Andersons pediatric cardiology 263
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maternalarteriesnormallyextendsbeyondthespiralarteriesandthedecidual
borderintotheradialarteriesofthemyometrium.8,9Arteriovenousshuntsalso
forminthematernalmyometriumunderneaththeplacenta,whichsupport
placentalcirculationbydecreasingmaternalsystemicvascularresistance.4
Thusthehumanplacentaformsfromtheinterweavingofmaternalandfetal
tissues,guidedbyacomplexinterplayofhormones,cytokines,andgrowth
factors.3,7Bytheendofthefirsttrimestertheplacentahasdevelopedintoits
definitivestate.Althoughtrophoblastinvasioncontinuesthrough19to20
weeks,thefetushasbecomedependentontheuteroplacentalcirculation.2
MechanismsandConditionsofPlacental
Dysfunction
Placentaldysfunctionisthedirectconsequenceofimpairedplacental
development.Itcantriggeramyriadofconditionsaffectingbothmotherand
fetus,includingmiscarriage,prematureruptureofmembranes,fetalgrowth
restriction,andthehypertensivedisordersofpregnancy,includingpreeclampsia.
Fordefinitionpurposes,preeclampsiaisadisorderofpregnancybelievedto
developduetoplacentaldysfunctionandischaracterizedbytheonsetof
maternalhypertensionandproteinuria.Asseverityprogressesitcanleadto
thrombocytopenia,hemolysis,hepaticdysfunction,renaldysfunction,peripheral
edema,andvisualdisturbances.Inthisadvancedform,somerefertothe
conditionasHELLPsyndrome(hemolysis,elevatedliverenzymes,andlow
plateletcount).Ifuntreated,preeclampsiacanleadtoseizures,atwhichpointit
isthenknownaseclampsia.Manyoftheseclinicalsymptomsarebelievedto
resultfromamaternalinflammatoryreactiontoplacentaldysfunctionwith
maternalendothelialdysfunctionandincreasedvascularreactivity.4,8
Manypathologicfindingsareassociatedwithplacentaldysfunction,which
canbelooselygroupedintothreecategories:defectivetrophoblastinvasionand
failureofspiralarterydilation,vascularlesionstermed“atherosis,”andlesions
ofthematureplacenta.However,howthesefindingsareinterrelated,andthe
rolestheyplayinthemechanismsofthevariousclinicalmanifestations,isstill
somewhatunclear.
Defectivetrophoblastinvasionandsubsequentfailureofspiralarterydilation
havebeenshowntobeassociatedinparticularwithearly-onsetpreeclampsia,
fetalgrowthrestriction,andprematureruptureofmembranes.2,4Beginningeven
beforefertilization,iftheuterinedeciduaisinsufficientlyprepared,trophoblast
invasionmaybesuboptimal.8,10Abnormaltrophoblastinvasionprevents
adequatespiralarteryremodelinganddilation,notonlyleadingtodecreased
flowintotheplacentabutlossofthepotentiallyoxygen-drivendeep
trophoblasticinvasionandarterialremodeling.8,9Inseverepreeclampsia,deep
placentationisseverelyaffected,withfewspiralarteriesdemonstratingfull
transformation,comparedto90%transformationinnormalpregnancies.10
Prematurelossofthespiralarterytrophoblastplugscanresultinmiscarriageor
preeclampsia,dependingonthelocationandtiming.8Normally,bloodflowfrom
spiralarteriesbeginsatthecenteroftheplacentafirst,andspreadstothe
margins;flowthatbeginsatthemarginsinsteadmayresultinhighoxidative
stressandvillousregression.Conversely,ifintervillousflowdoesnotreachthe
placentalmargins,therecanbechorionicregressionandsubsequentlyasmall
placenta.8
Atherosisisanothercommonfindinginstatesofplacentaldysfunction.Itcan
beseeninpreeclampsia,hypertensivediseasewithoutpreeclampsia,fetalgrowth
restrictionwithoutmaternalhypertension,andsystemiclupuserythematosus.2,9
Lipophageplaquesandfibrinaccumulateinspiralarteries,andfibrinoidnecrosis
occurs.Inadditiontophysicallyobstructingflow,theresultingvasculopathy
leadstoendothelialdisruptionandaprothromboticstate,aswellasaneurysm
formationintheweakenedarterialwalls.2,9
Overtime,macroscopiclesionsdevelopintheplacenta.Withoutadequate
dilationofthespiralarteries,maternalarterialbloodflowenterstheintravillous
spacewithgreatervelocity,creatingintervillouslakes.Theseabnormalpockets
oftenbecomelinedwiththrombusduetoalteredflowdynamics.Whensevere,
anchoringvillicanberuptured,pushingthechorionicplateawayfromthebasal
plate.Thisperpetuatesfurtherplacentaldisorderasfewerextravillous
trophoblastsareabletoreachthematernalsurfacetoremodelthespiralarteries.4
Asthestructureoftheplacentaisdisrupted,thedelicatebalanceofoxygen
andnutrientexchangeisalsoaffected.Intheclassicstateoffetalgrowth
restriction,uterinevenousbloodhashigheroxygencontentthannormal,which
maybeduetothehighervelocityofarterialbloodenteringastructurally
disruptedintervillousspaceresultinginsuboptimalgasexchange.4Moreover,
withoutspiralarteryremodeling,thevasocontractilityofthevesselsremains
intact.Thesearteriesarelessabletoprovideadequateflowtokeepupwith
increasingfetaldemandaspregnancyprogresses.2Theirvasoreactivitycanalso
causeepisodesofplacentalhypoxiaandreperfusion,leadingtooxidativestress,
apoptosis,andnecrosis.This,inturn,cantriggerorpromoteamaternal
hyperinflammatoryresponse.8
Noteverypregnancywithimperfectplacentationresultsinclinically
significantdisease,andtheclinicalmanifestationsofdiseasesarenotconsistent.
Althoughmanyofthesefindingscanbeseeninintrauterinegrowthrestriction
andpreeclampsia,notallfetusesofpreeclampticpregnanciesaregrowth
restricted.9
Lessdramaticaberranciesinplacentaldevelopmentneverthelesshavean
