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Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure
Author(s) -
Kato Masataka,
Hughes Robin D.,
Keays Richard T.,
Williams Roger
Publication year - 1992
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840150615
Subject(s) - fulminant hepatic failure , pathology , cerebral edema , fulminant , medicine , blood–brain barrier , brain biopsy , biopsy , central nervous system , transplantation , liver transplantation
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. (H EPATOLOGY 1992;15:1060–1066).