Brain Abscess GK

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Transcript of Brain Abscess GK

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Brain abscess

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CNS ABSCESSES• Focal pyogenic infections of the central nervous system

• Exert their effects mainly by:

 – Direct involvement & destruction of the brain or spinal

cord

 – Compression of parenchyma

 – Elevation of intracranial pressure

 – Interfering with blood &/or CF flow

• Include: !rain abscess" subdural empyema" 

intracranial epidural abscess" spinal epiduralabscess" spinal cord abscess

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BRAIN ABSCESS

•  #ccounts for $ % in %"

hospital admissions in '

(%)*+) cases/yr,

• -a.or improvements

realied in diagnosis &

management the last

century" & especially over

the past three decades"

with:

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BRAIN ABSCESS

0as uniformly fatal before the late %12s• -ortality down to 3*45 from 00II*%672s

 – Introduction of abx (penicillin" chloramphenicol888, 

 – newer surgical techni9ues

• -ortality down to *+5 over the past threedecades" with:

 – #dvent of C; scanning (%67," -<I

 – tereotactic brain biopsy/aspiration techni9ues

 – Further improvement in surgery

 –

=ewer abx (e8g8 cephalosporins" metronidaole88, – !etter treatment of predisposing conditions

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CHANGES IN EPIDEMIOLOGY OF

BRAIN ABSCESS(in the last 2! "eca"es#

 – -ar>ed drop in mortality overall

 – ?ower incidence of otogenic brain abscesses – improved treatment of chronic ear infections

 – 0ith increase in =o8 of immunosuppressedpatients:•  increased incidence of brain abscess seen in that

population (;ransplant" #ID"@, 

• -ore incidence of brain abscess caused by

opportunistic pathogens (fungi" toxo@,

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PA$HOPHYSIOLOGY

• !egins as localied cerebritis (%*+ w>s,

• Evolves into a collection of pus surrounded by a

well*vascularied capsule (3* w>s,

• ?esion evolution (based on experimental animal models,: – Days %*3: Aearly cerebritis stageB

 –

Days *6: Alate cerebritis stageB – Days %*%: Aearly capsule stageB

 – day%: Alate capsule stageB

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PA$HOGENESIS

•Direct spread from contiguous foci (*)5,

• ematogenous (+)*3)5,

• enetrating trauma/surgery (%5,

• Cryptogenic (%)*+5,

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DIREC$ SPREAD(from contiguous foci,

• ccurs by: – Direct extension through infected bone

 – pread through emissary veins" diploic veins" local

lymphatics

• ;he contiguous foci include:• titis media/mastoiditis

• inusitis

Dental infection (G%5," typically with molarinfections

• -eningitis rarely complicated by brain abscess 

(more common in neonates with Citrobacter diversus meningitis" of

whom 75 develop brain abscess,

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HEMA$OGENO%S SPREAD (from remote foci,

• ources: – Empyema" lung abscess" bronchiectasis"

endocarditis" wound infections" pelvic

infections" intra*abdominal source" etc@ –  may be facilitated by cyanotic D" #H-8

• <esults in brain abscess(es, at middle

cerebral artery distribution• ften multiple

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PREDISPOSING CONDI$ION & 

LOCA$ION OF BRAIN ABSCESS

titis/mastoiditis ;emporal lobe"Cerebellum

Frontal/ethmoid sinusitis Frontal lobe

phenoidal sinusitis Frontal lobe"

ella turcica

Dental infection Frontal temporal lobe8

<emote source -iddle cerebral arterydistribution (often multiple,

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 Micr'bi'l') '*

Brain Abscess

• Dependent upon:• ite of primary infection

• atient2s underlying condition

• eographic location

• 'sually streptococci and anaerobes

• taph aureus" aerobic =< common after

trauma or surgery• 3*4 5 are polymicrobial

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 redisposing Conditions & -icrobiology of

!rain #bscessPredisposing Condition  Usual Microbial Isolates 

Otitis media or mastoiditis Streptococci (anaerobic or aerobic),

 Bacteroides and Prevotella spp.,

 Enterobacteriaceae

Sinusitis (frontoethmoid or sphenoid) Streptococci, Bacteroides spp.,Enterobacteriaceae, Staph. aureus, Haemophilus 

spp.

Dental sepsis  Fusobacterium, Prevotella and

 Bacteroides spp., streptococci

Penetrating trauma or postneurosurgical S. aureus, streptococci,Enterobacteriaceae, Clostridium spp.

  PPID,2000

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PREDISPOSING CONDITION  USUAL MICROIAL ISOLATES

Lung abscess, empyema, bronchiectasis  Fusobacterium, ctinom!ces, Bacteroides

 Prevotellaspp., streptococci, "ocardia 

Bacterial endocarditis S. aureus, streptococci

ongenital heart disease Streptococci, Haemophilus spp.

 !eutropenia "erobic gram#negati$e bacilli, sper#illus 

%ucorales, Candidaspp.&ransplantation  sper#illus spp., Candida spp., %ucorales,

Enterobacteriaceae, "ocardia spp., $o%oplasma #ondii

 ' infection $o%oplasma #ondii, "ocardia spp.,

 &!cobacterium spp., 'isteria monoc!to#enes,

Cr!ptococcus neo(ormans

 PPID, 2000

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MICROBIOLOGY OF BRAIN ABSCESSAGEN$ FRE+%ENCY (,#

treptococci (S. intermedius" including S. anginosus, 4J7

Bacteroides and Prevotella spp8 +J

Enterobacteriaceae +3J33

Staphylococcus aureus %J%)

Fungi K  %J%)

Streptococcus pneumoniae G%Haemophilus influenzae   G%

rotooa" helminths L (vary geographically, G%

KMeasts" fungi ( Aspergillus #gents of mucor Candida Cryptococci Coccidiodoides

Cladosporium trichoides Pseudallescheria boydii)

Lrotooa" helminths (Entamoeba histolytica chistosomes aragonimus Cysticerci,

C;ID"+%

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CLINICAL MANIFES$A$IONS

• =on*specific symptoms

• -ainly due to the presence of a space*

occupying lesion• /#" =/H" lethargy" focal neuro signs " seiures

• igns/symptoms influenced by• ?ocation

• ie• Hirulence of organism

• resence of underlying condition

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CLINICAL MANIFES$A$IONS 

F !<#I= #!CE

eadache 75Fever )

 #ltered mental status )*4

;riad of above three G)

Focal neurologic findings )=ausea/vomiting +)*)

eiures +)J3)

=uchal rigidity +)

apilledema +)

 C!"#$%%&. PP"#$%%% 

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CLINICAL MANIFES$A$IONS

eadache

• ften dull" poorly localied (hemicranialN," non*

specific – #brupt" extremely severe /#: thin> meningitis" #8

 – udden worsening in /# w meningismus: thin> rupture

of brain abscess into ventricle (often fatal,

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LOCA$ION & CLINICAL FEA$%RES

• FRON$AL LOBE: /#" drowsiness" inattention"

hemiparesis" motor speech disorder" #-

• $EMPORAL LOBE: Ipsilateral /#" aphasia"visual field defect

• PARIE$AL LOBE: /#" visual field defects"endocrine disturbances

• CEREBELL%M: =ystagmus" ataxia" vomiting"dysmetria

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DIFFEREN$IAL DIAGNOSIS

• -alignancy –  #bscess has hypo*dense center" with surrounding smooth" thin*

walled capsule" & areas of peripheral enhancement8

 – ;umor has diffuse enhancement & irregular borders8

 – EC; (E; scan, may differentiate8 C< tooN

• CH#

• emorrhage

 #neurysm• ubdural empyema/ICEpidural abscess

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DIAGNOSIS

• igh index of suspicion

• Contrast C; or -<I

•Drainage/biopsy" if ring enhancinglesion(s, are seen

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IMAGING S$%DIES

• MRI  – more sensitive for early

cerebritis" satellite lesions"necrosis" ring" edema"especially posterior fossa &

brain stem• C$ scan• --. $c brain scan 

 – very sensitiveO usefulwhere C; or -<I not

available• S/0ll 1ra)  insensitive"

 – if air seen" considerpossibility of brain abscess

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LAORATOR! TESTSB*"! "BSESS

• Aspirate" +ram"-Bfungal stains cultures,

cytopathology (/#P* for &B)

• #C !ormal in 012 ( only moderate leu3ocytosis in 4 512

only 612 ha$e 7B 891,111)

CRP almost in$ariably ele$ated• ESR :sually moderately ele$ated

• C Often negati$e B:& Should still be done

LP  Contraindicated  in patients with known/suspected brainabscess Risk of herniation 15-30%

 I( done, may ha$e normal S- findings, but;

:sually ele$ated S- protein cell count (lymphs)

:nremar3able glucose S- cultures rarely positi$e

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$REA$MEN$• Combined medical & surgical

•  #spiration or excision

•  empirical abx

• Empirical antibiotics are selected based on:• ?i>ely pathogen (consider primary source" underlying

condition" & geography,

•  #ntibiotic characteristics: usual -ICs" C=

penetration" activity in abscess cavity

• -odify abx based on stains

• Duration: usually 4*1 w>s• after surgical excision" a shorter course may suffice

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 #rmstrong ID" -osby inc %666

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MEDICAL $REA$MEN$ 

ONLY• nly in pts with prohibitive surgical ris>:

 – poor surgical candidate" – multiple abscesses" – in a dominant location" –  #bscess sie G+8) cm – concomitant meningitis" ependymitis" – early abscess (cerebritisN, – with improvement on abx"

P!etter*vascularied cortical lesions more li>ely to respond to abx aloneQP ubcortical/white*matter lesions are poorly vasculariedQ

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C;ID"+%

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  E<I#? I-#I= I-<;#=; ;

-=I;< <E=E

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!efore <x

 #fter completion of <x

 #rmstrong ID"-osby inc %666

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 POOR PROGNOS$IC MAR3ERS• Delayed or missed diagnosis

• Inappropriate antibiotics8

• %ultiple, deep, or multi#loculated abscesses

• entricular rupture (<12=6112 mortality)

• -ungal , resistant pathogens.

•  !eurological compromise at presentation

• Short duration > se$ere "%S,•  *apidly progressi$e neuro. mpairment

• Immunosuppressed host

• oor localiation" especially in the posterior fossa (before C;,

%odified from &D,9116

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EPID%RAL ABSCESSES

• pinal intracranial (6:%,

• Intracranially" the dura is

adherent to bone

• ;rue spinal epidural

space is present

posteriorly throughout

the spine" thus posterior

longitudinal spread of

infection is common8 –  #nterior spinal epidural

very rare (usually below

?% & cervical,

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 #merican Family hysician #pril %" ++

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SPINAL EPID%RAL ABSCESS

IN$ROD%C$ION

• <are" 8+*%8+ per %" hospital

admissions

• -edian age ) yrs (3) yrs in IHD',

• ;horaciclumbarcervical

• -a.ority are ac9uired hematogenously

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COMMON PREDISPOSING

CONDI$IONS

• E-#;E=' <E#D: from remote

infections & w IHD'

• DI<EC; <E#D: Hertebral

osteomyelitis" dis>itis" decubitus ulcers"

penetrating trauma" surgery" epidural

catheters

• Hia paravertebral venous plexus: fromabdominal/pelvic infections

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PA$HOGENESISI=#? EID'<#? #!CE

• ften begins as a focal disc or disc*vertebral

 .unction infection

• Damage of spinal cord can be caused by: –

Direct compression – ;hrombosis" thrombophlebitis

 – Interruption of arterial blood supply

 – Focal vasculitis

 – !acterial toxins/mediators of inflammation

• Even a small E# may cause serious se9uelae

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MICROBIOLOGYI=#? EID'<#? #!CE

;he most common pathogens are:

• taph aureus 45

• treptococci %15

•  #erobic =< %35

• olymicrobial %5

(=ote: ;! may cause up to +)5 in some areas,

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CLINICAL MANIFES$A$IONSI=#? EID'<#? #!CE

Four clinical stages have been described:45 Fe6er an" *'cal bac/ 7ainO

25 Ner6e r''t c'.7ressi'n with nerve root

painO Ashooting painB

!5 S7inal c'r" c'.7ressi'n with

accompanying deficits in motor/sensory

nerves" bowel/bladder sphincter functionO

85 Paral)sis (respiratory compromise may alsobe present if the cervical cord is involved,8

"rmstrong, D, %osby inc,9111

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DIAGNOSISI=#? EID'<#? #!CE

(;hin>ing of it is >ey" in a pt with fever" severe" focal bac> pain,

• -<I" C;

•  #bscess drainage

•!lood cultures

• <outine ?abs rarely helpful• E<"C< usually elevated" !'; non*specific

• 0!C may or may not be elevated

• ? contraindicated

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D9D:I=#? EID'<#? #!CE

• -etastases

• Hertebral dis>itis and osteomyelitis

• -eningitis

• erpes Roster infection

• ther disc/bone disease

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$REA$MEN$I=#? EID'<#? #!CE

• Early surgical decompression/drainage(preferably within first +h,

•  #ntibiotics – Empiric abx should cover taph" strep" &

=<

 – Duration of <x : *4 wee>s

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 (E#/DE,

• 65 epidural abscesses are spinal

• -ost E# occur in thoracic (the longest,

• -a.ority of E# (75, are posterior to the cord

• -ost E# caused hematogenous spread &taph aureus is the leading cause8

• 6)5 DE are in intracranial

-a.ority of DE pts have associated sinusitis

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IN$RACRANIAL EPID%RAL

ABSCESS

• ?ess common & less acute than E#

• <ounded" well*localied (because dura is

firmly adherent to bone,

• Path'enesis  – Direct ext8 from contiguous foci (sinusitis"

otitis/mastoiditis,

 –  trauma"or surgery

IN$RACRANIAL EPID%RAL ABSCESS

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IN$RACRANIAL EPID%RAL ABSCESS

• MICROBIOLOGY: -icraerophillic trep"

ropioni" eptostrept" few aerobic g=<"fungi8 ostop: taph" =<8

• CLINICAL MANIFES$A$ION: from ?/ systmic

igns of infection

 – Fever" #" =/H" lethargy

• D:* ;hin> of it" imaging" drainage

• D9D1: ;umor" other IC#bscesses

• R1: urgery S abx

• M'rtalit) w appropriate <x G %5

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 S%BD%RAL EMPYEMA

%)*+ 5 of all focal intracranial infections• -otly a complication of sinusitis" otitis

media" mastoiditis8

-ost common complication of sinusitis(45 of such cases," mostly from

frontal/ethmoid sinusitis8

;rauma/post*op & rarely hematogenous• -F

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 S%BD%RAL EMPYEMA

Clinical Mani*estati'ns

• Fever 

• eadache

• Focal =euro defects

Homiting• -ental status changes• eiures

• -ass effect more common w DE than w ICE#

DT: C;" -<I (? contraindicated,

<x: urgery 8 #bx (3*4 w>s,

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(#rmstrong" ID"%666" -osby Inc,

S C

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PARASI$IC 

!<#I= #!CE

• ;oxoplasmosis

• =eurocysticercosis

•  #mebic

•  Echinococcal

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NOCARDIA BRAIN ABSCESS

• 'sually in immunosuppresed (C-I,

• )5 no >nown predisposing factor 

•  #ll pts w pulmonary nocardiosis should undergo

brain imaging to r/o subclinical C= nocardiosis• <x: ulfa (;/ invitro synergy," imipenem"

ceftriaxone" ami>acin" minocin – Duration of abx Ga year8

 –

 =eedle aspiration or surgical excision needed inmost8

• <elapse common

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BRAIN ABSCESS IN AIDS

• ;oxoplasmosis is the most common• eropositive

•  d/dx lymphoma

ften empiric <x given & biopsy only non*responders

• ?isteria" =ocardia" tb" fungi@

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BRAIN $B

• <are cause of brain abscess

• 'sually in immunocompromised

• ;uberculoma is a granuloma (not a true

abscess ,

• !iopsy/drainage (send for C< too ,

F%NGAL BRAIN ABSCESS

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F%NGAL BRAIN ABSCESS

(#spergillus" -ucor 888,

• I--'=C-<-IED

• oor inflammatory response" less

enhancement on C;8

• -ay present w much more advanced

disease (seiure" stro>e more common,

• igh mortality

• <x: aggressive surgery S antifungal

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BRAIN ABSCESS SE+%ELAE

• eiure in 3*45

• =euro deficits 3*)5

• -ortality *+5

YIELD OF C%L$%RES

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 YIELD OF C%L$%RESI=#? EID'<#? #!CE

'<CE MIE?D

•  #bscess fluid aspirate 65

• !lood culture 4+5

• CFK %65

'(P often contraindicated