Sinonasal polyposis is a chronic inflammatory disease characterized by bilateral, multiple, benign polypoid lesions originating from the nasal cavity and paranasal sinus mucosa. It affects approximately 1-4% of the adult population and typically begins in the ethmoid sinuses, potentially spreading to all sinuses. Histopathologically, edematous stroma, goblet cell hyperplasia, and prominent eosinophilic infiltration are typical. The disease shows strong association with chronic rhinosinusitis and may form Samter's triad (ASA triad/aspirin-exacerbated respiratory disease — AERD) together with asthma and aspirin intolerance. Infundibular obliteration, ostiomeatal complex obstruction, and bilateral ethmoid opacification are classic CT findings. Treatment includes nasal corticosteroids, systemic steroids, biologic agents (dupilumab, omalizumab) and functional endoscopic sinus surgery (FESS) when needed. Recurrence rate is high, with approximately 40-70% of patients experiencing relapse after surgery.
Age Range
20-70
Peak Age
45
Gender
Equal
Prevalence
Common
Sinonasal polyposis develops as a result of chronic activation of Type 2 immune response in the nasal and sinus mucosa; cytokines such as IL-4, IL-5, and IL-13 trigger eosinophilic infiltration and stromal edema. Eosinophilic degranulation causes epithelial damage and increased mucosal permeability through release of major basic protein (MBP) and eosinophil cationic protein (ECP), perpetuating edema formation — this intense edema translates to low density on CT and T2 hyperintense signal on MRI. Upregulation of vascular endothelial growth factor (VEGF) and impaired lymphatic drainage in polypoid tissue increase stromal fluid accumulation, contributing to polyp size increase. Mucosal edema and polyp tissue at the ostiomeatal complex level mechanically obstructs sinus drainage; this obstruction leads to secretion accumulation within the sinus, secondary bacterial infection, and mucosal thickening — seen as sinus opacification and air-fluid levels on CT. In Samter's triad, the shift of arachidonic acid metabolism toward the leukotriene pathway through cyclooxygenase-1 (COX-1) inhibition increases cysteinyl leukotriene (LTC4, LTD4, LTE4) production, exacerbating bronchospasm and nasal polyposis; polyposis follows a more aggressive course in these patients with significantly higher recurrence rates.
Diffuse polypoid soft tissue opacification in bilateral ethmoid sinuses together with ostiomeatal complex obliteration on CT is characteristic and diagnostic for sinonasal polyposis. This bilateral distribution pattern is the most important clue in differentiating from unilateral pathologies (inverted papilloma, unilateral fungal sinusitis, neoplasia). A Lund-Mackay score ≥12 (out of 24 total) reflects clinically significant polyposis.
CT demonstrates diffuse soft tissue density (25-45 HU) opacification in bilateral ethmoid sinuses. Ethmoid cells are filled with polypoid tissue and intercellular septa may be thinned or obliterated due to pressure. Remodeling may be seen at the ethmoid bulla, lamina papyracea, and fovea ethmoidalis levels but bone destruction is not expected. The opacification pattern may be homogeneous or show heterogeneous density due to secretions of different protein concentrations. In advanced cases, the ethmoid sinuses are completely opacified with extension to the frontal and sphenoid sinuses.
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Diffuse soft tissue density opacification is noted in bilateral ethmoid sinuses, with pressure-related thinning of intercellular septa; no bone destruction is identified.
Complete obliteration at the ostiomeatal complex (OMC) level is observed. The infundibulum, hiatus semilunaris, area around the uncinate process, and middle meatus are obliterated by polypoid tissue. OMC obstruction impedes drainage of the maxillary and frontal sinuses, predisposing to secondary sinusitis development. OMC anatomy is best evaluated on coronal CT sections and the Lund-Mackay scoring system provides standardized assessment of disease extent. Bilateral OMC obliteration is a typical finding of sinonasal polyposis, and in unilateral OMC obliteration, different etiologies (inverted papilloma, unilateral fungal sinusitis, neoplasia) should be considered.
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Bilateral ostiomeatal complexes are obliterated by polypoid soft tissue with completely obstructed infundibula and hiatus semilunaris; secondary mucosal retention is noted in bilateral maxillary sinuses.
In chronic polyposis, bone remodeling is observed due to long-standing pressure effect. The lamina papyracea may be laterally displaced and thinned, intercellular septa of ethmoid cells may be eroded or obliterated, and convexity of the nasal septum may be increased. This remodeling has smooth margins and cortical integrity is generally preserved. Bone destruction (irregular, permeative, or moth-eaten pattern) is not seen — this feature is the most critical CT finding in differentiating benign polyposis from malignant lesions. However, in advanced cases, focal defects in the lamina papyracea may be seen and this condition should be reported in surgical planning regarding orbital complication risk.
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Smooth-margined pressure-related remodeling/thinning is noted in bilateral interethmoidal septa and lamina papyracea, with no aggressive bone destruction identified.
On MRI T2-weighted sequences, sinonasal polyps characteristically demonstrate markedly hyperintense signal, and this CSF-like high signal reflects the intense edema content of the polyps. However, chronic proteinaceous/desiccated secretions accumulated within the sinus may show hypointense signal on T2 — this is described as a 'two-signal intensity' pattern: peripheral hyperintense polyps + central hypointense secretions. This two-component signal pattern plays a critical role in the differential diagnosis of sinuses showing homogeneous opacification on CT when evaluated with MRI. Desiccated secretions may show high density (>70 HU) on CT and can be confused with fungal sinusitis or calcification; MRI T2 hypointensity helps in this differentiation.
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Markedly hyperintense polypoid lesions on T2-weighted sequences are noted in bilateral ethmoid sinuses, with T2 hypointense signal in secretions accumulated in sinus lumina (two-signal intensity pattern).
On T1-weighted sequences, polyps typically show hypointense signal, while secretions within the sinus show variable signal depending on protein concentration. Serous secretions are hypointense on T1, mucoid secretions intermediate, and high-protein/desiccated secretions may be hyperintense on T1. On contrast-enhanced T1-weighted sequences, polyps show thin peripheral rim enhancement; this enhancement originates from the vascular plexus on the mucosal surface. Absence of solid enhancement supports the benign inflammatory nature of the lesion. On contrast-enhanced sequences, mucosal thickening and polyp surface enhancement allow differentiation from non-enhancing secretions within the obstructed sinus.
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On T1-weighted sequences, polypoid lesions show hypointense signal while secretions accumulated in sinus lumina demonstrate variable T1 signal intensity; thin peripheral enhancement is noted in polyps on contrast-enhanced T1 sequences.
On diffusion-weighted imaging, sinonasal polyps typically do not show restricted diffusion and high values are observed on ADC maps. This feature is important in differentiating from malignant tumors with high cellularity (SCC, lymphoma) and the viscous fungal elements of fungal sinusitis. However, desiccated secretions within the sinus may show restricted diffusion on DWI — this is related to increased viscosity rather than true cellular restriction. Therefore, correlation of ADC values with anatomical localization is necessary: restriction within the sinus lumen may be due to secretions, while restriction associated with bone destruction suggests malignant etiology.
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No restricted diffusion is noted in polypoid lesions on DWI with high values on the ADC map; low signal on both T2 and DWI is present in desiccated secretions accumulated in sinus lumina.
On endoscopic or transnasal ultrasonography, multiple hypoechoic or anechoic polypoid structures are seen in the nasal cavity. Polyps may be smooth-bordered, homogeneous, and in a grape-cluster-like configuration. Intranasal polyps demonstrate markedly hypoechoic appearance due to edematous stroma and show extension from mucosal pedicle into the nasal cavity. On Doppler examination, no significant vascularity is seen within the polyps; this low vascularity is a consistent finding in sinonasal polyposis. Although ultrasonography is limited in evaluating intrasinus pathology, it can demonstrate the presence and size of polyps in the nasal cavity; it may be used as a radiation-free preliminary assessment tool, particularly in pediatric patients and pregnancy.
Report Sentence
On transnasal ultrasonography, multiple hypoechoic polypoid structures are noted in bilateral nasal cavities, with no intrapolyp vascularity identified on Doppler examination.
Criteria
Most common subtype (80-85%). Characterized by prominent eosinophilic infiltration, elevated IL-5/IL-13, serum eosinophilia, and elevated total IgE. Association with asthma and allergic rhinitis is common.
Distinct Features
Shows prominent bilateral ethmoid-predominant involvement, dense mucoid secretions, and frequent recurrence on CT. Responds well to biologic therapy (dupilumab — anti-IL4Rα). Charcot-Leyden crystals may be seen on histology.
Criteria
Triad of asthma + aspirin/NSAID intolerance + nasal polyposis. Accounts for approximately 10-15% of all nasal polyposis patients. Cysteinyl leukotriene overproduction is pathognomonic.
Distinct Features
More aggressive course, high recurrence after surgery (70-90%), involvement of all sinuses, massive polyposis. Aspirin desensitization and leukotriene antagonists (montelukast) are important in treatment. Lund-Mackay score on CT is generally high (>18).
Criteria
Less common subtype (15-20%). Characterized by neutrophilic infiltration, low tissue eosinophilia, and normal serum IgE. Association with bacterial infection is more frequent.
Distinct Features
Response to biologic therapy is low. Recurrence rate after surgery is lower than the eosinophilic type. High density within sinuses may be seen on CT due to purulent secretions. Long-term low-dose macrolide (clarithromycin) therapy may be beneficial.
Criteria
Seen in 25-40% of cystic fibrosis patients. Associated with increased mucus viscosity and impaired mucociliary clearance related to CFTR gene mutation. Early age of onset is characteristic.
Distinct Features
CT may show sinus hypoplasia (especially frontal and sphenoid), medial bowing of the lateral nasal wall, and high-density mucocele-like secretions. When bilateral polyposis is detected in young children (<16 years), cystic fibrosis sweat test should be performed.
Distinguishing Feature
Allergic fungal sinusitis is characterized by metallic high-density (>70 HU) heterogeneous material within the sinus on CT, and this high density is related to calcium, iron, and manganese accumulation within fungal hyphae. In sinonasal polyposis, intrasinus density typically remains between 25-45 HU. AFS may also show unilateral or asymmetric involvement and bone remodeling is more prominent.
Distinguishing Feature
Inverted papilloma is usually unilateral (different from bilateral sinonasal polyposis) and demonstrates characteristic 'cerebriform' enhancement pattern on MRI. It shows intermediate signal on T2 (different from the marked hyperintensity of polyposis). Focal bone hyperostosis/sclerosis (attachment point = tumor origin) is seen in inverted papilloma but not in polyposis.
Distinguishing Feature
Antrochoanal polyp is unilateral, originates from the maxillary sinus, and shows a three-component structure (intramaxillary cyst + pedicle + intranasal polyp). Sinonasal polyposis is bilateral, multiple, and ethmoid-predominant. Allergic/eosinophilic association is usually absent in antrochoanal polyp.
Distinguishing Feature
Sinonasal lymphoma shows marked restricted diffusion on DWI (low ADC <0.7 × 10⁻³ mm²/s) with homogeneous moderate enhancement. Bone destruction is prominent and may show a 'bone replacement' pattern (infiltrating and displacing bone marrow). In polyposis, diffusion restriction and bone destruction are not expected.
Urgency
routineManagement
medicalBiopsy
Not NeededFollow-up
Medikal tedaviye yanıt değerlendirmesi için 3-6 ayda klinik ve endoskopik kontrol; cerrahi sonrası ilk yıl 3 ayda bir, sonrasında yıllık endoskopik takip; biyolojik tedavi altında yıllık BT ile yanıt değerlendirmesi.Sinonasal polyposis is a chronic inflammatory disease with medical approach forming the cornerstone of treatment. First-line treatment is intranasal corticosteroids (mometasone, fluticasone) and short-course systemic steroid regimens. Second-line biologic agents (dupilumab, omalizumab, mepolizumab) are effective in the eosinophilic phenotype. FESS is performed in cases refractory to medical treatment and provides drainage by opening sinus ostia. Postoperative topical steroid irrigation reduces recurrence. In Samter's triad patients, aspirin desensitization and leukotriene antagonists are recommended as adjunctive therapy. In unilateral polypoid lesions, malignancy and inverted papilloma should be excluded — biopsy may be required.
Sinonasal polyposis is managed with medical (intranasal steroids, short-course oral steroids) and surgical (FESS) treatment. Recurrence rate is high. Aspirin desensitization may be considered with Samter's triad. Unilateral polyposis requires malignancy exclusion. Biologic therapies (dupilumab) are emerging options.