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 Table of Contents  
Year : 2022  |  Volume : 10  |  Issue : 1  |  Page : 14-25

Approach to sinonasal masses: A comprehensive review

Department of Radiodiagnosis, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India

Date of Submission13-Feb-2022
Date of Decision18-Mar-2022
Date of Acceptance22-Mar-2022
Date of Web Publication23-Jun-2022

Correspondence Address:
Mahesh Kumar Mittal
Department of Radiodiagnosis, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi - 110 029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jhnps.jhnps_10_22

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The complex anatomy and exposure to various potential carcinogens lead to the development of tumors and tumor-like pathologies of the nose and paranasal sinuses. Delays in the diagnosis of sinonasal masses are common, leading to significant morbidity and mortality. Often the radiologist is the first person to recognize a neoplasm in a suspected inflammatory condition. Computed tomography and magnetic resonance imaging play a synergistic role in the assessment of pathologies in the sinonasal region, and their importance has become increasingly prevalent in the current scenario of coronavirus disease 2019 associated mucormycosis. Besides, imaging is essential for mapping the exact extent of the pathology and delineating vascular supply of hypervascular masses, thus facilitating the operating surgeon and interventional radiologist in management. The cases presented in this article have been accrued over the past three decades and analyzed as a retrospective observational study, with clinical, radiological, and pathological data having been extracted from the existing database in the institution. We present the imaging spectrum of sinonasal masses in the pediatric and adult population, highlight the key radiological features of the common pathologies and discuss an imaging template for reporting these masses, with special focus on the surgically relevant points to be included in the report. The educational goal of this review is to explore a meticulous and systematic imaging approach toward soft tissue lesions in the sinonasal region, which would enable the radiologist to reach a diagnosis or point toward the possible etiology and nature of the lesions.

Keywords: Computed tomography, magnetic resonance imaging, nasal cavity, nasal masses, paranasal sinuses

How to cite this article:
Reghunath A, Mittal MK, Thukral BB, Sinha M. Approach to sinonasal masses: A comprehensive review. J Head Neck Physicians Surg 2022;10:14-25

How to cite this URL:
Reghunath A, Mittal MK, Thukral BB, Sinha M. Approach to sinonasal masses: A comprehensive review. J Head Neck Physicians Surg [serial online] 2022 [cited 2022 Jun 28];10:14-25. Available from: https://www.jhnps.org/text.asp?2022/10/1/14/347980

  Introduction Top

Nasal masses may originate from the nasal ala, mucosa of the nasal cavity, the osseous/cartilaginous portion of the nasal septum, the turbinates, or the nasal bones. Lesions may also arise from the adjacent structures such as nasopharynx and secondarily involve the nose and paranasal sinuses by direct extension. Clinical symptoms of sinonasal malignancies simulate common inflammatory and infective conditions and are often overlooked. The restricted sinonasal space, its rich lymphatic supply, proximity to vital structures like the skull base, and orbits make the extra-compartmental spread of disease early. This aggressive nature of the malignancies along with late presentation leading to the large size of the masses heralds a poor prognosis. Besides, bone destruction, a typical feature of sinonasal malignancies is a painless process, and pain at presentation should raise a suspicion of nerve or skull base involvement.

Imaging of sinonasal masses is essential for evaluating their location and extent, especially the perineural, intracranial, and intraorbital spread. Computed tomography (CT) allows assessment of osseous remodeling/destruction while magnetic resonance imaging (MRI) enhances soft tissue characterization, facilitating accurate diagnosis. Approximately 80% of the malignant nasal cavity tumors are squamous cell carcinomas and they often arise from the maxillary sinus (25%–58%). About 10% of the malignant tumors are adenocarcinoma and adenoid cystic carcinoma.[1] Rhabdomyosarcoma is common below 6 years and accounts for 3%–4% of all pediatric malignancies. It is the most common solid tumor in children.[2] Benign soft tissue masses are usually inflammatory conditions such as polyps, granulomatosis with polyangiitis, and inverted papilloma.

The imaging features of various sinonasal masses can be very similar and it is often puzzling to the general radiologist to arrive at a definite conclusion as to whether the pathological process is benign or malignant and if malignant, to ascertain the probable cell line of origin. The aim of this pictorial essay is mainly to explore a simplified radiological approach to evaluate sinonasal soft tissue lesions, highlight the essential imaging pointers toward a malignant process, discuss a template for reporting such masses and illustrate the frequently encountered ones in the pediatric as well as the adult population, along with the characteristic imaging features of few lesions.

  Imaging Modalities and Role of Imaging Top

The imaging modalities routinely used in the assessment of sinonasal masses are radiographs, CT, and MRI. Water's view, Caldwell's view, Submentovertical view, lateral skull view are the commonly used radiographic views.[2] CT evaluation includes non-contrast and contrast-enhanced phases, which are best evaluated when they are reformatted to include three planes in both soft-tissue and bone algorithms.[2] CT angiography is useful for the assessment of highly vascular sinonasal masses. MRI sequences that are best for evaluating nasal masses include thin-section, fat-suppressed T1-weighted and T2-weighted imaging (T2WI), contrast-enhanced T1WI with fat suppression, and diffusion-weighted imaging.[2]

CT and MRI are the primary modalities for the assessment of tumor size, nature, extent, and invasion into adjacent structures such as anterior and middle cranial fossa, orbit, pterygopalatine fossa, palate, and infratemporal fossa.[3] Imaging also can suggest the malignant transformation of benign pathologies on follow-up imaging, by detecting new bone destruction, extension outside the sinonasal cavity, or change in the pattern of enhancement.[4] Ostia of the sinuses is usually blocked by the sinonasal tumors, and hence superimposing sinusitis, inflammatory changes, and retention cysts may not be differentiated from the primary mass on CT. However, these can be detected easily on contrast-enhanced MRI as very high homogenous T2W signal intensity soft tissues which do not enhance.[1]

  Radiological Approach to Evaluation of Sinonasal Pathologies Top

  1. Age of the patient: Congenital pathologies such as cephaloceles, nasal neuroglial heterotopias, dacryocystocele, dermoid cyst, and hemangioma are commonly encountered in children as compared to adults
  2. Spatial localization of pathology: The epicenter of the lesion may give a clue toward diagnosis, which for sinonasal masses could be the nose or paranasal sinuses themselves or adjacent spaces such as the nasopharynx, sphenopalatine foramen, orbit, clivus, and hard palate with secondary extension into the sinonasal region. Within the nose, the lesion may be centered around the cribriform plate, nasal septum, or along the lateral wall. For soft tissue lesions of the paranasal sinuses, laterality of involvement, size of the sinuses, nature of their contents, and involvement of the bony walls are beneficial in narrowing the differentials [Table 1]
  3. Lesion characterization: This includes the CT attenuation or MR signal intensity of the soft tissue lesion, presence of fat or calcification, diffusion restriction within the lesion, and the enhancement pattern on DCE-MRI. Inflammatory soft tissue lesions have higher T2-weighted signal intensity as compared to malignancies which have intermediate and heterogeneous T2 signal intensity.[2] On T2WI, significant hyperintensity is a feature of mucinous or cartilaginous tumors; isointensity is indicative of hypercellular tumors, and hypointensity is characteristic of tumors with fibrosis, calcification, or flow void.[3] Tumors with areas of T1W hyperintensity signify the presence of subacute bleed (methemoglobin), melanin, high amounts of protein, fat, and mineral elements.[3] Fat density/signal is seen in dermoid cyst while intralesional calcification may be seen in fungal sinusitis, dentigerous tumor, inverted papilloma, adenocarcinoma, olfactory neuroblastoma, ossifying fibroma, osteoma, osteosarcoma, and chondroid tumors.[3] Lesions with strong diffusion restriction are, abscess, hypercellular tumors or lesions with hemorrhage. High-ADC lesions indicate hypocellularity, mucus, cartilage, or fluid[3]
  4. The presence of flow voids in lesion and feeding arteries: suggest a highly vascular lesion such as juvenile nasopharyngeal angiofibroma, neuroendocrine carcinoma, hemangiopericytoma, esthesioneuroblastoma, renal cell carcinoma metastasis, thyroid carcinoma, or melanoma
  5. Pattern of bone involvement: Widespread bony destruction is a feature of high-grade malignancies, whereas permeative pattern of lytic bone lesions without frank destruction is typical of small round cell tumors. Benign lesions and low-grade malignancies demonstrate bony expansion owing to their slow and expansile growth pattern[3] [Table 2].
  6. Extent of the lesion: The intracranial, intraorbital, and perineural spread of lesion and dural invasion. Intracranial extension to the anterior cranial fossa may occur from frontal and ethmoidal sinuses while middle cranial fossa can occur from the sphenoid sinus.[5] Intraorbital spread may occur by the destruction of intervening bone from ethmoidal and maxillary sinuses, along the nasolacrimal duct from the nasal lesion, through inferior orbital fissure from the pterygopalatine fossa and infratemporal fossa, and through infraorbital foramen by maxillary growth involving the premaxillary region.[5] Pterygopalatine fossa involvement is seen as a replacement of its normal fat signal intensity by the lesion and it acts as a strategic location for the spread of pathology in different pathways [Table 3]
  7. Regional lymphadenopathy: significant in malignant pathologies.
Table 1: Radiologically relevant features of sinus predominant pathologies

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Table 2: Pattern of bone involvement in sinonasal pathologies

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Table 3: Various routes of spread of sinonasal pathology from pterygopalatine fossa

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  Imaging Appearances of Commonly Encountered Entities in Sinonasal Region Top

Describing the radiological appearances of the entire gamut of sinonasal soft tissue masses is beyond the scope of this article. However, the salient imaging features of few commonly encountered sinonasal masses are illustrated below with the help of images.

  Congenital Top

  1. Cephalocele: Cephalocele refers to the herniation of intracranial contents through a skull defect, which may involve the meninges and cerebrospinal fluid (meningocele) or the meninges, cerebrospinal fluid, and brain (encephalocele and meningoencephalocele)[2] [Figure 1]
  2. Dacryocystocele/Nasolacrimal duct mucocele: may be proximal (dacryocystocele) or distal (dacrocystocele with dilated nasolacrimal duct, intranasal mucocele below inferior turbinate)[2]
  3. Nasal neuroglial heterotopias: These are nonenhancing lesions without diffusion restriction, and without communication with the brain. Occasionally, they may be connected with a fibrous stalk to the brain[2]
  4. Dermoid cyst: A nasal dermoid may manifest as a tract or fistula, with or without dermoid [Figure 2] or epidermoid cysts. Dermoid cysts are seen in the midline, at the glabella, nasal dorsum, or tip of the nose. They appear bright on T2W sequences and may show fat or calcific signal within. Epidermoid cysts show diffusion restriction, unlike dermoid cysts. CT is useful in detecting intracranial extension and may demonstrate a large foramen cecum (>3mm) and/or a bifid/deformed crista galli in these cases[2]
  5. Hemangioma: Capillary hemangioma (also called pyogenic granuloma) is seen in the nasal cavity adjacent to the nasal septum in children and pregnant ladies and shows intense enhancement with washout and peripheral non-enhancing rim. Cavernous hemangioma is commonly seen in males and located along the lateral nasal wall with a typical centripetal filling-in pattern of enhancement[6],[7] [Figure 3].
Figure 1: Herniation of meninges and cerebrospinal fluid along with part of brain parenchyma through a defect in cribriform plate on the left side into ethmoid air cells and nasal cavity on the left side in 5 years old (a and b) and 10 years old (c and d) patients respectively, consistent with nasoethmoidal encephalocele

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Figure 2: NCCT of paranasal sinuses in a case of nasal dermoid with areas of fat and calcific density within, along with extension into the frontal lobe with a bifid cribriform plate (a and b)

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Figure 3: Noncontrast computed tomography scan (a) revealing a hypodense mass filling the right maxillary sinus in an 11-year-old patient. On arterial phase (b), patchy nodular contrast puddling noted within the lesion and lesion shows almost complete contrast filling in the venous phase (c). Features consistent with hemangioma

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  Inflammatory Top

  1. Sinonasal polyposis: Nasal polyps are secondary to chronic sinusitis and are often associated with bone sclerosis and thickening [Figure 4]. Antrochoanal polyp is seen as a mass with epicenter at the maxillary sinus ostium with a hypointense signal on T1W and hyperintense signal on T2WI, with peripheral enhancement. It radiologically simulates inverted papilloma and angiomatous polyp, however, bone destruction excludes antrochoanal polyp from the differential diagnosis[8]
  2. Mucocele: Benign, respiratory epithelial lined, cyst-like masses which develop from obstruction of the ostium of paranasal sinus [Figure 5]. The chronic mucus accumulation results in expansion of the sinus, with bone remodeling and sometimes erosion[2]
  3. Pott's puffy tumor: Osteomyelitis of frontal sinus with subperiosteal abscess[8] [Figure 6]
  4. Fungal sinusitis: Nodular mucoperiosteal thickening with hyperintense areas on NCCT and low signal contents within sinuses on T1WI, with markedly low signal areas on T2-weighted images, are characteristic of fungal rhinosinusitis, owing to mycelial iron and manganese. Fungal sinusitis can demonstrate an acute or chronic, invasive or non-invasive presentation. Invasive forms are seen in immunocompromised patients and is characterized by bone destruction, rapid extension into orbits, cavernous sinus, infratemporal fossa, cranial cavity, and brain through skull base partitions and foramina [Figure 7].[9] Extensive use of immunosuppressants and systemic immune alterations may have currently led to the development/exacerbation of rhino-orbito-cerebral mucormycosis in coronavirus disease 2019 patients.[10] The disease has a fulminant course and may be associated with subtle or aggressive bony erosion of sinus walls [Figure 8]
  5. Central giant cell granuloma: they predominantly affect the mandible, but can involve the maxilla with extension into the nasal cavity. They present as well-defined, T2 hypointense soft tissue masses causing bone erosion and remodeling, with occasional cystic components[2] [Figure 9]
  6. Granulomatosis with polyangiitis or Wegner's disease: early septal erosion is a hallmark with necrotizing lesions of nose and sinuses. Pulmonary and renal involvement is associated[8] [Figure 10]
  7. Langerhan's cell histiocytosis: They commonly present in children and adolescents as an expansile lytic lesion with enhancing soft tissue and “hair-on-end” periosteal reaction[2] [Figure 11]. It is often radiologically indistinguishable from metastatic neuroblastoma, lymphoma, and rhabdomyosarcoma.[2]
Figure 4: NCCT of paranasal sinuses showing hypodense polypoidal growth completely filling bilateral maxillary, ethmoidal sinuses, and both nasal cavities, along with infundibular widening and erosion of nasal septum in a case of inflammatory polyposis (a). Antrochoanal polyp in another patient originating from the right maxillary antrum and extending via ostium and infundibulum into the right nasal cavity and further into the posterior choana (b)

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Figure 5: Expansile, hypodense lesion of fluid attenuation involving sphenoid sinus (a and b) and right-sided frontoethmoidal sinuses (c and d) causing rarefaction and focal erosions of sinus walls in 2 different patients, consistent with mucocele of the paranasal sinus

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Figure 6: Lateral radiograph in a patient revealing frontal sinus osteomyelitis and expansion with periosteal elevation due to subperiosteal abscess in a case of Pott's puffy tumor

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Figure 7: NCCT of paranasal sinuses in a diagnosed case of fungal sinusitis in an uncontrolled diabetic reveals soft tissue thickening with hyperdense contents involving all sinuses, causing bony destruction and extending into right frontal epidural space (a and b). The soft tissue thickening appears T1 iso-hypointense to grey matter(c) and T2 hyperintense with few hypointense areas within (d)

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Figure 8: T1-weighted post gadolinium axial image (a) in a COVID-19 positive patient with left maxillary and sphenoid sinus mucormycosis depicts left cavernous sinus thrombosis (white arrow), while coronal image (b) shows extensive involvement of left infratemporal fossa, parotid gland (white arrowhead), and buccal space. Post contrast coronal magnetic resonance images (c and d) in another COVID-19 patient treated with steroids reveal right maxillary and ethmoid sinusitis with right subperiosteal extraconal abscess, displacing inflamed right medial rectus (asterisk) and inferior rectus muscles medially. Note the infarcted non-enhancing mucosa in right maxillary sinus (yellow arrow). KOH culture revealed mucormycosis

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Figure 9: Water's view radiograph (a) demonstrates homogenous opacification of the right maxillary sinus. NCCT reveals a honeycomb, multilocular appearance of the lesion involving the sinus and right hemi-maxilla with root resorption and erosion of cortex (b-d). Biopsy of the lesion depicted giant cells and hemosiderin deposits, classical of central giant cell granuloma

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Figure 10: A case of known granulomatosis with polyangitis, with soft tissue in the right nasal cavity and maxillary sinus, causing septal rarefaction and focal perforation and erosion of cribriform plate on right side as seen on NCCT (a). The soft tissue appears hyperintense on T2-weighted (b) and isointense on T1-weighted (c) images to muscle and shows homogenous post-contrast enhancement (d)

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Figure 11: Magnetic resonance imaging of paranasal sinuses in an 11-year-old boy demonstrating a soft tissue lesion with an isointense signal to cortex on T1-weighted imaging (a) with heterogeneous enhancement on the postcontrast scan (b) and heterogeneously hyperintense signal on T2-weighted imaging (c) with epicenter in the left orbit and adjacent frontal sinus, extending to ethmoid air cells. Note made of mucocele of the left maxillary sinus. Contrast-enhanced computed tomography (d) revealed heterogeneously enhancing lesion causing destruction of the left frontal sinus, left lamina papyracea, and orbit. On biopsy, the lesion was diagnosed as Langerhan's cell histiocytosis

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  Neoplastic Top

  1. Inverted papilloma: convoluted, “cerebriform,” or columnar pattern is characteristic on T2/STIR and post-gadolinium T1-weighted MR images. Focal hyperostosis of origin of inverted papilloma is often detected on CT [Figure 12]. Bone destruction, extension outside the sinonasal cavity, and necrotic component with the partial loss of cerebriform pattern of enhancement suggesting malignant transformation[4]
  2. Juvenile nasopharyngeal angiofibroma: Hypervascular mass centered in the sphenopalatine foramen, causing its widening and causing erosion of pterygoid lamina and bowing of the maxillary antrum posterior wall is typical [Figure 13]. It characteristically presents in adolescent males[9]
  3. Nasopharyngeal carcinoma: They are divided into three histopathologic types: keratinizing squamous cell carcinoma (seen in older adults); nonkeratinizing differentiated carcinoma; and non-keratinizing undifferentiated carcinoma (most common in children aged 10 – 19 years). It is seen as a mass centered at the fossa of Rosenmüller, with aggressive features such as bone erosion or sclerosis of the skull base, petroclival widening, intracranial extension, and metastatic cervical lymphadenopathy[2] [Figure 14]
  4. Ossifying fibroma: They appear as an expansile lytic lesion with areas of calcification/ossification within and thin sclerotic margin separating the lesion from adjacent bone is typical [Figure 15]
  5. Fibrous dysplasia: Craniofacial fibrous dysplasia presents as expansile lesions with a characteristic ground glass matrix.[2] However, the lesions may be pagetoid or sclerotic or cystic depending on the proportions of osseous/fibrous components[11] [Figure 16]. A variant of fibrous dysplasia affecting the maxilla and mandible is known as “cherubism,” where the bones are replaced by expansile lytic lesions, giving a “soap bubble” appearance [Figure 17]
  6. Ameloblastoma: Though common in the posterior mandible, around 15% may arise from the maxilla from the sinonasal epithelial lining.[12] They present as lytic expansile bony lesions with heterogeneously enhancing soft tissue components within and causing destruction and loosening of teeth [Figure 18]
  7. Squamous cell carcinoma: These are aggressive tumors commonly involving maxillary antrum, causing bone invasion and destruction. They are characteristically T2 hypointense and enhance less than sinus mucosa with larger lesions showing intratumoral necrosis and hemorrhage[4] [Figure 19]
  8. Adenocarcinoma: Imaging features are indistinguishable from squamous cell carcinoma.[4] However, adenocarcinomas have a predisposition to involve ethmoid air cells, have more well-defined margins, and tend to enhance more than mucosal lining[13] [Figure 20]. Mucin containing adenocarcinomas show occasional calcification, along with T2 hyperintensity and gradual enhancement[3]
  9. Salivary gland tumors: Mucoepidermoid and adenoid cystic carcinomas are the common tumors of salivary gland origin with extension to the sinonasal region. Mucoepidermoid carcinoma has an intermediate to low signal on T2W sequences and commonly involves the nasal cavity and maxillary antrum [Figure 21]. Adenoid cystic carcinoma appears hyperintense on T2WIs and has the greatest propensity for perineural invasion, most commonly involving the maxillary division of the trigeminal nerve.[9] Pleomorphic adenoma arises from the nasal septum and has a typical spherical morphology, without the destruction of surrounding tissue[4]
  10. Lymphoma: Lymphoma radiologically simulates other malignant lesions of the sinonasal and nasopharyngeal region, however, it shows significant diffusion restriction with lower ADC as compared to squamous cell carcinoma (ADC value 0.61 × 10−3 mm2/s)[11] [Figure 22]
  11. Neuroendocrine tumor: Four histologic phenotypes of neuroendocrine tumors have been described: Esthesioneuroblastoma, sinonasal neuroendocrine carcinoma, sinonasal undifferentiated carcinoma, and small-cell undifferentiated carcinoma.[9] These are highly enhancing tumors that appear “hot” on positron emission tomography (PET) scan and cause bone erosion[9] [Figure 23]
  12. Esthesioneuroblastoma: It is centered around the cribriform plate and shows avid, homogenous enhancement with areas of speckled calcification [Figure 24]. Peripheral/marginal cysts are typical when the mass shows the intracranial extension[3]
  13. Rhabdomyosarcoma: These masses appear isointense to skeletal muscle on T1W and slightly hyperintense on T2WI [Figure 25]. Intratumoral calcification and hemorrhage rarely occur[3]
  14. Malignant melanoma: The nasal septum is the most common origin site of nasal melanoma. The lesion appears hyperintense on T1-weighted and hypointense on T2-weighted images respectively[6] [Figure 26]
  15. Malignant bony neoplasms (Chondrosarcoma, Osteosarcoma, Ewing's sarcoma): On CT, chondrosarcomas typically have a matrix with scattered small rings forming calcifications while areas of abnormal ossification and woven bone formation are the hallmark of osteosarcomas. MRI typically demonstrates a high-intensity T2 signal for the chondroid matrix.[6] Ewing's sarcoma is identified as a large soft tissue mass without any specific matrix and is accompanied by an aggressive periosteal reaction[6] [Figure 27].
Figure 12: Soft tissue lesion completely filling right maxillary sinus and medially extending into the right nasal cavity with focal destruction of the lateral wall and extension into the right infratemporal fossa. The lesion shows typical cerebriform appearance on T2-weighted imaging (a and b), and appears isointense to muscle on T1 sequences (c) with inhomogeneous contrast enhancement (d), consistent with the diagnosis of inverted papilloma

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Figure 13: Computed tomography angiography in a case of juvenile nasopharyngeal angiofibroma revealing an arterially enhancing with epicenter in left sphenopalatine foramen extending to the infratemporal fossa, left-sided choana, and posterior nasal cavity (a) and left superior orbital fissure (b). Magnetic resonance imaging in another case of juvenile nasopharyngeal angiofibroma showing extension into cavernous sinus (c) by invasion through sphenoid sinus (d)

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Figure 14: Axial T1-weighted gadolinium-enhanced images (a-c) in a patient with nasopharyngeal carcinoma reveals an avidly enhancing lesion obliterating the left fossa of Rosenmuller (red arrow). The lesion is also seen extending anterosuperiorly to the left pterygopalatine fossa, laterally to the infratemporal fossa involving the pterygoid muscles and posteriorly to the ipsilateral carotid sheath and left side of the clivus

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Figure 15: Well-demarcated, predominantly hyperdense lesions with inhomogeneous areas of low density and scattered calcifications/ossified trabeculae within and peripheral sharp sclerotic margins in two different patients (a and b) with epicenter in the left maxillary sinus region, suggesting ossifying fibroma

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Figure 16: Frontal skull radiograph (a) demonstrating opacification and expansion of right-sided ethmoid air cells with the replacement of superior and medial wall of right orbit by ground-glass matrix lesion. NCCT of the paranasal sinus (b and c) revealing expansile lytic lesion involving the superomedial wall of right orbit and adjacent ethmoid sinus with areas of ground-glass attenuation areas within, suggestive of fibrous dysplasia

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Figure 17: Frontal (a) and lateral (b) skull radiographs demonstrating lucent expanded regions within the maxilla and mandible, giving a soap-bubble appearance. Coronal sections of the NCCT face of the patient revealed multiple, lytic expansile lesions diffusely involving walls of both maxillary sinuses reducing their sizes (c) and also affecting the rest of the maxilla and mandible (d), consistent with the maxillofacial variant of fibrous dysplasia or cherubism

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Figure 18: Frontal (a) and lateral (b) radiographs of the skull demonstrating a large lytic, expansile lesion involving the left maxillary sinus and maxilla on the left side associated with internal bony trabeculations and soft tissue, causing destruction and loosening of teeth. NCCT confirms the findings of radiographs (c). Contrast-enhanced CT (d and e) reveals a heterogeneously enhancing soft tissue lesion with internal necrotic areas in the lesion which was diagnosed as ameloblastoma on histology

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Figure 19: Heterogeneously enhancing mass lesion involving right maxillary sinus and extending to right ethmoid air cells along with bone destruction, in a biopsy-proven case of squamous cell carcinoma of paranasal sinuses (a and b)

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Figure 20: Heterogeneously enhancing lesion involving bilateral ethmoid sinuses in a case of biopsy-proven case of adenocarcinoma of paranasal sinuses (a and b)

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Figure 21: Heterogeneously enhancing lesion in the right side of nasopharynx extending into the posterior part of the right nasal cavity (a and b) with lytic permeative destruction of the right sided pterygoid root, pterygoid plates, post part of the right inferior turbinate, and also posterior wall of the right maxillary sinus (c and d) in a histologically proven mucoepidermoid carcinoma

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Figure 22: Soft tissue lesion which is isointense to cortex on T1 (a-c) and hypointense on T2-weighted(d) imaging, with extension into sphenoid and posterior ethmoid sinuses, sellar region, and cavernous sinuses, with heterogeneous contrast enhancement (e and f) in a case of nasopharyngeal lymphoma

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Figure 23: Contrast-enhanced, axial (a), sagittal (b), and coronal (c) images of the sinonasal region in the bone window demonstrate an enhancing mass lesion involving the right nasal cavity with extension to the opposite nasal cavity by eroding nasal septum. The lesion is also eroding the cribriform plate and causing retention of secretions in the right maxillary sinus by blocking the osteomeatal complex. The mass which shows avid uptake on positron emission tomography computed tomography (d) was found to be neuroendocrine tumor on histopathology

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Figure 24: Soft tissue lesion which appears hyperdense to gray matter on T1W sequences (a and b) epicentered in both nasal cavities and extending to epidural space through the cribriform plate, consistent with esthesioneuroblastoma in a child

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Figure 25: NCCT of the face in a child with left proptosis reveals a large soft tissue mass lesion with attenuation similar to muscle, centered in the left orbit, and ethmoid sinuses (a) with superior extension into anterior cranial fossa (b). On the post-contrast scan, the lesion shows a heterogeneous enhancement pattern (c and d). Biopsy revealed rhabdomyosarcoma

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Figure 26: Water's view of the paranasal sinus (a) revealing expansion of both nasal cavities and ethmoid sinuses, with greater opacification of the left side. On contrast-enhanced computed tomography (b and c), heterogeneously enhancing mass lesion is seen to fill the nasal cavities up to choana, ethmoid sinuses, and right maxillary sinus in a histologically proven case of sinonasal melanoma

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Figure 27: Two different patients with biopsy-proven Ewing's sarcoma of left nasal bone (a and b) and posterolateral wall of the left maxillary sinus (c)

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  Miscellaneous Top

Gossipyboma: Low-density mass with spongiform appearance, containing air and calcific foci within. The lesion may demonstrate a thin enhancing capsule on contrast-enhanced images and low signal with whorled stripes in center on T2WI[14] [Figure 28].
Figure 28: NCCT of paranasal sinuses (a and b) in a patient with past history of septoplasty reveals low-density mass with a spongiform appearance containing air bubbles and calcifications within. The lesion was surgically removed and found to be gossipyboma

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  Imaging Features of Sinonasal Malignancies Top

Imaging features in sinonasal soft tissue lesions which should raise the suspicion of malignancy are as follows:[5]

  1. Single site/compartment involvement or unilateral sinus pathology
  2. Contiguous multi-compartment disease with the destruction of the intervening boundary (bone/cartilage)
  3. Heterogeneously enhancing, soft tissue masses with areas of internal necrosis
  4. Intermediate to low signal intensity on T2-weighted images: although the most sinonasal malignancies follow this dictum, the notable exceptions are low-grade adenoid cystic carcinoma, chondrosarcoma, and malignant nerve sheath tumors which appear hyperintense on T2-weighted sequences
  5. Bone erosion/destruction
  6. Aggressive periosteal reaction
  7. Extracompartmental invasion to adjacent structures [Table 4]
  8. Dural invasion [Table 5].
  9. Perineural spread: Typical sites of perineural spread include the pterygopalatine fossa, pterygomaxillary fissure, foramen rotundum, vidian canal, inferior orbital fissure, and orbital apex[6] [Table 5]
  10. Significant lymphadenopathy with heterogeneous enhancement [Table 6].
Table 4: Extracompartmental extension of disease

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Table 5: Radiological features of dural invasion and perineural spread of sinonasal malignancy

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Table 6: Lymphatic drainage of sinonasal space

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A useful checklist of the structures to be looked at and the specific features to be assessed while reporting any case of sinonasal pathologies is formulated in [Table 7].[15],[16],[17],[18]
Table 7: Checklist for reporting of sinonasal masses

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  New and Emerging Entities Top

The fourth edition of the World Health Organization (WHO) Classification of Head and Neck Tumors released in 2017 classify benign tumors as sinonasal papillomas, respiratory epithelial lesions, salivary gland tumors, benign soft tissue tumors, or other tumors.[19] WHO 2017 also describes three new, well-defined entities, and few less-defined, emerging entities.[19] The new entities are seromucinous hamartomas, nuclear protein in testis carcinomas, and biphenotypic sinonasal sarcomas. Emerging entities include human papillomavirus-related sinonasal carcinomas, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 (SMAR CB1)– deficient sinonasal carcinomas, renal cell-like adenocarcinomas, and chondromesenchymal hamartomas.[19],[20] The imaging features of these new and emerging entities are described in [Table 8].[20]
Table 8: Imaging features of new and emerging entities in head and neck tumors

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  Conclusion Top

Soft tissue lesions of the sinonasal region may be majorly attributed to congenital, inflammatory, and neoplastic etiologies. Clinical examination and nasal endoscopy can only visualize the superficial extent of sinonasal pathologies. Cross-sectional imaging of sinonasal space not only plays a role in honing down differential diagnoses but is also an essential part of preoperative work-up to map the extent of surgical margins and plan radiotherapy as well as for angioembolization of vascular tumors to prevent massive bleeding. Many of the lesions have characteristic CT and MRI findings, while some have non-specific imaging findings requiring histopathology for final diagnosis. Nevertheless, imaging guides the clinician in determining whether medical/surgical intervention is essential.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17], [Figure 18], [Figure 19], [Figure 20], [Figure 21], [Figure 22], [Figure 23], [Figure 24], [Figure 25], [Figure 26], [Figure 27], [Figure 28]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]


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