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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 on theme: "Brain Abscess Dr. Safdar Malik. Definition Brain abscess is a focal suppurative infection within the brain parenchyma, typically surrounded by a vascularized."— Presentation transcript:

1 Brain Abscess Dr. Safdar Malik

2 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.

3 Epidemiology Relatively uncommon Incidence~.3-1.3:100000 person per year

4 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

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

6 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)

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

8 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: 10-13 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

9 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 11-12 days following onset of symptoms.

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

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

12 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)

13 MRI

14 CT Scan

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

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

17 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

18 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

19 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.

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


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