cns abscess (1)

8/3/2019 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

cns abscess (1)

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