Abstract
Gastrointestinal bleeding threatens the cirrhotic patient with exsanguination and a frequently fatal disturbance of the central nervous system. The understanding and treatment of blood loss is more advanced than the control of hepatic coma. In 1896 Nencki and Pawlow1indicted blood ammonia in meat intoxication. McDermott,2Mann,3and Levine4demonstrated that blood ammonia levels were frequently elevated after an Eck fistula. McDermott,2correlated these elevations with the episodic stupor following portal systemic anastomosis. An increase of blood ammonia is common in hepatic coma.5,6The experimental elevation of blood ammonia produced a neurological syndrome similar to hepatic coma.7-9Gastrointestinal administration of protein, especially blood, in these experiments confirms the clinical necessity of controlling blood loss, eliminating the blood lost, and reducing the metabolism of blood retained in the stomach and intestines. Blood digested in the gastrointestinal tract causes a prompt rise in the portal
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