Nasal Polyps — Symptoms, Causes & Treatment | MyMedicPlus

Nasal polyps are soft, non-cancerous, teardrop-shaped pedunculated growths that develop from the chronically inflamed mucosa lining the nasal passages and paranasal sinuses. They arise from persistent type 2 eosinophilic airway inflammation driven by cytokines including interleukin (IL)-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP) — resulting in accumulation of eosinophils, IgE, and inflammatory mediators within the mucosal tissue. Nasal polyps affect approximately 2-4% of the general population and are more common in adults than children (in children, bilateral nasal polyps should prompt testing for cystic fibrosis). They are significantly more prevalent in men than women, and in individuals with asthma. The condition is classified under the umbrella of chronic rhinosinusitis with nasal polyps (CRSwNP) — distinct from chronic rhinosinusitis without nasal polyps (CRSsNP) in its pathophysiology, inflammatory profile, treatment response, and biologic eligibility. Samter's triad (aspirin-exacerbated respiratory disease, AERD) — the combination of nasal polyps, asthma, and aspirin/NSAID sensitivity — occurs in approximately 10% of polyp patients and is particularly difficult to treat. Without consistent medical therapy, nasal polyps recur in 50-70% of patients after surgery within 5 years.

The pathophysiology of nasal polyps (chronic rhinosinusitis with nasal polyposis — CRSwNP) centres on dysregulated type 2 (T2) eosinophilic mucosal inflammation driven by innate lymphoid cells (ILC2s), IL-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP). Epithelial barrier disruption (from allergens, viruses, pollution, or microbiome dysbiosis) triggers TSLP and IL-33 release from epithelial cells, amplifying ILC2 and Th2 lymphocyte responses, leading to eosinophil recruitment, mast cell activation, and excessive type 2 cytokine production that drives mucosal oedema, goblet cell hyperplasia, and polyp formation. Associated conditions: asthma (concurrent in 40-60% of polyposis patients — the eosinophilic airway inflammation is contiguous, representing an 'united airway' disease); NSAID-exacerbated respiratory disease (AERD, previously called Samter's triad) — aspirin sensitivity, asthma, and nasal polyposis form a triad in approximately 10% of patients; caused by abnormal arachidonic acid metabolism with excessive cysteinyl leukotriene production when COX-1 is inhibited by aspirin or NSAIDs (diverting arachidonic acid to the leukotriene pathway); AERD patients experience severe bronchospasm and rhinorrhoea within 30-120 minutes of NSAID ingestion. Allergic rhinitis coexists in 50-60% of polyposis patients. Cystic fibrosis (CFTR gene mutations causing thick viscous secretions, impaired mucociliary clearance) produces bilateral nasal polyps in 40-50% of CF patients — and bilateral paediatric polyposis should always trigger CF testing. Primary ciliary dyskinesia (PCD — ciliary ultrastructure defects): bronchiectasis, sinusitis, and polyps. Genetic susceptibility: variants in ALOX5AP and PTGDR2. Non-type 2 CRSwNP (particularly in East Asian populations) may be neutrophilic rather than eosinophilic — different pathophysiology with lower biologic response rates.

The dominant and most troubling symptoms of nasal polyps relate to chronic nasal obstruction and loss of smell. Bilateral nasal blockage and congestion is typically chronic and progressive — patients breathe predominantly through the mouth and experience persistent nasal discharge (clear or mucopurulent). Anosmia (complete loss of smell) or hyposmia (reduced sense of smell) is caused by direct mechanical blockage of the olfactory cleft in the roof of the nasal cavity where the olfactory nerve endings are located — this is one of the most distressing and quality-of-life-impairing symptoms, affecting food taste, enjoyment, and safety (inability to detect gas, smoke, or spoiled food). Hypogeusia (reduced taste sensation) commonly coexists with anosmia as the senses are closely linked. Chronic postnasal drip causes constant throat clearing, cough, and sleep disruption. Facial pain or pressure is less prominent than in acute sinusitis. Snoring and sleep-disordered breathing worsen due to nasal obstruction. Chronic ear symptoms (eustachian tube dysfunction, hearing muffling) may occur from mucosal oedema. Unilateral nasal polyp or mass is a red flag — always requires urgent ENT referral with endoscopy and possible biopsy to exclude sinonasal carcinoma or inverted papilloma.

Diagnosis of CRSwNP requires: (1) symptoms for more than 12 weeks (bilateral nasal obstruction, hyposmia/anosmia, mucopurulent discharge or post-nasal drip); (2) objective evidence of chronic rhinosinusitis on endoscopy or CT. Anterior rhinoscopy (otoscope or speculum and headlight): may visualise pale, grey, translucent grape-like masses (polyps) in the nasal cavity — but limited to the anterior third of the nasal passage. Nasal endoscopy (rigid or flexible, usually 4mm 0° or 30° telescope in clinic): provides direct superior visualisation of all nasal structures, including middle meatus (the site where most polyps originate), the olfactory cleft, posterior nasal cavity, nasopharynx, and sinus ostia; scores polyp extent using Lund-Kennedy endoscopic scoring system (0-2 per side per feature); essential before biologic prescription. CT paranasal sinuses (non-contrast): confirms bilateral polyposis, assesses sinus opacification (Lund-MacKay CT score 0-24 — guides surgical planning), and identifies anatomical variants relevant to FESS planning (e.g., Haller cells, Onodi cells, depth of olfactory fossa — Keros classification); CT is the standard pre-surgical imaging. Nasal peak inspiratory flow (NPIF): objective measure of nasal airway obstruction at baseline and after treatment. Blood tests: FBC (peripheral eosinophilia above 300 cells/mcL suggests type 2 disease and better biologic response); serum IgE; allergen-specific IgE or skin prick testing for common aeroallergens (house dust mite, grass pollen, pet dander). In all children with bilateral nasal polyps: sweat chloride test (above 60 mmol/L diagnostic of cystic fibrosis) — bilateral paediatric polyposis is CF until proven otherwise. Nasal polyp biopsy: not routinely required but if unilateral polyp (raises concern for inverted papilloma or malignancy) or atypical appearance, biopsy and histopathology is mandatory.

Management of CRSwNP follows a step-up approach from medical to biological to surgical therapy. Step 1 — Topical corticosteroids (INCS): high-dose intranasal corticosteroid sprays or drops are the mainstay of long-term maintenance therapy — mometasone furoate 200mcg each nostril BD (400mcg/nostril/day); fluticasone propionate 200mcg/nostril/day; budesonide irrigation (via Neti pot or rinse bottle with corticosteroid added — delivers drug to the ethmoid sinuses more effectively than spray); these reduce polyp size, improve nasal symptoms and olfaction with long-term use, and reduce post-surgical polyp recurrence. Saline nasal irrigation (isotonic or hypertonic, 240ml volumes — Neti pot, NeilMed Sinus Rinse): improves mucociliary clearance, removes antigenic particles, and enhances INCS delivery when used before steroid spray — EPOS 2020 recommends as adjunct to INCS. Step 2 — Short-course systemic corticosteroids: prednisolone 0.5mg/kg/day (or 25-50mg) for 5-7 days rapidly shrinks polyps and restores olfaction within days — effective for acute exacerbations or pre-operatively; polyps return within weeks to months on stopping; limit to 2-3 courses per year due to systemic corticosteroid side effects. Antibiotics: 3-month low-dose doxycycline (an anti-inflammatory effect rather than antimicrobial) reduces polyp size and symptoms in non-type 2 CRSwNP — considered in neutrophilic/Asian-type CRSwNP. Step 3 — Biologic therapy (targeted IL-4/IL-13/IL-5 inhibition): dupilumab (Dupixent — anti-IL-4Rα, blocking both IL-4 and IL-13 signalling) is first-line biologic for moderate-severe CRSwNP inadequately controlled by INCS; SINUS-24 and SINUS-52 trials: 57% reduction in polyp score; 2.3-point improvement in SNOT-22; 65% improvement in olfaction (smell); NICE and FDA/EMA approved; self-administered by subcutaneous injection 300mg every 2 weeks; particularly effective in patients with severe anosmia and concurrent asthma. Mepolizumab (Nucala — anti-IL-5): reduces eosinophilic polyp inflammation; approved as add-on for CRSwNP. Omalizumab (Xolair — anti-IgE): approved for CRSwNP with allergic asthma. Step 4 — Functional endoscopic sinus surgery (FESS): performed under general anaesthesia, removes polyps endoscopically and opens sinus ostia to restore drainage and ventilation; surgery controls disease in 70-80% of patients at 12 months; however, polyp recurrence is common (30-50% at 5 years), particularly in patients with AERD, asthma, or high blood eosinophilia — biological therapy significantly reduces post-surgical recurrence rates. Aspirin desensitisation in AERD: gradual increasing aspirin dose challenge in a monitored setting — allows therapeutic aspirin use long-term and reduces polyp recurrence and sinus surgery frequency.

Persistent anosmia profoundly impairs quality of life, nutritional enjoyment, and safety — the inability to detect smoke, gas leaks, or spoiled food constitutes a real environmental hazard. Severe anosmia also causes depression and social withdrawal. Nasal polyps consistently worsen coexisting asthma control by increasing lower airway type 2 eosinophilic inflammation — treating CRSwNP improves both nasal symptoms and asthma outcomes simultaneously. In patients with AERD (aspirin-exacerbated respiratory disease), NSAID or aspirin exposure triggers severe bronchospasm and nasal congestion — all NSAIDs (ibuprofen, diclofenac, naproxen) must be avoided, and surgical procedures or medical conditions requiring anti-platelet agents need specialist guidance. Post-surgical recurrence is the major clinical challenge — polyps recur in 50-70% of patients within 5 years of FESS without ongoing medical therapy; early maintenance with intranasal corticosteroids and biologic therapy reduces reoperation rates. Extension of polyps into the orbit or intracranial space (rare in severe uncontrolled disease) can cause orbital cellulitis, optic nerve compression, or intracranial spread — emergency presentations requiring imaging and urgent surgical management. Nasal polyps in children are uncommon and when bilateral, strongly indicate cystic fibrosis (CF) — this diagnosis must be excluded by sweat chloride testing.

Long-term maintenance therapy is essential to prevent polyp recurrence after both medical and surgical treatment. Intranasal corticosteroid sprays (mometasone 200 micrograms daily, fluticasone propionate 200 micrograms twice daily, or budesonide nasal irrigation) should be used continuously and indefinitely — these are the cornerstone of relapse prevention, reducing polyp volume and anosmia recurrence. Nasal saline irrigation (isotonic or hypertonic) twice daily enhances mucociliary clearance, removes inflammatory mediators, and improves drug delivery to the sinuses. Avoidance of NSAIDs and aspirin in AERD patients is mandatory — all NSAIDs (ibuprofen, naproxen, diclofenac) must be avoided; paracetamol is the recommended alternative. Aspirin desensitisation (aspirin-exacerbated respiratory disease desensitization protocol — AERD-D) under specialist supervision with increasing oral aspirin doses achieves aspirin tolerance in 80-90% of patients, reducing polyp recurrence, improving anosmia, and lowering asthma exacerbation frequency. Optimal asthma treatment is essential — biologics (dupilumab, mepolizumab) simultaneously treat both asthma and nasal polyps in eligible patients. Post-FESS follow-up with endoscopy at 4-6 weeks and 3-6 months enables early detection of recurrence before symptoms return.

See a GP for: persistent bilateral nasal blockage, reduced or lost sense of smell (hyposmia or anosmia), chronic nasal discharge, or postnasal drip lasting more than 3 months — particularly if associated with asthma or aspirin sensitivity (Samter's triad). Request ENT referral for nasal endoscopy to confirm diagnosis and assess polyp extent. Seek urgent ENT referral within 2 weeks for: a unilateral (one-sided) nasal polyp or mass — unilateral nasal growths must be assessed urgently to exclude sinonasal malignancy or inverted papilloma; unexplained unilateral facial pain, blood-stained nasal discharge, or loosening of teeth. Seek emergency assessment for: acute sinusitis with periorbital swelling, proptosis (eye pushed forward), diplopia, or restricted eye movements (suggests orbital cellulitis — surgical emergency); severe headache, neck stiffness, or photophobia with sinusitis (possible meningitis). Children with bilateral nasal polyps require cystic fibrosis testing — nasal polyps are a common presenting feature of CF in children.