• Z Szychowska.
• Kliniki Chorób Zakaźnych Wieku Dzieciecego Akademii Medycznej im. Piastów Slaskich we Wrocławiu.
• Pol. Merkur. Lekarski. 1997 Apr 1; 2 (10): 291-4.

AbstractWith improved understanding of the pathophysiology of bacterial meningitis, a number of points in the deleterious inflammatory cascade have been identified as possible sites for modulation. Dexamethasone attenuates tissue injury by inhibiting host mediators at several steps in the inflammatory process. Animal and clinical trials have demonstrated that adjunctive corticosteroid therapy reduces the production of cytokines in the CSF. This results in decreased severity of the inflammatory process and fewer neurologic sequelae. However, routine use of steroids adjunctive treatment of bacterial meningitis remains controversial. Data support the use of adjunctive corticosteroid therapy in children with S. pneumoniae and H. influenzae type b meningitis. There is not sufficient evidence supporting the use of adjunctive corticosteroid therapy in patients with meningitis caused by N. meningitidis, which is the main cause of purulent meningitis in Poland. Also, the routine use of the dexamethasone in children and adult meningitis in Poland cannot presently be recommended. When using dexamethasone timing and dosage seems to be crucial. Administration before or with antibiotics is optimal for attenuating the subarachnoid space inflammatory response. The host's inflammatory response can be accompanied by the neuroendocrine response which is complex and its mediators are not well understood. Data indicate that the large component of the neuroendocrine response (e.g. inadequate secretion of ADH and large adrenocortical stress response) adversely affects the outcome from bacterial meningitis. So, the modulating effect of dexamethasone on both inflammatory and neuroendocrine response may be beneficial in bacterial meningitis and can probably be, achieved with sufficiently high dose of dexamethasone w has not yet been specified. Based on present pathophysiological and pharmacokinetic data, and to achieve maximum benefits and minimum complications, dexamethasone therapy started 10 min before the first dose of antibiotic and given every 12 h for only 2 days in a dose 0.8 mg/kg/day is suggested. Future studies of the pathogenesis and pathophysiology of bacterial meningitis may lead to the development of other adjunctive treatment strategies, improving the outcome of this serious disease.

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