Hepatic Encephalopathy

Hepatic encephalopathy is characterized by a range of neuropsychiatric abnormalities caused by the accumulation of neurotoxic substances in the bloodstream of patients with liver dysfunction. It is considered a diagnosis of exclusion. The condition differs in patients with chronic liver disease compared to those with acute liver failure or acute-on-chronic liver failure (ACLF), with distinctions in pathophysiological, clinical, and radiological features. Symptoms may result from liver insufficiency or the diversion of blood flow away from the liver (portosystemic shunting). The "meat-intoxication" syndrome observed in Eck fistula animals, an early model of portosystemic shunting, has been recognized since 1893. However, our understanding of hepatic encephalopathy has evolved from solely attributing it to hyperammonemia to acknowledging a complex interplay of factors, including systemic inflammation, gut dysbiosis, altered neurotransmitters, and other neurotoxins such as manganese. The International Society for Hepatic Encephalopathy and Nitrogen Metabolism defines the onset of overt hepatic encephalopathy as the appearance of disorientation or asterixis. Subtle signs, detectable only through specialized tests, characterize minimal hepatic encephalopathy, which affects up to 80% of patients with cirrhosis. Symptoms of hepatic encephalopathy range from confusion, personality changes, and disorientation to reduced consciousness. In the initial stages of hepatic encephalopathy, patients often exhibit a disrupted sleep-wake pattern, characterized by sleeping during the day and staying awake at night. As the condition progresses to intermediate stages, symptoms typically worsen, with increasing confusion, lethargy, and personality changes. In advanced stages, hepatic encephalopathy may lead to coma, which can be life-threatening. Among patients with cirrhosis and severe encephalopathy, the mortality rate exceeds 50% within the first year.