CNS ABSCESSES

Nov 10, 2003

Gebre K Tseggay, MD
 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 CSF flow
• Include: Brain abscess, subdural empyema,
intracranial epidural abscess, spinal epidural
abscess, spinal cord abscess
 BRAIN ABSCESS

• Accounts for ~ 1 in 10,000

hospital admissions in US
(1500-2500 cases/yr)
• Major improvements
realized in diagnosis &
management the last
century, & especially over
the past three decades,
with:
 BRAIN ABSCESS
• Was uniformly fatal before the late 1800’s
• Mortality down to 30-60% from WWII-1970’s
– Introduction of abx (penicillin, chloramphenicol...)
– newer surgical techniques
• Mortality down to 0-24% over the past three
decades, 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
CHANGES IN EPIDEMIOLOGY
OF 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 immunosuppressed

patients:
• increased incidence of brain abscess seen in that
population (Transplant, AIDS,…)
• More incidence of brain abscess caused by
opportunistic pathogens (fungi, toxo…)
 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”
 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
Predisposing Conditions & Microbiology of
Brain Abscess
Predisposing Condition
Otitis media or mastoiditis
Sinusitis (frontoethmoid or sphenoid)
Dental sepsis
Penetrating trauma or postneurosurgical
PPID,2000
Usual Microbial Isolates
Streptococci (anaerobic or aerobic),
Bacteroides and Prevotella spp.,
Enterobacteriaceae
Streptococci, Bacteroides spp.,
Enterobacteriaceae, Staph. aureus,
Haemophilus spp.
Fusobacterium, Prevotella and
Bacteroides spp., streptococci
S. aureus, streptococci,
Enterobacteriaceae, Clostridium spp.
PREDISPOSING CONDITION USUAL MICROBIAL ISOLATES

Lung abscess, empyema, bronchiectasis Fusobacterium, Actinomyces, Bacteroides

Prevotellaspp., streptococci, Nocardia
Bacterial endocarditis S. aureus, streptococci
Congenital heart disease Streptococci, Haemophilus spp.
Neutropenia Aerobic gram-negative bacilli, Aspergillus
Mucorales, 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
 MICROBIOLOGY OF BRAIN ABSCESS
AGENT FREQUENCY (%)
Streptococci (S. intermedius, including S. anginosus) 60–70
Bacteroides and Prevotella spp. 20–40
Enterobacteriaceae 23–33
Staphylococcus aureus 10–15
Fungi 10–15
Streptococcus pneumoniae <1
Haemophilus influenzae <1
Protozoa, helminths † (vary geographically) <1

*Yeasts, fungi (Aspergillus Agents of mucor Candida Cryptococci Coccidiodoides

Cladosporium trichoides Pseudallescheria boydii)
†Protozoa, helminths (Entamoeba histolytica, Schistosomes Paragonimus
Cysticerci) CTID,2001
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 MANIFESTATIONS
OF BRAIN ABSCESS
Headache 70%
Fever 50
Altered mental status 50-60
Triad of above three <50
Focal neurologic findings 50
Nausea/vomiting 25-50
Seizures 25–35
Nuchal rigidity 25
Papilledema 25

CTID,2001. PPID,2000
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
 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
 DIAGNOSIS

• High index of suspicion

• Contrast CT or MRI
• Drainage/biopsy, if ring enhancing
lesion(s) are seen
 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; useful
where CT or MRI not
available
• Skull x-ray : insensitive,
– if air seen, consider
possibility of brain abscess
 LABORATORY TESTS
BRAIN 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 Contraindicated in patients with known/suspected brainabscess

Risk 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
• 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]
CTID,2001
SERIAL IMAGING IMPORTANT TO
MONITOR RESPONSE
 Before Rx

After completion of Rx

Armstrong ID,Mosby inc 1999

 POOR PROGNOSTIC MARKERS
•Delayed 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

 EPIDURAL ABSCESSES
• Spinal > intracranial (9:1)
• Intracranially, the dura is
adherent to bone
• True spinal epidural
space is present
posteriorly throughout
the spine, thus posterior
longitudinal spread of
infection is common.
– Anterior spinal epidural
very rare (usually below
L1 & cervical)
American Family Physician April 1, 2002
 SPINAL EPIDURAL ABSCESS
INTRODUCTION
• Rare, 0.2-1.2 per 10,000 hospital
admissions
• Median age 50 yrs (35 yrs in IVDU)
• Thoracic>lumbar>cervical
• Majority are acquired hematogenously
 COMMON PREDISPOSING
CONDITIONS
• HEMATOGENOUS SPREAD: from remote
infections & w IVDU
• DIRECT SPREAD: Vertebral
osteomyelitis, diskitis, decubitus ulcers,
penetrating trauma, surgery, epidural
catheters
• Via paravertebral venous plexus: from
abdominal/pelvic infections
 PATHOGENESIS
SPINAL EPIDURAL ABSCESS

• Often begins as a focal disc or disc-vertebral

junction 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
 MICROBIOLOGY
SPINAL 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)
 CLINICAL MANIFESTATIONS
SPINAL EPIDURAL ABSCESS

Four clinical stages have been described:

1. Fever and focal back pain;
2. Nerve root compression with nerve root
pain; “shooting pain”
3. Spinal cord compression with
accompanying deficits in motor/sensory
nerves, bowel/bladder sphincter function;
4. Paralysis (respiratory compromise may also
be present if the cervical cord is involved).
Armstrong, ID, Mosby inc,2000
 DIAGNOSIS
SPINAL 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
 D/DX
SPINAL EPIDURAL ABSCESS

• Metastases
• Vertebral diskitis and osteomyelitis
• Meningitis
• Herpes Zoster infection
• Other disc/bone disease
 TREATMENT
SPINAL EPIDURAL ABSCESS

• Early surgical decompression/drainage

(preferably within first 24h)
• Antibiotics
– Empiric abx should cover Staph, strep, &
GNR
– Duration of Rx : 4-6 weeks
 (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
 INTRACRANIAL EPIDURAL
ABSCESS
• Less common & less acute than SEA
• Rounded, well-localized (because dura is
firmly adherent to bone)
• Pathogenesis:
– Direct ext. from contiguous foci (sinusitis,
otitis/mastoiditis)
– trauma,or surgery
 INTRACRANIAL EPIDURAL ABSCESS
• MICROBIOLOGY: Micraerophillic Strep,
Propioni, Peptostrept, few aerobic gNR,
fungi. Postop: Staph, GNR.
• CLINICAL MANIFESTATION: from SOL/ systmic
igns 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%
 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 from
frontal/ethmoid sinusitis.
• Trauma/post-op & rarely hematogenous
• M>F
 SUBDURAL EMPYEMA
Clinical 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)
(Armstrong, ID,1999, Mosby Inc)
 PARASITIC
BRAIN ABSCESS
• Toxoplasmosis
• Neurocysticercosis
• Amebic
• Echinococcal
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 <a year.
– Needle aspiration or surgical excision needed in
most.
• Relapse common
 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…
 BRAIN TB
• Rare cause of brain abscess
• Usually in immunocompromised
• Tuberculoma is a granuloma (not a true
abscess )
• Biopsy/drainage (send for PCR too )
 FUNGAL BRAIN ABSCESS
(Aspergillus, Mucor ...)

• IMMUNOCOMPROMISED
• Poor inflammatory response, less
enhancement on CT.
• May present w much more advanced
disease (seizure, stroke more common)
• High mortality
• Rx: aggressive surgery + antifungal
BRAIN ABSCESS SEQUELAE
• Seizure in 30-60%
• Neuro deficits 30-50%
• Mortality 4-20%
 YIELD OF CULTURES
SPINAL EPIDURAL ABSCESS

SOURCE YIELD
• Abscess fluid aspirate 90%
• Blood culture 62%
• CSF* 19%

*LP often contraindicated