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BRAIN ABSCESS. M.RASOOLINEJAD, MD DEPATMENT OF INFECTIOUS DISEASE TEHRAN UNIVERSITY OF MEDICAL SCIENCE. BRAIN ABSCESS. Focal & Suppurative Process in Brain Parenchyma. Anatomical Relationships of the Meninges. Bone Dura Mater Arachnoid Pia Mater Brain.

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BRAIN ABSCESS

M.RASOOLINEJAD, MD

DEPATMENT OF INFECTIOUS DISEASE

TEHRAN UNIVERSITY OF

MEDICAL SCIENCE


BRAIN ABSCESS

Focal

&

Suppurative Process

in Brain Parenchyma


Anatomical Relationships of the Meninges

  • Bone

  • Dura Mater

  • Arachnoid

  • Pia Mater

  • Brain

  • Epidural Abscess

  • Subdural Empyema

  • Meningitis


EPIDEMIOLOGY

  • Uncommon intracranial infections

  • Incidence 1:100,000/year

  • Predisposing conditions: Paranasal Sinusitis

  • Otitis Media

  • Dental infections

  • Immunocompromised pts Uncommon org

  • (T.gondii, Aspergillus spp, Nocardia spp, …)


ETHIOLOGY

  • Abrain abscess may develop:

  • Direct spread from a contagious cranial of infections

  • ( Paranasal sinusitis, Otitis media, Mastoiditis,…..)

  • 2. Following head trauma or Neurological procedure

  • 3. Hematogenous spread from remote site of inf

  • 4. No obivious primary source of inf ( 20-30% )

  • (Cryptogenic brain abscess )


ETHIOLOGY

  • Most common organisms are :

  • Paranasal sinusitis:Microaerophilic &

  • Anaerobic strep

  • Haemophilus spp

  • Bacteroides spp

  • Fusobacterium spp

  • Dental infections: Streptococci spp

  • Prevetella

  • Prophyromanas


ETHIOLOGY

Most common organisms are :

Otitis media & Mastoiditis:

Streptococci

Bacteroides spp

P. aeroginosa

Enterobacteriaceae

Hematogenous: S. Viridance

S. Aureous

Neurosergical procedure & open head trauma:

(S. aureous, Enterobactericeae, P. aeroginosa)


SOURSE OF BRAIN ABSCESS

  • Frontal lobe:Frontal & Ethmoidal & Sphenoidal sinuses

  • Dental infections

  • Temporal lobe: Middle ear, Mastoid, Maxillary sinuses

  • Cerebellum & Brain Stem: Middle ear & Mastoid

  • Posterior Frontal or Parietal lobes:

  • Middle Cerebral Artery

  • Gray- White matter

  • Often multiple


PATHGENESIS

  • Bacterial invasion of brain

  • (Parenchyma )

  • Preexisting or concomitant :

  • Ischemia &

  • Necrosis &

  • Hypoxia of brain tissue


PATHGENESIS

4 Stages Brain Abscess formation:

Stage 1

  • Early cerebritis ( days 1 to 3 )

  • Prevascular infiltration of inflammatory cells

  • Central core of coagulative necrosis

  • Marked edema surrounds the lesions


Early Cerebritis


Early cerebritis


PATHGENESIS

4 Stages Brain Abscess formation:

Stage 2

  • Late cerebritis ( days 4 to 9 )

  • Pus formation ( necrotic center )

  • Macrophages & Fibroblastrs

  • Thin capsule ( Fibroblast & Reticular fibers )

  • Marked edema around the lesions


Late Cerebritis


PATHGENESIS

4 Stages Brain Abscess formation:

Stage 3

  • Early Capsule formation ( days 10 to13 )

  • Capsule formation

  • Ring-enhancing capsule ( Imaging )


Early Capsule formation


PATHGENESIS

4 Stages Brain Abscess formation:

Stage 4

  • Late Capsule formation ( > 14 days )

  • Well formed necrotic center

  • Dense peripheral collagenous capsule

  • No cerebral edema

  • Marked gliosis & reactive astrocytes

  • Gliosis  Seizures


CLINICAL PRESENTATIONS

Brain abscess presents as an

Expanding Intracranial mass

  • Headache > 75%

  • Constant, Dull,

  • Aching sensation

  • Hemicranial or General

  • Progressive  Refractory

  • Fever: 50% & Low grade

  • Seizure: New onset

  • Focal or Generalized


CLINICAL PRESENTATIONS

  • Increased Intracranial Pressure:

  • Papilledema

  • Nausea

  • Vomiting

  • Drowsiness

  • Confusion

  • Meningismus:

  • When it has ruptured into

    Ventricle or subarachnoid space


CLINICAL PRESENTATIONS

  • Focal neurologic deficit > 60%

  • Frontal lobe Hemiparesis

  • Mental status, Drowsiness

  • Temporal lobe  Dysphasia

    Upper homonymous quadrantanopia

    Ipsilateral headache


CLINICAL PRESENTATIONS

  • Focal neurologic deficit > 60%

  • Cerebellar  Nystagmus, Ataxia

  • Dysmetria, vomiting

  • Brain stem  Facial weakness,

  • Fever, Hemiparesis, Dysphagia,

  • Vomiting, Headache, Fever


DIAGNOSIS

NEUROIMAGING STUDIES

  • Brain CT- Scan

  • MRI ( Early cerebritis, Posterior Fossa)

  • Steriotactic Needle aspiration

  • Lumbar puncture  Risk of Herniation

  • CSF  Non Specific

  • Peripheral leucocytosis: 50%

  • Elevated ESR: 60%


Left parietal abscess


Marked edema


Ring Enhancement


Multiple abscess in a 6 years old boy


Presumed source of polymicrobial abscess


Cerebellar Abscess


Mixed Abscess Location


T. Gondii Encephalitis


T. Gondii Encephalitis


T. Gondii Encephalitis


TREATMENT

SURGICOMEDICAL

  • Aspiration Or Open Drainage

  • Empirical Combination

  • Antimicrobial Therapy

  • Duration: 6 to 8 wks IV

  • Prophylactic Anticonvulsant Therapy

  • Glucocorticoids( Severe Edema & ICP )

  • Serial CT-Scan or MRI


ANTIMICROBIAL THERAPY

  • Otitis media & Mastoiditis:

  • Metronodazole & 3rd Cephalosporin

  • Sinusitis:

  • Metronidazole & 3rd Cephalosporine

  • Dental Sepsis:

  • Penicillin & Metronidazole


ANTIMICROBIAL THERAPY

  • Penetrating trauma &Neurosurgury:

  • Vancomycin & 3rd Cephalosporin

  • Bacterial endocarditis:

  • Vancomycin & Gentamycin

  • Nafcilline (Oxacillin) & Ampicillin

  • & Gentamycin

  • Unknown:

  • Vancomycin & Metronidazole &

    3rd Cephalosporin


PROGNOSIS

  • Successfully treatment 

  • Good prognosis

  • Seizures are a

  • common complication 70%


THE

END


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