Mandiga Pujyitha, Kommu Sharath, Bollu Pradeep C.
Genesys Regional Hospital
Marshfield Clinic Health System
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.
肝性脑病的特征是，肝功能不全患者血液中神经毒性物质蓄积导致一系列神经精神异常。它被认为是一种排除性诊断。与急性肝衰竭或慢加急性肝衰竭（ACLF）患者相比，慢性肝病患者的这种病症有所不同，在病理生理、临床和放射学特征方面存在差异。症状可能源于肝功能不全或血流从肝脏分流（门体分流）。自1893年以来，在门体分流的早期模型——艾克瘘管动物中观察到的“肉中毒”综合征就已为人所知。然而，我们对肝性脑病的理解已从单纯将其归因于高氨血症，发展到认识到多种因素的复杂相互作用，包括全身炎症、肠道菌群失调、神经递质改变以及其他神经毒素，如锰。国际肝性脑病和氮代谢协会将显性肝性脑病的发作定义为定向障碍或扑翼样震颤的出现。轻微肝性脑病仅通过专门测试才能检测到，它影响高达80%的肝硬化患者。肝性脑病的症状范围从意识模糊、性格改变、定向障碍到意识减退。在肝性脑病的初始阶段，患者通常表现出睡眠-觉醒模式紊乱，其特征是白天睡觉、晚上清醒。随着病情发展到中期，症状通常会恶化，意识模糊、嗜睡和性格改变会加剧。在晚期，肝性脑病可能导致昏迷，这可能危及生命。在肝硬化和重度脑病患者中，第一年的死亡率超过50%。
