Liver Complications

The incidence of liver complications associated with PN ranges from approximately 7% to 84%, and end-stage liver disease develops in as many as 15% to 40% of adult

patients on long-term PN. Patients often develop a mild increase in liver enzymes within 1 to 2 weeks of initiating PN, but this generally resolves when PN is discontinued. Severe liver complications include hepatic steatosis (fat deposition in liver), steatohepatitis (a severe form of liver disease characterized by hepatic inflammation that may progress rapidly to liver fibrosis and cirrhosis), cholestasis, and cholelithias-is.38

Hepatic steatosis usually is a result of excessive administration of carbohydrates and/or lipids, but deficiencies of carnitine, choline, and essential fatty acids also may contribute. Hepatic steatosis can be minimized or reversed by avoiding overfeeding, especially from dextrose and lipids.38 Carnitine is an important amine that transports long-chain triglycerides into the mitochondria for oxidation, but carnitine deficiency in adults is extremely rare and is mostly a problem in premature infants and patients receiving chronic dialysis. Choline is an essential amine required for synthesis of cell membrane components such as phospholipids. Although a true choline deficiency is rare, preliminary studies of choline supplementation to adult patients' PN showed reversal of steatosis.

Cholestasis is a common problem in patients who are dependent on PN. Factors that predispose PN patients to cholestasis include overfeeding, lack of bowel stimulation, bowel rest (decrease in cholecystokinin secretion), long duration of PN,

short-bowel syndrome, bacterial overgrowth and translocation, and sepsis. Patients may exhibit increased liver transaminases, increase alkaline phosphatase and gamma-glutamyl transferase concentrations, and mainly increased bilirubin concentrations with jaundice. The most sensitive marker of cholestasis is an increased serum conjugated bilirubin concentration of 2 mg/dL (34.2 |imol/L) or more.38 Cholestasis generally is reversible if PN is discontinued before permanent liver damage occurs. Serum liver enzyme concentrations may take up to 3 months to return to normal after discontinuing PN. Steps to prevent cholestasis associated with PN include early initiation of enteral or oral feedings, using a balanced PN formulation, avoiding overfeeding,

cyclic PN infusion, and treating and avoiding sepsis. Limiting IV lipid emulsion infusion to 1 or 2 times weekly at a dose no less than to prevent essential fatty acid deficiency may also decrease serum bilirubin concentrations and improve cholestas-is. Pharmacologic treatments include ursodeoxycholic acid (ursodiol), which may improve bile flow and reduce the signs and symptoms of cholestasis. However, ursodiol is only available in an oral dosage form, and absorption may be limited in patients with intestinal resections. If other measures are not successful, and bacterial overgrowth is thought to be contributing to cholestasis, courses of oral metronidazole, oral gentamicin, or oral neomycin have been used to reduce bacterial overgrowth.

Cholelithiasis can develop as a result of decreased gallbladder contractility, especially in the absence of enteral or oral intake. Lack of intestinal stimulation reduces secretion of cholecystokinin, a peptide hormone secreted in the duodenum that induces gallbladder contractility. The best prevention of cholelithiasis is early initiation of enteral or oral feeding, as stated earlier (to stimulate secretion of cholecystokinin, gallbladder contraction and emptying, and intestinal motility). Pharmacologic treatment with cholecystokinin-octapeptide (sincalide) to stimulate gallbladder contraction and bile flow does not prevent PN-associated cholestasis or improve serum conjugated bilirubin concentrations.

Monitor liver function tests, including serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, total bilirubin, and conjugated bilirubin, at the initiation of PN and regularly thereafter during PN therapy. The frequency of monitoring liver function tests depends on the presence or absence of liver disease. This varies from one to two times weekly in the acute setting to once weekly to once monthly in the stable home PN patient.

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