Parenteral nutrition in neonates — viva

Stem

The examiner hands you the prescription chart for a 780 g infant born at 26 weeks, now two hours old, with a umbilical venous catheter in place. The team asks you to start parenteral nutrition. [3]

Examiner: What is your opening approach to prescribing PN for this infant? [3]

Strong answer: I would frame PN as a bridge, not a destination, and begin early aggressive nutrition to prevent the catabolic crisis of extreme prematurity. Within the first hours of life I would start 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, then advance to the ESPGHAN targets over the first days. I would secure central access, protect the line with a dedicated lumen and a no-break policy, and set up the daily monitoring of glucose, weight, electrolytes, triglycerides and liver function. [4] [3]

Branch 1 — Definition and classification

Examiner: How do you classify parenteral nutrition, and how does that frame your prescription? [1]

Strong answer: I classify PN by three axes: route, indication and timing. By route, PN is central or peripheral, dictated by osmolarity — central access tolerates osmolarity above 900 mOsm/L and concentrated glucose, while peripheral nutrition must stay below 900 mOsm/L with glucose no stronger than 12.5%. By indication, the three groups are the nutritional bridge (the extreme preterm), the gastrointestinal or surgical group (NEC, gastroschisis, short bowel), and the critical-illness group. By timing, PN is early aggressive, standard or long-term. This infant is a central, bridge, early-aggressive case. [1]

Examiner probe: Why is the route dictated by osmolarity, and what access would you use here? [1]

Strong answer: Concentrated glucose and amino acids are hyperosmolar and sclerose peripheral veins, so any PN with glucose above 12.5% or an osmolarity above 900 mOsm/L must run centrally. For this infant I would use the umbilical venous catheter for the first days and then transition to a peripherally inserted central catheter for the duration of PN. [1]

Branch 2 — Targets and advancement

Examiner: What are the ESPGHAN targets, and how do you advance to them? [4]

Strong answer: The ESPGHAN 2018 targets are amino acids 3 to 3.5 g/kg/day, a glucose infusion rate of 10 to 12 mg/kg/min, lipid 3 to 3.5 g/kg/day, and energy around 110 to 135 kcal/kg/day. I start at roughly half the target — amino acids 1.5 to 2 g/kg/day, glucose infusion rate 4 to 6, lipid 1 to 2 — and advance daily, adding electrolytes, calcium, phosphate, trace elements and vitamins as the prescription and the infant allow. I monitor glucose each shift, weigh daily, run the metabolic panel, and check triglycerides when advancing lipid. [4]

Examiner probe: What does the evidence say about early amino acids? [3]

Strong answer: The te Braake study showed that amino acids started directly after birth prevent negative nitrogen balance and support protein accretion without the metabolic harm once feared, and the Cochrane review confirms the rationale for early amino acids in preterm infants. This is the evidence that makes early aggressive PN the standard for the ELBW preterm. [3]

Branch 3 — The PEPaNIC lesson (a trap)

Examiner: The PEPaNIC trial showed that late parenteral nutrition reduced infections and shortened stay in critically ill children. Why do you still start early PN in this preterm infant? [2]

Strong answer: PEPaNIC studied critically ill children in PICU, where late PN to day 8 reduced new infections and shortened stay. That is a real finding, but it does not extrapolate to the ELBW preterm, whose developmental need for early protein accretion is non-negotiable. For the very preterm, withholding early amino acids drives the catabolic crisis that PN exists to prevent — so I hold both truths: early PN for the preterm, and a late-PN strategy for the critically ill older child. [2]

Examiner probe: On day 28 of PN the conjugated bilirubin rises and the liver enlarges. What is happening, and what do you do? [5]

Strong answer: This is parenteral nutrition-associated cholestasis, now called IFALD, driven by the prolonged PN, the soybean-lipid load and the absence of enteral feeding. I would reduce the soybean lipid, switch to a mixed-oil or fish-oil (omega-3) emulsion — the Puder data show fish oil improves PN-associated liver injury — advance enteral feeding as aggressively as the residual bowel allows, treat any line sepsis, and involve hepatology and the intestinal-failure team early, because early modification can reverse IFALD whereas late disease can progress to irreversible liver failure. [6] [5]