Hypoglycemia develops at some time in almost 50 per cent of patients with ALF (MunozJ993). It should be prevented by a continuous infusion of 10 per cent glucose and must be considered during any deterioration in mental state. Both hyper- and hyponatremia may be present. The former is a consequence of treatment of cerebral edema with dehydration and is treated by judicious rehydration. Hyponatremia appears to be dilutional and is managed by volume restriction. Hypokalemia is present in approximately 50 per cent. It is closely related to the presence of metabolic alkalosis and may be both cause and result of this abnormality. It is treated with potassium supplementation, intravenously or via the nasogastric tube. Primary respiratory alkalosis is common in patients allowed to breathe spontaneously. It is a consequence of hepatic encephalopathy but the mechanism is unknown. No treatment is usually necessary. Metabolic alkalosis occurs in 25 to 50 per cent of patients; predisposing factors are hypokalemia and, perhaps, the liver's inability to synthesize urea. The treatment is correction of hypokalemia. Metabolic acidosis is common in patients with acetaminophen poisoning and is the most reliable indicator of a poor prognosis in this group. In other patients it is almost always associated with severe circulatory compromise. Management involves correction of the underlying cause, where possible. Nutritional therapy can be provided using conventional nutritional solutions, preferably by the enteral route. Caloric requirements are increased in ALF because of the markedly elevated basal energy expenditure. There is no evidence that protein restriction improves the outcome. Branched-chain amino acid solutions have not been shown to improve encephalopathy or overall mortality rate.
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