Abstract
Hepatic coma is a serious complication of advanced liver disease. It may occur secondary to hemorrhage from gastroesophageal varices, after operation for portal decompression, or in the final stages of hepatic decompensation. The prognosis varies with the severity of the underlying liver disease and the recuperative powers of the liver. Although the metabolic derangements associated with hepatic coma are not completely known, elevated levels of blood ammonia are found with reasonable consistency.1,2This has been recognized since 1896 when Nencki and Pawlow3related blood ammonia elevations with meat intoxication. McDermott and Adams,4Mann et al,5and Levine and Rigler6showed that blood ammonia levels often rose after portacaval anastomosis. Protein digestion in the gastrointestinal tract is a major source of ammonia. The products of digestion, including ammonia, are absorbed and carried by the portal vein. The normal liver can readily detoxify ammonia by converting it
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