Case Studies in Pediatric Critical Care (Jun 11, 2009)_(0521878349)_(Cambridge University Press)


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meningococcalsepticemia
narrowcomplextachycardia
Pneumocystisjiroveci
pneumonia(PJP)
ventilatorinducedlung
injury(VILI)
seealso
meningococcalsepticemia
casehistory
progressandmanagement
onPICU
treatmentpriortoPICU
complicationsand
initialassessmentatPICU
initialmanagementonPICU
circulatorysupport
earlygoal-directedtherapy
fluidmanagement
mixedandcentralvenous
oxygensaturation
myocardialdysfunction
pulmonaryedema
treatmentofshock
learningpoints
ongoingmanagementon
cardiorespiratorysupport
fluidmanagement
newertherapies
skinandlimbcare
publichealthissues
mixedvenousoxygen
saturation(SVO
modifiedBlalock
Taussig(BT)
shuntasalternativeto
modifiedGlasgowComaScore
forchildren
modifiedultrafiltration(MUF)
mosquito-bornediseases
denguehemorrhagic
fever(DHF)
multi-organfailure(MOF)
severemeningococcal
severepertussis
survivalrates
multipletrauma
abdominalinjury
cardiothoracicinjury
casehistory
fluidandbloodproduct
learningpoints
managementof
airwayandbreathing
secondarysurvey
temperaturecontrol
non-accidentaltrauma
orthopedicinjuries
spinalinjuries
seealso
traumaticbrain
injury(TBI)
oxygendelivery(cont.)
optimizationofsystemic
reducedbylowcardiac
sepsisinBMTpatient
oxygenationindices
Parkland/Baxterformula,
fluidresuscitation
pentamidineforPJP
percutaneousdrainageof
pericardialeffusion
casehistory
causesof
post-cardiacsurgery
recurrentpericarditis
renalfailure
diagnosisof
signsandsymptoms
techniquesfor
emergencypericardiocentesis
149
learningpoints
percutaneousdrainage
postdrainagecare
problemsinpractice
semi-urgentdrainage
surgicaldrainage
peritonealdialysis(PD)
hemolyticuremicsyndrome
hypothermicpatients
permanentjunctional
tachycardia(PJRT)
permissivehypercapnia
casehistory
progressonPICU
ansfertocardiacICU
136
extra-corporealmembrane
followingtransferto
laboratorydiagnosis
learning/practicepoints
pulmonaryhypertension
ventilatorysupport
plasmaexchange,aHUSand
plasticbronchitis
pneumococcalmeningitis,
incidenceof
,causingABM
pneumocystisjiroveci
pneumonia(PJP)
(TCA)poisoning
positiveend-expiratory
pressure(PEEP)
post-pericardiotomysyndrome
alkalinizationlowering
benefitsofdropin
restingenergyexpenditure
systemicinflammatory
responsesyndrome
systemicperfusion
improvementwith
managementof
pre-operativeoptimisation
systemicvascularresistance
tachycardia(SVT)
TCApoisoning
(TCA)poisoning
ventriculardysfunction
coarctationoftheaorta
failingfontan
hypoplasticleftheart
syndrome(HLHS)
patientswithTAPVC
ABC(airway,breathing,
circulation)of
abdominalinjury
acutebacterial
ABOmismatchheart
non-accidental
injury/trauma
ACE(angiotensin-converting
enzyme)inhibitors
acidosis,causesofin
TCApoisoning
activatedproteinC(APC)
acutebacterialmeningitis
antimicrobialtherapy
casehistory
cerebralperfusion
atrialseptaldefect(ASD),
restrictiveinHLHS
atrioventricularre-entry
tachycardia(AVRT)
atropine,treatmentof
atypicalhemolyticuremic
syndrome(aHUS)
distinguishingfromTTP
bacterialinfections
bonemarrowtransplant
burnwounds
HIV-infectedchildren
pericardialeffusion
seealso
acutebacterial
meningitis(ABM),
BerkowChartforestimationof
BerlinHeart
modifiedBlalock
Taussig(BT)shunt
bloodglucoseconcentration,
managementof
bloodpressure
managingfollowinghead
normalvaluesbyage
bloodtransfusion
forintractableshock
patientswithHUS
pediatricmultipletrauma
279
complicationsfollowing
freshfrozenplasma
guidelinesfor
initialfluidmanagement
packedredbloodcells
recombinantactivated
factorVII
uncross-matchedO
volumevaluesby
bodysurfacearea(BSA)
bonemarrowtransplant
allogeneicvs.autologous
casehistoryandexamination
highmortalityriskfollowing
infectionrisk
antibioticsandantifungals
higherforallogeneic
organismscausing
initialassessmentand
initialresuscitation
learningpoints
managementinPICU
outcomesinPICU
withdrawalofsupport
cardiothoracicinjury
severeburnsincreasinglevels
seealso
inotropicsupport
centralvenousaccess
centralvenousoxygen
saturation(ScvO
cephalosporinresistance
cerebralbloodflow(CBF)
hyperthermiaincreasing
hyperventilationdecreasing
managingfollowinghead
asmeasureofoxygenation
usingXenonCTto
cerebraledemainDKA
cerebraloxygenation,indirect
measureof
cerebralperfusionpressure
casesofABM
lowerlimitforchildrenwith
cerebralvenoussinus
thrombosis(CVST)
casehistory
clinicalpresentation
donororgans
ABOmismatchtransplant
limitedavailabilityof
dopamine,inotropicsupport
dressings/skingraftsfor
analgesiafordressing
factorsassociatedwith
diagnosisof
inducedaftercardiac
protectionofferedby
coldwater
ischemicbrain
evaluationof
managementof
initialassessmentand
learningpoints
progressinPICU
resuscitationfollowing
cardiacarrest
Haemophilusinfluenzae
,typeB
(Hib),causeofABM
headinjury
childdifferences
casehistory
cerebralperfusionpressure
emergencymanagement
factorsaffectingoutcome
intensivecaremanagement
intracranialpressure(ICP)
learningpoints
non-accidentalcauses
indicationsof
shakenbabysyndrome
progressinPICU
routinetherapyfor
transportationissues
seealso
traumaticbrain
injury(TBI)
heartfailure
acuteheart
heartsurgery
hearttransplantation
ABOmismatchtransplants
assessmentfor
forinfantswithHLHS
inotropicsupportwhile
orthotopic(OHT)forfailing
post-operativeacuterenal
survivalstatistics
hemolyticuremicsyndrome
atypicalHUS(aHUS)
plasmaexchange,role
casehistory
inPICU
contraindicationsandadvice
diarrheaassociatedHUS
antibiotictreatment
durationofhospital
outbreaksof
renalfailure
verotoxinscausing
incidenceof
initialassessmentand
learningpoints
hypoplasticleftheartsyndrome
casehistory
examinationand
managementin
progressinPICU
centralvenousaccess
extra-corporeallifesupport
immediatemanagement
learningpoints
optimizingsystemic
postnataldiagnosis
prenataldiagnosis
reasonsformortality
surgicaloptions
hearttransplantation
stagedsurgicalpalliation
survivalrates
glucagontreatment
headinjuries
patientsinsepticshock
pericardialeffusion
useofcorticosteroids
coldwaterprotection
diagnosisof
effectsoninjuredbrain
inducedaftercardiac
intracerebralhemorrhageswereobservedinanyofthepatientsreceivinganticoagulation
therapyand,despitethefactthattheRR95%CIincludes1,thereisapotentiallyimportant
reductionintheriskofdeathordependency.
Heparinisthemostcommonlyusedfirstlineoftreatmenttopreventlocalextensionof
thethrombusandpulmonaryembolism.Sebire
Chapter27:Managementofsagittalsinusthrombosisinachild
should,however,onlybeattemptedincenterswithstaffexperiencedininterventional
radiologyandshouldberestrictedtopatientswithpoorprognosis.
Treatmentofisolatedintracranialhypertension
Inpatientswhomonlyhavesymptomsofchronicintracranialhypertension,thefirstpriority
Chapter27:Managementofsagittalsinusthrombosisinachild
Themostcommoncausesofdeatharehemorrh
agicinfarctionwithraisedintracranial
pressure,cerebraledema,statusepilepticus
,sepsis,pulmonaryemboli,andseverityof
Chapter27:Managementofsagittalsinusthrombosisinachild
7.CrassardI,BousserMG.Cerebralvenous
JNeuroophthalmol
(2):156
8.deBruijnSF,BuddeM,TeunisseS,deHaan
RJ,StamJ.Long-termoutcomeofcognition
andfunctionalhealthaftercerebralvenous
sinusthrombosis.
(8):1687
9.deBruijnSF,StamJ.Randomized,placebo-
controlledtrialofanticoagulanttreatment
withlow-molecular-weightheparinfor
cerebralsinusthrombosis.
(3):484
10.deVeberG,AndrewM,AdamsC
Chapter27:Managementofsagittalsinusthrombosisinachild
Managementofsagittalsinus
thrombosisinachild
DavidJ.Grant
CerebralVenousSinusThrombosis(CVST)isaclinicallydiversediseaseinitscausation,
extent,andclinicalpresentation.Itsoutcomeisunpredictableandcanvarygreatlyamong
patients.
Thrombosisofthecerebralveinsandsinusesarecerebrovasculardisordersthatoccur
mostcommonlyinyoungadultsandchildren.Inchildrentheestimatedannualincidenceis
7per1millionchildren.
AprothromboticriskfactororadirectcauseisidentifiedinalmostallcasesofCVSTin
childrenandupto85%ofadults.
Themanagementpriorities,intheacutephase,aretostabilizethepatient,byoptimal
resuscitation,andprevention/reversalofcerebralherniation.Followingstabilization,atten-
tionshouldturntopreventingprogressionofthethrombusand/orthrombolysis.Treatment
shouldbestartedassoonasthediagnosisisestablishedandshouldaimtoreversethe
underlyingcause(ifknown),controlseizures,controlintracranialhypertension,andcom-
menceantithrombotics.Heparinshouldbethefirst-lineantithromboticagentused.
Casehistory
An18-month-oldgirlpresentedtoherprimarycarephysicianwitha1-dayhistoryof
AfterobtainingIVaccessandtakingbloods
forbloodcultures,C-reactiveprotein
(CRP),biochemistry,fullbloodcount,an
dclottingshewasresuscitatedbygivinga
20mlkg
normal(0.9%)salinefluidbolus.Herperfusionimprovedandshewas
commencedon0.45%salineplus5%dextrose
asintravenousmaintenancefluid.Full
maintenancerequirementsplus100mlkg
wasprescribedataratetorehydrateherover
a24-hourperiod.
TheresultsofherinitialCRP,biochemistry,fullbloodcount,andcoagulationscreenare
depictedin
Table27.1
.Shewasadmittedtothepediatricwardat16:00thatafternoonand
seemedtorespondwelltothefluidtherapy.Duringthenightthedoctorswereaskedto
reviewherbecauseshewasquitedifficulttorouse.Thesameregistrarwhomsawherinthe
emergencydepartmentreviewedherandfeltthatshewasmerelytiredaftertheeventsofthe
lastcoupleofdaysandthatshewassleepingasitwaslateatnight.Hecommentedthatifshe
Table27.1.
Resultsofinvestigations
Day2
09:3015:0020:15
Fullbloodcount
Hbgdl
WCC(x10
)14.4
PLT(x10
)280
APTTratio1.11.2
Fibrinogen4.23.6
SerumU&Es
mmoll
114113113136
mmoll
4.34.44.13.2
Urmmoll
2.62.62.01.6
Crmmoll
30302622
Osmolality305264262260290
Albumin2321
CRP(
5)75
UrineU&Es
mmoll
mmoll
Osmolality568
542521503
DipsticksNoprotein/blood
CTbrainwith
contrast:DGH
Noevidenceofcerebraledemaorhydrocephalus.
?Thrombusinsuperiorsagittalsinus
Thrombussuperiorsagittalsinuswithextensionintobothlateral
sinusesandextensivevenousinfarcts
Chapter27:Managementofsagittalsinusthrombosisinachild
wasathomeshewouldbesleepingnow.Hefeltnoneedtodiscusshercasewiththe
consultantoncall.
Bythefollowingmorningshestillhadareducedlevelofconsciousness,butwasnowalso
havingepisodesofbradycardia.Inviewofthesefindingsandthefactthatshecontinuedto
vomitdespiteherdiarrheahavingbeenresolvedandherclinicalhydrationstatusimproved,
therewasconcernthatshemayhavemeningitis.Itwasthereforedecidedtoperformafull
septicscreenincludingalumbarpuncture.
Thefluidobtainedfromthelumbarpuncturewasclearandcolorless,butflowedatarate
suggestingthatitwasunderincreasedpressureleadingtoconcernsthatshemayhaveraised
intracranialpressure.
Chapter27:Managementofsagittalsinusthrombosisinachild
Progressinthepediatricintensivecareunit
TheresultsofherbiochemistryonarrivalatPICUaredepictedin
Table27.1
(20:15).She
nowstarteddevelopingepisodesofbradycardiawithassociatedhypertension.Onexamina-
Fig.27.1.
Fillingdefectsinlateralandsagittalsinuses.
Chapter27:Managementofsagittalsinusthrombosisinachild
Cerebralvenoussinusthrombosis(CVST)isapoorlyunderstood,unpredictablecondition
Cortical veins
Superior
sagittal sinus
Straight
sinus
Transverse
sinuses
Jugular veins
Vein of Galen
and internal
cerebral veins
Fig.27.2.
mostfrequently
involvedinCVST.
Chapter27:Managementofsagittalsinusthrombosisinachild
CVSTinfiveEuropeancentersfoundclinicalriskfactorsinalltheirpatients.
childrenpresentingwithCVST,approximately40%haveknownpreviousillnesseswhile±
60%arepreviouslywellchildren.
Chapter27:Managementofsagittalsinusthrombosisinachild
Table27.2.
Chapter27:Managementofsagittalsinusthrombosisinachild
headache,vomiting,diffuseneurologicalsigns(76%),seizures(58%),focalneurologicalsigns
(42%),andcoma.
Focalneurologicalsignsthatdevelopsecondarytovenousthrombosismayoftenlocalize
toaunilateralhemisphereonlytobefollowedwithindaysbybilateralsigns.Thesemani-
festationsmaytaketheformofseizures,behaviouralsymptoms,orcoma.
Seizuresoccurinapproximately40%
60%ofpatientsandareusuallyfocal,butmay
generalize.Behavioralsymptomsaremostcommonlyfoundsecondarytothalamiclesions,
whichmayleadtocomaiftheyoccurbilaterally.Comacanalsobecausedbyunilateral
infarctsorhemorrhagesthatcompressthediencephalonandbrainstem.Ifleftuntreated,
thesepatientsdieduetocerebralherniation.
Involvementofthedeepvenoussystem(straightsinusanditsbranches)mayresultinthe
infarctionofbasalganglia,thalamus,hypothalamus,ventralcorpuscallosum,medialocci-
Chapter27:Managementofsagittalsinusthrombosisinachild
hematoma,subarachnoidhemorrhage,orseptationswithinthesinus.OtherCTfindings
mayincludeedemaofthebrain(focalorgeneralized),venousinfarction,parenchymal
hemorrhage,andsubduralhematoma.
Thespectrumofvenousinfarctsincludesunilateral
orbilateralinfarctsorhemorrhagesofthedeepgraystructures(secondarytothrombosis
ofthedeepcerebralveinsandstraightsinus)orthecortexandunderlyingwhitematter
(secondarytothrombosisofthesagittal,transverse,andsigmoidsinuses).
callysignificantresultswerefound.Theyfoundthatanticoagulanttherapyhadapooled
relativerisk(RR)ofdeathof0.33(95%CI0.08
1.21)andofdeathordependencyof0.46
(95%CI0.16
1.31).Whatis,however,importanttonoteisthatnonewsymptomatic
Chapter27:Managementofsagittalsinusthrombosisinachild
Allpatientsareatriskofinvasiveinfectionsfollowingbonemarrowtransplantation,
buttheriskishigheramongstallogeneicpatientsastheyreceiveamoreaggressiveinitial
myelosuppression.OtherriskfactorsforinfectionincludethedevelopmentofGraft-Versus-
HostDisease(GVHD)necessitatingtheuseofciclosporinand/orcorticosteroids,useofbone
marrowfromunrelateddonors,
thedegreeofmucosaldisruption,bacterialcolonization,
andreactivationoflatentviruses.
Infectiouspathogensfollowingallogeneictransplant,varyaccordingtothetimeelapsed
followingtheprocedure.Intheearly(pre-engraftment)timeperiod,theriskforbacterialand
fungalsepsisishighestforseveralreasons.Mucosalintegrityisdisturbedbytoxiccondition-
ingregimens,prolongedneutropeniaresultsfrommyelosuppressiveconditioning,andT
andB-cellsmaybedysfunctionalfrominducedimmounosuppressiontopreventGVHD.
Complicatingthesituationfurtheristheroutineuseofindwellingintravenouscathetersin
pediatricpatients.Theseconditionscombinetocreateanidealopportunityforinvasive
pathogens.
Theorganismscausinginfectionduringthepre-engraftmenttimeperiodaregenerally
endogenousbacteriaorfungithatcolonizetheintestinaltract.
Gram-positiveorganisms
areisolatedmorefrequentlythanGram-negatives.
Organismssuchas
Staphylococcus
epidermis
tendtobeassociatedwithindwellingcentrallines,whileotherssuchasviridans
Streptococci
Stomatococcusmucilaginosus
areassociatedwithchemotherapy-induced
mucositis.BacterialtranslocationofGram-negativeentericorganisms,suchas
Pseudomonas
aeroginosa,Escherichiacoli
spp.,isamajorissueastheseorganismstendtobe
moreaggressive,havehigherassociatedmortalityandarecommonlyresistanttoantibio-
Fungalinfectionscorrelatewiththedegreeanddurationofneutropeniaandgenerally
tendtooccurafteraperiodofantibiotictherapy.
Candida
spp.enterfromthegastro-
intestinaltractandmayberecoverablefrombloodcultures.
Aspergillus
,ontheotherhand,
entersviatherespiratorytractandisrarelyisolatedfrombloodcultures.Viralinfectionsin
thisearlyperiodincludethereactivationof
Herpessimplexvirus
andrespiratoryvirusessuch
RespiratorySynctialVirus
Parainfluenzatype3
.Ifrespiratoryvirusesprogress
toinvolvethelowerairwaysandcauseaninterstitialpneumonia,theyareahighriskfor
Chapter26:SepsisinaBMTpatientadmittedtoPICU
patientswithfever.Broad-spectrumantibioticsshouldbestartedbasedonthepatient
colonization,thecommunityantimicrobialresistancepatternsandthehospitalenviron-
Ourhospitalstandardantibioticsforfebrileneutropeniaincludepiperacillin/
tazobactamandtobramycin.Forpatientswithclinicallysuspectedsepsis,vancomycinis
addedempiricallytocoverforviridans
Streptococci
,particularlyifpatientshavesignificant
mucositis,and
Staphylococcusepidermis
Chapter26:SepsisinaBMTpatientadmittedtoPICU
follow-up(36%).
Similaroutcomeswerereportedinpatientsrequiringventilationfollow-
ingsepsis-inducedcardiovascularcollapse(38%survival).
Althoughthesurvivalissignifi-
cantlylowerthanthevastmajorityofPICUpatients,itisclearlynotfutileandtherapyis
indicated.Patientsthatdevelopmultiple-organfailurearemoreconcerning,withseveral
studiesdemonstratingverypooroutcomes.
Thepresenceofthreeormoreorgan
failureswasassociatedwithnosurvivorsinonestudy(0/5)
andonly10%survival(1/10)in
Athirdstudydemonstrated20%(4/20)survivalinpatientswithfailureoffouror
moreorgansystems.
Particularlypooroutcomeswerenotedforpatientswhorequired
renalreplacementtherapyforrenalfailure.
AttemptshavebeenmadetoquantifyriskformortalityinBMTpatientsrequiringICU
admission.
TheO-PRISM(oncologicalriskofmortality)scoreusesseverityofGVHD,
CRPlevel�(10mgdl
)andpresenceofmacroscopicbleedingcombinedwiththestandard
scoretoidentifypatientsathighestrisk.Althoughquitehelpfulinthatrespect,theO-PRISM
doesnothaveenoughofapositivepredictivevaluefordeathtorelyonitexclusivelytomake
clinicaldecisionsforwithdrawalofsupport.
Continuousveno-venoushemofiltration(CVVH)hasshownpromiseasanovelmethod
totreatARDSinBMTpatients
renalfailure.
Themainmechanismsareconsidered
tobeimprovedlungfunctionthroughremovaloflungandbodywater,andremovalof
solubleproinflammatorymediators.Ifconfirmedbyfurtherresearch,CVVHmayhavea
greatimpactonthefutureoutcomeofthesepatients.
Asageneralrule,wewouldadvocatethatallbonemarrowtransplantpatientsrequiring
intensivecaredeserveatrialofconventionalICUtherapy,solongasthefamilyiswell
informedoftheriskformortalityandagreestointervention.Moreinnovativetherapy
shouldbeevaluatedwiththefamilyonacase-by-casebasis.Prognosticdecisionsand
limitationstocareshouldbebasedonthedevelopmentandtemporalevolutionofmulti-
systemorganfailureandnotonaspectsontheBMTitself.
Withdrawalofsupport
Thedecisiontolimitorwithdrawsupportonapediatricpatientisquitedifficult.Thereisan
inherent(andappropriate)biastowardsgivingthepatientachancefor
Atthesame
timeparentsandhealthcareprofessionalsdonotwanttoprolongsufferingiftheycanonly
delaytheinevitable.Thedecisiontolimitorwithdrawsupportshouldideallybediscussed
withthefamilyjointlybytheoncologyandPICUteams.Theoncologistislikelytohavea
long-standingtrustingrelationshipwiththefamily,whiletheintensivecarephysicianisbest
toprovidecurrentstatusandprognosis.Ultimately,theparentsshouldguidewhentheright
timeistowithdrawsupport.Althoughdifficulttobepresentatthetimeofwithdrawal,most
familiesappreciatebeingwiththeirlovedoneatthetimeofdeath.Supportservicessuchas
closefamilymembers,pastoralservices,socialworkers,orotheralliedhealthprofessionals
(basedonthespecificsofthePICU)mayproveinvaluabletotheimmediatefamilyatthetime
ofgrieving.
Learningpoints
TheprimaryfocusinasepticpatientshouldbetheABCs:
Breathing
Circulation.
Chapter26:SepsisinaBMTpatientadmittedtoPICU
Patientsinsepticshockneedrapidfluidresuscitationwithbolusesof20mlkg
crystalloidorcolloidgivenoverminutes.
Inotropicsupportwithdopamine(ordobutamine)shouldbestartedafter60mlkg
volumeresuscitation.
Pediatricpatientsaremorelikelytopresentwith
coldshock
(vasoconstrictedwith
inadequatecardiacoutput)than
warmshock
(vasodilatedwithgoodcardiacoutput).
Second-lineinotropicsupportshouldgenerallybeadrenaline(epinephrine)forcold
shockandnoradrenaline(norepinephrine)orvasopressinforwarmshock.
Broad-spectrumantibioticsshouldbeinitiatedearlyinthecareofsepticpatientsfollo-
wingbonemarrowtransplantation(orotherimmunodeficiency).
TheperiodofhighestriskforsepsisisearlyafterBMT,priortoengraftment.
AlthoughGram-positiveorganismsaremorecommon,Gram-negativeshaveahigher
riskofsignificantmorbidityandmortality.
Patientsrequiringmechanicalventilationhavesignificantriskofmortality.Thisriskis
significantlylowerforpediatricpatientscomparedwithadults.
Pre-admissionBMTcharacteristicshavenoapparentinfluenceonICUoutcomes.
Limitationorwithdrawalofsupportshouldbeconsideredincaseswithadvancingmulti-
Chapter26:SepsisinaBMTpatientadmittedtoPICU
14.DevineSM,AdkinsDR,KhouryH
Chapter26:SepsisinaBMTpatientadmittedtoPICU
SepsisinaBMTpatient
admittedtoPICU
FarhanBhanjiandSamD.Shemie
BoneMarrowTransplant(BMT)recipientsadmittedtothepediatricintensivecareunit
(PICU)remainamongstthehighestriskformortality,particularlyiftheyrequireintubation
andmechanicalventilation.Negativeperceptionsexistamongstthehealthcareteamregar-
dingtheirprognosisdespiteimprovingoutcomesafterICUadmission.Paradoxically,ICU
outcomesarenotprincipallylinkedtofeaturesofBMTitself,butratherrelatedtotheseverity
andtemporalevolutionofMulti-organFailure(MOF),similartoanyICUpatient.
PatientsundergoingBMTareatparticular
lyhighriskfordevelopingoverwhelming
sepsisandshouldbestartedonbroad-spectrumantibioticsatthefirstsignsofinfection.
Aggressivefluidresuscitationisfrequentlynecessaryandshouldbeinstitutedrapidly.
Inotropicsupportandinvasivemechanicalven
tilationshouldbeprovided,asclinically
indicated,butthefamilyshouldbeinform
edofthesignificantriskformortality.
Considerationshouldbegiventowithdrawal
ofsupportornon-escalationintherapyif
thepatientdevelopsmultiple
systemorgandysfunction.
Casehistory
A3-year-oldboy,ontheoncologyward,wasinsecondremissionforAcuteLymphoblastic
Leukemia(ALL).HeunderwentanallogeneicBMT14daysagoandnowpresentswithpoor
perfusionandafeverof38.5°C(axillary).Thepatientwasevaluated2hoursearlierbythe
juniorresidentbecausehedidnot
lookwell
accordingtothebedsidenurse.Therewasno
historyofcough,runnynose,headache,vomiting,diarrhea,orurinarysymptoms.The
patientfeltwarmaccordingtotheparentsbutwasafebrile(37.6°Caxillary)atthattime.
Theyoungboydidnotfullycooperateforthetemperaturemeasurement,ashewasquite
Thechildlookedgenerallyunwellbutwasalertandprotectinghisairway.Hisrespiratory
ratewas35breathsperminutewithmoderatelyincreasedworkofbreathing.Airentrywas
sentforFBC,coagulationprofile(INR/PTT),U&E,glucose,venousbloodgas,livertrans-
aminases,bilirubin,C-reactiveprotein,andabloodculture.Bedsideglucosemeasurement
wasmildlyelevatedat9.1mmoll
.Afluidbolusof300mlof0.9%saline(20mlkg
)was
givenover15minuteswithnochangeinperfusion.Bloodpressureremainedconstantat
82/50mmHgandheartratedidnotchange.Thepatientappearedagitatedwithaslight
worseningofhisrespiratorystatus.Asecondfluidbolusof300mlwasstarted,whiletheICU
fellowwascalledandintubationmedicationswerebeingprepared.
Chapter26:SepsisinaBMTpatientadmittedtoPICU
saturationandculturesweresenttoassessforpossiblecolonization.Ventilationwasinsti-
tutedusingthePressureRegulatedVolumeControl(PRVC)mode,atarateof20anda
deliveredtidalvolumeof10mlkg
.ThePaCO
wasallowedtorise(permissivehyper-
capnia)solongasthepHremainedgreaterthan7.25.TheaimforPaO
wastoremain
Chapter26:SepsisinaBMTpatientadmittedtoPICU
Sinceitwaspossiblethatthepatientwouldnotbefedinthenextdayortwo,hewas
startedonranitidineforprotectionagainstgastrointestinalbleeding.Intravenousantibiotics
werecontinuedwithregularmonitoringoflevels.Dailylaboratorymonitoringincluded
serumureaandcreatinine,giventheriskofnephrotoxicity.Otherroutineinvestigations
includedadailyFBC,electrolytes,andlivertransaminases,alongwithbilirubin.Bloodgases
wereperformedasclinicallyindicated(i.e.changeinpatientstatusorventilator)atleastfour
timesperday.
OverthecourseofhisPICUstay,thepatient
Chapter26:SepsisinaBMTpatientadmittedtoPICU
Chapter26:SepsisinaBMTpatientadmittedtoPICU
Inotropicorvasopressortherapyshouldbeconsideredinsepticshockonlyafteradequate
initialfluidresuscitation.Thiscanbebasedonanage-appropriatecentralvenouspressureor
often,intheabsenceofcentralpressuremonitoring,onpresumedadequatefluidresuscita-
tion(40to60mlkg
ofcrystalloid).Adultstypicallydemonstratearelativedysfunctionin
vasomotortoneinresponsetosepsis.Theypresentwithgoodcardiacoutputbutlowblood
pressurewithwarmperipheriesandboundingpulses,theso-called
warmshock.
Children
donotbehavelikeadultsandrespondinamorevariablemannertoinfection.
importanttonoteisthatchildrenareoftenabletomaintainbloodpressure,despitefalling
cardiacoutput,throughelevationofsystemicvascularresistance.Thechildinthiscase
demonstratedaclassicexampleof
coldshock.
Thebloodpressurewaswellmaintained,
despitesignificantmyocardialdepressionandinadequatetissueoxygendelivery.Theheart
ratewasmarkedlyelevatedinanattempttomaintainmaximalcardiacoutputandtherewas
significantvasoconstrictiontomaintainbloodpressure.Infact,thedropinbloodpressureof
achildisalateandoftenworrisomefinding.Ageappropriatetablesexisttoestimateblood
pressurebutasimpleclinicaltooltoestimatethefifthpercentileforsystolicbloodpressure
is70+(age×2).
PICUmanagement
VentilationwasimplementedinthePRVCmodewithdeliveredtidalvolumesof10mlkg
AsthepatientdevelopedARDS,ventilationwaschangedtoreflectamorelung-protective
strategyof6mlkg
Initialuseofafractionofinspiredoxygenat1.0wastoimproveoxygen
deliverytoendorgans.Thiswasweanedasoxygendeliveryimproved.Transfusionofpacked
Chapter26:SepsisinaBMTpatientadmittedtoPICU
inferiorvenacava(IVC)andsuperiorvenacava(SVC)bloodhasadequatelymixed.In
children,centralSVO
(SVCorIVC)bloodmayserveasasurrogateformixedvenousblood
andisparticularlyusefulforobservingtrends.Ithasbeenadvocatedtoaimforasaturationof
70%intheSVCduringsepsistoensureadequateoxygendelivery.
Inthiscase,cardiovascularsupportwastitratedtoend-organperfusion,aimingforgood
Chapter26:SepsisinaBMTpatientadmittedtoPICU
SurgicalstrategiesforfailedFontancirculations
Fontanconversion
TherehasbeenconsiderablesuccesswithFontanconversionsforpatientswithfailingFontan
circulationsleadingtoreductioninrightatrialsize,abatementorimprovementinatrial
arrhythmias,resolutionofrightpulmonaryveincompression,resolutionofpleural
effusions,andclinicalimprovement(improvementinNYHAclassandexercisetoler-
ance).
,24,
Fontanconversionsaremostusefulinpatientswithatriopulmonary
Fontanswithabnormalitiesamenabletosurgicalrepairorinthosewitharrhythmiasrefractory
tomedicalmanagementorpacing(see
Figs.25.3
and25.4).Lesionsamenabletosurgical
interventionincludesystemicvenousbaffleobstruction,proximalpulmonaryarterydistor-
tions,rightpulmonaryvenousobstructionsecondarytoadilatedrightatrium,atrioventricular
valveregurgitation,andventricularoutflowtractobstruction.Seriesofconversionshave
includedtransitionstolateraltunnelbafflesorextracardiacconduits,bothaimedatstream-
liningflowthroughtheFontancircuitanddiminishingatrialsuturelinesthatpredisposethe
patienttoIART.Theseproceduresareoftenscheduledinconjunctionwithrightatrial
debulking,cryoablationorradiofrequencyablationoffocigeneratingatrialarrhythmias,
rightorbiatrialmazeprocedures,andepicardialpacemakerplacement.
,24,
,35,
OrthotopicHeartTransplantation(OHT)
Iftherearenodefectsamenabletotransca
RA
SVC
IVC

with stent
RPA
Fig.25.3.
FailingatriopulmonaryFontanwithsevere
rightatrialdilationandapreviousstentintheleft
pulmonaryartery.SVC=superiorvenacava,RPA=right
pulmonaryartery,LPA=leftpulmonaryartery,RA=right
atrium,IVC=inferiorvenacava
Chapter25:Managementofthepatientwithafailingfontan
entailsadditionalrisk;thesepatientshavehadprevioussurgeries(oftenmultiple),have
multipleadhesions,andanincreasedriskof
bleeding,haveincreasedlymphocytotoxic
antibodiessecondarytobloodtransfusions,andmayhaveelevatedpulmonaryvascular
resistancewhichcancausedifficultieswithr
ightventricularfailurepost-operatively.
Acaseseriesofcardiactransplantationinp
atientswithaFontancirculationdidnothave
anincreasedriskwhencomparedwithotherswithformsofcongenitalheartdisease.
Withtheseconsiderations,OHTmaybetheo
nlyviableoptionforsomepatientswitha
failingFontancirculation.
Overall,thepatientwithafailingFontancirculationpresentsadifficultclinicalchallenge
requiringvigilancetodiagnoserepairablelesionsasmedicaltherapyisoftenunsatisfying.
MedicaltherapyisaimedatimprovingsymptomatologyinapatientwithafailingFontan
suchasdecreasingedema,preventingcomplicationsfromthromboembolism,anddimin-
ishingthecontributionofarrhythmias.Preservationofventricularfunctionisalsoofpara-
mountimportanceasthiscanbeanominousfindingwithfewtherapeuticoptions.Blood
Fig.25.4.
Pre-andpost-operativeCXRsinapatientwhounderwentconversionfromanatriopulmonaryFontanto
alateraltunnelFontanwithrightatrialdebulkingandplacementofanepicardialpacemakershowingadecreasein
thecardiacsize.
Chapter25:Managementofthepatientwithafailingfontan
remainspalliativeandeventhe
perfectFontan
islikelytoeventuallyfail.Thefocusonthis
groupofpatientsistocontinuetoimprovemedicalandsurgicalmanagementinorderto
increaseboththedurationandqualityoflifeforthepatientwithaFontancirculation.
Learningpoints
Withrecentdecreasesinearlymortality,morepatientsaresurvivingtoexperience
associatedmorbiditiesrelatedtotheFontancirculation.
Post-operativeissuesfollowingaFontanoperationinclude:Fontanpathwayobstruction,
atrialarrhythmias,thromboembolism,progressivecyanosis,lowcardiacoutput,and
proteinlosingenteropathy.
FontanconversionsaremostusefulinpatientswithatriopulmonaryFontanswith
abnormalitiesamenabletosurgicalrepairorinthosewitharrhythmiasrefractoryto
medicalmanagementorpacing.
Chapter25:Managementofthepatientwithafailingfontan
15.JacobsML,PourmoghadamKK,GearyEM
Chapter25:Managementofthepatientwithafailingfontan
Fontanoperation.
JThoracCardiovascSurg
:863
38.ConteS,GewilligM,EyskensB,Dumoulin
M,DaenenW.Managementoflate
complicationsafterclassicFontan
procedurebyconversiontototal
cavopulmonaryconnection.
CardiovascSurg
:651
39.GambaA,MerloM,FiocchiR
Chapter25:Managementofthepatientwithafailingfontan
Managementofthepatientwith
afailingfontan
ofapalliativeprocedure
HeatherA.DickersonandAnthonyC.Chang
Thiscaseillustratesmanyofthepost-operativecomplicationsencounteredinthefollow-up
ofthepatientwhohashadaFontanprocedure.Withdecreasesinmortalityovertheyears,
morepatientsaresurvivingtoexperienceassociatedmorbiditiesofthispalliativeprocedure,
eveninthosewitha
perfect
Fontancirculation.
Theprocedurehasalsoexpandedto
palliatepatientswithelevatedpulmonaryvascularresistance,borderlinepulmonaryartery
anatomy,andthosewithcomplexsingleventricleanatomywithothercomplicatingfactors
historyrevealedthatshewashavingrecurrentpalpitationsthathadbeenprogressively
increasinginfrequencywithsomeepisodeslastinguptoanhour.Shehadnothadany
symptomsofchestpain,shortnessofbreath,orneurologicdeficits.Anechocardiogramat
thistimedocumentedthefindingspreviouslyseen,butalsoshowedathrombusalongthe
lateralrightatrialwallandmoderateleftventriculardysfunction.Pulseoximetrywas92%
onroomairandaCXRrevealedsmallbilateralpleuraleffusions.Hercoagulationstudies
werenormalexceptamildlyelevatedprothrombintimeandamildproteinCdeficiency.
SherequiredadmissionforheparinizationandeventualDCcardioversionafterresolutionof
herintracardiacthrombus.Shewasstartedonsotaloltocontrolheratrialarrhythmiasin
additiontowarfarinforanticoagulation.ShehadcontinuedepisodesofIARTrequiring
cardioversionandhersotalolwastransitionedtoflecainidewithoutsignificanteffect.She
hadworseningexerciseintolerance,wasunabletoworkandhadrecurrenceofherlower
extremityedema.Heralbuminandtotalproteinlevelswereonthelowendofthenormal
rangesandshedidnothaveelevationinherstool
1antitrypsin.Shedidnothavediarrhea.
Chapter25:Managementofthepatientwithafailingfontan
Post-operativeissuesfollowingaFontanprocedure
Fontanpathwayobstruction
FactorswhichcompromiseflowthroughtheFontancircuitwilldiminishcardiacoutputand
functionalstatusandleadtomanyofthemorbiditiesassociatedwiththiscirculation.
Associatedmorbiditiesoftencannotbereversedorimprovedwithoutaddressingobstruc-
tionintheFontanpathway.HemodynamicsindicativeofobstructionintheFontanpathway
includeanincreasedcentralvenouspressure(CVP)withalowleftatrialpressure(LAP)
resultinginanincreasedtranspulmonarygradient(CVP
LAP).Afterrulingouttreatable
pulmonaryproblems(pneumonia,poorventilation,pleuraleffusions),circulatorycauses
mustbeinvestigated.Obstructionmayoccurwithinthesystemicvenousbaffle,atthe
pulmonaryarteriessecondarytodistortionorasaresultofcompressionofthepulmonary
veins.BleedingaroundtheFontancircuitcancauseexternalcompressionaswellandpresent
asobstruction.Obstructioncanalsobesecondarytopulmonarythromboembolism.Allof
theseabnormalitiesincreasetheresistanceintheFontancircuitleadingtoincreasesinthe
systemicvenouspressurerequiredtomaintainflow.Theseobstructionsareoftenhardto
delineatebynon-invasivemeansduetopoorechocardiographicwindows,lowpressure
gradientswithnon-pulsatilevenousflowandthefactthatmanyobstructionsareinthe
distalpulmonaryvasculature.
RPA
LPA
RA
MPA
Stenosis
RA
Fig.25.1.
Atriopulmonary
Fontanwithstenosis
intheatriopulmonary
connection.RA=right
atrium,RPA=right
pulmonaryartery,
LPA=leftpulmonary
artery.
Chapter25:Managementofthepatientwithafailingfontan
previoussurgeriesorbycongenitalpulmonaryarteryanomaliesorstenoses.Someofthese
II
III
IV
3VF
aVL
aVR
V1
V2
V3
V6
V5
V3R
V4R
V7
Fig.25.2.
Intra-atrial
tachycardia(IART)
with2:1conduction
(seecolorplate
Chapter25:Managementofthepatientwithafailingfontan
Chapter25:Managementofthepatientwithafailingfontan
pressureandatrialpressureincreases.CausescanincludedistalobstructionsintheFontan
circuitasdelineatedabove.PulmonaryAVMsmayresultinintrapulmonaryshuntingof
venousblooddirectlyfromthesystemicveinstothepulmonaryveins.Theyaremorelikelyif
thepatienthasahistoryofaclassicGlennshunt,butcandevelopinitsabsence.Venoatrial
connectionscanbeabsentinitially,butdevelopinthefaceofworseninghemodynamicsas
thesevenousvesselsrecanalizeorenlargebecomingclinicallysignificant.Insomepatients
Chapter25:Managementofthepatientwithafailingfontan
contributedventriculardysfunctiontoventricularvolumeoverloadfromthepresenceof
aortopulmonarycollaterals;theyarereadilyaddressedinthecatheterizationlaboratory.
Diastolicventriculardysfunctioncanbesecondarytochronicunderloadingoftheventricle
Chapter25:Managementofthepatientwithafailingfontan
partoftheairwayisthesubglotticregionratherthanthevocalcordsandthedistancefrom
thevocalcordstothecarinaisrelativelyshortcomparedtotheadult.
Stepsinevaluationincludelookingforsignsofadequaterespiratoryeffortfollowedby
Table24.9.
Trachealtubesizebyage
Chapter24:Achildwithmultipletrauma
However,someanesthesiologistsusecuffedtrachealtubesinvirtuallyallchildren.After
trachealintubation,therigidcollarshouldbereplaced.Fiberopticintubationcanbe
consideredfordifficultintubationsbutisusuallylefttocliniciansaccustomedtoperforming
pediatricfiberopticintubations,andpreferablynotleftasarescuetreatmenttofaileddirect
laryngoscopy.Lastly,nasotrachealintubationisrarelyindicatedinthetraumapatientandis
contra-indicatedinthepresenceofbasilarskullornasalfractures.
Circulationisevaluatedbyfeelingperipheralandcentralpulsesandbyassessingperfu-
sionusingcapillaryrefillandbloodpressure.Whilepediatricpatientsbecomeprogressively
tachycardicasbloodlossoccurs,theyareabletomaintaintheirbloodpressureuntillosses
aregreaterthan25%ofcirculatingbloodvolume.
Afterthistime,decompensationcanbe
rapid.Bradycardiaisanominoussignandmaysignifysignificantcardiacinjuryorraised
intracranialpressure(ICP)aspartofCushing
striad(hypertension,irregularrespirations,
andbradycardia)insevereTBI.Regardlessofthecauseofbradycardiainyoungchildren,it
resultsindecreasedcardiacoutput(CO)astheyhaverelativelyfixedstrokevolume(SV).
Venousaccessisanintegralpartoftraumacareandadequateaccessdependsonthesize
ofthepatientaswellastheseverityofinjuries.Formostchildren,a22-gaugePeripheral
IntravenousCatheter(PIV)isadequatetobeginresuscitation.AlargersecondorthirdPIV
shouldthenbesought.
Typically,upperextremityveinsarepreferred.However,inthe
absenceofsignificantabdominaltrauma,saphenousveinsprovidealargeveininapredict-
ablelocationthatcanbeaccessedeitherpercutaneouslyorbycut-down.Atthetimevenous
Intheeventthatperipheralaccesscannotbeobtainedaftertwoattemptsor90secondsin
anemergentsituation,anintra-osseous(IO)lineshouldbeplacedwitheitherapackaged
intra-osseousneedleoranylargebore(18
16G)needle,suchasalargespinalneedle.
This
techniquehasclassicallybeenrecommendedforchildrenlessthan6yearsofage,butcanbe
effectivewellbeyondthisage.Theanteromedialsurfaceoftheproximaltibiaisthemost
commonsiteofinsertion,butanynon-traumatizedlongbonecanbeused.Ifthetibiais
chosen,theneedleisinserted2cmbelowand1
2cmmedialtothetibialtuberosity,usinga
twistingmotionuntilalossofresistanceisnoticedindicatingthetipoftheneedleisinthe
marrowcavity(
Fig.24.8
).Often,bonemarrowcanbeaspiratedwhentheneedleisinthe
Femur
Patella
Epiphyseal plate
Fig.24.8.
Intra-osseousvascular
Chapter24:Achildwithmultipletrauma
bonemarrow.Inabilitytoaspiratedoesnotn
ecessarilymeanimproperplacementaslong
asthereisnotevidenceofinfusedfluidinth
esofttissue.Theneedleneedstobesecuredto
thepatientaswellaspossiblerecognizingthetemporarynatureoftheIOlineuntilmore
definitiveaccesscanbeobtained.Substances
thatcanbeadministeredbythevenousroute
canbegivenbytheIOroute;includingcrystalloid,medications,blood,andblood
products.
Centralvenousaccesscanbeusedasvenousaccessaswellasanindicatorofvolume
status,butisbestplacedbyexperiencedpersonneltoavoidiatrogenicinjury.Thefemoral
routeisoftentheeasiesttoplacebutshouldbeavoidedwhenthereisInferiorVenaCava
injury(IVC)orsignificantliverinjurywithongoingbleeding.
Arteriallineplacementisoftenhelpfulandnecessaryandismostcommonlyperformed
confirmorruleoutinjuriessuspectedbytheexam.Insometraumacenters,itisroutinetodo
ascreeningultrasoundcalledFocusedAssessmentSonographyforTrauma(FAST)ofthe
abdomenandchestcavitytolookforfreefluid,indicatingtheneedforeitheradditional
studiesoroperativeinvestigation.Currently,however,thereisnotaconsensusontheutility
ofthisinchildren.
Thepediatricpatienthasalargersurfacetobodyratiocomparedtoadultsandtherefore
ismorepronetoheatloss.Thosepatientswhoarrivehyperthermicshouldbecooledto36
37°C.Normothermiashouldbesoughtinallpatientsexceptinthosewithrefractoryintra-
cranialhypertension,inwhichcasehypothermia(32
34°C)maybeconsidered(
Table24.2
Otherwise,patientsshouldbewarmedto36
37°Cwithwarmblankets,lights,warmedIV
fluids,andhumidifiedoxygen.
Learningpoints
Traumaisaleadingcauseofmortalityandperma
nentdisabilityinchildrenover1yearofage.
Traumaticbraininjuryisthemostcommoninjuryinchildrenfollowingblunttrauma.
InthepresenceoftraumaticbraininjuryitshouldbeassumedthatthechildhasaC-spine
injuryuntilprovenotherwise.
Chapter24:Achildwithmultipletrauma
Ribfracturesinyoungchildrenimplythatasignificantforcewasappliedtothechild
thorax.
Abdominalinjuriesarepresentin8%ofbluntpediatrictraumapatients,withtheliver
andspleenmostcommonlyinjured.
Pelvicfracturesinchildrenarerarelythecauseofhemodynamicinstability.
Injuriesoutofproportiontothereportedmodeofinjuryshouldalertthecliniciantothe
possibilityofnon-accidentaltrauma.
PediatrSurg
.1979;
(1):41
15.NewmanRJ,JonesIS.Aprospectivestudyof
413consecutivecaroccupantswithchest
JTrauma
(2):129
16.CooperA.Thoracicinjuries.
SeminPediatr
.1995;
(2):109
17.BaumVC.Cardiactraumainchildren.
PaediatrAnaesth
:110
18.DowdMD,KrugS.Pediatricbluntcardiac
injury:epidemiology,clinicalfeaturesand
JTrauma
(1):61
19.GainesBA,FordHR.Abdominalandpelvic
traumainchildren.
CritCareMed
.2002;
(Suppl):S416
20.GarciaVF,BrownRL.Pediatrictrauma
beyondthebrain.
CritCareClin
21.BondSJ,EichelbergerMR,GotschallCS
Chapter24:Achildwithmultipletrauma
Chapter24:Achildwithmultipletrauma
associatedabdominalandbackpain(
Fig.24.7
).Diagnosisismadewitheitherserialphysical
examinationsorfreeaironradiographorCT.AdditionalfindingonCTsuggestiveofbowel
injuryincludefreeintraperitonealfluidintheabsenceofsolidorganinjuryandbowelwall
thickening.Overall,CTispooratidentifyingisolatedbowelinjury.
Table24.3.
Liverinjuryscale
GradeInjurydescription
VIVascularHepaticavulsion
VLacerationParenchymaldisruptionof�75%ofhepaticlobe
Table24.4.
Spleeninjuryscale
GradeInjurydescription
VVascularHilarinjurywithdevascularizedspleen
LacertaionShatteredspleen
IVLacerationLacerationofsegmentalorhilarvesselsresultingindevascularizationof�25%of
IIIHematomaSubcapsularinvolving�50%surfaceareaorexpanding.Rupturedsubcapsularor
Chapter24:Achildwithmultipletrauma
Orthopedicinjuries
Orthopedicinjuriesotherthanspineinjuriesareverycommon,butarerarelythecauseof
death.However,interruptionofongoingbonegrowthfromtraumacanresultinsignificant
morbidity.Alsoongoinggrowthanddevelopmentcanmakeradiologicdiagnosisofbone
injuriesdifficultforcareprovidersnotaccustomedtonormalchangesofdevelopment.
Routinepelvicradiographsareappropriateforthepediatrictraumapatientastheyarefor
theadultpatient.Pelvicinjuriesareassociatedwithotherinjuriesnearly75%ofthetime.
Theirpresence,therefore,isanindicationofasignificantbluntforceandotherinjuries
shouldbesought.Unlikeadults,pelvicfracturesinchildrenarerarelythecauseofhemody-
namicinstability.
Untildefinitivefixation,temporarypelvicstabilizationcanbeachieved
withbedrest,apelvicsling,orexternalfixationasthemedicalconditionallows.
Openfracturesareurgentinjuriesthatneedtoberepairedwithin6hourstominimizethe
risksofinfection,furthersofttissue,andmuscleinjury,andnon-unionormalunionofthe
bone.Allfracturesshouldbesplintedassoonasmedicallypossibleafterthesecondary
traumasurvey.Irrigationanddebridementshouldbeperformedassoonaspossibleand,if
neurovascularinjuryispresent,definitiverepairshouldoccurwithin6hours.
Closedfracturescanappearlessconcerningthanopenfractures,butthiscanleadtoa
falsesenseofsecurityifongoingbloodloss,neurovascularcompromise,orcompartment
syndromeexist.Diagnosisbeginswiththephysicalexamduringthesecondarysurveyalong
withappropriateradiographstoconfirmthediagnosis.Initialtreatmentissplintingwhile
stabilizationandtreatmentofmorelife-threateninginjuriesoccursfollowedbydefinitive
repairandfixationwhenthepatienthasstabilized.
NAT,orchildabuse,resultsinover300deathseachyearintheUSA.Headinjuries,mainly
subduralhematomas,asaresultofblunttraumaorviolentshaking(ShakenBabysyndrome)
aretheleadingcauseofdeathamongchildrenlessthan1yearofage.
Whileitcan
Fig.24.7.
Seatbeltsyndrome(seecolorplatesection).
Chapter24:Achildwithmultipletrauma
trainedtoevaluateandnavigatethepublichealthsystemshouldbeconsulted.Inaddition,a
Table24.5.
Normalhemodynamicvaluesbyage
90thpercentile
systolicblood
5thpercentile
systolicblood
90thpercentile
diastolicblood
pressure(mmHg)
5thpercentile
diastolicblood
1year120105726948
3years110105786248
5years100108786748
8years90112827352
10years91117897554
13years85124957959
16years851311038160
ValuesareapproximateandadaptedfromUpdateonthe1987TaskForceReportonHighBloodpressureinChildren
andAdolescents.
.98(4)Oct1996,Reportofthetaskforceonbloodpressurecontrolinchildren.
.59
(5)Suppl.May1977,AdelsonPD.BrattonSL,CarneyNA
Table24.6.
Estimatedpediatricbloodvolumesbyage
Estimatedbloodvolume(EBV)(mlkg
Prematureinfant90
Full-terminfant80
3months
1year70
�1year70
Chapter24:Achildwithmultipletrauma
lactateorPlasma
LyteR
)bolusof20mlkg
,representingroughly25%ofcirculating
volume.Ifthisisunsuccessfulinrestoringnormalbloodpressure,asecond20mlkg
ofthesamesolutionshouldbegiven.Ifthepatienteitherhasongoingbloodlossorcontinues
tobehemodynamicallyunstable,PRBCshouldbegiven.Theoverallgoalsoffluidresusci-
tationaretorestorehemodynamicstabilityandensureorganperfusion.End-pointsinclude
normalheartrateandbloodpressureforage,decreasedskinmottling,increasedwarmthin
extremities,improvedsensorium,urineoutput�1mlkg
perh,increasedpulsepressure,
andcorrectionofsourcesofbloodloss.
Invirtuallyallhospitals,theadministrationofredbloodcellsisachievedwithblood
concentratessuchasPRBC,aswholebloodisrarelyneededoravailable.TypicalPRBC
preparationshaveahematocritofaround50%
75%.Fora10mlkg
bolus,thehematocrit
shouldincreasebyapproximately10%.
Bloodtransfusionshouldbegiventomaintainoxygen-carryingcapacitytothebody.
Table24.7.
Indicationsfortransfusionofpackedredbloodcells(PRBCs)inchildren
Clinicalsituation
Transfusionhematocritgoal(%)
Acutebloodlossw/hypovolemianotresponsivetoother
Emergencysurgerywithsignificantpre-operativeanemia�24
Intra-operativebloodloss
15%ormorethanmaximalallowable
bycalculation
Severepulmonarydisease
Cyanoticheartdisease
Theseend-pointsmaybealteredfordifferentclinicalsituations.AdaptedfromRoseffSD,NaomiLC,MannoCS.(2002).
Table24.8.
Chapter24:Achildwithmultipletrauma
whendecidingRBCtransfusion,regardlessoftheclinicalsituation.Othersattempttotake
intoconsiderationotherfactorslikeage,ongoingbloodloss,evidenceofcyanoticheartor
sicklecelldisease,andpooroxygendelivery,suchasincreasingserumlactate,whendeciding
totransfusePRBCs.Previouslyhealthychildrencantoleratehematocritswellbelow30%
beforeadversesequelaeareseen.
PRBCsthathavebeencross-matchedarethemostdesiredformofredbloodcell
replacement.However,inacute,life-threateningsituations,uncross-matchedOblood
shouldbeused.ThereisnostandardastowhentouseOnegativeversuspositiveblood.
Insomehospitals,OnegativebloodisreservedforfemalestoavoidalloimunizationtotheRh
Chapter24:Achildwithmultipletrauma
Achildwithmultiple
JoshuaC.UffmanandMonicaS.Vavilala
Traumaistheleadingcauseofmortalityinchildrenover1yearofageandasignificantcause
ofpermanentdisabilityintheUnitedStates.
Mostinjuriesaretheresultofblunttrauma
fromMotorVehicleCrashes(MVC),wherethechildiseitheranoccupantorisstruckbya
vehicle.TraumaticBrainInjury(TBI)isthemostcommoninjury,butabdominal,chest,
spine,pelvic,andlongboneinjuriesalsooccureitheralone,orinassociationwithTBI.Other
causesofinjuriesincludefalls,Non-AccidentalTrauma(NAT),andsports.
Casehistory
A7-year-oldmalewasbroughttotheemergencydepartment(ED)bytheEmergency
MedicalService(EMS)afterbeinghitbyacarwhileridinghisbicycle.Witnessesreported
fracture.Giventhephysicalexamfindingsandmechanismofinjury,computedtomography
(CT)ofthehead,neck,abdomenandpelviswithoralandintravenouscontrastwasplanned.
ThirtyminutesafterarrivalattheED,thepatientbecamerestlessandconfused.He
vomitedtwice.HisHRincreasedintothe150sandhisBPdecreasedto80/42mmHg.A
second20mlkg
bolusofnormalsalinewasgivenwithnoeffect.Hebecamemoresomnolent
anddevelopedintermittentepisodesofagitation.Laboratoryevaluationrevealedahematocrit
of24%.Twentymlkg
ofun-cross-matchedOnegativebloodwasgiven.HisBPimproved
to90/50mmHgbutHRremainedintheupper140swithnoimprovementinmentalstatus.
Thetraumateamdecidedtosecuretheairwaybyintubation.Preparationsincluded
Fig.24.1.
Right-SidedSubduralHematoma(SDH)with
nomid-lineshift.
Fig.24.2.
ComputedtomographyofGradeIVliver
Chapter24:Achildwithmultipletrauma
musclerelaxantand5mcgkg
intravenousfentanylgivenincrementally.Becauseofthe
SDH,theneedforgeneralanesthesia,andlikelyprolongedsedationallmakingneurological
assessmentdifficult,theneurosurgeonplacedaCaminofiberopticintraparenchymalintra-
cranialpressuremonitor(
Fig.24.4
).Initialintracranialpressure(ICP)was18mmHg
andcerebralperfusionpressure(CPP)45mmHg.Afterabdominalincision,alargeamount
ofbloodlossoccurredandtheBPdroppedto50/25mmHgandtheHRincreasedto175b
min
.Fourcross-matchedunitsofPRBCsweregivenoverthenext20minutes,whilethe
liverwaspackedandthepatientwasstabilized.BPincreasedto80/45mmHgandHR
decreasedto145bmin
.Repeathematocritwas25%andanadditional6unitsofPRBCs
Fig.24.3.
Fig.24.4.
ofCaminofiberoptic
intraparenchymal
intracranialpressure
Chapter24:Achildwithmultipletrauma
wereordered.Therewasnourineoutputovera30-minuteperiodand40mlkg
normal
salinewasadministeredincrementallytomaintainasystolicBP�90mmHgandCPP
�40mmHg.Coagulationstudiesrevealedplateletsof90000×10
andINRof1.8;
fourunitsofplateletsandfourunitsFreshFrozenplasma(FFP)weregiven.Allfluids,
Fig.24.5.
Radiograph.Antero-posteriorviewright
femurfracture.
Fig.24.6.
Lateralviewrightfemurfracture.
Chapter24:Achildwithmultipletrauma
Traumaticbraininjury
Traumaticbraininjury(TBI)isthemostcommoninjuryinchildrenfollowingblunttrauma.
Thistopicisdiscussedelsewhereinthisbook;howeveritisdifficulttoavoidabasic
discussionofTBIwhendiscussingpediatrictrauma,sinceitisrareforachildtohave
significantinjuriesfollowingtraumawithoutassociatedTBI.TheincreasedriskofTBIis
largelyduetotheirlargerhead-to-bodyratiothanadults,lesscentralnervoussystem(CNS)
myelination,andmorecompliantbones.Blunttraumacanresultinanacceleration
erationinjury,withcerebralcontusion,intracranialhemorrhage,orDiffuseAxonalInjury
(DAI).DAIistheresultoftissueshearing,usuallyatthejunctionoftwotissuetypesof
differingdensities,mostcommonlyatthegray
whitematterinterface.DAIisacommon
causeoflong-termdisabilityinpatientswithTBI.
DiagnosisofTBIstartswiththeassumptionofinjury,evenintheabsenceofneurological
deficits,aschildrenaremorelikelythanadultstohaveneurologicaldeficitspresentlateinthe
courseofinjury.ThemodifiedGCSishelpful:moreasatrendthananabsolutenumber.The
modifiedGCStakesintoaccountthechild
sageinthederivationoftheverbalandmotor
components(
Table24.1
).Ingeneral,TBIisgradedasfollows:mild(GCS13
15),moderate
(GCS9
12),andsevere(GCS9).InitialCToftheheadmayshowintracranialbleedingand
contusions,butpatientswithDAImayhaveanormalCTwithoutevidenceofinjuryuntil
muchlaterwhencerebraledemabecomesapparent.
ManagementofTBIiscomplexandcurrentrecommendationsaretheresultof
extrapolationfromadultstudiesinmostcases.In2003,theBrainTraumaFoundation
published
Guidelinesfortheacutemedicalmanagementofseveretraumaticbraininjury
ininfants,childrenandadolescents
PediatricCriticalCareMedicine
CriticalCare
andthe
JournalofTrauma
assimultaneoussupplements.Theyrecommend
preventinghypoxia,hypocarbia,andhyperc
arbia,maintainingSBP�fifthpercentilefor
ageandCPP�40mmHginchildrenwithsevereTBI(
Table24.2
).Whiletherecommen-
dationsareforsevereTBI,manyprovidersal
soextrapolatetheinformationtomoderate
headinjury.
Spinalfracturesandspinalcordinjury
Overall,traumaticspineinjuriesarelesscommoninpediatricthanadulttraumapatients,
withanincidenceof1%
MostspineinjuriesarearesultofMVCs,althoughfallsand
sports-relatedinjuriesarealsocommoncausesinyoungerchildrenandadolescentsrespec-
.OfallSpinalCordInjuries(SCI),5%occurinchildrenlessthan16yearsofage.
Despitethisapparentlowincidence,mortalityis15%
20%inC-spineinjuries(CSI)because
50%ofthesechildrenhaveassociatedTBI.InthepresenceofTBI,itshouldbeassumedthat
thechildhasaCSIuntilprovenotherwise.
Theageofthechildinfluencesthelevelofspineinjury.Inpatientsyoungerthan11years,
thelocationofSCIismorelikelytobeC1
C4whereaspatientsgreaterthan11yearsaremore
likelytohaveinjurytoC5
C7,similartoadults.
Injurytothethoracolumbarspineisrarein
children,accountingforonly10%
20%ofspineinjuries.Mostthoracicspineinjuriesare
fromMVCsorfallsresultingincompressioninjuries.
Chapter24:Achildwithmultipletrauma
Therearemanypostulatesastothedifferentpatternsofspineinjuryinchildren,but
anatomicandsocialdifferencesappearthemostlikelyexplanations.Inyoungerchildren,the
headrepresentsagreaterpercentageofbodyweightresultinginthefulcrumofmovement
beingC2
C3comparedtoadolescentsandadultswhereitisC5
C6.Inaddition,thecervical
spineislessabletoprovidesupportbecauseofgreatermuscleandligamentlaxityand
Table24.1.
ModifiedGlasgowComaScoreforchildren
Besteyeresponse(modificationforinfants)
4Eyesopenspontaneously(spontaneously)
3Eyesopentospeech(tospeech)
2Eyesopentopain(topain)
1Eyesdon
topen(don
topen)
Bestverbalresponse(modificationforinfants)
5Orientedandconverses(coos,smiles,babbles,andinteracts)
4Confused(irritableand/orinappropriateinteractions)
3Inappropriatewords(criestopainandinconsistentlyconsolable)
2Incomprehensiblesounds(moanstopainandinconsolable)
1None(none)
Bestmotorresponse(modificationforinfants)
6Obeysverbalcommands(normalspontaneousmovements)
5Localizespain(withdrawstotouch)
4Withdrawstopainfulstimulus(withdrawstopainfulstimulus)
3Abnormalflexion(abnormalflexion)
2Extensionposturing(extensionposturing)
1Nomotoractivity(nomotoractivity)
GCS13
15:Mildheadinjury.
GCS9
12:Moderateheadinjury.
GCS9:Severeheadinjury.
Modifiedfromtrauma.orgwebsite.
Chapter24:Achildwithmultipletrauma
Theexactprotocolforspineclearancevariesbyinstitutionandpractitionerbutusually
consistsoftheabsenceofradiologicalinjuryandabsenceofneurologicaldeficit.Ifdoubt
existsaboutaneurologicaldeficit,orifthepatientiscomatose,anMRIisperformedlooking
forevidenceofSCIWORA.Twenty-fivepercentofthetime,SCIWORApresentswellafter
theoriginalinjury
.Sincethoracolumbarinjuriesarerare,routinescreeningforinjuryisnot
recommended.
Thepresenceofthoracicorabdominaltraumashouldpromptaworkupfor
SCI,beginningwithplainradiographs.
TheroleofsteroidsinSCIiscontroversial.SeveralstudiescalledtheNationalAcute
SpinalCordInjuryStudy(NASCIS)I
Table24.2.
Recommendationsformanagementofseverepediatricheadinjury
Chapter24:Achildwithmultipletrauma
Cardiothoracicinjury
Thoracicinjuryaccountsforonly4%
10%ofpediatrictrauma,
Chapter24:Achildwithmultipletrauma
Abdominalinjury
Abdominalinjuriesarepresentin8%ofbluntpediatrictraumapatients,withthespleenand
liverbeingthemostcommonlyinjuredintra-abdominalorgans.
Comparedwiththeadult,
thechild
Chapter24:Achildwithmultipletrauma
useofextracorporeallifesupport.Thegoalofventilatorysupportistoprovideadequate
oxygentationandCO
removalatthelowestpossibleFiO
andpeak(ormean)airway
pressures
PermissivehypercapniareferstothepracticeofacceptinghigherlevelsofPaCO
(inthe
75mmHgrange)andassociatedrespiratoryacidosis(generallypH�7.2).Despitethe
Fig.23.5andFig.23.6.
Edema,ulceration,sloughingofairwaymucosaatthelevelofcarinaandlarynxas
seenonfiberopticbronchoscopy
.(ImagescourtesyofLeeWoodson,MD,Ph.D.;UniversityofTexasMedicalBranch,
BurnsHospital;Galveston,TX.)(Seecolorplatesection.)
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
Patientsshouldbeextubatedassoonastheupperairwayedemaisresolvedandthe
adequacyofgasexchangeisconfirmed.Aleakaroundtheendotrachealtubeanddirect
laryngoscopicand/orfiberopticvisualizationoftheairwayserveasclinicalguidesfor
resolutionofairwayedema.ItisacommonpracticeamongNorthAmericanpediatric
burncenterstousesteroidstodiminishairwayedemapriortoextubation.
Temperaturehomeostasisandnutritionalsupportforpediatricburnvictimsarecovered
elsewhereinthisbook
Severepainisaninevitableconsequenceofamajorburninjuryandanalgesicrequire-
mentsarefrequentlyunderestimated,especi
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
Non-accidentaltrauma
Childabusemustalwaysbeconsideredwhentreatingaburnedchild.Mostoftheseburns
occurinchildrenyoungerthan4yearsandinthosewithahistoryoftapwaterimmersion.
Thepatternofburninjuryshouldbecarefullyevaluatedwithspecialemphasisonthe
presenceofmultipleburns(recentorold),thepresenceorabsenceofsplashmarks,spared
ofburnarenotconsistentwiththehistory,historyofeventsleadingtotheinjurychanges
withrepeatedtelling,andthepatternofburnsisasdescribedabove.Whensuspicionis
aroused,thesocialworkerandchildwelfaredepartmentmustbecontacted.Duetothehigh
incidenceoffurtherinjuryanddeath,itisvitalthatallpersonscaringforburnedchildren
maintainanappropriateindexofsuspicionforthepossibilityofnon-accidentalburninjury.
Drugsandmaterialsusedinpatientswithburns
Silversulfadiazinecream1%
Manytopicalantisepticsandantibioticshavebeenutilizedastopicalagentsonburnwounds
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
BiobraneandIntegrawerethefirstFDA-approvedbiologicallybasedwounddressings.
Biobraneusesanultrathinsiliconefilmintowhichispartiallyimbeddedanylonfabric.The
nylonmaterialcontainsagelatinderivedfrompigtissuethatinteractswithclottingfactorsin
thewound.
Integraisatwo-layermembrane.Thebottomlayer,madeofsharkcartilageandcollagen
fromcowtendons,actsasamatrixontowhichaperson
sowncellsmigrateovertwotothree
weeks.Thecellsgraduallyabsorbthecartilageandcollagentocreateanewdermis,or
dermis.
Thisbottomlayerisapermanentcover.Thetoplayerisaprotectivesiliconesheet
thatispeeledoffafterseveralweeks.Athinlayeroftheautologousskinisthengraftedonto
theneo-dermis.
Themorerecentlyapprovedcellularwounddressingsaremadewithhumantissue.OrCel
ismadeoflivinghumanskincellsgrownonacowcollagenmatrix.TransCyteconsistsof
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
VolumeDiffusiveRespiratorvsconventional
ventilationforventilationofburnedchildren.
2001ABApaper.
JBurnCareRehabil
(6):444
10.CioffiWG,deLemosRA,CoalsonJJ
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
matchlungventilationtoperfusioninnormallungsbycausingpulmonaryarterialsmooth
muscleconstrictioninresponsetolocalizedalveolarhypoxiacausedbyairwayobstruction.
HPVisinhibitedbynitricoxide.Concomitantcutaneousburninjuryaggravatesthelung
damagebyreleasingpro-inflamatorymediatorsandcausinghydrostaticpulmonaryedema
secondarytotheloweredplasmaoncoticpressureresultingfromlossofplasmaproteininto
theinterstitialspace.TheendresultisamismatchedV/Qratioandhypoxemia.(
Fig.23.3
Thereisstrongevidencetosuggestthatmechanicalventilationcanworsenlung
damage(VentilatorInducedLungInjury,VILI).Severalfactorssuchasshearingforces
oflargetidalvolumesandexcessivepeakpressures(volutrauma,barotrauma),ahigh
(oxygentoxicity),repeatedopeningandc
losingofalveoliduetoinsufficientPEEP
contributetothedevelopmentofVILI.Inaddi
tion,thenon-homogeneousnatureofARDS
leadstolocalizedareasofover-inflationwithconventionalventilatorymodes.Over-
distensionofpartsoflunghasbeenshowntoproduceinterstitialedema,hyalinemem-
braneformation,andmicroatelectasis.
Carbonmonoxide(CO)poisoningisaleadingcauseofdeathinmajorburnswith
inhalationinjury.COhasa250-foldaffinityforhemoglobin(Hb)ascomparedwithO
.CO
displacesO
fromHbandalsoshiftstheO
Hbdissociationcurvetotheleftresultingin
impairmentofdeliveryofO
totissues(
Fig.23.4
COalsoinhibitscytochromeoxidasea3complexatthetissuelevelandthusinterferes
withaerobiccellularmetabolism.BindingofCOtocardiacandskeletalmusclesresultsin
directtoxicityandimpairedfunction,whilecentralnervousdemyelinationcanoccurbya
BronchoconstrictionFormation of exudateAirway casts
Fig.23.3.
Pathophysiologyof
tracheobronchial
damagebysmoke
inhalation
fromTraber
LD,HerndonDN:
Pathophysiologyof
smokeinahalation.In
HaponikEF,Munster
AM,eds.Respiratory
injury:Smokeinhalation
andburns.NewYork,
1990,McGraw-Hill)
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
ofCOHbandHbO
.Pulseoximetryisunreliableinthepresenceofcarbonmonoxide
oxygenadministrationresultsinfivefoldreductionofhalflifeofCOHbfrom2.5htoapprox-
imately40min.Hyperbaricoxygentherapyisfraughtwithpracticaldifficultiesoftransporting
criticallyillpatientsintohyperbaricchambe
rsand,althoughusefulinisolatedcasesofCO
poisoning,israrelyusedinthemanagementofcombinedburnandinhalationinjuryvictims.
102030405060
708090100110
Oxygen bound to hemoglobin (ml/100 ml)
Normal blood
40% Normal Hb
Fig.23.4.
Carboxyhemoglobin-
inducedchangesin
theoxygen
dissociationcurve
(Fein,Leff,A,Hopewell
PC.CritCareMed
1980;8:94
8.)
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
asecondchoice.Avenouscutdownmaybeperformedthroughunburnedorburnedskin,if
Table23.4.
BerkowchartforestimatingpercentofTBSAburnedinvariousagegroups
Area1year1
4years5
9years10
14years15yearsAdult
Head1917
Neck22
Ant.trunk1313
1313
Post.trunk1313
1313
Rbuttock2.52.5
2.52.5
Lbuttock2.52.5
2.52.5
Genitalia11
RUarm44
LUarm44
RLarm33
LLarm33
Rhand2.52.5
2.52.5
Lhand2.52.52.52.52.52.5
Rthigh5.56.588.599.5
Lthigh5.56.588.599.5
Rleg555.566.57
Lleg555.566.57
Rfoot3.53.53.53.53.53.5
Lfoot3.53.53.53.53.53.5
Total100100100100100100
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
aredressedwithsilversulfadiazine,finemeshgauze,andasimplegauzedressing.Wounds
arewasheddailytoremoveoldtopicalagentsandtissuedebris.Thisisdoneintapwaterwith
awashclothandsoap.Newtopicalagentisthenappliedinathinlayeranddressedwith
OptimalcareofpatientswithmajorthermalinjuriesasoutlinedbytheAmericanBurn
Associationrequiresanorganizedapproachbestdeliveredbyaspecializedburncenter
facility(
Table23.5
Inadditiontothegeneralobjectivesofimmediatecare,specialattentionmustbegivento
fluidresuscitationandmaintenanceoftheairwayandbodytemperature.
Fluidresuscitation
Childrenolderthan2yearswithmorethan20%TBSAburnsandallyoungerchildren
regardlessofburnsize,requireintravenousf
luidsforoptimalmanagement.Theobjective
ofresuscitationistoreplacefluidlossesand
restoreeuvolemiawiththeminimalamountof
fluidrequiredtomaintainorganfunction.Thefluidrequirementsmaybecalculatedusing
severaldifferentformulae,allofwhichach
ievegoodresults.Thereisnoconclusive
evidencere:
kindoffluid;
(howfast)togive;and
muchtogive.
fluidresuscitation(within2hoursofburninjury)helpsinlimitingthemorbidityand
mortalityinpediatricburnvictims.
TheParkland(Baxter)formulaprovidesasimple,
easilyrememberedbasisforresuscitation(4mlRinger
slactate[RL]/kgperpercentTBSA
burned;onehalftobegivenduringthefirst8hoursafterinjuryandtherestinthenext16
Table23.5.
AmericanBurnAssociation(ABA)criteriaformajorburninjuries
Partialthicknessburnsgreaterthan10%TBSA
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
resuscitationofburnvictims.Dextrose-containingfluidsandfreewatermaybeneededin
infantslessthan6monthsofage.Cardiogenicfailure,predominantlyleft-sided,isamajor
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
Thechildwiththermalinjury
andsmokeinhalation
SanjayM.BhanankerandSamR.Sharar
Burn-relatedinjuriesaccountforover1millionemergencyroomvisits,50000acute
admissions,and4000deathsintheUSAannually.Childrenbelow15yearsofageaccount
forapproximatelyathirdofburnadmissionsandburndeaths.Burnsaresecondonlyto
motorvehiclecrashesastheleadingcauseofdeathinchildrenolderthan1year.Flameburns
accountforaboutathirdofpediatricburnsandfrequentlyinvolveinhalationinjury.
Althoughburnsdirectlyaffecttheskin,largeburnsalterthephysiologicfunctionofalmost
allotherbodyorgansandcreateincreasedriskofinfectionanddeathdirectlyrelatedin
magnitudetoburnsize.
Casehistory
A4-year-oldboyandhis80-year-oldgrandmotherwerevictimsofanaccidentalhousefire.
Whilethegrandmothersuccumbedtoherinjuries
enroute
tohospital,theboywasbrought
tohospitalbytheparamedics.Hehadbeenresponsive,butdrowsy,atthesceneofthe
accident.Uponarrivalattheemergencydepartment,hebecameunresponsivetocommands,
butmovedallfourextremitiestopain.ABroselowlength-basedresuscitationtapewasused
toestimatehisweightat20kg.Hisinitialvitalsignswere:heartrate174bmin
,BP
88/40mmHg,respiratoryrateof50breathsmin
,tympanictemperature38.8
C.His
cervicalspinewasimmobilizedinanappropriatelysizedcervicalcollar.Hewasadministered
100%oxygenviaanon-rebreathingfacemaskandhistranscutaneousoxygensaturation
)was99%.Hehadflameburnsinvolvingchest,abdomen,bothhisupperextremities,
face,andpartsofhislowerextremities.Hecoughedupdark,carbonaceoussputum.Inview
ofhisunresponsivenessandpossibleinhalationinjury,theon-callanesthesiologistwas
consultedtohelpwithairwaymanagement.Intravenousaccesscouldnotbeobtained,soa
righttibialintra-osseousneedlewasplaced.FluidtherapywithRinger
slactatesolutionwas
commenced.Followingpre-oxygenation,arapidsequenceinductionwasperformedbythe
Table23.1.
Findingsonadmission
ExaminationAirwayclearbutedematous,sats99%on100%Oxygen
Respiratoryrate50min
Chestclear,bilateralairentry,coughingupdarksputum
Heartrate174bmin
,Capillaryrefilltime=3seconds
Normalheartsounds,BP88/40,peripheralpulsespalpable
Temperature38.8
52%TBSAburnswithsmokeinhalationinjury
InvestigationsWeight20kg(EstimatedusingBroselowtape)
FBCHb14.6gdl
,Plat410×10
WBC13.4×10
U+EsNa
138mmoll
4.2mmoll
,Cl
110mmoll
Urea15.9mmoll
,Creatinine100
moll
2.1mmoll
Glucose12.5mmoll
Albumin25gl
ArterialpH7.22,
50mmHg,HCO
16.2mmoll
bloodgasBE
11.4,carboxyhemoglobin30%
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
28breathsmin
tocorrecttherespiratorycomponentofacidosis.Hisparentsandpedia-
tricianwerecontacted.Historyobtainedfromthesesourcesrevealedthathewaspreviouslya
healthychild,hadnoknowndrugallergies,andwasnotonanymedication.
Hewasnursedinawarmroom(temperaturemaintainedat30
C).Theburnareaswere
cleansedanddressedwithsilversulfadiazine1%cream,andcoveredwithgauze.Highcaloric
enteralfeedswerecommencedviathenasogastrictube.Arterialbloodgasesweremonitored
frequentlytoassesstheadequacyofoxygenationandventilation.Adequacyoffluidresusci-
tationwasmonitoredbytrendingtheHR,BP,urineoutput,capillaryrefilltime,basedeficit,
andserumlactatelevels.
Twenty-fourhourslater,thepatientwasopeningeyes,andfollowingsimplecommands.
Hewasabletomovealltheextremitiesand,afteranegativephysicalexamination,the
cervicalcollarwastakenofftofacilitatethecareofburnareasinhisupperchestandneck.He
wasjudgedtobeinpainandthemorphineinfusionwasadjustedupwardsto0.2mgkg
Fig.23.1.
ChestX-rayshowingbilateraldiffuseinfiltrates
inachildwithsmokeinhalationinjury.
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
PEEPof12cmH
Table23.2.
Post-PICUcourse
Day9
14Dailydressingchangesinthe
tankroom
underdeepsedationprovidedbyan
anesthesiologist.Dailyrangeofmotionexercisesbyphysicaltherapisttotryand
preventdevelopmentofcontractures.
Day15TakentotheORforremovaloftheskinsubstitute,andautografting.Splitthicknessskin
graftsharvestedfromhisentirebackandscalpandappliedtotheburnareas.Hewas
broughttothePICUwithendotrachealtube
insitu
ashewashypothermic(esophageal
temperatureof34.6°C).Hewaswarmedgradually,weanedfromtheventilatorand
extubatedintheeveningonthesameday.Hewasstartedonsupplementaloral
transmucosalfentanyl(200mcg)asrequired,andhis4-hourlyoralmorphinedosewas
escalatedto50mg.
Day16Dischargedbacktothefloor(pediatricward)
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
surfacearea).DamagedskinisnolongerabletoretainheatandH
O,consequentlylarge
evaporativelossesensue.Combinationofthesemechanismsresultsinhypovolemicshock
acutelyfollowingburninjury.
Classificationofburndepth
First-degreeburnsaffectonlytheepidermisandarecharacterizedbyerythemaandedemaof
theburnedareaswithoutblisteringordesquamation.Second-degreeorpartialthickness
burnsinvolvetheepidermisandaportionofthedermis.Inmostcases,thesewoundscanbe
expectedtospontaneouslyhealin7to28days,althoughsurgicaltreatmentmaybenecessary
forextensiveordeepsecond-degreeburns.Painischaracteristicofpartialthicknessburns.
Third-degreeorfull-thicknessburnsextendentirelythroughboththeepidermisanddermis
andwillnothealspontaneously(
Table23.3
Table23.3.
Classificationofburndepth
BurnDepth
Superficial(first-degree)EpidermisonlyHealspontaneously
Partialthickness(Second-degree)Epidermisanddermis
Fullthickness
Third-degreeDestructionof
epidermisanddermis
Woundexcisionandgraftingnecessary
Fourth-degreeFascia,muscle,bone
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
Infectionprevention/control
Lossofbarrierfunctionofskinandbluntingofimmuneresponseresultinincreased
susceptibilitytoinfectionandbacterialovergrowthwithintheeschar.Sepsisisaleading
causeofdeathinpatientswhosurvivetheacuteburninjury.Cutaneousburntoxin,atoxic
lipidproteinisolatedfromburnedskin,is1000timesmoreimmunosuppressivethan
endotoxins.
Bowelpermeabilityisincreasedinburnpatients,leadingtotranslocationof
bacteriaandabsorptionofendotoxinsintothebloodstream.Burnwoundinfection,intra-
Major burns
Local mediators
Systemic mediators
Histamine
TNF
Cytokines
Systemic response
Contributing factors
(1) Immune suppression
+

Fig.23.2.
Pathophysiologyof
thermalinjury.
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
ofhypovolemiaanddecreasedcardiacoutput.Inaddition,increasedlevelsofcatecho-
lamines,angiotensin,vasopressin,andaldosteronecontributetorenalvasoconstriction.
Myoglobinuriaandsepsiscanalsoaggravaterenaldysfunction.Despiteanincreaseinthe
Chapter23:Thechildwiththermalinjuryandsmokeinhalation
therapyincludehypotensionandbradycardia,ofteneffectivelymanagedusingIVfluidsand
cardiacpacing.Inadditiontothewell-documentedlong-termsideeffectsofamiodarone
therapy,furtherlife-threateningarrhythmiashavealsobeenreported,hencetheneedfor
adequatemonitoring,pacingandresuscitationfacilities.
ThedegreeofcyanosisinTOFpatientsusuallydependsontheseverityoftheright
ventricularoutflowtractobstruction.
Pre-operativeconcernsincludeexclusionofco-existinganomaliesandsyndromes,of
whichtrisomy21and22q11aremorefrequentlyobserved.
ModifiedultrafiltrationhasbeenshowntoreduceICUstay.Itcanbeusedafter
cardiopulmonarybypasstoremoveexcessbodywaterandmayhaveadditionalanti-
inflammatorybenefits.
Phosphodiesteraseinhibitorssuchasmilrinonecanprovideincreasedventriculardia-
stolicrelaxationandinotropyfollowingTOFrepair.
Lowcardiacoutputstateisfrequentandmanagementprinciplescenteronreducing
oxygenconsumptionandincreasingoxygendelivery.
Post-operativecardiacarrhythmiais
commonandshouldbe
monitoredfor.
Junctionalectopictachycardiaisamalignantarrhythmiaandshouldbemanaged
providingthecatheterimages.
1.ShrivastavaS.Bluebabies:whento
IndJPaediatr
.2005;
2.ShinebourneEA,Babu-NarayanSV,
courseandoutcome.
CritCareMed
(9):1974
11.KaushalSK,RadhakrishananS,DagarKS,
IyerPU,GirotraS,ShrivastavaS,IyerKS.
Significantintraoperativerightventricular
31.ChowCK,AmosD,CelermajerDS.
Cerebrovasculareventsinyoungadults
Treatmentstrategies
Inrecentyearstherehasbeengrowingsupportforanearlycorrectiveprocedureinthe
firstfewmonthsoflife.
Thereareseveralperceivedbenefitsofearlycorrection:reduced
exposuretohypoxemiaandpolycythemia,duetoashorterintervalofright-to-leftshunting;
reducedrightventricularhypertrophy;normalpulmonaryflowandorgandevelopment;a
singleoperationandreducedrightventricularmuscleexcision.Also,adecreaseinshunt-
inducedleftventricularoverloadandareducedincidenceoflatearrhythmiashavebeen
reported.However,therehasbeensomeconcernovertheeffectsofprolongedbypassatthis
ageandincreasedoverallmortalityandmorbidityincludingaprolongedICUstay.
Oneof
thekeyissuesisthattherightventriculo-arterialjunctionmaybemoresuccessfullyrepaired
afterithasbeenallowedtodevelop.Delayedrepair(afterthefirst3monthsoflife)hasbeen
Thecourseofthecoronaryarteriesisabnormalin3%
8%.Ifthereisacoronaryartery
crossinganteriortotheRVOT,itmaybecompromisedbyatransannularincisionandaright
ventricle-pulmonaryarteryhomograftmaybepreferred.Thiswillrequirefurtherreplace-
mentasthechildgrows.
Thechildmayhavehadprevioussurgeryintheformofashuntprocedure.Theseare
usuallyperformedviaathoracotomy;however,amidlinesternotomyapproachmayhave
beenused,especiallyiftherehavebeenconcernswithseverespellingandtheneedforcardio-
pulmonarybypassorifacentralshunthasbeenused.Scarringandabnormalanatomy
resultsinalongersurgicaltimeandagreaterriskofhemorrhage.Additionalintravenous
accessanduseoftheantifibrinolyticagenttranexamicacidmaybeconsidered.
Additionalcongenitalabnormalitiesshouldbeexcluded.The22q11chromosomeabnor-
mality,foundinaround15%ofpatientswithTOF,
isoftenrelatedtoimmunedysfunction
andhypocalcemia.Ifpresent,thereisariskoftransfusion-relatedgraftversushostdisease.
-irradiationoftransfusedbloodmaybeusedtoremoveactiveT-cellsandmanycenterswill
usethisbloodroutinelywithoutcheckingpatientT-celllevels.Trisomy21carrieswithit
Pre-operativecyanosismaybemarkedduetoright-to-leftshuntingthroughtheVSDora
particularlyinterleukin8areremovedfromthecirculation,attenuatingthesystemicinflam-
matoryresponsetoCPBandreducingpost-operativecapillaryleak.Thereisevidencethat
MUFcanincreasesystolicfunction,increasediastoliccompliance,reducepost-operative
ventilatordaysandreduceinotroperequirementsinpediatricpatients.
Post-bypass
MUFneedstobeinstigatedwithcautionasitisoftenaccompaniedbyasignificantdrop
insystemicbloodpressureduetoalterationsinSVRcombinedwitharelativelypoorcardiac
functionpost-bypass.
Post-operativeconcerns
Intheimmediatepost-operativephaseimpairedrightventricularfunctionisfrequent.
Thismaymanifestitselfasventriculardiastolicdysfunctionoranacuterestrictivepicture
(so-calledrightventricularrestrictivephysiology)andappearstoincreasetheincidenceof
pleuraleffusions,lowcardiacoutputandpost-operativeICUstay.
Itcanbecharacterized
onechocardiographybyanterogradediastolicpulmonaryflowduringatrialsystole,i.e.the
stiffventricleisactingasaconduitforbloodflowfromtherightatriumtothepulmonary
arteryduringatrialsystole.Themechanismofrightventricularrestrictivephysiologyisnot
clear,butcontributingfactorsmayberelatedtoendomyocardialfibrosis,intra-operative
myocardialinjuryandoxidativestress.Itmaybeexacerbatedbypoorintra-operativecooling
duetotheanterioratrialposition,inadequatecardioplegiaofthehypertrophiedmuscle,
ordownregulatedantioxidantpropertiesofthechronicallyhypoxicmyocardium.
Thereis
alsoanassociationwiththeuseoftransannularpatches.
Prolongedcardiopulmonarybypassisassociatedwithasystemicinflammatoryresponse
andcapillaryleakagesyndromeandreducedmyocardialfunctionduetomyocardial
stunning.
ImmediatelyfollowingtherepairofTOF,thepulmonaryarterypressureswillusuallybe
higher.Pleuraleffusions,especiallyontherightside,arefrequentandintrapleuraldrainsare
usuallyinsertedperi-operatively.Thedrainsmayberemovedinthepost-operativeperiod
onceoutputhasdecreasedtoasuitablelevel.Inmostunitsthedrainswillberemovedbefore
Theassessmentofoxygendeliverytothetissuesisfundamentaltotheearlyrecognitionof
m
m
m
m
90
60
5
8
8
Fig.22.1.
Diagramof
oxygensaturations(circled)
Fig.22.2.
Progressintheoperatingroom
Followinganinhalationalinductionwithsevoflurane,nitrousoxide,andoxygen,vascular
accesswasobtainedandthetracheasuccessfullyintubatedfollowingtheadministration
ofpancuronium0.2mgkg
andfentanyl2mcgkg
.Arightinternaljugularcentral
withaninspiredoxygenfractionof50%.Venousoxygensaturation,takenfromthecentral
line,was76%.Intravenoussedationwasinstigatedusingmorphineandmidazolaminfu-
sions,andventilationwasachievedusingintermittentpositivepressureventilation.Dopamine
andmilrinoneinfusionswerecontinuedat5and0.25mcgkg
permin,respectively.A
standard12-leadECGwasobtainedaswellasanatrialelectrogram,takenbyconnectionof
theatrialpacingwiretotheelectrodeintheV1position;theinitialECGindicatedsinus
tachycardiaandrightbundlebranchblockwithnodiscernableischemicchanges.
Apost-operativechestX-rayindicatedgoodcentrallineanddrainposition,nopneumo-
thorax,andnoevidenceofcardiacfailure.Bloodwastakenforarterialbloodgasmeasure-
mentandanalysisofFBC,UandE,LFT,magnesium,calcium,andphosphate.Clinical
significantincreaseinperihilarvascularmarkingsconsistentwithcardiacfailure.Active
surfacecoolingwasemployedthroughuseofacoolingairblankettoachieveacoretemper-
atureof35°C.Avecuroniuminfusionwasinitiatedtopreventshiveringandsedation
increasedtoreduceanyfurtherendogenouscatecholaminerelease.Regularbloodgas
analysisthroughoutthenightallowedforaggressivecorrectionofpotassium,calcium,and
Fig.22.3.
24hoursfromthedrainswas140mland50mlfromtherightandleftintrapleuraldrains,
respectively.Aplanwasformulatedtoleavethedrains
insitu
.Threehoursaftertheamiodar-
oneloading,therewasachangeincardiacrhythmtosinustachycardiaatarateof140beatsper
minute,confirmedbyECG.Therewasanaccompanyingincreaseinarterialbloodpressureof
10mmHg.Serumlactatelevelsdroppedoverthenext2hoursto2mmoll
Despiteacontinuationoftheamiodaroneinfusion,therewasarecurrenceofthe
arrhythmialaterintheday.Thisepisodewasself-limitingandterminatedwithin45minutes.
Aftera6-hourperiodofsinusrhythm,theactivesurfacecoolingwasstoppedandthe
patientwasallowedtowarmto37°C.Thevecuroniuminfusionwasterminated.During
rewarming,theCVPdroppedfrom11to5mmHg,accompaniedbyadropinthemean
arterialpressureandanincreasedswingofthearterialwaveformonthemonitor.This
respondedtobolusesof5mlkg
humanalbuminsolution.Throughouttheremainderof
theday,thechild
sclinicalconditionimproved.Hewaswarm,wellperfusedwithacapillary
refilltimeoflessthan2seconds.Thedopamineinfusionwasweanedoveraperiodof4hours
andthemilrinonewasreducedto0.5mcgkg
permin.Thechilddevelopedadiuresisof4ml
perh,andstaffwereabletoweantheventilatoryparameterstoaninspiredoxygen
concentrationof35%,airwaypressuresof15/5andarespiratoryrateof18bmin
Day3
progressandwasdischargedhomeonthetenthpost-operativeday.Amiodaronewas
stopped1weekafterdischarge.Echocardiogram3monthslaterconfirmedpersistenceof
rightventriculardiastolicdysfunction;however,overallfunctionwasgood.Thechildhada
goodexercisetoleranceandwasabletofeedwithoutexcessiveshortnessofbreath.Therewas
noindicationofongoingcardiacfailure.
Casehistory3
A14-year-oldboyhadanidiopathicdilatedcardiomyopathy,whichwasdiagnosedwhenhe
was6yearsold.Nounderlyingcausehadbeenfound.Hehadbeenunderregularcardiac
Chapter21:ManagementofacuteheartfailureinPICU
Chapter21:ManagementofacuteheartfailureinPICU
Patientsareoftenadmittedforinotropicsup
portforworseningcardiacfunctioneither
duetodevelopmentofco-morbidityorbeca
usetheyarereachingapointwhentheir
cardiacoutputdecreasessufficientlytom
akethemsymptomatic.Thismayoccurunex-
pectedlyandmayindicateasuitabletimea
twhichcardiactrans
plantationshouldbe
considered.Onceapatienthasbeenlistedforcardiactransplantation,theremaybea
significantperiodoftimebeforeanappropr
iateorganbecomesavailable.Duringthis
period,itisoftennecessarytosupportcardiac
outputwithinotropes.Initially,dobutamine
isusedandmilrinoneeithersubstitutedoraddedtomaintainaninotropiceffectovera
numberofweeks.However,theinotropiceffectofdobutaminemaydecreaseduringthe
courseoftreatment.Recently,wehaveusedthecalciumsensitizingagentlevosimendanto
maintaincardiacoutputinasmallnumberofp
atients.Thisnovelagentdoesnotincrease
myocardialoxygenconsumpt
ion,preventingthedownwardspiraloftenseenwhenino-
tropictherapyiscommenced.Arecentreviewinadultpatientsdescribeditspotential
superioritytodobutamineinimprovingcar
diacoutput.However,somepatientswithin
Chapter21:ManagementofacuteheartfailureinPICU
myocarditisinthepediatricpopulation.
(1):252
5.MasonJW,O
ConnellJB,HerskowitzA
Chapter21:ManagementofacuteheartfailureinPICU
26.PackerM,CoatsAJ,FowlerMB
Chapter21:ManagementofacuteheartfailureinPICU
Managementofacute
heartfailureinpediatric
intensivecare
MatthewFentonandMichaelBurch
Inthischapterwepresentacompilationofthreeshortcasereports,eachrepresentinga
Chapter21:ManagementofacuteheartfailureinPICU
duetothehighspontaneousrecoveryrateassociatedwithacutemyocarditis.Arecentreview
onbehalfoftheCochranedatabasedidnotfindthatadministrationofintravenousimmuno-
globulinwasbeneficialinimprovingoutcomeinadultswithmyocarditisandaprospective
randomizedtrialinpediatricpatientsdidnotexist.Itwastheirconclusionthatimmunoglo-
bulinshouldnotbeincludedintheroutinetreatmentofmyocarditis.
However,itisstill
commonpracticetousehighdosemethylprednisoloneand/orimmunoglobulintotreatacute
heartfailureinchildren.Theimprovementinmyocardialfunctionmayberelatedtoa
reductioninthecytokineresponseseeninheartfailureandmaynotberelatedtotheresolution
ofmyocarditis.
Chapter21:ManagementofacuteheartfailureinPICU
notmatchedforbloodgroup.ThisisknownasanABOmismatchtransplant.
Under
normalcircumstancescardiactransplantationisperformedwithmatchingforbloodgroup
Chapter21:ManagementofacuteheartfailureinPICU
publishedfortheUK.
IntheUKthepediatricorgandonationrateislessthanthatinNorth
Americaand,aswehavediscussed,itisnotpossiblerealisticallytobridgeinfantswith
chronicleftventricularfailuretocardiactransplantation.Itiscrucialthatpediatricintensiv-
istsconsiderandrequestafamily
sconsentfororgandonationwhenachilddies.Untilnow,
thetimeframeavailabletobridgechildrentocardiactransplantationhasbeenlimitedbythe
useofECMObutitishopedthat,byusingaleftventricularassistdevice,suchastheBerlin
heart,thedurationofsupportwillbeextendedandincreasethechancesofreceivinga
suitabledonororganincreased.
Althoughkeepingachildaliveandwellenoughtoundertakehearttransplantationhas
beenthefocusofthediscussionsofar,itisimportanttorememberthatthechallengeto
maximizethedurationandfunctionofthecardiacgraftbeginsinthepost-operativedayson
theintensivecareunitearlyaftertransplantation.Currentstatisticsforpediatriccardiac
Chapter21:ManagementofacuteheartfailureinPICU
argininosuccinatesynthasedeficiency,andtoargininosuccinicacid,whichisexcretedin
argininosuccinatelyasedeficiency.Inbothcases,thereisincorporationofcarbamoylphos-
phate.Administrationofargininecan,therefore,leadtotheexcretionofcarbamoylphos-
Table20.2.
Chapter20:Theneonatewithhyperammonemia
Fig.20.2
).Glycine
-acyltransferasecatalyzesthereactionofbenzoatewithglycinetoform
hippurate,primarilyintheliverandkidney.PhenylbutyrateisfirstactivatedtoitsCoAester,
Chapter20:Theneonatewithhyperammonemia
alsoconsiderdiscontinuationofdialysisifitisineffective:iftheammonialevelremainsover
1000
moll
after24hoursofeffectivetreatment,the
ntheoutlookforthechildisverypoor.
Thelong-termmanagementofpatientswithureacycledisordersinvolvestheuseofa
Chapter20:Theneonatewithhyperammonemia
orcommencedimmediatelyonarrivalatPICUifthepatientisbroughtbythetransportteam
ofareferringhospital.
Drugsusedinpatientswithundiagnosedhyperammonemia
Loadingdose
Sodiumbenzoate250mgkg
Sodiumphenylbutyrate250mgkg
Argininehydrochloride600mgkg
Allmadeuptoavolumeof30mlkg
with10%dextroseandadministeredintravenously
over90minutes.
Maintenanceinfusion
Sodiumbenzoate250mgkg
Sodiumphenylbutyrate250mgkg
Argininehydrochloride600mgkg
L-carnitine100mgkg
Allaremadeuptoavolumeof30mlkg
with10%dextroseandadministeredintravenously
over24hours
Dialysistechniques
Dialysistechniquesshouldbeundertakeniftheplasmaammoniaconcentrationisgreater
than500
moll
orwhentheinitialplasmaammoniaisgreaterthan350
moll
anditis
nolowerafter3hoursofintravenousdrugtherapywithammonialoweringagents.
CVVHorHDshouldbeinstigatedinneonatesweighingmorethan2.5kgbutthese
techniquesmaynotbepossibleinverysmallbabiesandinthesecircumstancesPDmayhave
tobeconsidered.
Learningpoints
Attentionshouldinitiallyfocusonsecuringtheairwayandmaintainingthebreathing
andcirculationwhenapproachingthechildwithhyperammonemia.
Inbornerrorsofmetabolismshouldalwaysbeconsideredasadifferentialdiagnosisinthe
sickneonateastheinitialfeaturesofhyperammonemia(poorfeedinganddrowsiness)
maybepresentinmanydifferentdiseases.Thepresenceofarespiratoryalkalosisdueto
directstimulationoftherespiratorycentermaybesuggestiveofhyperammonemiaina
childotherwisethoughttobesufferingfromsepsis.
Allfeedscontainingproteinshouldbediscontinuedandintravenousglucoseshouldbe
administered.Intravenoustherapywithammonia-scavengingdrugsshouldbecommenced
wheneverhyperammonemiaisassociatedwithcentralnervoussystemsymptoms.
Allneonateswithsymptomatichyperammonemiashouldbeurgentlytransferredtoan
intensivecarefacilityofferingCVVHorhemodialysis.
CVVHorhemodialysisshouldbecommencediftheplasmaammoniaconcentrationis
greaterthan500
moll
orwhentheinitialplasmaammoniaisgreaterthan350
moll
andisnolowerafter3hoursofintravenousdrugs.
Chapter20:Theneonatewithhyperammonemia
1.MaestriNE,ClissoldDB,BrusilowSW.Long-
termsurvivalofpatientswith
Chapter20:Theneonatewithhyperammonemia
Fig.10.2
Fig.10.2
(j).SeriesofechocardiographimagesofobstructedTAPVC.RV=RightVentricle,LV=LeftVentricle,IVC=
InferiorVenaCava,Ao=Aorta,DV=DescendingVein,LPV=LeftPulmonaryVein,HV=HepaticVein,PVS=Pulmonary
Fig.23.5andFig.23.6.
Edema,ulceration,sloughingofairwaymucosaatthelevelofcarinaandlarynxasseenon
fiberopticbronchoscopy.(ImagescourtesyofLeeWoodson,MD,Ph.D.;UniversityofTexasMedicalBranch,Shriners
BurnsHospital;Galveston,TX.).
Fig.24.7.
SeatbeltSyndrome.
Fig.25.2.
Intra-atrialre-entranttachycardia(IART)with2:1conduction.
Theneonatewith
StephenD.PlayforandAndrewA.M.Morris
Ammoniaisformedprimarilyduringthedegradationofaminoacidsintheliver(
Fig.20.1
Table20.1
Thechildwastransferredtothepediatricwardandreassessedbytheconsultantpedia-
trician.Aplasmaammoniaandlactatespecimenweretakenalongwitharepeatcapillary
bloodgasspecimen:pH7.14,
19.8mmHg,HCO
5.7mmoll
,BE
20.6.Asthe
bloodgasresultwasbeingtelephonedbacktothewardthechildbegantohaveabnormal
|
Side chain
Fig.20.1.
Aminoaciddegradation.Ureacycledisordersinterferewiththe
conversionoftheaminogrouptourea.Defectsintheconversionofthe
Table20.1.
Findingsonadmission
ExaminationAirwayclear,sats97%inair,facemaskoxygen
Respiratoryrate85min
Chestclear,bilateralairentry
Heartrate130min
,Capillaryrefilltime=3seconds
Normalheartsounds,BP95/60,femoralpulsespalpable
Temperature34.7
InvestigationsWeight2.3kg(Birthweight2.7kg)
FBCHb16.2gdl
,Plat355×10
WBC13.4×10
143mmoll
4.3mmoll
Urea15.9mmoll
,Creatinine157
moll
1.1mmoll
,Cl
110mmoll
2.1mmoll
6.5mmoll
CapillarybloodgaspH7.01,
15.2mmHg,HCO
4.9mmoll
,BE
LumbarCSFglucose3.9mmoll
,CSFprotein2.2gl
WBC1.2×10
,RBC2.0×10
Noorganismsseen
Supra-pubicWBC0,RBC0
aspirateNoorganismsseen
Chapter20:Theneonatewithhyperammonemia
movementsofhislegs;bilateral,rhythmicalclonicjerkingofthelegswasnotedandoncloser
inspectionhiseyesweredeviatedtotheleft.Arepeatfingerprickbloodglucoseestimation
showedabloodglucoselevelof6.1mmoll
.Thechildwasadministeredintravenous
phenobarbitalatadoseof50mgover10minutes.Tenminutesafterthephenobarbital
hadbeenadministered,theabnormalmovementsceasedbutthechildwasnotedtobe
unresponsiveandpulseoximetryshowedasaturationof87%despite15lmin
ofoxygen.
Chapter20:Theneonatewithhyperammonemia
fewhourssawthebloodglucoselevelstabilizebetween7.7
9.5mmoll
.Thepediatric
Chapter20:Theneonatewithhyperammonemia
moll
.Thismaybefollowedbygruntingandhyperventilationduetodirect
stimulationoftherespiratorycentreinthemedullabytheammoniumion.Astheammonia
levelrisesfurther,seizuresmayoccurandthebabybecomescomatose.
Therearenospecificphysicalfindingsassociatedwithhyperammonemia.Affectedneo-
phosphate
succinate
Other amino acids
phenylbutyrate
or benzoate
Urine
1
3
4
5
cycle
Fig.20.2.
Theurea
cycleandthecause
ofhyperammonemia
inbranched-
chainorganic
acidemias.NAG=
Chapter20:Theneonatewithhyperammonemia
acidemiasarethecommonestofthesedisorders.Allcancauseseverehyperammonemia,
probablybyinhibiting
Chapter20:Theneonatewithhyperammonemia
Fig.2.1.
Fig.5.2.
CTscanofheadandXenonperfusionstudy
demonstratingaveragecerebralbloodflowsintherange
of50
70ml/100gpermin.Noareasofischemiaor
oligemiacouldbeidentified.
Fig.7.4.
ECG1hourlatershowingpolymorphousQRScomplexesleadingtoventriculartachycardia.
Fig.7.3.
ECGonarrivalinPICU.Rate90
120,QRS0.12
0.132s,QTc0.549s(normal0.45).
Fig.8.1.
Bloodsmearshowingschistocytes(redbloodcellfragmentation).
Fig.10.2
Fig.10.2
Pharmacologicaltherapy
Unfortunately,manyformsoftachycardiaareresistanttocardioversionorwillrapidlyrecur
afterrestorationofsinusrhythm.Insuchcasescommencinganantiarrhythmicagentmay
pharmacologicallycardioverttherhythm,maintainsinusrhythmaftercardioversionby
anothermeans,orprovideratecontrolofthetachycardia.Thechoiceofantiarrhythmic
agentwillvaryaccordingtothespecifictypeofarrhythmiaconcerned,andasuggested
approachtotreatmentisoutlinedin
Table19.2
,withdoseslistedin
Table19.3
RadiofrequencyAblation(RFA)inPICU
RFAreferstotheinterruptionofaccessorypathwaysandectopicfocibyusingradiofrequency
energytoheatthetipofanintracardiaccatheterpositionedagainsttheendocardialsurface
atthetargetarea.Thethermalenergyproducedatthetipcauseslocaltissuedestruction,
effectivelyblockingelectricalactivityatthesiteofthe
burn.
Becauseofconcernsregarding
theeffectofsuchendocardialscarringonthedevelopingheartandthenaturaltendencyfor
manyarrhythmiastoresolveinthefirstyearsoflife,ablationisgenerallyavoidedininfancy.In
children,itisusedwheresymptomsarepoorlycontrolledbyfirst-linemedicaltherapy.The
successrateinchildrenissimilartothatinadults,withcessationofthetachycardiain91%of
accessorypathwaysand87%ofectopicfoci.
Itisrare,butrecognized,forachildinintensivecaretorequireRFAasthevastmajority
ofSVTcanbecontrolledwithmedicaltherapy.Inthosewherecardioversioncannotbe
accomplishedsuchasatrialectopictachycardias,adequateratecontrolisusuallypossible,
Table19.2.
Suggestedapproachtotreatment
Acutetermination:IVadenosine
Chapter19:Refractorynarrowcomplextachycardiaininfancy
anditsneedmaybetransient.ForthesmallnumbersthathavearefractorySVTwith
significanthemodynamiccompromise,RFAmayprovidethebestwayofcontrollingthe
arrhythmia.Suchpatientsareoftenextremelyunwellwithprecarioushemodynamics,and
maynottoleratetherhythmmanipulationsinvolvedinRFA.Hemodynamicstabilitycanbe
obtainedbysupportingthecardiacoutputusingExtracorporealSupport(ECS).Insome
Table19.3.
Recommendeddrugdoses
Loading/Acutetermination
Adenosine0.1
0.4mgkg
Amiodarone5
7mgkg
over30
60min,or25mcg
for4hours
15mcgkg
perminIV
10mgkg
perdayPO
Atenolol1
2mgkg
perdayPO
Digoxin15mcgkg
then5mcgkg
after6hours5mcgkg
POorIVBD
Flecainide0.5
2mgkg
over5min
12mgkg
perdayPO
Nadolol1
5mgkg
perdayPO
Propafenone1.5
2mgkg
over3min
600mgm
perday
Propranolol0.1mgkg
over10min(repeatifneeded
upto3x)
0.3mgkg
1mgkg
POQDS
Sotalol0.5
2mgkg
over10min
8mgkg
perdayPO
Chapter19:Refractorynarrowcomplextachycardiaininfancy
1.TrohmanRG.Supraventriculartachycardia:
implicationsfortheintensivist.
CriticalCare
(10):N129
Chapter19:Refractorynarrowcomplextachycardiaininfancy
inpediatricpatients.
JAmCollCardiol
:1002
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Chapter19:Refractorynarrowcomplextachycardiaininfancy
chamberpacingatjustoverthetachycardiarate.Flecainideandprocainamide
canbe
usedasalternativestoamiodarone.
Slow conducting
Fig19.7.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
dysplasia,forinstance,canpresentwithaleftbundlebranchblockmorphologyven-
triculartachycardia.Ifindoubt,apediatric
cardiacelectrophysiologistshouldbeasked
toreview.
Generalmanagement
A12-leadECGofthetachycardiashouldbeobtained,ifpossiblewitharecordingof
anyterminationmechanism.Esophagealand/orepicardialrecordingsmaybeneeded.
Electrolytesshouldbenormalised.Afullmedicationhistoryshouldbecheckedandconside-
rationgiventopossibleingestion/administrationofotherproarrhythmicagents.Inotrope
infusionsshouldbereviewedasseveraltypesofSVT,particularlyautomatictachycardias,are
catecholaminesensitive.Anechocardiogramshouldbeobtainedtoidentifyanyunderlying
structuralabnormalityandassessventricularsizeandfunction.
leadsshouldberecordedduringanyelectricalorpharmacologicalattemptsatrestoringsinus
rhythm,asthepatternofterminationmayprovidethediagnosis.
Insomecasesthe12-lead
surfaceECGisnotadequate,andfurtherinvestigationssuchastransesophagealor,inthe
post-operativecardiacpatient,epicardialECGs,mayberequired.Inothersituationsphar-
macologicaltrials,particularlywithadenosine,canprovidevitalinformation.Rarely,more
advancedtechniquessuchasprogramedatrialpacingorfullelectrophysiologicalstudies
mayberequired.
ManyalgorithmsexisttofacilitatetheaccuratediagnosisofSVT.Allrelyonthe
identificationofthePwave,itsrelationtotheQRS,anditselectricalaxis.Manysplit
tachycardiasintoshortRPandlongRPgroups.
ShortRP
WherethePwaveisclosesttotheprecedingRwave(RP50%RRinterval),itissaidtobea
shortRPtachycardia.ThisgroupincludesAVRT,AVNRT,formsofatrialtachycardiawhere
Chapter19:Refractorynarrowcomplextachycardiaininfancy
TransesophagealECG
Specializedtransesophagealpacingwiresarenowproducedforadultsandchildrenthatare
wellsuitedtorecordingelectrocardiograms.
Ifthesearenotavailableeitherastraightfor-
wardtemporarypacingwireorquadripolarelectrophysiology,electrodesmakeverygood
substitutes.Thewireisintroducedlikeanasogastrictube.Thedistancecanbemeasured
againstthechildpriortoinsertionbyestimatingapointinthemid-axillarylinelevelwiththe
nipple.Onceinposition,thewireisconnectedtoa12-leadECGmachine(
Fig.19.8
Pacingleadshavetwoelectrodesallowingacquisitionofabipolarcardiogram,althoughit
ispossibletoconnectupjustoneoftheelectrodesandobtainaunipolarcardiogram.The
pacingleadelectrodesfortherightarmandrightlegelectrodes.LeadIIIwillshowthesurface
ECG,whilsttheotherlimbleadswillshowtheesophago-atrialECG.Alternatively,aunipolar
tracecanbeobtainedbysubstitutingoneofthepacingleadelectrodeswithV1,displayingthe
esophago-atrialECGonV1andtherestoftheECGwillbeanormalsurfaceECG.The
advantageofaquadripoleelectrodeisthattwoleadscanbeusedtorecordabipolaratrial
cardiogram,whilsttheothertwocanbeusedtopaceifneeded.Withthewireinposition,it
canbemovedupanddowntheesophagusuntilanoptimalrecordingisobtained(
Fig.19.8
Left arm
Epicardial wire (quadripole)
Lead III – surface ECG
Fig19.8.
PacingoftransesophagealelectrodeandECGtracesrecorded.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Complicationsofesophagealleadplacementarerare,althoughesophagealulcerationhas
beenreportedinadultandpediatricpatientswithlongtermuse�(60hours).Mildpressure
necrosisrelatedtoelectrodeplacementratherthanelectricalstimulationhasalsobeen
reported.
Theplacementofanesophagealelectrodealsoallowstheuseofprogramedstimulation
asadiagnostictoolorasawayofcardiovertingsometypesofSVT.
EpicardialECG
tingthepacingwiresfortheECGleadsasoutlinedabove.Aswithesophagealpacing,the
electrodecanalsobeusedforstimulationtohelpdiagnoseandtreatsomeformsofSVT.
Theadvantageofobtainingbipolarratherthanunipolarrecordingsbythesetechniquesis
theamplificationoftheatrialsignalrelativetotheQRScomplex.Indifficultdiagnosticcases
suchasAVNRT,thismayfacilitatedistinctionofthePwavefromtheQRSTcomplex.
Adenosine
NarrowcomplextachycardiasdifferintheirresponsetoAVnodeslowingorblock.This
canbeachievedbyvagalmaneuverssuchasvalsalva,carotidsinusmassage,orface
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Fromadiagnosticpointofview,adenosinewillblockAVnodeandaccessorypathway
conductionandthereforeterminatere-entrytachycardiassuchasAVRT,AVNRT,and
PJRT.PatientswithsinustachycardiawillshowAVnodeblockandslowingofthesinus
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Refractorynarrowcomplex
tachycardiaininfancy
TrevorRichens
Narrowcomplextachycardiasoccurfrequentlyinpatientsonpediatricintensivecareunits
(PICU).Althoughthemyocardialsubstrateforsupraventriculartachycardias(SVT)may
Heradmissioninamoribundstateremainedunexplained;howeverongoingproblems
withnarrowcomplextachycardiasraisedconcernsthatanarrhythmiamighthaveprecipi-
(b)
Fig.19.1(a).
ECG1.
Fig.19.1(b).
ECG2.
Fig.19.2.
Strip1.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
digoxinstarted,andshewasintubatedandventilatedpriortoDCcardioversion.One,2,and
5Jkg
synchronized,DCshocksweretried,againwithouteffectandhertachycardiarate
persistedat300bmin
Table19.1.
Earlyvitalsignsandbloodresults
VentilatedPre-ECMOOnECMO
Heartrate255200119
BP80/4565/4590/81
SaO29878100
RR282215
Toecoregap163.5
pH7.437.317.5
Lactate3
Na(mmoll
)136
K(mmoll
)5.6
Cl(mmoll
)101
U(mmoll
)13.7
Cre(µmoll
)515446
Ca(mmoll
)1.04
(mmoll
)2.39
Mg(mmoll
)1.08
Chapter19:Refractorynarrowcomplextachycardiaininfancy
2mgkg
wasadded,andshewastakentothecatheterlaboratoryforelectrophysiological
studiesandpossibleradiofrequencyabl
ationoftheculpritaccessorypathway.
AV node
Accessory
pathway
Fig19.3.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
formofJunctionalReciprocatingTachycardia(PJRT).However,inPJRTthereis
classicallynopre-excitationinsinusrhythm,mitigatingagainstthisbeingtheunder-
lyingmechanism.
TherefractorynatureofthearrhythmiainthischildsuggestsanAtrialEctopic
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Fast
Fig19.4.
typicalorslow-fast
PwaveconcealedinQRS.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
addressed.Digoxin,historicallywellestablishedinthetreatmentofnarrowcomplextachy-
cardia,isnotwithoutproblems.Accidentaloverdosingisnotunusual,sinusbradycardia
occursfrequentlyandventricularfibrillationhasbeenreportedevenintheabsenceofa
manifestaccessorypathway.
Closemonitoringoflevelsinunstablepatientsminimizes
theseproblems.
Itsmodestefficacyasasingleagent
improvesincombinationwith
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Lead ILead I
Lead aVFLead aVF
Fig19.5.
Atrialectopictachycardia
Pwaveaxisshift.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
circuitformsaroundthetricuspidvalve.
Theflutterratechangeswithage;inneonatesit
maybeasfastas400bmin
;however,duringinfancyandchildhoodthisslowstotheadult
flutterrateof300bmin
.MostAVnodeswillnotconductatsuchratesandthetransmitted
ventricularresponseistypicallyhalftheatrialrate,i.e.2:1block.Uncommonlyininfants,the
AVnodeconductstheatrialflutterratetotheventriclewithoutblockresultinginventricular
ratesinexcessof300bmin
.AtypicalECGfindingofsawtoothflutterwavesisseenwhere
2:1blockoccurs.
Antiarrhythmicagentsarerarelysucce
ssfulatterminatingARTandthefavored
approachisDCcardioversionoroverdrivepacing.
Atrialflutterinneonatesrarely
recursafterthefirstyear,
sotheneedforprophylacticpharmacologicaltherapyis
questionable.
ARTrelatedtosurgicalscarsgenerallyoccursinolderchildrenandis
oftenrefractorytomedicaltreatmentrequi
ringrevisionofthesurgicalrepairandcon-
currentinterventionaltreatment(surgicalor
Chapter19:Refractorynarrowcomplextachycardiaininfancy
Sinus rate slower than
unctional therefore only
occassionally depolarizes
ventricles
Fig19.6.
Chapter19:Refractorynarrowcomplextachycardiaininfancy
transmittedHIVinfection.
Theunintendedconsequenceisthatanincreasingpropor-
tionofchildrennewlyinfectedwithHIVh
avenotbeendiagnosedantenatally.These
Chapter18:ThechildwithHIVinfection
shouldbestartedwitha10
15mgkg
Chapter18:ThechildwithHIVinfection
HIV-infectedchildrenarealsoatriskforotherfungalinfections,suchas
albicans
andother
species,whichmayinvolvetheesophagus,trachea,andlungs.
Candida
maybeisolatedfromtheBALspecimenandnosocomialcandidemiaisassociated
withcentralvenouscannulae.Notethatwidespreaduseoffluconazoleprophylaxishas
resultedinanincreaseinfluconazole-resistantnon-albicansspecies,whichwouldrequire
amphotericinasafirst-lineagent.
ICUManagementofPJPinfectedchildren
TheprognosisofchildrenwhodevelophypoxicrespiratoryfailureduetoPJPhasimproved
considerablysincetheearlydaysoftheHIVepidemic,when�80%ofchildrendied.
Besides
high-doseco-trimoxazoleandsteroidtherapy,generalimprovementsinpediatricintensive
Chapter18:ThechildwithHIVinfection
Learningpoints
TheincidenceofverticallyacquiredHIVinfectionhasdeclinedrapidlyindeveloped
countries.
UndiagnosedHIVinfectionstillpresentswithlife-threateningopportunisticinfections
duringinfancy.
TheearlyclinicalandradiologicalfeaturesofPJPmaybenon-specific.
ThecardinalclinicalfeatureofPJPishypoxia.
EarlysteroidtherapymayaverthypoxicrespiratoryfailureinPJP.
Co-trimoxazoleisfirst-linetherapyforPJP.
Co-infectionwithviral,bacterial,andfungalorganismsiscommonandmaydelay
responsetotherapy.
Severityoflungdiseasemaybeassessedbyserialcalculationofoxygenationindex.
PICUsurvivalofchildrenwithPJPwhorequiremechanicalventilationhasimproved
substantially.
Medium-termoutcomeofHIV-infectedinfantswhosurvivePJPtobeestablishedon
ARTisrelativelygood.
1.SharlandM,GibbDM,Tudor-WilliamsG.
Advancesinthepreventionandtreatment
ofpaediatricHIVinfectionintheUnited
ArchDisChild
:178
2.WilliamsAJ,DuongT,McNallyLM
Chapter18:ThechildwithHIVinfection
carinii-relatedrespiratoryfailure.
JPediatr
:821
13.MontanerJS,LawsonLM,LevittN,
BelzbergA,SchechterMT,RuedyJ.
Chapter18:ThechildwithHIVinfection
ThechildwithHIV
MarkHatherill
perfused,withacapillaryrefilltimeof2s
econds.Hedidnotappearcyanosed,buthis
oxygensaturation(SaO
)was84%inroomair,87%innasalcannulaoxygen,and98%in
facemaskoxygen.Hisrespiratoryratewas60perminutewithnasalflaring.Hehadmild
costalrecessionbutnoaudiblewheeze.Bronchia
lbreathingwasheardatbothlungbases.A
2cmsoftliverwaspalpablebuttherewasnosplenomegaly.Chestradiographshowedair
bronchogramsinbothlowerlobes,butnohyperinflation,orlobarconsolidation(see
Fig.18.1
).Hewasinitiallyassessedasawell-nourishedinfantwithaviralorbacterial
bronchopneumonia.
Hewasadmittedtothehigh-dependencyareaofthegeneralpediatricwardforpulse
Fig.18.1.
Admissionchestradiographshowsair
bronchogramsinbothlowerlobes,butnohyperinflation,
atalectasis,orlobarconsolidation.
Chapter18:ThechildwithHIVinfection
CourseinPICU
Hewasnursedprone,sedatedwithintravenousmorphinebyinfusionat20mcgkg
perh
andoralclonidine5mcgkg
8-hourly.HewasinitiallyventilatedusinganSIMVrateof
25perminute,pressuresof24/8,andFiO
0.6.RepeatABGanalysisshowedpH7.39,
4.9kPa,
8.3kPa,andbasedeficit
1.6mmoll
,withSaO
96%.The
(mmHg)/FiO
ratiowascalculatedas104andtheoxygenationindex(OI)was11.
Oxygenationindex
FiO
mmHg
Itwasplannedtoreducebothventilatoryrateandpeakpressure,toleratinghypercapniaand
92%.Thepost-intubationchestradiographshowedadiffusebilateralinfiltrate
withagroundglassappearance(see
Fig.18.3
).Theendotrachealtubewasinanacceptable
position,butthenasogastrictubelayintheesophagusandwasadvanced.Thepossibilityof
PJPwasraisedinviewoftheworseninghypoxicrespiratoryfailure,andbothintravenous
co-trimoxazole7.5mgkg
6-hourlyandoralprednisone2mgkg
dailywerecommenced.
Anarterialcannulawasinsertedforcontinuousarterialbloodpressuremonitoringand
bloodsampling.Artificialmilkfeedswerestartedandtotalfluidintakewasrestrictedto
60mlkg
perday.Urineoutputwas1.3mlkg
perh.
ThefamilywerecounselledandconsentedtotestingforHIV.Bloodwassampledandan
HIVELISAwasrequested.Additionalinvestigationsincludedaserumalbumin24gl
,total
protein59gl
,andLDH1169Ul
.Theleukocytecounthadfallento20×10
,with31%
neutrophils,and35%immatureneutrophils,althoughtheserumprocalcitoninlevelwas
0.5mcgl
.Anon-directedbronchoalveolarlavage(BAL)wasperformedandlavagefluid
senttomicrobiologyformicroscopy,culture,and
Pneumocystisjiroveci
immunofluorescence,
andtovirologyforimmunofluorescenceandviralculture.Anechocardiogramshoweda
structurallyandfunctionallynormalheart.
Onday2,theadmissionBALsamplewasconfirmedpositivefor
Pneumocystisjiroveci
fluorescentantibody.Scantyneutrophilswerenoted,butnobacteriaoracid-fastbacilli.
Fig.18.3.
Thepost-intubationchestradiograph
showsadiffusebilateralinfiltratewithagroundglass
appearance.Theendotrachealtubeisinanacceptable
position,butthenasogastrictubeliesinthe
esophagus.
Fig.18.2.
Repeatchestradiographafter24hours
showsconsolidationinall4quadrants,withamilky
appearancesuggestiveofinterstitialdisease.
Chapter18:ThechildwithHIVinfection
TheHIVELISAwasalsoreportedaspositive.TheparentswerecounseledthattheELISA
testsuggestedperinatalexposuretoHIV,andalthoughnotdiagnosticininfants,the
presenceofanopportunisticinfection(PJP)washighlysuggestiveofHIVinfection.
Apolymerasechainreaction(PCR)testforHIVwassentandbothparentswereoffered
testing.
Onday3,SaO
fellbelow88%inFiO
0.75,withventilatorypressuresof20/8.Hewas
turnedproneagainandpressureswereincreasedto24/10,whichallowedagradualreduction
oftheFiO
to0.5,withSaO
Byday4,attemptstoweanventilationhadbeenunsuccessful.SaO
was88%inFiO
withpressuresof23/10,andanSIMVrateof25.The
was6.5kPa,anddespitepH7.36
4.9kPa,heappearedsweatyandtachypneic,withaspontaneousrespiratoryrateof
50perminute.The
ratiowas82andOIwas14.
Nogrowthhadbeenreportedfromtheadmissionbloodcultureat72hoursandtemper-
aturehadremained38°C.Totalleukocytecounthadfallento8×10
,with57%
neutrophilsand19%immatureneutrophils.Hemoglobinwas7.4gdl
andabloodtrans-
fusionwasordered.Thetroughgentamicinlevelwasappropriateat0.6mgl
,butthepeak
wassub-therapeuticat6.0mgl
andthedosewasincreased.TheHIVqualitativePCRwas
reportedtobepositive,confirmingthediagnosisofHIVinfection.TheBALandblood
culturewererepeated,andbloodwassampledforcytomegaloviruspp65antigen.
Chapter18:ThechildwithHIVinfection
1.6×10
RNAcopiesperml.ThefamilyagreetostartARTandstavudine1mgkg
12-hourly,
lamivudine4mgkg
12-hourly,andritonavir250mgm
12-hourlywerecommenced.
Thatafternoon,thevirologylaboratoryreportedthattheshellvialculturefromthe
Fig.18.4.
ChestradiographonHFOVshowsgoodlung
expansion.Therearefeaturesofearlyhoneycombing,
suggestiveoflungfibrosissecondarytovolutrauma.The
endotrachealtubeappearstoohigh.
Chapter18:ThechildwithHIVinfection
Table17.2.
WHOclassificationofdenguehemorrhagicfever(DHF)anddengueshock
syndrome(DSS)
DHFgradeHemorrhage
Table17.3.
Rangesofhematocritforage
Range(%)
Mean(%)
2weeks42
3months31
6months
6years33
4237
7years
12years34
4038
Male42
5247
Female37
4742
NelsonTextbookofPediatrics
,15thedn,p.1379.
Chapter17:Childwithdenguehemorrhagicfever
ManagementofgradeIandIIdenguehemorrhagicfever
Allcasesshouldbeadmittedformonitoring.Oralintakeshouldbeencouragedandinthose
whoaredrinkingpoorlyintravenousfluidsatmaintenanceratesof4
5mlkg
perhusing
D5%0.45%salineorD5%0.9%saline(inolderchildren)shouldbeadministered.Vital
signs,urineoutput,andconsciouslevelshouldbecloselymonitored.Hematocritshould
bemonitoredatleastonceadayormoreoftenifrequired.Non-steroidaldrugsoraspirin
shouldbeavoidedasithasbeenshowntoaggravateplateletdysfunctionandpredisposeto
severeandrefractorybleeding.
Chapter17:Childwithdenguehemorrhagicfever
Chapter17:Childwithdenguehemorrhagicfever
Additionalpoints
1.Insertionofnasogastrictubeandendotrachealtubecarriestheriskoftraumaand
hemorrhagetonasalpassagesandstomach.Ifitisnecessary,theoralrouteispreferable.
2.Insertionofintercostaldrainscarriestheriskoftraumaandhemorrhagetothelung.
Carefultitrationofintravenousfluidstoachievestablevitalsigns,withreductionof
intravenousfluidintakeoncestablevitalsignsareachieved,willlimittheaccumulation
oflargepleuraleffusions,ascites,andpositivefluidbalanceinchildren.Largepleural
effusionsduringtherecoveryphaseafter48hoursmayneedsmalldosesoffrusemide.
3.Insertionofcentralvenouslinecarriestheriskofhemorrhageandshouldnotberoutinely
inserted.
4.Theuseofcorticosteroidsinthetreatmentofshockhasfailedtoshowanybenefits.
5.Echocardiogramassessmentisrecommendedincasesofprofoundshockasasmall
percentagehavedecreasedfunctionrequiringinotropesandmayalsobeusefultoassess
volumestatus.
Learningpoints
Chapter17:Childwithdenguehemorrhagicfever
ofconsultation
.GenevaWHO1995.
(CID/FIL(Den)/IC.96.1).
3.KliksSC,NimmannityaS,NisalakA
Chapter17:Childwithdenguehemorrhagicfever
Childwithdengue
hemorrhagicfever
AdrianY.Goh
Dengueisthemostcommonandimportantmosquito-borneviralinfection
andcan
manifestasDengueFever(DF),whichisoftenaself-limitingfebrileillnessorlesscommonly
denguehemorrhagicfever(DHF).Themajorpathophysiologichallmarksthatdistinguish
DHFfromDFandotherdiseasesareincreasedvascularpermeabilityleadingtoplasma
leakageandcirculatorycollapse(DengueShockSyndrome/DSS).Managementinvolvesclose
Herrepeatbloodinvestigationsshowed:fullbloodcount:Hb15.4gdl
,PCV0.55,
Table17.1.
Clinicalandinvestigativefindingsonadmission
PastmedicalhistoryHealthyandwell
RegularmedicationsNone
AllergiesNoneknown
ExaminationAwakebutslightlyconfusedandagitated
Airwayclear,facemaskoxygen
Tachypneicrespiratoryrate40/min
Chestclear,bilateralairentry,Sats98%inair
Normalheartsounds,pulse140/min,BP100/80
Capillaryrefilltime=4seconds
Chapter17:Childwithdenguehemorrhagicfever
Fig.17.1
),whichconfirmedalargerightsidedeffusion.Herrepeatbloodinvestigationson
arrivalshowedaHBof12.8gdl
Fig.17.1.
Chestradiographonadmissiontopediatric
intensivecare.
Chapter17:Childwithdenguehemorrhagicfever
Prothrombinratio(PTr)2.6,partialthromboplastintime(pTT)135s,control36s,D-dimer
positive,urea19.6mmoll
,creatinine183µmoll
.Overthenext4hours400mloffresh
frozenplasmaand4unitsofcryoprecipitatewastransfused.
TwelvehoursfollowingadmissiontoPICUherarterialpressureremainedborderlinelow
at90/45mmHgwithcontinuingtachycardia,despitemassivetransfusionsofcrystalloids
ischemic),shewasstartedoncontinuousrenalreplacementtherapy(CRRT)at36hoursafter
admissionusingcontinuousveno-venoushemodiafiltration(CVVHDF).Abicarbonate
bufferedsolution(hemosol)wasusedbecauseofhersignificantliverdysfunction.Noanti-
coagulationwasusedbecauseofhercoagulopathy,withfilterlifebeingincreasedwithhourly
100mlflushesof0.9%saline.Fluidextractionwasgraduallyincreasedfrom200mlh
700mlh
Chapter17:Childwithdenguehemorrhagicfever
magneticresonanceimagingwithdiffusion-weightedimaging(MRI-DWI)revealednoabnor-
malityafter10daysofadmission.Shewastransferredtothegeneralwardforcontinuedcare,
whereshewasdischargedafteratotalhospitalstayof17days.Onfollow-upafter2monthsshe
hadreturnedtohernormalpre-illnessfunctionallevel.
Dengueisthemostcommonandwidespreadarthropod-bornearboviralinfectioninthe
worldtoday.
Thegeographicalspread,incidenceandseverityofdenguefever(DF)and
denguehaemorrhagicfever(DHF)areincreasingintheAmericas,South-EastAsia,the
EasternMediterraneanandtheWesternPacific.Some2500millionto3000millionpeople
liveinareaswheredenguevirusescanbetransmitted.Itisestimatedthateachyear50million
infectionsoccur,with500000casesofDHFandatleast12000deaths.
Therearefour
serotypesofdenguevirus(DEN1,DEN2,DEN3,DEN4),whichareantigenicallysimilar
butdifferentenoughtoelicitonlytransientcrossprotectionafterinfectionbyoneofthem.
Allfourserotypesmaycirculateconcurrently,butonemaypredominatedependingon
thesusceptibilityorimmunityofthepopulation.Therearetwodistincthostserological
responses,namelyprimaryandsecondary.Primaryresponseoccursinnon-immuneindi-
vidualsundergoingtheirfirstdengueinfection,whilstasecondary(anamnestic)response
occursinindividualshavingmemorycellsfrompreviousdengueinfection.Secondaryinfec-
tionisariskfactorforDHF,includingpassivelyacquiredantibodiesininfants.
Otherrisk
factorsincludevirusstrainandageofthepatients.
AlthoughDHF/DSScanoccurinadults,
mostcasesareinchildren15years,withcircumstantialevidencesuggestingthatcertain
populationgroupsaremoresusceptibletovascularleaksyndrome.
Initialassessmentandmanagement
Denguevirusinfectionmaybeasymptomatic,causeundifferentiatedfebrileillness,dengue
fever(DF)ordenguehemorrhagicfever(DHF).
DFisoftenanacutebiphasicfever,with
headaches,myalgia,arthralgia,rash,andleukopenia.Itiscommonlybenignbutmayocca-
sionallypresentwithatypicalhemorrhage(
Fig.17.2
).TheclinicalfeaturesofDHF/DSSare
Symptomatic
Dengue hemorrhagic fever
(plasma leakage)
fever
Without
hemorrhage
Unusual
hemorrhage
Dengue shock
syndrome
Dengue fever
syndrome
Fig.17.2.
Manifestationsofthe
Denguesyndrome.
Chapter17:Childwithdenguehemorrhagicfever
Ongoingmanagementofdrowninganditscomplications
Table16.3
givesalistofcomplicationsofdrowning.Theearlyliteratureondrowning
Table16.3.
Complicationsofdrowning
Decreasedcardiacindex
Hypothermiccardiacarrhythmia
Pulmonaryedema
AcuteRespiratoryDistressSyndrome(ARDS)
DisseminatedIntravascularCoagulation(DIC)
Acutetubularnecrosis
Hypoxicischemicencephalopathy
Cerebraledema
Basalgangliaand
watershed
cerebralinfarcts
Chapter16:Managementofa3-year-oldchildwithdrowning
outcome.
Also,aggressivetreatmentofintracranialhypertensionhasnotproventobe
beneficialtovictimsofnear-drowning.
Thus,ICPmonitoringisnotrecommendedfollow-
ingnear-drowning.
RepeatedclinicalneurologicexaminationincludingGlasgowComaScore(GCS)and
scaregiversrequestconfirmatorytesting.
Theroleofelectroencephalography(EEG)earlyfollowingdrowningisoftenlimiteddue
totheuseofsedativesandanalgesicsintheintensivecareunit.Aflatorseverelyattenuated
EEGorburstsuppressionduringtheinitial24hoursreflectstheinitialinsult.Apersistently
attenuatedrecordwithoutmedications,however,ispredictiveofapoorneurologicprog-
foundthat,inchildrenwithhypoxicischemicencephalopathy,adiscon-
tinuousEEG,thepresenceofspikesorepileptiformdischargeswereassociatedwithan
unfavorableoutcome.
Brainstemauditory-evokedresponsescanbealteredbybothcentralandperipheral
auditorydisorders,andareparticularlyvulnerabletohypoxiainyoungpatients.
Fisher
foundthat,drowningpatientswhoweredeclaredbrain-deadordied,exhibitedabnormal
brainstemauditory-evokedresponsemeasurementsonadmissionanduntildeath;however
Chapter16:Managementofa3-year-oldchildwithdrowning
Increasedbloodglucoseconcentrationsafterischemicinjurymayimpairneurological
recovery,andarecentrandomizedcontrolledtrialincriticallyilladultshassuggestedthat
Chapter16:Managementofa3-year-oldchildwithdrowning
Routineprophylacticantibioticsorcorticosteroidsarenotrecommended.
Initialclinicalneurologicalassessmentonarrivalinthehospitalemergencydepartment
orICUincludingbrainstemreflexesandGlasgowComaScoreandasubsequentMRI
scanofbrainperformedonday3
4areusefuloutcomepredictors.
Generalizedsupportivemeasuresandpreventionofanysecondaryhypoxic,hypotensive,
Chapter16:Managementofa3-year-oldchildwithdrowning
18.VannucciRC,BrucklacherRM,Vannucci
SJ.Effectofcarbondioxideoncerebral
Chapter16:Managementofa3-year-oldchildwithdrowning
alonecancauseSDH.Theterm
shakenbabysyndrome
hasbeenusedtodescribecasesof
Chapter15:ManagementofNAIonthePICU
ofprobability
.This51%likelihoodofNAIisverydifferentfromthecriminallevel(
reasonabledoubt
)neededtoconvict.Itisessentialthatallprofessionalsarebothprepared
tocommentclearlyontheissuesonwhichtheyhaveknowledgeaswellaslimitingthemselves
tosuchareas.Therefore,ifanopinionon
forexample
MRIfindingsisrequestedfrom
anintensivecaredoctor,itisusuallymoreappropriatetorefersuchanopiniontoa
neuroradiologist.
Medico-legalreportsarealwayswanted,andshouldbegeneratedclearlyandinatimely
manner.Aseniordoctorshouldreviewsuchreports.Finally,allPICUsshouldhaveclear
guidelinesclarifyinglocalproceduretobefollowedincasesofsuspectedNAI,withphone
Chapter15:ManagementofNAIonthePICU
10.MandelstamSA,CookD,FitzgeraldM
Chapter15:ManagementofNAIonthePICU
Managementofa3-year-old
childwithdrowning
MargridSchindler
ThedefinitionofdrowningagreedbythetaskforceoftheFirstWorldCongressondrowning
in2003is:
theprocessofexperiencingrespiratoryimpairmentfromsubmersionorimmer-
sioninaliquid.
Drowningisanimportantcauseofchildhoodmorbidityandmortality,
with27%ofdeathsfromunintentionalinjuryintheUnitedStatesbeingduetodrowningat
age1
4years.Malesaremorecommonlyinvolvedthanfemales.Themajorityofdrownings
occurinfreshwater.Ofinfant(1year)drownings,55%wereinbathtubs;amongchildren
notrespondingtopainfulstimuli.AchestX-rayshowedbilateralhazyopacificationofthe
lungfields.30mlof4.2%sodiumbicarbonatewasgivenviaanintra-osseousneedle.TheBP
driftedto55/42(mean47)andafemoralcentralvenouslinewasinserted;thecentralvenous
pressuremeasuredthroughthislinewas22mmHg.Anadrenalineinfusionwascommenced
at0.2mcgkg
perminwithgoodeffect.ArepeatABGshowedpH7.1,PaCO
50mmHg,
120mmHg,bicarbonate14mmoll
,BE
18,lactate14mmoll
,Na144mmoll
K6.4mmoll
,Hct33%,Glu18mmoll
.Afurther15mmolofsodiumbicarbonate,IV,
wasgivenandhewastransferredtoPICU.
Progressinthepediatricintensivecareunit
Inthepediatricintensivecareunit,hewassedatedandmusclerelaxedwithmorphineand
vecuroniuminfusionsandhewaskeptcooledto34
Cfor24hours.Cardiovascularlyhis
perfusionimprovedandacidosisresolved,buthecontinuedtorequireinotropicsupportfor
Chapter16:Managementofa3-year-oldchildwithdrowning
wouldrequireassistancewithbasicneeds,andthatoneofthepossibleoptionstoconsider
waswithdrawalofintensivecaresupporttoallowhimtodie.Theparentsstatedthattheyhad
Fig.16.1.
Chapter16:Managementofa3-year-oldchildwithdrowning
successfullyextubatedtoBiPAPviafacemaskatpressuresof15/8cmH
O,andcontinuedto
Table16.1.
Factorsassociatedwithunfavorableoutcome
Watertemperature�10
Durationofsubmersion�10minutes
Timetoeffectivebasiclifesupport�10minutes
Absentpulseonarrivalinemergencydepartment
MinimumbloodpH7.1
Bloodglucose�11mmoll
Absentpupillaryresponses
GCS5inemergencydepartmentorintensivecare
Chapter16:Managementofa3-year-oldchildwithdrowning
predictivesignificance.Therefore,fullresuscitationshouldbeattempted,atleastbriefly,in
alldrowningpatientsarrivinginemergencydepartments.
Theoutcomeofcardiacarrestinchildrenisdependentfirstandforemostontheduration
ofthecardiacarrest,butisalsoinfluencedbythelocationandcauseofthearrest.Theworst
outcomesoccursfollowingout-of-hospitalcardiacarrest.Sirbaugh
reviewed300pediatric
out-of-hospitalcardiacarrestsandonlyfounda2%survivaltodischarge,allwithsignificant
neurologicalsequelae.Similarly,Schindler
reviewed80out-of-hospitalcardiacarrestsand
founda7%survivalto12monthsafterdischarge,with50%ofsurvivorsbeinginapersistent
Chapter16:Managementofa3-year-oldchildwithdrowning
severecasescardiopulmonarybypasshasbeenused,butthisisonlyavailableintertiarycenters
providingpediatriccardiacsurgery.
Orlowski
notedthatwatercolderthan10
Caccountsforallreportedcasesofsurvival
afterprolonged�(15minutes)submersion,and16of17casesprobablyinvolvedwater
colderthan5
C.Eveninice-waterdrowning,hypothermiabynomeansguaranteessurvival.
Unlesscoolingoccursquickly,beforehypoxiabecomessevere,littleusefulcerebralprotec-
tionisprovided.Rapidcoolingofbodytemperatureduetopulmonarycoolingbyrapid
breathinginandoutofice-coldwater,gastriccoolingfromswallowedcoldwaterinaddition
tosurfacecooling(especiallyfromscalp,wherebloodvesselsdonotconstrict)isrequiredto
offerprotection.
Coolingthatoccursduringrescueandtransporttohospitalisoflittle
benefitandmayrenderdeepbodytemperatureonarrivalinhospitalanunreliableprog-
nosticindicator.
Hyperkalemiainseverelyhypothermicpatientsisusuallyindicativeof
asphyxialcardiacarrestbeforesignificantcoolingoccurred.
Evenincaseswithrapidcool-
Table16.2.
Chapter16:Managementofa3-year-oldchildwithdrowning
Managementofnon-accidental
injuryonthePediatricIntensive
CareUnit
RobertRossRussellandDuncanMcAuley
IntheUK2
3%ofchildrenareabusedeachyear,withseriousinjuryoccurringin1ina
Doctorsandalliedprofessionalshavingcontactwithchildrenshouldbeawareofthe
possibilityofabuse.In2003,LordLamingstatedthatthe
rigorousinvestigationand
managementofactualorpossibleabuseinchildrenrequiresthesystematic,comprehensive
andtimelydocumentationofconcerns,andevidencethattheyhavebeenproperlyaddressed
neurosurgicalevaluation.Arapidsequenceinductionwasperformed,usingthiopental
4mgkg
Fig.15.1.
CTscanshowingmixeddensitysubdural
collections.
Chapter15:ManagementofNAIonthePICU
Chapter15:ManagementofNAIonthePICU
4.Abnormalparentalaffect,suchaslackofconcern,hostility,orpreoccupationwiththeir
ownproblems
5.Abnormalappearanceofchildorabnormalinteractionwithparents
6.Directhistoryfromchild
7.Injuriesofdifferentages.
Someformsofinjuryarehighlyassociatedwithnon-accidentalinjury.Theseincludefinger-
Chapter15:ManagementofNAIonthePICU
innon-accidentalinjurywithspiralorobliquef
racturesbeingtypical.Longbonefracturesfrom
abuseareoftenatthedistalend(involvingthecorn
Table15.1.
Importantmedicalcausesofbruising
HemophiliaAorB
vonWillebrand
sdisease
sthromboasthenia
FactorXIIIdeficiency
DanlosandMarfan
ssyndromes
Chapter15:ManagementofNAIonthePICU
Iftheeffusionislargeorcausingcardiaccompromise,thendrainagewillberequired.
Drainagemayalsooccasionallyberequiredfordiagnosticpurposes.Inmostinstances,
drainagewillbeanelectiveorsemi-urgentprocedure,asinthiscase.Thiswould,usually,
beperformedbycardiologistsorcardiacsurgeons.Veryoccasionallyemergencypericardio-
centesiswillneedtobeperformed.Ifnoechocardiographyisavailable,thisshouldonlybe
doneasablindprocedureinadireemergency,forexample,acardiacarrestorneararrest
Chapter14:Pericardialeffusioninachild
1.Firstidentifythexiphisternum.
2.EnsureanECGisattached.
3.Takeanappropriatecannula(seeabove)withasyringeattached.
4.Insert1
2cmbelowxiphisternumatanangleof45degreestotheskinaimingcephaladly
andslightlytotheleft,imaginingyouareaimingatthetipofthescapula.Aspirateasyou
insertthecannula.
5.Assoonasyouaspiratefluid,advancethecannulaandremovetheneedle.
Fig.14.3.
Needlepositionforemergency
pericardiocentesis.
Chapter14:Pericardialeffusioninachild
consultantpediatriccardiacsurgeononcallwasadvisedthattheprocedurewastakingplace.
Chapter14:Pericardialeffusioninachild
Incasesofrecurrenteffusionapericardialwindowcanbemadetoallowcontinued
drainage.Thiswouldusuallybeperformedintheaterasasemi-electiveorurgentprocedure.
Percutaneousballoonpericardiotomyhasbeendescribedasanalterativetoasurgical
pericardialwindow.
Post-drainagecare
Thepatientshouldbecloselymonitoredhemodynamically,and,indeed,requireaperiodof
observationandventilationinanintensivecareorhigh-dependencyunitdependingontheir
clinicalcondition.RepeatECHOexaminationwillberequiredtomonitorpotentialrecur-
renceoftheeffusion.
Inourpatientthepost-operativeperiodwascomplicatedbythedevelopmentofpulmo-
naryhypertensiveeventswhenweattemptedtoweanthechildfromventilation.Thiswas
relatedtothepre-existingpulmonaryhypertension,secondarytoalargeVSD.Itdoes
demonstrate,however,thatpericardialeffusionsandcardiactamponadewillmostcom-
monlyexistalongsideotherpathophysiology.
Purulentpericarditis
Installationofstreptokinase,intothepericardium,hasbeendescribedinpurulentperi-
carditis.Thishelpstobreakdownfibrinandpreventthedevelopmentofconstrictive
pericarditis.
Withappropriatelytimedrecognitionandintervention,themortalityfrompericardial
effusionshouldbeextremelylowandrelatedtotheunderlyingcause.
Inourpatienttheeffusiondidnotrecurandthepulmonaryhypertensionslowlyresolved.
Feedingwasgraduallyestablishedandata6-monthreviewhewasthrivingandgaining
weight.
Recurrentpericardialeffusionisrareanddifficulttomanagewhenitoccurs.
Developmentofconstrictivepericarditispost-pericardialeffusionsisararebutserious
sequelae,usuallyoccurringinthefirstyearafterinitialpresentation.
Learningpoints
Signsandsymptomsofpericardialeffusionareoftennon-specificandthereforeaclinical
indexofsuspicionisnecessarytomakethediagnosis.
Agoodhistorywillidentifyriskfactorsforpericardialeffusion.
Recentcardiacsurgeryplacespatientsatahighriskinthefirstmonthaftersurgeryof
pericardialeffusionandpotentialcardiaccompromise.
Pericardialtamponadecanoccurearlyorlateafteranycardiacsurgicalprocedureeven
thosethatareconsidered
straight-forward
suchassecundumASDrepair.Ninety-seven
percentwillpresentwithin28daysofsurgery.
Inapatientwithalowcardiacoutputstateandsignsofaraisedcentralvenouspressurea
diagnosisofpericardialeffusionwithcardiactamponademustbeconsidereduntilitcan
beeliminated.
Echocardiographyisthedefinitivediagnostictestforpericardialeffusions.
Chapter14:Pericardialeffusioninachild
Theavailabilityofportableultrasounddevisesallowsaquickcheckforlargeeffusionsto
beperformedbynon-expertsinanemergencysituationandallowsrapiddifferentiation
fromsevereventriculardysfunction.
Co-existingpathophysiologyiscommonlypresent.
Problemsinpractice
Drainageofpericardialeffusionevenunderultrasoundguidanceisnotarisk-free
Chapter14:Pericardialeffusioninachild
Pericardialeffusioninachild
PatriciaM.Weir
Pericardialeffusioncanbethoughtof,simply,asexcessfluidwithinthepericardialsac.
Cardiactamponadecanbedefinedascompressionoftheheartduetoaccumulationoffluid
inthepericardium.Pericardialeffusionsarenotuncommoninpediatriccriticalcare.
Cardiactamponade,althoughmuchlesscommonthansimplepericardialeffusions,isan
emergencysituation,whichmustberecognizedanddealtwithimmediately.Pericardial
effusionhasmultiplepotentialcausesandavariablepresentation.Ahighindexofsuspicion
ofpericardialeffusionisthereforeveryimportanttopreventmissingthediagnosis.Failureto
recognizetheproblem,anddealwithitappropriately,mayresultinthedeathofthechild.
Presentationtoanemergencydepartmentofachildwithapericardialeffusionisararebut
potentiallylife-threateningevent.
Casehistory
A6-month-old,5kgboyunderwentapatchrepairofalargeVentricularSeptalDefect
(VSD).Hehadbeenbornat34weeks
gestationwithadegreeofintra-uterinegrowth
Chapter14:Pericardialeffusioninachild
Traumaisanuncommonbutimportantcauseofcardiactamponade,sinceitmaypresent
veryacutely,requiringurgentdecompression.Ahighindexofsuspicionisnecessaryandit
mustberememberedthattamponadeisfrequentlydescribedsecondarytocentralvenous
Table14.1.
Causesofpericardialeffusions
Post-cardiacsurgery
Early(blood)
Late(serous/inflammatoryexudates)
Chesttrauma
Chapter14:Pericardialeffusioninachild
foundinothercausesofmyocardialinjurybutrarelyinsuchhightiters.Shealsofoundhigh
levelsofantiviralantibodiesandtheorizedthateitherfreshviralinfectionorreactivationofa
virusmayplayapartinthedevelopmentofPPS.
Post-cardiacsurgery
Thepercentageofchildrenfoundtohavepericardialeffusionaftercardiacsurgeryis
reportedasbeingbetween13.6%and53%.Thislargerangeis,inpart,duetodifferences
indefinitionofpericardialeffusionandhowcarefullyeffusionshavebeenlookedfor.After
cardiacsurgery,earlypericardialcollectionsareusuallyduetopost-operativebleedingand
becomeevidentinthefirstfewhourspost-operativelyinPICU.Alternatively,theymay
presentdaystoweekslateraspartofaninflammatoryresponseknownasPPS.Thisconsists
offeverandsignsofpericardialinflammationusuallyoccurringmorethanaweekpost-
operatively.Arecentstudyof336childrenafteropenheartsurgeryfoundthat77(23%)of
thepatientshadpericardialeffusions.
Ofthese43wereclassifiedasmoderateorlargeand18
(5%)weresymptomatic;12children(4%)requireddrainage;and97%ofeffusionsoccurred
Chapter14:Pericardialeffusioninachild
Inless-developedpartsoftheworldinfectivepericardialeffusionsarenotuncommon.These
arepredominantlyStaphylococcalinfections,buteffusionshavealsobeendescribedsecon-
darytootherbacterialinfections,includingmycoplasma,tuberculosis,parasites,Familial
Mediterraneanfeverandviruses(Influenza,CMV,Adenovirus,Coxsackie).Theyarealso
foundasafeatureofacuterheumaticfever.CardiovascularinvolvementinHIViswell
describedespeciallyindevelopingcountriesandastudyfromThailandof27childrenwith
CVSsymptoms,principallydyspnea,foundthat44%hadpericardialeffusionsonECHO.
Otherinflammatorycauses
Pericardialeffusionsoccasionallyoccuraspartofasystemicinflammatoryresponseto
sepsis.Theyalsooccurwithamultitudeofinflammatoryandauto-immunetypesyndromes,
suchasnephroticsyndrome,granulomatousdisease,Kawasakis,collagenvasculardisorders,
Chapter14:Pericardialeffusioninachild
Commonsymptomsofpericardialeffusionarenon-specificmalaise,tiredness,dyspnea,
andvomiting.Thechildmaycomplainofchestpainorabdominalpainandfever.
Table14.2.
Diagnosisofpericardialeffusion
Non-specificmalaise,vomiting,fatigue
Pain:chestorabdominal
Iflarge:Lowcardiacoutputstate
poorperfusion,pro-
longedcapillaryrefilltime,
Muffledheartsounds
Pericardialrub
Pulsusparadoxus
Jugularvenousdistension
Low-voltageECG
ECG:STelevation,PRdepression
ChestX-ray
largeglobularheart
excessfluidseeninpericardialspace
Chapter14:Pericardialeffusioninachild
Inthiscaseearlyechocardiographywouldhavedemonstratedthepresenceofaneffusion,
allowingatimelyassessmentanddrainage.
Anelectrocardiograph(ECG)willclassicallyshowlowvoltagecomplexes.STsegment
elevationinallleadsotherthanV1andaVRareaspecificsignofpericardialinflammation.
PRdepressioninbothlimbandprecordialleadsofgreaterthan0.5mmhasbeendescribedin
adultsasbeingpresentin23%ofpatientswithasymptomaticpericardialeffusion.
ChestX-ray(
Fig.14.1
)mayshowanenlargedorglobularheart.Changeinheartsizemay
beacluetodevelopmentofeffusion,butcanbedifficulttoassessinchildrenifthefilmisnot
takenatthesamepointinrespiration.
ThedefinitivediagnosisismadebyECHO(
Fig.14.2
).Thiswillallowestimationofthe
sizeandpositionoftheeffusionandanassessmentofthepresenceorabsenceofcardiac
compromise.Incardiactamponade,fluidinterfereswiththediastolicfillingofthechambers
andthereforediastoliccollapseonECHOindicatescardiaccompromise.
Portableultrasounddevicesallowarapidcheckforlargeeffusionstobeperformedin
emergencysituationsbynon-cardiologicallytrainedpractitioners.
Onlyaroundhalfofcaseswillhavetheclassicalchangestoheartsounds,low-voltage
ECG,orhepatomegaly.
CTandMRIcanbothbeusefulforevaluatingloculatedorhemorrhagiceffusions,
pericardialmasses,andconstrictivepericarditisbutarenotsuitableintheacutesituation
withahemodynamicallyunstablechild.
Fig14.1.
APchestX-rayshowinglargeheart
secondarytopericardialeffusionandaright-sided
pleuraleffusion.
Pericardial effusion
Fig.14.2.
Echocardiographshowingapericardial
Chapter14:Pericardialeffusioninachild
ProgressonECMO
Fig.13.1.
ChestX-rayonECMO:thetipofthe
endotrachealtubeliesapproximately1cmabovethe
carinaandthetipoftheNGtubeliesbeneaththe
Chapter13:The2-month-oldwithseverepertussis
Epidemiology,presentation,andcomplications
Chapter13:The2-month-oldwithseverepertussis
Toxin(PT),fimbriae(FIM),lipopolysaccharide(LPS),andTrachealColonizationFactor(TCF).
Then,paralysisofciliaanddeathofciliatedcellsleadstodefectivemucociliaryclearance.
Releaseof
toxincausesfurtherdamagetorespiratorytractandinterfereswith
theimmuneresponsebypreventingmigrationoflymphocytesandmacrophagestoareasof
infection,andadverselyeffectingphagocytosisandintracellularkilling.Thisleadstothe
symptomsofwhoopingcoughand,ifthebacteriareachthealveoli,pneumoniadevelops,
whichhasahighmorbidity.Atautopsy,inflammationofthemucosalliningoftherespira-
torytractciliaryepitheliumisseenwithcongestionandinfiltrationofthemucosaby
lymphocytesandpolymononuclearleukocytesandinflammatorydebrisinthebronchi.
Ventilationofinfantswith
Evidencehassuggestedthatthediseaseprocessininfantswith
Pertussis
maybeattenuatedby
earlyinterventionforapneicepisodesandrespiratorydistressbyinstitutingventilatory
support.Ideally,thisshouldbedoneelectivelyandincontrolledconditions.
Intheemergencysituationwithevidenceofcardiovascularcompromise,careshouldbe
takenwiththechoiceofinductionagentasdrugswithmyocardialdepressantactivity
(thiopental,propofol,andmidazolam)mayworsenthesituation.Considerationshouldbe
30cmH
O,whileallowingpermissivehypercapniawithpH
arterial
�7.2andtolerance
ofoxygensaturationof�85%.
AttemptingtooptimizelungvolumeswithPEEPandprone
positioning,useofHFOVespeciallywhenameanairwaypressure�16cmH
Omaybehelpful.
Thereissomeevidencetosuggestthatadministrationofsurfactantmayimproveoutcomes.
Pulmonaryhypertensionin
Pulmonaryhypertensionisadevastatingcomplicationofsevere
Pertussis
infectioninyoung
infants.Itisparticularlydifficulttotreatandonlyrarelyrespondstoconventionaltherapies
suchasalkalizationandinhalednitricoxide.Mechanismsunderlyingthisintractableformof
pulmonaryhypertensionthatdifferfromthoseinotherformsofinfantrespiratoryfailure
havebeensuggested.Oneisthatextremeleukocytosispredisposestotheformationof
lymphocyteaggregatesinthepulmonaryvasculature,resultinginincreasedpulmonary
vascularresistanceviaobstructionratherthanvasoconstriction.
Severallinesofevidence
Chapter13:The2-month-oldwithseverepertussis
WhilethevalueofECMOinthesecasesofintractablepulmonaryhypertensionhasbeen
questioned,thereareundoubtedlyasignificantproportionofcasesof
Pertussis
forECMOwhodosurvive.
Thesemayrepresentmoreofabronchopneumonia/acute
respiratorydistresssyndromepathophysiologythanthesevereandresistantpulmonary
hypertensiondescribedabove.
ECMOshouldbeconsideredinthoseinfantsandchildrenthoughttohavepotentially
reversiblelungdiseasewhohavebeenventilatedforlessthan7days,andhenceavoided
irreversibleventilatorinducedlungdamage.
Chapter13:The2-month-oldwithseverepertussis
Chapter13:The2-month-oldwithseverepertussis
Post-operativemanagement
Muchofthepost-operativemanagementofthepatient(bothneonatalandtheolderchild)
followingcorrectionofaCoAiscommontoallcardiacsurgery.Thepatientremainssedated,
intubated,andventilatedwhiletheyareallowedtowarmup,recoverfromtheeffectsofthe
Chapter12:Coarctationoftheaortainaneonate
Thedevelopmentoflate,chronichypertensionisawell-establishedcomplicationofCoA.
Itwasoriginallythoughtthatrepairintheneonatalperiodorearlychildhoodwouldprevent
this;howeverthereisevidencetosuggestthattheelasticpropertiesoftheprestenoticaortaof
neonateswithcoarctationareprimarilyimpairedandthattheyremainabnormalevenafter
successfulsurgicalcorrection.
Follow-updataindicatesthatneonatesundergoingcoarcta-
tionrepairhaveasignificantincidenceofhypertensionby10yearsofage.
Recentresearch
intoapolymorphismoftheAngiotensin-ConvertingEnzyme(ACE)genehassuggestedthat
childrenwithaparticularACEgenotypemaybeatgreaterriskofdevelopinghypertension
followingcoarctationrepairininfancy.
PatientswithCoAthereforerequirelifelong
follow-upandcarefulmanagementduringsubsequentsurgeryandanesthesia.
Respiratoryfailure
Causesofpost-operativerespiratoryfailureinclude:
Cardiacfailure
Pleuraleffusions
Pneumothorax
Lobar/segmentallungcollapse
Pneumonia
Upperairwayobstruction.
AchestX-rayisessentialtoaidthemanagementofachildwhoeitherfailstoweanfrom
ventilationordevelopsrespiratoryfailureafterextubation.Pleuraleffusionsmaybedueto
thepresenceofblood,reactiveexudates,leftventricularfailure,orachylothorax.Achylo-
thoraxisthepresenceoflymphinthepleuralspacefollowingdamagetothethoracicductor
backpressurefromrightventricularfailure.Bothpleuraleffusionsandpneumothoracesmay
requirerepositioningorreplacementofintercostaldrains.Chylothoraxmaynecessitatethe
Chapter12:Coarctationoftheaortainaneonate
injurytothebowelsecondarytolowcardiacoutput.Thisisbroughtaboutbymucosal
hypoperfusionasthearterialsupplytothebowelarisesfromtheaortaintheabdomen,
belowtheareaofaorticnarrowing.Enteralfeedingcausesanincreaseinoxygendemandin
thegutmucosa.Ifthisincreaseddemandcannotbemetbecauseofapoorbloodsupply,bowel
ischemiamayresult.Acase-controlstudyofnecrotizingenterocolitisinneonateswithcon-
genitalheartdisease
foundthatdiagnosesofhypoplasticleftheartsyndromeandtruncus
arteriosuswereindependentlyassociatedwiththedevelopmentofNECbymultivariate
analysis,alongwithearliergestationalageoftheinfantandepisodesoflowcardiacoutput.
Forthisreason,babiesarecommonlynotenterallyfedafterCoArepair,especiallythosewho
hadadegreeofshockatpresentation.IntheabsenceofevidenceofNEC,feedingisusually
reintroducedaroundday2to5post-operatively.Whereenteralfeedingistobewithheldfor
morethanafewdays,parenteralnutritionwillbenecessary.
Othercomplications
Otheruncommoncomplicationsrelatedtocross-clampingtheaortaincludeischemiaofthe
spinalcordcausingparaplegiaandrenalfailureduetoacutetubularnecrosis.
Learningpoints
Earlydiagnosisandprompttreatmentareessential.
Examinationofthefemoralpulsesismandatoryinallsickneonates.
WhereaCoAissuspectedinanunwellneonate,prostaglandinE
orE
10ngkg
minmustbestartedimmediatelyinacloselymonitoredenvironment.
Contactregionalcardiothoracicunitimmediatelyforadviceandreferral
Consider:intubation,ventilation,inotropicsupport,fluidrestriction,anddiuresis.
Stopenteralfeedinguntilformallyassessed.
Followingrepair,femoralpulsesshouldberegularlyassessed.
Enteralnutritionshouldbereintroducedwithcautionespeciallywhentheneonateisor
hasbeencardiovascularlyunstable.
Hypertensionshouldbecarefullycontrolledpost-operatively.
TheauthorsaregratefultoDr.GrahamStuartforallowingustousetheechocardiogramin
Fig.12.1
1.BensonLN,McLaughlinPR.Coarctationof
theaorta.In:FreedomRM,YooS-J,Mikailian
MRT,WilliamsW,eds.
TheNaturaland
ModifiedHistoryofCongenitalHeartDisease
NewYork,BlackwellPublishing,2004.
2.SchwengelDA,NicholsDG,CameronDE.
Coarctationoftheaortaandinterrupted
aorticarch.In:NicholsDG,CameronDE,
GreeleyWJ,LappeDG,UngerleiderRM,
Chapter12:Coarctationoftheaortainaneonate
6.YounoszaiAK,ReddyVM,HanleyFL,
BrookMM.Intermediatetermfollow-upof
theend-to-sideaorticanastomosisfor
coarctationoftheaorta.
AnnThoracicSurg
:1631
7.QuaegebeurJM,JonasRA,WeinbergAD
Chapter12:Coarctationoftheaortainaneonate
The2-month-oldwithsevere
pertussis(whoopingcough)
)ofnormalsalinegiven
intravenouslywithamarkedimprovementinherperipheralperfusionandheartrate.
FurtherIVaccesswasthenobtainedviaanothercannulaandbloodsampleswereobtained
Table13.1
Adecisionwasmadetoinstituteartificialventi
lationbecauseofthefrequencyoftheepisodes
ofapnea.Anesthesiaandparalysiswasinducedwiththiopental(3mgkg
inspiredoxygen.Ventilationwascontinuedwithsynchronizedintermittentmandatory
ventilation(SIMV)at40breathsperminutewithapeakinspiratorypressure(PIP)of22cm
Oandapositiveend-expiratorypressureof4cmH
O.Anasogastrictube(NGT)wasthen
Table13.1.
Investigationssentduringresuscitationandresults
Testssent
Resultsonarrival
BloodgasVenouspH7.21,
9.8kPa,
6.4kPa,Bicarbonate29mmoll
,BE
HB7.8gdl
,Na
131mmoll
,K4.0mmoll
(post-intubationcapillary
gas:pH7.33
6.0kPa,
13.0kPa,BE
5mmoll
BloodcultureNegativeat48hours
UreaandelectrolytesNa+131mmoll
,K3.9mmoll
,Urea4.0mmoll
,Creatinine70
moll
Bloodglucose4.2mmoll
FullbloodcountHemoglobin8.0gdl
,whitecellcount24×10
,(differential71%
Chapter13:The2-month-oldwithseverepertussis
Furtherbloodculturesandabronchoalveolarlavageforimmunofluorescenceforrespi-
ratoryvirusesandmicroscopyandculturewerenegative.
ClarithromycinwascontinuedandmilkNGTfeedswerestarted,whichwerewell
tolerated.
Chapter13:The2-month-oldwithseverepertussis
Coarctationoftheaortaina
MattOramandAndrewWolf
CoarctationoftheAorta(CoA)isavascularabnormalityinwhichtheaortaisnarrowed,
mostcommonlyintheregionoftheductusarteriosusandleftsubclavianartery.Thisresults
inanobstructiontobloodflowtothelowerbody.ThepatientwithCoApresentingtothe
pediatricintensivecareunit(PICU)generallyfallsintooneoftwogroups.Theymay
presentintheneonatalperiod,whenclosureoftheductusarteriosusprecipitatessufficient
obstructiontocausesymptomsandsignsorlaterinchildhoodfollowingelectivesurgery.
Thosethatpresentintheolderchildareoftendiscoveredasanincidentalfindingofa
murmurorhypertensionwithorwithoutnon-specificsymptomssuchasfatigueorshort-
nessofbreathonexertion.
Casehistory
A5-day-oldboywasreferredfromtheneonatalintensivecareunit(NICU)ofaperipheral
hospitaltothecardiacsurgicalcenterformanagementofaCoA.Hehadbeendelivered
uneventfullyatfullterm,hadinitiallyappearedtobewellwithnosuspectedabnormality.On
thefifthpostnatalday,hewasreadmittedtohospitalhavingbeennotedtobefeedingpoorly,
vomiting,andbecomingprogressivelytachypnoic.
Examinationandinitialmanagement
Examinationrevealedatachycardiaof200beatsperminute,acapillaryrefilltimeof
5seconds,impalpablefemoralpulses,hepatomegaly,arespiratoryrateof80breathsper
Progressinthepediatricintensivecareunit
Chapter12:Coarctationoftheaortainaneonate
CoAisfoundinaround1in2000livebirths.CoAaccountsfor7%ofneonatespresenting
withcardiacdefects.Malesareaffectedmorecommonlythanfemales.Therearetwodistinct
sub-groupsofpatients,thosethatpresentintheneonatal(andindeedantenatal)periodand
thosewhopresentasolderchildrenoradults.
Fig.12.1.
2-Dechocardiogramortheaorticarch
showingaCoAattheoriginoftheleftsubclavian
artery(asc.ao
ascendingaorta,coarct
coarctation,
desc.ao
descendingaorta,l.subclavart
subclavianartery,PA
pulmonaryartery).
Chapter12:Coarctationoftheaortainaneonate
differenceinbloodpressurebetweenlimbsismorelikelyduetorandomvariationthan
andtheinfantwillstillrequireechocardiographytoconfirmorexcludethediagnosis
ofcoarctation.
Thedecreasedbloodflowdistaltothecoarctationleadstoregionaltissuehypoxia,
improved,leftventricularafterloadisreduced,invasiveproceduresareperformedmore
easily,andasaferinter-hospitaltransfercanbeundertaken.
ThekeyaspecttomanagementistheurgentdeliveryofintravenousProstaglandinE
orE
.Theseprostaglandinsusuallyactbyreopeningtheductusarteriosusandrestoring
aorticbloodflowdistaltotheCoA.Thisallowstimefortransferandstabilizationofthe
babypriortosurgery.Thestartingdoseof10ngkg
perminmayneedtobeincreasedto
50ngkg
perminifthereisnoimprovementinthephysiologicalstateofthebaby.
Itmustbeborneinmindthatthereisariskofapneainthenon-ventilatedneonate
receivingaprostaglandinE
orE
infusionaswellashypotensio
n,bradycardia,flushing,
fever,andcoagulopathy.Thereisalsoevidenc
etosuggestthatprostaglandinsmayrelieve
Table12.1.
InitialmanagementofthesickneonatewithasuspectedCoA
Airwayandbreathing
Provideoxygen
Considerintubationandventilation
Venousaccess(peripheral,intra-osseousorcentralvenous)
Checkbloodglucose
Checkfemoralpulses
CheckSpO
andBPinallfourlimbs
Differentialdiagnosis
Othercardiacabnormality
Chapter12:Coarctationoftheaortainaneonate
theobstructionofCoAbytheireffectonectopticductaltissuewithintheaortawithout
reopeningtheduct.
Thesickneonatewillusuallyreceivefluidbolusesduringtheinitialresuscitationefforts
whilstdiagnosticuncertaintyexists.However,thesepatientsarelikelytohavesomedegreeof
leftventricularfailureandoftenalsorightventricularfailure.Therefore,oncethediagnosis
ofCoAismade,itmaybenecessarytocommenceaninotrope,restrictfluids,andgive
Chapter12:Coarctationoftheaortainaneonate
pigmentedurineandherethefluidintakeshouldbeincreasedtoproduce2mlkg
perh
urineoutput.Occasionallyinthiscircumstancemannitol0.25mgkg
isindicatedto
enhanceurineoutputandpreventmyoglobinfromobstructingtherenaltubules.
Inflammatoryresponseandburncare
Patientswithsevereburnscanonlyrecoverwithdefinitivewoundclosure.Intensivecarecan
supportthepatientuntilcoverageisachieved.Theburnisthemajorpropagatorofthe
inflammatoryresponse.Earlyexcisionpromoteshealingandreducestheriskofinfection
therebyreducingtheeffectsofhypermetabolism.
Localtissuedamagecausesincreasedcapillarypermeabilityandedemawithapeakin
Chapter11:Criticalcareforachildwith80%burns
glucocorticoidsandglucagon.
Hyperglycemiaiscommonandisassociatedwithhigher
mortality.
Insulinresistanceandsuppressionincreasesthecatabolicprocessand,although
catabolismcannotbereversedbyaninsulininfusion,thereappearstobeareductioninacute
phaseproteinswithinsulin-inducedeuglycemia.
Thetemperatureneedstobemaintainedatnormothermiaormildpyrexiatoreduce
Chapter11:Criticalcareforachildwith80%burns
Analgesiaandsedation
Intheemergencysituationmorphineisthedrugofchoiceandshouldbetitratedtoachieve
adequatelevelsofanalgesia.Reducingpainassociatedwithburncarehasapositiveimpacton
bothlong-termemotionalsequelaeforthepatientaswellasapositiveimpactoncaregivers.
Acombinationofanopiateandabenzodiazepineismostfrequentlyused.Standardpain
assessmenttoolsforchildrenareusedintheabsenceofburnspecifictools.Toleranceresults
Chapter11:Criticalcareforachildwith80%burns
Unconsciouspatients,thosewith�80%TBSAburnsandsignsofinhalationburnshould
beintubatedandventilationoptimized.
Carbonmonoxidepoisoningusuallyresolveswithhigh-inspiredoxygenandeffective
ventilation.Hyperbaricoxygenshouldbeconsideredinseverecases�(15%COHb)and
wherethechambercaneasilybeaccessed.
Earlyburnresectionandcoveragereducescatabolism,pain,andriskofinfection.
Earlyenteralfeedingpromoteshealingandreducesgutpermeabilitytobacteria.
Highdosesofmorphineandmidazolamarerequiredandshouldbeweanedslowly.
1.SheridanR,RemensnyderJ,SchnitzerJ
Chapter11:Criticalcareforachildwith80%burns
21.EngravL,ColescottP,KemalyanN
Chapter11:Criticalcareforachildwith80%burns
Criticalcareforachildwith80%
HeatherDuncan
Childrenwhosustainburnstomorethan80%oftotalbodysurfacehaveahighmortality.Burn
shock,sepsisandrespiratoryfailurearemajorcausesofdeathinsevereburns.
Thekeyto
reducingmortalityandmorbidityisadequatefluidresuscitation,earlyburnexcisionand
dedicatedmultidisciplinaryteamcareforthesecomplexpatients.
Indedicatedburnscenters,
ifthepatientsurvives,thelong-termoutlookisgoodforphysicaldisabilityandqualityoflife.
Casehistory
Apreviouslywell2-year-oldgirlwastrappedinherroomduringahousefire.Shepresented
tothelocalaccidentandemergencydepartmentwithstridor,ahoarsecryandmoaningwith
Hemodynamically,shewasunstable,requiringongoingfluidbolusesfortachycardia
(180beatsmin
)andhypotension(65/35mmHg),inadditiontotheresuscitationand
maintenancefluids.Urineoutputwas0.5mlkg
perh.Anadrenalinfusion0.1mcg
perminwasstartedandbloodproductsordered.Theburnswerecleaned,dressedwith
Flamazineandcoveredwithgauzedressings.
Priortotransfer,thefemoralvenouslinewasrewiredandreplacedwithatriplelumen
centralline,asecondrightinternaljugulartriplelumenlinewasinsertedandtheintra-
osseouslinesremoved.The60-minuteroadambulancetransfer,backtotheregionalburn
centre,wasuneventful.Fluidresuscitationcontinuedandshewastransfusedwithaunitof
packedredcells.
Progressinpediatricintensivecareunit(PICU)
ShortlyafterarrivingattheregionalPICU,shewasreassessedbytheburnssurgeonbefore
undergoinga3-hourprocedureintheater,whichinvolvedescharotomyofbotharms,both
legs,andpartialexcisionoftheburn.TheTBSAwasreassessedto88%fullthicknessburns
Table11.1.
Summaryofclinicalexaminationandinitialinvestigationsatadmissionto
accidentandemergencydepartment
PastmedicalhistoryFitandwell
Fullyvaccinated
RegularmedicationsNone
AllergiesNoneknown
ExaminationSevereburns,estimated80%
Stridor,moaningwithpain
Adequateoxygenationwithfacemaskoxygen
Respiratoryrate48min
Heartrate156min
Bloodpressure120/60mmHg
Capillaryrefilltime�5seconds
Temperature35.8°C
Decreasedlevelofconsciousness;
respondingonlytopain
InvestigationsWeight15kg
Height100cm
FBCHb9.4gdl
,WBC×10
Chapter11:Criticalcareforachildwith80%burns
Fig.11.1
).HerfacialburnsweredressedwithPolyfaxandtheburnsonherlimbsandtrunk
weredressedwithFlamazineandgauze.
Fig.11.1.
Distributionofburnsbasedona
Browdertypebodymap.Thehatchedarea
representsfullthicknessburn.
Chapter11:Criticalcareforachildwith80%burns
(selenium,zinc,andcopper)weresupplementedintravenouslyandmonitoredroutinelyand
glutamine(0.5gkg
)wasaddedtofeeds.Persistentdiarrheawasproblematicwiththehigh
feedosmoticandvolumeload.After2weeksthefeedswereadjustedtodeliver120kcalkg
perdayand3.3g
perdayofproteinforpersistinghypoalbuminemia32gl
Anophthalmologyexaminationofhereyeswaspossibleafter48hours,whentheswelling
hadreduced.Therewasnoevidenceofcornealburnsandroutineeyecarewascontinued
withtheadditionoftopicalantibiotics.
Table11.2.
Volumesoffluidinmladministeredduringthefirst4dayspost-burnexcludingblood
productsadministeredforbloodlossduringsurgicalprocedures.Resuscitationvolumeswere
calculatedon80%TBSAburns
Timefromburn
1h1
8h8
24h24hDay2Day3Day4
Intravenousfluid
6004645522510470229519401030
Oralfeed
55055069014301725
6004645557511020299033702755
60045855210
254026242156
ExpectedfromParklandformula350
Chapter11:Criticalcareforachildwith80%burns
volumeresuscitationbutnotinotropicsupportand,inaddition,poortoleranceofenteral
feedsnecessitatedfourdaysofparenteralnutrition.
AtthetimeofdischargefromPICU,shewasawake,watchingherfavoritevideosandhad
asleep
wakecycle.
Thetreatmentofchildrenwith�80%burnshasadvancedoverthepast30yearswith
significantimprovementinmorbidityandmortality.Progresshasbeenmadeinthree
areas:burnresuscitation,earlyexcisionandclosure,andimprovedgeneralcriticalcare
techniques.Therearefewdouble-blindedrandomized,controlledtrials,butawealthof
caseseriesandlaboratoryevidence.
Initialassessmentandmanagement
Itisessential,duringtheinitialevaluation,tosystematicallyandthoroughlyexaminethe
childinordertoidentifythedegreeofinjuryandtoidentifyorexcludenon-burntrauma,
Chapter11:Criticalcareforachildwith80%burns
Bothsizeanddeptharefrequentlyunderestimatedoninitialexamination.Thewound
appearancewillchangeoverthesubsequentfewdays;accordingly,serialexaminationsare
Table11.3.
Adjustmentforcalculationoftotalbodysurfaceareainchildrenaccordingtoage.
Therelativelylargesurfaceareaoftheheaddecreasesandthesurfaceareaofthelegsincrease
frominfancytoadulthood
Age1yr1yr5yr10yr15yrAdult
A:Head19%17%13%11%9%7%
B:Thigh5.5%6.5%8%9%9%9.5%
C:Lowerleg5%5%5.5%6%6.5%7%
Chapter11:Criticalcareforachildwith80%burns
Chapter11:Criticalcareforachildwith80%burns
Fluidresuscitationformulaeprovideaguidebutareinaccurateinmostindividual
patientswithmorethan50%ofpatientsneedingresuscitationfluidinexcessofthe
Parklandformula.
Fluidprescriptionshouldbeadjustedaccordingtoarterialandcentral
Table11.4.
Fluidprescriptionforresuscitationandmaintenancebasedon80%TBSAusing
theParkland/BaxterformulacomparedwithprescriptionsfromtheShrinersHospitalsforChildren
FluidPrescription
CalculationFluidperdayFluidperhour
Resuscitation(Parkland/Baxter)
Hartmannssolution(orhalf
ssolution+half
HAS4.5%)
4×weight×%
15kg×80%×4
15kg×30ml
4800ml
2400ml
2400ml
8h300mlhr
24h150mlh
5%dextrose,0.9%saline,
20mmolKCll
10kg×4mlh
5kg×2mlh
80mlkg
perday50mlh
Totalvolume0
Totalvolume9
24h
2800ml
3200ml
350mlh
200mlh
ShrinersHospitalforChildren,Boston
8hrRinger
slactate+50mmol
16hrRinger
slactate
24hrRinger
slactate+12.5g
albuminl
4mlkgper%TBSA
1500mlm
5970ml
ShrinersHospitalforChildren,
slactate+12.5galbuminl
5000mlm
2000mlm
5460ml
Anextra30mlkg
perdaycouldbeaddedforinhalationburn.
BodySurfaceArea(BSA)iscalculatedas
(87(heightincm+weightinkg)
2600)/10000.HumanAlbuminSolution(HAS).
Chapter11:Criticalcareforachildwith80%burns
TAPVC.Theresultantphysiologyisquitevariable,andisdependentonthecombinationof
thevenousdrainagepatterns.
Physiologicconsiderations
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
Althoughoxygenisbeneficialinpatientswithhypoxemiacausedbypulmonaryedema,
indiscriminateadministrationshouldbeavoidedduetoitssignificantpulmonaryvaso-
dilatoryeffects.
AdministrationofprostaglandinE
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
Thevastmajorityofpatientsshowsignificantimprovementfollowingoperativerepair.
However,manypatientswillhavesignificantresidualbiventriculardysfunctionandpulmo-
naryhypertensionintheimmediatepost-operativeperioddependingontheirpre-operative
condition.Strategiesaimedatoptimizingbiventricularfunctionandpreventingpulmonary
hypertensionarethecornerstonesofpost-operativemanagement.Monitoringcentralvenous,
rightatrial,pulmonaryartery,and/orleftatrialpressuremonitoringisfrequentlyuseful.
TherehavebeenseveralreportsoftheuseofECMOinpatientswithTAPVC,inthepre-
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
anatomicalclassificationisapredictorofoutcome.
Thepresenceofsingleventricular
physiology,however,remainsapredictorofpooroutcome.
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
TheauthorsaregratefultoDr.RobMartin,BristolRoyalHospitalforChildrenforproviding
theechocardiogramsin
Fig.10.2
1.HancockFriesenCL,ZurakowskiD,
ThiagarajanR
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
shouldbeprolonged,orevenmoreaggressively,thepatientpre-oxygenatedandthen
disconnectedfromtheventilatoreveryhourfor30
60seconds,orevenforcedmanual
expirationofthechest.
Everyeffortshouldbemadetodiscontinuetheneuromuscularblockingagentswithin
24hoursbecauseoftheassociationoftheiruse,especiallyincombinationwithcortico-
steroids,withcriticalillnessmyopathy.
Heavysedationmayfacilitatethecessationofthe
musclerelaxants.
Formostpatients,thedurationofMVisamatterof1or2days.Duringtheweaning
process,thepatientcanbeallowedtobreathespontaneously.Synchronizedintermittent
mandatoryandpressure-supportventilationmodesarehelpfulinfacilitatingthepatient
cooperationwithMVandreductionofsedationatthesametime.Precipitationofbroncho-
spasmsduetoincreasingawarenessandthepresenceoftheendotrachealtubearoundthe
timeofextubationcanbeovercomebytheuseofshort-actingsedativeagentssuchas
Althoughthereisacasereportoftheuseofhighfrequencyoscillatoryventilation(HFOV)
inayoungchildwithSAA,
thereisagenerallackofevidencetosupporttheuseofhigh
frequencyventilationmodes,eitherHFOVorhighfrequencyjetventilation(HFJV),in
patientswithSAA.Itisbelievedthathighfrequencymodesmayworsenalveolardistension,
orthatvibrationmaytriggerfurtherbronchospasm,andtheirusehasthereforebeengenerally
discouraged.Similarly,giventherelativelyfavorableoutcomesandlowmortalityofchildren
withSAAmanagedinintensivecare,theadditionalsurvivalrateprovidedbyextracorporeal
membraneoxygenation(ECMO)ismostlikelymarginal,andconsideringthepotential
complicationspossiblyharmful.However,therecertainlyisaroleforECMOasrescuetreat-
mentinpatientswhocannotbestabilizedwhenmechanicallyventilated.
Complicationsofsevereacuteasthma
Failuretorecognizetheseriousnessofrespiratoryfailure,ortotreattheepisodeearlyand
appropriately,remainsthechiefcontributingcauseofpooroutcomeinSAA.Effortsshould
bemadetoavoidMVinSAA,sinceintubationandventilationofthesepatientsareassociated
withahigherincidenceofcomplicationscomparedtopatientsventilatedforothercausesof
respiratoryfailure.
CausesofmortalityintheventilatedchildwithSAAareacuteairleaks,
sepsis,andthelowcardiacoutputsyndrome.
Barotraumaisresponsibleforacuteairleakssuchaspneumothorax,interstitial,media-
stinal,orsubcutaneousemphysema,andcanoccurintheventilatedandnon-ventilated
patient,althoughrarelyinyoungerchildren.
Inadditiontothedirect,mechanicalheart
lunginteraction,arterialhypotensionandlow
cardiacoutputsyndromecanalsoarisefromhypoxemia,acidosis,andarrhythmias.The
lattermaybetriggeredbyacombinationofpredisposition,catecholaminergicdrugstim-
ulation,hypokalemia,hypoxemia,andacidosis.InchildrentreatedforSAA,supraventric-
ulartrachycardia(SVT)isprobablythemostcommonlyobservedarrhythmia.If
hemodynamicallyunstable,ornotself-limited,theSVTcanreportedlybeconvertedusing
intravenousadenosinedespitecontinuationoftheanti-asthmaticpharmacotherapy.Also,
thereisatheoreticalriskofventriculartachyarrhythmiastriggeredbybronchodilator
inducedprolongationoftheQT
time,whichunderlinestheimportanceofECGand
potassiummonitoring.
Criticalillnessmyopathy(CIM)isararecomplicationwhichpresentsasdifficultyin
weaningfromMV,andismostoftenreportedinpatientswithSAA,sepsis,orpost-transplant,
Chapter9:Managementofsevereacuteasthmainchildren
inassociationwithexposuretocorticosteroidsand/orneuromuscularblockingagents.
seemsthatthedurationofadministrationratherthanthetypeofmusclerelaxantisthemain
factorfordevelopmentofthemyopathy.Uponclinicalsuspicion,CIMisdiagnosedbasedon
electromyographicandbiopsyfindings.Mostpatientsfullyrecoverwithin3months,but
morbidityfromothercomplicatingillnessesisnotinsignificant.IftheSAAleadstocardio-
respiratorycollapserequiringresuscitationandintubation,thehypoxic
ischemicencephal-
opathyshouldbesoughtandassessedbyimagingandelectrophysiologicmeansforprognostic
purposesassoonasthepatienthasstabilised.
TheintensivecaremortalityofSAAisrelativelylow:1%
2%ofchildrenwithSAA
admittedtotheintensivecareunitattheRoyalChildren
sHospitalinMelbourne,Australia,
die(unpublisheddata2004).However,despiteacontinuouslydecreasingprevalenceofasthma
overthelastdecade,theabsolutenumberofpatientswithSAAadmittedtoourunit,aswellof
thoseneedingmechanicalventilation,andofasthma-relateddeaths,hasremainedunchanged
in20years.
Thiswouldsuggestarelativeincreaseinseverityandmortalityofchildhood
asthmaoverall.
Learningpoints
ClinicalevaluationisthemostimportanttoolforassessmentofthechildwithSAA,and
forguidanceoftherapy.
Itisthesignsofrespiratoryfailurethatshouldpredominantlyguidesecond-linetherapy
andmoreadvancedinterventions.
Considerover-treatmentwithbronchodilatorsinachildwhohasongoingrespiratory
Chapter9:Managementofsevereacuteasthmainchildren
responsetotreatment.
ActaPaediatr
:789
4.PlotnickLH,DucharmeFM.Combined
Chapter9:Managementofsevereacuteasthmainchildren
Theneonatewithtotalanomalous
pulmonaryvenousconnection
RobertMazor,GordonCohen,andLynnD.Martin
Patientswithtotalanomalousvenousconnection(TAPVC)accountfor1%
5%ofallcasesof
congenitalheartdisease.Anomalouspulmonaryvenousdrainageisfrequentlypartofa
Fig.10.1.
ChestX-ray.
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
chestX-raydemonstratedworseningofthediffuseparenchymalopacification.Becauseshe
continuedtohavesignificantisolatedatrialectopy,thecardiologyservicewasconsulted.
Arepeatechocardiogramdemonstratedaconfluenceofallfourpulmonaryveinsbehindthe
leftatrium.Therewasasinglevenouschannelarisingfromtheconfluencethattraveled
caudallythroughthediaphragmandconnectedtotheductusvenosus,wheretherewas
Table10.1.
Admissiondata
Vitalsigns:afebrile,HR-170,RR-40BPM,MAP-40mmHg,O
saturation93%
Intubated,musclerelaxed
Reasonablechestriseandaeration
Loudsecondheartsound,2/6systolicmurmur
Fullabdomen,liveredge4cmbelowcostalmargin
Cooldistalextremities
133meql
2.5meql
,HCO
22meql
106meql
,BUN
22mgdl
,Cr1.0mgdl
,Glu168mgdl
WBC17000mm
,Hct51%,Plat219000mm
Coag.panelPT14.4s,INR1.3,PTT53s,Fibrinogen209mgdl
,TT29s,D-dimer5mcgdl
ArterialbloodgaspH7.38,
33mmHg,
50mmHg,BD
InfectiousViralrespiratoryFAnasalwash-negative
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
incisionwasthenmadeintheleftatrium,alongtheleftatrialappendageextendingright-
ward,nearlytotheintratrialgroove.Anintraatrialcommunicationwascreatedbyremoving
thetissueinthefossaovalis.Creationofawide-openatrialseptaldefectwouldallow
adequatedecompressionoftheleftheartwhileonVA-ECMOandwouldprovideasource
ofright-to-leftshuntingintheeventofapulmonaryhypertensivecrisisafterseparatingfrom
ECMO.Thepulmonaryvenousconfluencewasthenanastamosedtotheleftatrium.Once
Fig.10.2(a)-(j).
SeriesofechocardiographimagesofobstructedTAPVC.RV=RightVentricle,LV=Left
Ventricle,IVC=InferiorVenaCava,Ao=Aorta,DV=DescendingVein,LPV=LeftPulmonaryVein,HV=Hepatic
Vein,PVS=PulmonaryVeins(for(c),(d),(h),and(j),seecolorplatesection).
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
patientwasbrieflytakenoffcardiopulmonarybypass,andthearterialcannulawasthen
connectedtothearterialsideoftheVA-ECMOcircuit.ECMOflowwasthencommenced.
Therightatriumwasdecannulated,hemostasiswasobtained,achesttubewasplacedinthe
mediastinumandthechestwasclosed.ThepatientwastransferredtotheCardiacIntensive
CareUnit(CICU)oninhalednitricoxide20ppm,dopamine5mcgkg
permin,and
milrinone0.7mcgkg
permin.
ClinicalcourseintheCICU
Overthenextseveraldays,thepatientshowedgradualimprovementofherbiventricular
functionwithdecreaseinestimatedpulmonaryarterypressuresasdeterminedbyserial
echocardiogram.ShewassuccessfullyweanedfromECMOsupportonpost-operativeday6.
Shewasstartedonsildenafil0.5mgkg
every4hoursandweanedoffinhalednitricoxideon
post-operativeday9.Shewasweanedfrommechanicalventilatorysupportandthetrachea
wasextubatedonpost-operativeday11.SheremainedintheCICUfor3additionaldaysfor
respiratorymonitoring,advancementoffeeds,andweaningofsedation.Shewasultimately
dischargedfromthehospitalonpost-operativeday20.Herdischargeechocardiogram
revealedgoodbiventricularpressure.Therewasmildturbulenceintheareaofthesurgical
anastamosiswithanestimatedpressuregradientof5mmHgacrossthatarea.
Outpatientcourse
Shewasasymptomaticatherinitial1-monthfollow-upvisit.Herhemodynamics,asassessed
byechocardiography,wereessentiallyunchangedfromdischarge.Routinefollow-upwas
Fig.10.2(a)-(j).
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
scheduledfor2months.Onemonthlater,shewasseenintheemergencydepartmentwith
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
confluencetojointhesystemicvenoussystem,typicallytheinnominatevein(
Fig.10.3(a)
Theverticalveinusuallyascendsanteriortotheleftpulmonaryarteryandleftbronchusand
remainsunobstructed.However,theverticalveincanbecomecompressedifitpasses
LVV
PVC
CS
PVC
PV
RA
Fig.10.3.
Thefourmostcommonanatomical
defectsinTAPVC.FromNichols
Chapter10:Theneonatewithtotalanomalouspulmonaryvenousconnection
Managementofsevereacute
asthmainchildren
ChristianStockerandMikeSouth
Asthmaisahighlyprevalentdiseaseinchildren,andisassociatedwithsubstantialmorbidity.
Acuteexacerbationsofasthmarangeinseverityfrommild,manageablewithoutpatientcare,
tolife-threatening,requiringintensivecareandmechanicalventilation(MV).Severeacute
asthma(SAA)referstoacutelife-threateningasthma
orstatusasthmaticus
ifthelower
airwayobstructioncausingsevererespiratorydistressand/orrespiratoryfailurepersists
despitetreatmentwithinhaledbronchodilators.
Bothacutelife-threateningasthmaand
SAAbearanincreasedriskofmortalityifnottreatedearlyandadequately.Mostchildren
admittedtothehospitalwithSAAimprovewithsupplementaloxygen,inhaled
2-agonists,
andsystemiccorticosteroids.However,someofthesechildrenfailtorespondtotheinitial
therapy.
Casehistory
A13-year-oldgirlwithahistoryofrecurrentexacerbationsofasthmawasbroughtto
to165min
Chapter9:Managementofsevereacuteasthmainchildren
severelyconfoundthesefindings.Inourexperience,thereisoftenover-relianceonthe
amountofwheezingheardonauscultationintheassessmentofseverity.
Signsofrespiratoryfailurearemoreusefulforassessmentofseverityoftheasthma,and
forguidanceofmanagementofthepatient.Thediagnosisofrespiratoryfailureisbasedon
theclinicalsignsforpooroxygenation
poorventilation,
thesequelaeofglobal
respiratoryinsufficiencyonthetwoothervitalorgansystems,thecentralnervousandthe
cardiovascularsystem.Thecardinalsignofpooroxygenationiscentralcyanosis.Signsof
poorventilationareinadequaterespiratoryrate,poorchestmovementoninspection,and
poorairentryonauscultation;talkingandcoughingrelyongenerationofanappropriate
tidalvolume(tidalvolume~chestmovement
airentry).Fromahemodynamicview-
point,thesignsoflowcardiacoutputstate(LCOS)suchastachycardia,prolongedcapillary
refilltime,coldandmottledskin,andperipheralcyanosisshouldbesought.Regardingthe
centralnervoussystem,both
decreased
increased
(agitation)levelofconsciousnessoccur
inthecontextofrespiratoryfailure.
First-linetreatmentforSAAinchildrenincludeshigh-doseinhaledbronchodilators
aerosolizedornebulized
2-agonistsandanticholinergics
andoralorintravenouscortico-
steroids.
Chapter9:Managementofsevereacuteasthmainchildren
recommended.Itissuggestedtoinfusesalbutamolat5mcgkg
forthefirsthourand
thencontinuingtheinfusionat1mcgkg
permin.
Foraminophyllinetherecommended
intravenousloadingdoseis10mgkg
over1hourfollowedbyaninfusionof1.1mgkg
h(children1
9yearsofage)or0.7mgkg
perh(children10
16yearsofage).Strict
Chapter9:Managementofsevereacuteasthmainchildren
IntubationandMechanicalVentilation(MV)
ThedecisionforendotrachealintubationandMVofpatientswithSAAshouldbecarefully
,aFEV
orpeakexpiratoryflowrate,orameasuredfallinsystolicbloodpressureon
inspiration(pulsusparadoxus).
Forintubation,fastandsafeairwayaccessisimperative.Therefore,arapidsequence
inductiontechniqueismandatory:sufficientpreoxygenationwith100%oxygen,application
Chapter9:Managementofsevereacuteasthmainchildren
HUS.
Recently,ithasbeenfoundthataHUSisadiseaseofcomplementdysregulationwith
50%ofcasesinvolvingcomplementregualatorygenemutations.
Initialassessmentandmanagement
Ahistoryofthepresentingillnessshouldbeacquired.Ofthosewiththetypicalandoutbreak
HUS,almostallwillhaveadiarrhealillness,withtheresthavingsomegastrointestinal
symptoms.Approximatelyhalfofthosewithdiarrheawillhavebloodintheirstools.Itis
importanttoobtainahistoryofurineoutput,notonlyforfluidbalancestatus,butalsoasan
indicatorofanuricrenalfailure.AhistoryofCNSinvolvement,alteredlevelofconsciousness
orseizures,isalsoimportantasitincreasesthelikelihoodofmortalityandmorbidity.A
familyhistoryandhistoryofrecentmedicationsmayprovideinformationhelpfulto
diagnosisinthosewithatypicaldisease.
AswithallcriticallyillchildreninitialassessmentshouldstartwiththeABCs(airway,
breathingandcirculation).Foranychildwithagastrointestinalillness,assessmentoffluid
statusanddegreeofdehydrationisalwaysimportant.Dehydrationisusuallydescribedas
Mild=
Moderate=
Severe=
Arecentweightisoneofthemostusefulwaystoassessthedegreeofdehydration.Clinical
assessmentofthedegreeofdehydrationusesthesignsandsymptomsofdecreasedurine
output,drymouth,decreasedskinturgor,sunkeneyesandorfontanelle,tachycardia,and
changesinCNSstatus.
Ausefulformulatoremembertomanagereplacementoffluidsindehydrationis:
Percentagedehydration
weightinkg
fluiddeficit
inml
Fluidgivenforresuscitationshouldalwaysbeisotonicandpatientsshouldbereassessed
immediatelyafterfluidboluseshavebeengivenandacloseeyekeptonelectrolytes.
Forthechildinthiscase,hisairwaywasclearandhewasbreathingspontaneouslywith
goodsaturations.Hewasreceivingoxygenviafacemaskasisappropriateforanyacutely
unwellchild.Hewastachycardicandhadsomemilddecreaseinhisperipheralperfusion.He
8shouldbe
intubatedforairwayprotection.Thisisespeciallyimportantduringtransportationofsick
Chapter8:Managementofhemolyticuremicsyndrome
NeurologicalinvolvementintheacutephaseofHUSoccursinaboutathirdtoafifthof
allcases.Theformsofacuteneurologyseenincludeseizures,alteredlevelofconsciousness,
irritability,orfocalneurology(e.g.hemiparesisoraphasia).Themortalityofthosewith
neurologicalinvolvementhasbeenreportedtobeashighas23%
andinmostseriesthe
majorityofthosewhodiehavesomeformofCNSinvolvement.
Thosewithseizures
haveahigherincidenceoflong-termneurologicalsequelae.
Electroencephalograms(EEGs)
tendtoshowapictureofgeneralizedslowingconsistentwithanencephalopathicpicture,
thosewithseizuresmayhaveadditionalfindings,someofwhichhaveaworseprognosisfor
long-termneurologicalsequalae.
TheexactpathophysiologyoftheneurologyseeninHUS
isnotknown.Ithasbeensuggestedthatitmaybemetabolicinorigin,
relatedtofocaltoxin
mediatedmechanismsresultinginfocalvascularendothelialinjuryortothewidespread
thromboticmicroangiopathythatisassociatedwiththeacuterealfailureandcolitis.
OnceachildwithHUShasbeenresuscitatedandhasstableelectrolytes,theaimshould
alwaysbetoprovideadequatenutritionwithenteralfeeding,orparenterallyifthegutisnot
abletobeused.
Theincidenceofpancreatitisispoorlydefined,asanamylaseisnotalwayscheckedinthe
acuteillness.Ithasbeenreportedtooccurasfrequentlyasin20%ofcases.
Itdoesnot
Table8.3.
GlasgowComaScale
GlasgowComaScale(4
15years)Children
sComaScale(4years)
ResponseScoreResponseScore
EyesEyes
Openspontaneously4Openspontaneously4
Verbalcommand3Reacttospeech3
Pain2Reacttopain2
Noresponse1Noresponse1
BestmotorresponseBestmotorresponse
Verbalcommand:
Spontaneousorobeysverbalcommand6
Obeys6
Painfulstimulus:
Painstimulus:
Localisespain5
Localisespain5Withdrawsinresponsetopain4
Flexionwithpain4Abnormalflexiontopain(decorticateposture)3
Flexionabnormal3Abnormalextensiontopain(decerebrateposture)2
Extension2Noresponse1
Noresponse1Bestverbalresponse
Bestverbalresponse
Smiles,orientedtosounds,followsobjects,interacts5
Orientatedandconverses5
CryingInteracts
Disorientatedandconverses4ConsolableInappropriate4
Inappropriatewords3InconsistentlyconsolableMoaning3
Incomprehensiblesounds2InconsolableIrritable2
Noresponse1NoresponseNoresponse1
Chapter8:Managementofhemolyticuremicsyndrome
appeartobeclinicallyapparentinthemajorityofcases,butendocrinepancreaticinsuffi-
ciencydoesoccur,bothacutelyandpermanently,withreportsoflong-terminsulin-
dependentdiabetesmellitusoccurring
soitshouldbeconsideredbothintheacute
phaseandinthefollow-upofpatientswithHUS.Inthiscasehisglucosewasnormalon
presentationandpancreaticinsufficiencywasnotaproblem.
Hypertensionispresentin~50%ofcasesofHUS.Ifhypertensionoccurs,ittypicallydoes
soasrenalbloodflowisincreasing,andisusuallytransient,buttreatmentisindicatedifit
persistsformorethan24
36hours.
Althoughthispatientdidnotrequireabloodtransfusionforhisanemia,anumberof
Chapter8:Managementofhemolyticuremicsyndrome
Roleofplasmaexchange
Chapter8:Managementofhemolyticuremicsyndrome
7.ElliotE,WilliamsK,RidleyG
Chapter8:Managementofhemolyticuremicsyndrome
Managementofhemolyticuremic
GabrielleA.Nuthall
Hemolyticuremicsyndrome(HUS)isanimportantcauseofacuterenalfailureinchildren.
Themajorityofcasesarediarrhea-associatedHUS,whichoccurssporadicallyand,less
commonly,inoutbreaks.Atypicalcases,whicharenotassociatedwithdiarrhea,also
occur.Treatmentismainlysupportiveanddesignedtosupportrenalfunctionuntilthere
isspontaneousrecovery.
Casehistory
Apreviouslywell19-month-oldboypresentedwitha4-dayhistoryofbloodydiarrhoea.He
hadbeenseenbyhisprimarycarephysicianonday2oftheillnessandstartedon
amoxycillin.Onthedayofadmission,hismotherwasnotsurewhenhehadlastpassed
wassentforFBC,UandEs,glucoseandabloodculture.Anarterialbloodgaswasalso
obtained.Hewasgivena240mlbolusofnormalsaline(20mlkg
)andstartedonmain-
tenancefluids.Hehadastatdoseofathird-generationcephalosporinandaChestX-Ray
(CXR),whichwasnormal.Forresults,see
Table8.1
Afterdiscussionwiththepediatricianoncall,itwasfeltmostlikelythathehadHUSand
Table8.1.
Findingsonadmission
PastmedicalhistoryFitandwell
RegularmedicationsNone
AllergiesNoneknown
ExaminationDecreasedlevelofresponsiveness
Airwayclear,facemaskoxygen
Spontaneousrespirations,RR32
Chestclearwithbilateralairentry,Sats99%inO
Normalheartsounds,HR161,BP80/42
Capillaryrefilltime=4seconds
Temperature36.8°C
InvestigationsWeight12kg
FBCWCC23.9×10
,Hb86gl
Chapter8:Managementofhemolyticuremicsyndrome
whitecellcount18.0×10
,Na
120mmoll
4.4mmoll
,glucose5.6mmoll
,urea
30mmoll
,creatinine0.47mmoll
andaniongap19.9,pH7.27,O
31.1kPa,CO
4.3kPa,
14.6mmoll
.Thecoagulationscreenwasnormal.Hewasgivenaseconddoseof
of15mmoloverhalfanhour.
Hehadnotpassedanyurinesincethetimeofhisarrivalinthepresentinghospitaland,
uponfurtherquestioningofhismother,maynothavepassedurineforupto48hoursbefore
admission.
Afterreviewofhisclinicalandlaboratoryfindings,theintensivecarespecialistand
pediatricrenalphysiciandecidedheneededrenalreplacementtherapy.Soonafterarrival,he
Chapter8:Managementofhemolyticuremicsyndrome
a2-monthlycreatinine,urineanalysis,andbloodpressurecheck,untiltheywereallnormal.
Followingthis,therecommendationwasforayearlycreatinine,urineanalysis,andblood
pressurecheck.
Hemolyticuremicsyndrome(HUS)isamajorcauseofacuterenalfailureinchildren.Inone
series60%ofchildrenpresentingtoaPICUwithacuterenalfailurerequiringrenalreplace-
menttherapyhaddiarrheaassociatedHUS.
HUSischaracterizedbymicroangiopathic
hemolyticanemia(anemiasecondarytoredbloodcellfragmentation),thrombocytopenia
andacuterenalimpairment(see
Fig.8.1
).TherearetwodistinctsubgroupsofHUS.The
majority(~90%)ofcasesareassociatedwithadiarrhealillnessandiscalledtypicalor
D+HUS.Asmallersubgroup,usuallycalledatypicalcases(aHUS),areassociatedwitha
Fig.8.1.
Bloodsmearshowingschistocytes(red
bloodcellfragmentation)(seecolorplatesection).
Chapter8:Managementofhemolyticuremicsyndrome
colitiswithcolonicperforation,pancreatitis,andcardiacfailurehaveallbeenreported.In
placeswhererenalsupportisavailableforacuterenalfailure,theseextrarenalmanifes-
tationsarenowthemajordeterminantsofmortality.Thepathophysiologyofthese
ismultifactorial,butwidespreadthromboticmicroangiopathyisconsistentlyfoundin
autopsyspecimens
andisthoughttoplayalargepartintheacuterenalfailureseen
withHUS.Predictorsofseverityandincreasedriskofmortalityareanelevatedwhitecell
count(�20×10
),aseveregastrointestinalprodrome,anuriaearlyinthecourse,
prolongedanuriaandneurologicalinvolvement.
Themajorityrequireahospitalstaywithsomerequiringintensivecaresupport.Inone
Australianstudy115childrenwithdiarrheal-associatedHUShadamediandurationof
medianof4days(1
18days).
Table8.2.
IncidenceofHUSacrosscontinents
Incidenceper100000
NewYork
0.51
15
0.36
1.71
15
0.71
1.35
15
0.64
GreatBritain
0.25
Chapter8:Managementofhemolyticuremicsyndrome
Itisthereforeimportanttorealizethatanacidosisdoesnotneedtobepresentforthepatient
toreceivethespecifictreatmentofalkalinization.Sodiumbicarbonateiseffectiveeveninthe
absenceofacidosis.
Treatmentstrategies
General
Aswithallemergencycases,lifesupportshouldbecommencedwithrapidassessmentand
managementofbasicfunctions;ensuringintegrityoftheairway,adequateventilationand
oxygenationandvolumesupportofthecirculation.Initiationofbaselineinvestigations
shouldbeundertakenearlytoassessbloodchemistryandgases,glucoselevel,bloodcultures
and,wherepoisoningsuspected,plasmaandurineassaysforeitherimmediatescreeningor
storageuntilthehistoryismoreclear.Itis,however,importanttorealizethatbloodlevelsof
TCAwillnotreflecttheloadofingesteddrugnortheclinicalseverity.Thisisduetodelayed
absorptionandvariabilityinproteinbinding.Therehasbeensomedebateastotheplaceof
gastriclavageandinstillationofcharcoal.Therationaleforgastriclavagewaspartlybasedon
thefactthatTCAswouldslowgastricemptyingduetotheiranticholinergicaction.However,
theconsensusappearstobethatitisonlyeffectiveifcarriedoutwithin1hourofthe
Chapter7:Tricyclicantidepressantpoisoninginchildren
occur,thentheQTcdidlengthensignificantlyandmostofthoseanimalsdevelopedVT.
Whenatriallypacedatahigherrate,alltheanimalsdevelopedVT.Acasewasthereforemade
fortheadministrationofbetablockingagents;however,theclinicalcontextofhypotension
andpoormyocardialfunctiondoesnotusuallypermitthis.
Hyperventilationhasbeenproposedasameansofalkalinization,butthismaylowerthe
seizurethresholdduetofurtherreducingcerebralbloodflowwheretheremayalreadybe
decreasedcardiacoutput.
Inanexperimentalmodel,raisingpHbyloweringthepartial
pressureofCO
wasnotaseffectiveasadministrationofbicarbonate
andBrownfoundthe
effectsofhyperventilationpartialandtransient.
Chapter7:Tricyclicantidepressantpoisoninginchildren
bicarbonatehadmosteffect,followedbytherespiratoryalkalosis,withthehighsodium
solutionhavingleasteffect.Inhis
invivo
experimentsinamitryptiline
toxicdogs,Brown
Chapter7:Tricyclicantidepressantpoisoninginchildren
half-livesof12
20hoursandsorelativelysimilartothoseofTCAs.However,theamount
(inmilligrams)ofthesepolyclonalantibodiesrequiredismanytimesthedrugburdenand
thereisacostimplicationindevelopingthesecommerciallyaswellascontendingwiththeir
knownpotentialforrenaltoxicity.
Learningpoints
Themainstayoftreatmentatalltimeswillbetoensurethereisaclearairway,efficient
ventilation,andgasexchangeandtheaddressingofanycirculatoryfailure.
Ifthereisanyrespiratorydepression,giventhedelayedprogressionoftheseTCApoison-
ings,thenintubationandventilationtoensurecontrolofgasexchangeshouldbeunder-
takenearly,withaviewtoensurethatthepatientiswelloxygenatedandnormocarbic.
Thecirculationshouldbesupportedwithvolumeinitiallyand,ifhypotensionorunder
perfusionarerefractorytothis,thenanadrenalininfusionshouldbecommenced,
rememberingthatitseffectsmaybebeneficialandadditivetothosesodiumbicarbonate.
Itcanbeadministeredperipherallywhilecentralaccessissecured.
MonitoringofECG,peripheralsaturations,andend-expiredCO
shouldbeestablished
earlyandtheQRSintervalshouldbeassessed.Ifthisis0.1secondsorgreater,then
sodiumbicarbonateshouldbeadministeredwithaviewtoalkalinizingthepatient(e.g.to
apHof7.45
evenintheabsenceofaninitialacidosis
Ifarrhythmiasoccuranddonotrespondtothesemeasures,thenconsidergivinglidocaine
orphenytoin.Itshouldberememberedthatanyantiarrhythmicagentotherthanthese
twoislikelytocausemoreproblemsthanitislikelytosolveandthisisborneoutbythe
clinicalcourseofourpatientwheretheadministrationofamiodaronewasill-advised.
Seizuresshouldbetreatedwithbenzodiazepines(lorazepam)andthiscanbefollowedby
aninfusionofmidazolamifthepatientisventilated.Phenytoin
beofbenefitin
treatingbothseizuresandarrhythmiasbuttheevidencedoesnotexisttosupportthis.
Pyrexiawillexacerbatetheacidosis,especiallywherethecardiacoutputispoor,and
shouldbetreatedactively.Thismayrequireongoingmusclerelaxationaspartofthe
ventilationstrategytofacilitatecooling.Ifmusclerelaxantsareused,thenprophylactic
anticonvulsantsshouldbegivenandtheEEGmonitored.
Atallstagesofthisprocess,theteamshouldseekandfollowtheadviceoftheirlocal
PoisonsCentretoensuretimelyandup-to-datepractice.Consequently,PoisonsCentres
mustensurethattheadvicetheygiveisconsistentwiththemostrecentevidence.
TheauthorwouldliketothankDr.JamesFraser,Dr.HeatherDuncan,Dr.Nigel
Chapter7:Tricyclicantidepressantpoisoninginchildren
3.SasynuikBI,JhamandasV,ValoisM.
EmergMed
:1052
4.BoehnertMT,LovejoyFH.ValueoftheQRS
durationversustheserumdruglevelin
predictingseizuresandventricular
arrhythmiasafteranacuteoverdoseof
tricyclicantidepressants.
NEnglJMed
:474
5.LiebeltEL,FrancisPD,WoolfAD.ECGlead
aVRversusQRSintervalinpredicting
seizuresandarrhythmiasinacutetricyclic
antidepressanttoxicity.
AnnEmergMed
:195
6.SegerDL,HantschC,ZavoralT
Chapter7:Tricyclicantidepressantpoisoninginchildren
Tricyclicantidepressantpoisoning
inchildren
IanA.Jenkins
Withthislastdevelopmentthepediatricintensivecareunit(PICU)teamweresum-
moned.Itwasdecidedtosecurethepatient
sairwaybyintubation.At10.20h,thechildwas
given50mgofthiopentaland20mgsuxamethonium.A4.5mmoralendotrachealtubewas
passedand,onauscultation,therewasgoodairentryonbothsidesofthechest.The
saturationswere96%.Inviewoftheresistantfitactivity,paraldehyde2mlinoliveoilwas
givenrectally.
Atthispointanotherepisodeofbradycardiaensued,47bmin
,andsocardiaccom-
pressionswerecommenced.Atropine200microgramswasgivenIV,followedbytwodoses
ofadrenaline100mcg,with240mlofhumanalbuminsolution(HAS)andbicarbonate
(0.5mlkg
).Thisperiodofcardiopulmonaryresuscitation(CPR)lastedapproximately
199819992000200120022003
Fig.7.1.
admissionsinEnglandwith
tricyclicpoisoningin
childrenunder14yearsold.
1991199219931994199519961997199819992000200120022003
Fig.7.2.
Antidepressantprescriptions1991
2003inEngland.
Chapter7:Tricyclicantidepressantpoisoninginchildren
Table7.1.
Summaryofinitialclinicalfindings
PastmedicalhistoryHealthy.Noknownmedicalconditions
RegularmedicationsNone
AllergiesNone
PresentinghistoryFounddrowsyandwithabnormalcry.Startedtofitat0900tilladmittedtoED.
Giventwo2.5mgdiazepamsuppositoriesbyparamedicambulancecrew
withnoapparenteffect
ExaminationAirwaypatent.Breathingpoor,apneascausedbyconvulsions.Saturationsnot
recorded.CRT4
5seconds,pulse120butpoorvolume.Peripheriescool,central
temperature35.8°C.Unresponsivetovoiceandpain.Norash,noneckstiffness
InvestigationsWeight10kg(estimate)
FBCHb10.9gdl
,WCC16×10
,Plats369×10
Urea6.5mmoll
,Creatinine50mcgl
,Na
144mmoll
,Cl
108mmoll
,K3.3mmoll
Liver&BoneChemistryCRP10mgl
,Mg
0.72mmoll
,Ca
1.83mmoll
,ALT14IUl
VenousBloodGaspH7.07,
24.3mmHg,
70.3mmHg,base
Chapter7:Tricyclicantidepressantpoisoninginchildren
Herheartratewas90
120,irregularinrateandvolume.TheQRSwasbroadenedand
therewasstillatendencytopolymorphism.TheQRSdurationwas0.12
0.132secondsand
theQTc0.549s(
Fig.7.3
Fig.7.3.
ECGon
arrivalinPICU.Rate
120,QRS
0.132s,QTc
0.549s(normal0.45)
(seecolorplate
Fig.7.4.
ECG1hour
latershowing
polymorphousQRS
complexesleadingto
tachycardia(seecolor
platesection).
Chapter7:Tricyclicantidepressantpoisoninginchildren
ThefirstwastreatedwithCPRimmediately,quicklyfollowedbyDCshocks
2Jkg
twice,then4Jkg
withagoodresult.Thesubsequenttwoepisodesweretreatedwithgiven
4J/kgdirectlywithgoodresults.
Duringthisperiod,advicefromtheRegionalPoisonsServicehadbeensought.Thiswas:
7.5withsodiumbicarbonate2mmolkg
perh.Thelactatedroppedfrom4to
1.8mmolkg
andtheCVPfrom11to6mmHg.At04.00htheheartrateincreasedto
145bmin
andthemorphologyindicatedsinusrhythm.Thepacingandthesodium
bicarbonateinfusionwereturnedoffand,inviewofapparentlighteningoftheconscious
state,amidazolaminfusionwasstartedat100mcgkg
perh.
Day2
At07.00h,theheartwasinsinusrhythm,145bmin
.Theamiodaroneinfusionwas
stopped.TheECGmarkerswere,inseconds:QRS0.12,PR0.12,QTc0.469.Thus,although
Chapter7:Tricyclicantidepressantpoisoninginchildren
anormalrhythmhadappeared,conduction,andrepolarizationwerestillabnormal.Arterial
bloodgas,6hoursafterthebicarbonateinfusionstoppedwas:pH7.4,pO
109mmHg(FiO
0.5,PEEP5),CO
41mmHg(ventilationpressures18/5,rate20),Baseexcess+0.1,bicar-
bonate24mmoll
,Na157mmoll
,K4.6mmoll
,ionizedCa1.01mmoll
.Urine
outputwasgood(4.8mlkg
perh),thelactate1.6mmoll
andthetemperatures36.5°C
central,36°Cperipheral.
Overthecourseoftheday,theFiO
couldbedroppedto0.4andspontaneousrespiratory
effortsweresuchthattheSIMVratewasturneddownto5breathsmin
.Therewasno
Chapter7:Tricyclicantidepressantpoisoninginchildren
theycalledtheambulance.Themotherhadbeenundertreatmentfordepression,taking
dosulepinuntilmonthbefore.Theywerekeptonthetopshelfofakitchencupboard,thought
tobeunreachablebyanyofthechildren(evenifstandingonachair).Onreturnfromhis
daughter
sadmissiontothehospital,thefatherfoundthedosulepininthenormalplace.There
wasonestrippresentintheboxwithsixtabletsremoved.Themotherthoughtthatthisshould
havebeenanintactstripbutcouldnotbecertain.Notabletsorfoilstripswerefoundinthe
bedrooms.Theirfriends
daughterwasbabysittingthenightbefore20.30
22.30h.Therehad
beennoproblemswiththechildrenreportedduringthatperiod,thechildrenhavingbeenput
tobedbeforetheparentswentout.Theotherchildrenwereseenandexaminedandtherewere
nocauseforconcerndetectable.Inviewoftheongoinguncertaintyregardingthemechanism
ofadministrationofthedrug,thematterwasreferredtotheChildProtectionTeam,including
PoliceandSocialServices,forfurtherinvestigationandmanagement.
Fivemonthslater
ShewasreviewedbytheCommunityPediatricServiceandwasbehavinganddeveloping
normally.IntheinterveningperiodshehadundergonebothahearingtestandanMRIofher
brain.Bothinvestigationswerereportedasnormal.
Arationalapproachtotreatmentdependsonanaccurateappreciationofthepharmacology
Chapter7:Tricyclicantidepressantpoisoninginchildren
plasmatheyarehighlyproteinboundbutthefreefractionincreaseswhentheplasmapH
decreases.Therefore,underconditionsofacidosis,moreisavailabletoberedistributedinto
thetissuesandexertgreatereffects.Plasmalevelsdonotreflectthetotalloadasthedrugis
highlyproteinboundandthefree(ionised)fractionwilldecreasewithariseintheplasma
pH.Generally,thisclassofdrughasalongeliminationhalf-life(e.g.amitryptiline=31
Chapter7:Tricyclicantidepressantpoisoninginchildren
cardiacmonitorandwasnotedtobeshocked,withtachycardiaandaprolongedcapillary
refilltime.Thiswastreatedappropriatelywith20mlkg
of0.9%saline,whichresultedinan
improvementinhercirculatorystatus.Thereisnoevidencefortheuseofcolloidsfortreating
shockinDKA.Anybolusesoffluidsusedaspartoftheinitialresuscitationshouldbe
subtractedinthefluiddeficitcalculations,eventhoughfluidisbeingadministeredrapidlyto
restorethecirculatingvolume.Abriefneurologicalassessmentshouldalsobemadeatadmis-
sionforsubsequentreference,eitherusingtheGlasgowComaScoreforchildren�4yearsof
ageortheAVPU(a=alert,v=respondstovoice,p=respondstopain,u=unresponsive)score.
InchildrenwithDKA,itisimportanttoobtaingoodintravenousaccessandcollectblood
samplesfor:
Bloodglucose
Plasmaureaandelectrolytes
Bloodgas
Fullbloodcount
Bloodcultures
Itisalsoessentialtocalculatetheserumosmolalityatregularintervals:
Serumosmolality
¼ð½
þ½
valuesinmmoll
Inthecasepresented,theinitialserumosmolalitywas366mOsml
(=144×2+65+13),
signifyingthatshewasveryhyperosmolar.MostchildrenpresentingwithDKAaretosome
degreehyperosmolar,butthedegreeofhyperosmolalityisawarningsignofthedegreeof
illness,andrapidfallsineffectiveosmolalityarebelievedtobeariskfactorfordevelopment
ofcerebraledema.
Theinitialfluidrequirementcalculationneedstoincludetheongoingmaintenance
requirementplusthereplacementfordehydration.Ongoingmaintenancefluidvaluesare
calculatedasfollows:
100mlkg
perdayforfirst10kgofbodyweight
50mlkg
perdayfornext10kgofbodyweight
20mlkg
perdayforweightabove20kg
Thefluiddeficitandreplacementfordehydrationiscalculatedasfollows:
Deficit
bodyweight
%dehydration
Thedeficitisusuallyreplacedover48hoursinthefirstinstance,
using0.9%saline.Onceany
degreeofshockhasbeentreatedappropriately,rapidintravenousfluidreplacementis
unnecessaryandincreasestheriskofcerebraledema.Ongoingurinarylossesarenot
addedtothefluidcalculation.Potassiumshouldbeinitiallyincludedintheintravenous
fluidsat40mmoll
unlessanuriaissuspected,orthereisevidenceofpeakedTwaves
characteristicofhyperkalemiaontheECGmonitor.InDKA,anuriaisveryrare,asthechild
isusuallypolyuricatpresentation.Potassiumisapredominantlyintracellularionandis
Rehydrationalonewillcausesomedecreaseinbloodglucoseconcentration,butinsulinis
therapy,
asseenbyafallinglucosewithoutaconcomitantriseinsodium.Ithasbeen
introductionofnoradrenalintoappropriatelyraisethebloodpressureandtheinsertionofa
OxfordStudyGroup.
inthedorsumoftherighthand.BloodwassentforFBC,UandE,glucose,venousblood
gasandbloodculture.Afluidbolusof400mlof0.9%salinewasgiven,followingwhich
herheartratefellto135min
andhercapillaryrefilltimedroppedto3seconds.Her
GlasgowComaScore(GCS)wasassessedas8/15(E2,M4,V2)asshewasonlyresponsive
topain.
Acalculationofherfluidrequirementsforthenext48hourswasmadebothintermsof
herongoingrequirementsandasreplacementforherdehydration,whichwasestimatedat
10%(ongoingrequirement=1500ml×2=3000ml
fluiddeficit=20×10×10=2000ml;
totalfluidreplacementover48hours=5000ml
104.2mlh
).Shewascommencedonan
intravenousinfusionof0.9%salinewith40mmoll
potassiumchlorideat104mlh
havingalreadypassedurine.Aninsulininfusionwasstartedat0.1unitskg
.Asecond
22Gcannulawasinsertedintothedorsumofherlefthandandshewasalsogivenadoseof
intravenousantibiotics(cefotaxime50mgkg
).Afteranhour,herbloodglucose,electro-
lytesandacid
basestatuswererechecked.
CaseStudiesinPediatricCriticalCare
Theresultsoftherepeatbloodswereasshown:glucose59mmoll
,Na
145mmoll
3.5mmoll
,pH6.85,
6mmHg,HCO
5.0mmoll
,BE
31.5.Afterinitially
beingsomewhatcombatativetoproceduresbeingperformedonher,ataround2hoursafter
arrivalintheemergencydepartment,itwasnotedbythenurselookingafterherthatshehad
becomeunresponsive.AformalreassessmentofherGlasgowComaScorewasfoundtobe
only3/15(E1,M1,V1).Herpupilswerenotedtobesize4,equalandequallyreactivetolight.
Table6.1.
Findingsonadmission
PastmedicalhistoryFitandwell
lumencentrallinecatheterwasinsertedintoherrightfemoralveinundersterileconditions,
usingtheSeldingertechnique.Theintracranialpressure(ICP)wasestimatedtobeatleast
20mmHg.Ashermeanbloodpressurewas65mmHg,anoradrenalininfusionwasstarted
at0.05mcgkg
perminasanattempttokeepitabove75mmHg,aimingforacerebral
perfusionpressure(CPP)of55mmHg.Throughoutthistimeherpupilshadremainedsize2,
equalandreactivetolight.
fluidsintheformof5%dextrose/0.9%salinewithpotassiumchloride.Itwasalsonotedthat
herserumphosphatelevelhadfallentolessthan0.3mmoll
,soshewasgivenadoseof
dipotassiumphosphate,whichbroughtitabove1mmoll
.Twofurtherdoseswereneeded
overthefollowing48hoursasagainthelevelseventuallyfellbelow0.5mmoll
By24hoursafterherinitialpresentationtohospital,thegirlremainedintubatedand
ventilated.Shestillhad+2ofketonesinurine,butherbiochemistrywasveryslowlyimproving
withtheresultsasshown:glucose11mmoll
,Na
157mmoll
3.9mmoll
,Cl
141mmoll
,pH7.18,
19.4mmHg,
97.4mmHg,HCO
7.0mmoll
,BE
20.In
viewofherongoinghypernatremiaandhyperchloremia,thefluidswerechangedoncemoreto
5%dextrose/0.45%salinewith60mmoll
potassiumchlorideat83mlh
.Overthefollow-
ing12hours,regularnursingobservationandhourlybloodscontinued,
At36hoursintoherhospitaladmission,herinfusionsofmorphineandmidazolamhad
beenofffor6hours,suchthatshewasabletowaketothepointthatshesuccessfully
extubated.Sheremainedsomewhattachypnoicwitharespiratoryrateof25to30breaths
perminute,andherbloodgaswasstillacidotic:pH7.21,
16.4mmHg,
117mmHg,
6.3mmoll
,BE
20.5.Althoughinitiallysomewhatconfused,overthesubsequent
hoursherconsciouslevelimprovedsuchthatshewasabletoholdsimpleconversationswith
bothherfamilyandhospitalstaff.By48hours,herbloodbiochemistryhadcontinuedtovery
slowlyimproveandherbloodculturesfromthelocalhospitalwerenegative,soantibiotics
werestopped.Insulinwascontinuedat0.1unitskg
ofdiabetesmellitusincludepolyuria,polydipsia,significantweightloss,weakness,and
tiredness,asmentionedinthecasediscussed.Achildmayalsocomplainofabdominalpain
andmayhavebeenvomiting.Thesesymptomscanbedifficulttoelucidateinayoungchild
orinfant,sopotentiallydelayingthediagnosis,withasubsequentworseninginclinical
Stress, infection or insufficient insulin intake
Hyperosmolarity
Decreased fluid intake
FFA to liver
Counterregulatory Hormones
Cortisol
Growth Hormone
Alkali Reserve
Gluconeogenic substrates
Glucosuria (osmotic diuresis)
Loss of water and electrolytes
Dehydration
Fig.6.1.
3.Surgicaltreatmentwithdecompressivecraniectomymaybeconsideredinpediatric
patientswithseveretraumaticbraininjury,diffusecerebralswelling,andintracranial
hypertensionrefractorytointensivemedicalmanagement.
Aggressivehyperventilationtherapyhasbeenusedinthemanagementofseverepediatric
headinjuryforrapidreductionofICPsincethe1970s.HyperventilationreducesICPby
inducinghypocapnia,whichleadstocerebralvasoconstriction,reducingcerebralbloodflow.
However,thevasoconstrictoreffectofhyperventilationlastslessthan24hoursinmost
patientsandsustainedhyperventilationmaybecomplicatedbyreboundhyperemia.The
managementstrategyofutilizinghyperventilationinchildrentocontrolICPwasbasedon
theimpressionthathyperemiawascommonafterpediatricheadinjury.Morerecentstudies
Chapter5:Childwithaheadinjury
Chapter5:Childwithaheadinjury
patientswithTBIhavedemonstratedbenefitonlong-termoutcome,eventhosespecifically
inchildrensuchastherecentinternationalHYP-HITstudy.
Hypothermiaisalsonot
withoutrisk.Possiblecomplicationsincludeelectrolyteabnormalities,cardiacarrhyth-
coagulopathyandincreasedinfections.Furthermore,rapidrewarmingcanexacer-
batetheaxonaldamagethatresultsfromtraumaticbraininjuryandthereforeinduced
hypothermiaisnotcurrentlyrecommendedasatreatmentstrategyforthemanagementof
traumaticbraininjury,unlessasacomponentofaresearchstudy.
Theuseofsteroidsisnotrecommendedinpediatricpatientswithseveretraumaticbrain
injury,astheyhavenotbeendemonstratedtoshowbenefit.TheCRASHtrial,amulticentre,
international,randomizedplacebo-controlledtrialevaluatedtreatmentwithcorticosteriods
in10008headinjuredadults(GCS14).Thisdatashowednoreductioninmortalitywitha
trendtoincreasedmortalityinthetreatmentarm.
Themanagementofsevereheadinjuriesmustbeviewedasacontinuumthatbeginsatthe
scenewithresuscitationandtheinitiationofcriticalcare,andendswithneurologicalrehabil-
itation.Protocolguidedintensivecaremanagementmayreducetheincidenceofsecondary
braininjuryaftersevereTBI,therebyimprovingsurvivalandoutcome.MonitoringofICP
andthecontrolofincreasedintracranialpressureisakeyfeatureoftheseprotocols,withthe
goalbeingtomaintainICPwithinthenormalrange.Thisisintendedtooptimizecerebral
perfusionpressure,oxygenation,andmetabolicsubstratedeliveryandtoavoidcerebral
herniationevents.Thefutureofheadinjurymanagementliesindirectingtherapyatthe
biochemicalandcellularresponsestothetraumainanattempttopreventtheriseinintra-
cranialpressure.
Learningpoints
Headinjuryisaleadingcauseofdeathinchildren.
Initialresuscitativeeffortsintheemergencydepartmentandongoingcriticalcaresup-
Chapter5:Childwithaheadinjury
1.MansfieldR.Headinjuriesinchildrenand
Crit.CareClinics
Chapter5:Childwithaheadinjury
26.AdelsonPD,BrattonSL,CarneyNA
Chapter5:Childwithaheadinjury
Childwithaheadinjury
sentfor
routinetraumapanel(FBC,bloodgroupandscreen,ureaandelectrolytes,creatinine,glucose,
liverfunctiontests,andalsoserumamylase).Theinitialchestx-rayandcervicalspineplain
filmswerenormal.Thesecondarysurveyfailedtoidentifyothersignificantinjuries.
Approximately60minutesafterhisarrivaltothehospital,thechildbecameunre-
sponsivewithdilatingsluggi
shpupilsbilaterally.Hewasintubatedwithasize5cuffed
onFIO
0.5,MAP75mmHgandanETCO
of35mmHg,Anticipatingproblemswithraised
intracranialpressureduringtheinterhospitaltransfer,thetransportteamtookextramannitol,
isotonoicfluidsforresuscitationandadopamineinfusionforfluidunresponsivehypotension.
Progressinpediatricintensivecareunit
Uponarrivalatthetertiaryhospital,hewastakenimmediatelyforarepeatheadCT(Fig.5.1)and
xenoncerebralbloodflowscan.Thebasalciste
rnswerenowpresent.Thexenonstudydemon-
stratedgenerouscerebralbloodflowvaluesforagerangingbetween45and80ml100g
minwithnoregionsofischemiaoroligemia.Thechildwasthentakentotheoperatingroomfor
placementofarightfrontalExternalVentricularDrain(EVD).OnreturntotheICU,hisinitial
ICPwas25mmHg.HewasmanagedaccordingtothePICUstandardheadinjuryprotocol
Table5.1
).Afemoralcentralvenouscatheterwasplaced.Heremainedoninfusionsof
midazolamandmorphineat200and40mcgkg
perh,respectivelyandparalyzedinter-
mittentlywithrocuroniumasrequiredICPspikesorforfightingtheventilatororcoughing
andsuctioning.AnEEGwasalsoarrangedonthedayofadmissiontoexcludesubclinical
seizureactivity.Fullenteralfeedswereestablishedbyday2.
Table5.1.
RoutinetherapyforchildrenwithheadinjuryandGCS8
Headinneutralposition,withheadofbedelevated30degrees
Isotonicsolutionsforintravascularvolumesupport(0.9%NS)
Normotension(age-relatednorms)
Normocarbia:PaCO
40mmHg
Normothermia:36
36.5ºC
Chapter5:Childwithaheadinjury
HisICUcoursewascomplicatedbyrefractoryraisedICPgreaterthan25mmHgand
seizure-likeactivity,despitethemidazolaminfusionandtherapeuticphenytoinlevels.
Fig.5.1.
CTscanofheadshowingdecreased
attenuationwithinthecortexconsistentwithdiffuse
axonalinjury.ArightfrontalEVDhasbeenplaced.
Fig.5.2.
CTscanofheadandXenonperfusionstudy
demonstratingaveragecerebralbloodflowsintherange
of50
70ml/100gpermin.Noareasofischemiaor
oligemiacouldbeidentified(seecolorplatesection).
Chapter5:Childwithaheadinjury
Chapter5:Childwithaheadinjury
approach.Allchildrenshouldreceive100%supplementaloxygenandbagandmaskassisted
ventilationasnecessary.Apneaatthesceneoftheaccidentsuggestsahighspinalcordinjury
requiringfurtherinvestigation.Anunresponsi
vechildwithhypoventilationshouldbeurgently
intubated.Furtherindic
ationsforendotrachealintubationarelistedin
Table5.3
.Rapidsequence
intubationshouldbeusedinmostcaseswithcer
vicalspineprecautionsmaintainedatalltimes.
Combativepatientsrequiringdiagnosticimagin
gshouldhavetheirairwaysecuredandventilation
supportedundergeneralanesthesiapriortoimaging.Oncetheairwayiscontrolled,ventilatory
managementshouldinitiallybeaimedatnormoxi
aandnormocarbia,monitoredcontinuouslyby
pulseoximetryandend-tidalCO
monitoring,respectively,andbyserialbloodgasmeasurement.
Immediateattentiontohypovolemiaandhypotensionisparamountassomestudiessuggest
thathypotensiontriplesthemortalityinpediatricbraininjuries.
Maintenanceofanormalfor
agemeanarterialpressureisthegoalintheED.Peripheralvascularaccesscanbedifficultto
obtaininchildrenduringtheinitialresuscita
tion,andintraosseousinfusionoffluidsand
medicationsisindicatedaftertwofailedattemptsatperipheralvenousaccess.Isotoniccrystalloid
Table5.2.
Factorsaffectingoutcomefollowingheadinjury
SeverityofinitialinsultincludingGCSatscene
Typeofinjury
Post-resuscitationGCS
Associatedinjuries
Extremesofage
Secondaryinjuries:
ElevatedICP
Table5.3.
Indicationsforendotrachealintubation
inchildrenwithheadinjury
AcuteincreaseinICPneedinghyperventilation
Inabilitytoprotectairway
Severethoracicorairwaytrauma
Priortotransportofpatient
CombativepatientspriortoCTscan
Chapter5:Childwithaheadinjury
solutionsarethefluidsofchoice(0.9%normalsa
line)duringacuteresuscitation.Freewaterand
glucosesolutionsshouldbeavoidedunlesshypoglycemiaisdemonstratedonabloodsample.
BloodpressureshouldbemonitoredintheERevery5minutes;however,itisimportant
torememberthatpediatricpatientsmaintaintheirbloodpressuredespitesignificanthypo-
volemia.Shockisalatesignofhypovolemia.Clinicalsignssuchasunexplainedtachycardia
andpoorpulsevolumeindicatetheneedforvolumeresuscitation.
Vasopressorsshouldnot
beusedintheinitialphaseofresuscitation.Iffluidsaloneareinsufficienttomaintainthe
sbloodpressureortachycardiapersists,considerongoinghemorrhageorspinalcord
injury.Infantsandsmallchildrencanbecomehypovolemicfromascalplacerationdueto
theirsmallcirculatorybloodvolume.
Fluidrestrictionintheacutephasesofresuscitationisneverindicatedinchildrenwitha
Table5.4.
GlasgowComaScale(GCS)Score
Children4yr
Ages4
15yrs
Eyeopening
4SpontaneousSpontaneousSpontaneously
3TospeechTospeechToverbalcommand
2TopainTopainTopain
1NoresponseNoneNone
Verbalresponse
5Coos,babblesOriented
social,smiles,followsobjects,
4IrritablecryConfused,disoriented,awareof
environment,consolablecries
3CriestopainInappropriatewords,inconsolable,
persistentcries
Inappropriatewords
2MoanstopainIncomprehensiblesounds,agitated,
restless,inconsolable
1NoresponseNoresponseNoresponse
Motorresponse
6Normalspontaneous
NormalspontaneousmovementsObeysverbalcommands
5WithdrawstotouchLocalizespainLocalizestopainfulstimuli
4WithdrawstopainWithdrawstopainWithdrawal
3AbnormalflexionAbnormalflexionAbnormalflexion(decorticate)
2AbnormalextensionAbnormalextensionExtension(decerebrate)
1NoresponseNoresponseNoresponse
Chapter5:Childwithaheadinjury
Oncethelife-threateninginjurieshavebeenaddressed,thesecondarysurveyshouldbe
Chapter5:Childwithaheadinjury
therearenostudiesthatclearlyidentifythebestapproach.Werecommendfollowinga
standardprotocolforthebasicmanagementandhaveincludedtheprotocolcurrentlyfollowed
inthePediatricIntensiveCareUnitatBritishColumbia
sChildren
sHospitalin
Table5.1
ThegenerallyacceptedPICUmanagementinvolvesmaintainingnormoxia,normocar-
bia,normovolemia,andnormothermia.Cervicalspineprecautionsshouldbecontinued
untilclearanceisconfirmedanddocumentedinthechartbyanexpertinthefield.
Table5.5.
StepwiseapproachtothetreatmentofacuterisesinICP
Step1Ensuretheairwayissecured,ventilationisappropriate,thebloodpressureisinthenormal
range,thepatientisnothyperthermicandnothavingaseizure.
Step2CSFdrainage
Ifaventriculardrainisinplaceitcanbeopenedandallowedtodrainfor5minutes.Insome
patientsitmaybenecessarytoleavethedrainopencontinuously.Ifthisoccursitis
importanttoturnthe3-waystopcockevery10
15minutestorecordtheactualICP.Therole
ofCSFdrainageistoreducetheintracranialfluidvolume,therebyloweringICP.
Step3Mannitol
IfopeningtheEVDfailstolowertheICPbecausetheCSFisn
tdraining,administermannitol
1gkg
.Maintainnormovolemiaatalltimes,andfollowelectrolytesclosely.
Discontinuemannitolifhypernatremiadevelops.
Step4Hypertonicsaline
Ifthepatientishyponatremic(sodium135mmoll
),hypertonicsalineshouldbecon-
sideredasanalternativetomannitol(1
5mlkg
3%salineinfusedover10
20minutes).
Avoidlargechangesinserumsodiumandmaintainserumosmolality310mmoll
Step5HyperventilationtoPaCO
35mmHgonlyduringacuteresuscitationforraised
intracranialpressure,orguidedbyJVBandcerebralflowstudies.
Chapter5:Childwithaheadinjury
duringtheemergencyresuscitationshouldbereplacedwithin24hours.Pressuresore
preventionfortheparalyzedpatientincludesfrequentturningfromsidetoside.
Prophylacticanticonvulsantshavenotbeenshowntobeusefulinpreventinglatepost-
traumaticseizuresandarenotcurrentlyusedroutinely.
MostchildrenwillrequirearepeatheadCTwithin24
48hours,orforanyunexpectedor
Chapter5:Childwithaheadinjury
cardiaccontractilityintheearlypost-operativeperiod.Dobutamineanddopamineareboth
appropriateforthisrole,thoughtheadditionalvasodilatationaffordedbydobutaminewould
makethisthedrugofchoiceformanyclinicians.
Intravenousvasodilatorsproducesystemicvasodilatationandthereforecandirectly
improvesystemicperfusionininfantswithHLHS.Also,throughtheirbeneficialeffectson
ventricularafterload,vasodilatorscanbeespeciallyusefulinmanagementofinfantswith
ventriculardysfunction,andtricuspidregurgitation.
TwomainclassesofintravenousvasodilatorsarecommonlyusedininfantswithHLHS.
modificationhasbeen
introducedandisincreasinglyusedincardiacsurgicalunitsaroundtheworld.Thisapproach
involvestheplacementofasmall(4
Theconduitoffersthepotentialadvantageof
maintenanceofdiastoliccoronaryperfusion,avoidingtheunwanteddiastolic
run-off
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
associatedwithaBTshunt,leadingtopreservationofmyocardialfunctioninpatientswitha
conduit.Thishypothesisissupportedbyanumberofobservationalstudieswhichhave
reportedahigherdiastolicpressureinpatientswithaconduit;
echocardiographicdata
demonstratingthatinfantswithconduitpalliationhavenodiastolicflowreversalinthe
isalsorarelynecessarywiththismodification.
Insomecenters,theoptionofhearttransplantationinearlyinfancyisofferedasan
alternativetostageIpalliation.Centersroutinelyperformingtransplantationhaveprevi-
ouslyreportedimpressiveearlysurvivalfigureswhichwouldfavorthisoptionoverstageI
palliation.
Forthesinglereasonoflimiteddonororgansupply,primarytransplantationis
notarealisticoptioninmostinstitutionsoutsideNorthAmerica.Ifavailable,transplantation
isnotaneasyoptioneither.Mostinfantsawaitingtransplantationrequirelong-termtherapy
withprostaglandinandmayneedrepeatedseptaldecompressions,andpotentiallyother
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
Insummary,survivalofpatientswithhypoplasticleftheartsyndromehasimproved
dramaticallyoverthelast20years,withmanycentersnowquotingasurvivalafterstageI
palliationofover75%.
However,mortalityfortheseinfantsremainshigherthanfor
othercongenitalheartdefectsrequiringsurgicalinterventionintheneonatalperiod.Three
mainreasonsforthishavebeenidentified:pre-operativeinstability,mainlycausedby
inadequatesystemicoxygendelivery,mortalityfollowingstageIpalliationandout-of-
hospitalmortalitywhilstwaitingforstageIIpalliation.
Pre-emptivemanagementaimed
atoptimizingsystemicperfusioninthepre-andpost-operativephaseandrefinementof
ThecirculationofinfantswithHLHSiscriticallydependentonapatentarterialduct.
ProstaglandinEshouldbestartedassoonaspossibleafterdelivery.
ArestrictiveASDshouldbesuspectedininfantswithsuspectedHLHSwhodonot
respondtoearlyresuscitationwithprostaglandin,ventilation,andinspiredoxygen.
HLHSpatientswithrestrictiveASDrequireurgentintervention(surgicalseptectomyor
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
seriouscongenitalheartdiseaseattermin
theUK.
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
flowinterchangeable?
24.HoffmanGM,GhanayemNS,KampineJM
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
Learningpoints
Acutebacterialmeningitis
despitedevelopmentsinantimicrobialtherapyandintensive
persistsinhavingbothahighmortalityandahighincidenceofresultantneuro-
logicalsequelae.
Outsidetheneonatalperiod,thetwomostlikelyorganismstocauseABMare
N.meningitidis
Ifthedifferentialdiagnosisincludesthepossibilityofherpesencephalitis,aciclovirshould
Table3.1.
Contraindicationstolumbarpuncture
Presenceofshock
GlasgowComaScore13
Signsofraisedintracranialpressure
Abnormalpupillarysigns
Abnormaltoneorposturing
Respiratoryabnormalities
Hypertension/relativebradycardia
LocalskininfectionoverLPsite
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
Managementofaneonatewith
hypoplasticleftheartsyndrome
UlfTheilenandLaraShekerdemian
Untillittleovertwodecadesago,HypoplasticLeftHeartSyndrome(HLHS)wasconsideredan
inoperableandfatalcondition,withmostdeathsoccurringinearlyinfancy,andalmostall
infantsdyingbeforetheirfirstbirthday.However,theadventofsurgicalpalliationandadvances
inperi-operativeintensivecare,havedramaticallychangedtheprognosisofthiscondition.
Whilstmanyofthesebabiesareantenatallydiagnosed,otherspresentwithclinicalsigns
ofsystemichypoperfusion,acidosisandhypotension,mostcommonlyduringthefirstdays
oflife.Theprimarygoalofearlyintensivecareoftheinfantwithaknownorsuspected
diagnosisofHLHSistoactpre-emptively,withmanagementaimedatoptimizingsystemic
oxygendeliveryandorganperfusion.Thereislittledoubtthatearlyintensivecareplaysakey
roleintheultimatesurvivalofthischallenginggroupofinfants.
ThiscasefollowstheearlyclinicalcourseofaninfantwithaprenataldiagnosisofHLHS,
transferredduringthefirstfewhoursoflifetoacardiaccenterforintensivecaremanage-
ment,surgery,andsubsequentpost-operativecare.
Casehistory
A30-year-oldladypresentedforaroutinefe
talanomalyscanduringanuncomplicated
pregnancy.Thefour-chamberviewofthefe
talheartsuggestedthattheleftheartwas
ShortlyafteradmissiontotheNICU,theinfantbecameapnoeicanddesaturated.Bag
maskventilationwasdeliveredusingair,withimmediateimprovementinsaturationsand
heartrate,andtheinfantwasgiven3mcgkg
fentanyland0.1mgkg
pancuroniumfor
intubation.Oralintubationwitha3.5endotrachealtubewasuncomplicatedanditwas
securedat9.5cmatthelips.Furtherperipheralintravenousaccesswasobtained,anda24G
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
StageIpalliationwasperformedonday4.Anesthesiawasinducedusingtheexisting
lines,deliberatelyavoidingtheneedforaninternaljugularline.Amodificationofthe
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
Theprimarygoaloftheperi-operativecareoftheneonateundergoingstageIpalliation
(Norwoodoperationoritsmodifications)istooptimizesystemicoxygendeliveryandorgan
perfusion.Thisisachievedusingexpertanticipatorycarecommencingbeforedelivery,
continuingpostnatallyintheneonatalunit,andsubsequentlyaftertransfertothecardiac
center.
Thiscaseillustratesaninfantinwhomprenataldiagnosisallowedforawell-planned
delivery,withappropriatecommunicationbetweenmedicalteams,promptmedicalinter-
vention,andearlytransfertothecardiacunit.Theinfantdid,however,encounteranepisode
oflowsystemiccardiacoutputbeforesurgery,whichwasassociatedwithpulmonaryover-
circulationandmildventriculardysfunction.Thepost-operativecoursewascomplicatedby
anearlyepisodeofreducedsystemicperfusion,duetoacombinationoffactors:arelative
anemia,myocardialdysfunction,andtricuspidregurgitation.Thisoccurredatatime-point
aftersurgerywherea
ofcardiacoutputistypicallyseen.Theseepisodesofcompro-
misedsystemicperfusionwerepromptlyaddressed,andappropriateinvestigationsand
interventionswereperformed.Moresignificantsequelaewerethereforeavoided.Thesub-
sequentpost-operativerecoverywasrelativelyslowbutnotunusualforthisgroupofinfants.
Diagnosisandimmediatemanagement
Prenataldiagnosisallowsformorecarefulplanningofdeliveryandimmediatepostnatalcare
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
shouldbecommencedinthedeliveryroom,orintheabsenceofaprenataldiagnosis,assoon
asthediagnosisissuspected.
EarlysurvivalininfantswithHLHSalsodependsonanon-restrictiveAtrialSeptalDefect
(ASD).AnimportantminorityofnewborninfantswithHLHSmayhavearestrictiveASD.
Thismayhavealreadybeendiagnosedonprenatalultrasoundexaminations,inwhichcase
deliveryshouldtakeplaceatacardiaccentrecapabletourgentlyinstitutecardiopulmonary
bypass.ArestrictiveASDshouldalsobesuspectedintheinfantwithHLHS,whorapidly
developsprofoundhypoxemiaandacidosis,unresponsivetousualmeasuressuchas
mechanicalventilation,highinspiredoxygenfractions,ornitricoxide.AchestX-ray
typicallyshowsseverepulmonaryvenouscongestion.
Theseinfantswilldiewithouturgentintervention,
andmustbetransferredwithoutdelay
tothepediatriccardiaccenter,inorderforurgentatrialdecompressiontobeperformed.
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
Table4.2
Table4.2.
GuidetoimmediaterespiratorymanagementofinfantspriortosurgeryforHLHS;if
ventilated,useinitiallyFiO
0.21,PEEP4
5cmH
Table4.1.
Indicationsforintubationofpre-operativeinfantswithHLHS
Apneasorsevererespiratorydistress
Chapter4:Aneonatewithhypoplasticleftheartsyndrome
A2-year-oldchildwithacute
bacterialmeningitis
StephenC.MarriageandLauraJ.Coates
Infectiousillnessesareconsistentlyoneofthemostfrequentcausesofunplannedadmission
topediatricintensivecare.Acutebacterialmeningitis
despitedevelopmentsinantimicro-
bialtherapyandintensivecare
persistsinhavingbothahighmortalityandahighincidence
ofresultantneurologicalsequelae.Thedevelopmentofhighlyefficaciousconjugatevaccines
hashadasignificantimpactontheincidenceofmeningitiscausedby
Haemophilusinfluen-
typeB,serogroupC
Meningococcus
Pneumococcus
inthosecountrieswithsufficient
resourcestohaveauniversalvaccinationschedule;
however,theirhighcostprecludes
theiruseinmanydevelopingcountries.Intensivecareunitswillcontinuetoseechildrenwith
acutebacterialmeningitis:inyounginfants;inchildrenbornincountrieswithoutuniversal
vaccination;inchildrenoffamilieswhooptnottochoosevaccinationandinchildrenwith
immunosuppression.Optimizingtheiracutemanagementandcarewillhelpminimize
mortalityandmorbidity.
Casehistory
A2-year-oldgirldevelopedavomitingillnesswhilstonholiday.Thevomitingbecame
markedandassociatedwithafever.Awayfromhome,thefamilysoughtmedicalattention
onlyafter36hourshadpassed.Shewasnormallyawellchildandhadnorelevantpast
medicalhistory.Thegirlwasseenbyaprimarycarephysician,whonotedthatthechildwas
hot,notveryresponsive,andnotabletorecognizeherparents.Noparenteralantibiotics
wereadministeredatthisinitialconsultation.Shewasreferredtotheemergencydepartment
ofthelocalhospital.
Onarrivalattheemergencydepartmentthechildwastriagedandimmediatelyreferred
totheon-callpediatricteam.Initialobservationsrevealedachildwithtachypneaof40
breathsmin
,atachycardiaof145beatsmin
,andacentralcapillaryrefilltimeof5
seconds.Therewasnorashandthebloodpressurewasnotmeasured.Thechildresponded
neithertovoicenorpainfulstimuli,althoughshedidspontaneouslyopenhereyes.Her
pupillaryresponsestolightweresluggish,butequal.Sheseemedunawareofhersurround-
ings.Acapillarybloodgasanalysisrevealedabasedeficitof
8.5withadegreeofrespiratory
compensation.
Apresumptivediagnosisofmeningoencephalitiswasmade.Shewasgivenhigh-flow
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
Intracranialpressurewasnotmeasureddirectly,butaninfusionofnoradrenalinewas
commencedat0.04mcgkg
perminandtitratedtoachieveameanarterialpressureof
75mmHg.
Assumingtheintracranialpressuretobe25mmHg,thiswouldgivearesultant
cerebralperfusionpressureof50mmHg.
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
resistancehasbecomeanincreasingproblemandvancomycinhastobeincludedaspartof
empirictherapyuntilsensitivitiesbecomeknown.
Aciclovirwasusedasanadditionalantiviralagentinthiscaseasthediagnosisofbacterial
meningitishadnotbeenconfirmed.Ifthedifferentialdiagnosisincludesthepossibilityof
cultures,andthroatswabstoconfirmthediagnosis.
Inthemajorityofcases,theclinical
conditionofthechildwillimprovesufficientlytoallowtheinvestigationmerelytobe
deferreduntilclinicallystable.Muchusefulinformationmaystillbederivedfromthe
investigationupto48hoursafterpresentation.
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
braininjury,althoughabsolutecriteriaforwhatconstitutesanadequateCPPhavenotbeen
Chapter3:A2-year-oldchildwithacutebacterialmeningitis
capillaryleakandpulmonaryedema.Thisoftenrequiresincreasingsupportwherethereis
ongoingcapillaryleakand,asthefluidmovesbackintotheintravascularspace,ventilation
maybeweaned.
Inotropicsupportiscontinuedinordertomaintainadequateend-organperfusion,
andmayrequireoptimizationindifferentclinicalcircumstances.Commonlyusedmethods
ofassessmentofthecirculation,suchascontinuousCentralVenousPressure(CVP)
monitoring,TransesophagealDopplermeasurementofcardiacoutput,
andindwelling
arterialmonitorsusingtheFickprinciple(PICCO
,Philips)areusefulinthemeasurement
ofcardiacindices(CardiacIndex,SystemicVascularResistance)insepticpatientsand
mayprovideausefulguidetomanagementofinotropesandfluids.
Nevertheless,oneof
themorevaluableguidestocardiacoutputremainsurineoutput.
Whereaninotrope
isrequired,dobutamineandadrenalinearetitratedtoeffect;wherevasoconstrictionis
required,forexample,inavasodilated(lowSVR)statewithawidepulsepressure,
noradrenalineistheagentofchoice.Onceagain,theseagentsareweanedastheshock
improves.
Fluidmanagement
Maintenancefluidsareadministeredat80%oftotalmaintenancefluidrequirements;our
fluidofchoiceis0.45%salinewith5%dextrose.Enteralfeedingshouldbeinstitutedearly.
Thismaybecarriedoutbyeitherthenasogastricornasojejunalroute.Wecommencetrophic
feedsearlyandthengradeuptofullenteralfeedswhentolerated.
Skinandlimbcare
Meningococcalsepticemiaischaracterizedbyahemorrhagicrash,whichmayprogressto
areasofconfluentpurpura.Areasoftheskinandlimbs
inparticularextremities
becomenecrotic.Acompartmentsyndromemaydevelopintheacutesituationwherethere
isseverecapillaryleakthreateningtheperfusionofunderlyingmuscle.Itisimportantto
involvevascular,orthopedic,andplasticsurgicalteamsearly.Fasciotomyshouldonlybe
performedifdeemedabsolutelynecessary,wherecompartmentpressureshavebeendem-
onstratedtobehighandarterialpulsesareabsent.Mostoftheskinandlimbnecrosisthat
occursisusuallyduetomicrovascularthrombosis,andfasciotomyrarely,ifever,hasany
Inordertohaveoptimalfunctionalrecoveryoflimbsandextremities,thedecision
toperformamputationanddebridementisbestmadeintheconvalescentphaseoftheillness
andmustinvolveamultidisciplinaryteamapproach.
Newertherapies
Muchworkhasfocusedontheuseoftherapeuticagentsthatactasadjunctstothecurrent
supportivetherapiesusedinthemanagementofmeningococcalsepticemia.Theadjunctive
agentsthathavebeenusedtomodulatetheinflammatoryresponseincludeanti-endotoxin
agents,suchasrecombinantbactericidal-permeabilityincreasingprotein(rBPI
anticoagulantssuchasAntithrombinIII
andActivatedProteinC(APC).Activated
ProteinCisanendogenousregulatorofcoagulationandinflammation.OnceProteinC
isactivatedbythethrombin
thrombomodulincomplex,itisabletoexertbothantithrom-
boticandprofibrinolyticeffects.Patientswithseveresepsishavebeendemonstratedto
haveareductionorabsenceofproteinC,whichisassociatedwithanincreasedriskof
morbidityandmortality.
Drotrecoginalfa(activated)isarecombinantformofhuman
APCandintherecentlypublishedPROWESStrial,
wasadministeredtoadultswith
Chapter2:Theinfantwithmeningococcalsepticemia
severesepsis.Thismulti-centredouble-blin
d,randomized,placebo-controlledtrialcom-
paredAPCtoplacebo.Thetrialdrugwasadministeredforatotalof96hours.Therewas
astatisticallysignificantreductionin28-dayall-causemortality,witharelativerisk
reductionof19.4%inthoseadultswhor
eceivedAPCwhencomparedwiththeplacebo
group.Thiswasthefirststudyofanadjuncti
vetherapyinseveresepsistoshowasurvival
advantageintheoverallpatientpopulation.APCisnowlicensedforuseinadultswith
severesepsis.
Chapter2:Theinfantwithmeningococcalsepticemia
Fig.2.3.
MeningitisResearchFoundationProtocol.
1.HealthProtectionAgencyHomepage.
MeningococcalReferenceUnitLaboratory
ConfirmedNeisseriaMeningitidis:England
andWales,byAgeGroup,1989/1990to
2.BooyR,HabibiP,NadelS
Chapter2:Theinfantwithmeningococcalsepticemia
medicalmanagementofseveretraumaticbrain
injuryininfants,childrenandadolescents.
PediatrCritCareMed
2003;
:S40-4.
25.Useofhyperventilationintheacute
managementofseverepediatrictraumatic
braininjury.FromGuidelinesfortheacute
medicalmanagementofseveretraumatic
braininjuryininfants,childrenand
PediatrCritCareMed
:S45
26.TibbySM,HatherillM,DurwardA,
MurdochIA.AretransoesophagealDoppler
Chapter2:Theinfantwithmeningococcalsepticemia
Theinfantwithmeningococcal
MehrengiseCooperandSimonNadel
Meningococcalsepticemiaisassociatedwithahighmorbidityandmortality.Followingthe
introductionofthemeningococcalCvaccine,therehasbeenareductionintheincidenceof
disease,withthemajorityofthediseasenowbeingcausedby
Neisseriameningitidis
groupB.
In2003
2004,969casesofmeningococcaldiseaseinchildrenunder15yearswerenotifiedto
theHealthProtectionAgencyinEnglandandWales.
Promptrecognitionandearlyaggres-
sivemanagementofchildrenhasbeenshowntoreducebothmorbidityandmortality,with
themajoritysurvivingwithoutlong-termsequelae.
Casehistory
Apreviouslywell10-month-oldboywasadmittedtohislocalhospitalhavingbeennon-
specificallyunwellfor2dayswithafever.Initialbloodresultswereunremarkableandhewas
admittedtothewardforobservation.Twohourslater,twopetechialspotswerenotedonhis
neck.Atthistime,hisheartrate(HR)was160bmin
;hewasnormotensiveandhadacapillary
refilltime(CRT)2seconds.Hecontinuedtobecloselyobserved.Fourhourslater,therashwas
Table2.1.
Bloodresults
Na(mmoll
K(mmoll
Cl(mmoll
Urea(mmoll
)3.9
Creatinine(µmoll
)38
Calcium(mmoll
)2.24
Bilirubin(µmoll
)16
Albumin(gdl
)39
CRP(mgl
AST(Ul
ALP(Ul
Hb(gdl
WBC(×10
Neutrophils(×10
)1.6
Chapter2:Theinfantwithmeningococcalsepticemia
Fig.2.1.
Fig.2.2.
pulmonaryedema.
Chapter2:Theinfantwithmeningococcalsepticemia
dobutamineandadrenalinewere10mcgkg
perminand2mcgkg
permin,respectively
duringtransfer,inordertomaintainameanarterialBP
55mmHg.Thiswasfelttobean
age-appropriatelevelofbloodpressureinordertotrytomaintainend-organperfusion.Two
further4.5%HASboluseswereadministered
enroute
ProgressandmanagementonPICU
OnarrivalonPICUhewasreviewed.Onexamination,hewasedematous,andhadareasof
confluentpurpuraoverhistrunkandneck;hisperipheralperfusionwasverypoor,witha
Table2.2.
InvestigationsandresultsonadmissiontoPICU
Na(mmoll
K(mmoll
Urea(mmoll
Creatinine(µmoll
)87
Calcium(mmoll
Bilirubin(µmoll
Albumin(gdl
CRP(mgl
Hb(gdl
WBC(×10
Neutrophils(×10
)1.7
Chapter2:Theinfantwithmeningococcalsepticemia
FollowinghisarrivalonthePICU,inthenext2hourshebecameprogressivelymore
difficulttooxygenateandventilatedespiteFiO
of1.0,highpeakinspiratorypressures,and
increasingpeakendexpiratorypressure.ABGanalysisshowed:pH7.18,pCO
8.0kPa,
10kPa,HCO
21mmoll
,BE
5mmoll
.HewasthencommencedonHighFrequency
OscillatoryVentilation(HFOV)withaninitialfrequencyof8Hz,meanairwaypressure
(MAP)26cmH
O,amplitude(
P)55,andFiO
0.8.Followingthis,oxygenationand
ventilationimproved.
Overthenext2hourshebecameprogressivelymorehypotensive,withdecreasing
diastolicBPandhisinotropicmanagementwaschanged
dobutaminediscontinued,and
noradrenaline(norepinephrine)commencedat0.5mcgkg
permin.Hydrocortisonewas
commenced(1mgkg
every6hours).Herequiredfurthercolloidbolusesintheformof
Table2.3.
Bloodresultsat24hours
Na(mmoll
K(mmoll
Urea(mmoll
Creatinine(µmoll
)75
Calcium(mmoll
)2.23
Bilirubin(µmoll
)19
Albumin(gdl
CRP(mgl
Hb(gdl
WBC(×10
Neutrophils(×10
)20.3
Chapter2:Theinfantwithmeningococcalsepticemia
after4days,andCVVHwasdiscontinuedafter6days,withfurosemidesupport.Hereceived
a7-daycourseofceftriaxone.
Hisextremitiesshowedchangesconsistentwithdrygangrene,andhewasreviewedbythe
orthopedic,vascularandplasticsurgeryteams.Itwasimportanttoallowtheischemicareas
todemarcateinordertoassesstheareasofviableskinpresent.
Hewasdischargedtothepediatricwardafter2weeksofintensivecare.Heinitiallyremained
Chapter2:Theinfantwithmeningococcalsepticemia
assessmentmayincludeserumrapidantigenscreen,EDTAbloodformeningococcalPCR,
bloodcultures,andthroatswabfor
Neisseriameningitidis
Featuresassociatedwithapoorprognosisare:age6months,theabsenceofclinicalor
laboratoryfeaturesofmeningitis,coma,hypotension,peripheralWBC10000/cm
,CRP
50mgl
,ESR10mmh
ofshockarenotpresent,allchildrenwithmeningococcalsepticemiawillhaveadegreeof
hypovolemia.Thisshouldbepromptlytreatedbyinfusingfluid;40
60mlkg
of0.9%saline
or4.5%HASmaybegiveninthefirsthourwithoutanincreasedriskofpulmonaryor
cerebraledema.
Thedegreeofhypovolemiaisusuallyunderestimated,anditisnot
uncommonforchildrenwithmeningococcalshocktorequireseveraltimestheircirculating
volumeoffluidresuscitationinthefirst24hours.Suchvolumescanonlybegivensafelywith
invasivemonitoringofcentralvenousandarterialpressure,continuousmeasurementof
urineoutputandcontinuousclinicalandlaboratoryassessment.Thisisbestundertakenbya
Chapter2:Theinfantwithmeningococcalsepticemia
usedonthepatientdescribed.Eachhasitsad
vantagesanddisadvantages,andthechoiceis
dependentontheclinicalscenario.Dobutamineandadrenalinehavebothinotropicandvaso-
dilatorproperties,dependingonthedosagesuse
d,andusuallyincreasecardiacoutput.However,
theymayalsoincreasemyocardialoxygenrequire
mentsandcausemyocardialfailure.Adrenaline
andnoradrenalinemayactasvasopressorsandi
ncreasesystemicvascularresistance.While
maintenanceofbloodpressureisimportant,vaso
pressorsmayworsenmyocardialfunctionin
thefaceofalowcardiacoutputstateseeninpre-terminalsepsis,andreduceperfusionto
ischemicareasofskinanddistalextremities,andtothesplanchniccirculation.Neweragents
beingevaluatedinthemaintenanceofthecirculat
ionincludevasopressinbyinfusionininotrope
unresponsivevasodilatationduetosepsis,an
dmilrinoneinlowcardiacoutputconditions.
AstudyoftheuseofEarlyGoal-DirectedTherapy(EGDT)insepticadultpatients
showedasignificantreductioninmortality,whencomparedwithstandardtherapy.
Chapter2:Theinfantwithmeningococcalsepticemia
Chapter2:Theinfantwithmeningococcalsepticemia
aerosolizedRibavirinwaspurportedtobeassociatedwithimprovedoxygenation,
improvedclinicalscores,anddiminishedlevelsofsecretorymediatorsofinflammation
associatedwithseverewheezinganddisease.
However,itsusewaslimitedinitiallybecause
ofexpenseand,overthelast20years,anumberofinvestigatorshavebeenunableto
convincinglyshowabeneficialeffectonclinicaloutcome.Morestudieshavebeenunder-
Chapter1:Respiratorysyncytialvirusbronchiolitis
Co-infectionandtheuseofantibiotics
Manystudiesinthedevelopedworldhavenotedthatbacterialco-infectionduringRSV
bronchiolitisisunusual.Despitethis,inchildrenwhorequirepediatricintensivecare,anti-
bioticuseisalmostuniversal.
Itisfrequentlysuggestedthatantibioticsmaybebeingover-
usedandthatmeasuresshouldbetakentoreducethis.
However,diagnosisofco-infection
canbedelayed,ismorecommoninchildrenrequiringintensivecareandisassociatedwitha
moreseverecourse.
Inaddition,arecentreporthassuggestedthattrachealcolonizationwith
Haemophilusinfluenzae
maybeassociatedwithaworsePICcourseinRSVbronchiolitis.
Co-infectionwith
Bordatellapertussis
Streptococcuspneumoniae
areunusual,butnot
rare,andshouldbeconsidered.Co-infectionwithvirusessuchashumanmetapneumovirus
andhumanbocavirushaverecentlybeenemergingasanotherpotentialcauseofmoresevere
illnessduringthebronchiolitisseason
andcanbediagnosedbyPCR.
Chapter1:Respiratorysyncytialvirusbronchiolitis
mortalityandestimatesofrespiratory
syncytialvirus-associateddeathsamongUS
children,1979
JInfectDis
(1):16
4.LangleyJM,LeBlancJC,SmithB,WangEE
Increasingincidenceofhospitalizationfor
bronchiolitisamongCanadianchildren,
JInfectDis
:1764
5.LangleyJM,WangEE,LawBJ
Chapter1:Respiratorysyncytialvirusbronchiolitis
25.O
MalleyBW.Mechanismsofactionofsteroid
NEnglJMed
1971;
:370
26.FauciAS.Mechanismsofcorticosteroid
actiononlymphocytesubpopulations.II.
Differentialeffectsofinvivohydrocortisone,
Chapter1:Respiratorysyncytialvirusbronchiolitis
combinationtherapywithaerosolized
ribavirinandintravenous
BoneMarrowTranspl
(7):751
47.SokolJ,JacobsSE,BohnD.Inhalednitric
oxideforacutehypoxemicrespiratory
failureinchildrenandadults.
DatabaseSystRev
2000;CD002787.
Chapter1:Respiratorysyncytialvirusbronchiolitis
Inpediatricintensivecare,asinmostareasofclinicalpractice,welearnbestbyexperience.
Notextbookcanhopetoreplacethelearningprocessthatoccursfromlonghoursofclinical
Respiratorysyncytialvirus
RoddyO
DonnellandMichaelRoe
RespiratorySyncytialVirus(RSV)bronchiolitisistheleadingcauseofadmissiontohospital
inchildrenundertheageof1yearindevelopedcountries.
RSVisidentifiedasthecausein
theoverwhelmingmajority(75%)ofcasesofbronchiolitis.However,othervirusessuchas
Casehistory
A10-month-oldfemaleinfantpresentedinJanuarytoherlocalhospitalwitha7-dayhistory
ofcough,mildpyrexia,andwheeze.Shehasahistoryofmultipleepisodesofcoughand
wheeze,someofwhichrequiredadmissiontohospital,thatweretreatedwithinhaled
bronchodilators
2agonistsandipratropiumbromide
andsteroids.
Shewasbornprematurelybycesareansectionat28weeks
gestationbecauseofmaternal
placentapraevia.Shehadabirthweightof1050grams.Intheneonatalperiod,shewas
managedwithnasalContinuousPositiveAirwayPressure(CPAP)andsupplementaloxygen
anddidnotrequireintubationandventilation.At8weeksofage(36weeks
post-conceptual
age),shewasdischargedhomeandrequirednosupplementaloxygen.Shehadreceivedall
CaseStudiesinPediatricCriticalCare
herroutineimmunizationstodate,hadnoknownallergies,andhadreachedappropriate
developmentalmilestones.
Onadmissiontolocalhospital:
Temperature37.8ºC
48breaths.min
Saturations88%
92%inair,risingto96%in2litresofoxygen
ChestModeratesubcostal/intercostalrecessionwidespreadexpiratorywheezeandfine
Investigations
ChestX-ray
Hyperexpandedwithareasofatelectasisinbothlungfields
Nasopharyngealaspirate
Negativeforrespiratoryviruses
Onthisadmissionshewastreatedwithoxygenandgivenatrialofsalbutamoland
ipratropiumbromideinhalersasmetereddoseinhalersusingaspacerdevice.Bothsalbuta-
molandipratropiumbromidewerefelttohavesometherapeuticbenefit.Shewasallowedto
continuewithnormalfeedingandappearedtotoleratefeedswell.
Overthenext24hours,therewereepisodesofincreasedrespiratorydistressandrising
oxygenrequirements.Oralclarithromycinwascommencedandfeedsweregivenbynaso-
gastrictube.
Bytheseconddayofadmission,respiratorydistresshadworsenedandtherewasan
increasingrequirementforoxygen.Enteralfeedswerediscontinuedandintravenousfluids
(80mlkg
perdayof0.45%salinewith5%dextrose)werestarted.Acapillarybloodgaswas
undertakenwhichshowed:pH=7.39,
=6.28kPa,BE=
3.1.NasalContinuousPositive
AirwayPressure(nCPAP)usingnasalprongswasstarted.
Chapter1:Respiratorysyncytialvirusbronchiolitis
Progressonpediatricintensivecareunit(
Table1.1
Onadmission,shehadastrikinglyprolongedexpiratoryphasewithwheezeandinspiratory
crackles.Sincesalbutamolhadappearedtobeassociatedwithimprovementatherreferring
hospital,asalbutamolinfusionwascommencedbeginningat1mcgkg
permin.Overthe
following12hours,oxygenrequirementsremainedhigh.Afterfurtherdiscussion,atrialof
HighFrequencyOscillatoryVentilation(HFOV)wascommenced.AfterinitiatingHFOV
therewasmarkedhemodynamicinstability,necessitatingincreasedinotropicandvaso-
Table1.1.
FindingsonadmissiontoPICU
Airway4.5uncuffedoralendotrachealtubefixed11.5cmatlips
BreathingBIPAP,Pressures28/6,rate24,
Inspiratorytime=0.8seconds
=70%
GaspH=7.32,
=6.65kPa,
=12.22kPa,BE=
CirculationPulse=136bmin
,BP=88/44mmHg(MAP=56)
Warmandwellperfused;peripheralcapillaryrefilltime2s
Dopamine@8mcgkg
perminGlucose=2.7mmoll
,therefore5mlkg
dextrosegiven
Urineoutput=2mlkg
perh
NeurologyPupilssmallbutequalandreactbrisklytolight
InvestigationsHb=9.4gdl
,WCC=11.4×10
,Plts=294×10
Na=140mmoll
,K=4.1mmoll
,U=1.3mmoll
,Cr=17
moll
,CRP=45mgl
Chapter1:Respiratorysyncytialvirusbronchiolitis
Extra-corporealmembraneoxygenation(ECMO)
AfterdecidingtoinitiateatrialofNO,thesupra-regionalECMOcenterwascontactedin
accordancewithournormallocalpractice.Dailycontactwasmaintained,butsheremained
Chapter1:Respiratorysyncytialvirusbronchiolitis
hydratewereusedfromthe12thPICUdayonwardstoallowweaningofintravenous
sedationandmanagewithdrawalsymptoms.
Weaninganddischarge
Shegraduallyimprovedafterthe10thdayofintensivecareandwasweanedsufficientlyto
allowelectiveextubationonthe16thdayafteradmission.Forthenextday,sherequireda
smallamountofsupplementaloxygen,whichwassteadilyreducedandthenstopped.Shewas
dischargedfromtheintensivecareunitafter17daysandwastransferredbacktoher
Chapter1:Respiratorysyncytialvirusbronchiolitis
Inthe1960sanumberofvaccinetrialswereundertakeninchildrenusingaformalin-
inactivatedpreparationofthevirus.Thisvaccinewascreatedusingthesametechniquesthat
hadprovensosuccessfulinvaccinatingagainstpolio.Inthesestudieschildrenshowedgood
serumantibodyresponsesandcell-mediatedlymphocyteresponsesaftervaccination.During
subsequentnaturalRSVinfection,however,illnessappearedtobeenhanced.
Therewere
increasedadmissionsandsomechildrendiedwithevidenceatpostmortemofavigorous
inflammatoryresponseinthelung.
Inthe1980sand1990s,withgreaterunderstandingoftheroleoflymphocytesandwith
animalmodels,itwaspossibletoshowthat,duringRSVinfection,bothCD4helperandCD8
Chapter1:Respiratorysyncytialvirusbronchiolitis
authorsfoundnobenefitsineitherlengthofstayorclinicalscoreininfantsandyoung
childrentreatedwithsystemicglucocorticoidsascomparedwithplacebo.Theyalsofound
Chapter1:Respiratorysyncytialvirusbronchiolitis
Managementofacuteheartfailure
inpediatricintensivecare
MatthewFentonandMichael
Burch
SanjayM.Bhananker
AssistantProfessorinAnesthesiology
UniversityofWashingtonSchoolofMedicine
HarborviewMedicalCenter
Seattle,WA
FarhanBhanji
StaffSpecialist,CriticalCareMedicine
TheMontrealChildren
sHospital
Montreal,Quebec
Canada
EmmaJ.Bould
PaediatricandNeonatalIntensiveCareUnits
GreatOrmondStreetHospitalforChildren
London,UK
MichaelBurch
ConsultantPaediatricCardiologist
DepartmentofCardiothoracicTransplant
RoddyO
ConsultantPaediatrician
PaediatricIntensiveCareUnit
Addenbrooke
sHospital
Cambridge,UK
MattOram
UlfTheilen
ConsultantinPaediatricIntensive
PaediatricIntensiveCareUnit
RoyalHospitalforSickChildren,
Edinburgh,UK
JoshuaC.Uffman
ActingAssistantProfessor
DepartmentofAnesthesiology
UniversityofWashingtonSchoolof
Medicine
AttendingAnesthesiologist,Children
Hospital&RegionalMedicalCenterand
HarborviewMedicalCenter
Seattle,WA
MonicaS.Vavilala
AssociateProfessor
DepartmentsofAnesthesiology,Pediatrics,
andNeurologicalSurgery(Adj)
UniversityofWashingtonSchoolof
Medicine
AttendingAnesthesiologist,Harborview
MedicalCenter
AttendingEmergencyPhysician,Children
Hospital&RegionalMedicalCenter
Seattle,WA
PatriciaM.Weir
ConsultantinPaediatricAnaesthesiaand
IntensiveCare
BristolRoyalHospitalforChildren
Bristol,UK
AndrewR.Wolf
ProfessorofPaediatricAnaesthesiaand
IntensiveCare
BristolRoyalHospitalforChildren
Bristol,UK
CaseStudiesinPediatric
CriticalCare
CaseStudiesinPediatric
CriticalCare
Editedby
Cambridge University Press
The Edinburgh Building, Cambridge CB2 8RU, UK
First published in print format
ISBN-13978-0-511-54033-2
up-to-date information which is in accord with accepted standards and practice at
information contained herein is totally free from error, not least because clinical
This publication is in copyright. Subject to statutory exception and to the
Cambridge University Press has no responsibility for the persistence or accuracy
Foreword
Respiratorysyncytialvirus
bronchiolitis
RoddyO
DonnellandMichaelRoe
Theinfantwithmeningococccal
septicemia
MehrengiseCooperandSimon
A2-year-oldchildwithacute
bacterialmeningitis
StephenC.MarriageandLauraJ.
Coates
Managementofaneonatewith
hypoplasticleftheartsyndrome
UlfTheilenandLara
Shekerdemian
Childwithaheadinjury

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