IN recent years numerous publications have dealt with the pathogenesis and treatment of hepatic coma. The protean nature of the neurologic disturbances associated with liver failure and the absence of specific neuropathological findings suggest that "hepatic coma" is metabolic in origin.1 Although deranged nitrogen metabolism and the effects of ammonia and amines on brain cells have been implicated in the pathogenesis of this encephalopathy2 it is clear that the syndrome is not due to any single agent. However, the management of these patients is based upon the known biochemical abnormalities3 and includes the elimination of all protein from the diet . . .
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Trey et al. (1966) studied this question.
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