CNS Abscess (1)
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CNS ABSCESSES
Nov 10, 2003
Gebre K Tseggay, MD
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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 spinalcord
Compression of parenchyma
Elevation of intracranial pressure
Interfering with blood &/or CSF flow
Include: Brain abscess, subdural empyema,
intracranial epidural abscess, spinal epiduralabscess, spinal cord abscess
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BRAIN ABSCESS
Accounts for ~ 1 in 10,000hospital admissions in US(1500-2500 cases/yr)
Major improvementsrealized in diagnosis &management the lastcentury, & especially overthe past three decades,
with:
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BRAIN ABSCESS
Was uniformly fatal before the late 1800s
Mortality down to 30-60% from WWII-1970s Introduction of abx (penicillin, chloramphenicol...)
newer surgical techniques
Mortality down to 0-24% over the past threedecades, with:
Advent of CT scanning (1974), MRI
Stereotactic brain biopsy/aspiration techniques
Further improvement in surgery
Newer abx (e.g. cephalosporins, metronidazole..) Better treatment of predisposing conditions
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CHANGES IN EPIDEMIOLOGYOF BRAIN ABSCESS
(in the last 2-3 decades)
Marked drop in mortality overall
Lower incidence of otogenic brain abscesses improved treatment of chronic ear infections
With increase in No. of immunosuppressedpatients:
increased incidence of brain abscessseen in thatpopulation(Transplant, AIDS,)
More incidence of brain abscess caused byopportunistic pathogens (fungi, toxo)
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PATHOPHYSIOLOGY
Begins as localized cerebritis (1-2 wks)
Evolves into a collection of pus surrounded by awell-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
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PATHOGENESIS
Direct spread from contiguous foci (40-50%)
Hematogenous (25-35%)
Penetrating trauma/surgery (10%)
Cryptogenic (15-20%)
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DIRECT SPREAD(from contiguous foci)
Occurs by: Direct extension through infected bone
Spread through emissary veins, diploic veins, locallymphatics
The contiguous foci include:
Otitis media/mastoiditis
Sinusitis
Dental infection (
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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
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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 arterydistribution (often multiple)
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Microbiology ofBrain Abscess
Dependent upon: Site of primary infection
Patients underlying condition
Geographic location
Usually streptococci and anaerobes
Staph aureus, aerobic GNR common after
trauma or surgery 30-60 % are polymicrobial
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Predisposing Conditions & Microbiology of
Brain Abscess
Predisposing 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., streptococciPenetrating trauma or postneurosurgical S. aureus, streptococci,
Enterobacteriaceae, Clostridium spp.
PPID,2000
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PREDISPOSING CONDITION USUAL MICROBIAL ISOLATES
Lung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, BacteroidesPrevotellaspp., streptococci,Nocardia
Bacterial endocarditis S. aureus, streptococci
Congenital heart disease Streptococci,Haemophilus spp.
Neutropenia Aerobic gram-negative bacilli,AspergillusMucorales, Candidaspp.
Transplantation Aspergillus spp., Candida spp., Mucorales,
Enterobacteriaceae,Nocardia spp.,
Toxoplasma gondii
HIV infection Toxoplasma gondii, Nocardia spp.,Mycobacterium spp.,Listeria
monocytogenes, Cryptococcus neoformans
PPID, 2000
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MICROBIOLOGY OFBRAIN ABSCESS
AGENT FREQUENCY (%)
Streptococci (S. intermedius, including S. anginosus) 6070
Bacteroidesand Prevotellaspp. 2040
Enterobacteriaceae 2333
Staphylococcus aureus 1015
Fungi* 1015
Streptococcus pneumoniae
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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
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CLINICAL MANIFESTATIONSOF BRAIN ABSCESS
Headache 70%Fever 50
Altered mental status 50-60Triad of above three
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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 ruptureof brain abscess into ventricle (often fatal)
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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
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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
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DIAGNOSIS
High index of suspicion
Contrast CT or MRI
Drainage/biopsy, if ring enhancinglesion(s) are seen
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IMAGING STUDIES
MRI more sensitive for early
cerebritis, satellite lesions,necrosis, ring, edema,especially posterior fossa &
brain stem CT scan 99m Tc brain scan
very sensitive; usefulwhere CT or MRI not
available Skull x-ray :insensitive,
if air seen, considerpossibility of brain abscess
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LABORATORY TESTSBRAIN ABSCESS
Aspirate:Gram/AFB/fungal stains & cultures, cytopathology (+/-PCR for TB)
WBC Normal in 40% ( only moderate leukocytosis in ~ 50%
& only 10% have WBC >20,000)
CRP almost invariably elevated
ESR Usually moderately elevated
BC Often negative BUT Should still be done
LP Contraindicatedin patients with known/suspected brainabscessRisk of herniation 15-30%
If done, may have normal CSF findings, but:
Usually elevated CSF protein & cell count (lymphs)
Unremarkable glucose & CSF cultures rarely positive
TREATMENT
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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
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Armstrong ID, Mosby inc 1999
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MEDICAL TREATMENTONLY
Only in pts with prohibitive surgical risk: poor surgical candidate, multiple abscesses, in a dominant location, Abscess size
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CTID,2001
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SERIAL IMAGING IMPORTANT TO
MONITOR RESPONSE
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Before Rx
After completion of Rx
Armstrong ID,Mosby inc 1999
POOR PROGNOSTIC MARKERS
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POOR PROGNOSTIC MARKERSDelayed or missed diagnosis
Inappropriate antibiotics.Multiple, deep, or multi-loculated abscesses
Ventricular rupture (80%100% mortality)
Fungal , resistant pathogens.
Neurological compromise at presentation
Short duration w severe AMS,
Rapidly progressive neuro. Impairment
Immunosuppressed host
Poor localization, especially in the posterior fossa (before CT)
Modified from CTID,2001
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EPIDURAL ABSCESSES
Spinal > intracranial (9:1)
Intracranially, the dura isadherent to bone
True spinal epiduralspace is presentposteriorly throughoutthe spine, thus posteriorlongitudinal spread of
infection is common. Anterior spinal epidural
very rare (usually belowL1 & cervical)
http://home.mdconsult.com/das/book/body/0/1005/I316.fig -
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American Family Physician April 1, 2002
SPINAL EPIDURAL ABSCESS
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SPINAL EPIDURAL ABSCESS
INTRODUCTION
Rare, 0.2-1.2 per 10,000 hospitaladmissions
Median age 50 yrs (35 yrs in IVDU)
Thoracic>lumbar>cervical
Majority are acquired hematogenously
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COMMON PREDISPOSINGCONDITIONS
HEMATOGENOUS SPREAD: from remoteinfections & w IVDU
DIRECT SPREAD: Vertebralosteomyelitis, diskitis, decubitus ulcers,penetrating trauma, surgery, epiduralcatheters
Via paravertebral venous plexus: fromabdominal/pelvic infections
PATHOGENESIS
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PATHOGENESISSPINAL EPIDURAL ABSCESS
Often begins as a focal disc or disc-vertebraljunction infection
Damage of spinal cord can be caused by:
Direct compression Thrombosis, thrombophlebitis
Interruption of arterial blood supply
Focal vasculitis
Bacterial toxins/mediators of inflammation
Even a small SEA may cause serious sequelae
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MICROBIOLOGYSPINAL EPIDURAL ABSCESS
The most common pathogens are:
Staph aureus >60%
Streptococci 18% Aerobic GNR 13%
Polymicrobial 10%
(Note: TB may cause up to 25% in some areas)
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CLINICAL MANIFESTATIONSSPINAL EPIDURAL ABSCESS
Four clinical stages have been described:1. Fever and focal back pain;2. Nerve root compression with nerve root
pain; shooting pain3. Spinal cord compression withaccompanying deficits in motor/sensorynerves, bowel/bladder sphincter function;
4. Paralysis (respiratory compromise may alsobe present if the cervical cord is involved).
Armstrong, ID, Mosby inc,2000
DIAGNOSIS
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DIAGNOSISSPINAL EPIDURAL ABSCESS
(Thinking of it is key, in a pt with fever, severe, focal back pain)
MRI, CT
Abscess drainage
Blood cultures
Routine Labs rarely helpful ESR,CRP usually elevated, BUT non-specific
WBC may or may not be elevated
LP contraindicated
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D/DXSPINAL EPIDURAL ABSCESS
Metastases
Vertebral diskitis and osteomyelitis
Meningitis Herpes Zoster infection
Other disc/bone disease
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TREATMENTSPINAL EPIDURAL ABSCESS
Early surgical decompression/drainage(preferably within first 24h)
Antibiotics
Empiric abx should cover Staph, strep, &GNR
Duration of Rx : 4-6 weeks
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(SEA/SDE)
90% epidural abscesses are spinal
Most SEA occur in thoracic (the longest)
Majority of SEA (>70%) are posterior to the cord
Most SEA caused hematogenous spread &Staph aureus is the leading cause.
95% SDE are in intracranial
Majority of SDE pts have associated sinusitis
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INTRACRANIAL EPIDURALABSCESS
Less common & less acute than SEA
Rounded, well-localized (because dura isfirmly adherent to bone)
Pathogenesis:
Direct ext. from contiguous foci (sinusitis,otitis/mastoiditis)
trauma,or surgery
INTRACRANIAL EPIDURAL ABSCESS
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INTRACRANIAL EPIDURAL ABSCESS
MICROBIOLOGY: Micraerophillic Strep,
Propioni, Peptostrept, few aerobic gNR,fungi. Postop: Staph, GNR.
CLINICAL MANIFESTATION: from SOL/ systmicigns of infection
Fever, HA, N/V, lethargy
DX:- Think of it, imaging, drainage
D/Dx: Tumor, other ICAbscesses
Rx: Surgery + abx
Mortality w appropriate Rx < 10%
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SUBDURAL EMPYEMA
15-20 % of all focal intracranial infections Motly a complication of sinusitis, otitis
media, mastoiditis.
Most common complication of sinusitis(60% of such cases), mostly fromfrontal/ethmoid sinusitis.
Trauma/post-op & rarely hematogenous M>F
SUBDURAL EMPYEMA
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SUBDURAL EMPYEMAClinical Manifestations
Fever
Headache
Focal Neuro defects
Vomiting Mental status changes
Seizures
Mass effect more common w SDE than w ICEA
DX: CT, MRI (LP contraindicated)
Rx: Surgery . Abx (3-6 wks)
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(Armstrong, ID,1999, Mosby Inc)
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PARASITIC
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PARASITICBRAIN ABSCESS
Toxoplasmosis
Neurocysticercosis
Amebic
Echinococcal
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NOCARDIA BRAIN ABSCESS
Usually in immunosuppresed (CMI)
>50% no known predisposing factor
All pts w pulmonary nocardiosis should undergo
brain imaging to r/o subclinical CNS nocardiosis Rx: Sulfa (T/S invitro synergy), imipenem,
ceftriaxone, amikacin, minocin Duration of abx
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BRAIN ABSCESS IN AIDS
Toxoplasmosis is the most common Seropositive
d/dx lymphoma
Often empiric Rx given & biopsy only non-responders
Listeria, Nocardia, tb, fungi
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BRAIN TB
Rare cause of brain abscess
Usually in immunocompromised
Tuberculoma is a granuloma (not a trueabscess )
Biopsy/drainage (send for PCR too )
FUNGAL BRAIN ABSCESS
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FUNGAL BRAIN ABSCESS(Aspergillus, Mucor ...)
IMMUNOCOMPROMISED
Poor inflammatory response, lessenhancement on CT.
May present w much more advanceddisease (seizure, stroke more common)
High mortality
Rx: aggressive surgery + antifungal
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BRAIN ABSCESS SEQUELAE
Seizure in 30-60%
Neuro deficits 30-50%
Mortality 4-20%
YIELD OF CULTURES
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YIELD OF CULTURESSPINAL EPIDURAL ABSCESS
SOURCE YIELD
Abscess fluid aspirate 90%
Blood culture 62%
CSF* 19%
*LP often contraindicated