重症肝炎与脑水肿关系甚为密切,近年统计急性重症肝炎约40～80%合并脑水肿,其中20%可发生脑疝,尤其年青病例或合并呼吸衰竭时,脑水肿及脑疝发生率更高,往往是重症肝炎患者死亡的重要原因。一、脑水肿的发生机理脑肿瘤、炎症或脑外伤等均可引起脑动静脉环流障碍,脑脊液贮积过多,则形成脑水肿。克拉佐(Klatzo)(1967年)提出脑水肿有二种病理变化:(1)脑毛细血管上皮细胞通透性亢进(血脑屏障功能被破坏),白质细胞外水份贮留,成为血管神经性水肿(Vasogenic edema);(2)由于缺氧、某种毒性物质作用,三磷酸腺苷(ATP)酶被抑制,依赖 ATP酶的钠泵功能减退,脑细胞膜离子交换异常,血管内皮细胞和神经细胞内液贮积,成为细胞毒性水肿(Cytotoxic edema)。目前认为脑水肿往往不是单 Severe hepatitis and brain edema is closely related to the recent statistics of acute severe hepatitis about 40 to 80% with cerebral edema, of which 20% can occur hernia, especially in young cases or respiratory failure, cerebral edema and hernia higher incidence , Is often an important cause of death in patients with severe hepatitis. First, the mechanism of cerebral edema Brain tumors, inflammation or traumatic brain injury can cause cerebral arteriovenous circulatory disorders, excessive storage of cerebrospinal fluid, the formation of cerebral edema. Klatzo (1967) suggested that there are two pathological changes in brain edema: (1) hypertrophic permeability of the brain capillary epithelium (blood-brain barrier function is destroyed), extra-corpus luteum of white blood cells are stored and become vascular nerves Vasogenic edema; (2) As a result of hypoxia, a kind of toxic substances, ATP is inhibited, dependent on the ATP pump of sodium pump dysfunction, brain cell membrane ion exchange abnormalities, vascular endothelial cells and nerve cells Liquid storage, as cytotoxic edema (Cytotoxic edema). At present, brain edema is often not a single