Vaquero Javier, Chung Chuhan, Cahill Michael E, Blei Andres T
Department of Medicine, Lakeside Veterans Administration Medical Center, Chicago, Illinois, USA.
Semin Liver Dis. 2003 Aug;23(3):259-69. doi: 10.1055/s-2003-42644.
Hepatic encephalopathy (HE) in acute liver injury signifies a serious prognosis. Brain edema and intracranial hypertension are major causes of death in this syndrome. Comparison of HE in acute liver failure (ALF) with that of cirrhosis allows recognition of important differences and similarities. A key role for ammonia in the pathogenesis of both HE and brain edema is now firmly supported by clinical and experimental data. Additional factors, such as infection, products of the necrotic liver, and synergistic toxins, may contribute to an altered mental state. A low plasma osmolarity, high temperature, and both high and low arterial pressure may affect brain water content. A combined derangement of cellular osmolarity coupled with cerebral hyperemia can explain the development of brain edema in ALF. Increasingly, study of the mechanisms responsible for brain swelling provides critical information for understanding the pathogenesis of HE.
急性肝损伤中的肝性脑病（HE）预示着严重的预后。脑水肿和颅内高压是该综合征的主要死亡原因。对比急性肝衰竭（ALF）中的HE与肝硬化中的HE，可以发现重要的差异和相似之处。目前，临床和实验数据有力地支持了氨在HE和脑水肿发病机制中的关键作用。其他因素，如感染、坏死肝脏的产物以及协同毒素，可能导致精神状态改变。低血浆渗透压、高温以及动脉压的高低变化都可能影响脑含水量。细胞渗透压的联合紊乱与脑充血可以解释ALF中脑水肿的发生。对脑肿胀机制的研究越来越多地为理解HE的发病机制提供关键信息。
