Liver failure nutrition support

Liver disease is managed conventionally, maintaining appropriate nutritional support and managing the complications of portal hypertension and hepatic failure as they occur. We counsel heterozygote parents of a PIZZ... 

In a retrospective study of the incidence of cholestasis and liver failure in 42 patients with intestinal resection in the neonatal period who subsequently became dependent on parenteral nutrition support, the effect of various associated clinical factors on the incidence and severity of cholestasis was determined (103). Cholestasis developed in 28 while they were receiving parenteral nutrition. In 21 patients, the raised direct bilirubin concentration returned to normal while they continued to receive parenteral nutrition. Seven patients progressed to liver failure. Patients without cholestasis had been dependent on parenteral nutrition for longer than patients with cholestasis. It was clear from this study that cholestasis in neonates with intestinal resection is not simply a function of the duration of exposure to intravenous nutrition. 

Hypokalemia is common in the patient with liver failure who has normal renal function. Poor nutritional intake and vomiting may initiate this disorder. Severe vomiting may lead to volume contraction metabolic alkalosis, with increased renal excretion of potassium. Secondary hyperaldosteronism, seen in the liver failure patient with intravascular depletion, also increases renal excretion of potassium. Loop diuretic therapy causes increased renal excretion of potassium, whereas diarrhea from lactulose therapy increases fecal excretion of potassium. All these conditions can lead to profound hypokalemia. Therefore, potassium requirements in the liver failure patient receiving specialized nutritional support often are increased substantially. 

The major controversy in nutritional support of the patient with liver failure has centered around the use of protein products. Modified amino acid solutions for PN (HepatAmine, others) are marketed for patients with liver failure and hepatic encephalopathy. They are enriched with BCAAs and have reduced amounts of AAAs and methionine. The products are formulated on the basis of the false neurotransmitter hypothesis, which concludes that hepatic encephalopathy may be due to increased AAA concentrations in the central nervous system. 

Moriwaki H, et al. Nutritional pharmacotherapy of chronic liver disease From support of liver failure to prevention of liver cancer. J Gastroenterol 2000 35(Suppl 12) 13-17. 

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