Allergic Rhinitis

Allergic rhinitis is an IgE-mediated inflammatory response of the nasal mucosa to an inhaled allergen — pollen, dust mites, animal dander, or mold — producing sneezing, rhinorrhea, nasal and ocular itch, and congestion, frequently alongside allergic conjunctivitis.^[1]

An early phase driven by mast-cell degranulation and histamine release produces the itch, sneeze, and rhinorrhea symptom cluster within minutes of exposure; a later, eosinophil-driven inflammatory phase over the following hours is chiefly responsible for nasal congestion, which is why congestion often responds better to an anti-inflammatory intranasal corticosteroid than to an antihistamine alone.^[2]

The Allergic Rhinitis and its Impact on Asthma (ARIA) classification describes allergic rhinitis by symptom pattern (intermittent or persistent) and severity (mild or moderate-severe) rather than by season alone, since seasonal and perennial exposure patterns do not reliably predict either the duration or the severity of symptoms — see Choose Initial Treatment for the full classification and the treatment tracks it drives.

Nasal and ocular symptoms

Nasal congestion, clear rhinorrhea, paroxysmal sneezing, and nasal itch are the hallmark symptoms, often with a sensation of postnasal drip. Ocular symptoms — itching, redness, tearing, and mild lid swelling (allergic conjunctivitis) — accompany nasal symptoms in most patients and can be as bothersome as the nasal symptoms themselves.

Physical examination findings

The nasal mucosa is typically swollen, pale, or bluish, and moist on examination with an ordinary otoscope. Other supportive findings include infraorbital edema and darkening ("allergic shiners"), a transverse nasal crease from repeated upward rubbing of the nose (the "allergic salute"), cobblestoning of the posterior oropharynx from chronic postnasal drip, and conjunctival redness or swelling.

Symptom pattern

Symptoms may follow a recognizable seasonal pattern tied to a specific pollen (tree, grass, or weed), or occur year-round (perennial), typically from indoor allergens such as dust mites, animal dander, or mold, flaring after specific exposures. See Choose Initial Treatment for how the ARIA intermittent/persistent and mild/moderate-severe classification is used to select therapy.

• Personal history of another atopic condition — asthma, atopic dermatitis, allergic conjunctivitis, or food allergy.
• Family history of allergy or atopy.
• Regular exposure to an environmental allergen the patient is sensitized to — seasonal (tree, grass, or weed pollen) or perennial (dust mites, animal dander, indoor mold).
• Occupational allergen exposure (e.g., laboratory animals, flour, latex).
• Concomitant use of ASA or NSAIDs, which can precipitate nasal symptoms in ASA-intolerant individuals.
• Certain medications that cause or worsen nasal congestion independent of allergy — ACE inhibitors, sildenafil, and other phosphodiesterase-5 inhibitors among them.
• Urban residence and higher-pollution environments.

Differentiating allergic rhinitis from its common mimics

Local allergic rhinitis is a distinct, increasingly recognized entity: patients have classic allergic symptoms and a positive response to allergy-directed therapy, but negative skin-prick and serum-specific IgE testing — the allergic response is confined to the nasal mucosa itself and is only demonstrable with a nasal allergen challenge. Consider it when convincing allergic symptoms persist despite negative standard allergy testing, rather than concluding the symptoms are not allergic in origin. Non-allergic rhinitis is a broader category of nasal symptoms without an IgE-mediated mechanism, including vasomotor rhinitis (above), rhinitis of pregnancy, drug-induced rhinitis, and rhinitis medicamentosa from decongestant overuse — consider these when symptoms do not fit an allergic pattern or fail to respond to allergy-directed therapy.

History

• Characterize symptoms — congestion, nasal itch, rhinorrhea, sneezing, postnasal drip, ocular symptoms — along with their frequency and severity.
• Establish the duration and pattern of symptoms (intermittent versus persistent) to apply the ARIA classification.
• Identify precipitating factors, including specific environmental allergens such as pollen and animal dander.
• Ask about personal or family history of allergy or atopy.
• Screen for comorbid conditions — sleep apnea or snoring, asthma, and conjunctivitis.
• Take a medication history: intermittent ASA or NSAID use can precipitate nasal symptoms in ASA-intolerant individuals, and some drugs (ACE inhibitors, sildenafil, and other PDE5 inhibitors) can cause nasal congestion independent of allergy.
• Ask about prior self-treatment, including over-the-counter products, and how well they controlled symptoms.

Physical examination

Examine the nasal mucosa (colour, anatomy) with an ordinary otoscope, and look for infraorbital edema (allergic shiners), conjunctival redness or swelling, a transverse nasal crease, cobblestoning of the posterior oropharynx, and evidence of postnasal drip.

Objective testing

In vitro measurement of allergen-specific IgE (ELISA, previously performed as RAST) is an acceptable alternative but is more expensive and less sensitive than skin testing.

Not indicated: measuring total serum IgE has little diagnostic value, since it does not correlate well with the presence of allergic disease.

• Prevent allergic symptoms from occurring by reducing exposure to the causative allergen(s).
• Suppress and control the symptoms produced by the allergic response — nasal and ocular.
• Avoid or minimize medication side effects, including any negative impact on daily activities.
• Minimize interference with school or work performance and attendance, leisure activities, and sleep.

Allergen avoidance

• Pollen: use air conditioning to allow windows to stay closed, reducing exposure; nasal filters worn during high-exposure activities have demonstrated efficacy in reducing nasal and ocular symptoms in clinical trials.
• Animal dander: removing pets from the home reduces perennial symptoms caused by that exposure.
• Dust mites: impermeable covers for the mattress and pillows may reduce exposure; historical trial evidence for this measure has been mixed, though a more recent trial in dust-mite-allergic asthmatic children showed a reduction in asthma-related emergency visits over the following year. Acaricides (products that kill mites) have shown minimal added benefit in reducing symptoms, and the long-term safety of regular acaricide use on bedding is not established.

Saline nasal irrigation

Intranasal saline sprays or irrigation systems help relieve symptoms by washing out mucus and inhaled allergen. Use only distilled water, or water that has been boiled and cooled, to prepare the solution, and clean the irrigation device routinely.

Ocular symptom relief

Lubricant eye drops, or cold or warm compresses, can reduce conjunctival symptoms without medication.

Correct intranasal spray technique — a major factor in real-world efficacy

Aim the spray toward the outer wall of the nostril (the turbinates), angled upward and laterally toward the tip of the ear — never medially toward the septum, which increases irritation and epistaxis risk while reducing the dose actually delivered to the affected mucosa.

Most devices need initial priming before first use, and re-priming if not used for a product-specific interval (commonly several days to weeks) — confirm the specific product's requirement, since an unprimed or under-primed device delivers less than the full labelled dose.

Use on a fixed daily schedule rather than only when symptoms flare, since continuous, consistent use is substantially more effective than as-needed use for an intranasal corticosteroid.

For a combination intranasal antihistamine/corticosteroid product, tilt the head slightly forward, not backward, during administration — tilting the head back allows the medication to drip into the throat, producing an unpleasant taste.

Allergen immunotherapy

Allergen immunotherapy (subcutaneous or sublingual) is the only currently available disease-modifying option — a specialist-directed course of escalating allergen exposure that can produce sustained benefit lasting years after treatment is stopped, unlike symptomatic drug therapy. It is administered and monitored by an allergist/immunologist, not initiated in primary care or by a pharmacist. Refer a patient with confirmed IgE-dependent sensitivity to a specific allergen that cannot be effectively avoided, and whose symptoms are difficult to control with standard pharmacotherapy.

Breastfeeding: preferred initial therapy is again a saline nasal spray or rinse. Second-generation antihistamines are generally considered safe, especially cetirizine and loratadine, along with intranasal and ophthalmic products; a theoretical reduction in milk supply is possible. Pseudoephedrine concentrates in breast milk, so a nasal decongestant is preferred over an oral one when a decongestant is needed — limit nasal decongestant use to a maximum of 5 days per episode. Intranasal corticosteroids are considered safe given low bioavailability. Montelukast concentrates in breast milk but is generally considered safe, and is commonly used directly in young children for asthma.

Pediatrics

Lower-volume nasal sprays (e.g., fluticasone furoate) tend to be better tolerated by children and are more effective than oral antihistamines for pediatric allergic rhinitis. If an antihistamine is used, a second-generation agent is strongly preferred, since sedating antihistamines are associated with drowsiness and learning impairment in children. Oral cough and cold preparations containing a decongestant, with or without a sedating antihistamine, should not be used in children under 6 years of age for allergic or viral rhinitis, per Health Canada's labelling decision based on limited efficacy evidence and reported adverse effects in this age group.^[6]

Intranasal corticosteroids and growth in children

Mometasone and fluticasone propionate have historically been favoured given low oral bioavailability and an absence of growth suppression with long-term use at recommended doses, though fluticasone propionate is scented and some children prefer an unscented product; mometasone and fluticasone furoate are both available unscented, and fluticasone furoate has the lowest spray volume of the intranasal corticosteroids. Budesonide dry-powder delivery is an alternative for a child who dislikes an aqueous spray, and had no measurable effect on growth at its standard once-daily dose in a controlled study. Growth suppression has been reported with high-dose beclomethasone (well above the standard recommended dose), with the lowest recommended dose of over-the-counter triamcinolone, and with double the usual approved pediatric dose of fluticasone furoate — whether this reduction is recovered over time is not established. Once-daily morning dosing may reduce growth-suppression risk relative to twice-daily dosing by more closely following the normal diurnal cortisol pattern, though comparative studies are still needed. Total corticosteroid burden should be considered when a child also uses an inhaled corticosteroid for asthma; regardless, always use the lowest effective intranasal corticosteroid dose in children.

Older adults

Avoid first-generation sedating antihistamines given anticholinergic burden, sedation, cognitive effects, and fall risk in this population.^[5] Among the second-generation agents, cetirizine is the most likely to cause some sedation, particularly at higher doses — consider a lower starting dose. Use oral or intranasal decongestants cautiously given a higher prevalence of hypertension, cardiovascular disease, benign prostatic hyperplasia, and hyperthyroidism in this population.

Hepatic and renal impairment

Reduce the starting dose of cetirizine to 5 mg daily in moderate hepatic or renal impairment, or in adults 65 years of age and older. Loratadine clearance is reduced in severe hepatic impairment — use a lower initial dose.

Reassess symptom control 2 to 4 weeks after starting or escalating an intranasal corticosteroid, since maximal effect takes this long even though some benefit can appear on the first day of use. Before concluding that a therapy has failed, confirm adherence and correct spray technique. If as-needed antihistamine use has become effectively daily, consider switching to a regularly scheduled intranasal corticosteroid instead. Reassess the diagnosis, including for a non-allergic or drug-induced cause, if symptoms persist despite confirmed adherence to an appropriate first-line regimen. Monitor growth in children on long-term intranasal corticosteroid therapy, particularly with an agent or dose associated with growth suppression, and use the lowest effective maintenance dose. For any patient using an intranasal decongestant, ask specifically about frequency and duration of use at follow-up to catch early rebound congestion. For a patient with a predictable seasonal pattern, plan to restart an intranasal corticosteroid 1 to 2 weeks before the next expected exposure period. Monitoring for a patient on allergen immunotherapy is specialist-directed.

1. Confirm adherence — was the medication actually used consistently as directed, particularly a daily intranasal corticosteroid rather than only as-needed use.
2. Confirm correct intranasal spray technique — aimed toward the outer wall of the nostril rather than the septum, and properly primed.
3. Reassess the diagnosis before assuming first-line therapy has failed — consider non-allergic rhinitis, local allergic rhinitis, vasomotor rhinitis, nasal polyps, rhinitis medicamentosa from decongestant overuse, or a drug-induced cause (an ACE inhibitor, a PDE5 inhibitor, or chronic ASA/NSAID use).
4. Step up per the treatment algorithm — switch to a combination intranasal antihistamine/corticosteroid product rather than empirically adding a separate oral antihistamine.
5. Add montelukast specifically if comorbid asthma or nasal polyps are present.
6. Consider a short 5 to 7 day course of oral prednisone for very severe breakthrough symptoms.
7. Refer to an allergist/immunologist per the criteria in Red Flags & Refer, including for consideration of allergen immunotherapy.

• Reaching for a first-generation sedating antihistamine as routine therapy, especially in older adults or in anyone whose occupation requires vigilance or concentration.
• Using an intranasal decongestant for more than 3 to 7 days, or without a concomitant intranasal corticosteroid — both increase the risk of rebound congestion (rhinitis medicamentosa).
• Expecting an intranasal corticosteroid to work immediately and abandoning it before a genuine, adherent 2 to 4 week trial.
• Relying on an oral antihistamine alone when nasal congestion is the predominant symptom — an intranasal corticosteroid is more effective for congestion specifically.
• Defaulting to a separate oral antihistamine as the step-up when an intranasal corticosteroid alone is inadequate, rather than a combination intranasal antihistamine/corticosteroid product with better supporting evidence.
• Not counselling correct spray technique and aim — directing the spray at the septum increases irritation and epistaxis risk while reducing the dose delivered where it is needed.
• Using an oral cough and cold combination product containing a decongestant and/or a sedating antihistamine in a child under 6 years of age.
• Missing a drug-induced or non-allergic cause of nasal congestion — an ACE inhibitor, a PDE5 inhibitor, chronic decongestant overuse, pregnancy, or hypothyroidism — when antihistamines and an intranasal corticosteroid are not working.
• Treating persistent unilateral symptoms, epistaxis, or facial pain as routine allergic rhinitis rather than investigating for a structural or neoplastic cause.
• Overlooking local allergic rhinitis in a patient with convincing allergic symptoms but negative skin-prick or serum-specific IgE testing.

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Intranasal corticosteroids

The mainstay of therapy for moderate-severe symptoms; more effective than an oral antihistamine or a leukotriene receptor antagonist, especially for congestion. A 2-4 week trial may be needed for maximal effect, though some benefit is often seen on the first day.

Second-generation (less-sedating) oral antihistamines

Preferred over first-generation agents for essentially every patient given a far lower sedation and anticholinergic burden.

First-generation (sedating) oral antihistamines

Generally avoid as routine therapy given sedation and anticholinergic burden, especially in older adults or safety-sensitive occupations — see Special Populations. Included here for completeness and for the uncommon situation where a second-generation agent genuinely cannot be used.

Antihistamine/decongestant oral combinations

Avoid in severe hypertension or coronary artery disease; use with caution in cardiovascular disease, diabetes, hyperthyroidism, prostatic hypertrophy, and angle-closure glaucoma. Avoid combination products with additional ingredients such as analgesics or expectorants, which have not been shown to add benefit in allergic rhinitis.

Oral decongestants

Note: oral phenylephrine's effectiveness for nasal congestion has not been well established, and — unlike pseudoephedrine — it is not available in Canada as a single-entity product or in combination with a less-sedating antihistamine.

Leukotriene receptor antagonists

Intranasal antihistamines

Faster onset than an intranasal corticosteroid (minutes rather than days), useful for breakthrough symptoms or the first 1-2 weeks of a new intranasal corticosteroid course.

Intranasal antihistamine/corticosteroid combinations

Shown to be superior to either component alone for moderate-severe symptoms; consider after intranasal corticosteroid monotherapy has failed a genuine trial, or when faster onset is important.

Intranasal decongestants

Never use beyond the stated duration limit, and always counsel this limit explicitly before dispensing — see Choose Initial Treatment and Common Errors for the rebound-congestion rationale.

Other intranasal therapies

Ophthalmic therapy for allergic conjunctivitis

Allergic conjunctivitis frequently accompanies allergic rhinitis; an oral or intranasal antihistamine, intranasal corticosteroid, or leukotriene receptor antagonist often improves ocular symptoms too, but a dedicated ophthalmic product can be added for insufficient relief.

Ophthalmic antihistamines and mast cell stabilizers

Regular use of a topical ophthalmic vasoconstrictor (e.g., naphazoline, oxymetazoline, or phenylephrine eye drops) is discouraged given the risk of rebound vasodilation with continued use.

Short-course oral corticosteroid

For very severe nasal symptoms only, as a brief bridge while other therapy takes effect — never a maintenance strategy for allergic rhinitis.

Evidence note: drug inventory, dosing, adverse effects, and comments reflect standard Canadian practice, cross-checked against the current ARIA-EAACI and Rhinitis 2020 practice-parameter evidence base.^[4][1]