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Brain Abscess and Empyema

Chapter 145 | Part 5: Infectious Diseases · Part 5 – Infectious Diseases: Bacterial · Chapter 145

Key Clinical Points

  1. Brain abscess is a focal, suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule.
  2. MRI with diffusion-weighted imaging (DWI) is superior to CT for diagnosis; abscess cavity shows restricted diffusion (high signal on DWI, low signal on ADC).
  3. Lumbar puncture (LP) is contraindicated in suspected brain abscess or empyema due to risk of herniation.
  4. Empirical therapy for community-acquired brain abscess: third- or fourth-generation cephalosporin (e.g., ceftriaxone) plus metronidazole.
  5. Neurosurgical drainage is indicated for multiloculated abscesses, neurosurgically inaccessible lesions, or small nonencapsulated abscesses.
  6. Neurocysticercosis is the most common parasitic cause of brain abscess worldwide; treatment depends on cyst stage (vesicular/colloidal vs. calcified).
  7. Subdural empyema (SDE) is a medical emergency requiring emergent neurosurgical evacuation; mortality is higher than brain abscess.
  8. Glucocorticoids should not be given routinely to patients with brain abscesses as they may delay encapsulation.
  9. Anticonvulsant therapy is indicated for patients with seizures and continued for at least 3 months after resolution of the abscess.
  10. Cranial epidural abscess accounts for <2% of focal suppurative CNS infections and is often smaller than SDE due to tight adherence of dura to skull.

1. DEFINITION & OVERVIEW

• Brain Abscess: A focal, suppurative infection within the brain parenchyma. ◦ Typically surrounded by a vascularized capsule. ◦ Cerebritis: Term for nonencapsulated brain abscess. • Subdural Empyema (SDE): Pus between dura and arachnoid membranes. • Cranial Epidural Abscess: Occurs in the space between the inner skull table and dura. • Suppurative Intracranial Thrombophlebitis: Involves septic venous thrombosis of cortical veins and sinuses.

1.1 Classification by Pathogenesis

• Direct spread from contiguous cranial site: Paranasal sinusitis, otitis media, mastoiditis, dental infection. • Trauma/Procedure: Following head tussle trauma or neurosurgical procedure. • Hematogenous spread: From remote infection. • Cryptogenic brain abscess: No obvious source in 25% of cases.

1.2 Classification by Location

• Otogenic: Temporal lobe (55–75%), cerebellum (20–30%). • Sinusitis-associated: Frontal lobes. • Dental infection-associated: Frontal lobes. • Hematogenous: Multiple, gray-white matter junction, middle cerebral artery territory.

2. EPIDEMIOLOGY

• Incidence: ~0.3–1.3:100,000 persons per year. • Predisposing Conditions: Otitis media, sinusitis, pyogenic infections, head trauma, neurosurgical procedures, and dental infections. • Pathogen Distribution (Immunocompetent): ◦ Streptococcus spp. (40%) ◦ Enterobacteriaceae (25%) ◦ Anaerobes (30%) ◦ Staphylococci (10%) • Pathogen Distribution (Immunocompromised): Nocardia spp., Toxoplasma gondii, Aspergillus spp., Candida spp., and Cryptococcus neoformans. • Regional Prevalence: ◦ Neurocysticercosis: Most common parasitic cause in Latin America. ◦ Tuberculoma: Major cause in India and East Asia.

2.1 Pathogen Distribution by Source

• Otitogenic: Streptococci, Bacteroides spp., Pseudomonas spp. • Paranasal sinusitis-associated: Streptococcus milleri, Haemophilus spp., Staphylococcus aureus • Dental infections: Streptococci, staphylococci, Bacteroides spp. • Hematogenous (endocarditis): Viridans streptococci or S. aureus • Lung infections: Streptococci, staphylococci, Bacteroides spp. • Urinary sepsis: Enterobacteriaceae, Pseudomonas aeruginosa • Penetrating trauma/neurosurgery: MRSA, Staphylococcus epidermidis, Clostridium spp. • Immunocompromised hosts: Nocardia spp., Toxoplasma gondii

3. ETIOLOGY & PATHOPHYSIOLOGY

• Pathogenesis Requirements: Bacterial invasion requires preexisting ischemia, necrosis, or hypoxemia in brain tissue. • Abscess Evolution Stages: ◦ Early cerebritis: days 1–3 ◦ Late cerebritis: days 4–9 ◦ Early capsule formation: days 10–13 ◦ Late capsule formation: day 14+ • Subdural Empyema Development: Via retrograde spread from septic thrombophlebitis or contiguous infection. • Cranial Epidural Abscess Origin: Craniotomy, compound skull fracture, or spread from frontal sinuses/middle ear/orbit.

3.1 Neurocysticercosis Pathophysiology

Definition (Harrison's 22e): Neurocysticercosis is a parasitic infection of the CNS caused by Taenia solium larvae. • Acquisition: Ingestion of T. solium eggs. • Localization: Cysts develop in brain parenchyma, subarachnoid/ventricular spaces. • Clinical Trigger: Degenerating cysts cause inflammation and seizures. • Management Note: Calcified lesions do not require treatment.

3.2 Toxoplasmosis Pathophysiology

Definition (Harrison's 22e): Toxoplasmosis is a parasitic infection caused by Toxoplasma gondii, acquired from undercooked meat or cat feces. • Primary Infection: Often asymptomatic. • Reactivation: Latent parasites may reactivate in immunocompromised hosts. • CNS Lesions: Typically multiple, located in deep white matter, thalamus, basal ganglia.

4. CLINICAL FEATURES

• Presentation: Expanding intracranial mass lesion with variable symptom evolution (hours to months). • Classic Triad: ◦ Headache (75%) ◦ Fever (50%) ◦ Focal neurologic deficit (>60%) • Symptom Characteristics: ◦ Headache: Constant, dull, aching, progressive. ◦ Fever: Absence does not exclude diagnosis. ◦ Seizures: Occur in 15–35%. • Location-Specific Deficits: ◦ Frontal lobe: Hemiparesis common. ◦ Temporal lobe: May present with dysphasia or quadrantanopia. ◦ Cerebellar: Nystagmus, ataxia; raised ICP signs (papilledema, vomiting) dominate.

4.1 Neurocysticercosis Clinical Presentation

• Primary Manifestation: New-onset partial seizures. • ICP Symptoms: Cysts in subarachnoid/ventricular spaces cause increased ICP. • Spinal Involvement: Spinal cysts mimic intraspinal tumors. • Inflammatory Response: Degenerating cysts elicit inflammatory response causing seizures.

4.2 Toxoplasmosis Clinical Presentation

• Symptoms: Headache, fever, seizures, focal deficits. • Lesion Distribution: Multiple in deep white matter, thalamus, basal ganglia, gray-white junction.

5. DIFFERENTIAL DIAGNOSIS

• General Mimics: Bacterial meningitis, viral meningoencephalitis, superior sagittal sinus thrombosis, acute disseminated encephalomyelitis, primary/metastatic brain tumors. • Rapid Progression Cases: Subdural hematoma, bacterial meningitis, viral encephalitis. • SDE Indicators: Nuchal rigidity is unusual with brain abscess but suggests SDE when associated with focal deficits and fever.

6. INVESTIGATIONS & DIAGNOSIS

• Neuroimaging: MRI superior to CT for early cerebritis and posterior fossa lesions. • Cerebritis Imaging: Low T1, irregular postgadolinium enhancement, high T2 signal. • Mature Abscess Imaging: Hypodensity with ring enhancement on CT; hyperintense central pus with hypointense capsule on T2-weighted MRI. • Diffusion-Weighted Imaging (DWI): Shows restricted diffusion in abscesses (high signal on DWI, low signal on ADC). • Lumbar Puncture: Contraindicated in focal infections due to herniation risk. • Etiology Confirmation: Gram stain/culture via stereotactic aspiration or surgical drainage.

6.1 Diagnostic Algorithm

  1. Clinical Suspicion: Based on headache, fever, focal deficits, seizures.
  2. Neuroimaging: MRI preferred over CT for early cerebritis and posterior fossa lesions.
  3. Imaging Interpretation: ◦ Cerebritis: Low T1, irregular postgadolinium enhancement, high T2 signal. ◦ Mature Abscess: Hypodensity with ring enhancement on CT; hyperintense central pus with hypointense capsule on T2-weighted MRI. ◦ DWI: Restricted diffusion (high signal on DWI, low signal on ADC).
  4. Lumbar Puncture: Avoid in focal infections due to herniation risk.
  5. Etiology Confirmation: Gram stain/culture via stereotactic aspiration or surgical drainage.
  6. Treatment Adjustment: Modify empirical therapy based on culture results.

7. MANAGEMENT & TREATMENT

  1. Initial Management: Combine high-dose parenteral antibiotics and neurosurgical drainage.
  2. Medical Therapy Alone: Reserved for inaccessible abscesses, small nonencapsulated lesions, or unstable patients.
  3. Antibiotic Duration: Minimum 6–8 weeks of parenteral antibiotics.
  4. Anticonvulsants: Indicated for seizures; continue ≥3 months after resolution of the abscess.
  5. Glucocorticoids: Avoid routinely (may delay encapsulation); use only for significant periabscess edema.
  6. Surgical Intervention: Required for multiloculated, neurosurgically inaccessible, or small nonencapsulated abscesses; SDE requires emergent neurosurgical evacuation.
  7. Empirical Therapy Selection: ◦ Community-acquired: 3rd/4th-gen cephalosporin + metronidazole. ◦ Penetrating trauma/neurosurgery: Ceftazidime + vancomycin. ◦ Hospital-acquired SDE: Carbapenem + vancomycin (Metronidazole not necessary with meropenem). ◦ Cranial epidural abscess: 3rd-gen cephalosporin + vancomycin + metronidazole.

7.1 Empirical Antibiotic Therapy

See Table 1 for specific regimens and durations.

7.2 Neurocysticercosis Treatment Regimen

• Albendazole monotherapy: 15 mg/kg/day (2 doses) for 10–14 days. • Combination therapy: Albendazole + praziquantel 50 mg/kg/day for 10–14 days. • Corticosteroids: Prednisone/dexamethasone prior to anticysticidal therapy. • Calcified lesions: No treatment required. • Antiepileptic therapy: Continue ≥3 months after resolution of the abscess.

8. PROGNOSIS & COMPLICATIONS

• Mortality: <15% with modern management. • Sequelae: Significant sequelae (seizures, weakness, aphasia) in ≥20% survivors. • SDE Prognosis: Depends on consciousness at presentation, empyema size, and treatment timing. • Long-term Sequelae: Seizures, hemiparesis occur in up to 50% of cases.

8.1 Sequelae and Follow-up

• Monitoring: Serial MRI/CT scans monthly or twice-monthly to monitor resolution. • Anticonvulsants: Continued ≥3 months post-abscess resolution. • Tapering: EEG-guided tapering of anticonvulsants. • Long-term Management: Antiepileptic therapy for seizures after edema resolution.

9. SPECIAL CONSIDERATIONS

• Meningeal biopsy: May be diagnostic in cryptogenic cases; use if imaging and culture results are inconclusive. • Biopsy Risks: Bleeding, infection, and increased ICP.

9.1 Diagnostic Yield of Meningeal Biopsy

• Utility: Identifying atypical pathogens. • Indication: Patients with negative imaging and persistent symptoms.

10. KEY PEARLS & CLINICAL TRAPS

• Contraindication: Never perform LP in focal CNS infections (risk of herniation). • Imaging Gold Standard: Use DWI to differentiate abscess from tumor (restricted diffusion is pathognomonic). • SDE Emergency: Subdural empyema requires emergent neurosurgical evacuation. • Steroid Warning: Glucocorticoids delay encapsulation. • Neurocysticercosis: Treatment depends on cyst stage; calcified lesions do not require treatment. • Imaging Signatures: ◦ Restricted diffusion on DWI = pathognomonic for abscess. ◦ Ring-enhancing lesion with peripheral edema = common MRI finding. ◦ Subdural empyema: crescent-shaped hypodensity on CT/MRI. ◦ Cranial epidural abscess: lentiform fluid collection adjacent to skull.

10.1 Imaging Signatures

• Restricted Diffusion: Pathognomonic for abscess (High signal on DWI, Low signal on ADC). • Ring-Enhancement: Characteristic of mature abscess with peripheral edema. • Subdural Empyema: Crescent-shaped hypodensity between dura and arachnoid. • Cranial Epidural Abscess: Located between skull table and dura.