NECROTIZING ENTEROCOLITIS AND TOTAL PARENTERAL NUTRITION-ASSOCIATED CHOLESTASIS

The proportion of patients with total parenteral nutrition (TPN)-assoc iated cholestasis (TPN-AC) who have necrotizing enterocolitis (NEC) ha s increased markedly in the past ten years. Little is known about how these diseases affect each other. We retrospectively studied 24 patien ts with NEC and bowel necrosis or perforation who required surgical in tervention. Patients were divided into two groups: those who had recei ved TPN (NEC + TPN, n = 17) and those who had not (NEC, n = 7). As cho lestasis was present clinically. or prolonged TPN was anticipated, liv er biopsy was done. Bile acid levels were measured in both serum and b ile in 13 patients. Six patients, who underwent bowel resection and en terostomy, had a second liver biopsy and measurement of bile acid leve ls at stoma closure. Our results showed that in 13 patients for whom b ile acid levels were measured (NEC + TPN, n = 6) (NEC, n = 7), serum b ile acid level was significantly elevated in both groups over normal f or age. Biliary bile acid levels were correspondingly depressed in bot h groups suggesting a failure of bile acid transport. All patients had abnormal liver histology, but the pattern of injury differed between the two groups. Those in the NEC group had biliary stasis and mild hep atocyte degeneration. In contrast. 15 of 17 in the NEC + TPN group had advanced injury specific for TPN-AC, All six patients managed on TPN and partial enteral feeding before a second biopsy had no change in bi le acid levels and progression of histologic injury. We conclude that NEC alone can cause functional cholestasis and histologic liver injury but does not cause the specific progressive damage caused by TPN. NEC map make the liver more susceptible to the effects of TPN. Partial en teral feeding does not halt or reverse this injury.