Hepatic encephalopathy in liver cirrhosis: pathogenesis, diagnosis and management

T Gerber, H Schomerus
Drugs 2000, 60 (6): 1353-70
The pathogenesis of hepatic encephalopathy (HE) is unknown. Many theories have been proposed. Most established therapies are based on such theories but since no theory has have ever been proved, therapies have to be considered empiric. The spectrum of HE ranges from minimal cerebral functional deficits, which can only be found by sensitive psychometric tests, to coma with signs of decerebration. HE has arbitrarily been divided into stages. A number of precipitating factors are known and the first line of therapy should always be the elimination of these factors. The differential diagnosis includes all states of impaired consciousness and deficits in cerebral function in patients with chronic liver disease, and clinical and biochemical tests to differentiate are indicated. The therapeutic options for HE include: protein restriction only for a limited time in comatous patients; nonabsorbable antibiotics (aminoglycosides), which because of adverse effects are also limited to higher grades of HE: intestinal cleansing which is applicable in all degrees of HE; lactulose, branched chain aminoacids and ornithin aspartate which have been proven to be effective and can be applied long term in patients with lower grades of HE.

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