Current Problems in Diagnostic Radiology 46 (2017) 441–451

Current Problems in Diagnostic Radiology

journal homepage: www.cpdrjournal.com

Imaging of Intracranial and Orbital Complications of Sinusitis and

Atypical Sinus Infection: What the Radiologist Needs to Know
Vinodkumar Velayudhan, DOa,n,1, Zeshan A. Chaudhry, MBBSa,1, Wendy R.K. Smoker, MDb,
Roman Shinder, MDc, Deborah L. Reede, MDa
a
Department of Radiology, State University of New York Downstate Medical Center, Kings County Hospital Center, Brooklyn, NY
b
Department of Radiology, University of Iowa Hospitals and Clinics, Iowa City, IA
c
Department of Opthalmology, State University of New York Downstate Medical Center, Brooklyn, NY

Sinusitis is a common disease. Complications, however, are less common and can be life threatening. Major complications occur from extension of disease
into the orbit and intracranial compartment and often require emergent treatment with intravenous (IV) antibiotics or operative intervention.
Immunocompromised patients with acute sinusitis are susceptible to atypical infections, such as invasive fungal sinusitis, which is a surgical emergency.
Therefore, it is important to accurately and promptly identify potentional complications of acute sinusitis to ensure appropriate treatment and minimize
negative outcomes. This article reviews the imaging features of a spectrum of complications associated with acute sinusitis and atypical infections.
& 2017 Elsevier Inc. All rights reserved.

Introduction Most cases resolve with symptomatic treatments without anti-

Rhinosinusitis is defined as inflammation of the paranasal sinus
and nasal cavity mucosa. It is a common disease frequently
encountered by primary care physicians in both adults and
pediatric patients. It affects an estimated 35 million people per
year and results in substantial morbidity.1 The annual direct
medical costs of treatment are approximately $5.8 billion.2 This
results in nearly 16 million office visits, more than 500,000
surgical procedures, and is reported to be the fifth leading
indication for antibiotic prescriptions by primary care pro-
viders.1-3
Most sinus infections are viral in origin and in the acute setting,
are usually secondary to viral upper respiratory tract infections.
Bacterial infection is the cause in only 2%-10% of cases4; an even
lesser number are fungal in origin. Other etiologies include allergic
and nonallergic rhinitis, chemical irritation (such as cigarette
smoke), and anatomical variants that predispose to obstruction.5
Isolated infection of the maxillary sinuses may be odontogenic in
origin in up to 20% of cases.6 Generally, children are more prone to
develop sinusitis and suffer complications because of anatomical,
immunological, and environmental factors.7,8
n
Reprint requests: Vinodkumar Velayudhan, DO, Divisions of Neuroradiology
and Emergency Radiology, Department of Radiology, State University of New York
Downstate Medical Center, Kings County Hospital Center, 450 Clarkson Ave,
Brooklyn, NY 11203.
E-mail addresses: Vin.Velayudhan@gmail.com, Vinodkumar.
Velayudhan@downstate.edu (V. Velayudhan).
1
Co-first authors. V.V. and Z.A.C. contributed equally to this work.
biotics, even if bacterial in origin.9 Viral and bacterial sinusitis
often cannot be differentiated based on symptoms, although
certain symptoms, such as purulent nasal discharge and pain,
suggest a bacterial origin. A consensus statement published in
Otolaryngology—Head and Neck Surgery in 2007 suggests a pre-
sumptive diagnosis of bacterial infection if symptoms last for more
than 10 days following an upper respiratory infection or worsen
within 10 days after initially improving.10
Pathophysiology and Anatomy
The paranasal sinuses are normally sterile. Mucosal edema can
cause narrowing and obstruction of the sinus ostia (Fig 1), which
leads to stasis of secretions and subsequent infection.
The periorbita and orbital septum are major barriers that limit
spread of infection into the orbit (Fig 2). The periorbita is the
periosteum of the bones that form the orbit. It is contiguous with
the periosteum on the inner surface of the skull and dura at the
optic foramen, superior orbital fissures, and ethmoid canals. The
periorbita is tightly attached to bone at the anterior margin of the
orbit and near openings for neurovascular fissures, foramina,
and canals.11 Elsewhere, the periorbita is loosely connected and
creates a potential space for subperiosteal collections. Anteriorly,
the periorbita extends into the eyelids and forms the orbital
septum.12,13
The orbital septum is located deep to the orbicularis oculi
muscle and attaches to the levator aponeurosis in the upper eyelid
and the tarsal plate in the lower eyelid. Infection may breach the
orbital septum through perforations for neurovascular structures.

http://dx.doi.org/10.1067/j.cpradiol.2017.01.006
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442 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451
Fig. 1. Maxillary sinus ostia. Coronal CT demonstrates the maxillary sinus ostia
(white arrows), the opening for the drainage pathway of each maxillary sinus.
The largest perforation is in the superomedial aspect of the orbital
septum for passage of the infratrochlear neurovascular bundle and
supraorbital vein to the eyelid.12,13
The periorbita appears low in signal on magnetic resonance
imaging (MRI) and is difficult to distinguish from the underlying
cortical bone.14 It is also difficult to visualize the orbital septum on
imaging. Its location, however, can be approximated as the area
just anterior to the orbital fat or near where the extraocular
muscles insert on the anterior globe.15
The orbit is bounded by frontal, ethmoid, and maxillary sinuses.
The parameningeal and periorbital location of the sinuses facili-
tates development of intracranial and orbital complications of
sinusitis. Spread of infection may be either direct or indirect.
Direct extension is often through neurovascular foramina, or
congenital and acquired osseous defects (Fig 3), which are com-
monly seen in the lamina papyracea that forms the medial orbital
walls and contains foramina for the anterior and posterior eth-
moidal arteries. Occasionally, no osseous defect is found.
Hematogenous spread is a form of indirect spread via a network
of valveless veins that drain the soft tissues of the face and orbits
(Fig 4). Thrombophlebitis of the veins that drain the face, sinuses,
and orbits are thought to be the major route for the spread of
infection to adjacent structures.7 Emissary veins located in the loose
connective tissue layer of the scalp communicate with the intra-
cranial compartment. Bidirectional flow of blood in these veins
promotes spread of infection anteriorly into the scalp or intra-
cranially. Infection commonly spreads retrograde into the orbits
because of thrombophlebitis of ophthalmic veins and smaller venous
tributaries that drain into the cavernous sinuses. Infection of specific
sinuses demonstrates a predilection for certain complications
(Table 1). Orbital complications are most commonly due to ethmoid
followed by frontal sinusitis. Intracranial complications typically
occur with frontal, ethmoid, and sphenoid sinus disease. Sphenoid
sinusitis may result in cavernous sinus thrombosis.
Fig. 2. Periorbita and orbital septum. (A) Sagittal illustration shows the location of the periorbita. (B) The periorbita continues anteriorly as the orbital septum (arrow) in the
upper eyelid, as demonstrated on the sagittal T1WI.
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Fig. 3. Direct spread of infection. Axial CT image demonstrates a defect in the left
medial orbital wall (lamina papyracea), a common location for dehiscence. Direct
spread of infection occurs through neurovascular foramina or via congenital and
acquired defects in bone.
Imaging Protocols
Plain radiography can detect and confirm the clinical diagnosis
of sinusitis. However, radiography has shown poor interobserver
agreement, a high false-negative rate and has been supplanted by
computed tomography (CT).16 CT is the initial test of choice for
evaluating complications of sinusitis as it is widely available and
more accurate in depicting sinus pathology, bony detail, and
anatomical relationships. For orbital complications of sinusitis,
helical CT should be performed ideally with IV contrast in the
axial plane with submillimeter collimation to produce isotropic
voxels. These data can then be reconstructed into high-quality
sagittal and coronal images. Though less sensitive than MRI,
contrast-enhanced CT (CECT) can be used to quickly assess for
intracranial complications, such as large extra-axial collections,
brain lesions, mass effect, and hydrocephalus. The patient may
then be triaged appropriately for emergent neurosurgical inter-
vention and for MRI.7
MRI is more sensitive in the evaluation of orbital and intra-
cranial complications of sinusitis.6,17 Orbital imaging should be
performed using a field of view that includes the nose and orbital
soft tissues anteriorly and extends posteriorly through the sella to
include the cavernous sinuses. T1-weighted images (T1WI) in the
axial and coronal planes can depict orbital anatomy and the
stranding and soft tissue thickening that occur with inflammation
and infection. Short-tau inversion recovery (STIR) or fat sup-
pressed T2-weighted images are useful in demonstrating edema
and fluid collections. Unless contraindicated, IV contrast should be
administered to differentiate abscess from phlegmon, evaluate for
venous thrombosis and for intracranial collections and meningitis.
Dedicated images of the brain should be obtained with any sinus
or orbit MRI to screen for these complications and others, includ-
ing cerebral infarction. The usage of specific MRI pulse sequences
is discussed as they relate to different disease entities later in this
article.
 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451 443

Imaging Findings of Sinustis

Acute sinusitis is usually clinically evident. Cross-sectional

imaging is typically indicated if intracranial or orbital complica-
tions are suspected or when evaluating immunocompromised
patients.18,19 An acutely infected sinus may demonstrate an air-
fluid level or aerosolized (frothy) secretions (Fig 5A). Mucosal
thickening is a nonspecific finding, commonly encountered on
imaging, and found incidentally in 20%-40% of magnetic resonance
(MR) examinations.6 It is usually indicative of chronic sinusitis,
especially with polypoid mucosal thickening, but may also occur
with acute sinusitis. Bone thickening and sclerosis are usually
associated with chronic sinusitis (Fig 5B and C). Inspissated
secretions in chronic sinusitis may appear hyperdense or calcified
on CT in bacterial and fungal disease. On MR, secretions demon-
strate progressively increased signal on T1WIs and low T2 signal as
the ratio of protein to water content increases.20

Fig. 4. Indirect spread of infection. Lateral illustration demonstrates the network of
communicating veins draining the face, sinuses, and orbits. Superior and inferior
ophthalmic veins drain directly into the cavernous sinus (CS). The infraorbital vein
can drain into the CS via the inferior ophthalmic vein and pterygoid plexus. The
deep facial vein drains into the pterygoid plexus and into the CS. (Color version of
figure is available online.)
Table 1
Infection of specific sinuses have a predilection for certain complications
Complications associated with infections of specific sinuses
Frontal and ethmoid sinusitis Sphenoid sinusitis
Complications of Sinusitis
Orbital involvement is the most common complication of acute
sinusitis. It is more common in children, and may be the first
presenting symptom of acute sinusitis in this population. Orbital
extension of sinus infection is the most common cause of unilat-
eral proptosis in children and the third most common cause of
proptosis in adults following thyroid eye disease and orbital
pseudotumor.7
Orbital infection is divided into 2 major categories: preseptal
(periorbital or superficial to the orbital septum) and postseptal
(deep to the orbital septum). In 1970, Chandler et al21 developed a
classification system of sinusitis complications, based on orbital
anatomy (Table 2). Following the advent of cross-sectional imag-
ing, modifications to this classification system were made.22,23

Orbital cellulitis and abscess Cavernous sinus thrombosis

and subperiosteal abscess
Meningitis
Epidural abscess
Subdural empyema
Frontal lobe abscess
Superior sagittal sinus
thrombosis
Pott puffy tumor (frontal)
Direct extension from the maxillary sinus to critical structures is rare.
Table 2
Meningitis The Chandler classification system of orbital complications of sinusitis. These
Temporal lobe and epidural abscess classifications do not represent a progression of disease as each category can have
Superior orbital fissure syndrome: proptosis, various underlying causes
orbital pain, and ophthalmoplegia (CNs III,
IV, and VI) þ numbness in ophthalmic Chandler classification
division of trigeminal nerve
Group I: preseptal cellulitis
Group II: orbital cellulitis
Group III: subperiosteal abscess
Group IV: orbital abscess
Group V: cavernous sinus thrombosis

Fig. 5. Acute vs chronic sinusitis. (A) Axial T2WI demonstrates right maxillary sinus air-fluid level (white arrow), suggestive of acute sinusitis. (B) Axial CT demonstrates
opacification of left sphenoid sinus with diffuse sclerosis and thickening of its walls (black arrow), indicating chronicity. (C) Axial CT demonstrates partial opacification of left
maxillary sinus with high-density material centrally (white arrow) and wall thickening (black outlined arrow) due to chronic sinusitis. Calcifications can be seen in
desiccated secretions from chronic sinusitis and in fungal sinusitis.

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Table 3
Clinical signs of postseptal involvement of orbital infections

Proptosis
Limitation of gaze/extraocular movement
Decreased visual acuity
Color vision defects
Afferent pupillary defect

The current classification divides orbital complications into 5

groups. Note that these do not represent progression of disease
as each complication can have different causes and occur exclusive
of the others. Fig. 7. Orbital cellulitis. Contrast-enhanced axial CT scan demonstrates maxillary
and ethmoid sinusitis with left orbital cellulitis. There is left preseptal soft tissue
swelling (white arrow) and postseptal extension (black arrow) consistent with
orbital cellulitis.
Preseptal Cellulitis

Preseptal cellulitis is an infectious, inflammatory edema in the
soft tissues anterior to the orbital septum. Patients present with
swelling of the eyelid and surrounding soft tissues. Because the
inflammation does not involve soft tissues deep to the orbital
septum, there should be no vision loss, restricted extraocular
movement, or other findings associated with postseptal involve-
ment (Table 3). Comprehensive clinical assessment is difficult
when there is significant swelling of the eyelids. The etiology is
most often due to a local skin infection (eg, insect bite, trauma, or
retained foreign body) in both adults and children and may also be
due to sinusitis in children.24 Most patients respond to treatment
with oral antibiotics. Surgery is indicated when there is an
associated eyelid abscess or progression to orbital abscess.
On imaging, preseptal cellulitis appears as swelling of the
eyelid (Fig 6). Periorbital soft tissue swelling may also be present.
The postseptal region, including the extraocular muscles, post-
septal fat, and lacrimal glands should be normal. Imaging findings
of edema on CT consist of eyelid soft tissue thickening and
increased density and stranding of the surrounding tissues. On
MRI, eyelid edema may be present and appear as low signal
reticulation on T1WI and hyperintense on fat suppressed T2
weighted or STIR images with corresponding enhancement.
Orbital Cellulitis
Orbital cellulitis represents inflammatory edema posterior to
the septum without abscess formation. It is usually due to acute
sinusitis. The vast majority of cases are secondary to acute ethmoid
sinusitis, typically involving the medial orbit. Patients can present
with eyelid edema, erythema, ptosis, chemosis, and proptosis.
There may be limited restriction of extraocular movement,
depending on the degree of inflammation. Visual acuity is usually
normal. Patients are typically febrile and have leukocytosis. Orbital
cellulitis can lead to serious neurologic and visual deficits. Treat-
ment consists of IV broad-spectrum antibiotics and sinus and
orbital drainage if indicated.
On imaging, orbital edema, diffuse or localized, is present
posterior to the orbital septum, with or without periorbital soft
tissue swelling (Fig 7). Inflammatory changes may involve extraco-
nal structures, intraconal structures, or both. Imaging shows
edema and enhancement, without a rim-enhancing fluid collec-
tion to indicate a discrete abscess. It is important to differentiate
between orbital and preseptal cellulitis because orbital cellulitis
generally requires hospital admission for IV antibiotics and possi-
ble surgical intervention.
Subperiosteal Abscess
A subperiosteal abscess (SPA) is a collection of purulent
material between the bone and periorbita. The most common
location is along the medial orbital wall, in association with
ethmoid sinusitis. It can also occur in the superior aspect of the
orbit, in association with frontal sinusitis, or rarely along the
orbital floor, associated with maxillary sinusitis.
A trial of IV antibiotics may be sufficient in children if the
collection is small and visual function is not impaired. Drainage of
the abscess and sinuses is performed in adults, older children,
immunocompromised patients, and those who fail to respond to
antibiotics. Urgent drainage is indicated when visual or neurologic
complications are suspected.
An abscess is best demonstrated on postcontrast CT and MR
where a rim-enhancing fluid collection is identified (Fig 8). A
collection along the medial orbital wall is readily identified on
axial images. However, a collection along the roof or floor is best
demonstrated in the coronal and sagittal planes. Diffusion-
weighted MR demonstrates restricted diffusion. A medial SPA
can displace extraocular structures and result in lateral dystopia
or proptosis or both. If proptosis is severe, tension may develop
with tethering of the posterior margin of the globe and stretching
of the optic nerve. This may lead to ischemic necrosis of the nerve,
an ophthalmic emergency. (Fig. 9B). Extraocular muscles may be
enlarged because of myositis and result in diminished ocular
movement.

Orbital Abscess

Fig. 6. Preseptal and postseptal cellulitis. Axial noncontrast CT in a patient with

preseptal and orbital cellulitis. Soft tissue swelling involving the left eyelid (white
An orbital abscess is a collection of pus that is not subperiosteal
arrows) consistent with preseptal cellulitis. Mild infiltration of the left retrobulbar in location, is less common than SPA and may be intraconal or
fat is also seen (black outlined arrow) consistent with orbital cellulitis. extraconal. Extraconal abscess is usually secondary to orbital

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 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451 445

Fig. 8. Subperiosteal abscess. (A) Illustration demonstrates the location of a subperiosteal abscess (black arrow) along the medial orbital wall beneath the periorbita (white
outlined arrow). (B) CECT shows a large peripherally enhancing subperiosteal abscess (asterisk) along the left medial orbital wall and anterior to the maxillary sinus with
proptosis. Left maxillary and ethmoid sinus opacification with a dehiscence (white arrow) in the wall of the maxillary sinus. (C) Clinical image (same patient) demonstrates
downward gaze restriction of the left eye consistent with postseptal involvement. (Color version of figure is available online.)

cellulitis or rupture of an SPA.6 Intraconal abscess is typically due
to penetrating trauma or surgical complications.25 Clinical symp-
toms are similar to those of orbital cellulitis. Stretching of the optic
nerve with ischemic necrosis, optic neuritis, or compression of the
optic nerve at the orbital apex can result in loss of visual acuity and
eventual blindness. Mass effect on cranial nerves (CNs) as they exit
the superior orbital fissure may result in ophthalmoplegia and
diplopia. Treatment consists of medical therapy and surgical
drainage of the orbital abscess and infected sinuses. Imaging
shows a rim-enhancing fluid collection with surrounding inflam-
matory changes. The collection should be clearly separate from
osseous structures to diagnose an orbital abscess (Fig 9).
Cavernous Sinus and Ophthalmic Vein Thrombosis
Preseptal soft tissues drain primarily into the systemic venous
circulation. Venous drainage of the midface, sinuses, and orbits is
via a rich network of valveless veins. These structures drain via the
superior and inferior ophthalmic veins into the cavernous sinuses.
The infraorbital and deep facial veins drain into the pterygoid
venous plexus, which communicates with the cavernous sinuses
via emissary veins within the foramen ovale and a tributary of the
inferior ophthalmic vein that courses through the inferior orbital
fissure (Fig 4).26
Cavernous sinus and ophthalmic vein thrombosis or thrombo-
phlebitis are commonly due to infections in the areas they drain.
Patients with cavernous sinus thrombosis are usually very ill and
may have multiple CN palsies, headache, fever and signs of
meningitis. Ophthalmologic findings, due to venous congestion,
include periorbital edema, proptosis, chemosis, and engorgement
of retinal veins with papilledema on fundoscopy. Restricted move-
ment or paralysis of extraocular muscles occurs because of
involvement of CNs III, IV, V1, and V2 that course in the lateral
wall of the cavernous sinus and CN VI within the cavernous sinus
proper (Fig 10).
Cavernous sinus thrombosis due to sinus infection is usually
treated with sinus drainage and high-dose IV antibiotics. Unlike
other forms of cerebral venous and systemic deep vein thrombosis,
the use of anticoagulants is controversial because of the risk of
intracranial and orbital hemorrhage.
On imaging, the normal cavernous sinus should demonstrate
lateral margins that are either straight or concave. Convex bulging
of the lateral wall is abnormal and should prompt further inves-
tigation to exclude pathologies such as, thrombosis, neoplasm,
carotid cavernous fistula, aneurysm, or tortuous internal carotid
artery (ICA).
Noncontrast CT may be normal. Abnormal findings include
cavernous sinus and sometimes superior ophthalmic vein enlarge-
ment, infiltration of the intraorbital fat, proptosis, and enlarge-
ment of extraocular muscles. On CECT, the lateral dural wall of the
cavernous sinus should enhance. After a sufficient delay of at least
45 seconds, venous structures of the cavernous sinus enhance
homogeneously and the cavernous ICA will not be visualized
separately.27 Thrombus may appear as a localized filling defect or
nonenhancement of the entire cavernous sinus.
MRI and contrast-enhanced magnetic resonance venography
are considered superior to CT venography in evaluating cavernous
sinus thrombosis.28 MRI demonstrates variable signal in the
cavernous sinus, often with high signal on fluid attenuation

Fig. 9. Orbital abscess. Axial (A) and coronal (B) CECT images in a patient with frontal sinusitis and orbital abscess. There is a fusiform extraconal collection (large white
arrow) with faint peripheral enhancement in the superior right orbit displacing the globe inferiorly. The collection is an orbital abscess and not subperiosteal as there is fat
plane (small white arrows) separating it from the orbital roof. There is tension on the right globe and optic nerve with tethering at the nerve insertion (white arrowhead).

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Fig. 10. (A) Anatomical basis of cranial neuropathies in CS thrombosis and sphenoid sinusitis. Coronal illustration demonstrates the location of the CNs III, IV, V1, and V2 in
the lateral dural wall of the CS and CN VI coursing within the sinus inferolateral to the cavernous ICA. Gaze palsy is related to involvement of these nerves, which supply the
EOM. (B) Coronal CT shows the relationship of the optic nerve canal (white arrow) coursing superior to the anterior aspect of the sphenoid sinus (asterisk). Optic neuropathy
and afferent pupillary defect are likely secondary to encroachment on or irritation of the optic nerve (CN II) in the optic canal above the sphenoid sinus. CS, cavernous sinus;
EOM, extraocular muscles. (Color version of figure is available online.)

inversion recovery (FLAIR) images. Filling defects or lack of
enhancement may be seen. On routine postcontrast images, the
only flow void present in the cavernous sinus is the ICA and should
not be confused with thrombus. On both CECT and MRI, the
cavernous sinus may be enlarged, with dilatation and thrombosis
of the superior ophthalmic vein (Fig 11).
frontal sinus. MRI demonstrates marrow edema and enhancement
due to osteomyelitis. A subgaleal abscess appears as a rim-
enhancing fluid collection, closely adherent to the outer table of
the frontal bone, with surrounding inflammatory changes on both
CT and MRI, as well as with restricted diffusion on diffusion-
weighted imaging (DWI) (Fig 13).

Pott Puffy Tumor Intracranial Complication of Sinusitis

In addition to orbital and intracranial complications, osteomye-
litis may occur, most often associated with frontal sinusitis.29
Frontal bone osteomyelitis with an associated subperiosteal or
subgaleal abscess involving the overlying scalp is termed the Pott
puffy tumor. It can also be seen in the posttraumatic setting. This
infection may spread intracranially resulting in meningitis, brain
abscess, and extra-axial empyemas. Intracranial spread of infection
can occur via 3 major pathways: (1) along valveless emissary veins
that cross the calvarium and allow for bidirectional spread into the
scalp or intracranially (Fig 12); (2) along nerves extending through
the meninges; and (3) through congenital or acquired osseous
defects.
Clinical presentation includes forehead swelling with pitting
edema and tenderness. Headache, fever, and nasal drainage may
also be present. Meningeal signs, altered mental status, and focal
neurologic findings strongly suggest intracranial involvement. MRI
is best for evaluation and should be performed if neurologic
complications are clinically suspected.
CT is highly sensitive in demonstrating sinusitis and associated
subgaleal abscesses in Pott puffy tumor and is often associated
with bone destruction involving the inner and outer tables of the
Potential intracranial complications include epidural and sub-
dural abscess or empyema, meningitis, cerebritis, brain abscess,
and dural sinus thrombosis. Although intracranial complications of
sinusitis are rare, they can cause serious neurologic deficits and
other morbidity and mortality. Overall, 30%-45% of patients have
residual long-term neurologic deficits.7,30,31 The true incidence is
difficult to determine because most cases of sinusitis are uncom-
plicated, treated in outpatient settings, and the literature often
contains only case reports and series of complicated cases. In all,
3%-6% of patients hospitalized with sinusitis develop intracranial
complications.32-35
Up to 45% of patients exhibit more than one focus of infection:
intracranial or orbital or both.31,36 Therefore, it is important to
maintain a high index of suspicion for intracranial involvement in
patients with orbital extension. However, those with intracranial
complications tend to have a longer duration of symptoms with
more complicated and protracted hospital stays. They typically
occur in older patients. The most common symptoms in both adult
and pediatric populations are fever and headache.30,36 Other
symptoms include seizures, altered mental status, focal neurologic
deficits, meningeal signs, and ocular complaints.32,33,36,37 However,

Fig. 11. Cavernous sinus and superior ophthalmic vein (SOV) thrombosis. (A) Axial CE T1WI demonstrates filling defects in the right cavernous sinus (white arrow) consistent
with thrombosis in this patient with ethmoid and sphenoid sinusitis (black arrows). (B) Axial CECT in the same patient demonstrates the absence of enhancement of the
right CS (black arrow) and a thrombosed SOV. CE, contrast enhanced; CS, cavernous sinus.

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 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451 447

Fig. 12. Anatomical basis for bidirectional spread of infection via emissary veins.
Illustration demonstrates emissary veins traversing the calvarium allowing for
spread of infection anteriorly into the overlying subgaleal layer of the scalp or
posteriorly into the intracranial compartment. (Color version of figure is available
online.)
some patients with intracranial spread may be asymptomatic and
detected only on imaging performed to evaluate the sinuses.
Extracranial complications, particularly intraorbital, usually dom-
inate the clinical presentation. This results in patients with
extracranial complications presenting earlier as intracranial com-
plications often have indolent, nonspecific, or clinically silent
features.
Extra-Axial Collections (Epidural Abscess and Subdural
Empyema)
Spread of infections from the frontal sinus to the anterior
cranial fossa results in the development of epidural abscess
(EDA) and subdural empyema (SDE). Older studies report SDE as
the most common complication; recent studies show EDA to
predominate.30,34,37
EDA occurs between the outer layer of the dura and the inner
table of the calvarium. Initially, EDA are clinically occult or present
with nonspecific symptoms such as headaches. This is likely owing
to the restricted space in which they develop, which slows
progression until they either penetrate the dura resulting in a
SDE or become large enough to cause significant mass effect and
elevated intracranial pressure. SDE, however, can rapidly spread
over the convexities and therefore can present more acutely with
worrisome neurologic findings, including neurologic deficits and
altered mental status.30 EDA seems to be more commonly
Fig. 14. Intracranial complications of sinusitis: empyema. Axial CE T1WI demon-
strates ethmoid and sphenoid sinusitis (small white arrows), thrombosis of the
right superior ophthalmic vein (large white arrow) and cavernous sinuses (not
shown), and bilateral extra-axial peripherally enhancing fluid collections (black
arrows) consistent with subdural empyemas anterior to the temporal lobes. CE,
contrast enhanced.
associated with intraorbital involvement.30 Treatment requires
surgical intervention.
Imaging findings of EDA include a low-density, lenticular-
shaped, extra-axial fluid collection on CT with an enhancing rim.
An epidural collection does not cross sutures, although they can
cross the midline. Adjacent mass effect and parenchymal edema
can be present. The appearance on MRI includes T2 hyperintensity
with variable T1 signal (depending on the relative proteinaceous
or hemorrhagic content) with surrounding rim enhancement
(Fig 14). Similar to other abscesses, there is often restricted
diffusion on DWI.
SDE often appears as a crescent-shaped, hypodense, rim-
enhancing collection that can cross sutures, but not the midline.
CT is often the first imaging study and may be negative in early
cases when collections are small. CECT is often sensitive enough to
visualize SDEs; however, it is not as sensitive as MRI, and may fail to
detect smaller collections.6,30 Mass effect is often secondary to
edema and ischemia, not necessarily from the extra-axial collec-
tion.36 This can cause effacement of the basilar cisterns and cortical
sulci. On MRI, T2-weighted images (T2WI) demonstrate a hyper-
intense collection with mass effect. The rim is often T1 hyperintense
on the noncontrast sequence. DWI may aid in differentiating
between SDE and EDA. Tsuchiya et al38 noted that, although SDE
demonstrated restricted diffusion, EDA had variable signal patterns,
often low or mixed, on the diffusion trace images.39

Fig. 13. Pott puffy tumor. Axial CE T1WI (A) demonstrates a rim-enhancing epidural fluid collection (white asterisk) with restricted diffusion on DWI (black arrow, B)
consistent with an abscess. There is adjacent dural enhancement in the interhemispheric fissure (outlined white arrows, A) and leptomeningeal enhancement in the sulci
(outlined black arrows, B) consistent with meningitis. This process extends anteriorly into the scalp with a subgaleal abscess, also demonstrating peripheral enhancement
(white arrow, A) and restricted diffusion (white arrow, B). CE, contrast enhanced.

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448 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451

enhancement occurs along cerebral convexities and dural reflec-

tions (Figs 13-15). Associated imaging findings include hydro-
cephalus and adjacent cerebral edema. Purulent exudate can
form in the subarachnoid space, with increased attenuation on
CT and incomplete suppression of cerebrospinal fluid signal on
FLAIR and restricted diffusion on MRI.40

Cerebritis and Cerebral Abscess

Spread from the extra-axial space to the parenchyma results in

Fig. 15. Intracerebral abscess. Coronal CE T1WI demonstrates a left supraorbital
mucopyocele filling and expanding a left supraorbital ethmoid air cell (asterisk)
and displacing the left globe (small white arrows). There is an intra-axial rim-
enhancing lesion in the left frontal lobe consistent with a brain abscess (large white
arrow). Linear dural-based enhancement over the superior left frontal lobe is
consistent with meningitis (black arrow). CE, contrast enhanced.
Reactive subdural effusions are a common complication of
meningitis, especially in infants, and can occur in cases of
complicated sinusitis. These effusions usually resolve without
treatment. Therefore, subdural effusion should be differentiated
from SDE. Both are hyperintense on T2 and show enhancement
along the cerebral surface of the lesion on postcontrast images;
however, SDE will demonstrate restricted diffusion.39,40
SDE is a neurosurgical emergency with mortality rates ranging
from 10%-70%.6 SDE progresses rapidly, spreading over the con-
vexities and often localizing in the supratentorial compartment. If
untreated, this will result in increased intracranial pressure,
development of focal neurologic deficits, seizures, and coma
within 1-2 days, thus underscoring the need for prompt diagnosis
and aggressive management, including urgent surgical
intervention.6,36
focal cerebritis and abscess formation, which is a rare complication
of intracranial spread of sinus disease. The frontal and parietal
lobes are most often affected.41
Initially cerebritis may develop with focal brain edema mani-
festing as low attenuation on noncontrast CT. MRI is more sensitive
for detection, particularly in the initial stages with increased signal
on T2 and FLAIR sequences. Patchy enhancement on postcontrast
sequences may or may not be seen in cerebritis. Frank abscess
formation will have the characteristic imaging features of a well-
defined, rim-enhancing fluid collection that demonstrates
restricted diffusion, with surrounding mass effect and vasogenic
edema (Fig 15). Rim enhancement is often thicker along the
cortical aspect of the abscess. Treatment should include surgical
drainage of the abscess, parenteral antibiotics, and definitive
management of the sinus disease.
Fungal Sinusitis
Fungal sinusitis is classified as noninvasive or invasive. Among
noninvasive disease, there are the following 2 subtypes: allergic
fungal sinusitis and mycetoma. Invasive fungal sinusitis is sub-
divided into the following 3 groups: acute fulminant, chronic
invasive, and granulomatous.42 The primary fungal pathogens are
Zygomycetes (Mucor spp) and Ascomycetes (Aspergillus spp). A
diagnosis of invasive fungal sinusitis requires histopathologic
evidence of hyphae penetrating the mucosa, submucosa, or bone
with invasion of blood vessels and prominent tissue necrosis.7,42,43

Noninvasive Fungal Sinusitis

Meningitis
Meningitis occurs most often in association with extra-axial
suppuration rather than in isolation. Although many studies report
either EDA or SDE as the most common complication of sinusitis,
others have found meningitis to be more common.41 It is fre-
quently secondary to sphenoid or ethmoid sinusitis. The most
common sequelae are seizure and hearing loss.
MR is more sensitive than CT for diagnosis. Leptomeningeal
enhancement occurs in cisterns and sulci and pachymeningeal
Allergic fungal sinusitis is the most common form of fungal
sinusitis.19,44 It occurs in patients with a history of atopy
(eg, asthma and allergic rhinitis) and is often found in association
with sinonasal polyposis.6 It is felt to represent a hypersensitivity
reaction to fungal pathogens, rather than an infection. The sinuses
contain material referred to as “allergic mucin,” inspissated secre-
tions that contain eosinophils, Charcot-Leyden crystals, and eosi-
nophilic degradation products. Mycetomas occur when these
secretions become superinfected with fungus and form a ball.6,19

Fig. 16. Allergic fungal sinusitis. CT images (A and B) demonstrate complete sinus opacification (with central high and peripheral low attenuation) in the frontal, maxillary,
and sphenoid sinuses (black arrows) with expansion of the ethmoid air cells (white arrows, B) and widening of the accessory maxillary sinus ostia (white arrow, A). This is
the classic appearance of allergic fungal sinusitis. Sinonasal polyposis often coexists and can have a similar appearance on CT. (C) Axial FLAIR image demonstrates markedly
diminished areas of signal (white arrows) with surrounding mucosal thickening in the frontal sinuses. (D) Axial CT scan in the same patient demonstrates corresponding
areas of high-density material within, and expansion of, the frontal sinuses (black arrows) with marked thinning and dehiscence of the posterior wall (white arrow).

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 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451 449

Fig. 17. Mycetoma. Coronal CT (A) demonstrates opacification of the right ethmoid and maxillary sinuses with a hyperdense, calcified lesion in the region of the medial wall
of the right maxillary sinus and ostiomeatal unit (black arrow). The lesion has markedly diminished signal on the coronal T2WI (B, white arrow). Inflammatory mucosal
thickening (B, black arrow) and intermediate signal secretions are also noted (B, asterisk). (Color version of figure is available online.)

Allergic fungal sinusitis is typically bilateral and involves multi-
ple sinuses. Sinuses may be expanded with varying degrees of
opacification and central high attenuation on CT corresponding to
allergic mucin, desiccated secretions, and fungal concretions
(Fig 16).6,45,46 Areas of low density along the margins of the sinus
lumen are due to mucosal thickening. Coexisting polyps may be
present and result in nodular mucosal thickening with expansion
of the sinuses and sinus ostia. Sclerosis of the sinus walls may be
seen because of chronic inflammation. Advanced cases of chronic
allergic fungal sinusitis may result in marked thinning and erosion
of sinus walls with intraorbital and intracranial extension.
On MRI, T1 signal is variable and may be high, intermediate, or
low signal. Metallic ions, including zinc and manganese, can
produce high T1 signal. Inflammatory mucosal thickening has high
T2 signal. Central markedly diminished signal or signal voids are
due to metallic ions, high protein, and low water content of
inspissated secretions (Fig 16).6,19 This can mimic an aerated sinus.
Polyposis and chronic allergic fungal sinusitis often coexist and
there is considerable overlap in the imaging appearances, espe-
cially on CT. However, polyposis and inflammatory mucosal
thickening demonstrate high T2 signal and enhancement, whereas
fungal elements and desiccated secretions have low T2 signal and
little, if any, enhancement.
Mycetomas (fungus balls) typically involve one sinus, usually
the maxillary sinus, and are hyperdense on CT because of matted
hyphae that may contain calcifications (Fig 17). The sinus walls
may be thickened because of chronic inflammation or thinned and
eroded from expansion or pressure necrosis from the mycetoma.
On MRI, the fungal elements in the center of the sinus demon-
strate markedly diminished or no signal on T2WI and variable T1
signal (Fig 17). Mycetomas do not enhance; inflammatory changes
along the walls of the sinus may enhance and appear hyperintense
on T2WI.
Treatment of chronic allergic fungal sinusitis is surgical removal
of the allergic mucin and restoration of sinus drainage. Topical
steroids are used postoperatively to suppress the immune
response and prevent recurrence. As this is a hypersensitivity
reaction, antifungal medication is not required. For mycetomas,
surgical removal of the fungal material and restoration of sinus
drainage are usually curative.19,44
Invasive Fungal Sinusitis
Acute (fulminant) invasive sinusitis is the most lethal form of
fungal sinusitis with a mortality rate of 50%-80%. It typically occurs
in diabetics and immunocompromised and severely neutropenic
patients. Disease typically progresses rapidly over days to a few
weeks with fungal invasion of the mucosa, submucosa, blood
vessels, and bones of the nasal cavity and sinuses. Skull base
invasion and intracranial and orbital extension are common.
Angioinvasion may involve the cavernous sinus, ICA, and its
branches.

Fig. 18. Invasive mucormycosis in a patient with acute myelogenous leukemia, neutropenia, and necrotic nasal ulcer. Coronal T2 images demonstrates right sided
pansinusitis (black arrows), opacification of the right nasal cavity (white arrows), and inflammatory changes in the right orbital fat (large white arrow, B) and masticator
space (circle, B).

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Fig. 19. Chronic invasive fungal sinusitis. (A) Axial CT using soft tissue window demonstrates bilateral maxillary sinus opacification with high-density material on the left
(black arrow) and marked infiltration of the fat anterior to the sinus (white arrow) in a patient with symptomatology for months. (B) Bone window image demonstrates
destruction of the anterior and medial walls of the left maxillary sinus (arrows). Axial T1WI without (C) and with contrast (D) in another patient with chronic symptoms
demonstrates effacement of the right pterygopalatine fossa and retromaxillary fat with enhancement (large white arrows). There is involvement of the cavernous sinuses
with lack of enhancement and enlargement on the right (small arrows, D).

Invasive fungal sinusitis initially produces significant unilateral
inflammatory changes and mucosal edema in the nasal cavity,
though this finding is nonspecific.19,47 Disease progresses from the
nasal cavity to the sinuses, orbits and intracranially to involve the
cavernous sinuses, brain, and meninges (Fig 18). The ethmoid and
sphenoid sinuses are more commonly involved.19 Sinus mucosal
thickening may be subtle or mild. As the disease progresses, sinus
opacification increases and bone destruction occurs. Premaxillary
or retromaxillary fat inflammation are important indicators of
invasive disease and can be seen in acute and chronic forms19
(Fig 19). Invasive disease tends to extend along vasculature.
Specifically, sphenoid sinus disease may result in cavernous sinus
thrombosis and compromise the ICA and can lead to cerebral
infarction with restricted diffusion on DWI (Fig 20). Invasive fungal
sinus disease should be considered whenever there is concurrent
involvement of the nasal cavity, sinuses, and orbits,6 particularly in
the immunocompromised.
Chronic invasive sinusitis occurs in immunocompetent or
mildly immunocompromised patients with a history of chronic
rhinosinusitis. It has a similar pattern of disease to fulminant
sinusitis but progresses over a longer time course, typically
months.
Granulomatous invasive sinusitis occurs primarily in North
Africa (in the Sudan) and Southeast Asia. It is rare in the United
States. This disease produces noncaseating granulomas with a
similar pattern of involvement as chronic invasive sinusitis.
Chronic and granulomatous invasive fungal sinusitis may be
indistinguishable on imaging and can present with similar findings
as advanced fulminant invasive disease. CT may demonstrate high
attenuation material within the sinus (much less commonly seen

Fig. 20. Invasive fungal sinusitis with angioinvasion and cerebral infarction. Coronal CE T1WI (A) demonstrates absent enhancement of the left cavernous sinus (white
arrow) consistent with thrombosis and narrowing of the left cavernous ICA. Axial DWI (B) demonstrates multiple left-sided watershed infarcts (white arrows) due to
compromise of the left ICA. CE, contrast enhanced.

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 V. Velayudhan et al. / Current Problems in Diagnostic Radiology 46 (2017) 441–451
in acute invasive disease) that appears isointense to hypointense
on T1WI and markedly hypointense on T2WI19,48 (Fig 19). Bony
destruction or sclerosis may be present with extension beyond the
sinus that can exceed the amount of disease within the sinus.48
Sclerosis due to chronic inflammation helps differentiate chronic
and granulomatous invasive forms from acute invasive disease.19
The mass-like appearance, bone destruction and transpatial
involvement of chronic and granulomatous invasive fungal sinus-
itis may mimic a neoplasm. Although it may not always be possible
to differentiate the two, the presence of calcifications, markedly
diminished T2 signal and lack of enhancement of the noninflam-
matory components favor the diagnosis of fungal sinus disease
over tumor.
For all forms of invasive fungal sinus disease, treatment is
aggressive surgical debridement and administration of systemic
antifungal medication. Reversal of diabetic ketoacidosis and neu-
tropenia improve mortality.19
Summary
Intracranial and orbital complications of sinusitis can have
significant morbidity, including vision loss and other serious
neurologic impairment and death. Radiologists should have a high
index of suspicion when interpreting sinus imaging and closely
examine the brain and orbits, particularly in patients with visual or
neurologic symptoms. Becoming familiar with common and
uncommon complications of sinusitis and patterns of spread of
disease will facilitate prompt and accurate diagnosis. In addition,
fungal sinusitis can have highly characteristic features and its
fulminant invasive forms need to be recognized in immunocom-
promised patients as disease can progress rapidly and result in
fatality. CT is the initial examination of choice and should be
supplemented with contrast-enhanced MRI to better characterize
orbital and intracranial complications seen on CT or if CT is
nonrevealing and clinical suspicion remains high.
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