Hepatobiliary complications in healthy, intra-abdominally infected, and high-output fistula rats receiving total parenteral nutrition.

Abstract

This study examines the pathophysiology of hepatobiliary complications induced by total parenteral nutrition (TPN) by using animal models that underwent cecal ligation to produce intra-abdominal infection and received an enterostomy to mimic a high-output fistula, which causes the interruption of enterohepatic circulation of bile salt. Aspartate transaminase was elevated after TPN (p < .05). Alkaline phosphatase was increased in animals receiving TPN plus an enterostomy (p < .05). Serum albumin was significantly decreased in animals receiving TPN plus undergoing cecal ligation or enterostomy (p < .05). Liver weight and liver protein and water content decreased in animals receiving TPN alone (p < .05). Liver water content increased in animals receiving TPN plus undergoing cecal ligation (p < .05). Liver lipid content increased after TPN and to a significant degree in rats receiving TPN plus undergoing cecal ligation or enterostomy (p < .05). Bile flow diminished after TPN and to a level reaching significance in animals receiving TPN plus undergoing cecal ligation or enterostomy (p < .05). Reduction of bile flow, decrease of biliary cholesterol secretion, and increase of biliary bilirubin secretion, which may be the cause of TPN-induced bilirubinate stones, were most significant in animals receiving TPN plus undergoing cecal ligation (p < .05). In conclusion, TPN can induce hepatic dysfunction and bilirubinate stones, but these complications are more common in animals with associated intra-abdominal infection or high-output fistula.