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UpToDate OfficialreprintfromUpToDate www.uptodate.com2015UpToDate

AuthorsMatthewWemple,MDMatthewHallman,MDAndrewMLuks,MD

SectionEditorPollyEParsons,MD

DeputyEditorGeraldineFinlay,MD

Neurogenicpulmonaryedema

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.Literaturereviewcurrentthrough:Mar2015.|Thistopiclastupdated:Apr02,2014.

INTRODUCTIONNeurogenicpulmonaryedema(NPE)isanincreaseinpulmonaryinterstitialandalveolarfluidthatisduetoanacutecentralnervoussysteminjuryandusuallydevelopsrapidlyaftertheinjury[1].Itissometimesclassifiedasaformoftheacuterespiratorydistresssyndrome(ARDS),butitspathophysiologyandprognosisaredifferent.

Theclinicalfeatures,differentialdiagnosis,diagnosis,etiology,pathogenesis,andtreatmentofNPEarereviewedhere.ARDSandnoncardiogenicpulmonaryedemaduetoothercausesarediscussedelsewhere.(See"Acuterespiratorydistresssyndrome:Clinicalfeaturesanddiagnosisinadults"and"Noncardiogenicpulmonaryedema".)

CLINICALPRESENTATIONNPEcharacteristicallypresentswithinminutestohoursofaseverecentralnervoussysteminsultsuchassubarachnoidhemorrhageortraumaticbraininjury.However,morerapidonset(immediate)anddelayedonset(hourstodays)havebeendescribed[24].Resolutionusuallyoccurswithinseveraldays[5].

Dyspneaisthemostcommonsymptom,althoughmildhemoptysisispresentinmanypatients.Thephysicalexaminationgenerallyrevealstachypnea,tachycardia,andbasilarrales.Chestradiographstypicallyshowanormalsizeheartwithbilateralalveolaropacities,althoughunilateralopacitieshavealsobeendescribed[68].HemodynamicmeasurementsareusuallynormalbythetimeNPEisdiagnosed,includingthebloodpressure,cardiacoutput,andpulmonarycapillarywedgepressure.

ThereisabroadrangeofseveritiesofNPEandmildcasesmayneverbedetected.WhileNPEcanbefulminantandcontributetodeath,mortalityismorecommonlyduetotheneurologicinsultthatprecipitatedtheonsetofNPE.

DIFFERENTIALDIAGNOSISTheclinicalfindingsofNPEmaybeconfusedwithaspirationpneumonitis.Reliabledifferentiationbetweenthesesyndromesisdifficultbecausetheyarebothcommoninsettingsofalteredconsciousness,suchaspostictalstates.NPEtendstodevelopmorerapidlythanaspirationpneumonia,whilefeverandfocalopacities,particularlyinthelowerlungzones,favoraspiration.Inaddition,NPEtendstoresolvemorerapidlythanlunginjuryrelatedtoaspiration,particularlyifaspirationpneumoniadevelops.

Othercausesofpulmonaryedemashouldalsobeconsidered,suchasheartfailureandacuterespiratorydistresssyndrome.(See"Evaluationofthepatientwithsuspectedheartfailure"and"Acuterespiratorydistresssyndrome:Clinicalfeaturesanddiagnosisinadults".)

DIAGNOSISDefinitivediagnosisofNPEisdifficultbecausetheclinicalsignsandroutinediagnostictestsarenonspecific.Thus,NPEisaclinicaldiagnosisbasedupontheoccurrenceofpulmonaryedemaintheappropriatesettingandintheabsenceofamorelikelyalternativecause.ThefollowingcriteriaforthediagnosisandclassificationofNPEhavebeenproposed,buthavenotbeenwidelyaccepted[9]:

BilateralopacitiesPaO /FiO ratio



ETIOLOGYTheprimaryprecipitantsofNPEareepilepticseizures,traumaticbraininjury,andcerebralhemorrhages(table1)[3,10].

EpilepticseizuresAmongallpatientswithepilepsytheoccurrenceofNPEisrare.However,severalcaseseriesreportedthatuptoonethirdofpatientswithfatalstatusepilepticushadclinicalevidenceofNPE,whileanautopsystudyfoundthat87percentofpatientswithepilepsyandunexplainedsuddendeathhadNPE[1012].ItisuncertainwhetherNPEwastheproximatecauseofdeathinthesestudies,butitisclearthattheNPEismorelikelywithincreasingseizureseverity.

NPEduetoepilepticseizuresgenerallyoccursduringthepostictalperiodanditmayoccurrepeatedlyinagivenindividual[3,13,14].(See"Convulsivestatusepilepticusinadults:Classification,clinicalfeatures,anddiagnosis".)

TraumaticbraininjuryBluntorpenetratingheadinjuryandneurosurgicalprocedurescancauseNPE[2,3,15].TheNPEisusuallyassociatedwithelevatedintracranialpressure(ICP),butraisedICPisnotanecessarycondition[16].TheincidenceofNPEintraumaticbraininjuryhasbeenestimatedat20percent,andappearstoincreasewithincreasingseverityofinjury[17].(See"Evaluationandmanagementofelevatedintracranialpressureinadults".)

CerebralhemorrhageNPEcancomplicateupto43percentofcasesofsubarachnoidhemorrhage[4,7,1821].Inaseriesof78casesoffatalsubarachnoidhemorrhage,31percenthadantemortemclinicalevidenceofNPEand71percenthadpathologicalevidenceofNPEatautopsy[18].Onsetistypicallywithinminutestohoursofthehemorrhagealthoughlateonsetdaysafterhemorrhageorrecurrenceafterapparentresolutionhavealsobeendescribed[22].NPEhasalsobeenreportedduringcoilembolizationofarupturedcerebralaneurysm[23].ThemostimportantriskfactorsforNPEfollowingsubarachnoidhemorrhagearetheclinicalandradiographicseveritiesofthehemorrhagesaswellasavertebralarterysourceofthehemorrhage[1,21].NPEcanalsobeseeninupto35percentofpatientswithintracerebralhemorrhage,withtheprimaryriskfactorsinsuchpatientsbeinghigherAcutePhysiologyandChronicHealthEvaluation(APACHE)IIscoresandincreasedlevelsofseruminflammatorymarkers[24].(See"Clinicalmanifestationsanddiagnosisofaneurysmalsubarachnoidhemorrhage".)

Otherlesscommonetiologiesarelistedinthetable(table1)[2528].

PATHOGENESISTheneurologicalstructuresthatarecriticaltothedevelopmentofNPEareknown.However,themechanismbywhichlesionsinthesestructuresleadtoNPEisnotwellunderstood.

NeurologicstructuresThemedullaoblongataandhypothalamusareconsideredthecriticalanatomicstructuresinvolvedinthepathogenesisofNPE.Theimportanceofthemedullaissupportedbytheobservationthatbilaterallesionsinthenucleusofthesolitarytract,areapostremaandlesionsintheA1andA5neuroadrenergicneurons(allofwhichareinthemedulla)cancausesystemichypertensionandNPE[2932].

Themedullaoblongataprobablyactsviathesympatheticcomponentoftheautonomicnervoussystem,assuggestedbythefollowingevidencefromanimalmodels[3335]:

Inadditiontotheroleofthemedullaoblongata,theoriesregardingthepathogenesisofNPEhavecenteredonthepotentialcontributionsofthehypothalamus,elevatedintracranialpressure,andactivationofthesympathoadrenalsystem[29,30,3345].Experimentalmodelshaveshown,forexample,thatinducinghypothalamiclesionsprecipitatesNPE[46],whileacaseseriesof22patientswithNPEfoundthathalfof

(ARDS)(eg,aspiration,massivebloodtransfusion,sepsis)

Alphaadrenergicblockade(eg,withphentolamine)canpreventthedevelopmentofNPE

NPEcanbepreventedbyspinalcordtransectionatorabovetheC7level,belowwhichsympatheticfibersleavethelateralpartofthecordtoformtheparaspinalsympathetictrunks

NPEcanbepreventedbydenervationbytransectionofthesplanchnicsympatheticfiberstothelungs

NPEmaybeproducedbystimulationofthecordattheC7C8level,withthecordandsympatheticnervesintact



themhadradiographicevidenceofhypothalamicinjury,afindingassociatedwithworseoutcome[47].

MechanismsofedemaformationNPErequiresacentralnervoussysteminjuryorevent(eg,seizure)thatalterstheStarling'sforcesinawaythatincreasesthemovementoffluidfromthecapillariestothepulmonaryinterstitium,increasesthepermeabilityofthepulmonarycapillaries,orboth(figure1).

CapillaryhydrostaticpressureIncreasedcapillaryhydrostaticpressureistheStarling'sforcethatismostlikelytocontributetoNPE,sinceitisunlikelythatacentralnervoussysteminjuryoreventcouldchangecapillaryorinterstitialoncoticpressurerapidly[3].ThisissupportedbytheobservationthatalveolarfluidhasalowfluidtoserumproteinratioearlyduringthecourseofNPE,consistentwithhydrostaticpulmonaryedema[48].

Experimentalstudiesusinganimalmodelsanduncontrolledobservationsinhumanssuggestseveralmechanismsbywhichpulmonarycapillaryhydrostaticpressuremayincreaseacutely:

DespitetheevidencethatincreasedpulmonarycapillaryhydrostaticpressureplaysaroleinNPE,therearelikelyadditionalcontributors.ThisnotionisbaseduponreportsofNPEoccurringwithlittleornoelevationinthepulmonarycapillarywedgepressureandintheabsenceofleftatrialorsystemichypertension[49].

PulmonarycapillarypermeabilityIncreasedpulmonarycapillarypermeabilitymaycontributetoNPE.ThisideaissupportedbythefindingofproteinrichedemafluidinanimalmodelsandsomepatientswithNPE,aswellastheobservationthatNPEcanoccurintheabsenceofthehemodynamicalterationsassociatedwithpulmonaryedema[4,48,62,63].

Asanexample,astudyusedthermalgreendyetechniquestomeasureextravascularlungwaterin18patientswitheitherheadtraumaorsubarachnoidhemorrhageand13controlpatients(traumapatientswithoutheadinjury)[4].Nineofthe18patientswithbraininjurieshadpulmonaryedema,definedasextravascularlungwatervaluesgreaterthantwostandarddeviationsabovethecontrolgroupmean.Thepulmonaryedemawasindependentofintracranialorpulmonaryvascularpressure,suggestingincreasedvascularpermeability.

Themechanismbywhichneuralinfluencesproducechangesinpulmonaryvascularpermeabilityhavenotbeenelucidatedwell.However,severalhypothesesexist:

Pulmonaryvenoconstrictionmayoccurwithintracranialhypertensionorsympatheticstimulation.Thisincreasesthepulmonarycapillaryhydrostaticpressure,producingpulmonaryedema[33,4952].Alphaadrenergicantagonistsmayattenuatetheeffect[53].

Excessivesystemicvenoconstrictionmayoccurleadingtoasignificantincreaseinvenousreturntotherightheartandpulmonarycirculation.Supportforthisconceptcomesfromanimalstudiesinwhichprophylacticphlebotomy(15percentofbloodvolume)priortoCNSinsultpreventeddevelopmentneurogenicpulmonaryedema[54].

Leftventricularperformancemaydeteriorateforseveralreasons:directmyocardialdamageorstunningsecondarytobraininjury,increasedafterloadduetosystemichypertension,andnegativeinotropicandchronotropicinfluencesofexcessivevagaltone[52,55,56].Thiscancausepassiveelevationoftheleftatrialandpulmonarycapillarypressures,leadingtopulmonaryedema[38,39,55,5761].

Epinephrineornorepinephrinemaydirectlyincreasevascularpermeability.SupportingthisideaaretheobservationsfromanimalmodelsthatalphaadrenergicblockadecanprotectagainstNPEandsympatheticstimulationcanproduceit[53].However,thehypothesisisimperfectbecausedirectinfusionofthesesubstancesintothepulmonarycirculationdoesnotproducesuchaneffect[64].

Alphaadrenergicagonistsreleasedinresponsetobraininjurymaycausethereleaseofasecondmediator,whichincreasesvascularpermeability(eg,endorphins,histamine,bradykinin)[3].

Aninitialrapidincreaseinpulmonaryvascularpressure(eg,duetopulmonaryvasospasmand/orincreasedsystemicvenousreturn)maycausepulmonarymicrovascularinjurywithasubsequentincreaseinpermeability[65].Thistheory,sometimescalledthe"blasttheory"issupportedbystudiesinrabbitsshowingthatpulmonarycapillariesaredamagedwhenpressuresexceed40mmHg[66].ItisalsosupportedbytheobservationthatpatientswithNPEfrequentlyhavemildhemoptysisorpulmonary



Inflammatorymechanismsmayalsocontributetoincreasedcapillarypermeability[45].Evidenceforinflammatoryresponsestoseverebraininjuryinclude:

Whethertheseobservedinflammatoryresponsespredisposetoedemaformationremainsasubjectofdebate.

TREATMENTTheoutcomeofpatientswithNPEisusuallydeterminedbythecourseoftheneurologicinsultandnottheNPE.Thus,treatmentshouldfocusontheneurologicaldisorderwhileNPEismanagedinasupportivefashion.ManyepisodesofNPEarewelltoleratedandmostresolvewithin48to72hours.

SupportivecareMostpatientswithNPEarehypoxemicandrequiresupplementaloxygen.Somepatientsmayrequiremechanicalventilation.

WhilemostpatientswithNPEarehypoxemicandrequiresupplementaloxygen,thereisinsufficientevidencetosupportspecificoxygenationgoals.Maintenanceofanoxyhemoglobinsaturation88percentorPaO 55mmHgisgenerallyacceptableinundifferentiatedlunginjury,butspecifictargetsinNPEshouldalsotakeintoconsiderationtheeffectthatrelativehypoxemiamayhaveontheunderlyingneurologicalinjury.

Oxygenationgoalsmaybeachievedinsomepatientswithnoninvasivemeasuressuchasoxygenbynasalcannulasimplefacemask,nonrebreathermask,orhighflowdeliverysystems,butmechanicalventilationmaybenecessaryinothercircumstances.Mechanicalventilationandthedecisiontointubateapatientarediscussedseparately.(See"Overviewofmechanicalventilation"and"Noninvasivepositivepressureventilationinacuterespiratoryfailureinadults"and"Thedecisiontointubate".)

MechanicalventilationinpatientswithNPEissimilartothatinpatientswithothercausesofrespiratoryfailure,althoughtherearesomeimportantdifferences:

IfICPelevationisaclinicalconcern,ICPmonitoringmaybeconsideredtoguidemechanicalventilation.

Singlecasereportsdocumenttheuseofproneventilation,inhalednitricoxide,andextracorporealmembranousoxygenation(ECMO)inpatientswithNPEandseverehypoxemia,butthereisnosystematicevidencesupportingabenefitfromthesepracticesinsuchcircumstances[7779].BecauseECMOcarriestheriskofintracranialhemorrhage,extremecaremustbetakenwithitsapplicationinpatientswithcentralnervoussysteminjury.(See"Proneventilation"and"Extracorporealmembraneoxygenation(ECMO)inadults".)

Maintenanceoflowcardiacfillingpressureswithdiureticsandlimitationofintravenousfluidsmaydecreasepulmonaryedema.However,caremustbetakentoavoidcompromiseofcardiacoutputandcerebralperfusion.Pulmonaryarterycatheterizationwashistoricallythoughthelpfulinguidingtherapy,buthassincefallenoutof

hemorrhage[2].ThehypothesisisimperfectbecausetherapiddevelopmentofacutepulmonaryhypertensionisnotanecessaryconditionforNPE[67,68]andinanimalmodelselevatedpulmonaryvascularpressuresdonotinvariablyleadtoNPE[69].

Excesscatecholaminescanthemselvesleadtothereleaseofinflammatorymediators[70,71].

S100B,aserumbiomarkerofbraininjury,hasbeenshowntoinducethereleaseofproinflammatorycytokinesinalveolartype1likecellsinvitro[72].

Braininjuryhasbeenassociatedwithincreasedintracranialproductionofproinflammatorymediatorsandsubsequentreleaseofthesemediatorsintothesystemiccirculation[73,74].

AratmodelofSAHdocumentedincreasedexpressionofendothelialactivationmarkersonpulmonaryendothelialcells,andincreasedpulmonaryTNFexpression,whichwasattenuatedbyadministrationoftheimmunemodulatorIFN.

2

Highlevelsofpositiveendexpiratorypressure(PEEP)canreducecerebralvenousreturnandworsenintracranialhypertension[75,76].(See"Positiveendexpiratorypressure(PEEP)",sectionon'Intracranialdisease'.)

Hypercapnia,whichisoftentoleratedinpatientswithARDS,cancausecerebralvasodilation,therebyincreasingcerebralbloodflowandpotentiallyincreasingICP[1].(See"Permissivehypercapnia",sectionon'Contraindications'.)



favoraspartofroutinefluidmanagement[5].(See"Pulmonaryarterycatheterization:Indications,contraindications,andcomplicationsinadults".)

TheutilityoflessinvasivemethodsofassessingcardiacfunctionandpulmonaryedematoguidetreatmentinNPEisnotwellstudied.Simultaneousassessmentofcardiacoutput,extravascularlungwater,globalenddiastolicvolume,andpulmonaryvascularpermeabilityusinglessinvasivehemodynamicmonitorshasbeenproposedasamethodtoguidemanagementdecisions,butthedataareinsufficienttosupportspecificrecommendations[80].Small,limitedstudieshavealsoevaluatedtheutilityoflungultrasoundexamsinNPE[81].

MedicationsAvarietyofmedicationshavebeenusedtotreatpatientswithNPE,buttheireffectivenessisunproven.Theseinclude:

AlphaadrenergicantagonistshavebeenshowntopreventNPEorhastenitsresolutioninanimalmodels,whilearecentreportdemonstratedrapidimprovementsinoxygenationfollowingadministrationofphentolamineinasinglepatientwithNPEduetoarupturedarteriovenousmalformation[53].However,unopposedalphaadrenergicantagonistsmayprecipitatesystemichypotensionandcerebralhypoperfusion,andintheabsenceofdatafromcontrolledtrials,routineuseoftheseagentscannotberecommendedatthistime.(See"Antihypertensivetherapytopreventrecurrentstrokeortransientischemicattack"and"Evaluationandmanagementofelevatedintracranialpressureinadults".)

OutcomesAlthoughmanyepisodesofNPEarewelltoleratedandmostcasesresolvewithin48to72hours,thedevelopmentofNPEisassociatedwithworselongtermoutcomes.Asanexample,arecentobservationalstudyof108patientswithnontraumaticintracranialhemorrhage,foundthatcomparedtothosewithoutNPE,thosewhodevelopedNPEhadahigheroneyearmortalityof(37versus14percent)[24].

SUMMARYANDRECOMMENDATIONS

Betaadrenergicantagonistsarethoughttoincreaselymphflow,decreaseedemaandreducehistamineinducedaugmentationofpulmonaryvascularpermeability[3]

Dobutamine,whichmayincreasecardiacoutput,decreasespulmonarycapillarywedgepressure,andpromotediuresis[82,83]

Chlorpromazinemayblockalphaadrenergicreceptorstoreduceedema[84]

Neurogenicpulmonaryedema(NPE)isanincreaseinpulmonaryinterstitialandalveolarfluidthatisduetoanacutecentralnervoussysteminjury.Itusuallydevelopsrapidlyfollowingtheinjury.(See'Introduction'above.)

NPEcharacteristicallypresentswithinminutestohoursofaseverecentralnervoussysteminsult.Dyspneaisthemostcommonsymptom,althoughmildhemoptysisispresentinmanypatients.Thephysicalexaminationgenerallyrevealstachypnea,tachycardia,andbasilarrales.Chestradiographstypicallyshowanormalsizeheartwithbilateralalveolarfilling,whilehemodynamicmeasurementsareusuallynormal.(See'Clinicalpresentation'above.)

NPEisaclinicaldiagnosisbasedupontheoccurrenceofpulmonaryedemaintheappropriatesettingandintheabsenceofamorelikelyalternativecause.(See'Differentialdiagnosis'aboveand'Diagnosis'above.)

TheprimaryprecipitantsofNPEareepilepticseizures,traumaticbraininjury,andcerebralhemorrhages(table1).(See'Etiology'above.)

ThetreatmentofNPEshouldfocusontreatingtheneurologicaldisorderwhileNPEismanagedinasupportivefashion.ManyepisodesofNPEarewelltoleratedandmostresolvewithin48to72hours.(See'Treatment'above.)

MostpatientswithNPEarehypoxemicandrequiresupplementaloxygen.Somepatientsmayrequiremechanicalventilation,whichdiffersfromthatforothercausesofrespiratoryfailureintwoways:permissivehypercapniaandhighlevelsofpositiveendexpiratorypressure(PEEP)shouldbeused



ACKNOWLEDGMENTTheeditorialstaffatUpToDate,Inc.wouldliketoacknowledgeFrankDrislane,MD,andJessMandel,MD,whocontributedtoanearlierversionofthistopicreview.

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Topic1610Version8.0



GRAPHICS

Causesofneurogenicpulmonaryedema

MajorcausesEpilepticseizures,particularlystatusepilepticus

Cerebralhemorrhage

Headinjury

MinorcausesGuillainBarrsyndrome

Multiplesclerosiswithmedullaryinvolvement

Nonhemorrhagicstrokes

Trigeminalnerveblock

Bulbarpoliomyelitis

Vertebralarteryligation

Rupturedspinalarteriovenousmalformation

Airembolism

Braintumors

Electroconvulsivetherapy

Inductionofgeneralanesthesia

Colloidcyst

Hydrocephalus

Reyesyndrome

Bacterialmeningitis

Viralmeningoencephalitis

Cervicalspinalcordinjury

Graphic57483Version2.0



Capillaryhemodynamicforces

Schematicrepresentationofthecapillaryandinterstitialfluidhydraulic(P)andoncotic()pressurescontrollingfluidmovementacrossthecapillarywallbetweentheplasmaandtheinterstitialfluid.Thearrowspointinthedirectionoffluidmovementinducedbyeachoftheforces.

Graphic66819Version1.0



Disclosures:MatthewWemple,MDNothingtodisclose.MatthewHallman,MDNothingtodisclose.AndrewMLuks,MDNothingtodisclose.PollyEParsons,MDNothingtodisclose.GeraldineFinlay,MDNothingtodisclose.Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobeprovidedtosupportthecontent.AppropriatelyreferencedcontentisrequiredofallauthorsandmustconformtoUpToDatestandardsofevidence.Conflictofinterestpolicy

Disclosures

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