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Subdural empyema and other suppurative complications of

paranasal sinusitis
Melissa K Osborn, James P Steinberg
Lancet Infect Dis 2007; 7: 6267
Division of Infectious Diseases,
Department of Medicine,
Emory University School of
Medicine, Atlanta, GA, USA
(M K Osborn MD,
Prof J P Steinberg MD)
Correspondence to:
Dr Melissa K Osborn, Division of
Infectious Diseases, Emory
University School of Medicine,
550 Peachtree St NE, 7th Floor
Medical Oce Tower, Atlanta,
GA 30308, USA.
Tel +1 404 686 8114;
fax 1 404 686 4841;
mkosbor@emory.edu

Suppurative intracranial infection, including meningitis, intracranial abscess, subdural empyema, epidural abscess,
cavernous sinus thrombosis, and thrombosis of other dural sinuses, are uncommon sequelae of paranasal sinusitis.
A high index of suspicion is necessary to identify these serious complications. We present a patient with subdural
empyema in whom the diagnosis was delayed, followed by a discussion of suppurative complications of sinusitis. The
case shows the rapid progression of subdural empyema, which represents a true neurosurgical emergency requiring
prompt diagnosis and management.

Case presentation
A 63-year-old white man presented to the emergency
department because of lethargy. The patient was well
until 4 days before admission when he complained of
cough, fever, and feeling poorly. Over the next few days,
he became progressively lethargic. In the emergency
department, the patient complained of neck pain but was
unable to relate other symptoms.
The patients past medical history was notable for
diabetes mellitus, hypertension, hyperlipidaemia, and
daily alcohol use. He had a remote history of posttraumatic splenectomy. 8 years ago, he had recurrent
episodes of pancreatitis eventually requiring drainage of
a pseudocyst. 5 years before admission, he was treated
for a group F streptococcal liver abscess. Medications at
the time of admission included quinapril hydrochloride,
hydrochlorothiazide, and gembrozil.

On examination, the patient was lethargic, but could be

aroused with verbal stimulation. His temperature was
372C, heart rate 66 beats per min, blood pressure
180/64 mm Hg, and respiratory rate 18 breaths per min.
His pupils were equal, round, and reactive, and his neck
was supple. The patient was oriented only to person and
place; cranial nerves were intact. His left arm was accid,
but the right arm and both legs showed normal strength.
The remainder of his physical examination was normal.
The white blood cell count was 22 200 per L with
26% band forms, 48% segmented neutrophils, and
10% lymphocytes; haemoglobin was 148 g/dL, and
platelets 453 000 per L. Chemistries were remarkable for
a sodium level of 129 MEq/L. Pre and post-contrast cranial
computed tomography (CT) (gure, AC) showed
extensive pansinusitis with a 1 cm right-sided subdural
uid collection, associated mass eect, and overlying soft-

Figure: Serial computed tomography scans showing progressive subdural collection

(A, B, C) Initial contrast CT scan showing subdural uid collection and near complete opacication of bilateral ethmoid and maxillary sinuses (indicated by *). There is
a heterogeneous patter of mixed hyperdense and hypodense signal overlying the right cerebral convexity. (D, E, F) Non-contrast cranial CT 6 hours later: subdural
empyema now easily visible, with midline shift and obliteration of the contralateral basilar cisterns (D), consistent with subuncal hernation.

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tissue swelling. The CT ndings were interpreted by the

neuroradiologist as suggestive of subdural haematoma.
The patient was admitted to the intensive care unit and
vancomycin, ceftriaxone sodium, and metronidazole
were started as empiric therapy for sinusitis with possible
meningitis. Because of the CT ndings, a lumbar
puncture was not done. 6 h after admission, the patient
deteriorated acutely, developed a dilated right pupil, and
required endotracheal intubation. Repeat cranial CT
without contrast showed progression of the right
subdural uid collection with increased right-to-left
midline shift of 18 cm and subuncal herniation
(gure, DF). At emergent craniotomy, a large subdural
empyema was evacuated. The patient also underwent
bilateral maxillary antrostomy, bilateral anterior
ethmoidectomy, and right sphenoidectomy. Gram stain
of the empyema showed many polymorphonuclear white
blood cells, many Gram-positive cocci, and rare
Gram-negative rods. Culture of the empyema grew
alpha-haemolytic Streptococcus spp. Sinus cultures from
operative specimens also grew alpha-haemolytic
Streptococcus spp and Fusobacterium spp. The antibiotic
regimen was changed to meropenem.
By hospital day 2, the patients sodium level had
returned to normal. He was febrile for several days post
evacuation of the empyema then remained afebrile.
Following surgical evacuation, his mental status waxed
and waned, but slowly improved, and he was extubated
on hospital day 10. The patient received 3 weeks of
parenteral antimicrobials and required a percutaneous
gastrostomy tube for feeding because of impaired
swallowing. At hospital discharge he could answer simple
questions and sit up with assistance but was unable to
walk. 1 year later, he was much improved and had only
mild residual left arm weakness. He developed a seizure
disorder and remained on anti-epileptic medications.

Review and discussion

The case shows the rapid progression of subdural
empyema and the need for prompt diagnosis and
aggressive management of this disease. Although the
presence of sinusitis, fever, altered level of consciousness,
focal neurological ndings, and compatible intracranial
imaging suggested this diagnosis, recognition was
delayed. This delay was possibly caused by several factors
including a low index of suspicion, occurrence in an
older man (which is somewhat atypical), and the
clinicians reliance on the interpretation of CT imaging
done by a radiologist who was unaware of the clinical
context. The rapid progression to herniation emphasises
the need for emergent neurosurgical intervention.

Intracranial complications of sinusitis

Bacterial sinusitis is common and resolves without
sequelae in the majority of cases. Suppurative
complications can occur, although they are much less
common since the advent of antibacterial agents.
http://infection.thelancet.com Vol 7 January 2007

Additionally, the use of CT and other cranial imaging has

allowed for earlier diagnosis and treatment of complicated
sinus disease. Because the intracranial suppurative
sequelae of sinusitis can be neurologically devastating,
clinicians should retain a high index of suspicion for this
uncommon but serious disease.
The suppurative complications of sinusitis can be
divided into orbital and intracranial infections. Orbital
complications include orbital cellulitis, subperiosteal
abscess (Potts puy tumour), orbital abscess, and
cavernous sinus thrombosis.1 Sinusitis, particularly of the
ethmoid air cells, is the most common cause of these
severe orbital infections. Orbital infections present with
periorbital oedema, chemosis, visual loss, restricted eye
movement, and proptosis. The latter three ndings help
to dierentiate orbital infections from preseptal cellulitis,
which is conned to structures anterior to the orbit.
Diplopia results from involvement of the cranial nerves,
most often the sixth cranial nerve. Orbital complications
of sinusitis and intracranial infection coexist in up to
45% of cases.2,3 Therefore, patients exhibiting orbital
signs should undergo cranial imaging.2
The intracranial complications of paranasal sinusitis
include subdural empyema, epidural abscess,
intracerebral (intraparenchymal) abscess, meningitis,
cavernous sinus thrombosis, and thrombosis of other
dural sinuses. It is not uncommon for a patient to exhibit
more than one focus of infectionintracranial or orbital,
or both.39 Most cases of sinusitis are uncomplicated and
occur in the outpatient setting. In view of the common
occurrence of sinusitis and the rarity of complications,
the incidence is presumed to be low, although precise
estimates are unavailable since many cases of sinusitis
do not present for medical treatment. The literature on
intracranial complications of sinusitis consists mainly of
case reports and single-institution case series, with the
exception of one large series involving two institutions.10
The small number of cases acquired at one institution
over many years is a testimony to their rarity. In patients
hospitalised with sinusitis, the reported rate of
intracranial complications varies from 37% to 476%.4,10
By selecting for severe sinus disease, these series clearly
overestimate the incidence of intracranial complications.
Overall, sinus disease is the presumed underlying cause
of about 10% of intracranial suppuration.8,9,11 Subdural
empyema, however, is much more strongly associated
with underlying sinusitis and is also the most common
sinusitis-associated intracranial infection.24,10,11 Most case
series of complicated sinusitis are in the surgical
literature. Since meningitis from sinusitis rarely requires
surgery, this complication might be under-represented in
these case series.
The pathogenesis of intracranial complications of
sinusitis includes two major mechanisms: direct
extension and, more commonly, retrograde thrombophlebitis via the valveless diploe veins. The close
anatomical proximity of the sinuses to the intracranial
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cavity allows for direct extension of infection to bone

(ie, osteomyelitis) and subsequent erosion into the
epidural space. On occasion, there is further penetration
of purulence through the dura to the subdural space.
Retrograde thrombophlebitis is facilitated by the shared
venous drainage of the sinuses and the intracranial
structures. Because these veins are valveless,
thrombophlebitis that begins in the veins draining the
sinuses can pass retrograde into the cavernous sinus and
other dural venous sinuses. If infection reaches the
subdural space, it spreads easily over the convexities of
the brain owing to a lack of septations. The implantation
of the arachnoid granules represents the only barrier in
this space. Contralateral spread under the falx cerebri can
occur. Thrombophlebitis associated with subdural
empyema can lead to venous stasis with thrombosis,
infarction, and subsequent cerebral inammation. The
resultant oedema is a major contributor to the
neurological deterioration seen with undrained subdural
pus.12 The pathogenesis of subdural empyema in infants
is dierent, with most cases resulting from infection of
subdural eusions that develop from an initial
meningitis.13
The clinical presentation of complicated sinusitis
depends on the site of bacterial seeding (table). The
presentation can be acute and fulminant with bacterial
meningitis, cavernous sinus thrombosis, and subdural
empyema. Brain abscesses and epidural abscesses
typically have a more indolent presentation, although
rupture of a brain abscess into the ventricular system can
precipitate an acute neurological deterioration. The
anatomical considerations mentioned above are
important determinants of the clinical course. For
example, purulence in the epidural space is constrained
by the dura, which is adherent to the calvarium.
Therefore, clinical presentation of epidural abscess is
insidious with fever and headache evolving over weeks.
By contrast, seeding of the subdural space leads to rapid
spread of purulence because of lack of anatomical
constraints.
Most complicated sinusitis occurs in young men in the
second or third decade of life, often with no underlying
medical problems.5,911 This predisposition for young men
has been explained by the vascularity of the diploic

system in this age group, which is at its maximum,10

as well as the continued development of the frontal sinus
that occurs during that time. The male to female ratio is
reported to be from 13/1 to 45/1. The most common
symptoms in patients presenting with intracranial
complications are fever and headache. Symptoms or
history of sinusitis may or may not be present.2,9,10,14
Altered mental status and focal neurological decits are
frequent. Seizures occur in 820% of cases.8,10,15 Other
symptoms include meningismus, decreased visual acuity
or other ocular complaints including photophobia.
Silent (asymptomatic) complications have also been
described,3 in which intracranial purulence is detected
incidentally when imaging is done to evaluate the
sinuses. Most intracranial complications result from
frontal, ethmoid, or sphenoid4,9,10 sinusitis; sinusitis is
often bilateral.1517 Sphenoid sinusitis is strongly associated
with cavernous sinus thrombosis,18 which manifests as
proptosis, periorbital oedema, and chemosis caused by
obstruction of the superior ophthalmic vein. Meningitis
arises most often from ethmoid or sphenoid sinusitis.19
Mortality from intracranial sinusitis-associated
infection in the pre-CT era was as high as 66%,11 but has
decreased to 27%.2,10,15 Many patients are left with
residual neurological decits, including seizure disorders,
particularly if diagnosis or intervention is delayed.10
Therefore, early diagnosis and treatment remain a
priority.

Subdural empyema
Much of the clinical presentation and epidemiology of
subdural empyema parallels that of intracranial
complications in general. Most cases occur in the second
decade of life5,7,17,2023 in patients who are otherwise healthy.
As with other intracranial complications, males have a
marked predisposition, with a male-to-female ratio of
3/1,7,2022,24 and as high as 8/1 for sinus-associated cases.6,24
Compared with other causes of intracranial suppuration, a
greater proportion of subdural empyemas (41% to 67%)
result from sinusitis.57,2022 Other causes of subdural
empyema include meningitis,5,21,25,26 otitis media,5,7 operative infection,9,27 previous head trauma,6,7,21,23,26 or bacteraemic seeding of a previous subdural haematoma.6,7,20,21
As mentioned above, many subdural empyemas in infants

Site of complication

Usual involved sinuses

Clinical presentation

Meningitis

Sphenoid, ethmoid

Acute and rapidly progressive; fever, meningismus, headache with or without signs of cerebral dysfunction

Subdural empyema

Frontal

Rapidly progressive; meningeal signs plus increased intracranial pressure; can lead to focal neurological
defects and coma in 24 to 48 h if untreated; seizures

Brain abscess

Frontal, ethmoid

Indolent with symptoms caused by increased intracranial pressure; classic triad of fever, headache, focal
neurological ndings present in only a minority; seizures

Cavernous sinus
thrombosis

Sphenoid, ethmoid,
frontal

Subacute when sinusitis is the underlying cause; periorbital swelling, fever, headache, diplopia, proptosis;
involvement of contralateral eye is a late nding

Epidural abscess

Frontal

Slowly growing, indolent onset; may be asymptomatic except for headache; signs of increased intracranial
pressure eventually develop

Table: Intracranial complications of bacterial sinusitis

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Panel 1: Common signs and symptoms in patients with

subdural empyema

Fever
Headache
Altered mental status
Hemiparesis
Nausea or vomiting
Seizures
Meningismus
Periorbital oedema
Papilloedema
Potts puy tumour
Other: dilated pupil, ocular palsies, cranial nerve palsies,
dysphasia or aphasia, eyelid abscess, homonymous
hemianopsia, cerebellar signs, hydrocephalus

occur when a subdural eusion related to meningitis

becomes infected. When sinusitis is the cause, the frontal
sinus is most often implicated,6,7,21 though pansinusitis and
involvement of the posterior ethmoid cells are also
common. Concomitant intracerebral abscess occurs in 6%
to 22% of cases6,20,22 and epidural abscess in 9% to 17%.6,22
The presenting symptoms of subdural empyema are
reective of increased intracranial pressure, meningeal
irritation, and cerebritis (panel 1).57,13,17,2022,24,26,28 If the
empyema is located in the frontal lobe, the clinical
presentation could be subtle changes in personality or
mood without focal neurological symptoms.2,9,24 The most
common symptoms are headache, fever, and neck
stiness. More ominous ndings can evolve rapidly and
include depressed level of consciousness, focal
neurological decits or cranial nerve palsies, hemiparesis,
papilloedema, vomiting, and septic shock. Rapid
progression is a hallmark of subdural empyema and
underscores the importance of prompt intervention;
subdural empyema is a true neurosurgical emergency.
Seizures occur in 2580% and are more common in
subdural empyema than with other intracranial
complications.
Radiographic imaging should be done in all patients in
whom subdural empyema is suspected. Although
magnetic resonance imaging (MRI) is more sensitive in
showing parenchymal abnormalities such as abscess,19
cranial CT is often the rst neuroimaging done because
of more widespread availability and the need for a rapid
diagnosis. It is also the test of choice for visualisation of
the paranasal sinuses and associated bony abnormalities.
In early cases of subdural empyema, CT might not show
a uid collection,6,17,24,26,28 so consideration should be given
to repeated CT imaging or MRI as the clinical scenario
dictates. When visualised on CT, the empyema appears
as a thin, hypodense subdural lesion, with linear
enhancement of the medial surface.25,26 The grey-matter/
white-matter interface is displaced inwardly.25 Mass eect
is generally caused by oedema and ischaemia rather than
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mass eect from the abscess.25 The oedema can cause

eacement of the basilar cisterns and attening of the
cortical sulci.25 The sinuses might appear opacied, with
air-uid levels and bony erosion evident in some cases.2
MRI appearance is similar; T1-weighted images show
mass eect and hypointense areas of purulence, which
are hyperintense on T2-weighted images.19 The abscess
usually has a hyperintense rim on non-contrast
T1-weighted images. Diusion-weighted images (DWI)
on MRI may be helpful in dierentiating subdural and
epidural empyemas.29,30 Subdural empyemas have high
signal on DWI, whereas epidural empyemas show several
patterns, most often low DWI signal, or mixed signals.
Benign subdural eusions have a low signal on DWI,
similar to cerebrospinal uid (CSF).29,30 Most empyemas
are located within the frontal lobe6,23,31 and can be
bilateral.5,6,26 Although rare, infratentorial empyemas have
also been described as complications of paranasal
sinusitis.32,33
Complete blood count almost universally reveals
leucocytosis, with increased polymorphonuclear cells and
band forms.5,7,17,2123 Erythrocyte sedimentation rate is often
less than 100 mm/h.7,21,22 Lumbar puncture in patients
with subdural empyema is contraindicated, particularly if
mass eect is present on CT or if the patient has
papilloedema.5 Neurological deterioration and transtentorial herniation after lumbar puncture are well
described, and have led to death.2,5,6,20 However, in patients
who have a lumbar puncture done, the CSF shows a
parameningeal formula, with elevated protein, normal
glucose, and pleocytosis with polymorphonuclear
predominance.5,7,13,2123 The CSF Gram stain usually does
not show organisms and CSF cultures are negative more
than 85% of the time.5,7,13,20,22,24 The CSF may be normal.20
Infections are often polymicrobial.8,20 Anaerobic Grampositive cocci, Streptococcus spp, Staphylococcus spp, and
anaerobic Gram-negative bacilli are the most commonly
isolated organisms from empyema material6,7,12,14,2123,26
(panel 2). No single organism predominates, although
members of the Streptococcus milleri group (including
Panel 2: Associated pathogens in subdural empyema
More common
Streptococcus milleri
Other streptococci and enterococci
Aerobic Gram-negative bacilli*
No growth
Less common
Streptococcus pneumoniae
Staphylococcus aureus, coagulase-negative staphylococci
Anaerobic Gram-positive cocci
Anaerobic Gram-negative bacilli
*Haemophilus inuenzae, Proteus spp, Escherichia coli, Pseudomonas spp, Klebsiella spp,
Acinetobacter spp, Salmonella spp, Morganella spp, Eikenella spp. Veillonella spp,
Peptostreptococcus spp, others. Bacteroides spp, Fusobacterium spp, Prevotella spp.

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Streptococcus anginosus, Streptococcus intermedius, and

Streptococcus constellatus) are over-represented.2,16,22,24,34
Anaerobes are more likely to be present if the empyema
is associated with sinusitis compared with other causes
of subdural empyema. The presence of anaerobes and a
conspicuous absence of pathogens associated with acute
sinusitis (Streptococcus pneumoniae, Haemophilus
inuenzae, Moraxella catarrhalis) suggest that most
subdural empyemas arise from chronic sinusitis.
Operative cultures do not yield growth in 753% of cases,
6,2022
presumably because of previous administration of
antibiotics or failure to use proper anaerobic culture
technique.
Antimicrobial therapy should be directed against the
aforementioned organisms and include broad-spectrum
activity against aerobic and anaerobic cocci and bacilli.
Recommended empiric therapy is a third-generation
cephalosporin plus metronidazole, which oers broad
coverage and good CSF and abscess penetration. Once
antimicrobial identication and susceptibility results are
available, antimicrobial therapy can be tailored to the
pathogens recovered from cultures. Antimicrobial therapy
in the case discussed may have been unnecessarily broad.
It should be recognised, however, that cultures might be
negative and continuation of empiric antimicrobial
therapy, including anaerobic coverage, is reasonable. The
appropriate duration of therapy has not been studied in
randomised, controlled trials, but available series suggest
at least 2 weeks of intravenous therapy should be given;
parenteral or oral therapy is frequently continued for up to
a total of 6 weeks of antimicrobials.6,13,22 If adjacent
osteomyelitis is present, prolonged parenteral therapy
should be considered (eg, minimum of 68 weeks).
Adjunctive care includes prophylactic anticonvulsants,10,15
and management of oedema and intracranial hypertension
with measures such as corticosteroids,10,15 ventriculostomy,
and intravenous mannitol.26
Surgical management of subdural empyema is an
integral part of therapy and should be done without delay.
Isolated medical management has been successful in
only a few case reports.6,22 The goals of surgical
intervention are decompression of the brain and complete
evacuation of purulence. There is controversy in the
neurosurgical literature regarding the preferred surgical
interventionburr hole versus craniotomy.6,24,35 Some
patients treated with a burr hole require additional
surgery or conversion to craniotomy.12,22,23,26,35 Currently,
both procedures are acceptable, and the determination of
which procedure to do should be made in consultation
with the neurosurgeon. Multiple burr holes with surgical
irrigation and decompressive craniectomy are other
surgical options.35 In addition to drainage of intracranial
purulence, denitive management of the infected sinuses
should be done, preferably at the same time as empyema
drainage. The choice of surgical approach depends on
the involved sinus and can include maxillary irrigation,
external frontoethmoidectomy, sphenoid sinusotomy,
66

Search strategy and selection criteria

A Medline search of the literature from 1966 to the present
was done to identify relevant English language articles.
Several search strategies were used. The search term
sinusitis was combined with (1) subdural empyema,
(2) brain abscess or epidural or intracranial or intracerebral,
(3) cavernous sinus thrombosis, (4) meningitis, and
(5) intracranial complications. Retrieved references were
manually reviewed for relevance, favouring case series and
larger studies over case reports. Studies of exclusively
pediatric cases were not included. The references of selected
papers were also reviewed.

antral washout, and frontal trephine. The development

of endoscopic sinus surgery had made this the most
popular otolaryngologic intervention in subdural
empyema in recent years.15
Before the availability of antibiotics, subdural
empyemas were almost always fatal, even with surgical
drainage. Antimicrobials decreased the mortality rate to
15641%.5,7,11,13,21 Although the impact of CT diagnosis on
mortality has not been studied directly, mortality rates
are lower (615%) since the advent of CT imaging.6,17,20,22
Survivors may exhibit substantial morbidity, including
seizures in 12375% of cases,17,20,21 hemiparesis in
1535%,6,12,17,21 and residual neurologic decits in nearly
half of cases.6,17

Conclusions
Although often considered a benign disease, paranasal
sinusitis can on rare occasions lead to serious, potentially
life-threatening complications. The astute clinician should
consider such complications in any patient presenting
with fever, headache, and neurological decits, regardless
of a history of sinusitis. Early diagnosis with aggressive
medical and surgical management can lead to improved
outcome, most notably for subdural empyemas that evolve
rapidly and are true neurosurgical emergencies.
Conicts of interest
We declare that we have no conicts of interest.
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