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Radiological imaging of inflammatory lesions in the nasal cavity and

paranasal sinuses

Article in European Radiology · May 2006

DOI: 10.1007/s00330-005-0068-2 · Source: PubMed

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Eur Radiol (2006) 16: 872–888
DOI 10.1007/s00330-005-0068-2 HEAD AN D NECK

H. B. Eggesbø
Radiological imaging of inflammatory lesions
in the nasal cavity and paranasal sinuses

Received: 27 June 2005

Abstract Paranasal sinus develop- primary modality in diagnosing and
Revised: 9 October 2005 ment and pneumatisation variants are mapping suspected inflammatory si-
Accepted: 14 October 2005 described, and rhinosinusitis and dif- nonasal disease. Magnetic resonance
Published online: 4 January 2006 ferent patterns of inflammatory sino- (MR) imaging is complementary to
# Springer-Verlag 2006 nasal diseases are reviewed. Other CT if fungal sinusitis, pyocele or
H. B. Eggesbø (*) inflammatory sinonasal diseases, e.g., malignancy are suspected.
Department of Radiology, fungal sinusitis, mucocele, pyocele
Aker University Hospital, and sinonasal manifestations in sys- Keywords Rhinosinusitis .
N-0514 Oslo, Norway
e-mail: [email protected] temic diseases, are briefly described. Inflammatory patterns . CT . MR
Fax: +47-23-033046 Computed tomography (CT) is the

Introduction Inflammatory lesions in the nasal cavity and paranasal

sinuses comprise a spectrum of diseases, and imaging plays
The purpose of radiological imaging in inflammatory a key role in the diagnostic evaluation, choice of treatment
lesions in the nasal cavity and paranasal sinuses is to con- and surgical planning. In this review, the main focus will be
firm the diagnosis, characterise the extent and localisation on CT and MR imaging of inflammatory patterns of
of disease and describe anatomical variants in order to se- rhinosinusitis. Fungal sinusitis and sinusitis in patients with
lect patients that may benefit from sinus surgery. Computed systemic diseases are also described.
tomography (CT) offers excellent delineation of the bony
anatomy and extent of sinus disease and serves as a “road
map” during surgical procedures. CT therefore is regarded Development of the paranasal sinuses
as the “gold standard” in paranasal sinus imaging. How-
ever, in the differential diagnosis between “simple” inflam- Paranasal sinus development starts during the third and
matory paranasal sinus disease caused by bacterial agents fourth foetal months as evaginations of the nasal mucosa
and, e.g., mucocele, pyocele, fungal sinusitis or neoplasm, [2]. The development of the sinuses is closely linked to the
magnetic resonance (MR) imaging plays an important role. development of the facial bones. All the sinuses reach adult
The normal paranasal sinus anatomy displays a wide size approximately at the age of 12 years [2–6]. During
spectrum of pneumatisation and bony variants. The com- childhood, maxillary sinus development occurs in succes-
plex anatomy challenges both radiologists reporting sino- sive stages. The sinuses develop rapidly until the age of 2–3
nasal disease and ear, nose and throat (ENT) surgeons years, and then a slower evolution is seen until the age of 7
performing functional endoscopic sinus surgery (FESS). In years. A new acceleration of development may be seen after
1929, Mosher [1], an ENT surgeon, wrote: “...if it was the age of 7–8 years [7, 8].
placed in any other part of the body, it would be an in- Factors that determine the development of the paranasal
significant and harmless collection of bony cells. In the sinuses are not exactly known, and related studies described
place where nature has put it, it has major relationships so in the literature are scarce. Chronic sinusitis in childhood
that disease and surgery of the labyrinth often lead to has been the most frequently suggested explanation of sinus
tragedy. Any surgery in this region should be simple but it aplasia or hypoplasia [9, 10]. Low O2 saturation and altered
has proven to be one of the easiest ways to kill a patient.” temperature [11] secondary to chronic sinusitis or sinonasal
 873

polyposis in young children, causing mouth breathing, may

contribute to reduced pneumatisation. Preceding pneuma-
tisation, red marrow must convert to yellow marrow.
Factors that influence the red-marrow conversion, e.g.,
anaemia, have been shown to reduce pneumatisation, espe-
cially of the sphenoid sinuses [11, 12]. Mucosal inflam-
matory processes activate osteoclastic and osteoblastic
activity, but the stimulus that initiates bone remodelling is
not clearly known [13]. In addition, sinus surgery has been
postulated to induce maxillary sinus hypoplasia [14, 15].
Excessive pneumatisation of the surrounding bone may
follow simultaneously with the development of the para-
nasal sinuses and is commonly seen in the normal popu-
lation: e.g., agger cells, i.e., pneumatisation of the most
anterior part of the maxillary bone, the agger mound, oc- Fig. 2 Coronal CT. Infraorbital (Haller) cells (arrows) may cause
curring in 60% of the normal population, concha bullosa, narrowing of the ethmoid infundibulum, hence sparse mucosal
i.e., pneumatisation of the concha media (Fig. 1) and Haller thickening may cause obstruction of mucociliary clearance
cells (Fig. 2), i.e., pneumatisation of the infra-orbital bone,
seen in approximately 30% of the normal population [16,
17]. Thus, the final structure of a person’s paranasal sinuses sphenoid sinuses, the mucosal lining should not be seen at
is as unique as a set of fingerprints [18]. CT in normal healthy persons [21].
The ethmoid sinuses may undergo cyclical changes re-
ferred to as the nasal cycle, and therefore mucosal thick-
Mucosal thickening and nasal cycle ening up to 2 mm is considered as a normal finding in the
ethmoid sinuses [21, 22]. The mucosal lining of the nasal
The nasal cavity is lined by stratified squamous- and res- cavity and turbinates also undergoes cyclical changes. At
piratory-type ciliated columnar epithelium and in some MR, the nasal mucosal volume and signal intensities are
places is separated by transitional epithelium. The paranasal shown to alternate from one side to the other several times
sinuses are also lined with respiratory epithelium, but this is during 24 h. When a topical vasoconstrictor is applied, the
thinner and has fewer serous and mucinous glands than the nasal cycle will be interrupted [23]. The nasal cycle is not
nasal cavity. Thickening of the mucosal lining of the nasal seen in all individuals and becomes less prominent with
cavity and sinuses may be due to inflammation or represent age. The maxillary, frontal and sphenoid sinuses are not
mucosal oedema or hyperplasia [19, 20]. Mucosal thicken- included in the nasal cycle.
ing of the maxillary sinus is common in asymptomatic
patients [21], therefore the mucosal lining is considered to
be normal when less than 4 mm [21, 22]. In the frontal and Mucociliary clearance

The function of the ciliated cells is to move mucous from

the sinuses to the choanae. The mucous consists of two
layers: (1) a superficial layer of nasal mucous with high
viscosity that serves to trap bacteria and particles in a sub-
stance rich with immune cells, antibodies and antibacterial
proteins and (2) an underlying sol layer with less viscosity
in which the cilia are able to beat [24]. In each sinus, the
ciliated cells beat in a specific direction. Therefore, each
sinus has its own characteristic mucous flow pattern [25].
The flow pattern may be interrupted when two ciliated sur-
faces come in contact and cause stagnation of the mucous in
the sinus cavity. Long-lasting stagnation then will cause
sinusitis. This is particularly relevant in the region termed
the ostiomeatal complex (OMC). The OMC refers to the
common final drainage pathway of the maxillary, anterior
ethmoid and frontal sinuses and is regarded as the key area
Fig. 1 Coronal CT. Pneumatisation of the middle turbinates termed of inflammatory sinonasal disease. The anatomical struc-
concha bullosa (arrows) may be a predisposing factor to inflamma- tures of OMC are the maxillary ostium, ethmoid infundib-
tory sinonasal disease ulum, ethmoid bulla, uncinate process, hiatus semilunaris
874

and the middle meatus [26]. Anatomical variants in the is increased in asthma, allergic rhinitis and viral respiratory
OMC may cause a predisposition to mucosal contact and infections, but reduced in sinusitis, cystic fibrosis, primary
obstruction of mucociliary clearance [27–32]. However, at ciliary dysfunction, chronic cough and after exposure to
imaging, pneumatisation variants are commonly displayed tobacco and alcohol [44, 45].
without concomitant obstruction of the drainage routes
[30], and opacification may be seen without pneumatisation
and anatomical variants [33, 34]. Nasal septal deviation Rhinosinusitis
may interfere with mucociliary clearance due to mechanical
obstruction of the OMC. It has also been postulated that Rhinosinusitis is replacing the term sinusitis because
nasal septal deviation may modify the airflow and then sinusitis is often preceded by rhinitis and rarely occurs
influence the ciliary activity [35]. without concurrent nasal airway inflammation [46–48]. In
Since many of the sinuses develop laterally and in- the 1997 Task Force on Rhinosinusitis’ definition of chron-
feriorly, such as the maxillary sinuses, the ciliated cells ic rhinosinusitis, only symptoms and signs were included
often move mucous against gravity towards the sinus [49]. Though a correlation between symptoms of rhinosi-
openings, and mucous produced just adjacent to a sinus nusitis and CT findings remains controversial [50–54],
ostium may move around the entire sinus cavity before most clinicians prefer CT imaging for the diagnosis and
leaving the ostium. This is one explanation why the surgical assessment of disease severity.
creation of accessory ostia at sites outside the physiological
ostia fails to improve sinus drainage. In fact, this sometimes
results in mucous draining from the natural ostia re-entering Acute rhinosinusitis
the sinus via the newly created opening and recycling
through the sinuses again. Therefore, the main goal of sur- Acute rhinosinusitis is a clinical condition with symptoms
gical intervention is to enlarge the natural sinus ostia and lasting less than 4 weeks, while subacute rhinosinusitis is
passageways of the paranasal sinuses, thus preserving the defined when the duration of symptoms is more than 4
normal pathway of mucociliary clearance [36]. This sur- weeks, but less than 12 weeks [47]. Diagnostic clues at
gical intervention is referred to as functional endoscopic imaging are air-fluid levels or air bubbles within the opac-
sinus surgery or FESS. From the sinus ostia, the frontal, ification at CT (Fig. 3), while MR will estimate the mucosal
anterior ethmoid and maxillary sinuses drain into the thickening and differentiate it from fluid or pus-filled
middle meatus, while the posterior ethmoid and sphenoid material in the sinus lumen [19]. The dominant water
sinuses drain into the superior meatus [26]. component in acute rhinosinusitis (95% water and 5%
proteins) reveals low signal intensity on T1W images and
high signal intensity on T2W images.
Inflammatory mediators

The role of cytokines and nitric oxide (NO) in sinonasal

inflammatory disease has been in focus for the last decade.
In acute sinusitis, the pro-inflammatory cytokines inter-
leukin-1beta, interleukin-6 and the neutrophil-chemoat-
tractant interleukin-8 may play a major role [37]. In chronic
sinusitis, interleukin-3 dominates the cytokine profiles,
giving support to a variety of inflammatory cells, while in
the pathogenesis of nasal polyposis, interleukin-5 is shown
to be the most important cytokine [37].
The most recent research on sinus function has focused
on the molecule NO [38]. In humans, NO is produced by
epithelial cells in the paranasal sinuses and is present in
sinus air in very high concentrations, close to the highest
permissible atmospheric pollution levels [39]. NO has been
shown to be toxic to bacteria, fungi and viruses at levels as
low as 100 parts per billion (ppb) [40]. Nasal concentra-
tions of this substance can reach 30,000 ppb, which some
researchers have proposed as a mechanism of sinus ster-
ilisation [39]. Another effect of sinonasally derived NO is
increased arterial oxygen tension and reduced pulmonary
vascular resistance [41]. NO has also been shown to up- Fig. 3 Coronal CT. Air-fluid levels or air bubbles within the
regulate ciliary motility [42, 43]. The concentration of NO opacification at CT is a diagnostic clue to an ongoing infection
 875

Recurrent rhinosinusitis cosity of the sinus content, a phenomenon that may explain
the loss of signal at both T1W and T2W imaging mim-
Acute rhinosinusitis is termed recurrent when there is icking an aerated sinus [57].
complete resolution between the acute episodes and the Fungal infection may superimpose on CRS. Fungal
patient has three or more episodes in 6 months or more than hyphae contain calcium and paramagnetic elements such as
four episodes in 1 year [47]. manganese and iron, which highly influence the MR signals
[58, 59]. An intermediate signal at T1W images and low
signal or signal void at T2W images are characteristic for
Chronic rhinosinusitis fungal infections. Another explanation for these signal in-
tensities can be a paramagnetic effect in longstanding
Chronic rhinosinusitis (CRS) is defined as inflammatory bacterial sinusitis. Bacteria produce their own proteins, so-
sinonasal disease lasting longer than 12 weeks [47]. It has called siderophores. These are iron-binding proteins whose
been postulated that the presence of bacterial biofilms on main task is to steal iron from the surroundings, e.g., from
the sinus mucosa may explain the refractory nature of some lactoferrin found on the mucosal surface. Siderophores bind
forms of CRS [24, 55]. In a biofilm, bacteria exist in com- iron in its ferric state, hence making a paramagnetic
plex, surface-attached organisations and communicate with siderophore-Fe3+ complex that may contribute to the high-
each other. Biofilms provide bacteria with distinct advan- to-intermediate signal intensity at T1W images and low or
tages, including antimicrobial resistance and protection loss of signal intensity at T2W images typically seen in
from host defences [56]. patients with cystic fibrosis (CF) [19].
The diagnostic clue at CT and MR imaging is the same
as for acute rhinosinusitis. Moreover, in longlasting si-
nusitis, the sinus secretions may become inspissated. At CT Complications of rhinosinusitis
imaging, this phenomenon is seen as opacification with
higher attenuation than in acute disease. New bone for- Serious complications of rhinosinusitis are becoming more
mation along the contours of the sinus cavity, i.e., osteitis, rare due to the use of antibiotics [60]. Osteomyelitis may
is a common CT finding associated with CRS (Fig. 4). occur in the bone marrow of diploetic bone. When localised
MR signal intensities are highly dependent on the pro- to the frontal bone secondary to frontal sinusitis, osteomy-
tein content. T1W signal intensities get brighter with elitis may present with a subperiosteal abscess, known as
protein content increasing to approximately 25%; thereaf- Pott’s puffy tumour [61].
ter, with increasing protein content a signal decrease is Orbital complications following sinusitis are more com-
observed. T2W signal intensities remain high and then de- mon than intracranial complications and are seen in approx-
cline progressively with increasing protein content [57]. At imately 3% of patients with sinusitis [20]. The ethmoid
protein concentrations above 25%, a cross-linking between sinuses are most often the source of infection (Fig. 5). The
the protein macromolecules occur, causing increased vis-

Fig. 5 Axial CT showing soft tissue masses in the right ethmoid

sinus with bony destruction of the lamina papyracea (arrow). The
ethmoid sinuses are most often implicated as the source of infection
Fig. 4 Coronal CT demonstrating new bone formation equal to for orbital complications due to the thin lamina papyracea and the
osteitis along the contours of the right maxillary sinus cavity in a valveless ethmoid veins that allow rapid access of infection into the
patient with long-lasting sinusitis orbit
876

thin lamina papyracea and the valveless ethmoid veins

cause a predisposition to the spread of infection into the
orbit [62]. Sphenoid, maxillary and frontal sinusitis, in
descending order, are less commonly the cause of orbital
infection. Retrobulbar neuritis may be due to ethmoid and
sphenoid sinusitis in 15–20% of the cases [63].
Intracranial complications of rhinosinusitis such as
meningitis, epidural abscess, subdural abscess, cerebritis
and cerebral abscess are rare. Only 3% of cerebral abscesses
are due to sinusitis [64]. Frontal sinusitis is the most
common origin of cerebral abscess [65, 66]. An intracere-
bral abscess may result from the direct spread of infection
from the sinuses or distant spread due to septic embolisation
[60]. Cavernous sinus thrombosis is a rare intracranial
complication of sinusitis, with ethmoid or sphenoid sinus-
itis as the predisposing factor [67].
MR imaging is superior to CT in depicting orbital and
intracranial complications [68].

Imaging modalities and methods

CT

CT is regarded as the “gold standard” in the primary

imaging of inflammatory sinonasal lesions [69]. The use of
coronal CT scans prior to FESS in order to map the
sinonasal bony anatomy and pneumatisation variants and
to evaluate the extent of disease is well documented [70–
72]. A minus with CT is the radiation dose. Many reports
exist on the reduction of the radiation dose, especially
focusing on sparing the lens of the eye and thyroid gland Fig. 6 Coronal CT, non-enhanced. Advanced soft tissue masses
[73–78]. Low-dose CT with limited scans outside the lens are demonstrated in both maxillary sinuses. a An intermediate
area is to be preferred for screening and has been shown to window width (WW), 2,000 HU, and level (WL), 200 HU, are
cause less radiation to the lens than plain X-rays [79]. commonly used for depiction of both bony anatomy and soft tissue
Using a high-resolution bony algorithm, the radiation dose masses. b By changing the window settings, the attenuation
differences between mucosal thickening and centrally fluid-filled
may be as low as 16 mAs per scan for diagnosing sinusitis sinuses are more clearly depicted
[80]. When CT is performed as a preoperative evaluation in
order to map the bony anatomy and localisation of opac-
ifications, continuous scans throughout the sinuses are ethmoid complex as well as the sphenoid sinuses [83, 84].
necessary. This may also be the case in posterior ethmoid and sphenoid
An intermediate window width (WW), 2,000 HU, and inflammatory processes.
level (WL), 200 HU, are commonly used for depiction of While CT is superior to demonstrate the bony anatomy,
both the bony anatomy and soft tissue masses (Fig. 6a). A the extent and anatomic localisation of inflammatory
better distinction of watery sinonasal secretions (Fig. 6b) lesions and complications such as sclerotic thickening of
from more viscous or desiccated secretions or neoplasm the bone and cortical destruction, CT has major limitations
may require a more narrow window setting [81]. The prone in the differentiation of soft tissue masses, such as mucosal
position is preferred to drain fluid away from the thickening from pus-filled areas and inflammatory from
ostiomeatal complex (OMC) in order not to obliterate the neoplastic processes [19, 20, 85–87]. Patient preparation
OMC falsely and for better delineation of the bony anatomy with nose blowing and topical nasal decongestion offers
[82]. However, when dental amalgam fillings are excessive, only a small reduction in mucosal thickening and therefore
a supine position with coronal reconstruction is preferred to has a limited effect on the diagnostic accuracy of CT
reduce artefacts. In the patients operated on, axial images imaging in CRS patients [88].
may offer a better visualisation of the anterior and posterior
 877

MR observer agreement compared to other scoring systems

[98]. Zinreich reviewed four CT staging systems (Kennedy
MR has the advantage of no radiation and superior tissue 1992, Levine and May 1993, Lund-Mackay 1993 and
characterization compared to CT [83, 87, 89]. MR may be Harvard 1994) and concluded that all classification systems
useful when CT has shown advanced opacification that can had major limitations due to the lack of sufficient gradation
be due to a pyocele [19], fungal sinusitis [90] or neoplastic to track the volume of the disease [101]. He therefore
disease [87] and to display lesions involving the orbit or proposed that in future classification systems, these factors
cranial compartment [91]. Coronal imaging with T1W and should be taken into account to increase the clinical value
T2W sequences may be sufficient in “simple sinusitis”. In of the staging. In the Lund-Mackay scoring system, each
order to differentiate mucosal thickening and regions of sinus group (frontal, anterior and posterior ethmoid,
pus-filled sinuses, fast short inversion time recovery (STIR) maxillary and sphenoid) is scored as 0 (no abnormalities),
images instead of T2W images have been shown to be 1 (partial opacification) or 2 (total opacification). The
valuable [19, 86]. If neoplasm or complications to inflam- OMC is scored 0 (not occluded) or 2 (occluded). Further,
matory processes are to be ruled out, additional imaging anatomic variants are noted as being present (1) or absent
planes and intravenous gadolinium are mandatory [89]. (0), but do not contribute to the sinus score.
Variation in MRI signals of the sinonasal secretions has
been shown to be related to many properties of the secre-
tions such as the viscosity, protein concentration, fat, Inflammatory patterns
temperature and paramagnetic properties of fungal infec-
tions or haemorrhage [19, 57, 59, 69, 72, 87, 92, 93]. In order to identify radiological patterns of sinonasal in-
flammatory disease and elucidate how these patterns would
influence the surgical approval of FESS, Sonkens et al.
Plain films [102] in 1991 reviewed 500 screening sinus CTs (SSCT).
The group identified five CT patterns of inflammatory
Plain films have a limited role in sinonasal imaging, but can paranasal sinus disease, in which the first three patterns can
depict the size of the sinuses, septal deviation and opac- be correlated to the obstruction of known mucociliary
ification. In acute rhinosinusitis, the demonstration of air- drainage routes. These five patterns are the following.
fluid levels can be diagnostic. However, in a paediatric
population plain films were shown to be inaccurate in 75%
of cases of inflammatory sinonasal disease [94]. Further, Infundibular pattern
plain films are inadequate in the evaluation of the OMC and
pneumatisation variants, and therefore insufficient in the This pattern involves disease limited to the drainage route
preoperative evaluation for planning FESS. Further, neo- of the maxillary sinus, with obstruction of the maxillary
plasm may be interpreted as inflammatory disease. The ostium and/or the ethmoid infundibulum (Fig. 7). Variants
radiation dose to the lens is almost equal to low dose CT. that may cause this inflammatory pattern are infraorbital
Hence, plain X-ray should be performed only in cases (Haller) cells, pneumatisation of the uncinate process and
where CT is unavailable [91]. an enlarged ethmoid bulla, which is the largest and most
constant ethmoid cell, lying cranially and posteriorly to the
hiatus semilunaris (the opening of the ethmoid infundib-
Ultrasonography ulum into the middle meatus).

Ultrasonography (US) has been recommended for the

diagnosis of acute rhinosinusitis [95], but the literature is Ostiomeatal complex (OMC) pattern
not sufficiently conclusive to definitively recommend US
in patients with symptoms of sinusitis [96]. US has been Inflammatory disease within the ipsilateral maxillary,
reported to be valuable in space-occupying lesions of the anterior ethmoid and frontal sinuses is termed OMC
anterior nasal fossa [97]. pattern (Fig. 8). Involvement of the frontal sinus in the
OMC pattern may be variable and depends on the insertion
of the anterior uncinate process. If superior insertion is to
Staging for rhinosinusitis the ethmoid roof or medially into the middle turbinate, the
frontal recess opens into the ethmoid infundibulum. In
Several CT staging systems for planning medical and these cases, inflammation may easily spread from the an-
surgical treatment as well as to monitor the therapeutic terior ethmoid sinuses in the caudal and cranial direction to
outcome in CRS have been proposed and evaluated [98, the maxillary and frontal sinuses. When insertion is lateral,
99]. The modified Lund-Mackay system [100] from 1993 attached to the lamina papyracea, the infundibulum is
has proved to have the highest level of both inter- and intra- closed superiorly by a blind pouch called the terminal
878

Sphenoethmoid recess (SER) pattern

The sphenoethmoid recess (SER) is the common drainage

route of the posterior ethmoid and sphenoid sinuses. A
small obstruction of the SER may involve only the
sphenoid sinus, while a larger obstruction may involve
the ipsilateral posterior ethmoid sinus as well (Fig. 9).

Sinonasal polyposis pattern

This pattern is caused by multiple polyps that commonly

originate in the ethmoid sinuses, from where they pro-
trude into the nasal cavity, the sinuses and choanae.
Fig. 7 Coronal CT. Sinonasal inflammatory disease of infundibular Irregular polypoid mucosal thickening in the maxillary,
pattern on the left side. In this pattern soft tissue masses are limited frontal and sphenoid sinuses are contemporaneous findings
to the maxillary sinus due to obstruction of the maxillary ostium or at imaging in advanced polyposis. Polyps in the nasal
the ethmoid infundibulum. On the right side, a hypoplastic cavity are demonstrated as smooth, soft tissue masses with
maxillary sinus is seen together with retraction of the posterior
fontanel that may mimic postoperative changes after medial downward convexity [103]. Other typical CT findings are
antrostomy. The uncinate process is not visualised, but located bulging of the ethmoid sinus walls that are seen together
below the infraorbital wall. The total opacification of the right with demineralisation of the bone, hence the bony anatomy
maxillary sinus mimics an infundibular inflammatory pattern is obscured in soft tissue masses. Another characteristic CT
finding is bilateral widening of the ethmoid infundibulum
due to polypoid tissue (Fig. 10).

recess. In this case, the frontal recess opens into the middle
meatus. This explains why infundibular inflammation does Sporadic (unclassifiable) pattern
not always result in frontal sinusitis in some patients.
Inflammatory disease limited to the frontal sinus is termed This pattern includes randomly located sinonasal mucosal
frontal recess inflammatory pattern and may be seen in changes that cannot be classified into the four previously
cases where the frontal recess drains directly into the described patterns, e.g., retention cysts, polyps (Fig. 11),
middle meatus. A frontal recess pattern is considered a mucocele and pyocele as well as mucosal changes found in
limited variant of the OMC inflammatory pattern [102]. the patients operated on.

Fig. 8 Coronal CT. Sinonasal inflammatory disease of ostiomeatal Fig. 9 Coronal CT. Sinonasal inflammatory disease of spheno-
complex (OMC) pattern. Soft tissue masses are seen in the ipsilateral ethmoid recess (SER) pattern. Bilateral sphenoid sinusitis due to
ethmoid and maxillary sinuses. The involvement of the ipsilateral mucosal thickening in the SER (arrows). Larger obstructions in the
frontal sinus in this pattern may be variable SER in this pattern will also involve the posterior ethmoid sinuses
 879

surgical groups reflecting the anatomical localisation, ex-

tent and technical considerations of surgical intervention,
as well as the risk of surgical complications of the surgery
required [102, 104].
Infundibular pattern, OMC pattern and sporadic pattern
are classified as “routine” surgical group, while sinonasal
polyposis and SER pattern are classified as “complex” sur-
gical group. In the infundibular pattern, infundibulotomy
alone or together with limited ethmoidectomy will usually
be sufficient, while the OMC pattern often requires more
extensive ethmoidectomy. The sporadic pattern, though
classified as belonging to the routine surgical group, often
requires tailored FESS if surgery is necessary. Sinonasal
polyposis is grouped as complex because surgery may be
extensive and located close to the lamina cribrosa and the
Fig. 10 Coronal CT. Sinonasal inflammatory disease of polyposis
pattern. Polypoid soft tissue masses are filling the nasal cavities, anterior ethmoid artery, increasing the risk of CSF leakage
maxillary and ethmoid sinuses. Note bulging of the sinus walls with and profuse bleeding. Furthermore, polyps that obscure
loss of bony sinus architecture and broadening of the ethmoid surgical bony landmarks complicate surgery. The SER
infundibulum bilaterally pattern is grouped as complex due to its posterior location,
making it more difficult to reach safely with the endoscope
In patients undergoing SSCT for suspected inflamma- [102].
tory sinonasal disease, infundibular and OMC patterns are
reported to be most common, each seen in approximately
25%. The SER and sinonasal polyposis patterns are less Retention cysts and polyps
common, and each is found in less than 10%. The sporadic
pattern is reported in 24%. Normal SSCT is common in Retention cysts and solitary polyps are usually asymptom-
patients suspected of having sinusitis and has been reported atic, incidental findings in the paranasal sinuses and are
in 27% [102]. In the normal population, only a few patients regarded as complications of inflammatory sinusitis [105,
have more than one inflammatory pattern, while this phe- 106]. Mucous retention cysts are more common than serous
nomenon is common in patients with an underlying sys- retention cysts and are caused by the obstruction of a
temic disease as in CF patients [33]. seromucinous gland, while serous retention cysts are due to
Each inflammatory pattern as described by Sonkens et al. the accumulation of fluid in the submucosal layer [107].
[102] can further be categorised into “routine” and “complex” Retention cysts are common in the maxillary sinuses and
are found on imaging studies in up to 9 to 35% [108, 109].
Unless they cause obstruction of the mucociliary path-
ways, they are of little clinical consequence. Further, max-
illary retention cysts commonly recur after surgery [110].
Gardner [111] suggested that the term pseudocyst should
be used instead of serous retention cyst since there is no
epithelium-lined cavity present beneath the sinus mucosa.
Sporadic polyps are a common asymptomatic finding. A
post-mortem study revealed polyps in one third of the
autopsies [112]. Most of the polyps originated from the
OMC where the initial stage of sinonasal polyposis seems
to take place. Polyps are, as retention cysts, due to the
accumulation of fluid in the mucosa. In addition to stroma,
eosinophils are the dominating cells [60, 109]. The
aetiology of nasal polyps still remains unclear, but is
believed to be a complication of chronic infection, either
allergic or infectious [60]. In association with allergy,
polyps are usually multiple.
Fig. 11 Coronal CT. Sinonasal inflammatory disease of sporadic At CT and MR imaging, retention cysts and solitary
pattern in a patient with previous right-sided FESS (medial polyps are seen as smooth, outwardly convex soft tissue
antrostomy). Soft tissue masses in the right maxillary sinus are
depicted as mucosal thickening. There is also sparse mucosal masses (Fig. 12). A further differentiation is not possible at
thickening in the left maxillary sinus and opacification in the right CT and MR imaging, and their presence has no clinical
anterior ethmoid sinus impact. The MR signal intensities of cysts and polyps
880

maxillary sinus [115, 116]. Histological, antrochoanal

polyps differ from inflammatory polyps in that they are
fibrotic, with minimal inflammation [115, 117]. Ethmo-
choanal and sphenochoanal polyps are rare [118, 119].

Mucocele and pyocele

A mucocele can develop in any sinus following obstruction

of the sinus ostium and is seen as a complication of CRS,
polyposis, FESS or trauma. A mucocele contains mucous
and desquamated epithelium. A slow expansion over time
may cause extension into neighbouring organs such as the
orbital and cranial compartments. The frontal sinuses are
most commonly the site of mucoceles (65%) (Fig. 14),
followed by the ethmoid sinuses (25%) and maxillary
Fig. 12 Coronal CT. A typical smooth, outwardly convex soft sinuses (10%), but they are rarely seen in the sphenoid
tissue mass in the left maxillary antrum typical for a retention cyst or
solitary polyp sinuses. If superimposed infection occurs in a mucocele, the
mucocele is turned into a pyocele.
CT findings of an expanded airless sinus cavity filled
depend on the content of protein and water. Therefore, with fairly homogeneous opacification equal to the mucoid
signal intensities in polyposis can be very variable [109]. secretion (CT attenuation10-18 HU) is diagnostic of a
MR imaging is not mandatory, but may sometimes be mucocele [109]. At MR imaging, a mucocele is seen as a
necessary in order to differentiate these lesions from ma- mass with high signal intensities equal to high watery
lignancy or aggressive benign disease. content as mucosal lining. A pyocele has an increased
A large cyst or polyp, especially in the maxillary sinus, protein content, including iron-loaded siderophores, hence
can be falsely interpreted as an air-fluid level and diagnosed signal intensities may be paramagnetic, i.e., have high or
as sinusitis. Air surrounding a soft tissue mass with a intermediate signal intensity at T1W images and low or
convex border suggests a cyst or polyp (Fig. 13). If polyps signal void at T2W or STIR images [19].
enlarge to fill the entire sinus, they may obstruct sinus
drainage and become symptomatic [109]. A true air-fluid
level is seen as a fluid level with a concave upward me- Atrophic rhinitis
niscus at the margins throughout the entire sinus or limited
by the mucosal thickening [109] (Fig. 13). Sinochoanal Atrophic rhinitis is characterised by atrophy of the nasal
polyps are polyps arising in a sinus and growing out of the mucosa and enlargement of the nasal space with paradox-
sinus ostia into the choanae [113, 114]. Most commonly ical nasal congestion accompanied by reabsorption of the
referred to is the antrochoanal polyp, which originates in the

Fig. 13 Coronal CT. Soft tissue masses in both maxillary sinuses.

On the right side, the mass has smooth convexity upward and Fig. 14 Coronal CT. Frontal sinus mucocele on the left side seen as
therefore is interpreted as a large cyst or polyp. On the left side, the an expanded airless sinus cavity with homogeneous attenuation with
air-fluid level is seen with a concave upward meniscus bony erosion of the orbital roof
 881

underlying bone [60]. Secondary atrophic rhinitis accounts

for the majority of cases and may follow trauma, intranasal
surgery granulomatous diseases, infection and radiation
exposure [120]. Primary atrophic rhinitis is an uncommon
condition that presents with crusts in the nose. The nasal
mucosa is dry and atrophic, and the nasal cavities are
abnormally wide. A significant decrease in the total phos-
pholipids compared to the normal population and also a
significant change in the phospholipid profile have been
shown in these patients [121]. Further, a dominant inher-
itance may be present [122].

Silent sinus syndrome

Silent sinus syndrome (SSS) was introduced as a term in

1994 by Soparkar et al. [123]. SSS occurs when a negative
pressure develops in the maxillary sinuses due to obstructed
drainage. With time, the sinus walls collapse, and enoph-
thalmos may occur. This condition can be distinguished
from maxillary sinus hypoplasia due to pneumatisation of
the molar eminence and the maxillary alveolar ridge.
Characteristic CT findings of opacification and collapse of
the antral walls with inward bowing of the orbital floor are
mandatory to make the diagnosis [124]. SSS usually occurs
during the third and fifth decades, and the patients present
with symptoms relating to enophthalmos. Soparkar et al.
reported that only 36% of the patients with SSS had a
known history of previous sinus disease [123].

Fungal sinusitis

Fungal sinusitis (FS) of the paranasal sinuses can be

categorised into the non-invasive and invasive varieties. In
non-invasive fungal sinusitis, the fungal elements are
limited to the lumen of the involved sinus, whereas in
invasive disease, fungal elements cross the mucosa to
involve the blood vessels and the bony, orbital and intra-
cranial structures to a variable degree [125, 126]. In im-
munocompromised or diabetic patients, a biopsy of the
mucosa and bone should always be considered to exclude
an invasive form [125]. Both non-invasive and invasive
forms of FS may be difficult to diagnose, but should be
considered in any patient with CRS, especially in the pres-
ence of focal or diffuse areas of hyperdensity and/or
punctuate calcifications at CT [127] (Fig. 15a). At MR,
typical low signal intensity at T2W images and intermediate
Fig. 15 Coronal CT shows advanced right-sided maxillary opaci-
signal intensity at T1W images may be seen (Fig. 15b and c). fication with destruction of the lateral nasal wall and soft tissue
The non-invasive form of FS can be classified as masses bulging into the nasal cavity (a). Note sparse, focal,
mycetoma (fungus ball) and allergic FS (AFS). The latter punctuate calcifications at the level of a broadened ethmoid
results from an IgE-mediated hypersensitivity reaction in infundibulum that may be a diagnostic clue to fungal sinusitis.
atopic individuals. Five diagnostic criteria for AFS have Coronal MR imaging with STIR (b) and T1W (c) sequences of the
same patient as in (a) demonstrates advanced mucosal thickening
been proposed [128], where radiological imaging with (arrows) and centrally a fungus ball (arrowheads). A sample from
opacification of one or more sinuses is included. AFS surgery revealed Aspergillus species
882

demonstrates highly specific radiographic appearances, and the cANCA test is negative [140, 141]. Idiopathic or
i.e., high attenuation in the central part of the sinus at CT, lethal midline granuloma used to be classified as a
which corresponds to a signal void using MR T2W granulomatous disease, but is now classified as lymphoma
imaging. These areas correspond to surgically proven thick [142, 143].
inspissated allergic mucin [129, 130].
Until 1997, there was no consensus for the classification
and diagnosis of invasive FS, and therefore deShazo [131] Sarcoidosis
proposed a new classification system based on a review of
the literature and their own study including 30 patients. Sarcoidosis is a systemic disease characterised by non-
Three invasive forms were proposed: (1) granulomatous, caseating epithelial granulomas. [144]. Nasal obstruction
(2) acute fulminant and (3) chronic invasive. The diagnostic and CRS are common in sarcoidosis and may be the initial
criteria for invasive FS were: (1) sinusitis confirmed by symptoms [144, 145]. Nodules equal to non-caseating
radiological imaging and (2) histopathological evidence of granulomas may frequently be depicted on the septum and
hyphal forms within the sinus mucosa, submucosa, blood turbinates. In contrast to WG, bony destruction is rarely
vessels or bone. CT findings in invasive fungal rhinosinus- seen, but when present sarcoidosis may mimic WG. Four
itis may be non-specific and the extent often under- diagnostic criteria for sinonasal sarcoidosis have been
estimated. If this entity is suspected using CT, then an suggested in which the radiological evidence of sinusitis is
early endoscopic examination with biopsy is mandatory. one of the criteria [146].
Most cases have superimposed bacterial infection, except
for the granulomatous invasive variant of FS [132].
There are conflicting reports in the literature about how Cocaine nose
often the sinuses are colonised by fungi [133, 134]. Fungi
and eosinophilic mucin appear to be common components Nasal snorting of cocaine crystals may cause destruction of
of nasal mucous in patients with CRS, and hence, the sig- the nasal mucosa and septa. Cocaine abuse should be sus-
nificance of fungus in CRS remains controversial [135, pected in patients with a palatal or nasal septal perforation
136]. of unknown etiology [147] (Fig. 16).

Nasal and paranasal sinus manifestations Cystic fibrosis

of systemic diseases
Cystic fibrosis (CF) is a life-shortening autosomal-reces-
Many systemic diseases involve the nasal cavity and sive disease with an incidence in Caucasians of 1/2,000–
paranasal sinuses [137]. It is therefore important to be 6,000 [148]. The genetic defect is due to mutations in a
aware of the fact that sinonasal disease may be part of a gene coding for a chloride channel named the cystic fi-
systemic disease. brosis transmembrane conductance regulator (CFTR) on
chromosome 7 [149]. A defect CFTR protein causes elec-

Wegener’s granulomatosis

Wegener’s granulomatosis (WG) is a necrotising granulo-

matous vasculitis involving the nasal cavity, sinuses, lungs
and kidneys. The aetiology is unknown. The only man-
ifestation may be sinonasal [138]. The nasal cavity is most
commonly involved, followed by the maxillary, ethmoid,
sphenoid and frontal sinuses [139]. In the initial inflam-
matory process of WG, it is not possible to differentiate
between mucosal inflammation and granulomatous tissue
using MRI. In the later stage of granulomatous transfor-
mation, granulomas can be depicted as low-signal-intensity
lesions at T1W and T2W images in the nasal cavity,
paranasal sinuses and orbits [139]. In a patient without a
clinical history of previous sinonasal surgery, a combina-
tion of bone destruction and new bone formation on CT,
especially when accompanied by a fat signal from the Fig. 16 Coronal CT. Septal defect in a patient due to snorting of
sclerotic sinus walls using MR, can be used as a diagnostic cocaine. Other differential diagnoses causing septal destruction,
tool for WG when the clinical diagnosis may be uncertain such as Wegener’s granulomatosis, must be ruled out
 883

trolyte transport disturbances resulting in thick mucous

formation that is 30-60 times thicker than normal [150].
The paranasal sinuses, lungs, pancreas and intestine are
most seriously involved [151]. The cilia function in CF
patients is reported to be intact [152, 153]. However, the
high mucus viscosity impairs normal cilia motility, re-
sulting in poor mucociliary clearance, obstruction of the
sinus ostia and CRS.
CF patients have hypoplasia of their sinuses and lack
pneumatisation variants [8, 16, 154, 155]. Hence, in CF
patients pneumatisation and anatomical variants rarely
interfere with the drainage routes [86, 156]. Thus, impaired
mucociliary clearance due to increased mucous viscosity
probably is the keystone in the pathogenesis of CRS in CF.
A characteristic CT finding in young CF patients is medial
bulging of the lateral nasal walls (LNW) (Fig. 17a).
Subsequently, the medial maxillary sinus wall bulges into
the nasal cavity and may reach the nasal septum and
obstruct the nasal cavities. Medial bulging of the LNW is
associated with decreased mineralisation of the LNW.
Different opinions exist about whether these changes
reflect bony destruction and osteitis [157], decalcification
[156, 158] or osteolysis [159] of the LNW. Another
explanation may be that the LNW never mineralises in
early childhood due to the development of a maxillary sinus
pyocele, which causes medial bulging of the LNW. Using
MR, the high signal at T1W images and the signal void at
STIR images are the diagnostic clues to suggest a pyocele
(Fig. 17b and c).
Two studies have suggested that a mutation in the CFTR
gene may play a role in the pathogenesis of sinonasal dis-
ease in the normal population [160, 161], while two other
studies have found no correlation [162, 163].

Immotile cilia syndrome

Immotile cilia syndrome is an autosomal recessive disease

with an incidence of 1/16,000 [137], of which 50% have
Kartagener’s syndrome, consisting of the triad: bronchiec-
tasis, CRS and situs inversus [164–166]. The frontal si-
nuses are usually hypoplastic [137].
Fig. 17 Coronal CT demonstrates characteristic CT findings in a
young CF patient with bilaterally medial bulging of the lateral nasal
Asthma and allergy wall (arrows) due to pyoceles (a). Coronal MR imaging using STIR
(b) and TW1 (c) sequences differentiate between mucosal thicken-
Asthma or allergy is a significant factor in the development ing (arrows) and pus-filled material centrally (arrowheads), where
CT only depicts homogeneous soft tissue masses. The patient was
of rhinosinusitis, and patients with asthma and allergy are operated on and S. aureus was cultured from both maxillary sinuses.
more likely to demonstrate disease on CT images compared Due to signal void in the pus-filled sinuses at STIR imaging,
to non-allergic patients [167–169]. complementary T1W imaging is mandatory

Gastrointestinal disease autoimmune, inflammatory bowel disease) are often as-

sociated with chronic mucosal inflammation, nasal obstruc-
Crohn’s disease (a granulomatous inflammatory bowel tion and occasionally septal perforation [137].
disease with unknown aetiology) and ulcerative colitis (an
884

Radiological report sinus, mimicking an infundibular inflammatory pattern,

while an infection of odontogenic origin may cause max-
In the radiological report describing inflammatory lesions illary sinusitis with extension also to the ethmoid and
in the nasal cavity and paranasal sinuses, it is important to frontal sinuses, mimicking an OMC inflammatory pattern.
be aware of sinonasal diseases mimicking inflammatory In advanced unilateral disease, a neoplastic process should
patterns of rhinosinusitis. Awareness of other nasal and always be ruled out, while with the finding of an isolated
paranasal diseases is especially important in long-lasting nasal septum pathology or bilateral advanced opacifica-
cases and a lack of response to medical treatment, e.g., an tions, a systemic disease should always be considered in the
antrochoanal polyp, may occlude the whole maxillary differential diagnosis.

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