Bacterial meningitis affects an estimated 15 000 infants and children in the United States each year. The case-fatality rates for these patients are from 5% to 10%; as many as 20% to 30% of survivors have long-term sequelae, the most common of which is hearing impairment.1 The reported incidence of hearing loss after meningitis has ranged from 5% to 20% of patients, depending on the selection of patients, techniques used to assess hearing, and etiology.2-5 In 1972 to 1977, Dodge and co-workers2 documented hearing loss in 31% of patients with Streptococcus pneumoniae meningitis, 10% with Neisseria meningitidis meningitis, and 6% with Haemophilus influenzae meningitis. Bilateral sensorineural hearing impairment occurred in 14%, 10%, and 3%, respectively. Newer antimicrobial agents with superior bactericidal activity in cerebrospinal fluid have not reduced morbidity and case-fatality rates compared with conventional therapy.
The pathophysiologic events 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, and increased intracranial pressure.6 These events can lead to decreased cerebral perfusion pressure with a resultant diminution in cerebral blood flow causing regional hypoxia and focal ischemia of brain tissue.
Because of its anti-inflammatory effects, corticosteroid therapy has been evaluated in experimental meningitis and in infants and children with meningitis. Dexamethasone produced significant reductions in intracranial pressure, brain edema, and lactate concentrations in cerebrospinal fluid in experimental H influenzae and S pneumoniae meningitis.7,8 In addition, the administration of dexamethasone was associated with decreased concentrations of prostaglandin E2 in cerebrospinal fluid and lowered mortality and clinically evident neurologic sequelae in rabbits with experimental pneumococcal meningitis.9
- Copyright © 1990 by the American Academy of Pediatrics