Menon, Gopi

2018-03-29T12:18:52Z

2018-03-29T12:18:52Z

2005

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.

http://hdl.handle.net/1842/29271

The University of Edinburgh

Annexe Thesis Digitisation Project 2018 Block 17

Already catalogued

Studies of nutrition and growth in infants with chronic cardiopulmonary disease

Thesis or Dissertation

Doctoral

MD Doctor of Medicine