The pathophysiological events that are believed to contribute to adverse outcome from bacterial meningitis include alteration of cerebral capillary endothelial cells that comprise the blood-brain barrier, cytotoxic and vasogenic cerebral edema, loss of autoregulation, and increased intracranial pressure.1 These alterations can lead to a reduction in cerebral perfusion pressure and diminution in cerebral blood flow. This results in regional hypoxia and focal ischemia of brain tissue, possibly manifested as neurologic sequelae, learning or developmental disabilities, or communication disorders.
A number of investigators are pursuing studies in experimental meningitis models to delineate the mechanisms involved in meningeal inflammation and how this response can be downregulated by dexamethasone phosphate and other drugs. Available evidence in experimental meningitis suggests that components of the bacterial cell wall (eg, lipooligosaccharide of Haemophilus influenzae type b and lipoteichoic acid of Streptococcus pneumoniae) that are elaborated in infection stimulate
McCRACKEN GH, LEBEL MH. Dexamethasone Therapy for Bacterial Meningitis in Infants and Children. Am J Dis Child. 1989;143(3):287–289. doi:10.1001/archpedi.1989.02150150041013
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