Brain abscess

A brain abscess is a focal intracerebral infection that begins as localized inflammation and undergoes central necrosis and liquefaction. It may be caused by the direct spread of sinus, ear, and/or dental infections, hematogenous spread from distant infective foci, or direct inoculation of pathogens following neurosurgical procedures or open skull fractures. Causative organisms can be bacterial, fungal, or parasitic and may include opportunistic pathogens. Clinical manifestations include headache, fever, neurological deficits, and features of elevated intracranial pressure. Brain imaging (MRI or CT) reveals one or more intraparenchymal ring-enhancing lesions. Diagnostic confirmation using direct sampling is often required to differentiate brain abscesses from tumors and other causes of intracranial lesions with ring enhancement. Treatment of brain abscesses typically involves surgical drainage or excision followed by systemic antimicrobial therapy.

• Sex: ♂ > ♀ ^[1]
• Mean age: 30–40 years ^[1]

Epidemiological data refers to the US, unless otherwise specified.

Common bacterial pathogens ^[1][2][3]

Some brain abscesses are polymicrobial, especially those due to contiguous or homogenous spread from otogenic, odontogenic, sinus, or skin infections. ^[2][4]

Atypical and opportunistic pathogens ^[1][2][3]

• In immunocompromised states
  • Opportunistic fungal infections, e.g.: Aspergillus, Candida, Mucormycosis, Cryptococcus neoformans
  • Nocardia spp.
  • Toxoplasma gondii (cerebral toxoplasmosis)
  • Mycobacterium tuberculosis (Tuberculoma)
• Parasites: e.g., Taenia soleum (neurocysticercosis), Echinococcus (hydatid cyst)

Entry of pathogens via contiguous spread, direct inoculation, or hematogenous spread can result in the following: ^[5]

• 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

Clinical features depend on the size and location of the lesion. ^[6]

• 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

Approach

Obtain infectious diseases and neurosurgery consults.

• Initial studies
  • Brain imaging (CT/MRI)
  • Laboratory studies, including blood cultures
• Confirmatory study: abscess sampling, usually done by neurosurgery
• Consider additional testing based on the suspected underlying cause.

Brain imaging ^[3][7]

Brain imaging is used as an initial test to confirm and characterize intracranial lesions, then to monitor treatment response.

• MRI brain with and without contrast (preferred)
  • T1 weighted: hypointense fluid collection, hyperintense ring enhancement, hypointense vasogenic edema
  • T2 weighted: hyperintense fluid collection, hypointense ring enhancement, hyperintense vasogenic edema
  • Diffusion weighted (DWI): hyperintense and diffusion-restricted necrotic center ^[3]
• CT head with IV contrast: intraparenchymal lesions with a central hypodense (necrotic) area and peripheral ring enhancement

Laboratory studies ^[3][7]

• Inflammatory markers: ↑ CRP; , ↑ ESR, leukocytosis ^[1][4]
• Blood cultures: Obtain prior to starting antibiotics. ^[3]
• HIV testing: Consider in all patients with nontraumatic brain abscesses. ^[7]
• CSF studies: not routinely obtained
  • CSF analysis: may be normal or show pleocytosis, ↑ protein, ↓ glucose
  • CSF cultures: often negative

Lumbar puncture is relatively contraindicated in patients with a suspected brain abscess and not routinely performed. ^[3][7]

Abscess sampling ^[7][8]

• Indication
  • Diagnostic confirmation (gold standard) and identification of causative organisms and their antibiotic sensitivities
  • May be combined with therapeutic abscess drainage or excision
• Timing: ideally within 24 hours of radiological diagnosis and prior to starting antibiotics ^[7][8]
• Procedure: See “Interventional management” in “Treatment.”
• Testing: Order tests in consultation with infectious diseases.
  • Gram stain and bacterial cultures
  • Other tests based on clinical suspicion: e.g., fungal culture

Additional testing ^[7]

Based on the suspected underlying etiology of brain abscess, e.g.:

• Contiguous spread: ENT examination, dental examination
• Hematogenous spread
  • Echocardiography: to assess for endocarditis
  • CT chest, abdomen, and pelvis: to assess for a distant source of infection
• Immunocompromised state: testing for opportunistic infections, e.g., tuberculosis, toxoplasmosis, cryptococcosis

• Other CNS infections ^[2]
  • Bacterial meningitis
  • Epidural abscess
  • Subdural empyema
• Differential diagnosis of intracranial lesions with ring enhancement
  • Brain abscess
  • Malignancy: primary brain tumors (e.g., primary CNS lymphoma; , glioblastoma), brain metastases
  • Subacute hemorrhage and/or infarction
  • Radiation necrosis
  • Demyelinating plaque

The differential diagnoses listed here are not exhaustive.

Approach

• Consult neurosurgery for abscess drainage or excision.
  • Recommended in most patients for diagnostic and therapeutic purposes ^[7]
  • May be deferred for small (< 2.5 cm) uncomplicated abscesses with a known pathogen ^[7][8]
• Initiate empiric antimicrobial therapy for brain abscess in consultation with infectious diseases.
  • Unstable patients: Start immediately.
  • Stable patients: Start within 24 hours of diagnosis, preferably after diagnostic sampling.
• Treat complications, e.g.: ^[2][7]
  • Dexamethasone for the management of elevated ICP
  • Acute seizure management

Interventional management

For diagnostic purposes and therapeutic decompression

• Indications include:
  • All pyogenic abscesses ≥ 2.5 cm
  • Abscesses causing brain shift and risk of herniation
  • Inadequate response to antimicrobial therapy
• Timing: as soon as feasible; preferably within 24 hours of diagnosis and prior to starting antibiotics
• Procedures
  • Abscess drainage (e.g., stereotactic aspiration) ^[2][8]
  • Surgical excision ^[2]

In patients with HIV and positive Toxoplasma IgG, abscess drainage may be deferred in favor of presumptive cerebral toxoplasmosis treatment. ^[7]

Antimicrobial therapy ^[2][7]

Consult infectious diseases as there is no clear consensus.

• Select regimen based on most likely source, suspected causative agents, and patient's immune status.
• Adjust treatment based on culture results.
• Duration of treatment is guided by infectious diseases; typically given IV for 4–8 weeks

In patients with HIV, consider empiric coverage with RIPE TB regimen if they have risk factors for tuberculosis, and treatment for cerebral toxoplasmosis if toxoplasma IgG is positive. ^[2]

Repeat brain imaging and seek specialist advice immediately if there is clinical deterioration. ^[7]

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