Abstract
A PECULIAR neurologic syndrome, combined with alteration in consciousness and culminating in coma, is one of the most serious manifestations of liver failure. Better understanding of the fundamental metabolic changes leading to the development of hepatic coma have resulted lately in improved methods of treatment and prevention. The accumulation of ammonia in the blood and tissues was shown to be at least one of the important factors in the causation of hepatic coma. The ammonia derives from nitrogenous substances of unknown nature which are produced by the normal bacterial flora in the bowel from dietary protein and are absorbed into the portal venous system. An inability of the failing liver to convert ammonia to urea and the presence of natural or artificial shunts between the portal and systemic venous bed, allowing for these substances to bypass the liver, are the two key factors, either one or both of which may result in accumulation of ammonia in the body.
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