Hepatic Encephalopathy, Hepatocerebral Intoxication, Portal-Systemic Encephalopathy
What is Hepatic coma?
Hepatic coma is loss of consciousness due to liver failure. Liver failure occurs because the liver tissue has been irreversibly and progressively destroyed (cirrhosis) as a result of infection, poison, or other disease. Hepatic coma is characterized as the final stage of hepatic encephalopathy, a condition in which the brain is poisoned by the toxic elements from the liver, which is no longer capable of properly filtering the blood to remove toxins. Bleeding into the intestinal tract may significantly increase the amount of protein in the bowel and may precipitate rapid development of hepatic coma.
How is it diagnosed?
History: A history of liver disease is present. Hepatic encephalopathy often follows a clearly identifiable precipitating event. The most common predisposing factor is gastrointestinal bleeding, which leads to an increase in the production of ammonia and other nitrogenous substances, which are then absorbed. Increased dietary protein may also precipitate hepatic encephalopathy. The syndrome may evolve over a period of days to weeks. Prior to coma, the individual exhibits a change in personality, confusion, drowsiness and tremulousness. An irregular flapping movement of the hands when the arms are extended (asterixis) is a common feature of hepatic encephalopathy. The individual may fall into a stupor and then a coma.
Physical exam: Examination of an individual experiencing hepatic coma shows a progressive involvement of the nervous system from higher to lower levels. The pupils usually still react to light and the brain stem reflexes are retained. Consciousness is progressively impaired.
Tests: Blood tests will show an increase in ammonia levels, an index of the degree of accumulation of toxins. Measurement of brain activity (EEG) will show abnormalities. Severe brain edema, which can be visualized by MRI, occurs commonly. There are no diagnostic liver function tests.
How is it treated?
Treatment of hepatic coma and encephalopathy is aimed at elimination or treatment of precipitating factors and lowering the blood ammonia levels by decreasing the absorption of protein and nitrogenous products from the intestine. Ammonia absorption can be decreased by the administration of a nonabsorbable disaccharide that acts as an osmotic laxative. Dietary protein restriction is necessary. In severe liver disease, liver transplantation is necessary.
What might complicate it?
Individuals who survive one or more episodes of hepatic coma are occasionally left with residual neurologic abnormalities, such as tremor of the head or arms, asterixis, grimacing, choreatic twitching of the limbs, dysarthria, ataxia of gait, or impairment of intellectual functioning. These symptoms may worsen with repeated attacks of stupor and coma.
In severe cases, the coma is irreversible and death occurs. If the underlying disease is reversible, treatment is usually effective.
Differential diagnoses include acute alcohol intoxication, sedative overdose, delirium tremens, Wernicke's encephalopathy, Korsakoff's psychosis, subdural hematoma, meningitis, and hypoglycemia.
Internist, neurologist and general surgeon.
Last updated 17 November 2011