Transcript CNS ABSCESSES CNS ABSCESSES • Focal pyogenic infections of the central nervous system • Exert their effects mainly by: – Direct involvement &

CNS ABSCESSES
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:
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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):
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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
Dental infection
Remote source
Frontal lobe,
Sella turcica
Frontal > temporal lobe.
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
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
PREDISPOSING CONDITION
USUAL MICROBIAL ISOLATES
Lung abscess, empyema, bronchiectasis
Bacterial endocarditis
Fusobacterium, Actinomyces, Bacteroides
Prevotellaspp., streptococci, Nocardia
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 spaceoccupying lesion
• H/A, N/V, lethargy, focal neuro signs , seizures
• Signs/symptoms influenced by
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Location
Size
Virulence of organism
Presence of underlying condition
CLINICAL MANIFESTATIONS
OF BRAIN ABSCESS
Headache
Fever
Altered mental status
Triad of above three
Focal neurologic findings
Nausea/vomiting
Seizures
70%
50
50-60
<50
50
25-50
25–35
Nuchal rigidity
25
Papilledema
25
CTID,2001. PPID,2000
CLINICAL MANIFESTATIONS
Headache
• Often dull, poorly localized (hemicranial?), nonspecific
– 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, thinwalled capsule, & areas of peripheral enhancement.
– Tumor has diffuse enhancement & irregular borders.
– SPECT (PET scan) may differentiate. CRP too?
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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
•ESR
•BC
•LP
almost invariably elevated
Usually moderately elevated
Often negative BUT Should still be done
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:
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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)
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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
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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)
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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
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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
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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 nonresponders
• 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
• Abscess fluid aspirate
• Blood culture
• CSF*
*LP often contraindicated
YIELD
90%
62%
19%