Kato M, Hughes R D, Keays R T, Williams R
Institute of Liver Studies, King's College Hospital, London, United Kingdom.
Hepatology. 1992 Jun;15(6):1060-6. doi: 10.1002/hep.1840150615.
Cerebral edema is a serious complication of the encephalopathy in fulminant hepatic failure. It is a major cause of death. The mechanisms responsible for its formation are unclear, and the aim of this study was to investigate the ultrastructural appearance of brain capillaries by scanning electron microscopy. Samples of cerebral cortex were obtained immediately after death from nine patients with fulminant hepatic failure (seven cases due to acetaminophen overdose, one caused by hepatitis B and one caused by non-A, non-B hepatitis) by needle biopsy at the site of insertion of an extradural pressure transducer to monitor intracranial pressure. The intercellular tight junctions between capillary endothelial cells were intact. The endothelial cells were swollen, with increased numbers of vesicles and vacuoles. The basement membranes were enlarged and vacuolized and the pericytes had increased numbers of vesicles and vacuoles, indicative of passage of fluid by this route. Marked intracellular swelling of the perivascular astroglial foot processes was present. Thus mainly cytotoxic mechanisms, with cellular swelling, and to a lesser extent vasogenic mechanisms, with altered blood-brain barrier permeability, appear to be involved in the cerebral edema of fulminant hepatic failure.
脑水肿是暴发性肝衰竭脑病的严重并发症,是主要死因。其形成机制尚不清楚,本研究旨在通过扫描电子显微镜观察脑毛细血管的超微结构。9例暴发性肝衰竭患者(7例因对乙酰氨基酚过量,1例因乙型肝炎,1例因非甲非乙型肝炎)死亡后,立即在硬膜外压力传感器插入部位经针吸活检获取大脑皮质样本,以监测颅内压。毛细血管内皮细胞间的紧密连接完整。内皮细胞肿胀,囊泡和空泡数量增加。基底膜增大并空泡化,周细胞的囊泡和空泡数量增多,表明液体通过该途径通过。血管周围星形胶质细胞足突存在明显的细胞内肿胀。因此,暴发性肝衰竭脑水肿主要涉及细胞毒性机制(伴有细胞肿胀),以及程度较轻的血管源性机制(伴有血脑屏障通透性改变)。