ACIDOSIS IN PREMATURE INFANTS DUE TO LACTIC ACID

Abstract
Sixteen premature infants were fed a proprietary lactic-acid milk preparation for 7 to 10 days and were compared to 16 control infants fed non-acidified half-skimmed milk. The experimental group gained less weight (6.5 gm/kg/day) than the controls (14.0 gm/kg/day). This poor weight gain in the experimental group was associated with the production of a metabolic acidosis, the average blood pH decreasing from 7.39 to 7.25, and the average carbon dioxide content in plasma decreasing from 19.6 to 14.8 meq/l. Corresponding averages in the control group showed no appreciable change. A similar study was carried out in six pairs of premature infants, with a formula of half-skimmed milk compared with the identical formula to which lactic acid was added. The results were similar to those in the first study with regard to the poor weight gain and decrease in carbon dioxide content in plasma of the infants fed the acidified milk. Addition of lactic acid to the feeding mixture was followed by a prompt increase in excretion of lactate in the urine, which corresponded to approximately 4% of the lactic acid fed. In four premature infants, 24-hour urine collections demonstrated an increase in excretion of sodium and ammonia, associated with the increased excretion of lactate. The increase in excretion of lactate is considered the major mechanism responsible for the observed acidosis. Studies with intravenous injection of racemic sodium lactate failed to show any deficiency in lactate metabolism in the premature infants. It is suggested that lactic-acid milks not be used for premature infants.
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