Nasal Polyps

Definition

Nasal polyps are soft, non-cancerous swellings of the lining of the nose and sinuses. They are not a disease in themselves but the visible endpoint of long-standing mucosal inflammation, and the correct diagnostic label is chronic rhinosinusitis with nasal polyps (CRSwNP) — chronic rhinosinusitis being nasal blockage or discharge plus facial pressure or reduced sense of smell, present for twelve weeks or longer, with polyps confirmed on examination of the nose.¹ The distinction from chronic rhinosinusitis without polyps matters, because the two behave differently, respond to different treatments and carry different recurrence risks.

Pathophysiology

Most nasal polyps in Australia and Europe are driven by type 2 inflammation — the same immune pathway that underlies eosinophilic asthma. Interleukin-4, interleukin-5 and interleukin-13 recruit eosinophils into the mucosa, drive local immunoglobulin E production and disrupt the epithelial barrier. Persistent oedema of the loose connective tissue beneath the epithelium, especially in the ethmoid sinuses and the middle meatus, produces the pale, gelatinous, grape-like swellings seen at endoscopy.²

Three consequences follow directly from the mechanism and explain most of the clinical course. Polyps arise where the inflammation is, so they are typically bilateral — a genuinely one-sided polyp is a different problem until proved otherwise. They involve the olfactory region high in the nasal cavity, which is why loss of smell is such a prominent and early feature. And because the inflammation continues after the polyps are removed, they recur unless the underlying type 2 inflammation is treated — the single most important point for a patient to understand.¹

A minority of cases are not type 2 driven, including polyps in cystic fibrosis and primary ciliary dyskinesia, where impaired mucociliary clearance is the dominant mechanism, and polyps in granulomatosis with polyangiitis, where the process is vasculitic.

Co-morbidities

The dominant associations are asthma — present in roughly half of people with nasal polyps and usually eosinophilic — allergic and non-allergic rhinitis, aspirin- or non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease, bronchiectasis, obstructive sleep apnoea and snoring, and depression and anxiety related to persistent symptoms and to the loss of smell. In children and young adults, polyps raise the possibility of cystic fibrosis or primary ciliary dyskinesia and should prompt testing.³

Prevalence

Nasal polyps affect around 2–4% of adults in population studies that used endoscopy rather than symptom questionnaires.⁴ They are twice as common in men, uncommon before the age of twenty, and peak in the fifties and sixties. Prevalence rises sharply in defined groups: about 7% of people with asthma, 15% of those with severe eosinophilic asthma, and the great majority of people with NSAID-exacerbated respiratory disease. In children, polyps are rare enough that their presence is itself an indication to look for an underlying diagnosis.³

Causes and risk factors

• Type 2 eosinophilic inflammation — the principal driver in most adult cases.²
• Asthma, particularly late-onset eosinophilic asthma.
• NSAID-exacerbated respiratory disease — the triad of polyps, asthma and reaction to aspirin or other NSAIDs; polyps in this group are more aggressive and recur faster.⁵
• Cystic fibrosis and primary ciliary dyskinesia — the main considerations in children and young adults.
• Occupational and environmental exposure — dust, fumes and smoke; smoking worsens outcomes and increases recurrence after surgery.
• Allergy is an aggravating factor rather than a cause: allergic rhinitis is common in this group, but treating allergy alone does not resolve polyps.

Chronic infection is not the underlying cause, which is why repeated antibiotic courses do not help and why the treatment is anti-inflammatory.¹

Symptoms

• Persistent nasal blockage, usually both sides, that does not come and go the way allergic symptoms do.
• Loss of the sense of smell — often the earliest and most complete symptom, and frequently the most distressing; taste is lost with it.
• Thick nasal discharge or post-nasal drip, with throat clearing and cough.
• Facial pressure or fullness rather than the sharp pain of acute infection.
• Mouth breathing, snoring and disturbed sleep, with daytime fatigue.
• Nasal voice, and reduced effectiveness of nasal sprays as the polyps enlarge and block access.
• Worsening asthma — deteriorating lower airway control frequently accompanies polyp growth.

How severity is judged

Three measures are taken, and they do not always agree: the endoscopic polyp grade (size and extent at endoscopy), the symptom burden — usually with the 22-item Sino-Nasal Outcome Test (SNOT-22), where a change of about nine points is clinically meaningful — and smell testing. A patient with modest-looking polyps and complete anosmia has severe disease. Formal severity assessment matters because it determines eligibility for surgery and for biologic therapy.³

When symptoms suggest something else

Diagnosis

Why diagnosis matters

Because the label determines the treatment. Polyps are routinely managed for years as "sinus infections" with recurrent antibiotics, or as hay fever with an antihistamine — neither of which treats type 2 inflammation. Meanwhile the two symptoms that respond well to correct treatment, loss of smell and coexisting asthma, are the two most likely to have become entrenched by the time the diagnosis is made.¹

How is it diagnosed?

The diagnosis requires twelve weeks or more of nasal blockage or discharge with facial pressure or smell loss, plus visible polyps. Polyps at the front of the nose may be seen with an otoscope, but most sit further back in the middle meatus, so nasal endoscopy by an ear, nose and throat surgeon is the practical standard for diagnosis, grading and monitoring.³

Imaging

Computed tomography (CT) of the sinuses is the imaging test of choice — it shows the extent of disease, the anatomy the surgeon needs, and complications, and is used for surgical planning rather than for making the initial diagnosis. Plain sinus X-rays have no role. Magnetic resonance imaging is added where a tumour, fungal disease or intracranial extension is suspected, or where the disease is one-sided.¹

Assessing the inflammatory type

Because treatment now targets type 2 inflammation directly, the markers of that pathway have become practically relevant: blood eosinophil count, total and allergen-specific immunoglobulin E, and tissue eosinophil count where polyp histology is available. These, together with coexisting asthma and NSAID sensitivity, define the group most likely to respond to biologic therapy — and the group most likely to recur after surgery alone.²

Investigations for related conditions

• Spirometry with reversibility testing in everyone — asthma is present in about half, and is frequently undiagnosed.⁶
• Sweat test and cystic fibrosis genetic testing in children, adolescents and young adults with polyps.
• Nasal nitric oxide and ciliary studies where primary ciliary dyskinesia is suspected — polyps with lifelong wet cough, glue ear and situs abnormalities.
• Antineutrophil cytoplasmic antibody (ANCA) testing where crusting, bleeding, destructive disease or systemic features suggest vasculitis.
• Smell testing and a validated symptom score, at baseline and after treatment, so response can be measured rather than recalled.
• Sleep study where snoring and unrefreshing sleep suggest obstructive sleep apnoea.

Management

Management and goals

The aim is control of a long-term inflammatory disease, not cure. Realistic goals: a nose that can be breathed through, as much sense of smell recovered as the disease allows, no need for repeated oral corticosteroids, stable asthma, and sleep that is not fragmented by obstruction. The single most useful expectation to set at the outset is that treatment continues after surgery. Polyps removed and left untreated grow back in a large proportion of patients.⁷

Treatment options

Surgery — what it does and does not do

Endoscopic sinus surgery removes polyps and opens the sinus drainage pathways, which relieves obstruction and — just as importantly — creates a cavity that topical treatment can actually reach. It does not remove the inflammation. Long-term audit data show meaningful and sustained improvement in symptoms and quality of life after surgery, alongside a substantial revision rate, with the highest recurrence in patients with asthma, NSAID sensitivity and high tissue eosinophil counts.⁷ The practical framing for patients: surgery buys a much better starting position, and medical treatment afterwards decides how long it lasts.

Biologic therapy

Monoclonal antibodies against the type 2 pathway have changed the outlook for severe recurrent disease. Dupilumab (against the interleukin-4 receptor alpha subunit) produces the largest effect on polyp size, nasal obstruction and sense of smell, and reduces both surgery and systemic steroid use.¹¹ Mepolizumab (against interleukin-5) and omalizumab (against immunoglobulin E) also improve polyp size and symptoms.^12,13 Access in Australia is through specialist prescribing against defined criteria, generally requiring severe disease with prior surgery or contraindication to it. Where asthma coexists, one agent may treat both conditions — which is a strong argument for assessing the upper and lower airway together rather than in separate clinics.⁶

Recognising deterioration

Increasing blockage, returning loss of smell, thicker or discoloured discharge, new facial pain or fever, or deteriorating asthma all indicate that control has been lost — and returning smell loss is often the earliest signal of recurrence. New one-sided symptoms, bleeding or visual change require urgent review rather than an adjustment of treatment.

Action plan

A written plan should name the daily saline and topical steroid regimen, the plan for post-operative rinsing where relevant, what to do about a flare and who to contact, the NSAID advice where that applies, the asthma action plan alongside it, and the review interval for endoscopy and smell testing. Everyone with NSAID-exacerbated respiratory disease needs their NSAID restriction documented and understood, including in over-the-counter medicines.⁵

Medications

Medications for nasal polyps

Correct use of medications

Two failures account for most apparent treatment resistance. The first is intermittent use of a topical steroid that only works when taken daily, and whose full effect on polyp size takes weeks to months. The second is delivery: a spray cannot reach polyps that are already blocking the nose, which is why rinsing first, correct aim away from the septum, and — after surgery — a high-volume rinse rather than a spray, make so much difference.⁹

Order of medications

Saline rinse first to clear mucus and crust, then the topical corticosteroid a few minutes later onto cleared mucosa. Where a corticosteroid is added into the rinse itself, that replaces the spray rather than adding to it. Oral corticosteroids are a rescue, not a step in the routine — a patient needing more than one or two short courses a year needs reassessment for surgery or biologic therapy rather than another course.¹⁰

Multi-system manifestations

Lower airway

Nasal polyps and asthma are the upper and lower expressions of one eosinophilic airway disease. Around half of people with polyps have asthma, and polyp-associated asthma tends to be later-onset, eosinophilic and harder to control. Polyp recurrence and asthma deterioration commonly occur together, and treatment of one benefits the other.⁶

NSAID-exacerbated respiratory disease

In this subgroup, aspirin and other NSAIDs provoke acute upper and lower airway reactions — nasal congestion, flushing, wheeze, sometimes severe bronchospasm — through abnormal arachidonic acid metabolism rather than an allergic mechanism. Polyps in this group are more extensive, recur faster, and warrant earlier consideration of biologic therapy or aspirin desensitisation. Recognition is a safety matter as much as a therapeutic one.⁵

Smell, taste, appetite and safety

Loss of smell is not a cosmetic complaint. It removes the enjoyment of food and often changes eating and weight, and it removes the ability to detect smoke, gas, and spoiled food. It is independently associated with reduced quality of life and with depressive symptoms, and it is one of the outcomes that responds best to effective anti-inflammatory treatment — which is a reason to treat early rather than to wait for obstruction to become severe.¹¹

Sleep and daytime function

Fixed nasal obstruction produces mouth breathing, snoring and fragmented sleep, with daytime fatigue and impaired concentration. It also reduces tolerance of continuous positive airway pressure therapy where obstructive sleep apnoea coexists, so nasal patency is part of managing the sleep disorder rather than a separate issue.³

Systemic eosinophilic disease

Polyps can be the presenting feature of eosinophilic granulomatosis with polyangiitis, and destructive or crusting disease can indicate granulomatosis with polyangiitis. Fever, weight loss, rash, neuropathy, kidney involvement or a rising eosinophil count on treatment should prompt investigation for systemic vasculitis rather than escalation of nasal treatment.³

Impaired mucociliary clearance

In cystic fibrosis and primary ciliary dyskinesia, polyps sit alongside chronic wet cough, bronchiectasis and glue ear, and the airway clearance needs of the lower airway dominate management. Polyps in a child or young adult should always raise this possibility.

Living with nasal polyps

The daily routine

Rinse and spray become long-term habits, like a preventer inhaler. Attaching them to an existing routine — morning shower and bedtime — is what makes them stick. Symptom scores and smell tracked over months are far more useful than day-to-day impressions, which are dominated by weather and sleep.

Cooking and eating without smell

Practical adaptations help: use texture, temperature, salt and acid rather than aroma; date-label leftovers rather than relying on smell; and install a smoke alarm on every level of the house and a gas detector where there is gas.

Exercise

Nasal obstruction forces mouth breathing during exercise, delivering cold, dry, unfiltered air to the lower airway and worsening exercise-induced symptoms in those with asthma. Exercise remains firmly recommended, with a warm-up, asthma treatment optimised, and a plan for high-pollen and dusty days.

Work

Dust, fumes, smoke and strong irritants aggravate the condition; where exposure is occupational, controls and respiratory protection are part of treatment. Smoking cessation matters twice over — it worsens symptoms and increases recurrence after surgery.

Surgery and recovery

Recovery from endoscopic sinus surgery usually takes two to three weeks, with crusting, blockage and blood-stained discharge in the early days. Sense of smell often improves within weeks, sometimes dramatically. High-volume saline rinsing after surgery is the part of the recovery plan patients most often abandon and the part that most affects the result.⁸

Prognosis

Nasal polyps are a chronic, relapsing inflammatory disease that is now well controllable in most people. Topical corticosteroid with saline achieves adequate control for many. Surgery produces large, sustained improvements in symptoms and quality of life, with a meaningful revision rate over the following years — highest in those with asthma, NSAID sensitivity and marked eosinophilia.⁷ Biologic therapy has substantially improved outcomes for severe recurrent disease, reducing polyp burden, restoring some sense of smell, and reducing both repeat surgery and oral steroid exposure.¹¹ Sense of smell is the least reliably recovered outcome, particularly where loss has been complete for a long time — the reason not to accept anosmia as something to live with before it has been properly treated.

Role of the physiotherapist

The inflammation is managed medically and surgically; the physiotherapist addresses what chronic obstruction has done to breathing and to the lower airway. That includes teaching high-volume saline rinsing and correct topical spray technique — the two most commonly mistaught elements of the whole treatment plan, and the ones that decide whether the drug reaches the mucosa.⁹ It includes breathing pattern retraining to restore nasal, diaphragmatic breathing after years of mouth breathing, which does not correct itself once the nose is clear. It includes checking inhaler technique and actively looking for the eosinophilic asthma present in about half of these patients, and airway clearance where bronchiectasis, cystic fibrosis or primary ciliary dyskinesia coexists. Where nasal obstruction contributes to snoring or sleep apnoea, breathing pattern and patency work supports both symptoms and therapy tolerance.⁶

Part 1 · References

1. Fokkens WJ, Lund VJ, Hopkins C, et al. European Position Paper on Rhinosinusitis and Nasal Polyps 2020. Rhinology 2020;58(Suppl S29):1–464.
2. Stevens WW, Schleimer RP, Kern RC. Chronic rhinosinusitis with nasal polyps. J Allergy Clin Immunol Pract 2016;4(4):565–572.
3. Orlandi RR, Kingdom TT, Smith TL, et al. International consensus statement on allergy and rhinology: rhinosinusitis 2021. Int Forum Allergy Rhinol 2021;11(3):213–739.
4. Johansson L, Åkerlund A, Holmberg K, Melén I, Bende M. Prevalence of nasal polyps in adults: the Skövde population-based study. Ann Otol Rhinol Laryngol 2003;112(7):625–629.
5. Kowalski ML, Agache I, Bavbek S, et al. Diagnosis and management of NSAID-exacerbated respiratory disease (N-ERD) — a EAACI position paper. Allergy 2019;74(1):28–39.
6. Global Initiative for Asthma. Global strategy for asthma management and prevention: 2026 update. GINA, 2026.
7. Hopkins C, Slack R, Lund V, Brown P, Copley L, Browne JP. Long-term outcomes from the English national comparative audit of surgery for nasal polyposis and chronic rhinosinusitis. Laryngoscope 2009;119(12):2459–2465.
8. Chong LY, Head K, Hopkins C, Philpott C, Burton MJ, Schilder AGM. Saline irrigation for chronic rhinosinusitis. Cochrane Database Syst Rev 2016;4:CD011995.
9. Chong LY, Head K, Hopkins C, et al. Intranasal steroids versus placebo or no intervention for chronic rhinosinusitis. Cochrane Database Syst Rev 2016;4:CD011996.
10. Head K, Chong LY, Hopkins C, Philpott C, Burton MJ, Schilder AGM. Short-course oral steroids as an adjunct therapy for chronic rhinosinusitis. Cochrane Database Syst Rev 2016;4:CD011992.
11. Bachert C, Han JK, Desrosiers M, et al. Efficacy and safety of dupilumab in patients with severe chronic rhinosinusitis with nasal polyps (LIBERTY NP SINUS-24 and LIBERTY NP SINUS-52): results from two multicentre, randomised, double-blind, placebo-controlled, parallel-group phase 3 trials. Lancet 2019;394(10209):1638–1650.
12. Han JK, Bachert C, Fokkens W, et al. Mepolizumab for chronic rhinosinusitis with nasal polyps (SYNAPSE): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Respir Med 2021;9(10):1141–1153.
13. Gevaert P, Omachi TA, Corren J, et al. Efficacy and safety of omalizumab in nasal polyposis: two randomized phase 3 trials. J Allergy Clin Immunol 2020;146(3):595–605.

References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.