Parenteral nutrition in neonates — formative SAQs

SAQ 1 (10)

A 780 g infant is born at 26 weeks' gestation. A umbilical venous catheter is sited at one hour of life and the team asks you to prescribe the parenteral nutrition for the first day. [2] [6]

1. Explain why the very preterm infant needs early aggressive parenteral nutrition. (3) [2]
2. State the day-one starting doses and the ESPGHAN advancement targets for amino acids, glucose (as a glucose infusion rate) and lipid. (4) [6]
3. Outline the daily monitoring schedule and the four complications you actively prevent. (3) [4]

Model answer

1. Most glycogen, fat and protein stores are deposited in the third trimester the infant never completed, so the very preterm carries the smallest reserve at the moment of highest metabolic demand; the fetal protein accretion rate is 3.5 to 4 g/kg/day, the most anabolic period of life. Withholding nutrition flips this anabolic state into negative nitrogen balance within hours, with loss of brain and somatic growth that does not fully recover, so early amino acids directly after birth are a developmental necessity. [2]
2. Day one starts amino acids at 1.5 to 2 g/kg/day, a glucose infusion rate of 4 to 6 mg/kg/min, and lipid at 1 to 2 g/kg/day. Advance over the first days to the ESPGHAN targets of amino acids 3 to 3.5 g/kg/day, glucose infusion rate 10 to 12 mg/kg/min, and lipid 3 to 3.5 g/kg/day, with energy around 110 to 135 kcal/kg/day. [6]
3. Daily monitoring covers glucose each shift, daily weight on a gestation-specific chart, the electrolyte and metabolic panel (sodium, potassium, chloride, bicarbonate, calcium, phosphate, magnesium), triglycerides when advancing lipid, and liver function from the second week. The four complications to prevent are catheter-related bloodstream infection, PN-associated cholestasis (IFALD), metabolic derangement (hyperglycaemia and lipid intolerance), and refeeding syndrome. [4]

SAQ 2 (10)

A term infant who had bowel resection for gastroschisis is on day 28 of parenteral nutrition. The conjugated bilirubin has risen to 120 micromol/L, the liver edge is palpable 4 cm below the costal margin, and the lipid is running at 3 g/kg/day of a pure soybean emulsion with no enteral feeds established. [5] [4]

1. What is the most likely diagnosis and what features support it? (3) [4]
2. List three causes of a rising conjugated bilirubin in a neonate that you would exclude before attributing it to PN. (3) [4]
3. Outline your stepwise management of the liver injury, including lipid modification and the enteral strategy. (4) [5]

Model answer

1. Parenteral nutrition-associated cholestasis, now termed intestinal failure-associated liver disease (IFALD). The features supporting it are the prolonged PN course (day 28), the rising conjugated bilirubin, the hepatomegaly, the high soybean-lipid dose, and the absence of enteral feeding — all established risk factors for IFALD. [4]
2. Biliary atresia (pale stools, dark urine, the postnatal timing); a congenital infection (TORCH); a metabolic or genetic cause such as alpha-1-antitrypsin deficiency or galactosaemia; and a bile-duct obstruction such as a choledochal cyst or sludge. [4]
3. Reduce the soybean-lipid load and switch to a mixed-oil or fish-oil (omega-3) lipid emulsion, which has been shown to improve PN-associated liver injury; advance enteral feeding as aggressively as the residual bowel allows, because enteral bile flow and trophic signalling protect the liver; treat any line sepsis, which itself worsens cholestasis; and involve the hepatology and intestinal-failure team early. For refractory disease, the pathway is home PN with cycling and consideration of bowel-lengthening surgery or transplant. [5]