Abstract

Hepatic encephalopathy is a frequent and serious complication of liver cirrhosis; the pathophysiology of this complication is not fully understood although great efforts have been made during the last years. There are few prospective studies on the epidemiology of this complication; however, it is known that it confers with high short-term mortality. Hepatic encephalopathy has been classified into different groups depending on the degree of hepatic dysfunction, the presence of portal-systemic shunts, and the number of episodes. Due to the large clinical spectra of overt EH and the complexity of cirrhotic patients, it is very difficult to perform quality clinical trials for assessing the efficacy of the treatments proposed. The physiopathology, clinical manifestation, and the treatment of HE is a challenge because of the multiple factors that converge and coexist in an episode of overt HE.

Highlights

  • Hepatic encephalopathy (HE) is a disturbance in the central nervous system (CNS) function due to hepatic insufficiency or portal-systemic shunting

  • Hepatic encephalopathy is a frequent and serious complication of liver cirrhosis; the pathophysiology of this complication is not fully understood great efforts have been made during the last years

  • A consensus has been reached indicating that the PSE index is not adequate for clinical follow-up and is not recommended for clinical trials

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Summary

Introduction

Hepatic encephalopathy (HE) is a disturbance in the central nervous system (CNS) function due to hepatic insufficiency or portal-systemic shunting. HE causes a spectrum of neurologic manifestations that develop in association with different liver diseases [1]. The nomenclature that several authors have used for HE is confusing For this reason several efforts have been made to reach a consensus, especially for the design of clinical trials [2]. Despite this limitation, from a clinical perspective, HE is generally classified according to the underlying liver disease and the evolution of the neurological manifestations (Table 1). HE develops in the absence of any sign of parenchyma liver disease and is caused solely by portal-systemic shunting of congenital or surgical origin.

Pathogenesis
Clinical Features
Methods for the Assessment of Hepatic Encephalopathy
Findings
Principles of Treatment
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