Hepatic Encephalopathy

Abstract

Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome characterized by global CNS dysfunction reSUlting in impaired consciousness and coma. The association of the syndrome with acute or chronic liver failure implicates a plethora of metabolic abnormalities and gut-derived toxins in its pathogenesis. Thus, it is difficult to ascribe the neurological and psychiatric manifestations of HE to the presence of a single agent or changes in a particular metabolic pathway. The manifestations of HE are determined by two principle components of the underlying liver disease: hepatocellular failure and systemic shunting of portal venous contents (BASILE et al. 1991 b). Significant portal venous shunting is often found in chronic liver disease. HE occurs most frequently in this setting, where it is a milder, more persistent and episodic variant of the syndrome. In contrast, fulminant hepatic failure (FHF) has no vascular component. HE associated with FHF shows an acute onset with delirium progressing to deep coma. While delirium and seizures are generally uncommon in HE, they may occur during the rapid evolution of HE due to FHF (PAPPAS 1986). Although some of the characteristics of HE associated with acute or chronic liver failure result from fundamental differences in the mechanism of pathogenesis, many findings regarding the pathogenesis and treatment of the syndrome are held in common. Finally, it is important to recognize that while many of the animal models of liver failure used in research emphasize one or the other component of liver failure, most clinical cases tend to have a mixture of both. Although a single, perfect animal model of this syndrome does not exist, the animal models in use have nonetheless provided valuahle insights into the pathogenesis of HE and allowed for the testing of new therapeutic modalities.