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Brain Abscess

Definition

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Brain Abscess

ETIOLOGY
1.Infection :
Infection spread by either direct or through veins (thrombophlibitis of diploic vein) Characterized by solitary and located superficially

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PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESS

Otitis/mastoiditis Temporal lobe, Cerebellum Frontal/ethmoid sinusitis Frontal lobe Sphenoidal sinusitis Dental infection Remote source Frontal lobe, Sella turcica Frontal > temporal lobe. Middle cerebral artery distribution (often multiple)

PATHOGENESIS
Direct spread from contiguous foci (40-50%) Hematogenous (25-35%) Penetrating trauma/surgery (10%) Cryptogenic (15-20%)

Predisposing Conditions & Microbiology of Brain Abscess

Predisposing Condition
Otitis media or mastoiditis

Usual Microbial Isolates

Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp., Enterobacteriaceae
Streptococci, Bacteroides spp., Enterobacteriaceae, Staph. aureus, Haemophilus spp. Fusobacterium, Prevotella and Bacteroides spp., streptococci

Sinusitis (frontoethmoid or sphenoid)

Dental sepsis

Penetrating trauma or postneurosurgical

S. aureus, streptococci, Enterobacteriaceae, Clostridium spp.

PPID,2000

PREDISPOSING CONDITION
Lung abscess, empyema, bronchiectasis

USUAL MICROBIAL ISOLATES

Fusobacterium, Actinomyces, Bacteroides Prevotellaspp., streptococci, Nocardia S. aureus, streptococci Streptococci, Haemophilus spp. Aerobic gram-negative bacilli, Aspergillus Mucorales, Candidaspp. Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp., Toxoplasma gondii Toxoplasma gondii, Nocardia spp., Mycobacterium spp., Listeria monocytogenes, Cryptococcus neoformans

Bacterial endocarditis
Congenital heart disease Neutropenia Transplantation

HIV infection

PPID, 2000

 Symptoms : 1. Head ache ( 90 %) 2. Change in conscious level ( 60 %) 3. FND ( 60 %)

Parietal lobe : hemiparesis Temporal lobe : dysphasia Cerebellar : ataxia and nystagmus

4.Fever (more than 50 %) 5. Nausea and vomiting ( 50 %) 6. Seizure ( 50 %) 7.Papilledema and meningismus
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LOCATION & CLINICAL FEATURES

FRONTAL LOBE: H/A, drowsiness, inattention, hemiparesis, motor speech disorder, AMS TEMPORAL LOBE: Ipsilateral H/A, aphasia, visual field defect

PARIETAL LOBE: H/A, visual field defects, endocrine disturbances

CEREBELLUM: Nystagmus, ataxia, vomiting, dysmetria

DIFFERENTIAL DIAGNOSIS
Malignancy
Abscess has hypo-dense center, with surrounding smooth, thin-walled capsule, & areas of peripheral enhancement. Tumor has diffuse enhancement & irregular borders. SPECT (PET scan) may differentiate. CRP too?

CVA Hemorrhage Aneurysm Subdural empyema/ICEpidural abscess

DIAGNOSIS
High index of suspicion Contrast CT or MRI Drainage/biopsy, if ring enhancing lesion(s) are seen

 Preceding antibody formation there is an area of necrosis which is seeded by bacteria

PATHOGENESIS AND HISTOPATHOLOGY OF BRAIN ABSCESS

Brain abscess formation are 4 stages 1.stage I:early cerebritis (day 1 to day 3) : Necrotic tissue ,local inflammatory response, marked edema This stage there is no demarcation between the lesion and surrounding brain
2.stage two (late cerebritis)(day 4-10): pus , maximum edema 3.stage three (early encapsulation)(day1013) :
Capsule limits spread of infection Capsule develops slowly in medial wall of abscess?

4.Stage four: late capsule stage ( >day 14)

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 Clinical presentation :

Occur in majorities in the first 2 decades of life Males more affected ( cause is unknown ) adults depend on immune status Infants : increase in head circumference , bulging fontanel , separation of cranial sutures , vomiting , irritability , seizures Signs of IICP and FND : 1. Edema 2. Cerebral tissue destruction

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Radiological characteristic
1. Brain CTS with contrast ring enhancement Multi loculation Multiplicity Finding of gas 2. MRI : T1 : necrotic center ( hypointence) Capsule ( hyperintence) Edema ( hypointence) T2 : necrotic center ( hyperintence) Capsule ( hypointence) Edema ( hyperintence
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Brain abscess. Axial fluid-attenuated inversion recovery (FLAIR) MRI of a left occipital-parietal brain abscess. The edema pattern (white arrows) surrounds the central abscess (A). A secondary (daughter) abscess is noted anterior to the primary abscess cavity.

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Brain abscess. Sagittal T1weighted spin-echo gadolinium-enhanced MRI demonstrates an enhanced mass within the right medial cerebellum (yellow arrow). The thick-walled cystic mass was opened. Nocardia organisms were cultured from within the abscess.

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Brain abscess. Axial T2weighted MRI in a patient with a right frontal abscess. Note the mass effect and surrounding edema. The wall of the abscess is relatively thin (black arrows).

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Brain abscess. Gadoliniumenhanced coronal T1-weighted MRI in a patient who presented with headache, fever, and diplopia. The right frontal lobe of the brain is shifted across the midline (double arrow) by an intracranial abscess (single black arrow) that has extended upward from the medial right orbit and medial ethmoid air cells (curved dotted arrow). Aspergillus organisms were recovered from the sinuses and brain tissue.

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Follow up CT weekly during antibiotic therapy And then monthly CT 2-3 week decrease size of abscess 3-4 months complete resolution of abscess 6-9 months no residual contrast enhancement
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Before Rx

After completion of Rx

Armstrong ID,Mosby inc 1999

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