Growth among infants with CHD is poor, and is multifactorial with multiple contributing factors. Unexplained hypophosphataemia has been reported among infants and children with complex medical needs consuming amino acid infant formula as the sole source of nutrition. The aim of this audit was therefore to review the incidence of hypophosphataemia among infants with CHD.

The use of an electronic patient record search for “amino acid infant formula”, “CHD”, and “cardiac” yielded 136 infants <12 months of age. Preterm infants (n=24), children with chromosomal abnormalities (n=4), those >1 year of age (n=11) and infants with a structurally normal heart (n=31) were excluded from the study. The remaining 66 infants with CHD were given amino acid infant formula.

In all, 1059 serum phosphate measures were available. After the introduction of amino acid infant formula, significantly more infants with CHD had episodes of hypophosphataemia: 15% (n=10/66) before treatment versus 29% (n=19/66) after treatment (p=0.049). Mean serum phosphate levels were significantly lower in infants with CHD following consumption of amino acid infant formula (2.0±0.5 versus 1.5±0.5 mmol/L following treatment (p<0.0001)). Infants with CHD and hypophosphataemia, associated with amino acid infant formula, use demonstrated significantly lower weight gain compared with those with normal phosphate levels (weight-for-age z scores −2.1±1.4 versus –0.9±1.5; p<0.0001).

After the introduction of an amino acid formula, weight gain was significantly lower among those infants with low phosphate levels. There was a significantly higher prevalence of hypophosphataemia among infants with CHD after the introduction of amino acid infant formula. Lower phosphate levels were associated with lower weight-for-age z scores. Infants with CHD are susceptible to poor weight gain; it is therefore, crucial the nutritional status of infants prescribed amino acid infant formula is more closely monitored to ensure adequate growth.