Pathogenesis and pathophysiology
Bacterial invasion of brain parenchyma
 Preexisting or concomitant areas of ischemia,
necrosis, or hypoxemia in brain tissue
 Intact brain parenchyma - relatively resistant
to infection
Evolution of abscess influenced by:
 Nature of infecting organism
 Immunocompetence of host
 Stages:
1. Early cerebritis stage (days 1-3)
o Perivascular infiltration of
inflammatory cells
o Surrounds a central core of
coagulative necrosis
o Marked edema surrounds
the lesion
2. Late cerebritis stage (days 4-9)
o Pus formation enlarges
necrotic center bordered by
inflammatory infiltrate of
macrophages and
fibroblasts
o Thin capsule of fibroblasts
and reticular fibers develop
o Edema becomes more
distinct
3. Early capsule formation (days 10-13)
o Capsule is better developed
on the cortical (than on the
ventricular) side of the
lesion
o Appearance of a ring-
enhancing capsule on
neuroimaging studies
4. Late capsule formation (day 14 and
beyond)
o Well-formed necrotic center
o Dense collagenous capsule
o Edema has regressed
o Marked gliosis w/ large no.
of reactive astrocytes
outside the capsule
 Seizures as a
sequela
Laboratory
NEUROIMAGING STUDIES
Cerebritis
 T1W MRI: area of low signal
intensity w/ irregular post-Gd
enhancement
 T2W MRI: area of increased signal
intensity
 CT scan: often not visualized; area
of hypodensity
Mature brain abscess
 Contrast-enhanced CT scan:
o Center: (focal)
hypodense
o Ring: enhanced
o Edema: hypodense
 Contrast-enhanced T1W MRI:
o Center: hypodense
o Ring: enhanced
o Edema: hypodense
 Contrast-enhanced T2W MRI:
o Center: hyperintense
o Ring: hypodense
o Edema: hyperintense
MICROBIOLOGIC DIAGNOSIS
 Gram’s stain and culture
 Abscess material obtained via CT-
guided stereotactic needle
aspiration
INFLAMMATORY MARKERS
 Peripheral leukocytosis (50%)
 Elevated ESR (60%)
 Elevated CRP (80%)
BLOOD CULTURES
 Positive in 10% of cases overall
 Positive in >85% (Listeria)
DIFFERENTIAL DIAGNOSIS
 Conditions that cause HA, FVR,
focal neurologic signs, and seizure
activity:
o Brain abscess
o Subdural empyema
o Bacterial meningitis
o Viral
meningoencephalitis
o Superior sagittal sinus
thrombosis
o Acute disseminated
encephalomyelitis
Management
OPTIMAL THERAPY
 High-dose parenteral antibiotics +
neurosurgical drainage
MEDICAL THERAPY
 Indications:
o Neurosurgically inaccessible
abscesses
o Small (<2-3 cm) or non-
encapsulated abscesses
(cerebritis)
o Condition is too tenuous to allow
performance of a neurosurgical
procedure
 Duration:
o Minimum of 6-8 wk (parenteral
antibiotic therapy)
 Condition:
o Community-acquired brain
abscess, immunocompetent host
 3rd or 4th-gen
cephalosporin (e.g.,
cefotaxime,
ceftriaxone,
cefepime; and
 Metronidazole
o Penetrating head trauma or
recent neurosurgical procedure
 Ceftazidime
(Pseudomonas spp.);
and
 Vancomycin
(Staphylococci); or
 Meropenem +
vancomycin
ASPIRATION AND DRAINAGE
 Under stereotactic guidance
COMPLETE EXCISION
 Craniotomy or craniectomy
o For multiloculated abscesses
o If stereotactic aspiration is
unsuccessful
PROPHYLAXIS
 Anticonvulsant therapy
o d/t high risk (35%) of focal or
generalized seizures
o Cont'd at least 3 mo after
resolution
o Withdrawal based on EEG results
CORTICOSTEROIDS
 Not given routinely
 IV dexamethasone 10 mg q6h
o For Px w/ substantial periabscess
edema, mass effect, inc. ICP
o Tapered as rapidly as possible
 To allow for natural
encapsulation of
abscess
SERIAL MRI OR CT SCANS
 Monthly or bimonthly
 Weekly if Px receiving antibiotic therapy
alone
PROGNOSIS
 Mortality rate <15%
 Significant sequelae (>20% of survivors):
o Seizures
o Persisting weakness
o Aphasia
o Mental impairment