Andersons pediatric cardiology 2094

AKI,Acutekidneyinjury.
FromWebbTN,GoldsteinSL.Congenitalheartsurgeryandacutekidneyinjury.
CurrOpinAnaesthesiol.2017;30(1):105–112.

CardiacSurgery–AssociatedAKIandOutcomes
ThisstrongassociationbetweenAKIaftercardiacsurgeryinchildrenandpatient
morbidityandmortalityhasbeendemonstratedrepeatedlyoverthepastdecade.
Reviewofthelargeststudies,eachcomprisingatleast400surgeries(Table
78.5),revealsmortalityratesrangingfrom8.9%to54%forpatientswho
developedAKIversus1.2%to6%forpatientswhodidnotdevelopAKI(allP
values<.0001).Inaddition,multiplestudiesdemonstratethatincreasedfluid
accumulationaftersurgerywasassociatedwithmortality,independentofserum
creatininebasedAKIstatus,11,17–19andoneshowedthattheassociationbetween
AKIandoutcomeswasstrengthenedwhenserumcreatinineconcentrationwas
correctedforthedegreeoffluidoverload,17suggestingthatfluidaccumulation
maymaskAKIseveritybydilutingtheserumcreatinineconcentration;thisisa
phenomenonthathasbeendescribedincriticallyilladults.20Moststrikingly,the
associationsobservedbetweenAKIand/orfluidoverloadandmortalityhave
beencontrolledforunderlyingheartdiseaseandoperativefactors,andinsome
studies,theassociatedriskformortalityishigherwithAKIdevelopmentthan
singleventricularphysiology.7,11BothAKIdevelopmentandexcessivepositive
fluidaccumulationhavealsobeenassociatedwithprolongedmechanical
ventilation/delayedextubation,increasedneedforinotropicsupport,and
intensivecareunitlengthofstay.11,21,22
Table78.5
OutcomeComparisonsforPatientsWith/VersusAcuteKidneyInjury
AfterCardiacSurgery
StudyAuthor
(Subjects)
Blinder7(n=
430)

MortalityRatesforAKI OR(95%CI)for
vs.NoAKI
MortalityWithAKI
11.6%vs.2.9%
Stage1(1.3;0.4–4.1)a
Stage2(5.1;1.7–15.2)
Stage3(9.5;2.5–30.7)
Chiravuri13(n= 54.4%vs.6%
AKI-RI(6.7;4.1–

VentilationTime(Median[IQR])for
AKIvs.NoAKI
5[3–7]vs.3[2–5]days

NA


494)
Toth12(n=
1510)

10.8)b
AKI-F(36.9;20–67.9)
8.9%vs.1.2%

NA

49[26–112]vs.33[15–76]hours

aAcuteKidneyInjuryNetworkcriteriausedforAKI.
b

PediatricmodifiedRIFLE(risk,injury,failure,loss,end-stagekidneydisease)3criteriausedfor
AKI.Thesecriteriauseddecreasesinestimatedglomerularfiltrationrate(eGFR)tostratifyAKI
severity.Risk:25%decrease;injury:50%decrease;failure:75%decreaseoraneGFR<35
mL/minper1.73m2;loss:persistentfailurefor4weeks;end-stagekidneydisease:persistent
failurefor>3months.
AKI,Acutekidneyinjury;CI,confidenceinterval;IQR,interquartilerange;NA,notavailable;OR,
oddsratio.

Interventions
Giventhatnephrotoxicmedicationavoidanceandfluidmanagementrepresent
thetwomodifiableriskfactorsforpatientswith,oratriskforAKI,systematic
riskassessmenttoguideinterventionsisparamount.Somerecommend
avoidanceofgreaterthan10%fluid(inliters)accumulationbasedonbody
weight(inkilograms)usingthefollowingformula23:

The10%fluidoverloadthresholdisbasedonnumerousstudiesofcriticallyill
childrenwithAKIwhoreceivedcontinuousrenalreplacementtherapy(CRRT),
whichobservedanassociationbetween>10%and20%fluidoverloadatCRRT
initiationandpatientmortality,independentofpatientseverityofillness.24,25
Threerecentstudiesinchildrenaftercardiacsurgeryshowthatavoidanceof
10%fluidoverloadwasassociatedwithincreasedsurvivaland/ordecreaseddays
ofmechanicalventilation.11,21,22Thestrategiestolimitfluidoverloadinthe
settingofAKIarefluidrestriction,administrationofdiuretics,andinitiationof
renalreplacementtherapy.26
WhilemodifiedultrafiltrationduringtheCPBprocedureiseffectiveat
minimizingfluidoverloaduponarrivaltothecardiacintensivecareunit,fluid
restrictionlikelyhaslittleutilityintheearlypostoperativeperiodaspatients

developcapillaryleakfromthesysteminflammationcausedbyCPBandthe
surgeryitself.Furthermore,fluidrestrictionlimitstheabilitytoprovideadequate
nutritionforanabolisminpatientswhoarehighlycatabolicandatriskforAKI
forupto72hoursduetothelowcardiacoutputstateassociatedwithlong
bypassdurations.Therefore,fluidrestrictionalone,withoutescalationtodiuretic
administrationortheinitiationofrenalreplacementtherapy,shouldonlybe
consideredinolderpediatricpatients(>1yearofage)withadequatenutritional
reserves.
Diuretic,especiallyloopdiuretic,administrationisnearlyubiquitousanda
“backbone”forpatientswithoratriskforAKIinthecriticalcaresettingwitha
goalofpreventingorreversingfluidoverload.27,28Loopdiureticsexhibittheir
effectbyblockingsodium,potassium,andchlorideresorptioninthethick
ascendinglimboftheloopofHenle.Increasedurinaryexcretionofsodium,
potassium,andfluidarebeneficialinthepatientwithAKI,andwheneffective,
canallowforprovisionofadequatenutrition-associatedvolumeswithoutthe
developmentoffluidoverload.Althoughsomedebateexistsregardingthe
superiorityofdifferentloopdiureticmedications(furosemidevs.ethacrynic
acid29),maximumdoseandadministration(intermittentbolusvs.continuous
infusion),adetaileddiscussionisbeyondthescopeofthischapter.However,itis
criticalforthecliniciantoestablishdailygoalsofdiuretictherapyintermsofnet
fluidbalancegiventheoptimalfluid,nutrition,andbloodproductneedsofthe
patient,andtobefirmintheirassessmentofdiureticresistance.Escalationof
diuretictherapytoachievethesegoals,includingtheadditionofathiazide
diuretic30shouldbemadeinasystematicandrationalfashion,withaclearsense
thatdiureticresistanceshouldnotbedefinedbyaparticularurineflowratein
mL/kgperhour,butwithanobjectiveaccountingofwhetherornotdiuretics
achievetheneededfluidbalance.Inaddition,potentandincreaseddiuretic
administrationisnotdevoidoftheconsequencesofototoxicity,severe

electrolytederangement,includingmetabolicalkalosis,29hyponatremia,
hypokalemia,andworseningoffunctionalAKIleadingtodecreasedrenal
perfusion.31
Recently,theconceptofthefurosemidestresstest(FST)hascodifiedan
objectivemetricfordiureticresistanceincriticallyilladults.32,33TheFSTusesa
standardizeddoseofintravenousfurosemide(1mg/kginnaivepatients,1.5
mg/kginpatientswithchronickidneydisease[CKD]orwhohavereceived
furosemide)andassessesurineoutput(UOP)inthe2hoursafteradministration.
Patientswhodidnothavemorethan200mL/hofUOPprogressedtoworsening