Brain Abscess Dr. Safdar Malik. Definition Brain abscess is a focal suppurative infection within the brain parenchyma, typically surrounded by a vascularized.

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Presentation transcript:

Brain Abscess Dr. Safdar Malik

Definition Brain abscess is a focal suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule. Cerebritis: is often employed to describe a nonnencapsulated brain abscess.

Epidemiology Relatively uncommon Incidence~.3-1.3: person per year

Etiology Brain abscess may develop by 1. Direct spread from a contiguous cranial site of infection 2. Head trauma, neurosurgical procedures 3. Hematogenous spread 25% cases : There isno primary source of infection

Predisposing conditions Otitis media Mastoiditis Paranasal sinusitis Pyogenic infection of chest or any other part of body Penetrating head injury Neurosurgical procedure Dental infection

In Immunocompetent persons: Streptococcus spp. (aerobic, Anaerobic and viridans) 40% Enterobacteriaceae (Proteus, E.coli, Klebsella) 25% Anaerobes (Bacteroides, Fusobacterium) 30% Staphylococci 10% Taenia solium(NCC) Mycobacterial infection (tuberculoma)

In immuno-compromised host Nocardia T gondii Aspergillus Candida C. neoformans

Stages 1. Early Cerebritis: 1-3days A perivascular infiltration of inflammatory cells around a central core of coagulation necrosis 2. Late Cerebritis: 4-9 days Pus formationin necrotic center which is surrounded by inflammatory cells and fibroblast 3. Early Capsule Formation: days A capsule that is better develop on corticalthen on ventricle side of lesion 4. Late Capsule Formation: beyond 14 days A well defined necrotic center surrounded by a dense collageous capsule

Clinical Presentation Typically presents as an expanding intracranial mass rather than as a infectious process Symptoms are gradual in onset Patients present weeks to month Usually presents days following onset of symptoms.

Symptoms Classical triad: seen in <50% patients Headache 75% Fever 50% Focal neurologic deficit 15-35%

Focal neurologic deficit Aphasia Hemiparesis Visual field defect Ataxia Nystagmus Seizures Raised ICP-Papilledema Meningismus Uncommon unless abscess rupture in ventricle

Investigations TLC, DLC ESR, CRP Blood cultures Neuroimaging studies: MRI: better esp can detect early stages of cerebritis CT Scan: a focal area of hypodensity surrounded by ring enhancementwith surrounding edema (hypodensity)

MRI

CT Scan

Microbiological Evaluation CT-guided stereotactic needle aspiration Gram’s Stain Culture : Aerobic, Anaerobic, Mycobacterial and fungal cultures Blood Culture LP: do not perform

D/D Bacterial Meningitis Meningoencephalitis Acute disseminated encephalomyelitis Empyema Saggital Sinus Thrombosis Primary or Secondary brain tumor CVA

Treatment Combination of high dose parentral antibiotics and neurosurgical drainage Third/fourth grneration cephalosporin+Metronidazole Patients with neurodurgery/Head trauma Vancomycin+Ceftazidine Meropenem+Vancomycin Modify antibiotics as per culture results Duration: Min 6-8 weeks

Prophylactic anticonvulsant Should continue atleast 3 months after resolution of abscess Role of steroids Not given routinely Usually reserved forof significant periabscess edema with mass effect and raise ICP Dexamethasone 10 mg 6 hrly

Aspiration and Drainage of the abscess under stereotactic guidance Craniotomy and Complete excision of a bacterial abscess: reserved for multiloculated abscess or in those where aspiration is unsucessful.

Prognosis Mortality rate <15% Neurological sequelae ≥20% of survivors