Vasomotor Rhinitis

The largest subgroup of nonallergic rhinitis, characterised by nasal obstruction and rhinorrhoea triggered by non allergic physical and chemical stimuli, with no demonstrable allergic sensitisation, infection or structural cause. It is also termed idiopathic rhinitis, which is a more honest label since the vasomotor mechanism is only partly established.

Pathophysiology

Three interacting mechanisms are recognised.

• Autonomic imbalance with parasympathetic predominance. The nasal mucosa receives parasympathetic secretomotor fibres travelling from the superior salivatory nucleus through the nervus intermedius, greater petrosal nerve and vidian nerve to the sphenopalatine ganglion, from which postganglionic fibres supply the glands and vessels. Increased cholinergic tone produces glandular hypersecretion and venous sinusoid engorgement. Sympathetic fibres from the superior cervical ganglion travel with the deep petrosal nerve and produce vasoconstriction; relative sympathetic underactivity contributes to congestion.
• Sensory nerve hyperreactivity. Trigeminal C fibres expressing transient receptor potential vanilloid 1 and transient receptor potential ankyrin 1 channels are activated by cold air, capsaicin, irritants and osmotic change, releasing substance P and calcitonin gene related peptide with neurogenic inflammation, and triggering a central parasympathetic reflex. This mechanism explains the trigger profile and is the rationale for capsaicin treatment and for neurectomy.
• Exaggerated nasal cycle. The normal alternating congestion and decongestion of the turbinates, occurring over 2 to 6 hours, becomes symptomatically apparent, producing the characteristic alternating obstruction.

Epidemiology: onset typically after the third or fourth decade, more common in women, with no atopic family history, and frequently precipitated by an upper respiratory infection or a chemical exposure.

• Nasal obstruction that alternates between sides and is markedly positional, worse on lying and worse on the dependent side.
• Watery rhinorrhoea, sometimes profuse enough to require constant tissue use.
• Postnasal drip, throat clearing and chronic cough.
• Absence of itch, absence of significant sneezing and absence of ocular symptoms. Their absence separates this from allergic disease more reliably than any test.
• Perennial symptoms with no seasonality and no relation to pets, dust or pollen.

Characteristic triggers

• Cold air and sudden temperature change, particularly moving from a warm building into cold air.
• Strong odours and irritants: perfume, cleaning products, bleach, paint, tobacco smoke, cooking odours.
• Changes in humidity and barometric pressure, so symptoms track weather change.
• Alcohol, particularly red wine and beer, through a vasodilatory mechanism rather than an allergic one.
• Spicy and hot food, producing gustatory rhinorrhoea.
• Bright light.
• Emotional stress and sexual arousal, both mediated autonomically.
• Exercise, which usually improves nasal patency through sympathetic activation, so worsening with exercise is atypical.

Examination

• Turbinates may be erythematous, boggy or normal. The appearance is not diagnostic.
• Clear secretions, and often visible pooling in the nasal floor.
• A normal middle meatus with no polyps and no purulence.
• Assessment of the septum, nasal valve and turbinate size, since structural obstruction commonly coexists and may be the more treatable component.
• Perform a Cottle manoeuvre and modified Cottle manoeuvre to assess nasal valve collapse, which is frequently missed in patients labelled vasomotor.

A diagnosis of exclusion supported by a characteristic trigger history.

• Nasal endoscopy in all patients, to exclude polyps, structural obstruction, neoplasm, adenoid hypertrophy and a cerebrospinal fluid leak.
• Skin prick testing or serum specific immunoglobulin E, which must be negative. Where testing is positive but clinical correlation is absent, the diagnosis may still be vasomotor rhinitis with incidental sensitisation.
• Nasal cytology to exclude non allergic rhinitis with eosinophilia syndrome, which requires a different treatment emphasis and responds well to corticosteroid.
• Nasal provocation testing where local allergic rhinitis is suspected, particularly in patients with a convincing allergic history but negative systemic testing.
• Medication review, since drug induced rhinitis mimics this condition exactly and resolves on withdrawal of the agent.
• Thyroid function testing.
• Beta 2 transferrin assay for unilateral watery rhinorrhoea.
• Computed tomography of the sinuses only where the endoscopy or history raises the possibility of sinus disease.
• Consider intranasal drug use, particularly cocaine, which is often not volunteered.

Treatment is directed at the dominant symptom, since no single agent addresses both obstruction and rhinorrhoea well.

General measures

• Trigger identification and avoidance where practical: scarf over the nose in cold weather, avoidance of strong chemical odours, moderation of alcohol.
• Nasal saline irrigation once or twice daily, which reduces symptom scores and is well tolerated.
• Humidification in dry environments.
• Smoking cessation and removal from irritant occupational exposure.
• Substitution of causative medications where identified.

Rhinorrhoea predominant

• Intranasal ipratropium bromide is the treatment of choice, 42 micrograms per nostril two or three times daily, titrated to effect and up to 84 micrograms per nostril in refractory cases. It blocks the cholinergic drive to the seromucous glands and has no effect on obstruction. Onset is within 15 to 30 minutes.
• For gustatory rhinorrhoea, administer 30 to 60 minutes before meals.
• Adverse effects: nasal dryness in up to 20 percent, crusting, epistaxis and headache. Systemic anticholinergic effects are minimal but caution applies in narrow angle glaucoma, bladder outflow obstruction and myasthenia.

Obstruction predominant

• Intranasal corticosteroid: mometasone furoate 100 to 200 micrograms per nostril once daily, or fluticasone propionate 100 micrograms per nostril twice daily. The evidence is weaker than in allergic rhinitis, and the response is more variable, but a 4 to 6 week trial is justified given the safety profile. Patients with nasal eosinophilia respond best.
• Topical decongestants provide relief but must be limited to 5 days, and this population is at particular risk of rhinitis medicamentosa because the underlying condition is chronic and the relief is immediate. Warn explicitly.

Mixed symptoms

• Intranasal azelastine 137 micrograms per nostril twice daily has established efficacy in vasomotor rhinitis, acting through mast cell stabilisation and effects on sensory nerve activation in addition to histamine antagonism. It is one of the few agents with positive trial evidence in this specific condition.
• Combination azelastine with fluticasone propionate in one device is the most effective medical option for patients with both obstruction and rhinorrhoea, and is a reasonable second line after single agent failure.
• Oral antihistamines have no established role and should be stopped if ineffective.

Capsaicin

• Intranasal capsaicin defunctionalises the trigeminal C fibres responsible for the sensory hyperreactivity, and is the medical treatment with the most specific mechanistic rationale in this condition.
• Administered as five applications over one day, or as a weekly series, after topical anaesthesia with lidocaine.
• Produces symptom reduction lasting 6 to 12 months, with repeat courses possible.
• Severe burning at the time of application is universal and limits its acceptability, and it is available in a limited number of specialist centres.

Surgical management

Reserved for patients who fail full medical therapy.

• Turbinate reduction for obstruction with genuine turbinate hypertrophy demonstrated after decongestion. Use tissue sparing techniques: submucosal diathermy, radiofrequency ablation, microdebrider assisted submucous resection, or submucous resection with mucosal preservation. Total or near total turbinectomy must not be performed, given the risk of atrophic rhinitis and empty nose syndrome.
• Septoplasty where deviation contributes to fixed obstruction. Explain that septoplasty will not address rhinorrhoea or the alternating component of the obstruction, since disappointed expectations after septoplasty for vasomotor symptoms are a frequent source of complaint.
• Posterior nasal neurectomy, in which the posterior nasal branches of the sphenopalatine nerve are divided endoscopically at the sphenopalatine foramen. It produces durable improvement in rhinorrhoea and obstruction in the majority, is more selective than vidian neurectomy, and avoids the dry eye that complicates the vidian approach.
• Cryoablation of the posterior nasal nerve, delivered endoscopically under local anaesthesia in the outpatient setting, which offers similar benefits with lower morbidity and is increasingly used.
• Vidian neurectomy, now largely superseded, carries a substantial risk of dry eye through interruption of lacrimal secretomotor fibres, along with palatal numbness and dryness.

Counselling and follow up

• Explain clearly that this is a chronic condition with treatments that control rather than cure, that triggers will continue to provoke symptoms, and that response varies between individuals so a stepwise trial of agents is necessary.
• Review at 6 to 8 weeks with each intervention before declaring failure.
• Reassess the diagnosis in non responders, specifically re examining for structural obstruction, nasal valve collapse, local allergic rhinitis, occult sinus disease and drug induced causes.