BRAIN ABSCESS

PRESENTED BY:-

JASPREET KAUR SODHI

BRAIN ABSCESS

• The advent of antibiotics and improved treatment of ear diseases has lead to a reduction in intracranial abscess formation ,but the incidence is still 2-3 patients /million/year

Brain Abscess

• Microorgansims reach the brain by• i. Direct extension• ii. Hematogenous spread• Iii. Direct inoculation from penetrating

trauma or neurosurgical intervention

Brain Abscess

• Younger patients affected (<40 years)• Presence of predisposing condition in 80%

of cases• Immunocompromised states from AIDS

and immunosuppressive drugs in organ transplant recipents

Most Common Pathogens

• Otitis media, mastoiditis Streptococci• Paranasal sinusitis Streptococci

• Pulmonary infection Strep, Actionomyces

• Dental Mixed, Bacteroides spp.• CHD Strep

• Penetrating/Post-crani S. aureus

• HIV Toxoplasma gondii• Transplant Aspergillus, Candida

BRAIN ABSCESS

• Causes :

1. complication of bacterial meningitis

2. bacterial endocarditis

3. pulmonary sepsis : peumonia……etc

4. other sepsis

Brain abscess cause a space occupying lesion in the brain

PREDISPOSING FACTORS

• Congenital heart disease (6.1%) • HIV infection (1.2%) • Immunosuppression (3.7%) • Diabetes mellitus (3.1%)

Brain Abscess

Pathophysiology• A collection of

infectious material within the tissue of the brain

• Infection • I-ICP • Brain shift

Brain Abscess

2 ways infection can enter the brain

• Direct invasion • Spread from nearby

sight– Sinuses– Ears– Teeth

Tongue piercing causes brain abscess• 13 December 2001 New Scientist • Parents now have another reason to frown on

tongue piercing - a potentially fatal brain abscess suffered by a young woman in Connecticut.

• The woman's tongue became sore and swollen two or three days after it was pierced, and she reported a foul-tasting discharge from the pierced region. The infection healed in a few days after she removed the stud from her tongue, but a month later she suffered severe headaches, fever, nausea and vomiting.

• A scan at the Yale University hospital revealed the brain abscess, which physicians drained. She recovered after six weeks of intravenous antibiotic treatment.

Brain Abscess

Clinical manifestations• I-ICP• Infection• Fever?

– Sometimes– Sometimes not!

PATHOGENESIS• Direct spread from contiguous foci (40-50%)

• Hematogenous (25-35%)

• Penetrating trauma/surgery (10%)

• Cryptogenic (15-20%)

DIRECT SPREAD(from contiguous foci)

• Occurs by:– Direct extension through infected bone– Spread through emissary veins, diploic veins,

local lymphatics

• The contiguous foci include:• Otitis media/mastoiditis • Sinusitis• Dental infection (<10%), typically with molar infections • Meningitis rarely complicated by brain abscess (more

common in neonates with Citrobacter diversus meningitis, of whom 70% develop brain abscess)

HEMATOGENOUS SPREAD (from remote foci)

• Sources:– Empyema, lung abscess, bronchiectasis,

endocarditis, wound infections, pelvic infections, intra-abdominal source, etc…

– may be facilitated by cyanotic HD, AVM.

• Results in brain abscess(es) at middle cerebral artery distribution

• Often multiple

PREDISPOSING CONDITION & LOCATION OF BRAIN ABSCESS

Otitis/mastoiditis Temporal lobe, Cerebellum

Frontal/ethmoid sinusitis Frontal lobe

Sphenoidal sinusitis Frontal lobe,

Sella turcica

Dental infection Frontal > temporal lobe.

Remote source Middle cerebral artery distribution (often multiple)

Microbiology of Brain Abscess• Dependent upon:

• Site of primary infection• Patient’s underlying condition• Geographic location

• Usually streptococci and anaerobes • Staph aureus, aerobic GNR common

after trauma or surgery• 30-60 % are polymicrobial

Brain Abscess

Medical Management• Antimicrobial therapy

– Large IV doses

• Surgery• Anti-convulsant

Brain Abscess

• Microorgansims reach the brain by• i. Direct extension• ii. Hematogenous spread• Iii. Direct inoculation from penetrating

trauma or neurosurgical intervention

PATHOPHYSIOLOGY• Begins as localized cerebritis (1-2

wks)• Evolves into a collection of pus

surrounded by a well-vascularized capsule (3-4 wks)

• Lesion evolution (based on experimental

animal models):– Days 1-3: “early cerebritis stage”– Days 4-9: “late cerebritis stage”– Days 10-14: “early capsule stage”– > day14: “late capsule stage”

STAGES

1. Early cerebritis stage (D1-3):focal area of inflammation and edema

2. Late cerebritis stage (D4-9):development of a necrotic central focus

3. Early capsule stage (D10-14):ring-enhancing capsule of well-vascularized tissue with early appearance of peripheral fibrosis

4. Late capsule stage (>D14):host defenses lead to a well-formed capsule

PATHOGENESISPATHOGENESIS•Bacterial invasion of brainBacterial invasion of brain (Parenchyma )(Parenchyma )•Preexisting or concomitant :Preexisting or concomitant : Ischemia &Ischemia & Necrosis & Necrosis & Hypoxia of brain tissueHypoxia of brain tissue

PATHOGENESISPATHOGENESIS

Early cerebritis ( days 1 to 3 )Early cerebritis ( days 1 to 3 )

Prevascular infiltration of inflammatory Prevascular infiltration of inflammatory cellscells

Central core of coagulative necrosis Central core of coagulative necrosis

Marked edema surrounds the lesionsMarked edema surrounds the lesions

Stage 1 Stage 1

Early CerebritisEarly Cerebritis

Early cerebritisEarly cerebritis

Late cerebritis( days 4 to 9 )Late cerebritis( days 4 to 9 ) Pus formation ( necrotic center )Pus formation ( necrotic center )

Macrophages & Fibroblasts Macrophages & Fibroblasts

Thin capsule( Fibroblast & Reticular Thin capsule( Fibroblast & Reticular fibers )fibers )

Marked edema around the lesions Marked edema around the lesions

Stage 2Stage 2

Late CerebritisLate Cerebritis

Early Capsule formation ( days 10 to13 )Early Capsule formation ( days 10 to13 )

Capsule formationCapsule formation

Ring-enhancing capsule ( Imaging )Ring-enhancing capsule ( Imaging )

Stage 3Stage 3

Early Capsule formationEarly Capsule formation

Stage 4 Stage 4

Late Capsule formation ( > 14 days )Late Capsule formation ( > 14 days ) Well formed necrotic centerWell formed necrotic center

Dense peripheral collagenous capsuleDense peripheral collagenous capsule

No cerebral edemaNo cerebral edema

Marked gliosis & reactive astrocytesMarked gliosis & reactive astrocytes

Gliosis Gliosis Seizures Seizures

CLINICAL PRESENTATIONSCLINICAL PRESENTATIONSBrain abscess presents as an Brain abscess presents as an Expanding Intracranial massExpanding Intracranial massHeadache > 75%Headache > 75% Constant, Dull, Constant, Dull, Aching sensationAching sensation Hemicranial or General Hemicranial or General Progressive Progressive Refractory RefractoryFever: 50% & Low gradeFever: 50% & Low gradeSeizure: New onset Seizure: New onset Focal or GeneralizedFocal or Generalized

CLINICAL PRESENTATIONSCLINICAL PRESENTATIONS

Increased Intracranial Pressure:Increased Intracranial Pressure:•PapilledemaPapilledema•NauseaNausea•VomitingVomiting•DrowsinessDrowsiness•ConfusionConfusionMeningismus:Meningismus:•When it has ruptured into When it has ruptured into Ventricle or subarachnoid spaceVentricle or subarachnoid space

CLINICAL PRESENTATIONSCLINICAL PRESENTATIONS

CLINICAL MANIFESTATIONS

• Non-specific symptoms• Mainly due to the presence of a space-

occupying lesion• H/A, N/V, lethargy, focal neuro signs ,

seizures

• Signs/symptoms influenced by • Location • Size• Virulence of organism• Presence of underlying condition

CLINICAL MANIFESTATIONSCLINICAL MANIFESTATIONS

OF BRAIN ABSCESS

Headache 70%

Fever 50

Altered mental status 50-60 Triad of above three <50Focal neurologic findings 50Nausea/vomiting 25-50

Seizures 25–35

Nuchal rigidity 25

Papilledema 25

CLINICAL MANIFESTATIONS

Headache • Often dull, poorly localized

(hemicranial?), non-specific–Abrupt, extremely severe

H/A: think meningitis, SAH.

–Sudden worsening in H/A w meningismus: think rupture of brain abscess into ventricle (often fatal)

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

Brain Abscess

Diagnostic findings• CT• MRI

DIAGNOSIS

• High index of suspicion

• Contrast CT or MRI

• Drainage/biopsy, if ring enhancing lesion(s) are seen

TREATMENT

• Combined medical & surgical• Aspiration or excision• empirical abx

• Empirical antibiotics are selected based on:• Likely pathogen (consider primary source, underlying

condition, & geography)• Antibiotic characteristics: usual MICs, CNS penetration,

activity in abscess cavity

• Modify abx based on stains• Duration: usually 6-8 wks

• after surgical excision, a shorter course may suffice

Armstrong ID, Mosby inc 1999

MEDICAL TREATMENT ONLY

• Only in pts with prohibitive surgical risk: – poor surgical candidate,– multiple abscesses,– in a dominant location,– Abscess size <2.5 cm– concomitant meningitis, ependymitis, – early abscess (cerebritis?) – with improvement on abx,

[Better-vascularized cortical lesions more likely to respond to abx alone]

[ Subcortical/white-matter lesions are poorly vascularized]

Treatment

• I.V. Antibiotics 6 weeks• Steroids• Surgical intervention: Stereotactic

aspiration vs. craniotomy

ANTIBIOTICS

• CEFTRIAXONE i.v 3-4 g/day• METRONIDAZOLE i.v 500 mg tds• + amoxicillin iv 2g 4 hourly (for middle ear

source)

If ENDOCARDITIS OR CONGENITAL HEART FAILURE DISEASES,

+ benzylpenicillin i.v 1.8-2.4 g 6hourly

IF A PENETRATING TRAUMA,

FLUCLOXACILLIN-i.v 2g 4 hourly.

GENTAMICIN –i.v 5 mg/kg/day(monitor levels)

ABSCESS DRAINAGE

• Primary excision of the whole abscess

• Burr hole aspiration of pus,guided by ultrasound & frameless sterotaxy,with repeated aspirations if required.

• Evacuation of abscess contents under direct vision, leaving capsule remnants.

TREATMENT OF INFECTION SITE

• Mastoditis and sinusitis require immediate surgery.

• Use of steroids is controversial.

• Conservative management

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BRAIN ABSCESS