Treatment with adjunctive dexamethasone is the most likely intervention to improve neurologic outcomes in this patient with a presumptive diagnosis of bacterial meningitis due to Streptococcus pneumoniae. Meningitis leads to severe central nervous system (CNS) inflammatory changes that may cause acute neurologic changes and result in permanent, long-term neurologic damage. Neurologic sequelae associated with pneumococcal meningitis include seizures, hearing loss, cranial nerve deficits, and paralysis. The glucocorticoid dexamethasone decreases inflammation in the CNS and leads to lower mortality, fewer short-term neurologic sequelae, and decreased hearing loss in pneumococcal meningitis when used as adjunctive therapy in developed countries. Because of these potential benefits, guidelines recommend early dexamethasone treatment of possible or suspected pneumococcal meningitis; it should be given approximately 15 minutes before administration of antimicrobial agents and should be continued for the duration of antibiotic therapy.

Of interest, several recent studies have investigated therapeutic hyperthermia as a possible treatment of severe bacterial meningitis, but results have been conflicting and data not definitive enough to recommend this therapy.

Although excess intravascular volume has been associated with poorer outcomes in patients with severe bacterial meningitis, no evidence supports the benefit of fluid restriction or diuresis in euvolemic patients early in the management of bacterial meningitis compared with maintaining normal intravascular volume.

Patients with meningitis frequently have increased intracranial pressure (ICP), and several interventions may lower the ICP, including maintaining the head of the bed at greater than 30 degrees, administering a hyperosmolar agent (such as glycerol), and placing a ventricular drain. However, monitoring and treating increased ICP are beneficial primarily in patients with bacterial meningitis who are stuporous or comatose, unlike this patient. The effect of interventions to lower ICP in patients without significant neurologic findings associated with meningitis is unclear.

Experimental animal models of pneumococcal meningitis have shown that infusions of mannitol modulate and reduce ICP. The mechanism for this effect on ICP may be related to reduction of hydroxyl radicals, which are implicated in CNS injury from ischemia and neuronal damage. The use of mannitol in this patient who has no clinical evidence of ICP is not appropriate.