimitingpathologic
increasesinICP.

FIGURE25710.

Diffuseaxonalinjurywithintraventricularblood.[ImageusedwithpermissionofJackFountain,Jr.,MD,
EmoryUniversityandGradyMemorialHospital.]

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FIGURE25711.

Diffuseaxonalinjurywithlossofthegreymatterwhitematterinterface.[ImageusedwithpermissionofDaniel
Curry,MD,PhD,TexasChildren'sHospitalandBaylorCollegeofMedicine.]

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PENETRATINGINJURY

Asabulletpassesthroughthebrain,itcreatesacavitythreetofourtimeslargerthanitsdiameter.Direct
penetrationofthebulletthroughthebrainsubstanceandthetransferofkineticenergycausethemajorityofthe
destruction(Figure25712).TheGCScanbeusedtopredicttheprognosisfornonintoxicatedpatientswitha
gunshotwoundtothebrain.PatientswithaGCSscoreof>8andreactivepupilshavea25%mortalityrisk,
whereasmortalityapproaches100%inthosewithaGCSscoreof<5.Patientswithapenetratinggunshotwound
tothebrainshouldbeintubatedandtreatedwithprophylacticantibiotics,suchasvancomycin,1gramIV,and
ceftriaxone,2gramsIV.

FIGURE25712.

Gunshotwoundtraversingthroughfrontallobesbilaterallynotebonefragments.[Imageusedwithpermission
ofThomasEgglin,MD,DirectorofEmergencyRadiologyandanAssociateProfessorofDiagnosticImagingat
theWarrenAlpertMedicalSchoolofBrownUniversity,Providence,RI.]

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Stabwoundshaveverylowenergyandimpartonlydirectdamagetotheareacontactedbythepenetrating
object.Patientswithpenetratinginjuryrequireadmission,broadspectrumantibiotics,andoperative
intervention.Leaveimpaledobjectsinplaceuntilcontrolledsurgicalremovalisfacilitated.

MILDTRAUMATICBRAININJURY
mTBI(oftencalledaconcussion)isimpairmentinbrainfunctionwithoutoverthemorrhageorother
grosslesions,iscausedbyanexternalforce,andresultsinaGCSscoreof14or15(alsoseechapter110
andTable2573).1Thediagnosisismadebyahistoryofanyalterationinconsciousnessatthetimeorshortly
aftertheincitingevent(accelerationdecelerationorbluntforce).Alterationinconsciousnessincludesthe
individual'saccountof"gettinghis/herbellrung,""seeingstars,"orbeingdazedorconfusedasaresultofthe
force.Thepresenceofamnesiafurthersupportsthediagnosisandisoftenassociatedwithmoresignificant
injury.

Signsandsymptomssuchasvomiting,headache,lossofconsciousness,focalneurologicdeficit,age>65years,
coagulopathy,and/ordangerousmechanismofinjuryarefactorsthatincreaseriskofseriousinjury(seeTables
2574,2575,and2576).26,27,30,36Thepresenceofalcohol,distractinginjuries,andotherbarrierstoobtaining
aclearhistoryoftheeventconfoundthesignsandsymptomsofmTBI.

PATHOPHYSIOLOGY

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Initsmildestform,mTBIisanionicshiftthatcausesamomentarydisruptioninfunction.Symptomrecoveryis
PhysicalSignsand
CognitiveSymptoms BehavioralChanges
rapid,andtheconcussiveinjuryresultsinnoobviousstructuraldamage.However,mildinsultscanalsocausea
Symptoms
temporaryupregulationofionchannels,especiallyalongaxons.37,38Afterasingleinjury,theionchannel
densityreturnstonormalovertime.Repeatedexposuretoinjury,however,greatlyincreasestherestingnumber
ofchannels.Anincreaseinthedensityofionchannelsleavesthebrainvulnerabletooveractivation,neuronal
toxicity,andcelldeath.

Inadditiontoionchannelupregulation,largeshiftsofbalanceinionconcentrationsmayleadtomitochondrial
dysfunctionanddepletionofintracellularenergystoresinmTBI.14,39,40,41Thisstatecreatesametabolic
"mismatch"duringwhichneuronaldysfunctionpersistsuntilrecoveryoccurs.Thispathwayisarecognized
patternofinjuryinmoderate/severeTBIandisthoughttoalsoplayaroleinmTBI.

Metabolicinsults,electrochemicalimbalances(calciuminfluxandsodiumandpotassiumshifts),and
mitochondrialdysfunctionalsoresultindamagetoaxonaltransportsystems.Structuralabnormalitiesarenot
alwaysidentifiedonMRIorCT.However,histopathologyshowsmicroscopicinjury.Indeed,evidenceof
damageondiffusiontensorimaginghasbeendemonstratedinhighschoolathletesafterasinglefootballseason,
evenwithoutclinicalsignsorsymptomsofaconcussion.42,43Chronictraumaticencephalopathy44is
hypothesizedtooccurasaresultofrepeatedexposuretoTBIinsports.45,46,47

Repetitiveconcussionscanresultinlongtermcognitivedeficitsandstructuraldamagetothebrain.48,49,50,51In
extremecases,whenasecondconcussionoccurspriortorecoveryfromthefirst,rapidonsetofcerebraledema
anddeathcanoccur,particularlyinathletesprematurelyreturningtoplay(secondimpactsyndrome).52

DIAGNOSIS

ThephysicalexaminationfindingsinisolatedmTBIareoftennormal.Currently,therearenoreliabletests
thatcanconfirmthediagnosisofconcussion.TheGCSlacksthedetailtoassessthefullspectrumofsignsand
symptoms.HeadCTscansareusuallynormal,andanormalscanonlyeliminatestheconcernforanunderlying
lesionrequiringsurgery.

PerformathoroughneurologicexaminationandobtaintheGCS.Focalfindingssuggestpotentialintracranial
pathologyorapostictalstate.Assessforsignsofglobalimpairment,suchasconfusion,perseveration,or
amnesia.53Observegaitandtestbalance.ThemostconsistentabnormalitiesinmTBIaresubtle
impairmentsincognitivefunction(seeTable2577).Thegoldstandardwrittenneuropsychological
examinationisimpracticaltoperformintheEDsetting.However,performsomeassessmentofcognition.

Clinicalsymptoms(Table25711)maybeginimmediatelyaftertheinsultormaybedelayedfordaystoweeks.
Therefore,thelackofobvioussignsandsymptomsatthetimeofevaluationdoesnotexcludemTBIifthe
historicalaccountisconsistentwithsuchinjury.Anothercomplicatingfactoristhatmanyofthesignsand
symptomsarenonspecificandoverlapwiththoseofotherconditions.

TABLE25711SignsandSymptomsofmTBI
PhysicalSignsand
CognitiveSymptoms BehavioralChanges
Symptoms
Attentiondifficulties Headaches Irritability
Concentrationproblems Dizziness Depression
Amnesiaandperseveration Insomnia Anxiety
Fatigue Sleepdisturbances
Shorttermandlongtermmemory
problems
Unevengait Emotionallability
Orientationproblems Nausea,vomiting Lossofinitiative

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PhysicalSignsand
CognitiveSymptoms BehavioralChanges
Symptoms
Alteredprocessingspeed Blurredvision Lonelinessandhelplessness
Alteredreactiontime
Problemsrelatedtojob,relationship,home,or
Calculationdifficultiesandproblemswith Seizures schoolmanagement
executivefunction

Note:At3monthsafterinjury,<30%aresymptomaticat1year,15%aresymptomatic.

Thepracticeofgradingconcussionsiswidelyemployedbutisnotevidencebased.Thereare>20different
classificationsystemsinexistence.54

Biomarkers

Serummarkersspecifictoneurologicinjurymayimprovefuturediagnosisandmanagement.36,55,56

Ofthebiomarkerscurrentlyunderstudy,S100B(calciumbindingproteinBantibody)istheonlyonethatis
relativelysensitive(94%to99%sensitive)fordetectingthepresenceofinjury,butonlyunderspecific
conditions.S100Bserumlevelsriseandfallrapidly,sotimefrominjurydeterminestherelevanceofanegative
finding.S100BisalsonotcurrentlyapprovedbytheU.S.FoodandDrugAdministrationformTBI.The
AmericanCollegeofEmergencyPhysiciansprovidesthefollowingguidance:"LevelCrecommendations.In
mTBIpatientswithoutsignificantextracranialinjuriesandaserumS100B<0.1g/Lmeasuredwithin4hours
ofinjury,considerationcanbegiventonotperformingaCT."57

CognitiveScreeningandPsychometrics

CognitivetestingintheEDiscurrentlylimitedtotheuseofbriefmemoryscreenssuchastheMiniCog(see
Figure2882)ortheQuickConfusionScale(seeTable2867).Othertools,primarilydevelopedforsports,
suchastheSportsConcussionAssessmentTool,theStandardizedAssessmentforConcussion,andothersimilar
instruments,havenotbeenvalidatedforEDuse.

Neuropsychologicaltesting58,59,60,61consistsofabatteryofindividualteststhatevaluateanumberofdomains
requiredfornormalbrainfunction,includingmemory,attention,concentration,executivefunction,andreaction
time.Severalofthesetestsareusedbysportsprogramstoassessrecoveryfromconcussion.Theyaremost
valuablewhenbaselinescoresareavailableforcomparison.

TREATMENTANDDISPOSITION

TheprimarytreatmentformTBIisrest.Makesurethepatientavoidsaspirinandnonsteroidalanti
inflammatorydrugsafteracuteinjury.EDtreatmentobjectivesaretoidentifypatientswhohaveintracranial
lesionsrequiringneurosurgicalinterventiontoadmitpatientswhoseconditionmightdeteriorateovertimeand
forthosedischarged,toprovideinstructionsforcognitiveandphysicalrestandprovidefollowupfor
reassessmentbeforereturntonormalactivities.

Whenthepatientissafefordischarge,oneofthemostimportant"interventions"istoprovidethorough
concussiondischargeinstructions.Atemplateisavailableat
http://www.cdc.gov/ncipc/tbi/Physicians_Tool_Kit.htm.Physicalandneurologicrestisneededuntilsymptoms
abatefully.Dischargethepatienttothecareofaresponsibleindividualandprovideinstructionstoboththe
patientandthatindividual.PatientswithmTBImaynotcomprehendorrememberdetaileddischarge
instructions.HavethepatientreturntotheEDforincreasingsymptoms,headaches,alteredmentalstatus,

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nausea,orvomiting.Referpatientsforfurtherevaluationandfollowupcare.Patientsatanincreasedriskfor
SportsRelated NonSportsRelated
reinjury,suchasathletes,shouldundergoaformalgraduatedreturntoactivityprogram(Table25712).

TABLE25712ReturntoActivityProgram
SportsRelated NonSportsRelated
Noactivity(restuntilsymptomfree) Noactivity(restuntilsymptomfree)
Lightaerobicexercise Lightaerobicexercise
Sportspecifictraining(noncontact) Moderateaerobicexercise
Noncontactdrills Returntonormalactivities
Fullcontactdrills
Gameplay

Note:Patientmustremainasymptomaticfor24hoursbetweeneachstep.Developmentofsymptomsatanylevel
requiresreturntotheprevioussymptomfreelevel.

ReturntoActivity

Symptomsreflectunderlyingmetabolicdysfunctionandarecurrentlytheonlyreliableguidetobrain
health.40,54Returntoplayorworkdecisionsarebasedonsymptomsandagraduatedevaluationprogram.

Assessmentsincorporateserialsymptomchecklists,neuropsychologicaltests(memoryandreactiontime
assessment),andabalanceevaluation(seeTable25712).54,62Becausethistypeofassessmentisnot
practicalintheED,EDcliniciansshouldnotprovidedefinitivereturntoactivitydirections.

SPECIALCONSIDERATIONS
POSTCONCUSSIVESYNDROME

Patientsoftenreportaseriesofphysical,emotional,andcognitivesymptomsinthedaysandweeksaftermTBI.
Theestimatedprevalenceofpostconcussivesyndromevarieswidely,withabout20%to40%ofpatients
reportingsymptomsat3monthsandabout15%at1year.63,64Themostcommonlyreportedpostconcussion
symptomsareheadache,dizziness,decreasedconcentration,memoryproblems,sleepdisturbances,irritability,
fatigue,visualdisturbances,judgmentproblems,depression,andanxiety.65Whenaclusterofsymptoms
becomeschronicaftermTBI,theyareoftencalledpersistentpostconcussivesymptomsorpostconcussion
syndrome.Clinicalfindingsatthetimeoftheinjurydonotreliablypredictthedevelopmentofpostconcussive
syndrome.Postconcussivesyndromesymptomscanoverlapthoseofposttraumaticstressdisorder.
Neuropsychologicaltestinganduseofasymptomchecklistarethecornerstonesofdiagnosisandmanagement.
Treatmentissymptomatic.ReferpatientstoaneuropsychologistormTBIclinic.

RECURRENTCONCUSSIONS

Threeormoreconcussionsposeariskforlongtermsequelae,especiallyinadolescentsandyoung
children.48,49,66Almostallcasesofsecondimpactsyndromehaveoccurredinyoungathletes.Chronic
traumaticencephalopathy,44characterizedbyearlyonsetofmemorylossanddepression,isaconcernin
professionalathletes.Pathologicallylargedepositsoftauproteinareseeninthebrainsofdeceasedchronic
traumaticencephalopathypatients.47Tauproteindepositshaverecentlybeendiscoveredeveninyouthfootball
playerswhodiedfromothercauses.

SECONDIMPACTSYNDROME
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Secondimpactsyndromeisararedisorderthatresultsinrapidcerebraledemaandhighmortality(60%to
80%).52Thepathophysiologyandthepredictorsarenotwellunderstood.Itishypothesizedthatoccurrenceofa
secondimpactbeforethebrainhasresetorrecoveredfromafirstmTBIcausesalossofautoregulationandion
imbalance,andleadstorapidcerebraledema.Thisexplanationfitswellwiththeconceptofenhanced
vulnerabilityduetometabolicdisturbances,energydemandmismatch,andionchannelupregulationaftera
concussion.67,68

ANTICOAGULATION

Anticoagulantsandantiplateletagentsincreasetheriskofintracranialhemorrhageafterinjury,especiallyinthe
elderly.

IntracranialhemorrhageinpatientstakingwarfarinandwhohaveanelevatedINRisassociatedwithahigh
mortalityrate(89%).69Ingeneral,patientswithheadtrauma,whoaretakinganticoagulantsorantiplatelet
agents,shouldundergoemergentheadCT.TheORfortheriskofintracraniallesionsaftermildheadinjuryin
patientstakinganyantiplatelettherapyis2.6.70Clopidogrelseemstobeapotentriskfactor.71Theeffectof
lowdoseaspirin(162mgorlesstakendaily)onpostheadinjurybleedinghasnotbeendetermined.

Patientswithintracranialhemorrhageneedimmediateanticoagulantreversal.PatientstakingWarfarinwhohave
anelevatedINRareoptimallytreatedwithplasmaor4factorconcentrate.Seechapters239,"Thromboticsand
Antithrombotics"and166,"SpontaneousSubarachnoidandIntracerebralHemorrhage"forfurtherdiscussion.

AnegativeinitialCTfindinginanasymptomaticTBIpatientreceivinganticoagulationorantiplatelettherapyis
reassuring,butdelayedhemorrhagemayoccurandisnoteasilypredicted.71

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USEFULWEBRESOURCES
AcuteConcussionEvaluation(ACE),EmergencyDepartment(ED)Versionv1.4
http://www.cdc.gov/ncipc/tbi/ACE_ED.pdf
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BrainTraumaFoundationhttp://www.braintrauma.org
HeadsUp:BrainInjuryinYourPracticeAToolKitforPhysicians,CentersforDiseaseControland
Prevention,NationalCenterforInjuryPreventionandControl
http://www.cdc.gov/ncipc/tbi/Physicians_Tool_Kit.htm

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