Rhinitis Medicamentosa

Also known as: Rebound congestion

Rebound nasal congestion caused by prolonged use of topical nasal decongestants, producing a self perpetuating cycle in which the patient uses the spray more frequently to relieve the congestion the spray itself is causing.

Pathophysiology

Topical decongestants are alpha adrenergic agonists that constrict the capacitance venous sinusoids of the nasal turbinates.

Imidazoline derivatives, that is oxymetazoline and xylometazoline, act predominantly on alpha 2 receptors, producing prolonged constriction of the venous sinusoids with a duration of 6 to 12 hours.
Sympathomimetic amines, that is phenylephrine and ephedrine, act predominantly on alpha 1 receptors with a shorter duration of 4 to 6 hours and more frequent rebound.

With repeated exposure, several processes combine:

Downregulation and desensitisation of alpha adrenergic receptors, with reduced responsiveness requiring higher and more frequent dosing.
Negative feedback reduction of endogenous noradrenaline release, so that when the drug wears off there is less endogenous vasoconstrictor tone than before, producing rebound vasodilation and congestion worse than the original.
Interstitial oedema, increased vascular permeability and reduced ciliary function.
Structural change with prolonged use: mucosal metaplasia, loss of ciliated cells, goblet cell hyperplasia, fibrosis and, in extreme cases, septal perforation.
Benzalkonium chloride, the preservative in most preparations, independently causes ciliotoxicity and mucosal injury and compounds the process.

Time course: rebound congestion typically develops after 5 to 10 days of continuous use, which is the basis for the universal 5 day limit on these preparations. Some patients develop it after as little as 3 days, and some tolerate longer, but the limit should be treated as absolute in advice given to patients.

Cocaine produces the same picture through alpha adrenergic effects with additional direct mucosal ischaemia, and causes septal perforation and midline destructive lesions. Ask about it directly in any patient with severe rhinitis medicamentosa and septal changes.

Severe nasal obstruction, which is the sole or dominant symptom. Rhinorrhoea, sneezing and itch are typically absent.
Progressive escalation of spray use, from once or twice daily to hourly, with a diminishing duration of relief.
Bottles used at night to enable sleep, and multiple bottles kept in different locations.
A history that begins with a legitimate short term indication such as a cold, sinusitis, air travel or the initiation of an intranasal steroid, followed by continued use for weeks, months or years.
Patients often minimise or are embarrassed about the extent of use, and specific direct questioning is required. Ask how many bottles are used per month.
Nasal dryness, burning, crusting and epistaxis.
Headache and sleep disturbance.
Anosmia in prolonged severe cases.

Examination

Beefy red, granular, oedematous inferior turbinates, which is the characteristic appearance and differs from the pale boggy mucosa of allergic disease.
Loss of the normal glistening mucosal surface, with a dry granular texture.
Poor or absent response to topical decongestant applied in clinic, which is a useful confirmatory test since the receptors are desensitised.
Crusting, and in advanced disease septal ulceration or perforation.
Assess for coexisting septal deviation and turbinate hypertrophy, since these frequently underlie the original symptom that prompted decongestant use and will need addressing.

Clinical, based on the history of decongestant use and the characteristic mucosal appearance.

Detailed medication history with specific enquiry about over the counter nasal sprays, which patients frequently do not consider medications and do not report unless asked directly by product name.
Nasal endoscopy to document mucosal appearance, exclude polyps and structural pathology, and assess the septum.
Failure to decongest with topical adrenergic agent in clinic, supporting receptor desensitisation.
Allergy testing to identify a coexisting allergic component, since many patients started decongestants for allergic rhinitis and will need that treated for the withdrawal to succeed.
Consider intranasal cocaine use and ask directly, particularly with septal ulceration or perforation.
Computed tomography of the sinuses only where sinus disease is suspected, since rhinitis medicamentosa alone does not require imaging.
Where septal perforation is present, exclude other causes: granulomatosis with polyangiitis with antineutrophil cytoplasmic antibody testing and urinalysis, syphilis serology, tuberculosis, sarcoidosis and malignancy, with biopsy of the perforation edge where the cause is not obvious. Do not assume perforation is drug related without excluding vasculitis.

Differential diagnosis

Chronic rhinosinusitis with or without polyps.
Untreated allergic or vasomotor rhinitis, which is frequently the underlying condition.
Structural obstruction from septal deviation, turbinate hypertrophy or nasal valve collapse.
Drug induced rhinitis from systemic medications.
Cocaine induced midline destructive lesion.

The treatment is withdrawal of the decongestant, and the clinical skill lies in making withdrawal tolerable, since abrupt cessation produces several days of severe obstruction and most unsupported attempts fail.

Explanation, which determines success

Explain the mechanism plainly: the spray is now causing the blockage it was bought to relieve, and each dose makes the underlying problem worse.
Set expectations: obstruction will worsen for 3 to 7 days after stopping, then improve, with mucosal recovery over 2 to 4 weeks and sometimes several months in long standing cases.
Warn that this is the point at which most people restart the spray, and that getting through this window is the entire treatment.
Address the shame that many patients feel, which contributes to concealment and to failed attempts.

Intranasal corticosteroid, started before or at the time of withdrawal

Mometasone furoate 200 micrograms per nostril twice daily, or fluticasone propionate 100 micrograms per nostril twice daily, initially at the higher end of the dose range and reduced after 4 to 6 weeks.
Start 3 to 7 days before stopping the decongestant where possible, so that it is already working when the rebound occurs.
It reduces the severity and duration of rebound congestion and treats any underlying inflammatory rhinitis.
Emphasise correct technique directed away from the septum, particularly in a mucosa that is already fragile and prone to bleeding.

Withdrawal strategy

Two approaches, chosen according to the patient:

Abrupt total cessation, which is faster and is preferred where the patient is motivated and adequately supported. Combine with intranasal steroid and consider a short course of oral corticosteroid.
Graduated withdrawal, either by stopping one nostril at a time so that the patient always has one patent side, or by progressively diluting the decongestant with saline, or by lengthening the interval between doses. Unilateral withdrawal is well tolerated and is a practical option for anxious patients.

Adjunctive measures

Oral corticosteroid for severe cases: prednisolone 20 to 30 mg daily for 5 to 7 days, or a short tapering course, which substantially reduces the rebound obstruction and improves the chance of successful withdrawal. Use the standard cautions in diabetes, peptic ulceration, hypertension and psychiatric illness.
Nasal saline irrigation two or three times daily, which relieves dryness, removes crusts and gives the patient something active to do in place of the spray. This behavioural substitution is genuinely useful.
Oral decongestant such as pseudoephedrine 60 mg three times daily for up to 5 days during the withdrawal period, in patients without hypertension, ischaemic heart disease, arrhythmia, hyperthyroidism or prostatic obstruction. This provides some relief without perpetuating the local receptor problem.
Sleep with the head elevated.
Humidification and emollient nasal preparations for dryness and crusting.
Treat the underlying condition: intranasal steroid and antihistamine for allergic rhinitis, ipratropium for vasomotor rhinorrhoea, and management of chronic rhinosinusitis.

Follow up and surgery

Review at 2 to 4 weeks to confirm cessation and mucosal improvement, and again at 3 months.
Most patients recover normal mucosal function within 4 to 12 weeks. Persistent obstruction beyond this suggests either continued covert use, or a genuine underlying structural or inflammatory problem.
Only after complete withdrawal and adequate medical therapy should surgery be considered. Turbinate reduction with tissue sparing technique and septoplasty are appropriate where genuine structural obstruction persists.
Operating on a patient still using decongestants is futile, since the mucosal changes will not resolve and the patient will resume spray use afterwards.

Prevention

Never prescribe or recommend topical decongestants for more than 5 days, and state the limit explicitly rather than assuming it is understood.
Provide a specific alternative for the underlying condition at the time of prescribing, so the patient has somewhere to go when the 5 days end.
Ask about over the counter nasal spray use in every patient presenting with nasal obstruction, since it will not be volunteered.

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

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.

Rhinitis Medicamentosa

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management