Jensen D M
Med Clin North Am. 1986 Sep;70(5):1081-92. doi: 10.1016/s0025-7125(16)30913-0.
Decompensation in the cirrhotic patient is typically manifested as hepatic encephalopathy or coma. This may be precipitated by azotemia, gastrointestinal bleeding, infection, hypokalemic alkalosis, excess dietary protein, or the use of sedative, tranquilizer, or analgesic medications. The pathogenesis of hepatic encephalopathy associated with portal-systemic shunting is unknown, but theories purporting major roles for ammonia, AAAs, false neurotransmitters, and GABA have been advanced. Treatment is aimed at removing precipitating factors and eliminating nitrogenous substances from the gastrointestinal tract.
肝硬化患者的失代偿通常表现为肝性脑病或昏迷。这可能由氮质血症、胃肠道出血、感染、低钾性碱中毒、过量饮食蛋白质或使用镇静剂、安定剂或镇痛药引发。与门体分流相关的肝性脑病的发病机制尚不清楚，但已提出氨、芳香族氨基酸、假性神经递质和γ-氨基丁酸起主要作用的理论。治疗旨在消除诱发因素并清除胃肠道中的含氮物质。
