brain abscess

Pathophysiology: Brain abscess formation progresses through stages—early cerebritis (1-3 days, poorly organized inflammation), late cerebritis (4-9 days, necrotic center), early capsule formation (10-13 days, collagen capsule begins), and late capsule (>14 days, well-formed capsule with gliosis). Common organisms depend on source: Streptococcus (viridans, milleri group) and anaerobes from sinus/dental/otogenic sources; Staphylococcus aureus from hematogenous spread/endocarditis/trauma; Toxoplasma gondii and other opportunists in HIV/AIDS patients (CD4 <100); fungal (Aspergillus, Candida) in immunocompromised hosts; Nocardia in immunocompromised. Often polymicrobial.

Clinical presentation: Headache (most common symptom), fever (present in only ~50%), focal neurologic deficits based on location, seizures, altered mental status, signs of increased ICP (papilledema, vomiting). Onset is typically subacute over days to weeks.

Diagnosis: Contrast-enhanced MRI is more sensitive than CT; shows a ring-enhancing lesion with central hypointensity (necrotic core) and surrounding vasogenic edema. Diffusion-weighted imaging helps distinguish abscess (restricted diffusion) from tumor. Lumbar puncture is generally contraindicated due to risk of herniation. Definitive diagnosis via stereotactic aspiration for Gram stain/culture.

Differential diagnosis: Must distinguish from primary/metastatic brain tumor (ring-enhancing lesions), toxoplasmosis (in HIV patients—multiple ring-enhancing lesions in basal ganglia), primary CNS lymphoma, and resolving hematoma.

Management: Empiric IV antibiotics (e.g., vancomycin + ceftriaxone/metronidazole) tailored to suspected source and culture results, typically for 6-8 weeks. Surgical aspiration or excision is often needed both for diagnosis and source control, especially for abscesses >2.5 cm or those causing mass effect. Corticosteroids may be used cautiously to reduce edema but can theoretically limit capsule formation and antibiotic penetration.

Complications: Herniation, ventricular rupture (intraventricular rupture carries high mortality), seizures, residual neurologic deficits.

High-yield associations: Otitis media/mastoiditis → temporal lobe or cerebellar abscess; sinusitis → frontal lobe abscess; hematogenous spread → often multiple abscesses at gray-white junction; congenital cyanotic heart disease (e.g., tetralogy of Fallot) with right-to-left shunt increases risk due to bypassing pulmonary filtration of bacteria.