妊娠期高血压疾病课件

HypertensiveDisorders

inPregnancyTengYinChengShanghaiJiaotongUniversityAffiliatedSixthPeople'sHospital,DeptofObs&GynContentsEtiology&PathogenesisClinicalfeaturesPhysiopathologyClassificationDiagnosisManagement234561IncidenceandRiskFactorsIncidenceCommonlyabout5percentMarkedlyinfluencedbyparityRelatedtoraceandethnicity—AgeneticpredispositionMainRiskFactorsNulliparous(初产妇)MultiplepregnancyHistoryofchronichypertensionMaternalageover35yearsObesityLowersocioeconomicstatus…EtiologyandPathogenesisNormal:vesselremodeling(血管重铸)ofthedeciduaandmyometriumtransformingintolarge-capacitance,low-resistancevesselsPreeclampsia:incompleteremodelinglimitedtothe

superficialdeciduamyometrialsegmentsremain

narrowFaultyPlacentation(胎盘形成不良)---StageIPathogenesisofpreeclampsiaGeneticfactorsimmunologicalfactorsMaternalvasculardiseaseEnvironmentalfactorsReduceduteroplacentalperfusionFaultyplacentationEndothelialactivationSystemicvasculardysfunctionCapillaryleakvasospasmHypertensionCerebraledema(eclampsia)EdemaProteinuriaCoagulationabnormalities(HELLP)Fetalgrowthrestriction(FGR)Physiopathology

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Basicchange:SystemVasospasm（全身小动脉痉挛）Hemorrhage,edema,hyperemia充血,thrombosis

Visualdisturbances:blurredvision,blindness,retinaldetachment（视网膜脱落）Reducedrenalperfusionandglomerularfiltration肾小球滤过率

Proteinuria;increaseduricacid;oliguriaIschemia,edema→elevatedserumtransaminases(ALT,AST,AKP..);jaundice（黄疸）Subcapsularhematoma(肝包膜下出血)orhepaticrupturePhysiopathologyPeripheralvascularresistance↑,cardiacoutput↓(低排高阻),bloodpressure↑Cardiacfailure(心力衰竭),pulmonaryedema(肺水肿)

Bloodvolume↓,hematocrit↑(HCT,红细胞压积)

,bloodconcentration

Hypercoagulability(高凝),thrombocytopenia(血小板减少)PlacentalischemiaandhypoxiaHigh-resistancecircuitwithdecreasedbloodFetalgrowthrestriction,fetaldistress(胎儿窘迫)WHATLINKSSTAGE

1&2?Theoryexploration:Genetics/AbnormallipidmetabolismEndocrinedysfunctionInflammationNotallwomenwithreducedplacentalperfusiondeveloppreeclampsia…

Whatlinksstages1and2?Reducedplacentalperfusionmustinteractwithmaternalfactorstoresultinpreeclampsia.Stage1???Stage2Roberts,J.M.,GammillH.S.(2005)Diversemanifestationsarepossible:maternalandfetal/placentalfactorsmayvaryinproportion.

Inawomanwithmany

predisposingfactors,evenaminorreductioninplacentalperfusionissufficientforstage2todevelop.Inawomanwithfewpredisposingfactors,aprofoundreductioninplacentalperfusionmayberequiredforpreeclampsiatodevelop.

Roberts,J.M.,GammillH.S.(2005)PredisposingfactorsReducedplacentalperfusionMicrosoftOffice2000Whatdoweknow?Weknowthatabnormalitiesinlipidmetabolismhaveageneticbasis.Wehavelearnedthatpreeclampsiaischaracterizedbyprofoundlipidabnormalitiessuchashypertriglyceridemia…Gratacos,E.(2000)MicrosoftOffice2000Couldabnormallipidmetabolismbeageneticfactorlinkingthestagesofpreeclampsia?

Stage1Stage2AbnormallipidmetabolismPreeclampsiaischaracterizedbymetabolicabnormalitiessimilartothosepresentinatherosclerosis:HypertriglyceridemiaReducedHDLcholesterolPredominanceofsmall-denseLDLcholesterolwhichhaveanincreasedpotentialtocauseendothelialcelldamageascomparedtolarger,morebuoyantLDL’s.GratacosE.,2000.Mostofthesuggestedlinkagescouldcontributetoorbestimulatedbyoxidativestress.Oxidativestressisproposedasrelevanttomanydiseases.Evidencesupportsthepresenceofoxidativestressinpreeclampsia:ProteinproductsofoxidativestresspresentinmaternalandfetaltissuesAntibodiestooxidativelymodifiedLDL’spresentinmaternalandfetaltissuesConcentrationsofcertainantioxidantsreducedinpreeclampticwomen.

Roberts,J.M.,GammillH.S.(2005)Insummary:Hypertriglyceridemiaandpredominanceofsmall-denseLDL’spriortopregnancycouldbeonepredisposingfactorfordevelopingpreeclampsia.Oxidativestressandinflammation maytriggerthematernaldisease.GratacosE.,(2000)MicrosoftOffice2000CouldendocrinedysfunctionbeafactorlinkingStage1andStage2?Stage1Stage2EndocrinedysfunctionStudieshaverepeatedlydemonstratedthatmetabolicabnormalitiesprecedetheclinicalsignsofpreeclampsia:InsulinresistanceandassociatedhyperinsulinemiaGlucoseintoleranceHypertriglyceridemiaThissuggeststhatinsulinresistanceanddyslipidemiamaybefactorsinvolvedinthedevelopmentofpreeclampsia.Innes,etal.(2005)Similaritiesbetweentheriskfactorsforpreeclampsiaandcardiovasculardiseaseinclude:InsulinresistanceDyslipidemia-decreasedHDLlevelsand elevatedtriglyceridelevelsTheseriskfactorsarethoughttoplayacausalroleinthedevelopmentofendothelialdysfunction,acharacteristicfeatureofpreeclampsiaandcardiovasculardisease.Innes,etal.(2005)“Preeclampsiaisassociatedwithanexcessiveinflammatoryresponsecomparedwithnormalpregnancy.”InastudydonebyBraekke,et.al(2005)inflammatorymarkers(calprotectin,CRP)wereevaluatedinmaternalandfetalserumandamnioticfluid.Braekke,K.,Holthe,Ml,Harsem,N.,Fagerhol,M.,Staff,A.,2005InflammatoryMarkers:Calprotectin:IsaproteinreleasedbyactivatedneutrophilsC-reactiveprotein(CRP):IsaproteinproducedbytheliverProductionisstimulatedbyinflammatorycytokinesBraekke,K.et.al.(2005)MicrosoftOffice2000CalprotectinandC-reactiveprotein(CRP),markersofinflammation,areelevatedinpreeclampsia.Theconcentrationofcalprotectininthematernalplasmaofpreeclampticwomenwashigherthaninthecontrolgroup(normalpregnantwomen).NostatisticallysignificantdifferenceincalprotectinlevelswasnotedbetweenwomenwithmildandseverepreeclampsiaBraekke,K.etal.(2005)C-reactiveprotein:Hasbeenusedtoevaluatelow-gradeinflammationasacardiovascularriskfactor

Braekkeetal.2005MicrosoftOffice2000CRPlevelsinthematernalplasmaofpregnantwomen:Correspondtoalow-gradeinflammationinpreeclampsiaandinnormalpregnancy.

Braekkeetal.2005MicrosoftOffice2000Concentrationsofcalprotectininbotharterialandvenousumbilicalplasma,andamnioticfluidweremuchlowerthaninmaternalplasmaCRPlevelsinfetalcirculationwere1/100ofmaternalCRPlevels.Noinflammatoryresponsewasnotedinthefetalcirculation.Braekkeetal.2005Theoretically,“Calprotectinconcentrationscouldplayaroleinthepathophysiologyofpreeclampsiathroughaugmentedplacentalcelldeathorreducedtrophoblastinvasion(stage1)”Braekkeetal.2005Whatstimulatestheinflammatoryresponse(activatestheneutrophils)inpreeclampsia?Researchershavebeenunabletodeterminewhyorexactlywheretheneutrophilsbecomeactivated.Maternalorplacentafactorstriggeringmaternalinflammationdonotappeartobetransferredintothefetalcirculation.

Braekkeetal.2005Futureimplications:Furtherresearchisneededtoevaluatetheroleofcalprotectininpregnancyorpregnancycomplications.Willcalprotectinconcentrationsbeused topredictpreeclampsiabeforetheonsetofclinicalsymptomsorasamarkeroftheclinicallyestablisheddisease?

Braekkeetal.2005ClassificationGestationalHypertensionBP≥140/90

mmHgforfirsttimeduringpregnancyNoproteinuriaBPreturntonormal<12weeks’postpartumFinaldiagnosismadeonlypostpartum（产后）Preeclampsia

BP≥140/90mmHgafter20weeks’gestationProteinuria300mg/24hoursor≥1+dipstick

EclampsiaSeizuresthatcannotbeattributedtoothercausesinawomanwithpreeclampsiaClassificationPreeclampsiaSuperimposedonChronicHypertensionNew-onsetproteinuria≥300mg/24hoursinhypertensivewomenbutnoproteinuriabefore20weeks’gestationAsuddenincreaseinproteinuriaorbloodpressureorplateletcount<100×109/LChronicHypertensioninPregnancyBP≥140/90mmHgbeforepregnancyordiagnosedbefore20weeks’gestationOrHypertensionfirstdiagnosedafter20weeks’gestationandpersistentafter12weeks’postpartumDiagnosis

HistoryHypertensionProteinuriaEdemaAssistantexaminationDiagnosisofseverepreeclampsiaCentralnervoussystem:headache,visualchanges,comaSubcapsularhematomaorhepaticrupture:epigastricdiscomfortorpersistrightupperquadrantpainHepaticimpairment:elevatedhepaticenzymesSystolicpressure≥160mmHg,ordystolicpressure≥110mmHgThrombocytopenia:<100×109/LProteinuria:≥5g/24hoursOliguria:<500ml/24hours(少尿)CerebralvascularcomplicationsIntravascularhemolysis:anemia,jaundice,LDH↑(血管内溶血)CoagulationdisordersFGR(胎儿生长受限)orOligohydramnion(羊水过少)ManagementPrinciplesSedation(镇静)Antihypertension(降压)Antispasm(解痉)Diuresis(利尿)TerminationofpregnancyManagementGeneralmanagementBedrestFrequentfetalandmaternalmonitoringSedationDiazepam(地西泮，安定)Hibemation(冬眠药物)pathidine派替啶,chlorpromazine氯丙嗪promethazine异丙嗪ManagementAntispasm(解痉)

：Topreventseizures

Magnesiumsulfate（硫酸镁）MechanismDoseregimenloadingdose:5g,5-10minutescontinuousinfusion:20-25g,1-2g/hourtotaldailydose:25-30