Acute fulminant hepatitis leads to complex biochemical and circulatory disturbances including coma. These can be predicted to some extent by knowledge of the functions of the normal liver cells. Ineffective haemostasis, coma, hypoglycaemia, electrolyte abnormalities, hypotension and renal circulatory failure are particularly important.
Management should be governed by the abnormalities found in the individual patient. Fluid overload and sedation must be avoided. More complex methods of temporary hepatic support such as exchange transfusion or perfusion of the isolated pig's liver should only be considered after simpler methods of correction have been attempted for a reasonable period of time and found wanting.
The prognosis of acute hepatocellular failure reaching the stage of deep coma is very poor, the mortality being about 80-90%.
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