management of intracranial hypertension

29/4/2015 ManagementofIntracranialHypertension

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2452989/ 1/17

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NeurolClin.AuthormanuscriptavailableinPMC2009May1.Publishedinfinaleditedformas:

NeurolClin.2008May26(2):521541.doi:10.1016/j.ncl.2008.02.003

PMCID:PMC2452989NIHMSID:NIHMS56358

ManagementofIntracranialHypertensionLeonardoRangelCastillo,MD,ShankarGopinath,MD,andClaudiaS.Robertson,MD

DepartmentofNeurosurgery,BaylorCollegeofMedicine,OneBaylorPlaza,Houston,TX77030,USA*Correspondingauthor.Emailaddress:[email protected](C.S.Robertson)

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Thepublisher'sfinaleditedversionofthisarticleisavailableatNeurolClinThisarticlehasbeencorrected.Seethecorrectioninvolume26onpagexvii.

SeeotherarticlesinPMCthatcitethepublishedarticle.

Abstract

Effectivemanagementofintracranialhypertensioninvolvesmeticulousavoidanceoffactorsthatprecipitateoraggravateincreasedintracranialpressure.Whenintracranialpressurebecomeselevated,itisimportanttoruleoutnewmasslesionsthatshouldbesurgicallyevacuated.Medicalmanagementofincreasedintracranialpressureshouldincludesedation,drainageofcerebrospinalfluid,andosmotherapywitheithermannitolorhypertonicsaline.Forintracranialhypertensionrefractorytoinitialmedicalmanagement,barbituratecoma,hypothermia,ordecompressivecraniectomyshouldbeconsidered.Steroidsarenotindicatedandmaybeharmfulinthetreatmentofintracranialhypertensionresultingfromtraumaticbraininjury.

Intracranialhypertensionisacommonneurologiccomplicationincriticallyillpatientsitisthecommonpathwayinthepresentationofmanyneurologicandnonneurologicdisorders.Theunderlyingpathophysiologyofincreasedintracranialpressure(ICP)isthesubjectofintensebasicandclinicalresearch,whichhasledtoadvancesinunderstandingofthephysiologyrelatedtoICP.Fewspecifictreatmentoptionsforintracranialhypertensionhavebeensubjectedtorandomizedtrials,however,andmostmanagementrecommendationsarebasedonclinicalexperience.

Intracranialpressure

Normalvalues

Innormalindividualswithclosedcranialfontanelles,centralnervoussystemcontents,includingbrain,spinalcord,blood,andcerebrospinalfluid(CSF),areencasedinanoncompliantskullandvertebralcanal,constitutinganearlyincompressiblesystem.Thereisasmallamountofcapacitanceinthesystemprovidedbytheintervertebralspaces.Intheaverageadult,theskullenclosesatotalvolumeof1450mL:1300mLofbrain,65mLofCSF,and110mLofblood[1].TheMonroeKelliehypothesisstatesthesumoftheintracranialvolumesofblood,brain,CSF,andothercomponentsisconstant,andthatanincreaseinanyoneofthesemustbeoffsetbyanequaldecreaseinanother,orelsepressureincreases.Anincreaseinpressurecausedbyanexpandingintracranialvolumeis

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distributedevenlythroughouttheintracranialcavity[2,3].

ThenormalrangeforICPvarieswithage.Valuesforpediatricsubjectsarenotaswellestablished.Normalvaluesarelessthan10to15mmHgforadultsandolderchildren,3to7mmHgforyoungchildren,and1.5to6mmHgforterminfants.ICPcanbesubatmosphericinnewborns[4].Forthepurposeofthisarticle,normaladultICPisdefinedas5to15mmHg(7.520cmH O).ICPvaluesof20to30mmHgrepresentmildintracranialhypertensionhowever,whenatemporalmasslesionispresent,herniationcanoccurwithICPvalueslessthan20mmHg[5].ICPvaluesgreaterthan20to25mmHgrequiretreatmentinmostcircumstances.SustainedICPvaluesofgreaterthan40mmHgindicatesevere,lifethreateningintracranialhypertension.

Cerebraldynamicsoverview

Cerebralperfusionpressure(CPP)dependsonmeansystemicarterialpressure(MAP)andICPbythefollowingrelationship:

Asaresult,CPPcanbereducedfromanincreaseinICP,adecreaseinbloodpressure,oracombinationofbothfactors.Throughthenormalregulatoryprocesscalledpressureautoregulation,thebrainisabletomaintainanormalcerebralbloodflow(CBF)withaCPPrangingfrom50to150mmHg.AtCPPvalueslessthan50mmHg,thebrainmaynotbeabletocompensateadequately,andCBFfallspassivelywithCPP.Afterinjury,theabilityofthebraintopressureautoregulatemaybeabsentorimpaired,andevenwithanormalCPP,CBFcanpassivelyfollowchangesinCPP.

WhenCPPiswithinthenormalautoregulatoryrange(50150mmHg),thisabilityofthebraintopressureautoregulatealsoaffectstheresponseofICPtoachangeinCPP[68].Whenpressureautoregulationisintact,decreasingCPPresultsinvasodilationofcerebralvessels,whichallowsCBFtoremainunchanged.ThisvasodilationcanresultinanincreaseinICP,whichfurtherperpetuatesthedecreaseinCPP.Thisresponsehasbeencalledthevasodilatorycascade.Likewise,anincreaseinCPPresultsinvasoconstrictionofcerebralvesselsandmayreduceICP.Whenpressureautoregulationisimpairedorabsent,ICPdecreasesandincreaseswithchangesinCPP.

Intracranialhypertension

Causesofintracranialhypertension

Thedifferentcausesofintracranialhypertension(Box1)canoccurindividuallyorinvariouscombinations.InprimarycausesofincreasedICP,normalizationofICPdependsonrapidlyaddressingtheunderlyingbraindisorder.Inthesecondgroup,intracranialhypertensionisduetoanextracranialorsystemicprocessthatisoftenremediable[911].ThelastgroupiscomposedofthecausesofincreasedICPafteraneurosurgicalprocedure.

Box1.Causesofintracranialhypertension

Intracranial(primary)

BraintumorTrauma(epiduralandsubduralhematoma,cerebralcontusions)NontraumaticintracerebralhemorrhageIschemicstroke

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HydrocephalusIdiopathicorbenignintracranialhypertensionOther(eg,pseudotumorcerebri,pneumoencephalus,abscesses,cysts)

Extracranial(secondary)

AirwayobstructionHypoxiaorhypercarbia(hypoventilation)Hypertension(pain/cough)orhypotension(hypovolemia/sedation)Posture(headrotation)HyperpyrexiaSeizuresDrugandmetabolic(eg,tetracycline,rofecoxib,divalproexsodium,leadintoxication)Others(eg,highaltitudecerebraledema,hepaticfailure)

Postoperative

Masslesion(hematoma)EdemaIncreasedcerebralbloodvolume(vasodilation)DisturbancesofCSF

Intracranialhypertensionsecondarytotraumaticbraininjury

Specialfeaturesshouldbeconsideredinpatientswithtraumaticbraininjury(TBI),inwhichlesionsmaybeheterogeneous,andseveralfactorsoftencontributetoincreasetheICP[12]:

1. Traumaticallyinducedmasses:epiduralorsubduralhematomas,hemorrhagiccontusions,foreignbody,anddepressedskullfractures

2. Cerebraledema[13]3. Hyperemiaowingtovasomotorparalysisorlossofautoregulation[14]4. Hypoventilationthatleadstohypercarbiawithsubsequentcerebralvasodilation5. HydrocephalusresultingfromobstructionoftheCSFpathwaysoritsabsorption6. Increasedintrathoracicorintraabdominalpressureasaresultofmechanicalventilation,posturing,

agitation,orValsalvamaneuvers

Afterevacuationoftraumaticmasslesions,themostimportantcauseofincreasedICPwasthoughttobevascularengorgement[14].Recentstudieshavesuggestedthatcerebraledemaistheprimarycauseinmostcases[15].

AsecondaryincreaseintheICPoftenisobserved3to10daysafterthetrauma,principallyasaresultofadelayedhematomaformation,suchasepiduralhematomas,acutesubduralhematoma,andtraumatichemorrhagiccontusionswithsurroundingedema,sometimesrequiringevacuation[16].OtherpotentialcausesofdelayedincreasesinICParecerebralvasospasm[17],hypoventilation,andhyponatremia.

Neurologicintensivecaremonitoring

Intracranialhypertensionisanimportantcauseofsecondaryinjuryinpatientswithacuteneurologicandneurosurgicaldisordersandtypicallymandatesspecificmonitoring.Patientswithsuspectedintracranialhypertension,especiallysecondarytoTBI,shouldhavemonitoringofICPmonitoringofcerebraloxygenextraction,aswithjugularbulboximetryorbraintissuePO ,mayalsobeindicated.Braininjuredpatientsalsoshouldhaveclosemonitoringofsystemicparameters,includingventilation,oxygenation,electrocardiogram,heartrate,bloodpressure,temperature,bloodglucose,andfluidintakeandoutput.Patientsshouldbemonitoredroutinelywithpulseoximetryandcapnographytoavoidunrecognizedhypoxemiaandhypoventilationor

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hyperventilation.Acentralvenouscathetercommonlyisneededtohelpevaluatevolumestatus,andaFoleycatheterisemployedforaccurateurineoutput.

Intracranialpressuremonitoring

ClinicalsymptomsofincreasedICP,suchasheadache,nausea,andvomiting,areimpossibletoelicitincomatosepatients.Papilledemaisareliablesignofintracranialhypertension,butisuncommonafterheadinjury,eveninpatientswithdocumentedelevatedICP.Inastudyofpatientswithheadtrauma,54%ofpatientshadincreasedICP,butonly3.5%hadpapilledemaonfundoscopicexamination[18].Othersigns,suchaspupillarydilationanddecerebrateposturing,canoccurintheabsenceofintracranialhypertension.CTscansignsofbrainswelling,suchasmidlineshiftandcompressedbasalcisterns,arepredictiveofincreasedICP,butintracranialhypertensioncanoccurwithoutthosefindings[19].

Typesofmonitors

TheventriculostomycatheteristhepreferreddeviceformonitoringICPandthestandardagainstwhichallnewermonitorsarecompared[20].Anintraventricularcatheterisconnectedtoanexternalpressuretransducerviafluidfilledtubing.Theadvantagesoftheventriculostomyareitsrelativelylowcost,theoptiontouseitfortherapeuticCSFdrainage,anditsabilitytorecalibratetominimizeerrorsowingtomeasurementdrift.Thedisadvantagesaredifficultieswithinsertionintocompressedordisplacedventricles,inaccuraciesofthepressuremeasurementsbecauseofobstructionofthefluidcolumn,andtheneedtomaintainthetransduceratafixedreferencepointrelativetothepatientshead.Thesystemshouldbecheckedforproperfunctioningatleastevery2to4hours,andanytimethereisachangeintheICP,neurologicexamination,andCSFoutput.Thischeckshouldincludeassessingforthepresenceofanadequatewaveform,whichshouldhaverespiratoryvariationsandtransmittedpulsepressure.

Whentheventriclecannotbecannulated,otheralternativescanbeused.DifferentnonfluidcoupleddevicesareavailableforICPmonitoringandhavereplacedthesubarachnoidbolt.Themicrosensortransducerandthefiberoptictransducerarethemostwidelyavailable.Thesetransducertippedcatheterscanbeinsertedinthesubduralspaceordirectlyintothebraintissue[21].Themainadvantagesofthesemonitorsistheeaseofinsertion,especiallyinpatientswithcompressedventricleshowever,noneofthetransducertippedcatheterscanberesettozeroaftertheyareinsertedintotheskull,andtheyexhibitmeasurementdriftovertime[22].SubduralandepiduralmonitorsforICPmeasurementsarelessaccuratecomparedtoventriculostomyorparenchymalmonitors.

Forsurgicalpatients,theICPmonitormaybeinsertedattheendofthesurgicalprocedure.ICPmonitoringiscontinuedforaslongastreatmentofintracranialhypertensionisrequired,typically3to5days.AsecondaryincreaseinICPmaybeobserved3to10daysaftertraumain30%ofpatientswithintracranialhypertension[16]secondarytodevelopmentofdelayedintracerebralhematoma,cerebralvasospasm,orsystemicfactorssuchashypoxiaandhypotension.

Typesofintracranialpressurewaveforms

ThevariationsseeninthenormaltracingofICPoriginatefromsmallpulsationstransmittedfromthesystemicbloodpressuretotheintracranialcavity.Thesebloodpressurepulsationsaresuperimposedonsloweroscillationcausedbytherespiratorycycle.Inmechanicallyventilatedpatients,thepressureinthesuperiorvenacavaincreasesduringinspiration,whichreducesvenousoutflowfromthecranium,causinganelevationinICP.

Pathologicwaveforms

AstheICPincreases,cerebralcompliancedecreases,arterialpulsesbecomemorepronounced,andvenouscomponentsdisappear.PathologicwaveformsincludeLundbergA,B,andCtypes.LundbergAwavesorplateauwavesareICPelevationstomorethan50mmHglasting5to20minutes.Thesewavesareaccompaniedbya



simultaneousincreaseinMAP,butitisnotclearlyunderstoodifthechangeinMAPiscauseoreffect.LundbergBwavesorpressurepulseshaveanamplitudeof50mmHgandoccurevery30secondsto2minutes.LundbergCwaveshaveanamplitudeof20mmHgandafrequencyof4to8perminutetheyareseeninthenormalICPwaveform,buthighamplitudeCwavesmaybesuperimposedonplateauwaves[23].

Indicationsforintracranialpressuremonitoring

MonitoringofICPisaninvasivetechniqueandhassomeassociatedrisks.Forafavorablerisktobenefitratio,ICPmonitoringisindicatedonlyinpatientswithsignificantriskofintracranialhypertension[12](Box2).PatientswithTBIwhoareparticularlyatriskfordevelopinganelevatedICPincludethosewithGlasgowComaScaleof8orlessaftercardiopulmonaryresuscitationandwhohaveanabnormaladmissionheadCTscan.Suchabnormalitiesmightincludelowdensityorhighdensitylesions,includingcontusionsepidural,subdural,orintraparenchymalhematomascompressionofbasalcisternsandedema[24].Patientswhoareabletofollowcommandshavealowriskfordevelopingintracranialhypertension,andserialneurologicexaminationscanbefollowed.

Box2:IndicationsforICPMonitoring

GCSScore:38(afterresuscitation)

1. AbnormalAdmissionHeadCTScan

a. Hematomab. Contusionc. Edemad. Herniatione. Compressedbasalcisterns

2. NormalAdmissionHeadCTScanPLUS2ormoreofthefollowing

a. Age>40yearsb. Motorposturingc. Systolicbloodpressure



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Themostcommoncomplicationofventriculostomycatheterplacementisinfectionwithanincidenceof5%to14%colonizationofthedeviceismorecommonthanclinicalinfection[25].Astudyfoundnosignificantreductionininfectionrateinpatientsundergoingprophylacticchangeofmonitorsbeforeday5,comparedwiththosewhosecatheterswereinplacefor5daysormore.[26].FactorsthatarenotassociatedwithinfectionareinsertionofthecatheterintheneurologicICU,previouscatheterinsertion,drainageofCSF,anduseofsteroids.Inagroupofpatientswithprolongedventriculardrainageof10daysormore,anonlinearincreaseindailyinfectionratewasobservedovertheinitial4daysbutremainedconstantdespiteprolongedcatheteruse[27].Useofantibioticcoatedventriculostomycathetershasbeenshowntoreducetheriskofinfectionfrom9.4%to1.3%[28].Othercomplicationsofventriculostomycathetersarehemorrhagewithanoverallincidenceof1.4%,malfunction,obstruction,andmalposition.

Intracranialpressuretreatmentmeasures:briefsummaryofgoalsoftherapy

1. MaintainICPatlessthan20to25mmHg.2. MaintainCPPatgreaterthan60mmHgbymaintainingadequateMAP.3. AvoidfactorsthataggravateorprecipitateelevatedICP.

AnoverallapproachtothemanagementofintracranialhypertensionispresentedinFig.1.

Fig.1Diagramofdiagnosisandtreatmentofintracranialhypertension.

Generalcaretominimizeintracranialhypertension

Preventionortreatmentoffactorsthatmayaggravateorprecipitateintracranialhypertensionisacornerstoneofneurologiccriticalcare.Specificfactorsthatmayaggravateintracranialhypertensionincludeobstructionofvenousreturn(headposition,agitation),respiratoryproblems(airwayobstruction,hypoxia,hypercapnia),fever,severehypertension,hyponatremia,anemia,andseizures.

Optimizingcerebralvenousoutflow

TominimizevenousoutflowresistanceandpromotedisplacementofCSFfromtheintracranialcompartmenttothespinalcompartment,elevationoftheheadofthebedandkeepingtheheadinaneutralpositionarestandardsinneurosurgicalcare.SomeauthorshaveadvocatedkeepingthepatientsheadflattomaximizeCPP[7].OtherstudieshaveshownareductioninICPwithoutareductionineitherCPPorCBFinmostpatientswithelevationoftheheadto30[29].Stillotherauthorshaveobservedthatelevationoftheheadto30reducedICPandincreasedCPP,butdidnotchangebraintissueoxygenation[30].ThereductioninICPaffordedby15to30ofheadelevationisprobablyadvantageousandsafeformostpatients.Whenheadelevationisused,thepressuretransducersforbloodpressureandICPmustbezeroedatthesamelevel(attheleveloftheforamenofMonro)toassessCPPaccurately.

Increasedintraabdominalpressure,ascanoccurwithabdominalcompartmentsyndrome,alsocanexacerbateICPpresumablybyobstructingcerebralvenousoutflow.SeveralcasereportshaveobservedimmediatereductionsinICPwithdecompressivelaparotomyinsuchcircumstances.Aretrospectivereportindicatedthatevenwhenabdominalcompartmentsyndromeisnotpresent,abdominalfascialreleasecanreduceeffectivelyICPthatisrefractorytomedicaltreatment[31].

Respiratoryfailure



Respiratorydysfunctioniscommoninpatientswithintracranialhypertension,especiallywhenthecauseisheadtrauma.HypoxiaandhypercapniacanincreaseICPdramatically,andmechanicalventilationcanaltercerebralhemodynamics.OptimalrespiratorymanagementiscrucialforcontrolofICP.

Thirtysixpercentofcomatoseheadinjurypatientspresentwithhypoxiaandrespiratorydysfunctionrequiringmechanicalventilationonadmission.Pneumoniaandpulmonaryinsufficiencyoccurin42%and28%ascomplicationsduringhospitalization.In227spontaneouslybreathingpatientswithneurologicdisorders,mostwithintracranialhypertension,NorthandJennettfoundthat60%hadbreathingabnormalities,includingperiodicrespirations,tachypnea,andirregularbreathing[32].Periodicbreathingwasnotcorrelated,however,withanyparticularanatomicsiteoftheneurologicinjury.PeriodicepisodesofhypoventilationcanprecipitateincreasedICP[33].ControlledventilationtomaintainanormalPaCO caneliminatethiscauseofintracranialhypertension.

MechanicalventilationalsocanhaveadverseeffectsonICP.PEEP,whichmaybeneededtoimproveoxygenation,canincreaseICPbyimpedingvenousreturnandincreasingcerebralvenouspressureandICP,andbydecreasingbloodpressureleadingtoareflexincreaseofcerebralbloodvolume.ForPEEPtoincreasecerebralvenouspressuretolevelsthatwouldincreaseICP,thecerebralvenouspressuremustatleastequaltheICP.ThehighertheICP,thehigherthePEEPmustbetohavesuchadirecthydrauliceffectonICP.TheconsequencesofPEEPonICPalsodependonlungcompliance,andminimalconsequencesforICPusuallyareobservedwhenlungcomplianceislowasinpatientswithacutelunginjury[34].

Sedationandanalgesia

AgitationandpainmaysignificantlyincreasebloodpressureandICP.Adequatesedationandanalgesiaisanimportantadjuncttreatment.Nosedativeregimenhasclearadvantagesinthispatientpopulation.Ingeneral,benzodiazepinescauseacoupledreductionincerebralmetabolicrateofoxygen(CMRO )andCBF,withnoeffectonICP,whereasthenarcoticshavenoeffectonCMRO orCBF,buthavebeenreportedtoincreaseICPinsomepatients[35].Oneconsiderationinthechoiceofsedativeshouldbetominimizeeffectsonbloodpressurebecausemostavailableagentscandecreasebloodpressure.Hypovolemiapredisposestohypotensivesideeffectsandshouldbetreatedbeforeadministeringsedativeagents.Selectionofshorteractingagentsmayhavetheadvantageofallowingbriefinterruptionofsedationtoevaluateneurologicstatus.

Fever

Feverincreasesmetabolicrateby10%to13%perdegreeCelsiusandisapotentvasodilator.FeverinduceddilationofcerebralvesselscanincreaseCBFandmayincreaseICP.FeverduringthepostinjuryperiodworsensneurologicinjuryinexperimentalmodelsofTBI[36].InanobservationalstudyinpatientswithTBI,Jonesandcolleagues[37]foundasignificantrelationshipbetweenfeverandapoorneurologicoutcome.Whileapatientisatriskforintracranialhypertension,fevershouldbecontrolledwithantipyreticsandcoolingblankets.Infectiouscausesmustbesoughtandtreatedwithappropriateantibioticswhenpresent.

Hypertension

Elevatedbloodpressureisseencommonlyinpatientswithintracranialhypertension,especiallysecondarytoheadinjury,andischaracterizedbyasystolicbloodpressureincreasegreaterthandiastolicincrease.Itisassociatedwithsympathetichyperactivity[38].Itisunwisetoreducesystemicbloodpressureinpatientswithhypertensionassociatedwithuntreatedintracranialmasslesionsbecausecerebralperfusionisbeingmaintainedbythehigherbloodpressure.Intheabsenceofanintracranialmasslesion,thedecisiontotreatsystemichypertensionismorecontroversialandmayneedtobeindividualizedforeachpatient.

Whenpressureautoregulationisimpaired,whichiscommonafterTBI,systemichypertensionmayincreaseCBFandICP.Inaddition,elevatedbloodpressuremayexacerbatecerebraledemaandincreasetheriskofpostoperativeintracranialhemorrhage.

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Systemichypertensionmayresolvewithsedation.Ifthedecisionismadetotreatsystemichypertension,thechoiceofantihypertensiveagentisimportant.Vasodilatingdrugs,suchasnitroprusside,nitroglycerin,andnifedipine,canbeexpectedtoincreaseICPandmayreflexivelyincreaseplasmacatecholamines,whichmaybedeleterioustothemarginallyperfusedinjuredbrain.Sympathomimeticblockingantihypertensivedrugs,suchasblockingdrugs(labetalol,esmolol)orcentralactingreceptoragonists(clonidine),arepreferredbecausetheyreducebloodpressurewithoutaffectingtheICP.Agentswithashorthalflifehaveanadvantagewhenthebloodpressureislabile.

Treatmentofanemia

AnecdotalcaseshavebeenreportedofpatientswithsevereanemiapresentingwithsymptomsofincreasedICPandsignsofpapilledema,whichresolvewithtreatmentoftheanemia[39].ThemechanismisthoughttoberelatedtothemarkedincreaseinCBFthatisrequiredtomaintaincerebraloxygendeliverywhenanemiaissevere.AlthoughanemiahasnotbeenclearlyshowntoexacerbateICPafterTBI,acommonpracticeistomaintainhemoglobinconcentrationataminimumof10g/dL.Inviewofalargerandomizedtrialofcriticallyillpatientsthatshowedbetteroutcomewithamorerestrictivetransfusionthresholdof7g/dL[40],theissueofoptimalhemoglobinconcentrationinpatientswithTBIneedsfurtherstudy.

Preventionofseizures

Theriskofseizuresaftertraumaisrelatedtotheseverityofthebraininjuryseizuresoccurin15%to20%ofpatientswithsevereheadinjury.SeizurescanincreasecerebralmetabolicrateandICP,butthereisnoclearrelationshipbetweentheoccurrenceofearlyseizuresandaworseneurologicoutcome[41].InpatientswithsevereTBI,50%ofseizuresmaybesubclinicalandcanbedetectedonlywithcontinuouselectroencephalographicmonitoring[42].Significantriskfactorsforlaterseizuresarebraincontusions,subduralhematoma,depressedskullfracture,penetratingheadwound,lossofconsciousnessoramnesiaformorethan1day,andage65yearsorolder.

Inarandomizedclinicaltrial,phenytoinreducedtheincidenceofseizuresduringthefirstweekaftertrauma,butnotthereafter[43].Basedonthisstudy,seizureprophylaxisforpatientswithseverebraininjuryisrecommendedforthefirst7daysafterinjury.Treatmentwithanticonvulsantsbeyond7daysshouldbereservedforpatientswhodeveloplateseizures[44].

Measuresforrefractoryintracranialhypertension

ForpatientswithsustainedICPelevationsofgreaterthan20to25mmHg,additionalmeasuresareneededtocontroltheICP.Emergentsurgicalmanagementshouldbeconsideredwheneverintracranialhypertensionoccurssuddenlyorisrefractorytomedicalmanagement.

Medicalinterventions

Heavysedationandparalysis

Routineparalysisofpatientswithneurosurgicaldisordersisnotindicatedhowever,intracranialhypertensioncausedbyagitation,posturing,orcoughingcanbepreventedbysedationandnondepolarizingmusclerelaxantsthatdonotaltercerebrovascularresistance[45].Acommonlyusedregimenismorphineandlorazepamforanalgesia/sedationandcisatracuriumorvecuroniumasamusclerelaxant,withthedosetitratedbytwitchresponsetostimulation.Althoughadisadvantageofthistherapyisthattheneurologicexaminationcannotbemonitoredclosely,thesedativesandmusclerelaxantscanbeinterruptedonceaday,usuallybeforemorningrounds,toallowneurologicassessments.

Majorcomplicationsofneuromuscularblockadearemyopathy,polyneuropathy,andprolongedneuromuscularblockade.Myopathyisassociatedwiththeuseofneuromuscularblockingagents,particularlyincombinationwith



corticosteroids[46].Polyneuropathyhasbeenobservedinpatientswithsepsisandmultipleorganfailure.Prolongedneuromuscularblockadeisseeninpatientswithmultipleorganfailureespeciallywithkidneyandliverdysfunction.Recommendationstominimizethesecomplicationsarelimitingtheuseanddoseofneuromuscularblockingagents,trainoffourmonitoring,measuringcreatinephosphokinasedaily,andstoppingthedrugdailytoevaluatemotorresponse[47].

Hyperosmolartherapy

Mannitolisthemostcommonlyusedhyperosmolaragentforthetreatmentofintracranialhypertension.Morerecently,hypertonicsalinealsohasbeenusedinthiscircumstance.Afewstudieshavecomparedtherelativeeffectivenessofthesetwohyperosmoticagents,butmoreworkisneeded.

IntravenousbolusadministrationofmannitollowerstheICPin1to5minuteswithapeakeffectat20to60minutes.TheeffectofmannitolonICPlasts1.5to6hours,dependingontheclinicalcondition[48].Mannitolusuallyisgivenasabolusof0.25g/kgto1g/kgbodyweightwhenurgentreductionofICPisneeded,aninitialdoseof1g/kgbodyweightshouldbegiven.Arterialhypotension(systolicbloodpressure



Hyperventilation

HyperventilationdecreasesPaCO ,whichcaninduceconstrictionofcerebralarteriesbyalkalinizingtheCSF.TheresultingreductionincerebralbloodvolumedecreasesICP.Hyperventilationhaslimiteduseinthemanagementofintracranialhypertension,however,becausethiseffectonICPistimelimited,andbecausehyperventilationmayproduceasufficientdecreaseinCBFtoinduceischemia.

Thevasoconstrictiveeffectoncerebralarterioleslastsonly11to20hoursbecausethepHoftheCSFrapidlyequilibratestothenewPaCO level.AstheCSFpHequilibrates,thecerebralarteriolesredilate,possiblytoalargercaliberthanatbaseline,andtheinitialreductionincerebralbloodvolumecomesatthecostofapossiblereboundphaseofincreasedICP[57,58].Forthisreason,themosteffectiveuseofhyperventilationisacutelytoallowtimeforother,moredefinitivetreatmentstobeputintoaction.Whenhypocarbiaisinducedandmaintainedforseveralhours,itshouldbereversedslowly,overseveraldays,tominimizethisreboundhyperemia[59].

HyperventilationdecreasesCBF,butwhetherthisreductioninflowissufficienttoinduceischemiaininjuredbrainiscontroversial.OneprospectivestudyshowedthatacutelyreducingPaCO fromanaverageof36mmHgto29mmHgreducedglobalCBFandsignificantlyincreasedthevolumeofbrainthatwasmarkedlyhypoperfuseddespiteimprovementsinICPandCPP[60].Diringerandcoworkers[61]showedsimilarchangesinCBFwithmoderatehyperventilation,butdidnotobserveanychangesinregionalCMRO evenwhenCBFwasreducedtolessthan10mL/100g/minininjuredbraintissue,suggestingthatenergyfailureassociatedwithcerebralischemiawasnotoccurring.

Althoughhyperventilationinducedischemiahasnotbeenclearlyshown,routinechronichyperventilation(toPaCO of2025mmHg)hadadetrimentaleffectonoutcomeinonerandomizedclinicaltrial[59].Theauthorsofthisstudyrecommendedusinghyperventilationonlyinpatientswithintracranialhypertension,ratherthanasaroutineinallheadinjuredpatients.ThisviewisreinforcedinTBIguidelines.

Barbituratecoma

Barbituratecomashouldonlybeconsideredforpatientswithrefractoryintracranialhypertensionbecauseoftheseriouscomplicationsassociatedwithhighdosebarbiturates,andbecausetheneurologicexaminationbecomesunavailableforseveraldays[62].Pentobarbitalisgiveninaloadingdoseof10mg/kgbodyweightfollowedby5mg/kgbodyweighteachhourfor3doses.Themaintenancedoseis1to2mg/kg/h,titratedtoaserumlevelof30to50g/mLoruntiltheelectroencephalogramshowsaburstsuppressionpattern.Althoughroutineuseofbarbituratesinunselectedpatientshasnotbeenconsistentlyeffectiveinreducingmorbidityormortalityaftersevereheadinjury[63,64],arandomizedmulticentertrialshowedthatinstitutingbarbituratecomainpatientswithrefractoryintracranialhypertensionresultedinatwofoldgreaterchanceofcontrollingtheICP[65].

ThemechanismofICPreductionbybarbituratesisunclear,butlikelyreflectsacoupledreductioninCBFandCMRO ,withanimmediateeffectonICP.StudiesbyMesseterandcolleagues[66,67]havesuggestedthatthereductioninICPwithbarbituratesiscloselytiedtotheretentionofcarbondioxidereactivitybythebrain.Complicationsoccurringduringtreatmentwithbarbituratecomaincludehypotensionin58%ofpatients,hypokalemiain82%,respiratorycomplicationsin76%,infectionsin55%,hepaticdysfunctionin87%,andrenaldysfunctionin47%[68].Hypotensioncausedbypentobarbitalshouldbetreatedfirstwithvolumereplacementandthenwithvasopressorsifnecessary.Experimentalstudiessuggestthatforthetreatmentofhypotensionassociatedwithbarbituratecoma,volumeresuscitationmaybebetterthandopamine[69]becausedopamineinfusionincreasedcerebralmetabolicrequirementsandpartiallyoffsetthebeneficialeffectsofbarbituratesonCMRO .

Hypothermia

AlthoughamulticenterrandomizedclinicaltrialofmoderatehypothermiainsevereTBIdidnotshowabeneficialeffectonneurologicoutcome,itwasnotedthatfewerpatientsrandomizedtomoderatehypothermiahadintracranial

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hypertension[70].ApilotrandomizedclinicaltrialofhypothermiainchildrenwithTBIproducedsimilarfindingsnoimprovementinneurologicoutcome,butareductioninICPduringthehypothermiatreatment[71].Althoughroutineinductionofhypothermiaisnotindicatedatpresent,hypothermiamaybeaneffectiveadjunctivetreatmentforincreasedICPrefractorytoothermedicalmanagement.

Steroids

Steroidscommonlyareusedforprimaryandmetastasticbraintumors,todecreasevasogeniccerebraledema.Focalneurologicsignsanddecreasedmentalstatusowingtosurroundingedematypicallybegintoimprovewithinhours[72].IncreasedICP,whenpresent,decreasesoverthefollowing2to5days,insomecasestonormal.Themostcommonlyusedregimenisintravenousdexamethasone,4mgevery6hours.Forotherneurosurgicaldisorders,suchasTBIorspontaneousintracerebralhemorrhage,steroidshavenotbeenshowntohaveabenefit[73,74]andinsomestudieshavehadadetrimentaleffect[75,76].

TheCRASHtrial[75]isarecentlycompleted,large(>10,000patientsenrolled),placebocontrolledrandomizedclinicaltrialofmethylprednisolonefor48hoursinpatientswithTBI.Administrationofmethylprednisoloneresultedinasignificantincreaseintheriskofdeathfrom22.3%to25.7%(relativerisk1.15,95%confidenceinterval1.071.24).ThistrialconfirmedpreviousstudiesandguidelinesthatroutineadministrationofsteroidsisnotindicatedforpatientswithTBI.

Surgicalinterventions

Resectionofmasslesions

IntracranialmassesproducingelevatedICPshouldberemovedwhenpossible.Acuteepiduralandsubduralhematomasareahyperacutesurgicalemergency,especiallyepiduralhematomabecausethebleedingisunderarterialpressure.Brainabscessmustbedrained,andpneumocephalusmustbeevacuatedifitisundersufficienttensiontoincreaseICP.Surgicalmanagementofspontaneousintracerebralbleedingiscontroversial[77].

Cerebrospinalfluiddrainage

CSFdrainagelowersICPimmediatelybyreducingintracranialvolumeandmorelongtermbyallowingedemafluidtodrainintotheventricularsystem.DrainageofevenasmallvolumeofCSFcanlowerICPsignificantly,especiallywhenintracranialcomplianceisreducedbyinjury.ThismodalitycanbeanimportantadjuncttherapyforloweringICP.Ifthebrainisdiffuselyswollen,theventriclesmaycollapse,andthismodalitythenhaslimitedutility.

Decompressivecraniectomy

Thesurgicalremovalofpartofthecalvariatocreateawindowinthecranialvaultisthemostradicalinterventionforintracranialhypertension,negatingtheMonroKelliedoctrineoffixedintracranialvolumeandallowingforherniationofswollenbrainthroughthebonewindowtorelievepressure.Decompressivecraniectomyhasbeenusedtotreatuncontrolledintracranialhypertensionofvariousorigins,includingcerebralinfarction[78],trauma,subarachnoidhemorrhage,andspontaneoushemorrhage.Patientselection,timingofoperation,typeofsurgery,andseverityofclinicalandradiologicbraininjuryallarefactorsthatdeterminetheoutcomeofthisprocedure.

SahuquilloandArikan[79]reviewedtheevidenceintheliteratureforstudiesevaluatingtheeffectivenessofdecompressivecraniectomyafterTBI.Theyfoundonlyonesmallrandomizedclinicaltrialin27childrenwithTBI[80].Thistrialfoundareducedriskratiofordeathof0.54(95%confidenceinterval0.171.72),andariskratioof0.54fordeath,vegetativestatus,orseveredisability6to12monthsafterinjury(95%confidenceinterval0.291.07).Alloftheavailablestudiesinadultsareeithercaseseriesorcohortswithhistoricalcontrols.ThesereportssuggestthatdecompressivecraniectomyeffectivelyreducesICPinmost(85%)patientswithintracranial



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hypertensionrefractorytoconventionalmedicaltreatment[81,82].BrainoxygenationmeasuredbytissuePO andbloodflowestimatedbymiddlecerebralarteryflowvelocityalsoareusuallyimprovedafterdecompressivecraniectomy[83,84].Reportedcomplicationsincludehydrocephalus,hemorrhagicswellingipsilateraltothecraniectomysite,andsubduralhygroma[81].Acasereportofparadoxicalherniationalsohasbeenreportedafteralumbarpunctureinapatientwithadecompressivecraniectomy[85].

Therearelimitedresultsfromrandomizedtrialstoconfirmorrefutetheeffectivenessofdecompressivecraniectomyinadults.Reportssuggest,however,thatdecompressivecraniectomymaybeausefuloptionwhenmaximalmedicaltreatmenthasfailedtocontrolICP.ThereareongoingrandomizedcontrolledtrialsinTBI(RescueICP[86]andDECRAN).InapooledanalysisofrandomizedtrialsinpatientswithmalignantMCAinfarction,decompressivesurgeryundertakenwithin48hofstrokewasassociatedwithreducedmortalityandanincreasedproportionofpatientswithafavourablefunctionaloutcome[87].

Summary

EffectivetreatmentofintracranialhypertensioninvolvesmeticulousavoidanceoffactorsthatprecipitateoraggravateincreasedICP.WhenICPbecomeselevated,itisimportanttoruleoutnewmasslesionsthatshouldbesurgicallyevacuated.MedicalmanagementofincreasedICPshouldincludesedation,drainageofCSF,andosmotherapywitheithermannitolorhypertonicsaline.Forintracranialhypertensionrefractorytoinitialmedicalmanagement,barbituratecoma,hypothermia,ordecompressivecraniectomyshouldbeconsidered.SteroidsarenotindicatedandmaybeharmfulinthetreatmentofintracranialhypertensionresultingfromTBI.

Acknowledgments

ThisarticlewassupportedbyNIHgrantP01NS38660.

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