Abstract
After primary neurologic damage due to a traumatic, ischemic, hypoxic or metabolic event, a secondary lesion may arise, worsening it and becoming a vicious circle. Locally, the initial energetic breakdown or the tissue mechanical disruption set off a number of biochemical chain reactions leading to a derangement of molecular structures and liberating toxic mediators. Globally, these reactions are responsible for brain edema and disorders of microcirculation (1).
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© 1996 Springer-Verlag Italia, Milano
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Corte, F.D., Piazza, O., Clemente, A., Pennisi, M.A. (1996). Pathophysiology and Monitoring of Cerebral Edema. In: Gullo, A. (eds) Anaesthesia, Pain, Intensive Care and Emergency Medicine — A.P.I.C.E.. Springer, Milano. https://doi.org/10.1007/978-88-470-2203-4_51
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DOI: https://doi.org/10.1007/978-88-470-2203-4_51
Publisher Name: Springer, Milano
Print ISBN: 978-3-540-75014-7
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