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Hyperalimentation with amino acid and casein hydrolysate solutions. Mechanism of acidosis.

Four premature infants aged 1 to 2 weeks and one 10-year-old child who developed metabolic acidosis (base excess [BE], —9 to —17 mEq/liter) with continuous intravenous amino acid alimentation for extended periods were studied before, during, and after the development of acidosis, to test the hypothesis that the acidosis is secondary to the excessive hydrogen ion (H+) intake from these casein hydrolysate and amino acid infusates. The net acid excretion (NAE) consisted of the sum of urinary titratable acid plus ammonium ion (NH 4 + ) minus bicarbonate radical (HCO 3 - ). The net acid input (NAI) consisted of the endogenous acid production plus the exogenous acid intake from the amino acid infusion. In all cases, metabolic acidosis developed whenever the NAI exceeded the NAE, and recovery occurred whenever the infusates were stopped or continued with a half-strength solution, allowing the NAE to exceed the NAI.