Andersons pediatric cardiology 233
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FIG.9.1 Freedomfromprenatalterminationofsupraventricular
tachycardia(SVT)oratrialflutter(AF).Slowercardioversionratestoa
normalrhythmweresignificantlyassociatedwithanincessantversus
intermittent(presentin<50%ofobservationtime)tachycardiapattern(A),
thepresenceoffetalhydropsatthetimeofarrhythmiadetection(B),anda
diagnosisofAFwhencomparedwithotherformsofsupraventricular
tachyarrhythmia(C).(FromJaeggiE,CarvalhoJS,DeGrootE,etal.
Comparisonoftransplacentaltreatmentoffetalsupraventricular
tachyarrhythmiaswithdigoxin,flecainideandsotalol:Resultsofanonrandomizedmulticenterstudy.Circulation.2011;124[16]:1747–1754.)
VentricularTachycardia
VTinthefetusisrareandreportsarescarce.8,51–57Theechocardiographic
diagnosisisbasedonatachycardiawithhigherventricularthantheatrialrates
andnorelationbetweenventricularandatrialevents(AVdissociation).Ifthere
is1:1retrogradeAVnodalconduction,itisusuallynotpossibletodifferentiate
aregularVTfromSVAbyfetalechocardiography.58Treatmentandprognosis
dependonthecauseandpatternoftheVTandthehemodynamicconsequences.
Acceleratedidioventricularrhythmisaventricularrhythmthatisslightlyfaster
thanthesinusrateandisconsideredabenignformofVT.Theseratesare
usuallyseenlateingestationandgenerallydonotrequiretreatmentprenatallyor
postnatally.Intheabsenceofapredisposingcondition,idiopathicVTisarare
causeoftachyarrhythmiainthefetus.51,58Itismorecommonlyseeninyoung
patientsafterbirthandthenusuallyhasabenigncourse,althoughtreatmentmay
berequired.59IdentifiableassociationswithVTincludeacutecardiac
inflammation,cardiactumors,andionchannelopathies.Anti-Roantibody-
mediatedcarditisshouldbesuspectedifrunsofVTareobservedinafetuswith
anewdiagnosisofcongenitalcompleteheartblock(CHB).Transplacental
maternaldexamethasonemaythenbeusedtoeasetheinflammationandtostop
thetachycardia.60ThemostcommonpredisposingconditionleadingtofetalVT
isLQTS.Itisalikelycauseifsinusbradycardiaorsecond-degreeheartblock
andafastVT(torsadedepointes)coexist.57Withthearrivaloffetal
magnetocardiography,ithasbecomepossibletodetectfetalQTcprolongation
noninvasively.Iffetalmagnetocardiographyisunavailable,thediagnosisof
LQTSisconfirmedbypostnatalECGandtestingforLQTSknownmutations.
Treatment
Perinataldataontreatmentandoutcomearelimitedandvarybetween
conditions.ForfetalVTgreaterthan200beats/min,short-termmaternal
intravenousmagnesiumhasbeenrecommendedasthefirst-linetransplacental
medication(seeTable9.1).11,55OthertreatmentoptionstocontrolafetalVT
mayincludeintravenousmaternallidocaineaswellasoralβ-blockerand
mexiletine.54,56IntheabsenceofLQTS,amiodarone,flecainide,orsotalolmay
alsobeuseful.
Thyrotoxicosis
Fetalhyperthyroidismorthyrotoxicosisisanotherrareyetpotentiallylifethreateningcondition.Itshouldalwaysbeconsideredinthedifferential
diagnosisofalong-VAtachycardiaofupto200beats/min,whichincludesAET
andPJRT.Itismostcommonlyobservedinthyroidautoimmunedisorderssuch
Gravesdisease.ThematernaldiagnosisofGravesdiseaseissuggestedby
physicalsigns―suchasexophthalmos,anenlargedthyroidgland,and
exaggeratedreflexes―andisconfirmedbyfindingmarkedlyelevatedlevelsof
thyroidhormone.Transplacentalpassageofmaternalthyroid-stimulating
immunoglobulins(TSIs)leadstofetalthyroidglandstimulationandtheclinical
manifestationsofthisdisorder,includingfetalhydrops,restrictionofgrowth,
andgoiter.61Becausefetaltachycardiaandrestrictedgrowthmayresultfrom
otherpathologicprocesses,somehaveadvocatedsamplingofumbilicalbloodto
measurethelevelsofthyroid-stimulatingantibodies,thyroid-stimulating
hormone,andFT4fordefinitivediagnosis.62Ifthyrotoxicosisgoesunrecognized
anduntreated,theriskoffetalmortalityandseverecomplicationsishigh.
Treatment
Themainstayofprenataltreatmentisinhibitionoftheexcessivefetalsynthesis
ofthyroidhormonebypropylthiouracil(PTU)andslowingofthefetalheartrate
byβ-blockade.63
Propylthiouracil.
PTUdoesnotaffectthereleaseofthyroxin.TherapidityofresponsetoPTU
thereforedependsontheamountofcolloidstoredinthethyroidgland.Thedrug
isgenerallywelltolerated,withsideeffectsoccurringinabout1%oftreated
adults.Adverseeventsaremainlyrelatedtotheskinandincluderash,itching,
abnormallossofhair,anddermalpigmentation.Agranulocytosis,nausea,
vomiting,lossoftaste,jointormuscleaches,numbness,andheadacheareother
possiblereactions.Theagentcrossestheplacentaandmayproducefetal
hypothyroidismevenifitisadministeredinrelativelylowdoses.62Tolimitthis
risk,treatmentwithPTUshouldbetitratedtothelowestpossibledoseto
maintainthematernalindexforfreethyroidinthehighnormalrange.Thefetal
responsecanbemonitoredbyserialmeasurementofthefetalheartrateandby
directmeasurementofT4andthyroid-stimulatinghormoneinthefetalcord
blood.Ultrasonographymaypermitassessmentofchangesinthesizeofthe
thyroidgland.InfantsborntomotherswithGravesdiseaseshouldbeclosely
followedbyapediatriciantoassessanythyroidaldysfunction.PTUwas
previouslyconsideredasafemedicationforuseduringgestation.Arecent
Danishstudyrevealedthat2%to3%ofchildrenexposedtoPTUearlyin
gestationdevelopedbirthdefects(neckcystsandurinarytractabnormalities)
associatedwiththistherapy.64
Propranolol.
Propranololorasimilarmaternalβ-blockermaybeusedtoslowfetalsinus
tachycardia,thusreducingtheriskofhigh-outputcardiacfailure.Propranololis
rapidlyandcompletelyabsorbed,withlevelspeakingintheplasmafrom1to3
hoursafteroralingestion.Thedrugreadilycrossestheplacenta.β-Blockadeis
contraindicatedinthepresenceofseverematernalbradycardia,high-degree
atrioventricularblock,severeasthma,orbronchospasm,theRaynaud
phenomenon,andotherperipheralvasculopathies.Pharmacologicβ-blockadeis
consideredrelativelysafeforthefetus,althoughsideeffectshavebeenreported
inneonatesfollowingtheuseofpropranololinpregnancy,includingrestricted
