Mineral balance studies were performed in 61 sick preterm infants given parenteral fluids only. Their gestational ages varied from 24 to 35 weeks, and 50 required mechanical ventilation. Two consecutive balance studies were performed; the first from admission to 48 hours in all babies given maintenance fluids of 10% Dextrose, and the second from 48 hours to 7 days in those babies given intravenous feeding (IVN). At the beginning and end of each balance period, the baby was weighed and an arterial blood sample taken for blood gases, electrolyte, urea, creatinine and protein determinations. During the balance period all urine was collected and analysed for electrolyte, urea, and creatinine composition, and all fluid intake was recorded. The balance of a mineral was calculated as the difference between parenteral intake and urine output. Infants requiring IVN were allocated alternatively to regimen X or regimen Y, which had the same calcium content of 9.5 mmol/L, but different phosphate contents, regimen X containing 7.3 mmol/L and regimen Y 11.6 mmol/L. In those infants requiring prolonged IVN, 12–24 hour balance studies were performed at weekly intervals after day 10.
1. Phosphate deficiency developed in infants given regimen X, who had higher urine calcium excretion, lower percentage calcium retention and lower plasma phosphate levels than those given regimenY. These differences were apparent by day 7 and persisted after day 10. In infants given regimen Y, mean calcium retention from admission to day 7 was 3.9 mmol/kg, and after day 10 was 0.9 mmol/kg/day.
2. In the first 48 hours, urine output and creatinine clearance varied widely and were lower in infants with higher oxygen requirements at 48 hours. Ten babies had severe oliguria with outputs less than 10 mL/kg/day. Creatinine clearance was directly related to gestational age, mean arterial blood pressure, and plasma protein concentrations on admission. After 48 hours, urine output and creatinine clearance increased considerably.
3. In the first 48 hours, metabolic acidosis was produced by increased plasma non‐protein metabolisable acid concentrations, which were associated with low creatinine clearances, and were thought to be due to lactic acid accumulation in response to decreased tissue perfusion. At 7 days, metabolic acidosis was of similar severity but was produced by decreased plasma non‐metabolisable base concentrations, caused by increased urine loss of net base, and not directly by IVN.
4. A simple model was constructed for either estimating the net movement of a substance into or out of the extracellular fluid (ECF) space, referred to as production or uptake respectively, or for estimating change in the fraction of body weight made up by ECF, referred to as ECF fraction.
5. Hyperkalaemia developed in 5 infants at 48 hours, and was caused by a combination of severe oliguria and high rates of potassium production. Potassium production was directly related to urea production, which varied widely over the first 48 hours, low rates being found i...
