INTRODUCTION

Hepatic encephalopathy describes the spectrum of potentially reversible neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of unrelated neurologic and/or metabolic abnormalities. The term implies that altered brain function is due to metabolic abnormalities that occur as a consequence of liver failure. The full reversibility of symptoms after improvement of liver function is considered to be direct proof of this causal relation.

This definition is easy to apply in previously healthy patients presenting with acute liver disease and overt neuropsychiatric symptoms. It is more difficult to apply to patients with chronic liver diseases who have only mild to minimal signs of altered brain function, particularly in settings in which the underlying cause of the liver disease may be associated with neurologic manifestations (such as alcoholic liver disease or Wilson's disease). The problem in defining hepatic encephalopathy precisely is not just a matter of semantics, but has major implications in the design and evaluation of clinical studies on diagnosis and treatment of this syndrome.

A generally accepted nomenclature could provide a solution to this debate and provide a standard for clinical studies. To achieve this goal, the World Organization of Gastroenterology (OMGE) commissioned a Working Party to reach a consensus in this area. A group of experts proposed a consensus statement at the 11th World Congress of Gastroenterology in Vienna in 1998 (table 1) [1]. A classification of hepatic encephalopathy has also been proposed (table 2).

CLINICAL MANIFESTATIONS

Patients with hepatic encephalopathy (HE) usually have advanced chronic liver disease and thus have many of the physical and laboratory stigmata associated with severe hepatic dysfunction. Physical findings may include muscle wasting, jaundice, ascites, palmar erythema, edema, spider telangiectasias, and fetor hepaticus. Some of these findings (such as muscle wasting, spider telangiectasias, and palmar erythema) are usually absent in previously healthy patients with fulminant hepatic failure since their development requires a relatively longer period of hepatic dysfunction. (See "Acute liver failure in adults: Etiology, clinical manifestations, and diagnosis".)

The history may reveal a precipitating cause. These include: