Brain Abscess

**1. Risk Factors for Brain Abscess

A brain abscess is a focal collection of pus within the brain parenchyma. In approximately 20% of cases, no predisposing factor is identified; however, in the majority of children, distinct risk factors facilitate bacterial entry into the brain through contiguous spread, hematogenous dissemination, or direct inoculation.

A. Contiguous Spread (Direct Extension)

Infections in the head and neck region can erode through bone or spread via valveless emissary veins to the brain.

• Otitis Media and Mastoiditis: A common cause, particularly associated with temporal lobe or cerebellar abscesses.
• Sinusitis: Infections of the frontal, ethmoid, or sphenoid sinuses can extend intracranially, typically causing frontal lobe abscesses,.
• Dental Infections: Molar infections can lead to intracranial spread.
• Orbital Cellulitis: Can extend posteriorly to involve the frontal lobe.
• Meningitis: Rarely, bacterial meningitis (e.g., Citrobacter koseri or Proteus mirabilis in neonates) may complicate into abscess formation.

B. Hematogenous Dissemination (Metastatic Spread)

Bacteria travel through the bloodstream from a distant focus.

• Congenital Cyanotic Heart Disease (CCHD): Right-to-left shunts (e.g., Tetralogy of Fallot) allow bacteria to bypass pulmonary macrophage filtration and seed the brain. This is a major risk factor in children >2 years of age,.
• Pulmonary Infections: Lung abscess, empyema, bronchiectasis, and arteriovenous malformations (AVMs),.
• Infective Endocarditis: Septic emboli can cause multiple microabscesses.

C. Direct Inoculation

• Head Trauma: Penetrating head injuries or compound depressed skull fractures,.
• Neurosurgical Procedures: Post-operative infections.
• Foreign Bodies: Ventriculoperitoneal (VP) shunts or other hardware.

D. Immunodeficiency

• Children with HIV/AIDS, malignancy, or those on immunosuppressive therapy are at risk for opportunistic pathogens (fungi, Toxoplasma, Nocardia).

**2. Clinical Features of Brain Abscess

The clinical presentation is variable and depends on the location, size, number of lesions, and the host's immune status. The classic triad of fever, headache, and focal neurologic deficit is present in less than 50% of patients.

• Raised Intracranial Pressure (ICP):
  • Headache: The most common symptom (>70%), often severe and unrelenting,.
  • Vomiting: Often projectile, associated with raised ICP.
  • Papilledema: Suggests a mass effect and chronicity; seen in older children.
  • Altered Sensorium: Ranges from lethargy and irritability to stupor and coma; indicates severe cerebral edema or herniation.
• Fever: Low-grade or intermittent; notably absent in 40–50% of patients at presentation.
• Focal Neurological Deficits: Occur in 50% of cases and depend on the site:
  • Frontal lobe: Hemiparesis, behavioral changes, seizures.
  • Temporal lobe: Aphasia, visual field defects (homonymous hemianopia).
  • Cerebellum: Ataxia, nystagmus, dysmetria, and hydrocephalus due to 4th ventricle compression.
• Seizures: Focal or generalized seizures occur in 25–50% of patients and may be the presenting sign.
• Neonates: Present non-specifically with poor feeding, lethargy, irritability, bulging fontanelle, and seizures.

3. Etiology of Brain Abscess

The microbiology correlates strongly with the predisposing condition. Streptococci are the most predominant organisms.

4. Investigations

1. Neuroimaging (Diagnostic modality of choice)

• MRI Brain (Contrast-Enhanced): Superior to CT for early diagnosis (cerebritis stage), posterior fossa lesions, and differentiating abscess from tumor.
  • Findings: A ring-enhancing lesion with a hypointense center (T1) and hyperintense center (T2) surrounded by perilesional edema.
  • Diffusion-Weighted Imaging (DWI): Shows restricted diffusion (bright signal) within the abscess cavity, which helps distinguish pus from necrotic tumors (which typically do not restrict diffusion).
• CT Scan (Contrast-Enhanced): Rapid and useful for unstable patients.
  - Findings: Hypodense center with a contrast-enhancing uniform rim and surrounding low-density edema.

2. Microbiological Diagnosis

• Abscess Aspiration: Stereotactic aspiration of pus is critical for Gram stain, culture (aerobic, anaerobic, fungal, mycobacterial), and PCR (16S rRNA) to guide targeted therapy.
• Blood Cultures: Positive in only ~28% of cases but should be obtained before antibiotics.

3. Laboratory Tests

• CBC/ESR/CRP: Leukocytosis is present in only 60%; ESR/CRP may be elevated but are non-specific.

4. Lumbar Puncture (LP)

• Contraindication: Generally contraindicated in large focal abscesses due to the risk of brain herniation,.
• CSF Findings: If done safely (rarely), may show elevated protein, mild pleocytosis, and normal glucose. Cultures are usually negative unless the abscess has ruptured into the ventricle.

Treatment of Brain Abscess

Management involves a combination of medical therapy and neurosurgical intervention.

1. Medical Management (Antimicrobial Therapy)

Antibiotics must penetrate the blood-brain barrier and abscess cavity. High-dose IV therapy is required for 4–8 weeks.

• Empiric Therapy (Pending cultures):
  • Standard Regimen: 3rd Generation Cephalosporin (Ceftriaxone or Cefotaxime) + Metronidazole (for anaerobic coverage).
  • Suspected Staphylococcal Infection (Trauma/Surgery): Add Vancomycin.
  • Pseudomonas Risk (Otogenic): Use Ceftazidime or Cefepime or Meropenem instead of Ceftriaxone.
  • Neonates: Add Ampicillin if Listeria is suspected (though rare in abscess).
• Targeted Therapy (Examples):
  • Streptococci: Penicillin G or Ceftriaxone.
  • S. aureus (MSSA): Nafcillin/Oxacillin.
  • MRSA: Vancomycin or Linezolid.
  • Anaerobes: Metronidazole.
  • Toxoplasma: Pyrimethamine + Sulfadiazine.

2. Surgical Management

• Aspiration (Stereotactic or CT-guided): The procedure of choice for most abscesses. It is diagnostic (culture) and therapeutic (decompression).
• Excision (Craniotomy): Reserved for:
  • Multiloculated abscesses.
  • Abscesses containing foreign bodies or bone fragments (post-traumatic).
  • Fungal abscesses (often resistant to medical therapy).
  • Refractory cases that re-accumulate despite aspiration.
• Medical-Only Treatment: May be considered only if:
  • Small abscess (<2.5 cm).
  • Multiple small abscesses.
  • Early stage (cerebritis).
  • Location is inaccessible/eloquent cortex where surgery poses high risk.
  • Requirement: Must have close clinical and serial neuroimaging monitoring.

3. Supportive Care

• Intracranial Pressure (ICP) Management: Head elevation, mannitol, or hypertonic saline for acute spikes.
• Corticosteroids (Dexamethasone): Not routine as they may reduce antibiotic penetration and capsule formation. Used only if there is significant mass effect causing impending herniation or severe edema.
• Anticonvulsants: Seizures are common; prophylactic levetiracetam or phenytoin is often recommended, especially for frontal/temporal lesions, and should be continued for at least 3 months.

4. Prognosis

With modern imaging and antibiotics, mortality is <10%. However, long-term sequelae (seizures, hemiparesis, cognitive deficits) occur in ~30% of survivors. Rupture of the abscess into the ventricles is associated with high mortality (ventriculitis).