I. Etiology and pathophysiology
  1. Four main modes of origin (20-40% of cases have no identifiable origin)
    1. Direct extension from infection elsewhere (e.g. sinus; mastoid process)
    2. Venous seeding from sinuses, mastoid, or middle ear
    3. Direct trauma
    4. Vascular spread from distant location
  2. Etiologic organisms
    1. Bacterial (including TB)
      1. Staph aureus in absence of local head/neck infection or trauma suggests hematogenou seeding from another site, particularly endocarditis
    2. Fungal
    3. Protozoan
    4. In immunocompromised individuals can see opportunistic organisms: toxoplasma, listeria, nocardia, aspergillus, cryptococcus, coccidioides
II. Clinical features
  1. Headache
  2. Seizures
  3. Fever (absent in most cases at time of presentation)
  4. Focal neurologic defects
  5. Altered mental state
  6. Mortality is 5-30%; 1/3 of survivors will have moderate-to-severe cognitive impairment
III. Diagnosis
  1. Clinical presentation as above
  2. Peripheral WBC count may be elevated but not always (about 60% of cases)
  3. CRP is elevated in about 90% of cases
  4. CT with contrast: Hypodense center and enhancing outer ring
  5. MRI (more sensitive; can help differentiate from tumor)
  6. Lumbar puncture is contraindicated in suspected brain abscess due to potential increased intracranial pressure and thus herniation
  7. Gold standard = aspiration with culture
IV. Treatment
  1. Drainage (usually open)-May be unnecessary for solitary lesions < 1cm in diameter
  2. Antimicrobial therapy x 4-8wks; monitor progress using brain imaging
  3. Prophylactic anticonvulsant Rx
  4. Glucocorticoids-Sometimes used if there is substantial mass effect though little evidence of benefit exists as of 2012

(Sources include Core Content Review of Family Medicine, 2012)