Nonallergic Rhinitis

Chronic nasal symptoms of obstruction, rhinorrhoea and postnasal drip in the absence of demonstrable allergic sensitisation, structural abnormality or infection. It accounts for roughly a quarter to a third of all rhinitis, and a further group have mixed allergic and non allergic disease.

Subtypes, which determine treatment

• Vasomotor or idiopathic rhinitis, the largest group, driven by autonomic dysregulation with parasympathetic predominance and sensory nerve hyperreactivity, mediated in part by transient receptor potential channel activation on trigeminal C fibres.
• Non allergic rhinitis with eosinophilia syndrome, characterised by perennial symptoms with more than 20 percent eosinophils on nasal cytology despite negative allergy testing, frequently associated with polyps, asthma and aspirin sensitivity, and notably responsive to intranasal corticosteroid.
• Drug induced rhinitis: angiotensin converting enzyme inhibitors, beta blockers including ophthalmic preparations, alpha blockers, phosphodiesterase 5 inhibitors, aspirin and nonsteroidal anti inflammatory drugs, oral contraceptives, chlorpromazine, gabapentin, and cocaine.
• Rhinitis medicamentosa from topical decongestant overuse.
• Hormonal rhinitis: pregnancy, particularly the second and third trimesters, resolving within 2 weeks of delivery; puberty; the menstrual cycle; oral contraceptives; and hypothyroidism, which produces mucosal oedema through glycosaminoglycan deposition.
• Occupational non allergic rhinitis from irritants including chlorine, ammonia, solvents, grain dust and cold air.
• Gustatory rhinitis: profuse watery rhinorrhoea within minutes of eating, particularly hot or spicy food, mediated purely by a cholinergic reflex.
• Atrophic rhinitis, primary and secondary.
• Senile or geriatric rhinitis, with watery anterior rhinorrhoea in the elderly from cholinergic hyperreactivity and loss of mucosal support.
• Local allergic rhinitis, in which allergen specific immunoglobulin E is produced locally in the nasal mucosa with negative skin tests and negative serum specific immunoglobulin E. It accounts for a meaningful proportion of patients previously labelled non allergic, and responds to immunotherapy.

• Nasal obstruction, frequently alternating between sides and changing with posture, which reflects an exaggerated nasal cycle.
• Watery rhinorrhoea, often profuse.
• Postnasal drip with throat clearing and cough.
• Absence of nasal, ocular and palatal itch, and relatively little sneezing. Itch and sneezing point to an allergic mechanism, and their absence is the most useful discriminating historical feature.
• Absence of conjunctival symptoms.
• Perennial rather than seasonal pattern, without relation to allergen exposure.
• Onset typically in adulthood, often after the fourth decade, in contrast to allergic rhinitis which usually begins in childhood or adolescence.
• No personal or family history of atopy, eczema or asthma in most.

Trigger pattern, which is diagnostic in vasomotor rhinitis

• Sudden temperature change, particularly moving from warm to cold air.
• Strong odours: perfume, cleaning products, smoke, paint, cooking smells.
• Changes in humidity and barometric pressure.
• Alcohol.
• Bright light, causing sneezing in the photic sneeze reflex.
• Emotional stress and sexual arousal.
• Exercise.

Examination

• Turbinates that are erythematous or normal in colour rather than the pale boggy appearance of allergic disease, though this distinction is unreliable in practice.
• Clear secretions.
• Assess for septal deviation, turbinate hypertrophy, polyps and structural obstruction.
• Examine for signs of hypothyroidism.
• In atrophic rhinitis: a wide roomy nasal cavity, foul greenish crusts, and paradoxical obstruction despite the enlarged airway.

Diagnosis is by exclusion of allergic and structural causes, together with recognition of the characteristic trigger pattern.

• Detailed history of triggers, medication, occupation, hormonal status and drug use including intranasal cocaine.
• Nasal endoscopy in every patient, to exclude polyps, structural obstruction, neoplasm and cerebrospinal fluid leak.
• Skin prick testing or serum specific immunoglobulin E, which must be negative to make the diagnosis. Remember that a positive test only confirms sensitisation, and clinical correlation with symptoms is required.
• Nasal cytology, showing eosinophilia above 20 percent in non allergic rhinitis with eosinophilia syndrome, which identifies a corticosteroid responsive group.
• Nasal allergen provocation testing where local allergic rhinitis is suspected, which is the only way to make that diagnosis. Measurement of nasal specific immunoglobulin E in nasal lavage supports it.
• Thyroid function testing.
• Beta 2 transferrin or beta trace protein assay on nasal fluid where unilateral clear watery rhinorrhoea raises the possibility of a cerebrospinal fluid leak, particularly if it increases on bending, straining or with a history of head injury or previous sinus surgery.
• Computed tomography of the sinuses where structural disease or rhinosinusitis is suspected, not routinely.
• Culture and, in atrophic rhinitis, specific culture for Klebsiella ozaenae, together with iron studies and syphilis serology where secondary causes are considered.

Differential diagnosis

• Allergic rhinitis, distinguished by itch, sneezing, seasonality, ocular symptoms and positive allergy testing.
• Chronic rhinosinusitis, distinguished by facial pressure, smell loss and objective findings.
• Cerebrospinal fluid rhinorrhoea.
• Sinonasal malignancy and inverted papilloma, in unilateral disease.
• Granulomatosis with polyangiitis and sarcoidosis, with crusting, granulation and septal perforation.
• Nasal obstruction from septal deviation, turbinate hypertrophy, nasal valve collapse and adenoid hypertrophy, which is structural rather than inflammatory and requires surgical rather than medical treatment.

Treatment is symptom directed, since there is no single unifying pathology.

General measures

• Identify and avoid triggers where practical: temperature extremes, strong odours, alcohol.
• Nasal saline irrigation with large volume isotonic solution once or twice daily, which is effective, safe and inexpensive, and particularly useful in atrophic and crusting disease.
• Humidification in dry environments.
• Smoking cessation.
• Review and where possible substitute causative medications, in discussion with the prescribing clinician. Angiotensin converting enzyme inhibitors and beta blockers are the commonest offenders and are frequently overlooked.

Pharmacological treatment by dominant symptom

Obstruction dominant:

• Intranasal corticosteroid, which is effective in vasomotor rhinitis and highly effective in non allergic rhinitis with eosinophilia syndrome: mometasone furoate 100 to 200 micrograms per nostril once daily, or fluticasone propionate 100 micrograms per nostril twice daily, used continuously with the same technique instructions and the same 2 week onset expectation as in allergic disease.

Rhinorrhoea dominant:

• Intranasal ipratropium bromide 42 micrograms per nostril two to three times daily, titrated to effect, which is the specific treatment for watery rhinorrhoea and is highly effective in vasomotor, gustatory and senile rhinitis. Adverse effects are dryness, crusting and epistaxis. Caution in narrow angle glaucoma and prostatic obstruction, though systemic absorption is minimal.
• For gustatory rhinitis, ipratropium taken 30 to 60 minutes before meals is the treatment of choice.

Mixed symptoms:

• Intranasal azelastine 137 micrograms per nostril twice daily, which is effective in non allergic rhinitis through mechanisms beyond histamine antagonism, including effects on sensory nerves and mast cell stabilisation. It is one of the few agents with proven efficacy in vasomotor rhinitis.
• Combination azelastine with fluticasone propionate in a single device for patients with both obstruction and rhinorrhoea.
• Oral antihistamines are generally ineffective in non allergic rhinitis and should not be continued if they produce no benefit.

Capsaicin

Intranasal capsaicin causes defunctionalisation of trigeminal C fibres through transient receptor potential vanilloid 1 receptor overstimulation. Administered as a series of applications, it produces sustained symptom reduction in idiopathic rhinitis lasting months. It is intensely irritant at the time of application and requires topical anaesthesia, and it is available in a limited number of centres.

Local allergic rhinitis

Treated as allergic rhinitis with intranasal corticosteroid and antihistamine, and allergen immunotherapy is effective, which is the practical reason to make the diagnosis.

Atrophic rhinitis

• Nasal irrigation with large volume alkaline saline several times daily to remove crusts, which is the mainstay.
• Glucose in glycerine 25 percent nasal drops or emollient preparations to reduce crusting and odour.
• Topical or systemic antibiotics for secondary infection, directed by culture, with ciprofloxacin or a culture directed agent for Klebsiella ozaenae.
• Correct iron deficiency and treat underlying causes.
• Surgical narrowing procedures, including submucosal implants, Young procedure with nasal vestibule closure, and medial displacement of the lateral nasal wall, for severe refractory primary atrophic rhinitis.
• Secondary atrophic rhinitis and empty nose syndrome following excessive turbinate resection are managed with humidification, irrigation and, in selected cases, submucosal implant augmentation of the turbinate remnant. Prevention through conservative turbinate surgery is far more effective than any treatment.

Surgical management

• Reserved for structural contributors: septoplasty for a deviated septum, and turbinate reduction for hypertrophy refractory to medical therapy.
• Turbinate reduction should be tissue sparing: submucosal diathermy, radiofrequency ablation, or submucous resection with preservation of the mucosa and as much of the turbinate as possible. Total turbinectomy should not be performed, since it causes atrophic rhinitis and empty nose syndrome, which are far worse than the original complaint and effectively untreatable.
• Vidian neurectomy and posterior nasal nerve section, which interrupt the parasympathetic supply, produce durable relief of rhinorrhoea in severe refractory vasomotor rhinitis. Vidian neurectomy risks dry eye from interruption of the lacrimal secretomotor fibres, and posterior nasal neurectomy, which is more distal and selective, largely avoids this and is the preferred modern approach. Cryoablation of the posterior nasal nerve is a less invasive alternative performed under local anaesthesia.

Follow up

Review at 6 to 8 weeks. Reassess adherence and technique. Where medical treatment fails entirely, re examine the diagnosis, obtain endoscopy and imaging, and consider local allergic rhinitis and structural obstruction before offering neurectomy.