HYPOTHESES:
(1) Nutritional status is impaired in symptomatic congenital heart disease (CHD) in
infancy, and this is related to an inadequate positive energy balance. (2) Undernutrition
Hypotheses
(1) Nutritional status is impaired in symptomatic congenital heart disease (CHD) in
infancy, and this is related to an inadequate positive energy balance. (2) Undernutrition
precedes the development of bronchopulmonary dysplasia (BPD) in preterm infants, and
there is a subsequent persistent deficit in energy balance, bone mineral content (BMC)
and growth
OBJECTIVES:
To study (1) the effect of CHD on growth and energy balance in infancy (2)
macronutrient intake prior to the development of BPD (3) the effect of BPD on energy
balance and BMC and the effect of dexamethasone used to treat BPD on BMC.
BACKGROUND
Poor growth is seen :commonly in chronic disease of the heart and lungs (CCPD) and is
important because: (a) the disease and its treatment may compromise nutrition (b) good
nutrition may influence the outcome of the condition and adult health. Body growth in
infants is dependent upon a sufficiently positive balance of protein and energy, and
certain micronutrients are important for aspects of specific organ development. There are
few previous studies looking at specific aspects of nutrition in young infants with CCPD.
METHODS:
CHD Energy balance measurements were carried out on 21 infants with CHD, post-term
age [median (range)] 49 days (-9 to 246) and in 9 controls, post-term age 35 days (-14 to
86). Energy intake (EI) and losses (EL) were measured by bomb calorimetry (18 CHD, 5
control), resting energy expenditure (REE) by indirect calorimetry over several hours (14
CHD, 9 control), and anthropometry performed. Metabolizable energy intake (MEI) was
calculated as EI-EL, and energy available for deposition (EAD) as MEI-REE. BPD 195 consecutive infants of <32 weeks gestation had weekly anthropometry and
records of achieved nutritional intake. 54 of these had dual energy X-ray absorptiometry
of the forearm for bone mineral content (BMC). Case control studies were done on nested
cohorts within this group: (1) macronutrient intake and growth in 20 babies with BPD
and 20 gestation and birthweight matched controls, (2) BMC in 10 babies with BPD and
10 gestation and birthweight matched controls, (3) BMC in 15 BPD babies treated with
dexamethasone and 15 untreated BPD controls. In a separate convenience sample of 4
infants with BPD and 4 preterm controls El and EL were determined by bomb
calorimetry.
RESULTS:
CHD There was a fall with age in z-score for body size: for weight 1SD in 21 days,
length 1SD in 43 days and head circumference 1SD in 37 days. Weight gain over 5 days
[median (quartiles)] was less in cardiac infants [ll.Og/d (2.5-16.7)] than in controls
[39.0g/d (20.0-47.5)], P=0.0034. There was no statistically significant difference in EI,
EL, or MEI between the groups. Sleeping oxygen uptake [SV02, median (range)] was
similar in CIID infants [9.93ml/kg/min (7.7-13.88)] and controls [9.23ml/kg/min (7.5-
11.66)], with the highest values in 3 of 4 infants with persistent cardiac failure and
pulmonary hypertension. Respiratory quotients were similar. SVo2/kg correlated
inversely with log [summed skinfold thicknesses] (r2=0.671; P=0.0001) and with body
mass index. There was a positive correlation in CHD infants between weight gain and
MEI %RDA (r2 =0.28, P=0.024), and energy available for deposition (r2 =0.43, P=0.05).
BPD BPD infants had lower early macronutrient intake than controls [median
(quartiles)]: for first week EI, BPD = 262 kJ/kg/d (210-282), control = 347 kJ/kg/d (293-372), P=0.003. BPD infants had a lower proportion ofEI as enteral feeds than controls in
the first 2 weeks [median (quartiles)]: BPD = 68% (31.3-79.2), control = 91% (78.0-
93.0), P=0.0025. The rate of weight gain [slope (95% CI)] was less in babies with BPD
[151.5 g/week (135.5-167.6)] than in controls [192.2 g/week (178.5-205.9)], P<0.05.
There was no demonstrable difference in z-score values for weight, length, head
circumference or body mass index at discharge. In the small sample studied, there was no
difference in EI, EL, or MEI. For MEI, BPD = 592 kJ/kg/d (425-741), control = 565
kJ/kg/d (527-737). For all babies measured (n=54), BMC at birth [median (quartiles)]
was 1.79mg/mm (1.57-2.03), with a fall in the first 5 weeks by 0.23mg/mm (0.09-0.41),
followed by a rise, with a value at 10 weeks of 1.99mg/mm (1.69-2.16). There was no
detectable difference between the BPD and control groups. Dexamethasone had no effect
on the postnatal trend in BMC, but was associated with slower forearm growth: length
increase in 5 weeks [median (quartiles)] for steroid group =7.54mm (0.6-7.6), for
controls =11.6 (5.4-24.5), P=0.019.
CONCLUSIONS:
CHD There appears to be a progressive postnatal deterioration of nutritional status in
hospitalized infants with CHD. This is associated with a tendency to lower energy intake,
and in addition raised REE in some infants. Availability of energy appears to be a
limiting factor for growth in this group.
BPD There is a shortfall of nutrient intake in the first two weeks, particularly via the
enteral route, in preterm infants who later develop bronchopulmonary dysplasia. The
subsequent rate of weight gain is slower for several weeks in these babies. There appears
to be no abnormality of energy intake or losses. There is a large deficit in BMC in
preterm infants at term, with no additional effect of BPD. Systemic steroid treatment
slows linear growth, without any apparent effect on bone mineralization.