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Mineral balance studies in sick preterm intravenously fed infants during the first week after birth. A guide to fluid
C G Aiken1, R A Sherwood, I J Kenney
1Trevor Mann Baby Unit, Royal Sussex County Hospital, Brighton, England.
Insights
Phosphate deficiency occurred in preterm infants receiving intravenous feeding (IVN) regimen X, highlighting the importance of phosphate content in IVN for mineral balance in sick neonates.
Area of Science:
- Neonatal Medicine
- Pediatric Nutrition
- Intensive Care
Background:
- Sick preterm infants often require parenteral fluids and intravenous nutrition (IVN).
- Mineral balance is critical for neonatal outcomes, especially in mechanically ventilated infants.
Purpose of the Study:
- To assess mineral balance, specifically calcium and phosphate, in sick preterm infants receiving different intravenous feeding regimens.
- To evaluate the impact of IVN phosphate content on mineral retention and acid-base status.
Main Methods:
- Mineral balance studies were conducted in 61 preterm infants (24-35 weeks gestation).
- Two balance periods: initial 48 hours with maintenance fluids, followed by 7 days of IVN (regimen X or Y).
- Regimens differed in phosphate content (X: 7.3 mmol/L, Y: 11.6 mmol/L) but had identical calcium (9.5 mmol/L).
Main Results:
- Phosphate deficiency developed in infants on regimen X, with higher urine calcium, lower calcium retention, and lower plasma phosphate compared to regimen Y.
- Renal function (urine output, creatinine clearance) was initially low and related to oxygen requirements and gestational age, improving after 48 hours.
- Metabolic acidosis in the first 48 hours was linked to increased non-protein acids; at 7 days, it was associated with base loss via urine.
Conclusions:
- IVN phosphate content significantly impacts calcium and phosphate balance in preterm infants.
- Renal function and acid-base status in sick preterm infants are dynamic and influenced by fluid management and underlying conditions.
- Optimizing IVN composition is crucial for preventing mineral deficiencies and managing acid-base disturbances in vulnerable neonates.
Abstract:
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 regimen Y. 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.(ABSTRACT TRUNCATED AT 400 WORDS)