Hepatic Encephalopathy of ALF

In acute (fulminant) liver failure, hepatic encephalopathy is always present to same extent, and develops due to a precipitous decrease in hepatic function. It is important to determine whether the abnormal mental status in ALF is due to cerebral edema or if it develops in the absence of increased brain water. Clinical examination and radiological methods are limited tools for making this determination, and in hepatic coma, it is frequently necessary to directly measure the intracranial pressure. The importance of confirming or excluding the presence of cerebral edema or intracranial hypertension lies in the different management strategies. In encephalopathic patients without cerebral swelling, management is not significantly different from that described above for chronic cirrhotic hepatic encephalopathy. In contrast, the presence of cerebral edema requires the use of mannitol therapy, infusion of barbiturates, and preparation for urgent liver transplantation. Dietary protein is often withheld while energy substrates are administered intravenously. Bowel cleansing with oral lactulose is reasonable in patients with ALF and mild encephalopathy (stages I and II). Lactulose enemas are better suited for patients with more severe encephalopathy who are less able to cooperate with oral medications and have a risk of aspiration. Correction of metabolic factors and precipitating factors is not different in the ALF patient. Elective endotracheal intubation is recommended at the transition of stage 3 to 4 hepatic encephalopathy in ALF, to minimize risk of pulmonary aspiration and respiratory arrest.

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