BRAIN ABSCESS

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BRAIN ABSCESS

• November 20, 2006
• Gebre K Tseggay, MD

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BRAIN ABSCESSIntroduction

• Brain abscess is rare but life-threatening
  infection.
• Accounts for 1 in 10,000 hospital admissions in
  US (1500-2500 cases/yr)
• It was uniformly fatal before the late 1800s
• Advances in diagnosis management the last
  century, especially over the past three decades
  have lead to a significantly lower mortality.
• 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
• Advances in radiography CT scanning (1974), MRI
  
• Advances in surgery
• Stereotactic brain biopsy/aspiration techniques
• 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)

• Lower incidence of otogenic brain abscesses
• With increase in of immunocompormised patients
  (transplant, AIDS,), increased incidence of
  brain abscess seen in that population, including
  those caused by opportunistic pathogens (e.g.,
  fungi, toxo, Nocardia)

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PATHOGENESIS

• Direct spread from contiguous foci (40-50)
• Hematogenous spread (25-35)
• Penetrating trauma/surgery
  (10)
• Cryptogenic
  (15-20)

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DIRECT SPREAD

• From
• 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)
• By
• Direct extension through infected bone
• Spread through emissary/diploic veins, local
  lymphatics

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HEMATOGENOUS SPREAD (from remote foci)

• From
• empyema, lung abscess, bronchiectasis
• endocarditis,
• wound infections,
• pelvic infections, intra-abdominal source, etc
• may be facilitated by cyanotic HD, AVM.
• Abscess mostly at middle cerebral artery
  distribution, and often multiple

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PREDISPOSING CONDITION LOCATION OF
ABSCESS
Otitis/mastoiditis Temporal lobe, Cerebellum
Frontal/ethmoid sinusitis Frontal lobe
Sphenoidal sinusitis Frontal lobe, Sella turcica
Dental infection Frontal gt temporal lobe.
Remote source Middle cerebral artery distribution (often multiple)
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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 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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PREDISPOSING CONDITION USUAL MICROBIAL
ISOLATES Otitis media or mastoiditis Streptoco
cci (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
Prevotella spp., 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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PATHOPHYSIOLOGYof Brain Abscess

• 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 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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Cerebritis
http//pathology.mc.duke.edu/neurop
ath/cnslecture
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Effect of Brain Abscess

• Direct destruction
• Compression of parenchyma
• Elevation of intracranial pressure
• Interfering with blood /or CSF flow

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CLINICAL MANIFESTATIONSBrain Abscess

• Usually non-specific symptoms
• Manifestations are influenced by
• Location of abscess
• Size of abscess
• Virulence of organism
• Presence of underlying condition

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Clinical manifestations according to abscess
location

• Frontal lobe abscesses Headache Drowsiness I
  nattention Mental function deterioration Hemip
  aresis Motor speech disorder
• Temporal lobe abscesses Ipsilateral
  headache Aphasia Visual field defects
• Parietal lobe abscesses Headache Visual field
  defects Endocrine disturbances
• Cerebellar abscesses Nystagmus Ataxia Vomiti
  ng Dysmetria

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CLINICAL MANIFESTATIONS OF BRAIN
ABSCESS Headache 70 Fever 45-50 Focal
neurologic findings gt60 Triad of above
three lt50 Altered mental status
lt70 Nausea/vomiting 25-50 Seizures 2535
Nuchal rigidity 25 Papilledema 25
PPID,2005
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HEADACHE in Brain Abscess

• Usually non-specific, dull, and poorly localized.
• If abrupt extremely severe headache consider
  meningitis or SAH.
• Sudden worsening in H/A w meningismus consider
  rupture of brain abscess into ventricle.

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Diagnostic work-up

• MRI is the procedure of choice
• more sensitive especially for early cerebritis,
  satellite lesions, necrosis, ring, edema,
  especially for posterior fossa brain stem
  abscesses
• CT scan with contrast enhancement is 95
  sensitive
• Skull roentgenograms usually normal
• Biopsy or aspiration needed for definitive
  diagnosis
• Laboratory findings often not helpful
• Lumbar puncture contraindicated

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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 always elevated
• ESR Usually moderately elevated
• BC Often negative, BUT Should still be done
• AVOID LP!! Risk of herniation 15-30
• May even have normal CSF findings, but
• Usually elevated CSF protein cell count
  (lymphs)
• Unremarkable CSF glucose
• CSF culture rarely positive

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• PPID, 2005

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MRI of the brain reveals a 2-cm, round,
ring-enhancing lesion in the right lentiform
nucleus with associated vasogenic edema and
midline shift to the left. A, T1-weighted image
reveals an ill-defined area of low attenuation.
B, T1-weighted image after administration of
gadolinium, which reveals ring enhancement of the
abscess. C, T2-weighted image demonstrates
hypointensity of the rim of the abscess with a
large area of high signal intensity consistent
with cerebral edema. PPID,2005
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DIFFERENTIAL DIAGNOSIS

• Malignancy
• Abscess has hypodense center, with surrounding
  smooth, thin-walled capsule, areas of
  peripheral enhancement.
• Tumor has diffuse enhancement irregular
  borders.
• PET scan may differentiate.
• CRP??
• CVA
• Hemorrhage
• Aneurysm
• Subdural empyema
• Epidural abscess

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TREATMENT

• Medical surgical
• Obtain Neurosurgical Consult ASAP
• Aspiration or excision
• Antibiotics
• Initially selected based on
• -Likely pathogen considering primary source,
  underlying condition, geography
• -Antibiotic characteristics MICs for usual
  pathogens, CNS penetration, activity in abscess
  cavity
• Duration of abx usually 6-8 wks
• After surgical excision, a shorter course may
  suffice

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Antibiotics

• Empiric abx based on
• Likely pathogen
• considering primary source,
• underlying condition,
• Geography
• Antibiotic characteristics
• MICs for usual pathogens,
• CNS penetration,
• activity in abscess cavity
• Later, specific abx based on cultures
• Duration of abx usually 6-8 wks (/-po abx)
• After surgical excision, a shorter course may
  suffice

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Armstrong ID, Mosby inc 1999
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ANTIBIOTICS TREATMENT ONLY (WITHOUT SURGERY)

• Only in pts with prohibitive surgical risk
• poor surgical candidate,
• multiple abscesses
• a dominant location
• Abscess size lt2.5 cm
• concomitant meningitis, ependymitis
• early abscess (cerebritis?)
• In pt already showing improvement on abx

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• MONITOR RESPONSE CLOSELY WITH SERIAL IMAGING

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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
• Poor localization, especially in the posterior
  fossa
• Ventricular rupture (80100 mortality)
• Fungal , resistant pathogens
• Degree of neurological compromise at
  presentation
• Rapidly progressive neuro. impairment
• Immunosuppressed host
• Extremes of age
• Modified from CTID,2001

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SPINAL EPIDURAL ABSCESS
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SPINAL EPIDURAL ABSCESSINTRODUCTION

• 0.2-2.8 per 10,000 hospital admissions
• Incidence has doubled in the past 2 decades (with
  increasing spinal instrumentation, IVDU, aging
  population)
• Median age 50 yrs (35 yrs in IVDU)
• Thoracic gt lumbar gt cervical

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SPINAL EPIDURAL ABSCESSES

• A true spinal epidural space is present
  posteriorly throughout the spine, thus posterior
  longitudinal spread of infection is common.
• Anterior spinal epidural abscess is very rare
  (usually seen below L1 or cervical).

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American Family Physician April 1, 2002
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Predisposing Factors for Epidural Abscess

• Diabetes mellitus
• Intravenous drug abuse
• Alcoholism
• Spinal procedure or surgery
• Spinal trauma
• Chronic renal failure
• Malignancy
• Immunodeficiency
• Systemic source of infection
• AFP Vol. 65/No. 7 (April 1, 2002)
• NEJM 20063552012-20 Nov 9,2006

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PATHOGENESIS Spinal Epidural Abscess

• HEMATOGENOUS SPREAD from remote infections
  IVDU
• DIRECT SPREAD from 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 caused by
• Direct compression
• Thrombosis, thrombophlebitis
• Interruption of arterial blood supply
• Focal vasculitis
• Bacterial toxins/mediators of inflammation
• Even a small epidural abscess 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
• TB may cause up to 25 in some areas

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CLINICAL MANIFESTATIONS SPINAL EPIDURAL
ABSCESS Four clinical stages have been described
Stage I Fever and focal back pain Stage II
Nerve root compression with nerve root
pain Stage III Spinal cord compression with
accompanying deficits in motor/sensory nerves,
bowel/bladder sphincter function Stage IV
Complete Paralysis Armstrong, ID, Mosby
inc,2000
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DIAGNOSIS SPINAL EPIDURAL ABSCESS

• High index of suspicion in a pt with fever
  severe focal back pain.
• MRIgtCT
• Radionuclide studies (may identify the affected
  site)
• Abscess drainage(definitive dx)
• Blood cultures ( in 60, especially w S. aureus)
  
• Routine Labs rarely helpful
• ESR,CRP usually elevated, BUT non-specific
• WBC may or may not be elevated
• LP not advisable

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YIELD OF CULTURESSPINAL EPIDURAL ABSCESS

• Abscess fluid aspirate 90
• Blood culture 62
• CSF 19
• But, LP not advisable (may be c/b meningitis,
  subdural abscess, not very helpful anyway)

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TREATMENTSPINAL EPIDURAL ABSCESS

• Treatment of choice Surgical drainage as soon as
  possible systemic antibiotics.
• Empiric Abx for Staph (MRSA) GNR
• Duration of Rx at least 6 weeks
• If associated w infected SCS, remove all
  hardware.
• Monitor neurologic function closely

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Factors That Affect Outcome in Spinal Epidural
Abscess

• Pts neurologic status immediately before surgery
  NEJM Nov.9,2006
• Agegt60 years
• Degree of thecal sac compressiongt50
• Duration of cord symptoms gt72 hours
• Co-morbid conditions
• 
  Khanna RK, Malik GM, Rock JP, Rosenblum ML.
  Neurosurgery
  199639958-64

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Spinal Epidural AbscessComplications

• Mortality 5
• Paralysis 4-22
• Paralysis existing for more than 24-36 hrs
  unlikely to reverse.
• Darouiche NEJM Nov. 9, 2006

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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/ systemic signs
  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
• Mostly a complication of sinusitis, otitis media,
  mastoiditis.
• Most due to sinusitis (60 of such cases), mostly
  from frontal/ethmoid sinusitis.
• Trauma/post-op rarely hematogenous
• MgtF
• 95 SDE are in intracranial
• Majority of SDE pts have associated sinusitis

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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 ...)

• In 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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CTID,2001
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• The valveless venous network that interconnects
  the intracranial venous system and the
  vasculature of the sinus mucosa provides an
  alternative route of intracranial bacterial
  entry.
• Thrombophlebitis originating in the mucosal veins
  progressively involves the emissary veins of the
  skull, the dural venous sinuses, the subdural
  veins, and, finally, the cerebral veins.
• By this mode, the subdural space may be
  selectively infected without contamination of the
  intermediary structure a subdural empyema can
  exist without evidence of extradural infection or
  osteomyelitis.