Parenteral Amino Acid and Metabolic Acidosis in Premature Infants

Abstract

Background: Aggressive parenteral nutrition (PN) including amino acids is recommended for low-birth-weight infants to prevent energy and protein deficit. Their impact on acid-base homeostasis has not been examined. Methods: We investigated the impact of dose and duration of parenteral amino acids, with cysteine, on acid-base parameters in 122 low-birth-weight infants. Premature infants ≤32 weeks, ≤1850 g, and receiving parenteral amino acids at 1.5 g/kg/d for an extended period (>24 hours), or 3 g/kg/d for a short (5 hour), extended (24 hour), or prolonged (3–5 days) duration were included in the study. Data were obtained at age 0–3 days (n = 43) or, when clinically stable, age 3–5 days (n = 49). Data from 30 infants, matched for birth weight and gestational age, receiving PN during the first 5 days after birth were also obtained. Acidosis was defined as pH <7.25. Results: Acidosis was evident in all infants between 2 and 5 days after birth. Infants with large patent ductus arteriosus (PDA) exhibited significantly (p < .05) lower pH early, had higher blood urea nitrogen levels (26 ± 9 vs 18 + 8 mg/dL; p < .05), and had greater weight loss (∼17% of birth weight) when compared with infants without PDA. Gestational age, weight loss, and patent ductus arteriosus accounted for 65% of variance in acidosis. Conclusions: Low-birth-weight infants develop metabolic acidosis between 2 and 5 days after birth, irrespective of dose and duration of parenteral amino acid administration. Careful management of parenteral fluids and comorbidities may lower the incidence of acidosis and promote protein accretion.

The association between early parenteral amino acid administration at 1.5 and 3.0 g/kg/d and blood acid-base status was examined in 122 low birth weight (LBW) infants. The data show that all LBW infants develop metabolic acidosis independent of amino acid dose between 2 and 5 days after birth, which is exaggerated by associated comorbidities.

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