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PATHOPHYSIOLOGY
Subdural empyema is a collection of pus between the
dura mater and the arachnoid mater. It is usually unilateral and
has a tendency to spread rapidly through the subdural space
until limited by specific boundaries (eg, falx cerebri, tentorium
cerebelli, base of the brain, and foramen magnum). It accounts
for 20% of all cases of intracranial abscesses. The infection is
more common in men, who may account for as many as 80% of
cases. Approximately two thirds of patients are aged between
10 and 40 years. In infants, SDE is most commonly a
complication of purulent meningitis.5,6 In older children, the
source of SDE is typically direct extension of sinusitis or otitis
media.1,3,5 9 Other causes include spread of infection from
distant sites (viz, lungs). Subdural empyema can develop after a
cranial surgery or after a trauma, particularly in cases where
there is a compound depressed fracture.1,2,4,10 Subdural
empyema have been reported after secondary infection of a
subdural effusion or hematoma.1,2,5 The infection can spread
from mastoid or middle ear infections by eroding the tegmen
tympani11 and from the frontal air sinus by erosion of its
posterior wall.12 The infection can also spread by retrograde
septic thrombophlebitis.8 Subdural empyema, which is associated with venous sinus thrombosis and thrombophlebitis, may
cause cerebral abscess or infarction.13,14 Subdural empyema
may also occur after surgery; in rare cases, it is associated with
septicemia because of the valveless diploic veins.15 As the SDE
progresses, it behaves like an expanding mass lesion, which
occur after trauma-associated increased intracranial pressure
and cerebral intraparenchymal penetration. Cerebral edema and
hydrocephalus also may be present secondary to disruption of
blood flow or cerebrospinal fluid (CSF) flow caused by the
increased intracranial pressure. Thrombosis of the cortical
veins or cavernous sinuses or from septic venous thrombosis
of contiguous veins in the area of the SDE may lead to
cerebral infarction.
MICROBIOLOGY
The rate of success in culturing bacteria from
surgically evacuated pus varies from 54% to 81%.3,12,16
Common causative organisms are anaerobes, aerobic streptococci, staphylococci, Haemophilus influenzae, Streptococcus pneumoniae, and other gram-negative bacilli (Table 1).17
The most common organisms in intracranial SDE secondary
to paranasal sinusitis are anaerobic and microaerophilic
streptococci, in particular those of the Streptococcus milleri
group (S. milleri and Streptococcus anginosus).4,7,9,18,19
Staphylococcus aureus is seen in 7% cases of SDE
associated with sinusitis and is commonly seen in postoperative/posttraumatic SDE.1,9,20 Pseudomonas aeruginosa or
Staphylococcus epidermidis may be present in cases related
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Agrawal et al
Trauma
Otitis media
Neonates
Organisms
a-hemolytic streptococci
Anaerobic streptococci
Nonhemolytic streptococci
S. aureus
Bacteroides species
Enterobacteriaceae
S. aureus
S. epidermidis
Enterobacteriaceae
a-hemolytic streptococci
P. aeruginosa
Bacteroides species
S. aureus
S. aureus
S. epidermidis
S. pneumoniae
Klebsiella pneumoniae
H. influenzae
Escherichia coli
S. pneumoniae
Neisseria meningitidis
Enterobacteriaceae
Group B streptococci
Listeria monocytogenes
CLINICAL FEATURES
Stephanov et al26 described SDE as the most
imperative of neurological emergencies, which, if not
treated immediately, is associated with high risk of status
epilepticus, spreading cortical venous and cortico-venous
sinus thrombosis, fulminating cerebritis, brain swelling,
cerebral coning, and ultimately leads to death. It is difficult
to clinically differentiate between meningitis and SDE. The
diagnosis of SDE is based on a strong clinical suspicion
(Table 2).1,7,27 The commonest clinical presentation is a triad
of fever, sinusitis, and neurological deficits, with a fulminant
and rapid downhill course.1,7 9 Other symptoms include
headache, nausea/vomiting, first-time seizures, and mentalstatus changes.8,9,20,28 Headache, initially focal, is a
prominent early symptom in as many as 90% of patients.
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INVESTIGATIONS
Laboratory Studies
In addition to physical findings, laboratory data may be
helpful in determining which patient might benefit from
imaging of the brain.32,33 White blood cell count, erythrocyte
sedimentation rate, and C-reactive protein level can be
markedly elevated and may be useful screening tools to
decide which patient should be imaged.28 Children with
hyperglycemia or diabetes may be at increased risk for
sinogenic intracranial empyema.28
Lumbar Puncture
Lumbar puncture is contraindicated if there is raised
intracranial pressure because of the possibility of cerebral
herniation. However, lumbar puncture will be helpful to rule
out meningeal infection when increased intracranial pressure
has been excluded. Cerebrospinal fluid findings may suggest
the presence of infection (Table 4).1,30
Imaging Studies
Computed tomography (CT) and magnetic resonance
imaging (MRI) have been the mainstays of the imaging
diagnosis of SDE.5,34
CT Scan
High-resolution, contrast-enhanced CT scanning is the
standard technique for quick and noninvasive diagnosis of
SDE. If MRI is unavailable, a contrast-enhanced head CT
with axial and coronal planes should be obtained. Nonenhanced CT alone lacks sensitivity, and a normal study may
be falsely reassuring.28,32,35 On the CT scan, the empyema
may be manifested by a hypodense area over the hemisphere
or along the falx. The margins are better delineated with the
infusion of contrast material (Fig. 1). It will also delineate
cerebral involvement. Cranial bone involvement can also be
seen with CT scan. Computed tomographic scan is the
modality of choice if the patient is comatose or critically ill,
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Physical Examination
Aphasia or dysarthria
Seizure
Sinus tenderness, swelling, or inflammation
Papilledema and other features of increased ICP, such as
nausea/vomiting, mental status changes, and gait disturbance
Homonymous hemianopsia
Palsies of cranial nerves III, V, or VI, especially if the abscess is near
a petrous portion of the temporal bone, causing facial pain and lateral
rectus muscle weakness
Fixed dilated pupil on the ipsilateral side due to compression
of cranial nerve III
Other Tests
Cranial Ultrasound
Cranial ultrasound has been helpful in differentiating
SDE from anechoic reactive subdural effusion in infants with
Bacterial meningitis
Brain abscess
Cerebral thrombophlebitis
Epidural abscess
Acute necrotizing hemorrhagic leukoencephalopathy
Focal embolic encephalomalacia due to bacterial endocarditis
Management
Early and accurate diagnosis, timely surgical intervention, and appropriate antibiotic therapy are the keys to a
more favorable clinical outcome. Treatment in virtually all
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151
Agrawal et al
Antibiotics
Because intracranial SDEs may contain multiple
organisms, provisional antibiotic therapy for intracranial
SDE, where the organism is unknown, should be directed
against S. aureus, microaerophilic and anaerobic streptococci, and gram-negative organisms.9,28,48 51 Antibiotics should
include the following: (1) nafcillin, oxacillin, or vancomycin; plus (2) a third-generation cephalosporin; plus (3)
metronidazole. Provisional antibiotic therapy for spinal
SDEs should be directed against S. aureus and streptococci
and should include nafcillin, oxacillin, or vancomycin.9
FIGURE 1. High-resolution CT scanning showing a hypodense area over the left cerebral hemisphere. The margins are
better delineated with the infusion of contrast material.
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Complications
Complications of SDE include seizures; cerebral
infarction; cavernous sinus thrombosis from septic thrombosis of adjacent cerebral veins; hydrocephalus from
compressed cerebrum resulting in interference with CSF
flow; cerebral edema; cranial osteomyelitis, primarily in
adjacent cranial bones; and residual neurological deficits
(eg, hemiparesis and aphasia).
CONCLUSIONS
Subdural empyema is associated with the high
incidence of morbidity (ie, neurological deficits) because
very ill patients who would have died in the past now survive
with deficits. Early diagnosis and treatment, more accurate
localization with head CT scan, early sinus drainage, and
recognition of the prominent role of anaerobes in the disease
have reduced the mortality rate in SDE.
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2. Hlavin ML, Kaminski HJ, Fenstermaker RA, et al. Intracranial
suppuration: a modern decade of post-operative subdural empyema
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3. Nathoo N, Nadvi SS, van Dellen JR, et al. Intracranial subdural
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cases and review. Clin Infect Dis. 1995;20:372 386.
5. Rich PM, Deasy NP, Jarosz JM. Intracranial dural empyema. Br J
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