Nasal Polyps

Benign oedematous outgrowths of sinonasal mucosa arising most often from the ethmoid sinuses and prolapsing into the middle meatus and nasal cavity. They are a manifestation of chronic rhinosinusitis rather than a disease in themselves, and their presence defines the polyp phenotype of chronic rhinosinusitis.

Prevalence and associations

Around 1 to 4 percent of the general population. Associations that must be actively sought:

Asthma in 40 to 65 percent of polyp patients.
Aspirin exacerbated respiratory disease, comprising asthma, polyps and nonsteroidal anti inflammatory drug sensitivity, in around 10 percent. This subgroup has more aggressive disease, higher recurrence and a distinct treatment pathway.
Cystic fibrosis, which must be excluded in every child with nasal polyps, where the prevalence of polyps is 20 to 50 percent. Polyps in a child are cystic fibrosis until proven otherwise.
Primary ciliary dyskinesia.
Allergic fungal rhinosinusitis.
Eosinophilic granulomatosis with polyangiitis.
Non steroidal exacerbated disease and, in some series, allergic rhinitis, though the association with atopy is weaker than commonly assumed.

Pathology

Polyps are oedematous stroma with a loose extracellular matrix, sparse blood vessels and glands, and dense inflammatory infiltrate. In Western populations the infiltrate is predominantly eosinophilic with type 2 cytokines interleukin 4, 5 and 13, local immunoglobulin E production frequently against Staphylococcus aureus superantigens, and reduced tissue plasminogen activator with excess fibrin deposition producing the characteristic oedema. In East Asian populations a higher proportion are neutrophilic with a type 1 or type 3 profile, which is less corticosteroid responsive.

The critical rule on laterality

Bilateral polyps are inflammatory disease. Unilateral polyps are a neoplasm until proven otherwise and require imaging and histology in every case. The differential includes inverted papilloma, juvenile nasopharyngeal angiofibroma in an adolescent male, antrochoanal polyp, squamous cell carcinoma, adenocarcinoma, olfactory neuroblastoma, lymphoma, melanoma, encephalocele and meningocele. Never remove a unilateral nasal mass in clinic without imaging, since biopsy of an encephalocele or an angiofibroma has catastrophic consequences.

Antrochoanal polyp: a solitary polyp arising from the maxillary sinus, passing through an accessory ostium and extending posteriorly into the choana and nasopharynx. It occurs in younger patients, is unilateral, is not associated with eosinophilic disease, and does not respond to steroid. Treatment is complete surgical removal including the maxillary antral origin, since incomplete removal causes recurrence.

Progressive bilateral nasal obstruction, which is the dominant symptom and is typically constant rather than alternating.
Hyposmia progressing to anosmia, which is often complete and is frequently the most distressing symptom for patients. It results both from mechanical obstruction of the olfactory cleft and from inflammatory damage to the olfactory neuroepithelium.
Loss of taste as a consequence.
Rhinorrhoea and postnasal drip, usually mucoid.
Facial pressure rather than severe pain.
Sleep disturbance, snoring, mouth breathing and fatigue.
Recurrent acute exacerbations with purulent discharge.
Poorly controlled asthma, which frequently improves when the polyps are treated.

Examination

Pale, greyish, translucent, grape like masses in the middle meatus, insensitive to touch, which distinguishes them from a hypertrophic middle turbinate, which is sensitive and bleeds.
Polyp grading 0 to 3 per side as described under chronic rhinosinusitis.
Broadening of the nasal dorsum and hypertelorism in massive long standing polyposis, indicating bone remodelling and requiring imaging.
Assess smell formally.
Examine the chest and ask specifically about nonsteroidal anti inflammatory drug reactions, since the aspirin exacerbated group must be identified.

Red flags

Unilateral polyp or mass.
Bleeding, which polyps rarely cause.
Facial pain that is severe and unilateral.
Proptosis, diplopia, epiphora or reduced vision.
Facial numbness in the infraorbital distribution.
Cranial neuropathy.
A polyp in a child, which requires cystic fibrosis testing.
A polypoid mass in an adolescent male with epistaxis, which is angiofibroma until excluded and must never be biopsied without imaging.

Nasal endoscopy after decongestion, defining polyp origin, grade and extent, and assessing the postnasal space.
Non contrast computed tomography of the sinuses, which stages the disease using the Lund Mackay score, defines the anatomy for surgery, and identifies bone erosion or expansion that would suggest neoplasm, mucocele or fungal disease. Obtain this before any surgery.
Magnetic resonance imaging where the computed tomography shows bone erosion, expansion, orbital or skull base involvement, unilateral disease, or where malignancy, fungal disease, mucocele or an encephalocele is suspected. It distinguishes tumour from retained secretions, which computed tomography cannot.
Histology of tissue removed at surgery in every case, and specifically before or at removal of any unilateral lesion.
Objective smell testing with a validated instrument, both at baseline and to measure response.
Blood eosinophil count and total immunoglobulin E, for endotyping and biologic eligibility.
Skin prick testing or specific immunoglobulin E for aeroallergens.
Sweat chloride testing and cystic fibrosis genetics in all children with polyps and in adults with bronchiectasis, pancreatic insufficiency or male infertility.
Nasal nitric oxide screening and ciliary studies for primary ciliary dyskinesia.
Antineutrophil cytoplasmic antibody, urinalysis, renal function and eosinophil count where vasculitis is suspected, particularly with asthma, peripheral eosinophilia and mononeuritis.
Immunoglobulins and specific antibody responses where infection is recurrent.
Aspirin challenge under supervision where aspirin exacerbated respiratory disease is suspected and desensitisation is contemplated.
Symptom scoring with the Sino Nasal Outcome Test 22 at baseline and follow up.

Medical therapy first, with surgery for failure, and lifelong maintenance therapy in every case because polyps are a manifestation of persistent inflammation that surgery does not cure.

Foundation medical therapy

Intranasal corticosteroid used continuously and indefinitely: mometasone furoate 200 micrograms per nostril twice daily, or fluticasone propionate 100 micrograms per nostril twice daily. Higher doses are appropriate in polyp disease than in rhinitis.
Corticosteroid delivered by high volume irrigation gives markedly better distribution to the sinuses than a spray, particularly after surgery. Budesonide 0.5 mg respule added to 240 mL saline irrigation once or twice daily is widely used, with counselling about the possibility of systemic absorption in prolonged use and periodic consideration of adrenal function in patients on high doses long term.
Nasal saline irrigation, high volume, at least twice daily.
Steroid drops applied in the head down and forward position to reach the olfactory cleft, for anosmia.
Smoking cessation.

Oral corticosteroid

Prednisolone 0.5 mg/kg daily, generally 25 to 50 mg, for 5 to 10 days, or a tapering course over 2 to 3 weeks.
Reliably shrinks polyps and restores smell, with benefit lasting weeks to a few months.
Limit to a maximum of one or two courses per year. Cumulative exposure causes avascular necrosis of the femoral head, osteoporosis, diabetes, cataract, glaucoma, hypertension, weight gain and mood disturbance.
The need for repeated courses is an indication to escalate to surgery or biologic therapy, not to keep prescribing steroid. Patients who have had multiple courses should have bone density and glucose assessment.

Aspirin exacerbated respiratory disease

Strict avoidance of aspirin and nonsteroidal anti inflammatory drugs, with paracetamol and selective cyclo oxygenase 2 inhibitors as alternatives, the latter after supervised challenge.
Aspirin desensitisation followed by maintenance aspirin, commonly 650 mg twice daily and often reduced to 325 mg twice daily for tolerability, reduces polyp recurrence, reduces the need for revision surgery and improves asthma control. It requires supervised graded challenge in a specialist unit with resuscitation facilities, and it is contraindicated in peptic ulceration, bleeding disorders, pregnancy and severe uncontrolled asthma. Adherence must be lifelong, since desensitisation is lost within days of stopping.
Montelukast 10 mg daily as an adjunct, which is more effective in this subgroup than in unselected polyp disease.

Biologic therapy

For severe type 2 polyp disease, usually after surgery or where surgery is contraindicated.

Dupilumab 300 mg subcutaneously every 2 weeks, which produces the largest reductions in polyp score and the most reliable recovery of smell, and simultaneously treats asthma and atopic dermatitis. Monitor for conjunctivitis and transient blood eosinophilia.
Omalizumab, dosed by weight and total immunoglobulin E, every 2 to 4 weeks.
Mepolizumab 100 mg subcutaneously every 4 weeks.
Assess at 4 to 6 months against defined response criteria and discontinue non responders.

Antibiotics and antifungals

Antibiotics only for acute bacterial exacerbations, culture directed where possible, for 7 to 14 days.
Long term macrolide therapy has less evidence in polyp disease than in non polyp chronic rhinosinusitis, and is most useful in patients with low immunoglobulin E and neutrophilic disease.
Topical and systemic antifungals have no established role in ordinary polyp disease and should not be used.

Surgery

Indications: failure of appropriate medical therapy including a trial of oral corticosteroid; complications such as mucocele, orbital involvement or bone erosion; unilateral disease requiring histology; and to create access for topical therapy in extensive disease.

Endoscopic polypectomy with ethmoidectomy as the minimum, since simple polypectomy alone without addressing the ethmoid has high recurrence.
Complete or full house functional endoscopic sinus surgery with maxillary antrostomy, complete ethmoidectomy, sphenoidotomy and frontal recess clearance for extensive disease.
Extended approaches for severe eosinophilic disease: the endoscopic modified Lothrop or Draf III procedure for the frontal sinus, and reboot surgery with removal of diseased mucosa down to periosteum, which reduces recurrence at the cost of prolonged crusting and the need for meticulous postoperative care.
Image guidance navigation for revision surgery, frontal and sphenoid disease, distorted anatomy and skull base or orbital proximity.
Antrochoanal polyp requires removal of the antral origin, through a middle meatal antrostomy with an angled endoscope, or with an additional canine fossa or inferior meatal approach where the origin cannot be reached.

Postoperative care, which determines recurrence rates

Saline irrigation from day 1 or 2, high volume, twice daily.
Topical corticosteroid resumed at 1 to 2 weeks, preferably as steroid irrigation.
Oral corticosteroid in the early postoperative period for eosinophilic disease, which reduces early recurrence.
Endoscopic debridement at 1 to 2 weeks and as needed thereafter.
Emphasise from the outset that surgery removes polyps but does not cure the disease, and that stopping topical treatment leads to recurrence. This must be said before surgery, not afterwards.

Follow up

Endoscopic review at 2 weeks, 6 weeks, 3 months, then 6 to 12 monthly. Track polyp grade, symptom score and smell. Recurrence occurs in up to 40 percent within 5 years in eosinophilic disease, and revision surgery is needed in around 20 percent. Escalate to biologic therapy rather than to repeated oral steroid courses or repeated surgery in patients with rapid recurrence.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Oral Leukoplakia

A predominantly white patch or plaque of the oral mucosa that cannot be characterised clinically or pathologically as any other definable disease, and which carries an increased risk of malignant transformation. It is a clinical diagnosis of exclusion, and the term carries no histological meaning by itself.

Epidemiology and risk

Global prevalence around 2 to 3 percent, higher in populations with heavy tobacco and areca nut use.
Malignant transformation rate of approximately 1 to 3 percent per year, with a cumulative rate of around 5 to 12 percent overall, and substantially higher in specific subgroups.
Around 15 to 20 percent already contain dysplasia at first biopsy, and a small proportion contain invasive carcinoma.

Factors predicting malignant transformation, which determine surveillance intensity

Non homogeneous appearance, particularly speckled or erythroleukoplakia, with transformation rates several times higher than homogeneous lesions.
Presence and grade of epithelial dysplasia. Severe dysplasia and carcinoma in situ carry the highest risk, though transformation occurs in non dysplastic lesions too.
Site: the floor of mouth, the ventrolateral tongue and the soft palate complex are high risk. The buccal mucosa and hard palate are lower risk.
Size greater than 200 mm squared.
Female sex.
Non smokers, that is idiopathic leukoplakia, which paradoxically has a higher transformation rate than smoking associated leukoplakia.
Long duration.
Proliferative verrucous leukoplakia.
Candida infection within the lesion.

Aetiological factors

Tobacco in all forms: smoking, smokeless tobacco, and reverse smoking with the lit end in the mouth, which produces palatal lesions with high transformation rates.
Areca nut and betel quid, with or without tobacco, which also causes oral submucous fibrosis.
Alcohol, which acts synergistically with tobacco.
Chronic candidal infection, in hyperplastic candidiasis.
Human papillomavirus, particularly types 16 and 18, in a proportion.
Chronic trauma, though frictional keratosis is a separate entity that resolves when the cause is removed.
Idiopathic in a significant proportion, which is the group with the highest risk.

Clinical subtypes

Homogeneous: uniformly flat, thin, white, with a smooth or finely wrinkled surface and well defined margins. Lower risk.
Non homogeneous, which comprises:
Speckled or erythroleukoplakia: mixed white and red, which is the highest risk pattern.
Nodular: small polypoid white outgrowths.
Verrucous or exophytic: wrinkled or corrugated surface.
Proliferative verrucous leukoplakia: a distinct and dangerous entity occurring predominantly in older women who are often non smokers, characterised by multifocal, progressive, spreading white lesions that become verrucous and are highly resistant to treatment, with a transformation rate of 60 to 100 percent over 10 to 20 years and a strong tendency to recur after excision. It requires lifelong intensive surveillance.

Usually asymptomatic and detected incidentally by a dentist or clinician, which is why routine oral examination matters.
Roughness or a sensation of thickening.
Pain, burning or ulceration, which suggest dysplasia, malignant change or superadded candidal infection, and which are late features.
A patch that cannot be wiped or scraped off, which is the finding that distinguishes it from candidiasis and from debris.

Examination

Systematic examination of the entire oral cavity with good lighting and gauze, including the lateral and ventral tongue lifted with gauze, the floor of mouth, the retromolar trigone, the buccal mucosa stretched flat, and the gingivae. The floor of mouth and ventrolateral tongue are the high risk sites and are the areas most often examined inadequately.
Palpate every lesion. Induration is the single most important finding and indicates invasion until proven otherwise.
Record site, size in millimetres, appearance, whether homogeneous or non homogeneous, and photograph.
Palpate the neck for lymphadenopathy.
Examine for evidence of the causative habit: tobacco staining, betel staining, and dental trauma.

Red flags indicating probable malignancy

Induration on palpation.
Ulceration.
Erythematous component, that is speckled leukoplakia.
Rapid change in size or appearance.
Pain.
Bleeding.
Cervical lymphadenopathy.
Loosening teeth or numbness.
Any of these mandate urgent biopsy and referral on a suspected cancer pathway.

Biopsy is mandatory in every case. Leukoplakia is a clinical term and the management is determined entirely by the histology.
Incisional biopsy from the most clinically suspicious area: the erythematous, nodular, ulcerated or indurated part, since dysplasia is heterogeneous within a lesion and biopsying the homogeneous white area produces false reassurance. Where the lesion is large or multifocal, take multiple biopsies from several sites.
Excisional biopsy for small lesions where complete removal is feasible.
Adjuncts including toluidine blue staining, autofluorescence and brush cytology may help select the biopsy site in a large or multifocal lesion, but none replaces scalpel biopsy and none should be used to avoid biopsy.
Histological grading of dysplasia as mild, moderate or severe, or as low grade and high grade in the binary system, assessing architectural and cytological features: loss of polarity, drop shaped rete pegs, increased and abnormal mitoses, nuclear pleomorphism, hyperchromatism, increased nuclear to cytoplasmic ratio and abnormal keratinisation.
Periodic acid Schiff staining for candidal hyphae, since candidal leukoplakia may partially regress with antifungal treatment and requires re assessment afterwards.
Human papillomavirus testing where the histology suggests it.
Full examination of the upper aerodigestive tract with flexible endoscopy in patients with tobacco and alcohol exposure, given the field change effect and the risk of synchronous primary tumours.
Cross sectional imaging where malignancy is confirmed or strongly suspected.
Full blood count, haematinics and glucose.

Differential diagnosis and the discriminating feature

Frictional keratosis: a clear mechanical cause such as a sharp tooth, denture flange or cheek biting, resolving within 2 to 4 weeks of removing the cause. If it does not resolve, biopsy it.
Candidiasis: pseudomembranous plaques wipe off; hyperplastic candidiasis does not and requires biopsy.
Oral lichen planus: bilateral, symmetrical, with lacy Wickham striae.
Lichenoid reaction: unilateral, adjacent to an amalgam restoration or related to a drug.
Leukoedema: a diffuse greyish white filmy appearance of the buccal mucosa that disappears when the mucosa is stretched, which is a normal variant particularly in darker skinned individuals.
White sponge naevus: a hereditary autosomal dominant condition with diffuse thick white folded mucosa from childhood.
Hairy leukoplakia: vertically corrugated plaques on the lateral tongue, Epstein Barr virus related, strongly associated with HIV.
Smoker keratosis of the palate, that is nicotinic stomatitis: a white palate with red punctate inflamed minor salivary duct openings, which is not premalignant in conventional smokers but is in reverse smokers.
Squamous cell carcinoma.
Chemical burn, and morsicatio buccarum from chronic cheek biting.
Syphilitic leukoplakia of the tongue dorsum in tertiary syphilis.

Management centres on removing the cause, obtaining histology, treating dysplastic lesions, and lifelong surveillance, since transformation occurs both at treated sites and at new sites.

Risk factor elimination, which is the foundation

Complete tobacco cessation in all forms, with structured support including behavioural intervention and pharmacotherapy with nicotine replacement, varenicline or bupropion. Around half of leukoplakias regress or resolve within 6 to 12 months of cessation, so this is genuinely disease modifying rather than merely advisable.
Complete cessation of areca nut and betel quid.
Reduction or cessation of alcohol.
Remove chronic trauma: smooth sharp cusps, adjust dentures, treat sharp restorations.
Treat candidal infection with a systemic antifungal course such as fluconazole 50 mg daily for 2 to 4 weeks, then reassess. Candidal leukoplakia may substantially improve, but the residual lesion must still be biopsied.
Optimise oral hygiene and arrange regular dental care.

Management by histology

No dysplasia: risk factor elimination and observation with review at 3 to 6 months initially, then 6 to 12 monthly. Re biopsy if the appearance changes. Consider excision for high risk sites, non homogeneous appearance or large size even without dysplasia.
Mild dysplasia: risk factor elimination, review at 3 to 6 months, with excision considered particularly at high risk sites or if the lesion is non homogeneous or persists after habit cessation.
Moderate dysplasia: excision is generally recommended, with close surveillance thereafter.
Severe dysplasia and carcinoma in situ: excision with clear margins, followed by intensive surveillance.
Invasive carcinoma: manage on the head and neck cancer pathway.

Treatment modalities

Surgical excision with a scalpel, which provides a complete specimen for histology and remains the standard where the diagnosis or completeness of excision matters. Defects may be left to granulate, closed primarily, or reconstructed with a split skin or buccal fat pad graft depending on size and site.
Carbon dioxide laser excision or ablation, which offers good haemostasis, a clean field and reduced scarring and postoperative pain. Excision is preferable to ablation, since ablation destroys the specimen and precludes histological assessment of the margins.
Cryotherapy and electrocautery, which similarly destroy the specimen and are less favoured.
Photodynamic therapy in selected cases.
Recurrence after excision occurs in 10 to 35 percent, and new lesions arise at other sites because the whole mucosa is at risk from field change. Excision reduces but does not eliminate the risk of transformation, and this must be stated clearly to the patient so that they continue to attend for surveillance rather than assuming they are cured.

Medical treatment

No topical or systemic agent has established efficacy in preventing malignant transformation. Retinoids, both topical and systemic, produce regression in some lesions but with high relapse on cessation and significant toxicity including teratogenicity, hyperlipidaemia and mucocutaneous adverse effects. Beta carotene, vitamin E, lycopene, green tea extract, bleomycin and other agents have been studied without convincing evidence of a reduction in transformation. Patients should not be offered these as an alternative to excision or surveillance.

Proliferative verrucous leukoplakia

Requires an aggressive approach with wide excision of accessible lesions, though recurrence is near universal.
Lifelong surveillance at 3 to 6 monthly intervals with repeated biopsy of any changing area.
Counsel the patient explicitly about the very high transformation rate, since these patients require sustained engagement with follow up over decades.

Surveillance

Every patient with leukoplakia requires long term follow up, including those whose lesion has been excised and those whose lesion resolved after habit cessation.
Interval: 3 monthly for high risk lesions, dysplasia and proliferative verrucous leukoplakia; 6 monthly for intermediate risk; annually for low risk homogeneous lesions with no dysplasia in a patient who has stopped their habit.
At each visit: full oral examination with palpation, measurement and photography, and biopsy of any change in appearance, texture, size or symptoms.
Examine the whole upper aerodigestive tract periodically in patients with tobacco and alcohol exposure.
Teach the patient self examination and give clear instructions to present promptly with any ulcer lasting more than 3 weeks, any lump, any bleeding, or any change in an existing patch.
Discharge is generally not appropriate, since transformation occurs years and sometimes decades after initial presentation.

Nasal Polyps

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management