Brain Abscess

What is brain abscess?

Focal collection within brain parenchyma

Pathogenesis?

 Direct  20-60% of the cases  Focal abscess  Hematogenous  Multiple abscesses  No identifiable souces in 20-40% of the cases

Primary sources in direct spread and distribution of abscess

   Otitis media – inferior temporal lobe and cerebellum Frontal or ethmoid sinuses – frontal lobe Dental caries – frontal lobe  Foreign bodies - bullet

Primary sources hematogenous spread

 Chronic pulmonary infections – lung abscess and empyema  Skin infection  Intrabdominal and pelvic infection   Bacterial endocarditis Cyanotic congenital heart disease – most common in children

Microbiology

Clues to the primary source

Anaerobics

 Usually mouth flora   May be from pelvic or intraabdominal infections – multiple abscesses Examples – anaerobic streptococci, bacteroides species, fusobacterium

Aerobics

  Gram positive    Staphylococcus aureus – neurosurgery and trauma Streptococcus milleri – proteolytic enzymes that cause necrosis Others – viriddans streptococci, microaerophilic streptocci Gram negative   Usually from trauma or neurosurgery Klebsiella pneumoniae, Pseudodomonas species, E. coli, and Proteus species

Immunocompromised hosts?

 Opportunistic infections  Toxoplasma gondii   Listeria Fungi – Aspergillus, cryptococcus neoformans, coccidiodidides immitis, Candida albicans

Immigrants

  Parasites Cysticercosis – 85% of brain infection in Mexico city

Symptoms?

 Headache – most common  Neck stiffness  Associated with occipital abscess    Abscess leaks into lateral ventricle Altered mental status – cerebral edema Vomiting – increased intracranial pressure

Physical finding?

  Fever – not very reliable, since only 45-50% present Focal neurological deficit – days or weeks after onset of headache    Seizure   25% of the cases May be first manifestation of brain abscess  Grand mal in frontal infection Third or sixth cranial palsy – increased intracranial pressure Papilledema – cerebral edema

Tests?

 CT scan with contrast  MRI with gadolinium diethylenetriamine  Lumbar puncture  Contraindicated  Analysis   WBC < 500/mm 3 with predominately lymphocytes WBC > 1,000/mm 3 consistent with meningitis but not improved with antibiotics, consider MRI for ruptured abscess

Treatment options?

 Antibiotics – 6 to 8 weeks  Surgical drainage

Antibiotics?

       Penicillin G – aerobic and anaerobic streptococci from mouth flora Metronidazole – against anaerobes but not aerobes, good intralesional penetration Ceftriaxone or cefotaxime – Enterobacteraciae, particular chronic ear infection Ceftazidime – neurosurgery and p. aeruginosa Oxacillin or nafcillin – head trauma or neurosurgery, mainly staphylococcus aureus coverage Vancomycin – MRSA Aminoglycosides – poor blood brain barrier, not use

Indications for surgical drainage?

 No clinical improvement within a week  Depressed sensorium  Increased intracranial pressure  Progressive increase in the ring diameter of the abscess

Surgical approach

 Needle aspiration   Prefer approach because of less neurological deficit Under ultrasound or CT guided  Surgical excision  More neurological deficit   Prefer in traumatic abscess, particularly with foreign body,and encapsulated fungal abscess Advantages: shorten antibiotics to 2 to 4 weeks and less relapse

Steroid use?

 Mainly for mass effect  Disadvantages  Reduce contrast enhancement on CT scan  Slow capsule formation  Increase risk of rupture  Decrease penetration of antibiotics

Complications

  Neurological deficits – commonly seizure with frontal lesion Poor prognosis – mortality rate up to 30%  Rapid progression of the infection  Severe mental changes  Rupture into ventricle