Andersons pediatric cardiology 2218

8–12months
12–16months
16–20months
20–24months
2–10years

0.28–0.37cm/wk
0.24–0.33cm/wk
0.21–0.29cm/wk
0.19–0.26cm/wk
5–8cm/y

0.08–0.11cm/wk
0.04–0.08cm/wk
0.03–0.06cm/wk
0.02–0.04cm/wk
N/A

Table86.6
EstimatedEnergyandProteinRequirementsforChildren60
RecommendedDietary
Allowance
0–6months
108
7monthsto1 98
year
1–3years
102
4–6years
90
7–10years

70
11–14years
Male
55
Female
45
15–18years
Male
47
Female
40
Age

EnergyRequiredforCatch-upGrowth
(kcal/kgperday)
120–150+
110–140

Protein(g/kgper
day)
2.2–3.5
1.5–2.5

100–120
80–100
60–90

1.2–2.0
1.2–1.5
1.2–1.5

55–60
45–60

1.0–1.5
1.0–1.5

45–55
45–55

1.0–1.5
1.0–1.5

Specialconsiderations:Estimatedneedsmaybeaffectedbyventilation,sedation,ormechanical
support.

Table86.7
EstimatedFluidRequirements61
Weight(kg)
1–10kg
11–20kg
>20kg

Fluid
100mL/kgperday
1000mL+50mL/kgforeachkg>10kg
1500mL+20mL/kgforeachkg>20kg

Table86.8
FormulasforChylothorax(HighMedium-ChainTriglycerideand/or

LowLong-ChainTriglycerideContent)
Formula

Type

Liquidconcentrate30
Enfaporta
(MeadJohnson) calories/ounce
Powder

MCT:LCT
Ratio
83:17

PercentCaloriesFrom
LCTFat
7.8

LCTFatg/100
Calories
0.9

80:20

7.6

0.82


Lipistarta

(Néstle)
Monogena
(Nutricia)
Portagena,b
(MeadJohnson)
Tolerexc
(Néstle)
VivonexPediatricc
(Néstle)
VivonexTENc
(Néstle)

Powder

83:17

4.5

0.5

Powder

87:13

5.5

0.6

Powder

0:100

2

0.2

Powder

70:30

7.5

0.87

Powder

0:100

3

0.3

a

Containsmilkproteins.

bLong-termusage:Portagenpowderisnotnutritionallycomplete.Ifusedlongterm,

supplementationofessentialfattyacidsandultra-tracemineralsshouldbeconsidered
(manufacturer'snotation).

cElemental,100%freeaminoacids.

LCT,Long-chaintriglyceride;MCT,medium-chaintriglyceride.
Datafrommanufacturers'productlabelsasofApril2018.Pleasenoteproductcompositionmay
bechangedbythediscretionofmanufacturers.

EtiologyofMalnutrition
InadequateNutrientIntake
Inadequatecaloricandproteinintake,includingunderestimatednutrient
requirementsorenergyimbalance,isfrequentlycitedasamajorcontributing
factortogrowthfailureandmalnutritioninchildrenwithcongenitally
malformedhearts.22Itisalsooneofthemostmodifiablefactorsassociatedwith
favoredgrowth.23,24Disorderedoralfeedingskillsandinadequateoralintake
mayalsosignificantlycontributetoinadequatecalories.Thefeedingpatternsof
neonateswithCHDhavebeencomparedwithmatchedsubgroupsofinfantswith
structurallynormalhearts.15,25Forinfantswithcongenitallymalformedhearts,
oralfeedingdemandsincreasedamountsofenergy.Feedingintolerancecanbe
attributedtoaninabilitytoexpendsufficientenergyonfeeding,asexhibitedby
tachycardia,tachypnea,shortnessofbreath,andvomiting.
Othercontributingfactorsinclude:

■Earlysatiety


■Decreasedgastriccapacitycausedby
hepatosplenomegaly
■Delayedgastricemptyingtime
■Dysmotility
■Uncoordinatedsuck
■Abnormalpatternsofswallowingandbreathingdue

totachypnea.
Inaddition,fluidrestrictionsanddiuretictherapyaspartofthemedical
managementmayhinderprovisionofadequatecaloricintake.

Hypermetabolism
Theenergyavailableformetabolismisthesumoftotalenergyexpenditureand
energystored.Basalmetabolicraterepresentsthemajorcomponentoftotal
energyexpenditure.Ingeneral,childrenhaveahighermetabolicratethanadults,
placingthemathighriskforenergeticdeficienciesduringepisodesofacute
illness.15,26Childrenwithcongestiveheartfailurehavebeenreportedtohaveup
tofivetimeshigherbasalmetabolicratesthanchildrenwithoutcardiac
disease.22Theelevatedbasalmetabolicrateislikelyduetotheincreased
workloadofthecardiacandrespiratorysystems.Restingenergyexpenditurehas
beenshowntobeincreasedinmalnourishedinfantswithcongestivecardiac
failure.15Frequentrespiratoryinfectionsandfeverwillalsocontributetoastate
ofhypermetabolismbecausethepresenceofinflammationmaypromote
catabolism.27

Malabsorption
Theetiologyofmalabsorptionismultifactorialandcontributestomalnutritionin
childrenwithCHD.MalabsorptioncanresultfromGItissuehypoxia,which
mayleadtofeedingintolerance,limitedcaloricintake,anddecreasednutrient
utilization.28Thosewithcardiaclesionsresultinginright-sidedcardiacfailure
andincreasedsystemicvenouspressuremaydevelopedemaoftheintestinal
wallandmucosalsurfacesorpoorsplanchnicperfusion.Thesealterationsinthe