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Brain Abscess and Empyema

Chapter 145 | Part 5: Infectious Diseases

KEY CLINICAL POINTS

  • Brain abscess is a focal suppurative infection in the brain parenchyma, typically surrounded by a vascularized capsule.
  • Empyema refers to a collection of pus in the subdural space between the dura and arachnoid membranes.
  • Neurocysticercosis is the most common parasitic CNS infection, caused by Taenia solium eggs.
  • Diagnosis relies on neuroimaging (MRI/CT) with contrast, and treatment includes antibiotics, anticonvulsants, and surgical drainage.
  • Subdural empyema (SDE) is a medical emergency requiring emergent neurosurgical drainage.

1. DEFINITION & OVERVIEW

A brain abscess is a focal, suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule. The term cerebritis is often used for nonencapsulated abscesses. Subdural empyema (SDE) is a collection of pus between the dura and arachnoid membranes. Cranial epidural abscess is a suppurative infection in the potential space between the inner skull table and dura. Suppurative intracranial thrombophlebitis refers to septic venous thrombosis of cortical veins and sinuses.

Stages of Neurocysticercosis

Stage MRI/CT Findings Key Features
Vesicular Cystic lesion with scolex (small hypointense nodules), no significant edema Active parasitic infection
Colloidal Peripheral enhancement on postcontrast imaging, substantial T2 edema Degenerating cyst with edema
Granulonodular Homogeneous enhancement on postcontrast imaging, no surrounding edema Granulomatous reaction
Nodular-Calcified Parenchymal brain calcifications Nonviable parasites

Stages of Brain Abscess Development

Stage MRI/CT Findings Key Features
Early Cerebritis (Days 1–3) Low T1 signal, irregular postgadolinium enhancement, high T2 signal Inflammatory infiltration, no capsule
Late Cerebritis (Days 4–9) Enlarged necrotic center with inflammatory infiltrate Pus formation, edema
Stage MRI/CT Findings Key Features
Early Capsule Formation (Days 10–13) Ring-enhancing capsule on imaging Capsule development on cortical side
Late Capsule Formation (Day 14+) Well-formed collagenous capsule, gliosis Encapsulated abscess with gliotic reaction

1.1 Brain Abscess

A focal, suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule. Cerebritis describes nonencapsulated abscesses.

1.2 Subdural Empyema

A collection of pus between the dura and arachnoid membranes, often secondary to sinusitis, head trauma, or neurosurgical procedures.

1.3 Cranial Epidural Abscess

A suppurative infection in the potential space between the inner skull table and dura, often secondary to craniotomy, skull fractures, or sinus infections.

2. EPIDEMIOLOGY

Brain abscess incidence: ~0.3–1.3:100,000/year. Subdural empyema accounts for 15–25% of focal suppurative CNS infections. Neurocysticercosis is the most common parasitic CNS infection globally. Risk factors include immunocompromise (HIV, organ transplant), sinusitis, otitis media, head trauma, and neurosurgical procedures.

2.1 Brain Abscess

Incidence: ~0.3–1.3:100,000/year. Common in immunocompromised patients (HIV, organ transplant) and those with sinusitis/otitis media.

2.2 Subdural Empyema

Accounts for 15–25% of focal suppurative CNS infections. Predominantly affects young males due to sinus anatomy.

2.3 Neurocysticercosis

Most common parasitic CNS infection globally. Prevalent in Latin America, immigrants from Latin America, and India/East Asia.

3. ETIOLOGY & PATHOPHYSIOLOGY

Brain abscess: Bacterial (Streptococcus, Bacteroides, Pseudomonas), fungal (Candida, Aspergillus), or parasitic (Neurocysticercosis, Toxoplasma). Subdural empyema: Streptococci, staphylococci, Enterobacteriaceae. Neurocysticercosis: Taenia solium eggs. Pathophysiology involves direct spread, hematogenous spread, or contiguous spread from sinus/ear infections. Cerebritis precedes capsule formation.

3.1 Brain Abscess

Causes: Direct spread (sinusitis, otitis media), hematogenous spread (endocarditis, lung infections), or contiguous spread. Common pathogens: Streptococcus, Bacteroides, Pseudomonas.

3.2 Subdural Empyema

Causes: Sinusitis (frontal/ethmoid/maxillary), head trauma, neurosurgical procedures. Pathophysiology: Retrograde spread from septic thrombophlebitis or contiguous spread from intracranial infections.

3.3 Neurocysticercosis

Causes: Ingestion of Taenia solium eggs. Pathophysiology: Parasitic cysts in brain parenchyma or subarachnoid space, leading to inflammation and edema.

4. CLINICAL FEATURES

Classic triad: headache, fever, focal neurologic deficit. Seizures (15–35%), hemiparesis, dysphasia, nystagmus, ataxia. Increased ICP (papilledema, vomiting, confusion). Neurocysticercosis: Seizures, increased ICP, spinal mimic of tumors. Toxoplasma encephalitis: Headache, fever, seizures, focal deficits.

4.1 Brain Abscess

Headache (75%), fever (50%), focal deficits (60%), seizures (15–35%). Late stages: Increased ICP, hemiparesis, aphasia.

4.2 Subdural Empyema

Fever, headache, focal deficits, nuchal rigidity. Rapid progression to altered mental status, mass effect, and herniation.

4.3 Neurocysticercosis

New-onset partial seizures (70%), increased ICP, seizures from degenerating cysts. Spinal mimic of tumors.

5. DIFFERENTIAL DIAGNOSIS

Brain abscess: Subdural empyema, bacterial meningitis, viral encephalitis, brain tumor, superior sagittal sinus thrombosis. Subdural empyema: Brain abscess, epidural empyema, bacterial meningitis, acute disseminated encephalomyelitis. Neurocysticercosis: Brain tumor, tuberculoma, toxoplasma encephalitis.

5.1 Brain Abscess vs. Subdural Empyema

Abscess: Focal mass, ring-enhancing capsule. Empyema: Crescent-shaped hypodense lesion, mass effect disproportionate to size.

5.2 Neurocysticercosis vs. Brain Tumor

Cysts with scolex on MRI vs. solid mass. Neurocysticercosis may mimic tumors with calcifications.

6. INVESTIGATIONS & DIAGNOSIS

Neuroimaging (MRI/CT) with contrast. MRI superior for early cerebritis; CT for posterior fossa. CSF analysis avoided in suspected empyema. Lumbar puncture contraindicated in abscess/empyema. Serology for Toxoplasma, cryptococcal antigen, and neurocysticercosis. Gram stain/culture of abscess fluid.

6.1 Neuroimaging

MRI with gadolinium: Best for early cerebritis and capsule visualization. CT for posterior fossa and calcifications. Diffusion-weighted imaging shows restricted diffusion in abscesses.

6.2 CSF Analysis

Avoided in suspected empyema/abscess due to risk of herniation. May show pleocytosis, low glucose, elevated protein in meningitis.

6.3 Serology

Toxoplasma IgG, cryptococcal antigen, neurocysticercosis ELISA/PCR.

7. MANAGEMENT & TREATMENT

Antibiotics (cefotaxime, ceftriaxone, vancomycin, metronidazole), anticonvulsants (phenytoin, levetiracetam), surgical drainage. Neurocysticercosis: Albendazole (15 mg/kg/day) + praziquantel (50 mg/kg/day). Subdural empyema: Emergent drainage, broad-spectrum antibiotics. Cranial epidural abscess: Surgical drainage, antibiotics.

7.1 Brain Abscess

Antibiotics (third-gen cephalosporin + vancomycin/metronidazole). Surgical drainage for multiloculated abscesses. Anticonvulsants for seizure prophylaxis.

7.2 Subdural Empyema

Emergent neurosurgical drainage (craniotomy/burr-hole). Empirical antibiotics: Cefotaxime, vancomycin, metronidazole. Duration: 3–4 weeks.

7.3 Neurocysticercosis

Albendazole (15 mg/kg/day) for 10–14 days. Praziquantel for >2 viable cysts. Corticosteroids to reduce inflammation.

8. PROGNOSIS & COMPLICATIONS

Modern mortality <15% for brain abscess. Long-term sequelae: Seizures (20%), hemiparesis, aphasia, cognitive impairment. Subdural empyema mortality <5%. Neurocysticercosis: Seizures, increased ICP, hydrocephalus. Toxoplasma encephalitis: High mortality in immunocompromised patients.

8.1 Brain Abscess

Mortality <15% with timely treatment. Seizures, hemiparesis, and cognitive deficits in 20% of survivors.

8.2 Subdural Empyema

Mortality <5% with emergent drainage. Complications: Herniation, meningitis, brain abscess.

8.3 Neurocysticercosis

Seizures, increased ICP, hydrocephalus. Risk of status epilepticus and cerebral edema.

9. SPECIAL CONSIDERATIONS

Pregnancy: Avoid corticosteroids, use anticonvulsants cautiously. Pediatrics: High risk of seizures, need for anticonvulsants. Elderly: Increased risk of complications from surgery. Immunocompromised: Higher risk of fungal/parasitic causes.

9.1 Pregnancy

Avoid corticosteroids; use anticonvulsants (phenytoin, levetiracetam) for seizure prophylaxis.

9.2 Pediatrics

High seizure risk; early anticonvulsant therapy. Neuroimaging critical for diagnosis.

9.3 Immunocompromised Patients

Higher risk of fungal/parasitic causes (Candida, Aspergillus, Neurocysticercosis). Need for broad-spectrum antibiotics.

10. KEY POINTS & CLINICAL PEARLS

  1. Brain abscess: Ring-enhancing lesion on MRI, treat with antibiotics and drainage. 2. Subdural empyema: Crescent-shaped hypodense lesion on CT, emergent drainage required. 3. Neurocysticercosis: Cysts with scolex on MRI, treat with albendazole. 4. Avoid lumbar puncture in suspected abscess/empyema. 5. Anticonvulsants for seizure prophylaxis in all cases.