Hepatobiliary abnormalities and parenteral nutrition

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral elimentation (continuous or bollous) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.