High lipid, low dextrose parenteral nutrition allows patient to achieve nutritional autonomy: A case report

Prolonged use of parenteral nutrition can eventually lead to liver abnormalities. Causative factors include decreased enteral stimulation, high intakes of intravenous dextrose, proinflammatory 100 % soybean oil-based lipids, and increased burden on liver through 24-h infusions. We present a case report of a patient who received parenteral nutrition modifications to address liver dysfunction.

Our patient was a 37-year-old African American male with a past medical history including refractory Crohn's disease complicated by multiple small bowel obstructions, several bowel surgeries, left lower quadrant colostomy placement, short bowel syndrome, severe protein calorie malnutrition, parenteral nutrition dependence, and elevated liver function tests. He was admitted for nutritional optimization before a planned takedown of multiple chronic enterocutaneous and perianal fistulas. His home parenteral nutrition order contained high amounts of dextrose (69 % kcal), and low amounts of 100 % soybean oil (11 % kcal).

Due to an elevated alkaline phosphatase level at baseline (1746 U/L), the Registered Dietitian maximized protein, decreased the dextrose by 62.5 %, and changed to SMOFlipid (a fish-oil containing lipid) at >1 g/kg/day to address liver abnormalities. Within 1.5 months of changing parenteral nutrition to high SMOFlipid (>30 % kcal) with low dextrose (<30 % kcal) content, alkaline phosphatase levels declined by 62 %, prealbumin levels increased by 56 %, and c-reactive protein levels decreased by 62 %.

Parenteral nutrition modifications led to reversal of chronic liver dysfunction. This patient ultimately underwent a successful high-risk fistula takedown procedure, allowing for complete weaning of parenteral nutrition and achievement of sustained nutritional autonomy.