Abstract
AbstractThe coma which develops during acute hepatic failure has been attributed to the accumulation of toxic metabolites, since coma is potentially fully reversible without residual sequelae and there are no important structural changes in the brain of these patients [1]. Removal of these toxins might accelerate arousal and thereby improve survival by preventing cerebral edema and other complications of coma. Ultimately these complications are often the cause of death in many instances of acute hepatic failure, even in patients whose livers are beginning to regenerate [2].
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