PregnancyInducedHypertensionProf.DuanTao,M.D.Shanghai1stMaternityandInfantHospitalPregnancyInducedHypertensionDefinition：ToxemiaGestosisPreeclampsia-EclampsiaPregnancyInducedHypertensionEPHSyndromeTheoriesaboutcauses

StillUnknown:Utero-placentalischemia:Neuro-endocrinology：PGI2/TXA2Immunology-hereditary：ChronicDIC：TheoryPrimipaternity:

RobillardPY.EurJObstetGynecolReprodBiol,1999.Dekker:392multiparousPIHwomen,22-25%havenewpartners,3.4%incontrolgroup.MyTheoryTriggerofftheory：TheopenShieldinChicagoLying–InHospitalDiagnosisHypertensionofpregnancy:BP

140/90mmHgALONEorWITHmildoedema(after20wksofgestation)DiagnosisAmericanWayPreeclampsiaI)Mildpreeclampsia

BP:

140/90mmHg,but<160/110mmHg,

Edema:mild

Proteinuria:Trace/1+DiagnosisII)

Severepreeclampsia

BP:

160/110mmHg

Edema:marked

Proteinuria:2+ormore

Diagnosis

Withheadache,visualdisturbances,abdominalpain,oliguria,thrombocytopenia,bilirubin,liverenzymes,

creatinine,foetalgrowthretardation,pulmonaryoedemaEclampsia

SeverepreeclamsiawithCONVULSIONDiagnosisChineseway:Mildpreeclampsia

BP:

140/90mmHg,but<150/100mmHg,orwithanelevationof30/15mmHg

Edema:and/or

Proteinuria:TraceDiagnosisModeratepreeclampsia

BP:

150/100mmHg,but<160/110mmHg,Edema:and/or

Proteinuria:1+DiagnosisSeverepreeclampsia

BP:

160/110mmHg

Edema:and/or

Proteinuria:2+~4+PathophysiologyVasospasm“haemorrage&necrosis”endorganchangesReducedplacentalperfusion

IUGR&foetaldeathIncreasedcardiacoutputIncreasedextracellularfluidvolumePathophysiologyHaemoconcentrationHypercoagulability-DIC-reducedclottingfactors-bleedingReducedGFRoligouria-anuriaNoelectrolyticimbalancePathophisiologySeriousComplications:HellpsyndromeAbruptioplacentaePulmonaryoedemaAcuterenalfailurePathophysiologySeriousComplications:CerebralhaemorrhageVisualdisturbances&blindnessHepaticruptureElectrolyticimbalancePostpartumcollapseDifferential

DiagnosisChronichypertensionessential/renal/others

Mostlyobese,elderly,parous&likelytobeonantihypertensivedrugsUsuallypreexists/appearsearly(<20wks)&persistspostpartumEndorgandamagemaybepresentDifferential

DiagnosisDiagnosticconfusion:10of24(42%)womeninitiallythoughttohavehadeclampsiawerelaterfoundtohavehadothercerebro-vascularpathology-hypertensiveencephalopathy,cerebralhemorrhage,orcerebralinfarction.Suspectedeclampsia,unresponsivetoMgso4therapywarrantsapromptneuroimagingstudy.AmJObstetGynecol.1997;176:1139-1148Cure/preventprogression-ClosemonitoringReducebloodpressure-tatrget-140/90mmHgPromotefoetalmaturityProlongpregnancy(34-36weeks)ToachievefoetalmaturityterminationDelivery-bestday,bestway&bestplacePrevent/managecomplicationsOBJECTIVESOFMANAGEMENTLookforappearanceofominousfeaturesDaily-recordb.P4times,monitorurineoutput&testforproteinuriaquali./QuantAlt.Day-bodyweightEvery4thday-uricacid,plateletcount,liverfunctionWeekly-creatinineMATERNALMONITORINGDaily-clinicalfoetalmonitoring-fhs,fundalht.Abdominalgirth,amnioticfluid,foetalmovementcount,C.T.GUltrasound-onadmission&then3weeklyforfoetalbiophysicalparameters,placentaandamnioticfluidvolumeDopllerultrasonographyforplacentalbloodflowvelocityevery4thdayL/sratioformaturityFOETALMONITORINGAnticonvulsionThehistoryofMgSO4：Magnesiumsulfateinthetreatmentofeclampticconvulsion: 1)Itwasfirstusedtocontroltetanicconvulsionsinearly1900s.ThemodernobstetricuseofMgso4wasfirstpopularizedbyPritchard:IM10gload,then5g/4hrs(1955)Anticonvulsion2)Zuspanrecommendedcontinuousintravenousinfusion:4gload,then1g/hr(1966) (ThisregimenwasusedintheUnitedStatesbefore1980s,andiscurrentlyusedinEuropeandSouthAfrica,itwasfoundtoproducelevelslessthan4.8mg/dlinthemajorityofwomentreated).Anticonvulsion3)SibaimodifiedIVinfusion:6gload,then2g/hr(1981)4)PritchardrecommendedthattheappropriateserumlevelsofMgso4fortreatmentofeclampticconvulsionswere3.5-7Meq/L(or4.2-8.4mg/dl)(1979)Anticonvulsion5)Magnesiumlevelmg/dl=1.2xmagnesiumlevelMeq/L6)Ifthepatientsweretreatedaccordingtotherecommendedregimen,10%oftheeclampticseizureswillrecurAnticonvulsionTheusageofMgSO4：1)15-22.5g/d1.5-2g/hr2)I.M.VsI.V.3)I.V./day，I.M./night

25%MgSO420ml+2%Lidocaine2ml4)TheeffectofMgSO4：BP/Proteinuria/EdemaAttentions：patellarreflex/respiratory/urineoutputSedativesDiazepam：10mgIVPethedine:100mgChloropramazine:50mgAntihypertensivesApresoline：αblocker/25mg+5%GS500mlCaptopril：ACEIIblocker，bannedbecauseoffetaldamage.Nifedipine：Calciumchannelblocker,quick/shortlasting,10mgq6h.AntihypertensivesLabetalol：αandβblocker,

50-100mg+5%GS500mlNitroprussidesodium：Verypotent,butwithtoxiceffect.

50mg+5%GS500mlRigitine：α-blocker，firstchoiceforPIHpatientswithcardiacdisease.

10-40mg+5%GS500mlCaveats

for

antihypertensive

therapy1)Thereisgreatindividualvariabilityinresponsetothesedrugs,andtheydonotlowerbloodpressurepredictably,precisely,orsmoothly.2)Loweringbloodpressuretoorapidlyorexcessivelymayproducefetaldistress,particularlyinthesettingofIUGRoranabnormalfetalheartratetracing.Caveats

for

antihypertensive

therapy3)Epiduralanesthesiawilllowerthebloodpressureapproximately15%,frequentlyabrogatingtheneedforantihypertensivemedication.4)Thegravidawithchronicrenalinsufficiencyhashypertensionthatismoredifficulttocontrol,inpartduetovolumeexpansion.Caveats

for

antihypertensive

therapy5)Severehypertensionwithoutproteinuriashouldpromptaurinescreenforcocaine.6)Withprolongedunconsciousness,papilledema,lateralizingsigns,seizuresonmagnesiumsulfate,orseizuresmorethan48hoursafterdelivery,aCTscanshouldbeperformedtoruleoutintracranialhemorrhage.Volume

ExpansionChoicebetweencrystalloidandcolloid.DiuresisFurosemide:10-20mg/ivMannitol：20%250ml，within15’-20’Management

of

EclampsiaMafiaLookprotocolformanagingeclampsia

1）Convulsionsarecontrolledorpreventedwithaloadingdoseof6gMgso4in100ml5%dextroseinRinger’slactatedsolution,givenover15minutes,followedbyamaintenancedoseof2g/hr,thedoseisadjustedaccordingtopatellarreflexesandurineoutputintheprevious4-hourperiod.Management

of

Eclampsia2)Diuretics,plasmavolumeexpanders,andinvasivehemodymnamicmonitoringarenotused.3)Inductionand/ordeliveryisinitiatedwithin4hoursaftermaternalstabilization.Management

of

Eclampsia4)Mgso4iscontinuedfor24hrsafterdeliveryor,ifpostpartum,24hrsafterthelastconvulsion.Insomecases,theinfusionmaybecontinuedforlonger. *WitlinandSibai.Hypertensivediseasesinpregnancy.In:Medicineofthefetusandmother,2nded.ReeceEA,HobbinsJ(eds).Philadelphia,PA.Lippincott-Raven,1998,997-1020.HintDAMMCALDD:DiazepamA:ApresolineM:MgSO4M:MannitolC:ChlorpremazineA:AntibioticsL:LasixD:Digitalis

1)at36weeks:-inallcontrolledcases2)after32weeks:-forfoetalsalvageDecreasedfoetalmovementSevereIUGRwitholigohydramniosLatedecelerationwithpoorvariabilityReversedumbilicaldiastolicbloodflowDELIVERYTREATMENTBESTDAY-WHEN?DELIVERYTREATMENTBESTDAY-WHEN?3)anytime:-ifprogressiveinspiteof

treatment,when-Bp>160/100mmHgUrineoutput<400ml/24hoursPlateletcount<50,000/cmmSerumcreatinineincreasesprogressivelyLdh>1000iu/l1)Inductionwithoxytocin:-after36weeksIffoetalconditionisgoodCervixisfavourable/cerviprimeApplicationofforceps/ventouseDELIVERYTREATMENTBESTWAY-HOW?DELIVERYTREATMENTBESTWAY-HOW?

2)ByC-S:Ifterminationbefore36weeksIncasesofmaternal/fotaljeopardyAnaesthesia-general/epidural/spinal–betterlefttoanaesthetistDELIVERYTREATMENTBestplace-where?High-riskpregnancyunit/tertiaryhospital/wellequippedhospital2)neonatalcare:-PresenceofpaediatricianisamustIncubatorishelpfulPOSTPARTUMTREATMENT1)PPH:-bepreparedtofaceitUterineatony/DIC-FDP/bleedingdisorderOxytocics/uterinemassage/packing/uterinearteryligation/internaliliacarteryligation/hysterectomyPOSTPARTUMTREATMENT3)Drugs:-Judicioususeofantihypertensives,ivfluids,diuretics,&diazepaminthefirst48hours4)Followupfor6weeksTORCHSyndromeWhyTORCH?T:ToxoplasmaO:Others(Treponemapallidum,syphilis)R:RubellaVirusC:CytomegaloVirusH:HerpesSimplexVirusTORCHSyndromeCharacteristics:Mother---Minimal/Flu-likeFetus---Fatal/malformatiomRiskPopulation:WayoffetalInfection:1.Intrauterineinfection2.Birthcanalinfection3.PostpartuminfectionTORCHSyndromeEffectonthemother:minimalEffectonthefetus:1.Toxoplasma:Abortion,fetaldeath,cranialmalformation,neuraldysfunction.2.Others(Treponemapallidum,syphilis):Abort