Brain abscess

A brain abscess is a focal, suppurative lesion that may occur in one or more regions of the brain. It may be caused by the direct spread of sinus, ear, and/or dental infections, inoculation of pathogens following open skull fractures, and/or hematogenous spread from infective foci. During the course of the disease, the infected brain tissue softens and is subsequently encapsulated by granulation tissue. Clinical manifestations include headache, fever, neurological deficits, seizures, nausea, vomiting, and other features of raised intracranial pressure. Given these clinical findings, the main differential diagnosis is primary or metastatic brain tumor. Contrast CT reveals an intraparenchymal lesion with a hypodense center and peripheral ring enhancement. Treatment of brain abscesses involves surgical drainage of the abscess followed by systemic antibiotic therapy.

• Primary source of infection
  • Contiguous spread of an infection (most common cause)
    • Can be otogenic (e.g., otitis media, mastoiditis)
    • Sinus (e.g., sinusitis): most commonly seen in men and caused by Streptococcus milleri
    • Oral (e.g., dental infection)
    • Meningeal (e.g., meningitis)
  • Direct injection, e.g., head trauma, neurosurgery
  • Hematogenous spread, e.g., patients with cyanotic heart disease (least common cause): multiple abscesses located in the middle cerebral artery distribution at the gray-white junction
• Pathogens: brain abscesses are most commonly polymicrobial ^[1]
  • Most common pathogens
    • Viridans streptococci (often secondary to sinusitis)
    • Staphylococcus aureus
    • Coagulase-negative staphylococci
  • Less common pathogens
    • Obligate anaerobes; , e.g., Bacteroides species, (mainly due to dental infections)
    • Gram-negative aerobic bacteria, e.g., Enterobacteria, Pseudomonas species
    • Parasites, e.g., neurocysticercosis in patients from Latin America, Sub-Saharan Africa, and Asia
  • In immunocompromised states: Toxoplasma, Aspergillus, Candida, Mucormycosis (also known as Zygomycosis), Cryptococcus

• Initial infection: entry of pathogens via contiguous spread, direct inoculation, or hematogenous spread can result in the following ^[2]
  • Early cerebritis
    • Occurs during the first 3–5 days
    • Infiltration of neutrophils and cerebral edema
  • Late cerebritis
    • Occurs after 2–3 weeks
    • Necrosis, liquefaction, and infiltration of macrophages
    • Eventually results in the formation of a fibrotic capsule around the lesion
  • Spread patterns
    • Hematogenous spread of pathogens is associated with multiple brain abscesses.
    • Single abscess is associated with contiguous spread (e.g., otitis media/mastoiditis).
• Common sites of contiguous spread ^[3]
  • Temporal lobe and cerebellum (from otogenic infections)
  • Frontal lobe (from sinus infections)

Clinical features depend on the size and location of the lesion. ^[4]

• Dull persistent headache (a ruptured abscess is associated with a sudden worsening of headache and meningism)
• Focal neurological deficits (commonly oculomotor nerve palsy or abducens nerve palsy secondary to increased intracranial pressure)
• Symptoms of increased intracranial pressure (e.g., vomiting, papilledema, altered mental status)
• Fever
• Generalized or focal seizures

• Laboratory tests
  • ↑ CRP, ↑ ESR
  • Leukocytosis
  • Blood cultures
  • Lumbar puncture
    • Contraindicated in the presence of raised intracranial pressure (risk of uncal herniation)
    • Typical findings include elevated protein, normal glucose, sterile cultures, and high WBC
• Imaging (CT/MRI)
  • Best initial diagnostic test
  • Used to confirm the diagnosis and to localize the lesion (as well as size and number of lesions)
  • Can be used to monitor response to treatment
  • Findings include: intraparenchymal lesions with a central hypodense (necrotic) area and peripheral ring enhancement
    • T1-weighted with contrast agent: central hypointense (necrotic) lesions with ring-formed contrast enhancement, potentially in the perifocal hypointense regions (perifocal edema)
    • T2-weighted: central hyperintense region (necrosis) with an isointense rim and perifocal hyperintense regions (perifocal edema)
    • Diffusion-weighted imaging (DWI): hyperintense areas
• Biopsy (and drainage): microscopic examination and culture
  • Best confirmatory test
  • Entails either craniotomy for complete excision or image-guided aspiration
  • Distinguishes an abscess from a tumor
  • Cultures also determine the infective organism and its antibiotic sensitivities.
• Electroencephalography: striking focal lesions with potential for epileptic seizures

Other intracranial lesions with ring enhancement:

• Neurocysticercosis
• Toxoplasmosis
• Primary CNS lymphoma
• Brain metastases
• Subacute hemorrhage and/or infarction
• Tuberculomas
• Radiation necrosis
• Demyelinating plaque

The differential diagnoses listed here are not exhaustive.

• Early surgical drainage and biopsy of the abscess
• Empiric antibiotic therapy for pyogenic brain abscess: IV antibiotic therapy for 6–8 weeks
  • Indications
    • Antibiotic therapy without surgical drainage may be attempted if brain abscess < 2.5 cm, history of symptoms < 1 week, and no signs of ICP
    • In all other cases antibiotic therapy should be started immediately after abscess biopsy/drainage
  • Initial empirical therapy; (e.g., third-generation cephalosporin PLUS metronidazole with/without vancomycin)
  • Specific antibiotics may be used once the causative organisms and their antibiotic sensitivities are known.
• Intracranial pressure management: e.g., dexamethasone
• Seizure prophylaxis (e.g., anticonvulsants) ^[3][4]

• If treated early
  • High survival rates
  • Low rates of residual neurological sequelae
• Multiple, deep, ruptured, or inadequately treated abscesses have a poor prognosis.