Hepatobiliary complications associated with TPN: an enigma.

Despite the fact that the clinical experience with TPN has been gathered from patients of all age groups suffering from a variety of underlying diseases running very different clinical courses and often complicated by a number of septic metabolic and therapeutic problems, certain points can be made with regard to predisposing factors. 1) Prematures and neonates are particularly at risk. 2) Cholestasis occurs earlier and has a greater chance of leading to chronic liver disease in surgical patients. 3) Hepatobiliary abnormalities are more likely to develop after a prolonged period of TPN and are less frequent in patients who are also receiving oral feedings. Definition of the mechanism of hepatobiliary complications remains a problem. Although calcium bilirubinate appears to be responsible for sludge and stones, there is as yet no explanation for the presence of large amounts of indirect-reacting bilirubin in gallbladder and hepatic bile in patients on TPN. The pathogenesis of cholestatic liver disease remains an enigma; the lack of normal gastrointestinal stimuli for bile formation, abnormalities of bile acid metabolism, and sepsis might play roles, but attention has recently been attracted to amino acid toxicity and this possibility deserves further study.