Electron microscopic study of brain capillaries in cerebral edema from fulminant hepatic failure

Authors

  • Masataka Kato,

    1. Institute of Liver Studies, King's College Hospital and School of Medicine and Dentistry, Denmark Hill, London SE5 9RS, United Kingdom
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  • Robin D. Hughes,

    1. Institute of Liver Studies, King's College Hospital and School of Medicine and Dentistry, Denmark Hill, London SE5 9RS, United Kingdom
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  • Richard T. Keays,

    1. Institute of Liver Studies, King's College Hospital and School of Medicine and Dentistry, Denmark Hill, London SE5 9RS, United Kingdom
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  • Dr. Roger Williams

    Corresponding author
    1. Institute of Liver Studies, King's College Hospital and School of Medicine and Dentistry, Denmark Hill, London SE5 9RS, United Kingdom
    • Institute of Liver Studies, King's College Hospital, Denmark Hill, London SE5 9RS, UK
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Abstract

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. (HEPATOLOGY 1992;15:1060–1066).

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