HEPATIC COMA, characterized by a flapping tremor, disturbed consciousness, and electroencephalographic changes, may occur in patients with cirrhosis of the liver or with portacaval shunts.1 It is generally believed that under such circumstances toxic substances absorbed from the intestine may escape the normal detoxification processes in the liverand hence enter the systemic circulation and reach the brain. The identity of the toxic agent (or agents) in hepatic coma has not been fully established, but considerable evidence has accrued to implicate ammonia in this respect. Ammonia is normally present in appreciable amounts in the portal vein, due to intestinal absorption of ammonia derived from the bacterial breakdown of nitrogenous foodstuffs. Ordinarily this ammonia, together with the endogenous ammonia arising from the deamination of amino acids, is converted to urea by the liver, but in the presence of liver disease, or if the liver is bypassed, appreciable amounts may enter the
AMMONIA TOXICITY AND HEPATIC COMA. JAMA. 1959;169(10):1076. doi:10.1001/jama.1959.03000270058013
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