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KMID : 0381219750070060375
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Journal of RIMSK
1975 Volume.7 No. 6 p.375 ~ p.378
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Hepatic Coma
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Abstract
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In the pathogenesis of hepatic coma, many factors have been shown to be the actual cause. Most studies have shown that ammonia is an important factor of exogenous hepatic coma. Ammonia absorbed from the intestine is not metabolized by the liver before reaching the cerebral circulation. Many patients with hepatic coma have elevated systemic arterial and venous blood levels of ammonia.
Many toxic substances other than ammonia, such as indol and phenol, are involved in the genesis of hepatic coma. The liver is believed to produce substances that are essential for normal brain metabolism, and in liver failure these may be reduced. Such decreased essential factors may induce endogenous hepatic coma.
In the prevention of hepatic coma careful use of diuretics, sedative or tranquilizer and the prevention of infection are necessary. There are several basic steps in therapy including general measures such as providing nitrogen-sparing calories, reduction of blood ammonia level, ncaprotein diet, evacuation of colonic contents by laxatives and fleet enema, administration of necmycin to decrease the intestinal production and absorption of ammonia, and correction of the factors that potentiate or compound coma including hypokalemia, infection, anemia and gastrc ntestinal bleeding. And some heroic measures such as exchange blood transfusion, hemodialysis, extracorporeal pig-liver perfusion, and liver hemotransplantaticn have been tried and produced temporary improvement of mental and neurologic function in scme cases.
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