Neurogenic Pulmonary Edema
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UpToDate Official reprint from UpToDate www.uptodate.com ©2015 UpToDate Authors Matthew Wemple, MD Matthew Hallman, MD Andrew M Luks, MD Section Editor Polly E Parsons, MD Deputy Editor Geraldine Finlay, MD Neurogenic pulmonary edema All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Mar 2015. | This topic last updated: Apr 02, 2014. INTRODUCTION — Neurogenic pulmonary edema (NPE) is an increase in pulmonary interstitial and alveolar fluid that is due to an acute central nervous system injury and usually develops rapidly after the injury [1 ]. It is sometimes classified as a form of the acute respiratory distress syndrome (ARDS), but its pathophysiology and prognosis are different. The clinical features, differential diagnosis, diagnosis, etiology, pathogenesis, and treatment of NPE are reviewed here. ARDS and noncardiogenic pulmonary edema due to other causes are discussed elsewhere. (See "Acute respiratory distress syndrome: Clinical features and diagnosis in adults" and "Noncardiogenic pulmonary edema" .) CLINICAL PRESENTATION — NPE characteristically presents within minutes to hours of a severe central nervous system insult such as subarachnoid hemorrhage or traumatic brain injury. However, more rapid onset (immediate) and delayed onset (hours to days) have been described [24 ]. Resolution usually occurs within several days [5 ]. Dyspnea is the most common symptom, although mild hemoptysis is present in many patients. The physical examination generally reveals tachypnea, tachycardia, and basilar rales. Chest radiographs typically show a normal size heart with bilateral alveolar opacities, although unilateral opacities have also been described [68 ]. Hemodynamic measurements are usually normal by the time NPE is diagnosed, including the blood pressure, cardiac output, and pulmonary capillary wedge pressure. There is a broad range of severities of NPE and mild cases may never be detected. While NPE can be fulminant and contribute to death, mortality is more commonly due to the neurologic insult that precipitated the onset of NPE. DIFFERENTIAL DIAGNOSIS — The clinical findings of NPE may be confused with aspiration pneumonitis. Reliable differentiation between these syndromes is difficult because they are both common in settings of altered consciousness, such as postictal states. NPE tends to develop more rapidly than aspiration pneumonia, while fever and focal opacities, particularly in the lower lung zones, favor aspiration. In addition, NPE tends to resolve more rapidly than lung injury related to aspiration, particularly if aspiration pneumonia develops. Other causes of pulmonary edema should also be considered, such as heart failure and acute respiratory distress syndrome. (See "Evaluation of the patient with suspected heart failure" and "Acute respiratory distress syndrome: Clinical features and diagnosis in adults" .) DIAGNOSIS — Definitive diagnosis of NPE is difficult because the clinical signs and routine diagnostic tests are nonspecific. Thus, NPE is a clinical diagnosis based upon the occurrence of pulmonary edema in the appropriate setting and in the absence of a more likely alternative cause. The following criteria for the diagnosis and classification of NPE have been proposed, but have not been widely accepted [9 ]: ® ® Bilateral opacities ● PaO /FiO ratio <200 ● 2 2 No evidence of left atrial hypertension ● Presence of CNS injury (severe enough to have caused significantly increased intracranial pressure) ● Absence of other common causes of acute respiratory failure or acute respiratory distress syndrome ●
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Transcript of Neurogenic Pulmonary Edema
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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
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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
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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
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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'.)
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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
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ACKNOWLEDGMENTTheeditorialstaffatUpToDate,Inc.wouldliketoacknowledgeFrankDrislane,MD,andJessMandel,MD,whocontributedtoanearlierversionofthistopicreview.
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
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GRAPHICS
Causesofneurogenicpulmonaryedema
MajorcausesEpilepticseizures,particularlystatusepilepticus
Cerebralhemorrhage
Headinjury
MinorcausesGuillainBarrsyndrome
Multiplesclerosiswithmedullaryinvolvement
Nonhemorrhagicstrokes
Trigeminalnerveblock
Bulbarpoliomyelitis
Vertebralarteryligation
Rupturedspinalarteriovenousmalformation
Airembolism
Braintumors
Electroconvulsivetherapy
Inductionofgeneralanesthesia
Colloidcyst
Hydrocephalus
Reyesyndrome
Bacterialmeningitis
Viralmeningoencephalitis
Cervicalspinalcordinjury
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Capillaryhemodynamicforces
Schematicrepresentationofthecapillaryandinterstitialfluidhydraulic(P)andoncotic()pressurescontrollingfluidmovementacrossthecapillarywallbetweentheplasmaandtheinterstitialfluid.Thearrowspointinthedirectionoffluidmovementinducedbyeachoftheforces.
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Disclosures:MatthewWemple,MDNothingtodisclose.MatthewHallman,MDNothingtodisclose.AndrewMLuks,MDNothingtodisclose.PollyEParsons,MDNothingtodisclose.GeraldineFinlay,MDNothingtodisclose.Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressedbyvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobeprovidedtosupportthecontent.AppropriatelyreferencedcontentisrequiredofallauthorsandmustconformtoUpToDatestandardsofevidence.Conflictofinterestpolicy
Disclosures
