Nutritional support of patients with severe hepatic failure

Abstract

The pathophysiology, etiology, and metabolic alterations of severe hepatic failure and nutritional support of patients with this condition are reviewed. Hepatic failure encompasses a broad range of acute and chronic processes; complications may be fatal or quite minimal. Cirrhosis refers to all types of chronic diffuse liver disease. While hepatocytes regenerate in cirrhotic patients, eventually the parenchymal and vascular architecture of the liver is disrupted, leading to a syndrome of hepatic insufficiency. Normal metabolic processes deteriorate, and serum amino acid imbalances and fat intolerance may develop. Aromatic amino acids, which are normally catabolized by the liver, accumulate in the serum, and branched-chain amino acid deficiencies develop as these amino acids are broken down for energy by peripheral muscle. Hepatic encephalopathy often develops in these patients. Successful nutritional support of the patient with severe hepatic failure depends on correction of the specific metabolic abnormalities occurring. Parenteral nutrition with Hepatamine (American McGaw), a product with more branched-chain amino acids and less aromatic amino acids than other amino acid solutions, is useful in patients with altered serum amino acid profiles who develop hepatic encephalopathy. Patients in whom factors other than altered amino acids are primary causes of encephalopathy may not respond to Hepatamine. Enteral nutritional products with amino acid compositions similar to Hepatamine [Hepatic-Aid II (McGaw), Travasorb-Hepatic (Travenol Laboratories)] may be used in patients with encephalopathy, but they must be supplemented to provide complete nutrition.(ABSTRACT TRUNCATED AT 250 WORDS)