Pathogenesis, Clinical Manifestation, and Diagnosis of Hepatic Encephalopathy

Abstract

The pathogenesis of hepatic encephalopathy (HE) by general consensus is now considered to be a complex multifactorial process. Rather than simply a manifestation of direct ammonia neurotoxicity, HE is now believed to be the result of astrocyte swelling and oxidative stress caused by ammonia and other putative neurotoxins. Mediators of inflammation have also been shown to promote the expression of HE. The clinical manifestations of HE have been known for decades, and clinical evaluation still represents the primary method for diagnosing the overt forms of HE. A minimal form of HE is now recognized, which can be diagnosed by standard psychometric tests. Despite its clinically subtle nature, this form of HE is associated with significant reduction in quality of life. Minimal HE appears to be reversible with standard HE therapy. Detection needs to be simplified so that all physicians can diagnose its presence. This article reviews the pathogenesis, clinical classifications, and diagnosis of HE.