Fetuses receive a continuous infusion of parenteral nutrients via the placental circulation. The fetus receives a high carbohydrate, high protein, low fat intake from the mother. Amino acids are used by the fetus for rapid protein accretion and as an oxidizable energy substrate.
Trophamine is the amino acid solution used to provide parenteral protein intake to neonates at Vanderbilt.
Adequate protein is essential for growth in the neonate. Research indicates that when adequate protein is provided to the premature infant it has long term growth benefits with increases in linear and OFC growth post discharge. The following table serves as a guide to provide adequate protein intake according to current weight of the preterm infant.
From: Reynolds and Thureen. 2007
Initiating parenteral protein intake
To stem catabolism, premature infants < 1500g birthweight should be started on admission iv fluids containing 40g/L Trophamine. This amount of Trophamine provides 2-3g/kg amino acids and 2 g/kg amino acids to a 500g infant when administered at a typical rate of 100 ml/kg/d.
>1500g infants can begin Trophamine in TPN at 3 g/kg/d.
Advancing parenteral amino acid intake
Amino acid intake should be advanced in 1 g/kg/d increments daily to a goal of 3 g/kg/d in most infants. Extremely-low-birth-weight infants may be advanced to 3.5 g/kg/d (or even 4 g/kg/d amino acid intake those <750g birthweight) in consultation with the patientís attending.
Amino acid intakes of >3g/kg/d should not be used in infants experiencing metabolic acidosis or in infants with azotemia (BUN .40) due to dehydration or renal insufficiency. Furthermore, to optimize protein accretion, one should strive to maintain a non-protein calorie : nitrogen ratio of 150-200:1. Non-protein caloric intake should be provided as a balance of carbohydrate and fat. To achieve an appropriate NPC:N ratio, one should aim to provide 30 kcal/kg non-protein calories for every 2 g/kg/d amino acid intake.
When the patient it tolerating an enteral intake of > 50 mL/kg/d, the parenteral amino acid intake should be decreased to 2 g/kg/d and kept at that amount until TPN is discontinued (once an enteral intake > 100 mL/kg/d is achieved.)
Cysteine may be a conditionally essential amino acid in neonates important in the synthesis of endogenous antioxidants. However, cysteine is not stable in routine TPN preparations and must be added separately. Cysteine is added as Cysteine HCl (30mg/g protein) and may contribute to a metabolic acidosis in VLBW infants.
Cysteine should not be added to TPN until the patient is tolerating a protein intake of 3 g/kg/d without a metabolic acidosis (pH < 7.3 or base deficit > -6 mEq/L.) In a patient who develops an unexplained metabolic acidosis after the first weeks of life, other etiologies should be sought; however, cysteine may need to be eliminated from the TPN until the problem is corrected.
Zlotkin SH, Bryan MH, Anderson GH. Intravenous nitrogen and energy intakes required to duplicate in utero nitrogen accretion in prematurely born human infants. J Pediatr 1981; 99: 115-120.
Rivera A Jr, Bell EF, Bier DM. Effect of intravenous amino acids on protein metabolism of preterm infants during the first three days of life. Pediatr Res 1993; 33: 106-111.
Thureen PJ, et al. Protein balance in the first week of life in ventilated neonates receiving parenteral nutrition. Am J Clin Nutr 1998; 68: 1128-1135.
Van Goudoever JB, et al. Immediate commencement of amino acid supplementation in preterm infants: Effect on serum amino acid concentration and protein kinetics on the first day of life. J Pediatr 1995; 127: 458-465.
Laine L, et al. Cysteine usage increases the need for acetate in neonates who receive total parenteral nutrition. Am J Clin Nutr 1991; 54: 565-567.
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