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Treatmentofaneurysmalsubarachnoidhemorrhage

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Treatmentofaneurysmalsubarachnoidhemorrhage
Authors
RobertJSinger,MD
ChristopherSOgilvy,MD
GuyRordorf,MD

SectionEditor
JoseBiller,MD,FACP,
FAAN,FAHA

DeputyEditor
JanetLWilterdink,MD

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.

Literaturereviewcurrentthrough:Jul2015.|Thistopiclastupdated:Oct10,2013.

INTRODUCTIONAneurysmalsubarachnoidhemorrhage(SAH)isoftenadevastatingevent.Approximately
10percentofpatientswithaneurysmalSAHdiepriortoreachingthehospital,25percentdiewithin24hoursof
SAHonset,andabout45percentdiewithin30daysonlyonethirdofpatientswillhaveagoodoutcomeafter
treatment[13].
ThemostimportantpredictivefactorsforacuteprognosisafterSAHinclude[46]:
Levelofconsciousnessandneurologicgradeonadmission
Patientage(inversecorrelation)
Amountofbloodoninitialheadcomputedtomography(CT)scan(inversecorrelation)
Amongpatientswhoreachthehospitalalive,muchofthesubsequentearlymortalityiscausedbythecommon
complicationsofaneurysmalSAH,whichincluderebleeding,vasospasmanddelayedcerebralischemia,
hydrocephalus,increasedintracranialpressure,seizures,andcardiaccomplications.Therapeuticadvances
haveaddedtothearmamentariumfortreatingthesemalignantprocesses[1].Areductionofcasefatalityrates
from1971to2002inonestudyandfrom1981to1986and2002to2008inanotherstudymayreflectan
improvedapproachtomanagementoverthesetimeperiods.However,withsomeexceptions,highquality
clinicaltrialstosupportthesetreatmentsaregenerallylacking.
ThetreatmentofaneurysmalSAHanditscomplicationsisreviewedhere.Otheraspectsofthisillnessare
discussedseparately.(See"Clinicalmanifestationsanddiagnosisofaneurysmalsubarachnoidhemorrhage"
and"Unrupturedintracranialaneurysms".)
CRITICALCAREMANAGEMENTPatientswithaneurysmalSAHaremostappropriatelycaredforinhigh
volumecenterswithexperiencedstaffthatincludesneurovascularsurgeons,endovascularspecialistsand
neurointensivecareservices[7].Observationaldatasuggestthatsuchcentershaveimprovedoutcomeswith
lowermortality[812].
AcutemedicalcareApatientpresentingwithaneurysmalsubarachnoidhemorrhage(SAH)isadmittedto
anintensivecaresettingforconstanthemodynamicandneurologicmonitoring[13].PatientswithSAHareat
riskforhemodynamicinstabilityandneurologicdeterioration.Inonestudy,neurologicworseningoccurredin35
percentofpatientswithinthefirst24hoursofadmissionandheraldedtheonsetofcomplicationsandpoor
outcomes[14].Pulmonaryedemaandcardiacarrhythmiascomplicate23and35percentofSAHcases
respectively[15].(See"Clinicalmanifestationsanddiagnosisofaneurysmalsubarachnoidhemorrhage",
sectionon'Cardiacabnormalities'.)
IndicationsforendotrachealintubationincludeaGCS8(table1),elevatedICP,pooroxygenationor
hypoventilation,hemodynamicinstabilityandrequirementforheavysedationorparalysis.
Deepvenousthrombosis(DVT)prophylaxiswithpneumaticcompressionstockingsisstartedpriorto
aneurysmtreatment[16].Subcutaneousunfractionatedheparin5000unitsthreetimesdailycanbeaddedfor
DVTprophylaxisoncetheaneurysmistreated.
Intravenousfluidadministrationshouldtargeteuvolemiaandnormalelectrolytebalance.Hyponatremia,in
particular,iscommonsodiumlevelsshouldbecheckedatleastdaily(See'Intravenousfluids'belowand
Close
'Hyponatremia'below.).

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Patientsaregivenstoolsofteners,keptatbedrest,andgivenanalgesia(eg,morphinesulfate)todiminish
hemodynamicfluctuationsandlowertheriskofrebleeding.Prophylactictherapyforgastrointestinalulcersis
typicallyprovided.
PhysiologicderangementsoccurfrequentlyintheacutephaseofSAHandmightworsenthediffusebrain
injury.Acohortstudyof413patientsidentifiedfourvariablesthatwereindependentlyassociatedwith
increasedriskofdeathordisabilitythreemonthsafterSAH[17]:

Hypoxemia(arterioalveolargradient>125mmHg)
Metabolicacidosis(serumbicarbonate<20mmol/L)
Hyperglycemia(serumglucose>180mg/dL[10mmol/L])
Bloodpressureinstability(MAPof<70or>130mmHg)

Otherstudieshavealsonotedthattheseandothermedicalcomplications,renalinsufficiency,fever,and
anemiaarealsocommonafterSAHandareassociatedwithpooroutcomes[15,18,19].Correctionofthese
physiologicderangementsinpatientswithSAHissuggested[16],althoughnostudieshaveconfirmedthe
benefitofsuchtreatments:
HyperglycemiahasbeenassociatedwithapooroutcomeafterSAHinmanystudies[2023].Onestudy
foundthattheuseofanaggressivehyperglycemiamanagementprotocolappearedtoimproveglycemic
controlandneurologicoutcomeshowevertheuseofahistoricalcontrolgrouplimitsthevalidityofthis
study[24].Nobloodglucosetargetshavebeenspecificallyidentifiedforintervention.The2011American
StrokeAssociationguidelinessuggestcarefulglucosemanagementwithstrictavoidanceof
hypoglycemia[7].
FeverofinfectiousandnoninfectiousoriginisacommoncomplicationofSAH,particularlyinthosewitha
higherneurologicgrade,andisassociatedwithapoorprognosis[25,26].Inonenonrandomizedstudy,the
useofexternalcoolingdevicesinpatientswithfeverafterSAHappearedtobeassociatedwithimproved
outcomes[27].
AnemiaiscommonafterSAH,occurringin18percentofpatientsduringtheirhospitalstayinonereport
[28].Moststudiessuggestthatanemiaisassociatedwithworseoutcomes,whilehigherhemoglobin
levelsareassociatedwithfewercerebralinfarctionsandimprovedoutcomes[2932].Agoalhemoglobin
fortransfusionhasnotbeendefinedinpatientswithSAH[7]someexpertsrecommendatargetabove8
to10g/dl[33],however,onerandomizedtrialfoundthatahighertransfusiongoal(11.5g/dlversus10
g/dl)appearedtobesafe[34].
TroponinlevelsandECGshouldbecheckedonadmission[33].Ifpositive,followuplevelsand
echocardiogramtoevaluatepossibleleftventricularfunctionshouldbeconsidered.
HypothalamicpituitarydysfunctioniscommonafterSAH,buttheclinicalimplicationsandappropriate
treatmentisuncertain[35].RoutineadministrationofglucocorticoidsisnotrecommendedafterSAH,but
maybeconsideredinpatientswhoareunresponsivetovasopressortherapyforvasospasm[33]
AntithromboticdiscontinuationAlthoughtherearefewdata,mostexpertsfavorreversalofall
anticoagulationforacuteSAHuntiltheaneurysmisdefinitivelyrepairedbysurgeryorcoiling[3638].
GuidelinesfromtheAmericanHeartAssociation/AmericanStrokeAssociationissuedin2006recommendthat
allanticoagulantsandantiplateletagentsshouldbediscontinuedafterSAH[38].Inaddition,anyanticoagulant
effectshouldbereversedimmediatelywithappropriateagentssuchasvitaminK,freshfrozenplasma,or
unactivatedprothrombincomplexconcentrate,whichisalsocalledfactorIXcomplex.Weusethetherapeutic
approachthatisrecommendedforwarfarinassociatedintracerebralhemorrhage.(See"Reversalof
anticoagulationinwarfarinassociatedintracerebralhemorrhage".)
IntracranialpressurePatientswithSAHoftendevelopincreasedintracranialpressure(ICP)thatisusually
duetoacutehydrocephalusandreactivehyperemiaafterhemorrhage.(See"Clinicalmanifestationsand
diagnosisofaneurysmalsubarachnoidhemorrhage",sectionon'Hydrocephalus'.)
Wegenerallyplaceaventriculostomyinappropriatepatients(eg,thosewithenlargedventriclesonCTor
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WFNS3(table2)),thisallowsdirectmeasurementofintracranialpressureandalsoallowstreatmentby
drainageofCSFwhenappropriate.Whilesomeconcernhasbeenraisedaboutprecipitatingrebleedingwith
abruptloweringofICP,thishasnotbeensubstantiatedinclinicalstudies[39].(See"Intraventricular
hemorrhage",sectionon'Externalventriculardrain'and"Evaluationandmanagementofelevatedintracranial
pressureinadults",sectionon'ICPmonitoring'.)
Patientswithoutaventriculostomycanbemanagedmedicallywithosmotictherapyanddiuresis.
Hyperventilationisgenerallyavoidedbecauseitmayprecipitateorexacerbatevasospasm.Theuseof
hypertonicsalinehasbeenevaluatedinpatientswithelevatedICPrelatedtotraumaticbraininjuryandappears
tolowerICPandmayimprovecerebralperfusion.Asmallobservationalstudyin16patientswithpoorgrade
SAHsuggeststhatitmayalsobeusefulinthissettingbutfurtherstudyisrequired[40].(See"Evaluationand
managementofelevatedintracranialpressureinadults",sectionon'Osmotictherapyanddiuresis'.)
Insomecases,decompressivecraniectomymaybeneededforICPcontrol,inthesettingofintracerebral
hemorrhageand/orseverecerebraledema.(See"Evaluationandmanagementofelevatedintracranialpressure
inadults",sectionon'Decompressivecraniectomy'.)
BloodpressurecontrolTheoptimaltherapyofhypertensioninSAHisnotclear.Nobloodpressuretarget
hasbeendefinedinacuteaneurysmalSAHwithanunsecuredaneurysm.The2012AmericanStroke
Associationguidelinessuggestthatadecreaseinsystolicbloodpressureto<160mmHgisreasonable[7].
Whenbloodpressurecontrolisnecessary,theuseofvasodilatorssuchasnitroprussideornitroglycerinshould
beavoidedbecauseoftheirpropensitytoincreasecerebralbloodvolumeandthereforeintracranialpressure.
Labetalol,nicardipine,enalaprilarepreferred.
Whileloweringbloodpressuremaydecreasetheriskofrebleedinginapatientwithanunsecuredaneurysm,
thisbenefitmaybeoffsetbyanincreasedriskofinfarction.Cerebralperfusionpressure(CPP)equalsthe
meanarterialpressure(MAP)minustheICP.Thus,withincreasedICP,cerebralperfusionmaybeimpaired,
andincreasesinMAPmaybetheonlymeanstomaintainCPPatalevelnecessarytopreventinfarction.One
studysresultssuggestthatthisCPPthresholdmaybe70mmHg[41].Inonereportof134patientswithSAH,
80receivedantihypertensivetherapytolowerthediastolicpressurebelow100mmHg[42].Thepatientsgiven
antihypertensivetherapyhadalowerincidenceofrebleeding(15versus33percent)thatwasoffsetbyahigher
incidenceofinfarction(43versus22percent).
IntheabsenceofICPmeasurement,antihypertensivetherapyisoftenwithheldunlessthereisasevere
elevationinbloodpressure[43].Thepatientscognitivestatusmaybeausefulguideifthepatientisalert,
thenCPPisadequate,andloweringthebloodpressuremaydecreasetheriskofrerupturewetypicallykeep
thesystolicbloodpressureinsuchpatientsbelow140mmHg.Incontrast,antihypertensivetherapyis
generallywithheldinthosewithaseverelyimpairedlevelofconsciousnesssincetheimpairmentmaybedue
toareducedCPP.
AntiepilepticdrugtherapyTheuseofantiepilepticdrugs(AEDs)topreventseizuresinpatientswithSAH
hasbeenawidelydebatedtopic[7,44,45].Manyexpertsbelievethatseizureprophylaxisinthesettingofan
unsecuredaneurysmisreasonable,giventherelativelylowriskassociatedwithAEDadministrationversusthe
potentialdeleteriouseffectsofseizuresonanalreadydysautoregulatedbrain[4,46].However,evidencefroma
largecaseseriessuggeststhatAEDexposuretophenytoinmaybeassociatedwithworseneurologicand
cognitiveoutcomeafterSAH[47].Therefore,theuseofAEDsforseizureprophylaxisafterSAHshould
probablybeminimizedwheneverpossibleandphenytoinisgenerallyavoided.
Thedecisiontotreatwithantiepilepticagentsmaybebasedinpartuponthedistributionofbloodonaxial
imagingstudies.AlowerimpetustostartAEDsiswarrantedinthesettingofperimesencephalicbloodwithout
corticallayering,sincethispatternofhemorrhageisassociatedwithaparticularlygoodprognosis.Incontrast,
initiationofAEDsinhigherriskpatientswithpoorneurologicgrade,unsecuredaneurysmandassociated
intracerebralhemorrhagemaybereasonable[7].(See"Clinicalmanifestationsanddiagnosisofaneurysmal
subarachnoidhemorrhage",sectionon'Seizures'.)
ContinuationofAEDtherapymaynotbenecessaryinmostpatientsafterundergoinganeurysmalclipping
followingaSAH,especiallythosewithoutacuteseizureswhopresentwithagoodgrade(see'Seizures'
below).
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AntifibrinolytictherapyAntifibrinolyticagents(eg,tranexamicacid,epsilonaminocaproicacid)havebeen
investigatedinthepreventionofrebleedingafteraneurysmalSAH.Whiletheseagentsdonothavean
establishedroleinthemanagementofaneurysmalSAH,the2012AmericanStrokeAssociationguidelines
statethatwhendefinitivetreatmentoftheaneurysmisunavoidablydelayedandtherearenoother
contraindicationstotreatment,shorttermtherapy(<72hours)withtranexamicacidoraminocaproicacidis
reasonable[7].
Ametaanalysisofninetrialsconcludedthatalthoughantifibrinolytictreatmentreducestheriskofrebleeding
(oddsratio[OR]0.55,95%CI0.420.71),itdoesnotshowanyevidenceofreducingpooroutcomedefinedas
death,vegetativestate,orseveredisability(OR1.12,95%CI0.881.43)[48,49].Inearliertrialsthislackof
overallbenefitappearedtobeduetoanincreasedriskofcerebralischemiainpatientstreatedwith
antifibrinolyticagentswhichoffsetthereductioninrebleeding.
Inonesubsequentlypublishedrandomizedclinicaltrialinvolving505patients,tranexamicacidwas
administeredimmediatelyafterSAHdiagnosisanddiscontinuedwhentheaneurysmwasoccluded(allwithin
72hours,70percentwithin24hours)[50].Rebleedingwaslowerinthetreatedgroup(2.4versus10.8percent).
However,therewasnosignificantimpactonclinicaloutcomes(mortality,GlasgowOutcomeScore)atsix
months.
Thereareongoingstudiesinvestigatingapotentialroleforotherhemostaticagents(eg,thethrombininhibitor
argatroban)inaneurysmalSAH[51].
ANEURYSMTREATMENTAfteraneurysmalSAH,thepatientisatsubstantialriskofrebleeding:3to4
percentinthefirst24hoursand1to2percenteachdayinthefirstmonth[2].Reruptureisassociatedwitha
mortalitythatisestimatedtobe70percent.Aneurysmrepairistheonlyeffectivetreatmenttopreventthis
occurrenceandshouldbeperformedwithin24to72hourswhenpossible[7].Patientsinwhomaneurysm
treatmentisnotpossibleormustbedelayedmaybecandidatesforantifibrinolytictherapy.(See'Antifibrinolytic
therapy'above.)
ThemostcommonlyusedtreatmentoptionsforaneurysmrepairafterSAHaresurgicalclippingand
endovascularcoiling.Aneurysmtreatmentisdiscussedinmoredetailseparately.(See"Treatmentofcerebral
aneurysms".)
PREVENTIONOFVASOSPASMANDDELAYEDCEREBRALISCHEMIASymptomaticvasospasm
andcerebralinfarctionareanimportantcontributorstounfavorableoutcomesafterSAH[5,52,53].Clinically
significantvasospasmoccursinapproximately20to30percentofpatientswithaneurysmalSAH,anditis
thoughttoberelatedtospasmogenicsubstancesgeneratedduringthelysisofsubarachnoidbloodclots[52].It
typicallybeginsnoearlierthandaythreeafterhemorrhage,reachingapeakatdaysseventoeight.(See
"Clinicalmanifestationsanddiagnosisofaneurysmalsubarachnoidhemorrhage",sectionon'Vasospasmand
delayedcerebralischemia'.)
Preventionofvasospasmisimportant,becausetreatmentcanbedifficult.(see'Symptomaticvasospasm'
below).
Inordertomitigatethiscomplication,allpatientsshouldreceivenimodipine,andeuvolemiashouldbe
maintained.
MonitoringSymptomaticvasospasmanddelayedcerebralischemiaaremanifestedclinicallybyadecline
inneurologicstatusincludingtheonsetoffocalneurologicabnormalities.(See"Clinicalmanifestationsand
diagnosisofaneurysmalsubarachnoidhemorrhage",sectionon'Vasospasmanddelayedcerebralischemia'.)
TranscranialDoppler(TCD)sonographyisusefulfordetectingandmonitoringvasospasminSAH[7,5456].
VelocitychangesdetectedbyTCDtypicallyprecedetheclinicalsequelaeofvasospasm.Dailyrecordingsoffer
awindowofopportunitytotreatpatientspriortoclinicaldecline.However,itisanoperatordependent
technologythathasimperfectsensitivityandspecificity.Ingeneral,digitalsubtractionangiographyisrequired
todiagnosevasospasmandinstitutetreatment.(See'Symptomaticvasospasm'below.)
AccumulatingdatasuggestthatarterialnarrowingonCTangiographyandbrainperfusionasymmetry
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demonstratedonCTperfusion(CTP)scanningintheacutestageofSAHmaybeusefulandhighlysensitive
methodsforpredictingdelayedcerebralischemia[5760].Theuseofthistechniqueasamonitoringtoolmay
belimitedbyrisksofrecurrentdyeloadsandradiationexposure[7].Afindingofperfusiondiffusionmismatch
onMRImaybeanothermethodofdetectingbrainareasatriskofinfarctioninthissetting[61].Theclinical
utilityofeitherofthesemethodsremainstobeestablished.
NimodipineNimodipine60mgeveryfourhoursisadministeredtoallpatientswithaneurysmalSAH,
ideallywithinfourdaysofSAH.Thetypicaldoseis60mgeveryfourhoursbymouthornasogastrictube.
Nimodipinemustbegivenorallyorbynasogastrictubeinadvertentintravenousadministrationhasbeen
associatedwithseriousadverseevents,includingdeath.Treatmentiscontinuedfor21days.
ThecalciumchannelblockernimodipinewasinitiallystudiedinpatientswithSAHasameanstoprevent
vasospasm.However,despitethevasodilatoryeffectsofnimodipineoncerebralvessels,thereisno
convincingevidencethatnimodipineaffectstheincidenceofeitherangiographicorsymptomaticvasospasm
[6267].Nevertheless,nimodipinehasbeendemonstratedtoimproveoutcomesinSAHandisthestandardof
careinthesepatients[6265,6870].
MetaanalysesofrandomizedtrialsofprophylacticnimodipineadministeredforSAHhaveconsistentlynoteda
benefit[66,67,71]:
NimodipinetreatmentcomparedwithplaceboimprovedtheoddsofagoodoutcomeafterSAHby1.86
(99%CI1.073.25)[66].
Nimodipinereducedtheoddsofdeficit,mortality,orbothattributedtovasospasmby0.46,anditreduced
theinfarctionrateonCTby0.58(99%CI0.380.90)[66].
Overallmortalitywasslightlyreducedinthenimodipinegroup,butthetrendwasnotstatistically
significant[66,67,71].
ThetreatmenteffectofnimodipineinindividualtrialswaspositivelycorrelatedwiththeseverityofSAH
[66].
Thenumberneededtotreat(NNT)withnimodipinetopreventonepooroutcomewas13(95%CI830)
[67].
Bloodpressurefluctuationsarecommonafteradministrationofnimodipine.Thus,bloodpressuremonitoringis
essentialtoavoidhypotensionanddecreasedcerebralperfusionpressure.Nimodipinecanalsotemporarily
reducebraintissuepO2inpatientswithpoorgradeSAH[72],althoughtheclinicalimportanceofthisproperty
isunknown.
ThemechanismofbenefitofnimodipineinSAHisunknown.Putativemechanismsincludeneuroprotectionvia
reductionofcalciumdependentexcitotoxicity,diminishedplateletaggregation,dilationofsmallarteriesnot
visibleonangiograms,inhibitionofischemiatriggeredbyredbloodcellproducts,orsomecombinationofthese
actions.
IntravenousfluidsHypovolemiaisariskfactorforischemiccomplicationsandshouldbeavoided[73,74].
Euvolemiaisthegoalofintravenousfluidmaintenance,usuallywithnormalsaline,whichshouldbemonitored
bydocumentationoffluidinputandoutput.Routineplacementofcentralvenouscathetersformonitoring
volumestatusisnotnecessaryinmostpatients[33].
HemodynamicaugmentationHemodynamicaugmentationdoesnotappearusefulforthepreventionof
vasospasm,butmaybeappropriateinthetreatmentofsymptomaticvasospasm.(See'Symptomatic
vasospasm'below.)
Followinganeurysmalocclusion,hyperdynamictherapy,includingmodesthemodilution,inducedhypertension
(withpressoragentssuchasphenylephrineordopamine),andhypervolemia(socalled"tripleH"therapy),has
beenusedtotrytopreventvasospasm[75,76].SystematicreviewsoftripleHtherapyforprophylaxisof
vasospasmhavefoundthattherehavebeenfewwelldesignedprospectivestudieswhicharesmallanddonot
providestrongevidenceofbenefitofthistherapeuticapproach[77,78].Apreliminarystudysuggestedthatuse
ofsophisticatedhemodynamicmonitoringofcardiacoutputmayimprovetheefficacyofthisapproach[79].
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StatinsGuidelinesfromtheAmericanStrokeSocietyandotherexpertopinionstatethatdespitelackof
conclusiveevidenceofbenefit,itisreasonabletoadministerstatintherapytopatientsafterSAHtoprevent
vasospasm[7,33,80].Themechanismbywhichstatinsmightreducedvasospasmisuncertainitisbelieved
thattheseagentshavethepotentialtoimprovecerebralvasomotorreactivitybyupregulatingendothelialnitric
oxidesynthase,increasecerebralbloodflow,andattenuatevasculopathy[8184].
Itremainsuncertainthatstatintherapyreducestheincidenceofvasospasm,delayedcerebralischemia,poor
neurologicoutcome,ormortality.Whilefindingsfromatleastthreesmallrandomizedplacebocontrolledtrials
suggestedthatstatintreatmentisbeneficialforpreventingvasospasmandimprovingoutcomeafterSAH[85
87],subsequentlyperformedstudiesandmetaanalysesusingdifferentmethodologiesandinclusioncriteria
havehadmixedresults[8890].Largerplacebocontrolledtrialsarestillneededtoconfirmthatstatintreatment
iseffectivetherapyforSAH.
Nevertheless,giventheavailabledatasuggestingbenefitandtherelativesafetyofstatins,wesuggest
initiatingstatintreatment(pravastatin40mgdailyorsimvastatin80mgdaily)within48hoursofaneurysmal
SAHandcontinuinguntildischargefromintensivecare.Inaddition,wesuggestcontinuingstatintherapyafter
SAHforpatientswhoweretakingstatinspriortoSAH.
OtherinvestigationalapproachesAnumberofagentsareunderinvestigationforthepreventionof
vasospasmafterSAH,includingendothelinreceptorantagonists,magnesiumsulfate,andnicardipine
prolongedreleaseimplants.
Endothelin(ET)receptorantagonistsEndothelin1(ET1)isa21aminoacidpeptidethatactsasa
directandpotentvasoconstrictor[91,92].TheactionofET1ismediatedmainlythroughtwomajor
endothelinreceptors,ETAandETB.ETAreceptorsarelocatedonvascularsmoothmusclecellswhere
theymediatebothvasoconstrictionandsmoothmusclecellproliferation.Incomparison,ETBreceptors
arefoundprimarilyonvascularendothelialcellsandmediatevasodilationviathereleaseofendothelium
derivednitricoxide.ETBreceptorsarealsolocatedonvascularsmoothmusclecellswheretheymediate
vasoconstriction.
TheinvestigationaldrugclazosentanisaspecificETreceptorantagonistthathasamuchhigheraffinity
fortheETAthantheETBreceptors[93,94].ClazosentanthereforepotentlyinhibitstheETAreceptor
mediatedvasoconstrictioneffectofET1andminimallyinhibitstheETBreceptormediatedvasodilation.
TheCONSCIOUS2trialincluded1147patientsandfoundnodifferenceinmortalityorfunctional
outcomesbetweenpatientsrandomizedtoclazosentanversusplacebo[95].Theseresultspromptedthe
CONSCIOUS3studytobestoppedprematurelysimilarly,clazosentantreatmentwasnotassociated
withimprovedoutcomesinthisstudy[96].Potentialbenefitsofclazosentanappeartobeoffsetinpartby
anincreaseinadverseeffectsofclazosentan:pulmonarycomplications,hypotension,andanemia[97
99].
MagnesiumWhilemagnesiumsulfatetherapyhasbeenproposedasameanstopreventvasospasm,
thelargestrandomizedtrialof1204patientswithSAHfoundthattreatmentwithintravenousmagnesium
sulfatewasnotassociatedwithimprovedclinicaloutcomes[100].Similarly,ametaanalysispublishedin
2013thatincluded13trials,concludedthatwhileprophylacticintravenousmagnesiumwasassociated
withareductionindelayedcerebralischemia,clinicalneurologicoutcomeswerenotimprovedwith
treatment[101].
IntrathecalthrombolysisVasospasmisbelievedtobeproducedbyspasmogenicsubstances
generatedduringthelysisofsubarachnoidbloodclots,whichcauseendothelialdamageandsmooth
musclecontraction[92].Theobservationthatthevolumeofbloodproximatetothemajorcerebralblood
vesselsappearstocorrelatewiththeincidenceofvasospasm,delayedcerebralischemiaandoutcomes
afterSAHprovidetherationaleforusingintrathecalthrombolysistoacceleratesubarachnoidblood
clearance.Intrathecalthrombolysismaybeperformedintraoperativelyatthetimeofsurgicalaneurysm
clippingorbydirectinfusionbymicrocatheterintothecisternamagnaorlumbarcistern.
Ametaanalysisoffiverandomizedtrialsthatincluded465patientsconcludedthatintrathecal
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thrombolysiswasassociatedwiththereductionintheincidenceofpooroutcomes,aswellas
angiographicvasospasmandchronichydrocephalus,withoutanincreaseinhemorrhagicorinfectious
complications[102].However,nonstandardizedtechniquesusedacrossstudiesandmethodological
flawsintheirperformancecontributetoasubstantialriskofbiasandlimittheabilitytodrawfirm
conclusionsabouttheefficacyofthisapproach.Adefinitivetrialisrequired.
LumbardrainAtreatmentapproachthatincludedinsertionofalumbardraintoreducethebloodloadin
thespinalfluidwasevaluatedinarandomizedstudyof210patients[103].Treatedpatientshada
reducedprevalenceofischemicneurologicdeficitsandimprovedoutcomesatday10butnotat6
months.
NicardipineNicardipineprolongedreleaseimplants(NPRIs)arepolymersthatareloadedwith
nicardipineandimplantedintothebasalcisterns,incontactwiththelargearteriesofthecircleofWillis,
thuspermittinglocaldeliveryofconstanthighdosesofnicardipinetotheintracranialvessels.Ina
preliminaryrandomizedcontrolledtrial,implantationofNPRIswasassociatedwithasignificantreduction
inangiographicvasospasm,andimprovedclinicaloutcome[104].
PhosphodiesteraseinhibitorsPhosphodiesteraseinhibitorsarebelievedtohavepotentialvasodilatory
effectsandmayattenuatecerebralvasospasm.Inarandomizedtrialof109patientswithSAH,cilostazol
administrationwasassociatedwithareducedincidenceofsymptomaticandangiographicvasospasm
clinicaloutcomesweresimilarbetweenthetwogroups[105].Adefinitiveclinicaltrialisneeded.
AngioplastyWhileballoonangioplastyofthebasalcerebralbloodvesselsappearstobeaneffective
treatmentfortreatmentofcerebralvasospasm,ithasnotasyetbeenfoundtobeausefulprophylactic
approach.AphaseIIrandomizedtrialof85patientsfoundthatprophylacticangioplastywasnot
associatedwithsignificantreductionsintheincidenceofdelayedischemiaorvasospasm,norwith
improvedoutcomes[106].
AntiplatelettherapyhasbeenstudiedasatherapytoreducedelayedcerebralischemiainSAH.Ameta
analysisofsevenrandomizedtrialsfoundthatantiplatelettherapywasassociatedwithanonsignificanttrend
towardimprovedoutcomesasmallnonsignificantreductioninbrainischemiawasbalancedbya
nonsignificantincreaseinhemorrhagiccomplications[107].
MANAGEMENTOFCOMPLICATIONSMedicalandneurologiccomplicationsarecommonafterSAHand
contributesubstantiallytotheoverallprognosis.(See'Acutemedicalcare'aboveand"Clinicalmanifestations
anddiagnosisofaneurysmalsubarachnoidhemorrhage",sectionon'Cardiacabnormalities'.)
Patientsarecarefullymonitoredforchangesintheirclinicalcondition.Achangeinneurologicstatus(seizure,
newfocalneurologicdeficit,reducedlevelofconsciousness)istypicallyfurtherevaluatedwithCTscan(which
canidentifyrebleeding,cerebralinfarction,hydrocephalus),angiography(toidentifysymptomaticvasospasm),
and/orEEG(todetectsubclinicalseizures).Medicalcomplicationscanalsocontributetoachangein
neurologicstatus.
SymptomaticvasospasmAnimportantdistinctionmustbemadebetweenangiographicvasospasm,which
isseenin30to70percentofangiogramsperformedatdaysevenafterSAH,andclinicalorsymptomatic
vasospasm,whichisseenin20to30percentofpatients[52,108,109].Symptomaticvasospasmisassociated
withaclinicaldeclineandportendsapoorerprognosis.Symptomaticvasospasmmaynotbeidentifiableon
cerebralangiographyasmicroperforatorspasmdefiestheresolutionofevenstateoftheartangiography.
Isolatedangiographicvasospasmtraditionallyhasnotbeentreated.However,angiographyisusedtoidentify
patientswithsymptomaticvasospasmwhomightbenefitfromtreatment.Inoneseriesinwhichangiograms
wereperformedsystematicallyin381patients92daysafteraneurysmalSAH,thepresenceandseverityof
vasospasmcorrelatedwiththepresenceofcerebralinfarctiononCT[110].
Aggressivetherapyofvasospasmcanonlybepursuedaftertheaneurysmhasbeentreatedwithsurgeryor
intraluminaltherapy.Followinganeurysmalocclusion,treatmentoptionsinclude:
Hemodynamicaugmentationhasnotbeenevaluatedinrandomizedclinicaltrialshowever,incase
seriesofpatientswithsymptomaticvasospasm,thisapproachhasbeenassociatedwithimproved
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cerebralbloodflowandreversalofischemiainmorethanhalfofpatients[111113].
Traditionallythisapproach,socalled"tripleH"therapy,includedmodesthemodilution,induced
hypertensionandhypervolemiainstitutedinanefforttoraisethemeanarterialpressureandthereby
increasecerebralperfusion.Morerecently,thefocushasshiftedtowardmaintenanceofeuvolemiausing
crystalloidorcolloidsolution,andinducedhypertensionwithvasopressoragentssuchasphenylephrine,
norepinephrine,ordopamine[2,7,33].Bloodpressureaugmentationshouldprogressinastepwisefashion
withassessmentofclinicalstatusateachmeanarterialpressurelevel[33].
Theadditionofinotropicsupportwithagentssuchasdobutamineormilrinonehavsbeenreportedtobe
helpfulinpatientswhodonotappeartorespondtopressorsalone[33].
Patientstreatedwithhemodynamicaugmentationneedtobemonitoredforcomplicationssuchaspleural
orcerebraledemaandvolumeoverload.
Thisapproachdoesnotappeartobehelpfulasaprophylaxisagainstvasospasm.(See'Preventionof
vasospasmanddelayedcerebralischemia'above.)
Balloonangioplastyhasbecomethemainstayoftreatmentatmanycentersforsymptomaticfocal
vasospasmofthelargercerebralarterieswhichisrefractorytohemodynamicaugmentation,again
despiteanabsenceofclinicaltrialdata[114,115].
Intraarterialadministrationofvasodilatorsaregenerallyusedfordiffusevasospasminvolvingsmaller
arterialbranches.Agentsreportedaseffectiveforimprovingvasospasmincaseseriesinclude
intraarterialnicardipine[116],milrinone[117],papaverine[118120],nimodipine[121],verapamil[122],and
intrathecalnitroprusside[123].
Intraarterialvasodilatortherapyandangioplastyalsomaybeusedincombination[119,122].
HydrocephalusHydrocephalusisacommoncomplicationofSAHandmayoccurasearlyasthefirst
hourstodaysafterSAHorcanbealatecomplication.HydrocephalusisidentifiedbyCTscanperformedina
patientwithdeterioratingneurologicconditionafterSAH.(See"Clinicalmanifestationsanddiagnosisof
aneurysmalsubarachnoidhemorrhage",sectionon'Hydrocephalus'.)
VentriculardrainplacementcanimprovetheclinicalgradeofpatientspresentingwithSAH[2].Drainageshould
beconsideredforpatientswhohaveadeterioratinglevelofconsciousness,evidenceofincreasedintracranial
pressureandforthoseinwhomnoimprovementinhydrocephalusoccurswithin24hours[124].(See
'Intracranialpressure'above.)
ExternaldrainageofCSFisoftencomplicatedbyventriculitis,particularlywhendrainageiscontinuedformore
thanthreedays[125].Althoughearlierreportssuggestedthatthefrequencyofrebleedingwasincreasedwith
externalventriculardrainageforacutehydrocephalusafteraneurysmalSAH[125,126],thesestudieshad
methodologiclimitations[127],andlaterreportshavefoundnoassociationofexternaldrainagewiththeriskof
rebleeding[39].Lumbardrainageisanalternativebuthasbeenlesswellstudied.
Althoughdataarescant,surgicalandendovasculartreatmentsappeartobeassociatedwithcomparablerisks
ofdevelopingshuntdependenthydrocephalus[128,129].
Approximatelyonehalftotwothirdsofpatientswithacutehydrocephalusdevelopchronicshuntdependent
hydrocephalus.TheneedforlongtermCSFdiversionisassessedinthesubacuteperiodbyattemptsat
weaningventriculardrainage.(See"Evaluationandmanagementofelevatedintracranialpressureinadults".)
HyponatremiaHyponatremiafollowingSAHmaybeduetoinappropriatesecretionofantidiuretichormone
(SIADH)orrarely,tocerebralsaltwastingthesearephysiologicallydistinctandaretreateddifferently.(See
"Clinicalmanifestationsanddiagnosisofaneurysmalsubarachnoidhemorrhage",sectionon'Hyponatremia'.)
PatientswithSIADHareeuvolemic.WhiletherapyofasymptomatichyponatremiainSIADHusually
consistsofwaterrestriction,fluidrestrictionisnotdesirableinpatientswithSAHasitincreasestherisk
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ofvasospasmrelatedischemicinjury.Thus,hyponatremiaistreatedwithisotonicsaline,or,ifnecessary,
hypertonicsaline[130].(See"Treatmentofhyponatremia:Syndromeofinappropriateantidiuretichormone
secretion(SIADH)andresetosmostat".)
CerebralsaltwastingislesscommonthanSIADHinthissettingandischaracterizedbyvolume
depletion,whichleadstothereleaseofADH.Itisusuallytreatedwithinfusionsofisotonicsaline.
RestorationofeuvolemiawillsuppressthereleaseofADH.(See"Cerebralsaltwasting".)
Aprotocolformanaginghyponatremiausing3percentNaClsolutionsinpatientswithSAHispresentedinthe
Table(table3).
SeizuresPatientswithacuteseizuresafterSAHaretreatedwithAEDstopreventrecurrence.Agentssuch
asphenytoin,levetiracetam,carbamazepine,andphenobarbitalaretypicallyused.(See"Initialtreatmentof
epilepsyinadults".)
GeneralizedconvulsivestatusepilepticusisunusualafterSAH,occurringin0.2percentofpatientsinone
study[131].However,withincreaseduseofcontinuousEEGmonitoring,nonconvulsivestatusepilepticusand
subclinicalseizureshavebeenrecognizedasapotentialcontributortoprolongedimpairmentofconsciousness
inpatientsafterSAH.Inoneseries,subclinicalseizuresweredocumentedbycontinuousrecordingin7
percentofpatientsafterSAH[132,133].DiagnosisofNCSEandsubclinicalseizuresrequiresahighindexof
suspicion,aspatientsmostatriskofNCSEarealsothosewithpoorneurologicgradeandotherneurologic
complicationsofSAH,makingitdifficulttodetectsubclinicalseizures.Thediagnosisandmanagementof
NCSEisdiscussedseparately.(See"Nonconvulsivestatusepilepticus".)
AEDsareusuallycontinuedforapproximatelysixmonthsinpatientswhohaveexperiencedanacuteseizure
followingSAH,althoughtherearenostrictguidelines.Whileacuteseizuresareariskfactorfordeveloping
epilepsy,mostpatientsdonotrequirelongtermAEDs.(See'Neurologicmorbidity'below.)
PROGNOSISOutcomeaftertreatmentofaneurysmalsubarachnoidhemorrhage(SAH)isaffectedby
potentialbraininjuryfromtheSAHandsubsequentcomplications,aswellasbyrisksrelatedtoneurosurgery
(see"Treatmentofcerebralaneurysms").
Riskfactorsforallnegativeoutcomesincludeadvancedage,theclinicalorradiologicseverityoftheSAHon
presentation,andtheoccurrenceandseverityofcomplications.
MortalitySubarachnoidhemorrhage(SAH)isassociatedwithahighmortalityrate[134].Asystematic
reviewfoundthattheaveragecasefatalityrateforSAHwas51percent[135].Approximately10percentof
patientswithaneurysmalSAHdiepriortoreachingthehospital,25percentdiewithin24hoursofSAHonset,
andabout45percentdiewithin30days[3].
SurvivorsofaneurysmalSAHhaveanincreasedmortalityratecomparedtothegeneralpopulation(SMR1.6)
[136140].IntheISAT,theriskofdeathatfiveyearswaslowerintheendovasculartherapygroupthaninthe
surgicalgroup[136].Inonecohortstudy,theexcessmortalityriskappearedtobeattributedtocerebrovascular
events[139].Theriskofnonfatalvascularevents(stroke,myocardialinfarction)isalsoincreased(RR1.5)in
survivorsofaneurysmalSAH[138].
NeurologicmorbidityLongtermcomplicationsofSAHincludeneurocognitivedysfunction,epilepsy,and
otherfocalneurologicdeficits.
SeveralstudiessuggestthatSAHsurvivorshavehighratesofmemoryandneurocognitiveimpairment
[1,7,141146].Thelargestprospectiveevaluationofneuropsychologicalfunctionevaluated873survivorsof
SAH[144].Atthreemonthsafteraneurysmalclipping,globalimpairmentwaspresentinapproximately20
percentofallpatientsandin16percentofthosewiththebestpreoperativecondition.Detailed
neuropsychologicaltestingofpatientsfollowingsurgicallytreatedSAHhascommonlyshowncognitivedeficits,
evenamongpatientsmakinganotherwisegoodneurologicrecovery[147].Theimportanceofthese
neuropsychologicaldeficitstolongtermmorbidityiscontroversial,buttheyareoftenpermanent[53,148].
ThelocationoftheaneurysmresponsibleforSAHdoesnotappeartoinfluencecognitiveoutcome[1],butthe
occurrenceofvasospasm,delayedcerebralinfarction,andothercomplicationsdoes[53,149].IntheISAT,the
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proportionofsurvivorswhoreachedindependentstatusweresimilarinthosetreatedwithendovasculartherapy
versussurgicalclipping[136],however,amongthegroupthatwasnototherwisedisabled(mRS>2)the
proportionofthosewithcognitiveimpairmentat12monthswashigherinthosetreatedsurgicallythanwith
endovascularcoiling[141].
Depression,anxiety,andsleepdisturbancesarealsocommonandcontributetodecreasedqualityoflifethese
maybemoreamenabletotreatment[143,145,150].
TheincidenceoflateepilepsyafterSAHisunclear.Inaretrospectivereportof472patientswithaneurysmal
SAHwhohadundergonesurgicalclippingoftheaneurysmbetween1994and2000andwerefollowedforat
least12months,lateepilepsyoccurredinonly23(4.9percent)[151].Patientspresentingwithapoorgrade
hadahigherincidenceofepilepsy(9.6and12.5percentofthosegrades3and4,respectively),asdidthose
withassociatedcerebralinfarctionorsubduralhematoma.IntheISATtrial,25of612patients(4percent)hada
diagnosisofepilepsyata12monthassessmenttheratewaslowerinpatientstreatedwithendovascular
coiling,ascomparedtosurgicalclipping[141].PatientswhohavehadacuteseizuresafterSAHaresomewhat
morelikelytodevelopepilepsythanthosewhodonot.Themanagementofepilepsyisdiscussedseparately.
(See"Initialtreatmentofepilepsyinadults"and"Overviewofthemanagementofepilepsyinadults".)
AnosmiamaycomplicateSAH.Studiessuggestthatthisisamorefrequentcomplicationinpatientswho
undergogoaneurysmclipping(oneinthreepatients)thaninthosewhoundergoendovascularcoiling(oneinsix
patients),andthatrecoveryismorelikelyinendovascularlytreatedpatientsaswell[152,153].Intraventricular
hemorrhageisariskfactorforthiscomplication.Anosmiaisalessfrequentcomplicationofnonaneurysmal
perimesencephalichemorrhage[154].
AneurysmrecurrenceandlaterebleedingPatientswhosurviveaneurysmalSAHhaveasmallbut
enduringriskofrecurrentSAHwhichcanoccurdespitesuccessfulendovascularorsurgicaltreatmentofthe
rupturedaneurysm.RecurrentSAHmayresultfromrecurrenceofthetreatedaneurysm,ruptureofanotherpre
existinganeurysminapatientwithmultipleaneurysms,anddenovoaneurysmformation.Theriskofthese
eventsandrecommendationsformonitoringandtreatmentarediscussedseparately.(See"Laterecurrenceof
subarachnoidhemorrhageandintracranialaneurysms".)
ScreeningoffamilymembersFirstdegreerelativesofpatientswithSAHhaveatwotofivefold
increasedriskofSAHcomparedwiththegeneralpopulation[155,156].Itmaybereasonabletoscreensome
familymembersforthepresenceofcerebralaneurysm.Thisissueisdiscussedindetailseparately.(See
"Screeningforintracranialaneurysm".)
INFORMATIONFORPATIENTSUpToDateofferstwotypesofpatienteducationmaterials,TheBasics
andBeyondtheBasics.TheBasicspatienteducationpiecesarewritteninplainlanguage,atthe5thto6th
gradereadinglevel,andtheyanswerthefourorfivekeyquestionsapatientmighthaveaboutagiven
condition.Thesearticlesarebestforpatientswhowantageneraloverviewandwhoprefershort,easytoread
materials.BeyondtheBasicspatienteducationpiecesarelonger,moresophisticated,andmoredetailed.
Thesearticlesarewrittenatthe10thto12thgradereadinglevelandarebestforpatientswhowantindepth
informationandarecomfortablewithsomemedicaljargon.
Herearethepatienteducationarticlesthatarerelevanttothistopic.Weencourageyoutoprintoremailthese
topicstoyourpatients.(Youcanalsolocatepatienteducationarticlesonavarietyofsubjectsbysearchingon
patientinfoandthekeyword(s)ofinterest.)
Basicstopics(see"Patientinformation:Hemorrhagicstroke(TheBasics)"and"Patientinformation:
Subarachnoidhemorrhage(TheBasics)")
BeyondtheBasicstopics(see"Patientinformation:Strokesymptomsanddiagnosis(Beyondthe
Basics)"and"Patientinformation:Hemorrhagicstroketreatment(BeyondtheBasics)")
SUMMARYANDRECOMMENDATIONS
AneurysmalSAHisassociatedwithahighmorbidityandmortality.Whileadeclineincasefatalityrates
inrecentyears,aswellastheobservationofimprovedoutcomesinhighvolumecenterssuggestthat
recommendationsforcriticalcareoutlinedinthistopicarebeneficialforpatientswithSAH,highquality
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clinicaltrialstosupportthesetreatmentsaregenerallylacking.Withtheexceptionoftherecommendation
fornimodipinetreatment,mostarebasedonobservationalevidencealone.(See'Introduction'above.)
PatientswithaneurysmalSAHareadmittedtoanintensivecaresettingforcontinuoushemodynamicand
neurologicmonitoring.Initialmanagementincludesbedrest,analgesia,pneumaticcompressionstockings,
anddiscontinuationofantithrombotics.Hypoxemia,metabolicacidosis,hyperglycemia,cardiovascular
instabilityarecommoncomplications,worsenoutcomeandshouldbepreventedandpromptlytreated.
(See'Acutemedicalcare'above.)
Aventriculostomyisplaceinpatientswithelevatedintracranialpressure(ICP)withacutehydrocephalus
andallowsmeasurementandtreatmentofelevatedICP.(See'Intracranialpressure'above.)
TheoptimaltherapyofhypertensioninSAHisnotclear.Whileloweringbloodpressuremaydecreasethe
riskofrebleeding,thisbenefitmaybeoffsetbyanincreasedriskofinfarction.Adecreaseinsystolic
bloodpressureto<160mmHginthesettingofanunsecuredaneurysmisreasonable.Agentssuchas
labetalol,nicardipine,andenalaprilarepreferred.(See'Bloodpressurecontrol'above.)
Nimodipine(60mgbymouthornasogastrictubeeveryfourhours)hasbeendemonstratedtoimprove
neurologicoutcomesinSAH.Treatmentisstartedwithinfourdaysofonsetandiscontinuedfor21days.
ThemechanismofbenefitofnimodipineinSAHisunknown.(See'Nimodipine'above.)
Prophylacticantiepilepticdrug(AED)therapyisnotrequiredinallpatients,butmaybeconsideredin
somewithunsecuredaneurysmsandlargeconcentrationsofbloodatthecortex.Seizuresshouldbe
treatedpromptly.ContinuationofAEDtherapymaynotbenecessaryinpatientswithoutacuteseizures
aftertheaneurysmissecured.AEDsareusuallycontinuedforapproximatelysixmonthsinpatientswho
haveexperiencedanacuteseizure(withinsevendays)followingSAH.(See'Antiepilepticdrugtherapy'
aboveand'Seizures'above.)
Aneurysmalrebleedingisassociatedwithaveryhighmortality.Surgicalclippingandendovascularcoiling
areeffectiveinpreventingrebleedingandgenerallyshouldbeperformedearly.Shorttermuseof
antifibrinolyticagentstopreventrebleedingcanbeconsideredinthosewhoseaneurysmtreatmentis
unavoidablydelayed.(See"Treatmentofcerebralaneurysms"and'Antifibrinolytictherapy'above.)
Clinicallysignificantvasospasmcomplicates20to30percentofaneurysmalSAHandisassociatedwith
delayedcerebralischemiaandworseneurologicoutcome:(See'Preventionofvasospasmanddelayed
cerebralischemia'aboveand'Symptomaticvasospasm'above.)
Hypovolemiaisariskfactorforischemiccomplicationsandshouldbeavoided.
Thereislimiteddatatosuggestthathyperdynamictherapyisofvalueinthepreventionof
symptomaticvasospasmbutmaybeusedtoamelioratedocumentedvasospasminapatientwitha
securedaneurysm.Hyperdynamictherapyemploysmaintenanceofeuvolemiawithinduced
hypertensionwithpressoragents.
Clinicalvasospasmthatpersistsdespitehyperdynamictherapymaybetreatedbypercutaneous
intraarterialangioplastyorintraarterialadministrationofvasodilators.Thereislimiteddata
suggestingthattheiruseimprovesclinicaloutcomes.
Limiteddatasuggeststhatstatintherapy(pravastatin40mgdailyorsimvastatin80mgdaily)may
reducetheincidenceofvasospasm,delayedischemicdeficitsandmortality.
HydrocephalusisacommoncomplicationofSAH.Placementofaventriculardrainshouldbeconsidered
inpatientswithimpairedlevelofconsciousnessandprogressiveornotimprovinghydrocephalus.Some
patientsmayrequireplacementofapermanentshunt.(See'Hydrocephalus'above.)
HyponatremiaiscommonafterSAHusuallyduetoSIADH.Aprotocolformanaginghyponatremiainthis
settingispresentedintheTable(table3).(See'Hyponatremia'above.)
Mortalitywithinthefirst30daysafterSAHapproaches50percentandisattributedlargelytotheeffects
ofinitialandrecurrentbleeding.ThemostimportantpredictivefactorsforacuteprognosisafterSAH
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include:levelofconsciousnessandneurologicgradeonadmission,patientage,amountofbloodoninitial
CTscan.(See'Mortality'above.)
SAHsurvivorshavehighratesofmemory,mood,andneurocognitiveimpairment.Somepatientshave
otherfunctionalneurologicimpairmentsandepilepsy.(See'Neurologicmorbidity'above.)
PatientswithaneurysmalSAHareatenduringriskofrecurrentSAH,despiteaneurysmtreatment.(See
"Laterecurrenceofsubarachnoidhemorrhageandintracranialaneurysms".)
FirstdegreerelativesofpatientswithSAHhaveatwotofivefoldincreasedriskofSAHcomparedwith
thegeneralpopulation.Screeningoffamilymembersforthepresenceofcerebralaneurysmisdiscussed
indetailseparately.(See"Screeningforintracranialaneurysm".)
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
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GRAPHICS
Glasgowcomascale(GCS)

Score

Eyeopening
Spontaneous

Responsetoverbalcommand

Responsetopain

Noeyeopening

Bestverbalresponse
Oriented

Confused

Inappropriatewords

Incomprehensiblesounds

Noverbalresponse

Bestmotorresponse
Obeyscommands

Localizingresponsetopain

Withdrawalresponsetopain

Flexiontopain

Extensiontopain

Nomotorresponse

Total

TheGCSisscoredbetween3and15,3beingtheworst,and15thebest.Itiscomposedof
threeparameters:besteyeresponse(E),bestverbalresponse(V),andbestmotor
response(M).ThecomponentsoftheGCSshouldberecordedindividuallyforexample,
E2V3M4resultsinaGCSscoreof9.Ascoreof13orhighercorrelateswithmildbrain
injuryascoreof9to12correlateswithmoderateinjuryandascoreof8orless
representsseverebraininjury.
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WorldFederationofNeurologicalSurgeonssubarachnoid
hemorrhagegradingscale
Grade

GCSscore

Motordeficit

15

Absent

13to14

Absent

13to14

Present

7to12

Presentorabsent

3to6

Presentorabsent

GCS:GlasgowComaScale.
Basedupondatafrom:ReportofWorldFederationofNeurologicalSurgeonsCommitteeonaUniversal
SubarachnoidHemorrhageGradingScale.JNeurosurg198868:985.
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Protocolformanagementofhyponatremiainpatientswith
subarachnoidhemorrage
ForNalevel<133mEq/Loradecreaseof6mEq/Lin24to48hours:
1.NaCltabs3gPO/NGTevery6h
2.Initiate3percentNaClinfusionat20mL/hIV
3.CheckserumNaevery6hours
a.IfNa<130mEq/L:
Increaserateby20mL/h(maxrate=80mL/h)
Ifonholdatpresent,initiate3percentNaClinfusionat20mL/hIV

b.IfNa=130to135mEq/L:
Increaserateby10mL/h(maxrate=80mL/h)
Ifonholdatpresent,initiate3percentNaClinfusionat10mL/hIV

c.IfNa=136to140mEq/L:
Nochange

d.IfNa140mEq/L:
Holdinfusion

Reproducedfrom:WooCH,RoaVA,SheridanW,FlintA.Performancecharacteristicsofaslidingscale
hypertonicsalineinfusionprotocolforthetreatmentofacuteneurologichyponatremia.Neurocrit
Care200911:228,withkindpermissionfromSpringerScience+BusinessMediaB.V.Copyright
2009.
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Disclosures
Disclosures:RobertJSinger,MDNothingtodisclose.ChristopherSOgilvy,MDNothingto
disclose.GuyRordorf,MDNothingtodisclose.JoseBiller,MD,FACP,FAAN,FAHANothingto
disclose.JanetLWilterdink,MDNothingtodisclose.
Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,these
areaddressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsfor
referencestobeprovidedtosupportthecontent.Appropriatelyreferencedcontentisrequiredofall
authorsandmustconformtoUpToDatestandardsofevidence.
Conflictofinterestpolicy

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