Cerebral edema is a serious complication of the encephalopathy in fulminant hepatic failure. .[t is a major cause of death. The mechanisms responsilble 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 vacnolized and the pericytes had increased numbers of vesicles and vacuoles, indicative of passage of fluid kiy 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. (HEPATOLOGY 1992; 15: 1060-1066.)
Cerebral edema is a major complication in patients with fulminant hepatic failure, occurring in 86% of patients in grade I11 or IV encephalopathy, and is the most frequent immediate cause of death (1-3). The mechanisms responsible for the development of cerebral edema in liver failure, which is defined as an abnormal accumulation of fluid in the brain parenchyma producing a volumetric enlargement of the tissue, ;are not clear. From studies of cerebral edema due to other causes, two main possible mechanisms for edema formation have been elucidated -cytotoxic and vasogenic (4, 5 ) . In the cytotoxic type, of which ischemic brain edema is an example (6), increase in cellular water content results from impaired cellular metabolism and osmoregulation. In brain edema due to cold injury,