Parenteral Amino Acid and Metabolic Acidosis in Premature Infants

Abstract

OBJECTIVE: Aggressive parenteral nutrition 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. PATIENTS AND 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, <1850g and receiving parenteral amino acids at 1.5g·kg -1 ·d -1 for an extended period (>24h), or 3g·kg -1 ·d -1 for a short (5h), extended (24h) or for 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 thirty infants matched for birth weight, and gestational age and receiving parenteral nutrition during the first five 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<0.05) lower pH early, had higher blood urea nitrogen levels (26 ± 9 vs. 18+8 mg/dl, p<0.05) and had greater weight loss (∼17% of birth weight), when compared with babies 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 2-5 days after birth irrespective of dose and duration of parenteral amino acid administration.. Careful management of parenteral fluids and co-morbidities may lower the incidence of acidosis and promote protein accretion.Précis-The association between early parenteral amino acid administration at 1.5 and 3.0g·kg -1 ·d -1 and blood acid base status was examined in 122 low birth weight infants. The data show that all LBW infants develop metabolic acidosis independent of amino acid dose between 2-5 days after birth, which is exaggerated by associated co-morbidities.

Response of Chicken Ductus Arteriosus to Hypercarbic and Normocarbic Acidosis

“…Moreover, the incidence of patent DA does not appear to be augmented in the preterm newborns exposed to permissive hypercarbia [40] . On the other side, respiratory acidosis requiring increased ventilator rates and peak airway pressures is frequently observed in infants with patent DA [1,2] , and it has been reported that a correlation between metabolic acidosis and large patent DA exists [7] . In the present study, we demonstrated that clinically accepted acidosis produces significant relaxation of the DA.…”

“…Respiratory and metabolic acidosis are frequent events in the clinical course of very preterm infants [1][2][3][4][5][6][7] . Changes in pH can have a profound influence on pulmonary and systemic vascular resistance, and on the reactivity of the vessels to agonists.…”

Effect of Aggressive Early High-Dose Intravenous Amino Acid Infusion and Early Trophic Enteral Nutrition on Very Low Birth Weight Infants

“…However, previous study from Ridout et al showed no relationship between BUN and amino acid intake [15]. Jadhav looked at the relationship between metabolic acidosis and amino acid intake but did not find a correlation [16]. There is no scientific reason to explain why VLBW infants should not be offered 3 to 3.5 g/kg/d of amino acids immediately after birth.…”

Application of Parenteral Nutrition in Premature Infants

“…Современные данные, оценивающие аминокислот-ный состав парентерального питания, свидетельствуют о том, что аминокислоты могут быть быстро введены без метаболических нарушений даже у больных детей, не вызывая ацидоз [41,42]. Необходимо подобрать такое количество белка, которое позволит избежать его большего дефицита, который обычно возникает в 1-ю нед жизни новорожденного.…”