CNS ABSCESSES

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CNS ABSCESSES
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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 CSF flow
• Include Brain abscess, subdural empyema,
  intracranial epidural abscess, spinal epidural
  abscess, spinal cord abscess

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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

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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 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

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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)

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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
• gt 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,
  local lymphatics
• The contiguous foci include
• Otitis media/mastoiditis
• Sinusitis
• Dental infection (lt10), typically with molar
  infections
• Meningitis rarely complicated by brain abscess
  (more common in neonates with Citrobacter
  diversus meningitis, of whom 70 develop brain
  abscess)

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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
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Microbiology of Brain 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 Streptococ
ci (anaerobic or aerobic), Bacteroides and
Prevotella spp., Enterobacteriaceae Sinusiti
s (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 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
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MICROBIOLOGY OF BRAIN ABSCESS AGENT
FREQUENCY () Streptococci (S. intermedius,
including S. anginosus) 6070 Bacteroides and
Prevotella spp. 2040 Enterobacteriaceae 23
33 Staphylococcus aureus 1015 Fungi
1015 Streptococcus pneumoniae
lt1 Haemophilus influenzae lt1 Protozoa,
helminths (vary geographically)
lt1 Yeasts, fungi (Aspergillus Agents of mucor
Candida Cryptococci Coccidiodoides Cladosporium
trichoides Pseudallescheria boydii)Protozoa,
helminths (Entamoeba histolytica, Schistosomes
Paragonimus Cysticerci) CTID,2001
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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 MANIFESTATIONS OF BRAIN
ABSCESS Headache 70 Fever 50 Altered
mental status 50-60 Triad of above
three lt50 Focal neurologic
findings 50 Nausea/vomiting 25-50 Seizures
2535 Nuchal rigidity 25 Papilledema 25
CTID,2001. PPID,2000
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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
  rupture of 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 enhancing lesion(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 useful where CT or MRI not
  available
• Skull x-ray insensitive,
• if air seen, consider possibility of brain
  abscess

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• 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 gt20,000)
• 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

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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 TREATMENT ONLY

• Only in pts with prohibitive surgical risk
• poor surgical candidate,
• multiple abscesses,
• in a dominant location,
• Abscess size lt2.5 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

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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
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• POOR PROGNOSTIC MARKERS
• Delayed or missed diagnosis
• Inappropriate antibiotics.
• Multiple, deep, or multi-loculated abscesses
• Ventricular rupture (80100 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 gt intracranial (91)
• 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)

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American Family Physician April 1, 2002
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SPINAL EPIDURAL ABSCESSINTRODUCTION

• Rare, 0.2-1.2 per 10,000 hospital admissions
• Median age 50 yrs (35 yrs in IVDU)
• Thoracicgtlumbargtcervical
• Majority are acquired hematogenously

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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

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PATHOGENESISSPINAL 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

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MICROBIOLOGYSPINAL EPIDURAL ABSCESS

• The most common pathogens are
• Staph aureus gt60
• Streptococci 18
• Aerobic GNR 13
• Polymicrobial 10
• (Note TB may cause up to 25 in some areas)

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• CLINICAL MANIFESTATIONS
• SPINAL EPIDURAL ABSCESS
• Four clinical stages have been described
• Fever and focal back pain
• Nerve root compression with nerve root pain
  shooting pain
• Spinal cord compression with accompanying
  deficits in motor/sensory nerves, bowel/bladder
  sphincter function
• Paralysis (respiratory compromise may also be
  present if the cervical cord is involved).
• Armstrong, ID, Mosby inc,2000

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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

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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 (gt70) 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 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

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• 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 lt 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 from frontal/ethmoid
  sinusitis.
• Trauma/post-op rarely hematogenous
• MgtF

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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 BRAIN ABSCESS

• Toxoplasmosis
• Neurocysticercosis
• Amebic
• Echinococcal

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NOCARDIA BRAIN ABSCESS

• Usually in immunosuppresed (CMI)
• gt50 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 lta year.
• Needle aspiration or surgical excision needed in
  most.
• Relapse common

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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 true abscess )
• Biopsy/drainage (send for PCR too )

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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

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BRAIN ABSCESS SEQUELAE

• Seizure in 30-60
• Neuro deficits 30-50
• Mortality 4-20

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YIELD OF CULTURESSPINAL EPIDURAL ABSCESS

• SOURCE YIELD
• Abscess fluid aspirate 90
• Blood culture 62
• CSF 19
• LP often contraindicated