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    Brain Abscess

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    Fitrie Desbassarie
    Brain abscesses are caused by bacterial or fungal infections that spread from contiguous sites like the sinuses or middle ear, or from distant sites via the bloodstream. Common symptoms include headache, altered mental status, and focal neurological deficits. Diagnosis is made through CT or MRI imaging showing a ring-enhancing lesion. Treatment involves intravenous antibiotics tailored to the identified pathogen and sometimes surgical drainage. Follow up imaging is needed to monitor resolution of the abscess over several months.

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    Brain Abscess

    Uploaded by

    Fitrie Desbassarie
    201 views27 pages
    Brain abscesses are caused by bacterial or fungal infections that spread from contiguous sites like the sinuses or middle ear, or from distant sites via the bloodstream. Common symptoms include headache, altered mental status, and focal neurological deficits. Diagnosis is made through CT or MRI imaging showing a ring-enhancing lesion. Treatment involves intravenous antibiotics tailored to the identified pathogen and sometimes surgical drainage. Follow up imaging is needed to monitor resolution of the abscess over several months.

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    radiologi. brain. abscess

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    Brain abscesses are caused by bacterial or fungal infections that spread from contiguous sites like the sinuses or middle ear, or from distant sites via the bloodstream. Common symptoms include headache, altered mental status, and focal neurological deficits. Diagnosis is made through CT or MRI imaging showing a ring-enhancing lesion. Treatment involves intravenous antibiotics tailored to the identified pathogen and sometimes surgical drainage. Follow up imaging is needed to monitor resolution of the abscess over several months.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    201 views27 pages

    Brain Abscess

    Uploaded by

    Fitrie Desbassarie
    Brain abscesses are caused by bacterial or fungal infections that spread from contiguous sites like the sinuses or middle ear, or from distant sites via the bloodstream. Common symptoms include headache, altered mental status, and focal neurological deficits. Diagnosis is made through CT or MRI imaging showing a ring-enhancing lesion. Treatment involves intravenous antibiotics tailored to the identified pathogen and sometimes surgical drainage. Follow up imaging is needed to monitor resolution of the abscess over several months.

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    24/7/2013

    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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    Brain Abscess

    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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