Hypoxic-ischemic encephalopathy (adults and children)

Neurologic injury is caused by hypoxia (secondary to carbon monoxide toxicity, near drowning, etc.) or interruption of blood flow (usually from ... ×RecentEditsLogInArticlesSignUpCasesCoursesQuizDonateAbout×MenuSearch ADVERTISEMENT:Radiopaediaisfreethankstooursupportersandadvertisers.BecomeaGoldSupporterandseenoads. ArticlesCasesCoursesLogIn LoginSignup {"url":"/signup-modal-props.json?lang=us\u0026email="} ArticlesCasesCoursesQuizAboutRecentEditsGoad-freeSearch Hypoxic-ischemicencephalopathy(adultsandchildren)LastrevisedbyDrYahyaBaba◉on23Apr2022EditarticleViewrevisionhistoryReportproblemwithArticleCitation,DOI&articledataCitation:DiMuzio,B.,Baba,Y.Hypoxic-ischemicencephalopathy(adultsandchildren).Referencearticle,Radiopaedia.org.(accessedon28May2022)https://doi.org/10.53347/rID-14025DOI:https://doi.org/10.53347/rID-14025Permalink:https://radiopaedia.org/articles/14025rID:14025Articlecreated:16Jun2011byDrBrunoDiMuzio◉◈Revisions:61timesby17users-seefullrevisionhistorySystem:CentralNervousSystemSections:-Tags:hypoxic-ischemicencephalopathy,cerebrovasculardisease,refsSynonyms:hypoxic-ischemicbraininjuryHypoxic-ischaemicencephalopathyGlobalhypoxic-ischaemicinjuryHypoxic-ischemicinjuryinolderchildrenandadultshypoxicbraindamageHypoxic-ischaemicinjuryinchildrenandadultsHypoxic-ischemicbraindamageHypoxic-ischaemicbraindamageURLofArticle Hypoxic-ischemicencephalopathy inadultsandolderchildren(i.e.notneonates), alsoknownasglobal hypoxic-ischemicinjury, isseeninmanysettingsandoftenhasdevastatingneurologicalsequelae.Foradiscussionofneonatalhypoxia,refertoneonatalhypoxic-ischemicencephalopathy. Onthispage: Article: Epidemiology Clinicalpresentation Pathology Radiographicfeatures Differentialdiagnosis Seealso References Images: Casesandfigures Imagingdifferentialdiagnosis EpidemiologyHypoxic-ischemiccerebralinjuryoccursatanyage,althoughtheetiologyissignificantlydifferent: olderchildren:drowningandasphyxiationremaincommoncauses adults:moreoftenaresultofcardiacarrestorcerebrovasculardisease,withsecondaryhypoxemia/hypoperfusion1,3 ClinicalpresentationPatientstypicallypresenttohospitalfollowinganacuteevent(near-drowning,asphyxia,cardiac/respiratoryarrest).Theyareusuallyintubatedandhaveahistoryofprolongedresuscitation.PathologySevereglobalhypoxic-ischemicinjuryinadultshasahighlyvariablepatternofinvolvement.Mostoftenitinvolvesthecortexfairlydiffuselyalongwiththedeepgreymatterstructures,particularlybasalganglia,however,manyotherpatternsareobserved4: diffusecorticalanddeepgreymatterincludingperirolandiccortex(mostcommon) diffusecorticalanddeepgreymattersparingtheperirolandiccortex perirolandiccortex(primarymotor/sensory)andmedialoccipitallobes(primaryvisualcortex)  isolatedbasalganglia watersheddistribution diffusewhitematter cerebellum Thepredominanceofgreymatterinjuryisduetoitshighmetabolicrequirementforoxygenandglucosetosupplyalargenumberofsynapses.Thismakesgreymattermoresusceptibletohypoxic-ischemicinjury1. Italsocontainsmostofthedendriteswherepostsynapticglutamatereceptorsarelocated.Theyarethereforethesitesmostsusceptibletotheeffectsofglutamateexcitotoxicity(i.e.,damagetonervecellsbyexcessivestimulationbyglutamate).Neurologicinjuryiscausedbyhypoxia(secondarytocarbonmonoxidetoxicity,neardrowning,etc.)orinterruptionofbloodflow(usuallyfromcardiacarrestorhanging).Thereareoftensecondaryeffectsofhypoxiaoncardiacmyocytes,causingreducedcardiacoutputandcausingfurthersecondaryneurologicalinjury.Hypoxiaalonerarelycausessignificantbraindamageunlessitisprofoundandprolonged.Althoughcerebellarinjurycanbeseeninneonates,ittendstobemorecommoninolderpatients.Thereasonforthispredilectionisnotentirelyclear,butithasbeensuggestedthattherelativeimmaturityofPurkinjecells(whicharenormallyexquisitelysensitivetoischemicdamage)inneonatessomehowprotectsthecerebellarcortex1.RadiographicfeaturesCT diffuseedemawitheffacementoftheCSF-containingspaces decreasedcorticalgreymatterattenuationwithalossofnormalgrey-whitedifferentiation decreasedbilateralbasalgangliaattenuation reversalsign: reversalofthenormalCTattenuationofgreyandwhitematter,demonstratedwithinthefirst24hoursinasmallnumberofthesepatients ithasbeenproposedthatthisfindingisduetothedistensionofdeepmedullaryveinssecondarytopartialobstructionofvenousoutflowfromtheelevatedintracranialpressurecausedbydiffuseedema theresultisthatthecerebralwhitematterisofhigherattenuationthanthecorticalgreymatter whitecerebellumsign: hasbeendescribedinatleastonestudyasacomponentofthereversalsignandinwhichthereisdiffuseedemaandhypoattenuationofthecerebralhemisphereswithsparingofthecerebellumandbrainstem,resultinginapparenthighattenuationofthecerebellumandbrainstemrelativetothecerebralhemispheres linearhyperdensityoutliningthecortexaswellaslinearcorticalenhancement(laterandlessevidentsigns)correspondtocorticallaminarnecrosis pseudosubarachnoidhemorrhage: cerebraledemaandaresultantdecreaseinparenchymalattenuationandswellingandengorgementanddilatationofthesuperficialvenousstructuresduetoanincreasedintracranialpressureresultinthesubarachnoidspaceappearingfilledwithbloodthatappearshyperdense.  Boththereversalsignandthewhitecerebellumsignindicatesevereinjuryandapoorneurologicoutcome1,3.MRIDiffusion-weightedMRimagingistheearliestimagingmodalitytobecomepositive,usuallywithinthefirstfewhoursafterahypoxic-ischemiceventduetoearlycytotoxicedema.Duringthefirst24hours,theremayberestricteddiffusioninthecerebellarhemispheres,basalganglia,orcerebralcortex(inparticular,theperirolandicandoccipitalcortices)1,3.Thethalami,brainstemorhippocampimayalsobeinvolved.Diffusion-weightedimagingabnormalitiesusuallypseudo-normalizebytheendofthe1stweek1.Asinyoungerpatients,conventionalT1andT2weightedimagesareoftennormalordemonstrateonlyverysubtleabnormalities.Intheearlysubacuteperiod(24hoursto2weeks),conventionalT2weightedimagestypicallybecomepositiveandshowincreasedsignalintensityandswellingoftheinjuredgreymatterstructures1.T1hyperintensitiesindicatingcorticallaminarnecrosisbecomeevidentaftertwoweeks.Thishyperintensesignaldoesnotrepresenthemorrhage,anditisbelievedtobecausedbytheaccumulationofdenaturedproteinsindyingcells.ThishyperintensitycanalsobeseenwithinafewdaysonFLAIR3. Differentialdiagnosis molybdenumcofactordeficiency:veryrarelethalgeneticdiseaseSeealso neonatalhypoxic-ischemicencephalopathy carbonmonoxidepoisoning braindeath Quizquestions {"containerId":"expandableQuestionsContainer","displayRelatedArticles":true,"displayNextQuestion":true,"displaySkipQuestion":true,"articleId":14025,"mcqUrl":"https://radiopaedia.org/articles/hypoxic-ischaemic-encephalopathy-adults-and-children/questions/1598?lang=us"} References1.HuangBY,CastilloM.Hypoxic-ischemicbraininjury:imagingfindingsfrombirthtoadulthood.Radiographics.28(2):417-39.doi:10.1148/rg.282075066-Pubmedcitation2.HanBK,TowbinRB,Decourten-myersGet-al.ReversalsignonCT:effectofanoxic/ischemiccerebralinjuryinchildren.AJNRAmJNeuroradiol.10(6):1191-8.AJNRAmJNeuroradiol(abstract)-Pubmedcitation3.FaanARMD,ResnickSJ.PracticalNeuroimaginginStroke.Saunders.(2009)ISBN:0750675373.ReaditatGoogleBooks-FinditatAmazon4.MuttikkalT&WintermarkM.MRIPatternsofGlobalHypoxic-IschemicInjuryinAdults.JournalofNeuroradiology.2013;40(3):164-71.doi:10.1016/j.neurad.2012.08.002-Pubmed Promotedarticles(advertising) ADVERTISEMENT:Supportersseefewer/noads CasesandfiguresCase2Case2Dragheretoreorder.Case3:hypoxicbraininjuryCase3:hypoxicbraininjuryDragheretoreorder.Case4:globalHIECase4:globalHIEDragheretoreorder.Case5:neardrowning-DWICase5:neardrowning-DWIDragheretoreorder. Case6Case6Dragheretoreorder.Case7Case7Dragheretoreorder.Case8Case8Dragheretoreorder.Case9:corticallaminarnecrosisCase9:corticallaminarnecrosisDragheretoreorder.Case10Case10Dragheretoreorder.Case11:T1inversionrecoveryCase11:T1inversionrecoveryDragheretoreorder.Case12Case12Dragheretoreorder.Case13:lossofcaudateheaddensityCase13:lossofcaudateheaddensityDragheretoreorder.Case14Case14Dragheretoreorder.Case15:basalgangliaandvisualcortexCase15:basalgangliaandvisualcortexDragheretoreorder.Case15:motorcortexCase15:motorcortexDragheretoreorder.Case16Case16Dragheretoreorder.Case17:globalHIECase17:globalHIEDragheretoreorder.Case18Case18Dragheretoreorder.Case19:noncontrastCTCase19:noncontrastCTDragheretoreorder.Case19:T2MRICase19:T2MRIDragheretoreorder.Case20Case20Dragheretoreorder.ImagingdifferentialdiagnosisMetachromaticleukodystrophyMetachromaticleukodystrophyDragheretoreorder. Loadingmoreimages... 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