The pathogenesis of bacterial meningitis involves a cascade of neuroinflammatory events. Bacterial components (lipopolysaccharide in gram-negatives, peptidoglycan/teichoic acid in gram-positives) activate toll-like receptors on meningeal macrophages and microglia, triggering NF-κB-mediated production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and chemokines (CXCL8). This inflammatory cascade disrupts the blood-brain barrier through matrix metalloproteinase activation, leading to vasogenic edema. Neutrophil degranulation releases reactive oxygen species that cause neuronal apoptosis (cytotoxic edema). Purulent exudate obstructs CSF flow through the arachnoid villi, causing communicating hydrocephalus (interstitial edema). The combined effect raises ICP, reduces cerebral perfusion pressure, and can trigger transtentorial herniation. Adjunctive dexamethasone targets this inflammatory cascade by inhibiting cytokine production. The clinician must prescribe empiric and targeted antibiotic regimens, manage ICP, interpret CSF results, coordinate prophylaxis, and manage long-term sequelae including sensorineural hearing loss, cognitive deficits, and epilepsy.