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Article
August 14, 1967

Treatment of Hepatic Failure and Coma

Author Affiliations

From the Department of Surgery, Harvard Medical School, and Sears Surgical Laboratories and Fifth (Harvard) Surgical Service, Boston City Hospital.

JAMA. 1967;201(7):547-548. doi:10.1001/jama.1967.03130070067022
Abstract

The liver is the site where most of the important metabolic functions are carried out. Hepatic failure, therefore, involves almost every known synthesis and function. Clinically, it is characterized by jaundice, ascites, progressive emaciation, flap of hands, and physical weakness leading to ataxia and mental confusion. This is followed by stupor, deep coma, and finally death.

The rapidly expanding research into hepatic physiology has provided a basis for much of the modern treatment of hepatic failure. Biochemically, with involvement of most synthetic pathways, there is a deficit in protein synthesis characterized by anemia, reduced serum albumin, and reduced plasma clotting factors. The latter includes reduced fibrinogen and low prothrombin levels aggravated by poor vitamin K absorption. Serum globulins are first increased, then decreased. There is usually an increase in serum bilirubin from either obstruction of the biliary tree or inability to metabolize bilirubin breakdown products. Prolonged hyperglycemia is commonly observed

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