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Systemiceffectsofperinatalasphyxia
OfficialreprintfromUpToDate
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Systemiceffectsofperinatalasphyxia
Authors
LisaMAdcock,MD
asfixianeonatal
AnnRStark,MD

SectionEditor
LeonardEWeisman,MD

DeputyEditor
MelanieSKim,MD

Remove

Contributordisclosures
Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:Jul2016.|Thistopiclastupdated:Nov11,2014.
INTRODUCTIONPerinatalasphyxiaresultsfromcompromisedplacentalorpulmonarygasexchange.Thisdisorder
canleadtohypoxia(lackofoxygen)andhypercarbia(increasedcarbondioxidelevels)intheblood.Severehypoxia
resultsinanaerobicglycolysisandlacticacidproductionfirstintheperipheraltissues(muscleandheart)andthenin
thebrain.Ischemia(lackofsufficientbloodflowtoallorpartofanorgan)isbothacauseandaresultofhypoxia.
Hypoxiaandacidosiscandepressmyocardialfunction,leadingtohypotensionandischemia.Ischemiacanimpair
oxygendelivery,causingfurthercompromise,aswellasdisruptdeliveryofsubstrateandremovalofmetabolicand
respiratorybyproducts(eg,lacticacid,carbondioxide).
Thesystemiccomplicationsofperinatalasphyxiaarereviewedhere.Hypoxicischemicencephalopathy(HIE),
includingpathogenesis,pathology,diagnosis,prognosis,andtreatment,isdiscussedelsewhere.(See"Etiologyand
pathogenesisofneonatalencephalopathy"and"Clinicalfeatures,diagnosis,andtreatmentofneonatal
encephalopathy".)
TIMINGOFINJURYAsphyxiacanoccurbefore,during,orafterbirth.Basedonareviewofmultiplestudiesthat
haveexaminedthetemporalrelationshipbetweenobstetriceventsandneonataloutcomes,predominantlyhypoxic
ischemicencephalopathy(HIE)interminfants,theproportionofconditionsthatoccursineachtimeperiodcanbe
estimated[1].
Antepartumevents,suchasmaternalhypotensionortrauma,accountfor4to20percentofcases.Intrapartumevents,
suchasplacentalabruptionorumbilicalcordprolapse,areseenin56to80percent.Evidenceofintrapartum
disturbance(eg,meconiumstainedamnioticfluidorseverefetalheartrateabnormalities)occursin10to35percent,
usuallyinassociationwithanantenatalriskfactor,suchasdiabetesmellitus,preeclampsia,orintrauterinegrowth
restriction(IUGR).Inapproximately10percentofcases,apostnatalinsultoccurs,usuallycausedbysevere
cardiopulmonaryabnormalitiesorassociatedwithprematurity.
However,thetimingofinjuryoftenisdifficulttoestablishforanindividualinfant,inpartbecauseantepartumand
intrapartumeventsmaynotleadtosignsthataredetectableinthefetus.Inaddition,afetuswhohassufferedan
antepartuminsultmaybeatincreasedriskofincurringfurtherintrapartuminjury.
RISKFACTORSAvarietyofmaternal,obstetric,andneonatalconditionspredisposethefetusandnewbornto
asphyxia.Theseriskfactorsareassociatedwithreducedbloodflowand/oroxygenationtothetissues.Examplesof
conditionsoreventsinwhichperinatalasphyxiamayoccurarelistedbelow.
Antepartumconditions
Abnormalmaternaloxygenation(eg,severeanemia,cardiopulmonarydisease)
Inadequateplacentalperfusionand/orgasexchange(eg,maternalhypertensionorseverehypotension,placental
insufficiencycausedbyvasculardisease)
Congenitalinfectionoranomalies
Intrapartumevents
Interruptionofumbilicalcirculation(eg,trueknot,cordprolapse,cordavulsion)
Inadequateplacentalperfusionand/orgasexchange(eg,placentalabruption,uterinerupture,severematernal
hypotension,abnormaluterinecontractions)
Traumaticdelivery(eg,shoulderdystocia,difficultbreechextraction)
Abnormalmaternaloxygenation(eg,pulmonaryedema)
Postnataldisorders
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Persistentpulmonaryhypertensionofthenewborn(see"Persistentpulmonaryhypertensionofthenewborn")
Severecirculatoryinsufficiency(eg,acutebloodloss,septicshock)
Congenitalheartdisease(see"Identifyingnewbornswithcriticalcongenitalheartdisease"and"Cardiaccauses
ofcyanosisinthenewborn")
Infantsatincreasedriskforperinatalasphyxiaalsoincludethoseborntodiabeticmothersorwithsevereintrauterine
growthrestriction(IUGR).Indiabeticwomen,vasculardisease,manifestedbynephropathy,maycontributetothe
asfixianeonatal Remove
developmentoffetalhypoxiaandsubsequentperinatalasphyxia.InfantswithsevereIUGRwhoaredeprivedof
oxygenandnutrientsmayhaveadifficultcardiopulmonarytransitionwithperinatalasphyxia,meconiumaspiration,
and/orpersistentpulmonaryhypertension.(See"Infantofadiabeticmother"and"Infantswithfetal(intrauterine)growth
restriction".)
FetalbiophysicalprofileThefetalbiophysicalprofilescore(BPSorBPP)isanoninvasiveandaccuratemeansof
predictingthepresenceoffetalasphyxia.Thistestinvolvesthesonographicassessmentoffourdiscretebiophysical
variables(fetalmovement,fetaltone,fetalbreathing,amnioticfluidvolume),andtheresultsofnonstresstesting.A
compromisedfetustypicallyexhibitslossofaccelerationsofthefetalheartrate(FHR),decreasedbodymovementand
breathing,hypotonia,and,lessacutely,decreasedamnioticfluidvolume.Iffetalasphyxiaisdetected,appropriate
interventionmaypreventadversesequelae.(See"Thefetalbiophysicalprofile".)
ORGANINVOLVEMENTAllorganscanbeaffectedbyperinatalasphyxia.Hypoxicischemicencephalopathy
(HIE)isthemostwidelystudied,asithasthemostserioussequelae.Incontrasttothepersistenceofneurologic
injury,dysfunctionofotherorganscanresolvebeforehospitaldischarge[1].(See"Etiologyandpathogenesisof
neonatalencephalopathy"and"Clinicalfeatures,diagnosis,andtreatmentofneonatalencephalopathy",sectionon
'Prognosis'.)
Informationonthesystemiceffectsofperinatalasphyxiacanbeextractedfromdatafromthecontrolgroupsofclinical
trialsstudyingtheeffectsofhypothermiaontheoutcomeofHIE.Thescopeoforganinvolvementinperinatalasphyxia
variesamongstudiesdependinginpartuponthedefinitionsusedforasphyxia,asdemonstratedbythefollowingtrials
ininfantswithgestationalage36weeks.
Inthefirsttrial,inclusioncriteriawereApgarscoreoffiveorless,needforcontinuedresuscitation,orsevereacidosis
(umbilicalcordbloodpHlessthan7orabasedeficitof16mmol/Lorgreater),andevidenceofmoderatetosevereHIE
byneurologicassessment(eg,lethargy,stupor,coma,hypotonia,orabnormalreflexes)[2].Systemiceffectsandtheir
incidencesinthecontrolgroupduringthehospitalcourseincludedthefollowing:

Respiratorydistress(78percent)
Abnormalrenalfunction(70percent)
Elevatedliverfunctionstudies(53percent)
Hypotension(52percent)
Hypocalcemia(43percent)
Prolongedcoagulationtimes(42percent),plateletcountbelow100,000/microL,coagulopathy(14percent)
Metabolicacidosis(23percent)
Hypoglycemia(17percent)

Inthesecondtrial,inclusioncriteriaincludedsevereacidosis(cordbloodpHlessthan7,orabasedeficit16mmol/L)
andevidenceofHIEbyneurologicassessment[3].Inthisstudy,theincidenceofsystemiceffectsduringthehospital
courseinthecontrolgroupwaslowerthaninthepreviouslydiscussedtrial.

Hypotensionrequiringinotropicsupport(33percent)
Persistentpulmonaryhypertension(22percent)
Oliguria(22percent)andanuria(4percent)
Hepaticdysfunction(15percent)
Hypoglycemia(15percent)andhypocalcemia(19percent)
Disseminatedintravascularcoagulopathy(11percent)

Inthethirdtrial,inclusioncriteriaincludedtenminuteApgarscore5or10minutesofresuscitation,severeacidosis
(cord,arterialorcapillarypH<7,orabasedeficit16mmol/L),andmoderatetosevereencephalopathy(definedas
lethargy,stupor,orcoma),whichwereaccompaniedbyhypotonia,abnormalreflexes,absent/weaksuck,clinical
seizures,oranabnormalamplitudeintegratedelectroencephalogram(aEEG)[4].Systemiceffectsandtheirincidences
inthecontrolgroupincludedthefollowing:
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Persistenthypotension(83percent)
Intracranialhemorrhage(50percent)
Abnormalcoagulation(45percent)
Pulmonaryhypertension(6percent)
Pneumonia(3percent)
Airleak(2percent)
Remove
asfixianeonatal
Pulmonaryhemorrhage(2percent)
Arrhythmia(2percent)
Reportedvariationsinsystemiceffectsofasphyxiamightberelatedtochangingpracticesinthemanagementofthese
infants(evenwhencontrollingforhypothermia)aswellasdifferencesinthecriteriausedtodefineasphyxia.
ENCEPHALOPATHYHypoxicischemicencephalopathy(HIE)isthemostseriouscomplicationofperinatal
asphyxia,andtheneurologicsequelaeoftenpersist[1].IssuesrelatedtoHIEarediscussedseparately.(See"Etiology
andpathogenesisofneonatalencephalopathy"and"Clinicalfeatures,diagnosis,andtreatmentofneonatal
encephalopathy".)
MYOCARDIALDYSFUNCTIONAsphyxiamaycausemyocardialischemia,whichusuallyistransient,butmay
rarelyresultincardiogenicshockanddeath.Thisconditiontypicallypresentsasimpairedmyocardialcontractility,
decreasedcardiacoutput,andtricuspidinsufficiency,althoughsomeinfantshavesignsofrespiratorydistress,heart
failure,orshock[5].
ClinicalfeaturesPhysicalexaminationinaffectedpatientsshowstachypnea,tachycardia,andhepatomegaly
consistentwithheartfailure.Systemicbloodpressuremaybelowandcapillaryrefilldelayed,reflectingreduced
peripheralperfusion.However,normalbloodpressurecanbepresentininfantswithpoorcardiacoutput,a
phenomenonrelatedtoelevatedperipheralvascularresistance[6].Manyinfantshaveasystolicmurmurthatisloudest
atthelowerleftsternalborder,typicaloftricuspidinsufficiency.
DiagnosisThechestradiographtypicallyshowscardiomegaly.Theappearanceofpulmonarybloodflowdepends
uponwhethertheleftorrightventricleispredominantlyaffected.Ifleftheartfailurepredominates,thelungfields
usuallyarediffuselyhazy,withpulmonaryvenouscongestion.Iftherightsideismoreaffected,pulmonarybloodflow
maybereducedbyrighttoleftatrialshunting,andpulmonarycongestionmaybeabsent.
TheECGmayshowsignsofischemia,withdiffuseSTTwavechanges.ThemostcommonfindingisSTdepression
inthemidprecordium,withpersistentlyinvertedTwavesovertheleftprecordium.ECGabnormalitiesstillpresentat72
hoursoflifemaybeassociatedwithanincreasedriskofmortality.
Thediagnosisofmyocardialdysfunctionmaybeconfirmedbyechocardiographicfindingsofdecreasedleftventricular
ejectionfractionanddecreasedshorteningfraction[7].Echocardiography,whichshouldbeobtainedinallinfantsin
whommyocardialdysfunctionissuspected,isessentialtoexcludestructuralheartdisease.Italsodistinguishesright
toleftatrialshuntingcausedbymyocardialdysfunctionduetopersistentpulmonaryhypertensionofthenewbornfrom
asphyxia,whichisimportantsincemanagementdiffers.(See"Persistentpulmonaryhypertensionofthenewborn".)
Functionalechocardiographyandotheradvancedechocardiographictechniques(myocardialperformanceindexorTei
index)appeartobemoresensitivethanroutineechocardiographymeasurementsinidentifyingcardiacimpairmentin
asphyxiatednewborns,buttheirrelationtolongtermoutcomesremainsuncertain[6,8].
Nolaboratorytestreliablydetectscardiacdamageinperinatalasphyxia.LevelsofcreatininekinaseanditsMB
fractionincordbloodorvenoussamplesinthefirst12hoursafterbirthdonotdistinguishinfantswithandwithout
asphyxiaandarenotspecificforcardiacdamage[9,10].Neonatallevelsmaybeelevatedinthefirstdayoflifedueto
gestation,weight,andtypeofdelivery[8].However,elevationofcardiactroponinTandIlevelsisspecificforcardiac
dysfunction,occursduringthefirst12hoursofage,andappearstocorrelatewiththeseverityofasphyxiaand
neurodevelopmentat18months[7,1013].Inonestudy,troponinTlevelsinasphyxiatedinfantswerenotonly
significantlyhigherthanincontrolinfants(0.17versus0.03mcg/L),butatroponin0.15mcg/Lpredictedmortality(100
percentspecific,70percentsensitive)[8].
ManagementManagementissupportive.Patientswithrespiratoryfailurerequiremechanicalventilation.Ventilator
pressuresshouldbeaslowaspossibletominimizelimitationstovenousreturnandcardiacoutput.Metabolic
abnormalities,suchashypoglycemia,hypocalcemia,andacidosis,shouldbecorrected.Fluidsarerestricted,and
diuresisispromoted.Inotropicagentsusuallyareneeded[5].Severelyaffectedpatientsmayrequireafterload
reduction.
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RENALDYSFUNCTIONRenaldysfunctionoftenaccompaniesperinatalasphyxia.Thepresentationandcourse
dependupontheseverityanddurationofthehypoxicischemicevent.Severeasphyxiaresultsindiffusetubular
dysfunctionwithimpairedreabsorptionofsodiumandwateranddecreasedglomerularfiltrationrate[14].Amilderinsult
maycauseatransientlossofrenalconcentratingability.
DiagnosisAcuterenalfailure,oracutekidneyinjury(AKI),canbedifficulttodiagnosefollowingasphyxiafora
varietyofreasons,includingthelackofaconsensusdefinition.AKIshouldbesuspectediftheserumcreatinine
concentrationisincreased(>1to1.5mg/dL,88to133micromol/L)and/ortheurineoutputisreduced(<0.5mL/kgper
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hour).However,renalfailureafterperinatalasphyxiamaybenonoliguricinupto50percentofneonates,andserum
creatininelevelscanbehighlyvariableinthefirstdaysoflife[15].
Inonereport,renalfunctionwasevaluatedin66asphyxiatedinfantswithgestationalage36weeksandfiveminute
Apgarscores6[16].Acuterenalfailure,definedasserumcreatininelevel>1.5mg/dL(133micromol/L),occurredin
20of33infantswhowereconsideredtohavesevereasphyxia.Ofthese,renalfailurewasnonoliguric,oliguric,or
anuricin60,25,and15percent,respectively.Inanotherprospectivecasecontrolledstudyof70asphyxiatedinfants,
33patients(47percent)exhibitedrenalfailure,ofwhich7wereoliguricand26werenonoliguric[17].
Thediagnosis,evaluation,andmanagementofAKIarediscussedseparately.(See"Acutekidneyinjury(acuterenal
failure)inthenewborn".)
OutcomeInformationislimitedontheoutcomeofrenaldysfunctionafterperinatalasphyxia.Theprognosisof
patientswithintrinsicrenaldiseasedependsupontheextentoftheinjury.Ininfantswithasphyxia,urinaryexcretionof
proteinanduricacidareelevatedandmaycorrelatewithdiseaseseverityandshorttermoutcome[18].Oliguricrenal
dysfunctionisassociatedwithgreatermortalitythannonoliguricAKI[15,17].(See"Acutekidneyinjury(acuterenal
failure)inthenewborn"and"Acutekidneyinjury(acuterenalfailure)inthenewborn",sectionon'Prognosis'.)
PULMONARYDISORDERSSeveralpulmonarydisordersareassociatedwithperinatalasphyxia.Theyinclude
pulmonaryedemaandacuterespiratorydistresssyndrome,whicharepresentedhere,andmeconiumaspiration
syndromeandpersistentpulmonaryhypertensionofthenewborn(PPHN),whicharediscussedseparately.(See
"Clinicalfeaturesanddiagnosisofmeconiumaspirationsyndrome"and"Persistentpulmonaryhypertensionofthe
newborn".)
PulmonaryedemaPulmonaryedemamayoccurduetomyocardialdysfunction.Infantshavesignsofrespiratory
distress,includingcyanosis,tachypnea,nasalflaring,andgrunting.Signsofcardiacdysfunctiontypicallyarepresent.
Thechestradiographshowsanenlargedheart,normaltoincreasedlungvolume,andprominenthilarvascular
markings.(See'Myocardialdysfunction'above.)
Infantswithrespiratoryfailuremayrequireoxygensupplementationand/ormechanicalventilation,andtreatmentofthe
underlyingmyocardialdysfunction.Thedisorderresolvesinafewdaysinmostcases[19].Occasionalinfantsdevelop
hemorrhagicpulmonaryedema.
AcuterespiratorydistresssyndromeSomeinfantsdevelopsevererespiratorydistressafterasphyxiathatisnot
associatedwithmyocardialdysfunction,althoughitmayoccurwithPPHN[20,21].Thisconditionissimilartoacute
respiratorydistresssyndrome(ARDS)thatoccursinolderchildrenoradults.Themechanismappearstobeincreased
pulmonarycapillarypermeabilitytoplasmaproteins,whichleadstoinactivationofsurfactant.
Infantspresentwithsignsofrespiratorydistressandcyanosis.Theradiographicappearanceissimilartorespiratory
distresssyndromeinprematureinfants,withreducedlungvolumesanddiffusebilateralalveolaropacificationwithair
bronchograms[20,21].Treatmentissupportive,withsupplementaloxygenand/ormechanicalventilation,using
increasedlevelsofpositiveendexpiratorypressure.Someinfantsmaybenefitfromsurfactanttreatment,althoughthis
hasnotbeenwellstudied[22].
GASTROINTESTINALDYSFUNCTIONGastrointestinalcomplicationsafterperinatalasphyxiaincludefeeding
intolerance,necrotizingenterocolitis,andhepaticdysfunction.
FeedingintoleranceFeedingintolerancemaypresentasabdominaldistension,delayedgastricemptying,and
gagging.Theseabnormalitiesappeartobecausedbytransientdisturbancesinintestinalmotoractivitypatterns,which
mayresultfromlossofneuralregulationand/orinhibitionofmotorcontrol[23].
NecrotizingenterocolitisAlterationsinintestinalbloodflowcanfollowperinatalasphyxiaandpersistforupto
threedays[24].Thesechangesmayleadtoischemiaandsubsequentdevelopmentofnecrotizingenterocolitis(NEC).
TheincidenceofNECincreaseswithdecreasinggestationalage.NECtypicallypresentsafteroneweekofagein
prematureinfants,andinthefirstfewdaysafterbirthinterminfants[25].Signsincludebloodystools,oftenwith
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mucus.(See"Clinicalfeaturesanddiagnosisofnecrotizingenterocolitisinnewborns"and"Pathologyand
pathogenesisofnecrotizingenterocolitisinnewborns".)
ManagementAfterperinatalasphyxia,feedingsoftenaredelayedforfivetosevendays,oruntilintestinal
motilityappearsnormalandstoolscontainnoblood.However,theefficacyofthisapproachinpreventingNEChasnot
beenevaluated.
HepaticdysfunctionIschemiacaninterferewithsynthetic,excretory,anddetoxifyingfunctionsoftheliver.These
asfixianeonatal Remove
functionsshouldbeassessed.
Transaminasesfrequentlyareelevatedforseveraldaysafterbirth[26],andreducedsynthesisofclottingfactorsmay
resultinprolongationofprothrombinandactivatedpartialthromboplastintimes,sometimesassociatedwithclinical
bleeding.Severelyaffectedinfantsmaydevelophypoglycemia,andserumglucosevaluesshouldbemonitored.
Cholestaticjaundiceorhyperammonemiamayoccur.
HEMATOLOGICDISORDERSInfantswithperinatalasphyxiamayhavebleedingdisorders.Causesinclude
disseminatedintravascularcoagulation(DIC),impairedsynthesisofclottingfactors,andthrombocytopenia.In
particular,perinatalasphyxiaisanassociatedriskfactorforthrombocytopenia[3,27,28].Inonestudyofinfantsgreater
thanorequalto35weeksgestationadmittedtotheneonatalintensivecareunit(NICU)withasphyxia(cordbloodpH
<6.99and/orbasedeficitof16mmol/Lormore),affectedpatientsweremorelikelytohavethrombocytopenia(defined
asaplateletcountlessthan150,000/microL)comparedwithmatchedcontrols(31versus5percent)[28].The
underlyingmechanismremainsuncertain[28,29].(See"Disseminatedintravascularcoagulationininfantsand
children",sectionon'Neonates'.)
Theplateletcountshouldbemonitored,andpatientswiththrombocytopeniaorclinicalbleedingshouldbeevaluatedfor
DIC.Plateletsandfreshfrozenplasmacanbeprovidedasneeded.(See"Disseminatedintravascularcoagulationin
infantsandchildren",sectionon'Neonates'and"Disseminatedintravascularcoagulationininfantsandchildren",
sectionon'Treatment'.)
SUMMARYANDRECOMMENDATIONSPerinatalasphyxiaresultsfromcompromisedplacentalorpulmonarygas
exchange,whichmayresultinneonatalhypoxiaandtissue/organinjury.
Avarietyofmaternal,obstetric,andneonatalconditionspredisposethefetusandnewborntoasphyxia,which
canoccurbefore,during,orafterbirth.(See'Timingofinjury'aboveand'Riskfactors'above.)
AntepartumfactorsMaternalconditions(eg,anemia,hypertension,diabetes,severehypotension,or
trauma),placentalinsufficiency,congenitalinfectionoranomalies,orsevereintrauterinegrowthrestriction.
IntrapartumconditionsTraumaticdeliveriesorabnormalitiesofumbilicalcirculation,placentalperfusion,or
maternaloxygenation.
Perinatalasphyxiacanaffectallorgans.(See'Organinvolvement'above.)
Hypoxicischemicencephalopathyisthemostseriouscomplicationofperinatalasphyxia,andneurologic
sequelaemaybepersistent.(See"Etiologyandpathogenesisofneonatalencephalopathy"and"Clinical
features,diagnosis,andtreatmentofneonatalencephalopathy".)
Asphyxiamaycausemyocardialischemia,whichusuallyistransient,butmayrarelyresultincardiogenic
shockanddeath.Myocardialischemiatypicallypresentsasimpairedmyocardialcontractility,decreased
cardiacoutput,andtricuspidinsufficiency,andinseverecases,respiratorydistress,heartfailure,orshock.
Thediagnosisofmyocardialdysfunctionisconfirmedbyechocardiography.Inaffectedneonates,the
managementissupportivewiththeuseofmechanicalventilationinpatientswithrespiratoryfailure,
correctionofmetabolicabnormalities,theuseofinotropicagentanddiuretics,andfluidrestriction.(See
'Myocardialdysfunction'above.)
Acutekidneyinjury(AKI)oftenaccompaniesperinatalasphyxia.ThepresentationandcourseofAKI
dependupontheseverityanddurationofthehypoxicischemicevent.Severeasphyxiaresultsindiffuse
tubulardysfunctionwithimpairedreabsorptionofsodiumandwateranddecreasedglomerularfiltrationrate.
Amilderinsultmaycauseonlyatransientlossofrenalconcentratingability.AKIshouldbesuspectedifthe
serumcreatinineconcentrationincreasesand/ortheurineoutputisreduced.(See'Renaldysfunction'above
and"Acutekidneyinjury(acuterenalfailure)inthenewborn".)
Severalpulmonarydisordersareassociatedwithperinatalasphyxiaincludingpulmonaryedema,acute
respiratorydistresssyndrome,meconiumaspirationsyndrome,andpersistentpulmonaryhypertensionof
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thenewborn.(See'Pulmonarydisorders'above.)
Gastrointestinalcomplicationsafterperinatalasphyxiaincludefeedingintolerance,necrotizingenterocolitis,
andhepaticdysfunction.(See'Gastrointestinaldysfunction'above.)
Infantswithperinatalasphyxiaareatincreasedriskforbleedingdisorders,duetothrombocytopenia,
reducedsynthesisofclottingfactors,anddisseminatedintravascularcoagulation.(See'Hematologic
disorders'above.)

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