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Review Article

A Review of Subdural Empyema and Its Management

Amit Agrawal, MCh,* Jake Timothy, FRCS,y Lekha Pandit, MD,z Lathika Shetty, MD,x
and J.P. Shetty, MDk
Abstract: Subdural empyema is a collection of purulent material
between the dura mater and the arachnoid mater. It is a lifethreatening complication of paranasal sinusitis, otitis media, or
mastoiditis. The classic clinical syndrome is characterized by acute
febrile illness that is punctuated by rapid progressive neurological
deterioration, and, if left untreated, it will eventually lead to coma
with fatal outcome. High-resolution contrast-enhanced computed
tomographic scanning has revolutionized the diagnosis of subdural
empyema; however, gadolinium-enhanced magnetic resonance
imaging provides greater clarity of morphological detail. Treatment
of patients with subdural empyema consists of immediate surgical
evacuation only in rare circumstances where there are contraindications to surgery or significant mortality risks avoided;
conservative treatment is advised. The antibiotics should be given
for a period of 3 to 6 weeks with close monitoring of clinical status.
Aggressive management of subdural empyema has reduced the
mortality rate; still, it 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. We discuss
the etiopathology and diagnosis of subdural empyema and its
(Infect Dis Clin Pract 2007;15:149 153)

ubdural empyema (SDE) is a life-threatening infection

that was first reported in the literature approximately 100
years ago. Subdural empyema is an intracranial focal
collection of purulent material located between the dura
mater and the arachnoid mater. It has also been referred to as
subdural abscess, pachymeningitis interna, and circumscript
meningitis.1 Left untreated, SDE is invariably fatal. Since
the introduction of antibiotics, the mortality rate for this
infection has decreased significantly and now ranges from
14% to 28%.2,3 In the preantibiotic era, the mortality rate
approached 100%; this still may be the case in developing
countries. However, in the developed world, the mortality
rate has improved tremendously, and it is approximately 6%
to 35%.4 Rapid recognition and the early institution of
appropriate treatment and neurosurgical intervention give the
patient a good chance of recovery with little or no
neurological deficit.

*Department of Surgery, B.P. Koirala Institute of Health Sciences, Dharan,

Nepal; yLeeds General Infirmary, Leeds, United Kingdom; zDepartments
of Neurology, xRadiology and kPathology, K.S. Hegde Medical
Academy, Mangalore, India.
Address correspondence and reprint requests to Amit Agrawal, MCh,
Department of Surgery, B.P. Koirala Institute of Health Sciences,
Dharan, Nepal. E-mail:
Copyright n 2007 by Lippincott Williams & Wilkins
ISSN: 1056-9103/07/1503-0149

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.

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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Infectious Diseases in Clinical Practice  Volume 15, Number 3, May 2007

Agrawal et al

TABLE 1. Site of Infections and Organisms Commonly Isolated

in SDE
Source of Initial Infection
Paranasal sinuses


Otitis media

Postneurosurgical wound infection

Bronchogenic spread
Meningitis (infant or child)


a-hemolytic streptococci
Anaerobic streptococci
Nonhemolytic streptococci
S. aureus
Bacteroides species
S. aureus
S. epidermidis
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
Group B streptococci
Listeria monocytogenes

to neurosurgical procedures, and Salmonella species have

been detected in patients with advanced acquired immune
deficiency syndrome; multiple organisms may be present
simultaneously. Spinal SDEs are almost invariably caused by
streptococci or by S. aureus.9 In children, SDE is commonly
secondary to H. influenzae or S. pneumoniae meningitis.21
Nontyphoidal Salmonella organisms have been reported in
SDE in children recently.22 24 However, in adults, nontyphoidal Salmonella organisms have been found in the
setting of advanced acquired immune deficiency syndrome

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.


Later, the headache becomes diffuse. As the infection

progresses, focal neurological signs may appear. If untreated
symptoms may progress over several days to include
drowsiness, increasing stupor and eventually, coma. Seizures, either focal or generalized, have been reported in as
many as 50% of patients. Examination often reveals a
temperature greater than 388C (100.58F). Aphasia may occur
when the dominant hemisphere is involved. Meningismus is
present in 80% to 90% of the patients. Occasionally, palsies
of the third and sixth cranial nerves occur. In addition, more
than 85% of the patients have contralateral motor deficits.
Certain conditions that must be considered in the differential
diagnosis of SDE (Table 3) and these conditions can usually
be distinguished by clinical findings, lumbar puncture, brain
imaging, and appropriate laboratory studies.29 31

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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Subdural Empyema and Its Management

TABLE 2. Symptoms and Signs in a Patient With SDE


Physical Examination

 Fevertemperature above 388C (100.58F)

 Headacheinitially focal and later generalized
 Recent history (<2 wk) of sinusitis, otitis media, mastoiditis,
meningitis, cranial surgery or trauma, sinus surgery,
or pulmonary infection
 Confusion, drowsiness, stupor, or coma
 Hemiparesis or hemiplegia
 Seizurefocal or generalized
 Nausea or vomiting
 Blurred vision (amblyopia)
 Speech difficulty (dysphasia)
 History of intracerebral abscess
(recent or in the past)

 Mental status changesconfusion, drowsiness, stupor, and coma

 Meningismus or meningeal signs
 Hemiparesis or hemisensory deficits

Aphasia or dysarthria
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

ICP indicates intracranial pressure.

and MRI is not possible or is contraindicated.36,37 Computed

tomographic scan may miss intracranial SDEs detectable by
MRI. Conversely, occasional spinal SDEs may be detected
by CT myelography where MRI finding is negative.9

meningitis accompanied by complex features (eg, increased

echogenicity in the convexity collections, presence of hyperechoic fibrinous strands or thick hyperechoic inner membrane, and increases in echogenicity of the pia-arachnoid).

Magnetic Resonance Imaging

Other Tests

The diagnostic procedure of choice for intracranial and

spinal SDE is MRI with gadolinium enhancement.9,28,32,35,38
A fluid collection surrounded by a contrast-enhancing rim is
characteristic of SDE. The MRI is superior to CT in
demonstrating extraaxial fluid and its rim enhancement.5
Diffusion-weighted imaging has proved to be more sensitive
than conventional MRI in detecting the intraaxial involvement.39,40 Magnetic resonance imaging studies demonstrated
convexity and interhemispheric collections that have a low
signal on T1 weighted images and a relatively high signal on
T2 weighted images. Related cerebral edema seems hyperintense on T1 weighted scans.5

Radionuclide brain scanning and angiography have

been helpful in diagnosing SDE, but they are not nearly as
effective as CT scanning.

Cranial Ultrasound
Cranial ultrasound has been helpful in differentiating
SDE from anechoic reactive subdural effusion in infants with

TABLE 3. Differential Diagnosis of SDE

Bacterial meningitis
Brain abscess
Cerebral thrombophlebitis
Epidural abscess
Acute necrotizing hemorrhagic leukoencephalopathy
Focal embolic encephalomalacia due to bacterial endocarditis

Early and accurate diagnosis, timely surgical intervention, and appropriate antibiotic therapy are the keys to a
more favorable clinical outcome. Treatment in virtually all

TABLE 4. Lumbar CSF Findings

 Increased white blood cell count (predominantly
polymorphonuclear neutrophils). A significant increase
(>50/mL) may be seen, although a slightly elevated cell count
of 5 20 mL (reference range, 0 5/mL) does not rule
out the possibility of SDE.
 Increased protein level greater than 100 mg/dL may be
seen (reference range, 20 40 mg/dL), although less
substantial elevations (50 90 mg/dL) do not rule out the
possibility of SDE.
 Decreased glucose levels of 40 mg/dL (reference range,
50 80 mg/dL) or less usually are seen. The CSF glucose
levels should be normalized with a blood glucose level
obtained concurrently.
 Occasionally, the CSF is normal and sterile in these cases.
 The specific CSF findings should be compared with the
accepted normal values of the treating physicians laboratory.

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Agrawal et al

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.

cases of intracranial or spinal SDE requires prompt surgical

drainage and antibiotic therapy. Pus from the empyema
should always be sent for anaerobic, and aerobic, culture.9,14
Treatment of patients with SDE consists of immediate
surgical evacuation. Subdural empyema should be treated
surgically except in extremely rare circumstances where
there are contraindications to surgery or significant mortality
risks avoided. Imaging can accurately localize the collection
pus that can be evacuated by burr hole placement, but wide
craniotomy with irrigation is the procedure of choice because
it improves the outcome in SDE by allowing wide exposure,
adequate exploration, and better evacuation of subdural
purulent material.41,42 Complete evacuation of pus and
eradication of the source of infection is the goal of
treatment.1,20,36,43 Urgent evacuation of infected material
by a neurosurgeon and otolaryngologist team either simultaneously or at the earliest possible opportunity for
eradicating the source of infection results in cure and a
significant decrease in recollection and reexploration.1,44,45
Occasionally, medical management may suffice.46,47

TABLE 5. Prognostic Factors Associated With SDE

Unfavorable prognostic factors
 Encephalopathy or coma at the time of presentation
 Elderly or younger than 10 years
 Delay in starting antibiotics
 Sterile cultures
Favorable prognostic factors
 Craniotomy as surgical modality (rather than burr holes)
 Early treatment (surgery and antibiotics)
 Young age (10 20 yrs is optimal)
 Patient is alert, awake, and oriented at the time of presentation
 Paranasal sinus as source of initial infection
 Isolation of aerobic streptococci in the culture
 Aerobic streptococci isolated


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).

Follow-Up and Prognosis

Delay in surgery leads to clinical worsening and poor
results. Of the patients operated within 72 hours, 10%
became disabled as against 70% if the surgery took place
after 72 hours.52 Patient education should emphasize
compliance with medicationboth antibiotics and antiepileptic drugs. Intravenous antibiotics for a total period of 3 to
6 weeks can be administered on either an inpatient or
outpatient basis. Certain prognostic factors are identified in
SDE (Table 5). Outcome is dependent on the preoperative
level of consciousness,47,52,53 timing and aggressiveness of
treatment,19,31,45 and the rapidity of progress of disease.47

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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