MD Notes

creation date: 2025-09-08 16:16
tags: Pathologies

Allergic Rhinitis

Background

Definitions

Allergic rhinitis, sometimes referred to as allergic rhinosinuitis, is characterized by inflammation of the nasal mucosa leading to paroxysms of symptoms.

Allergic rhinitis is highly prevalent, especially in resource-abundant/urban areas, and is associated with other atopic conditions:

Local allergic rhinitis refers to allergic rhinitis without detectable specific IgE by allergen-specific skin prick testing.

In some terminology, allergic rhinitis is referred to as “seasonal” for symptoms that occur at a particular time of the year or “perennial” which occurs year-round.

Etiology

A number of allergens can cause allergic rhinitis.

Seasonal allergens include:

  • Pollen from trees (spring), grasses (early summer), and weeds

Perennial allergens include:

  • Dust mites
  • Cockroaches
  • Mold spores
  • Animal dander

Pathogenesis

IgE production
The genesis of allergic reactions begin with exposure to an allergen, of which allergen-specific IgE are produced. This marks the sensitization of the immune system to the allergen and subsequent inhalation of said allergen will trigger symptoms of allergic rhinitis.

Genetic disposition may increase the propensity to produce high levels of IgE in response to inhaled allergen. Additionally, atopy increases likelihood of Th2 lymphocytes responses.

The sensitization process can take several ears to occur.

Mast cell and basophil activation
IgE produced after sensitization reside on receptors found on mast cells and basophils which are cross-linked by allergens that results in rapid degranulation. This releases chemical mediators that stimulate blood vessels, nerves, and glands to cause the clinical manifestations of allergic rhinitis.

Effects of mediators
In the context of allergic rhinitis, histamine contributes to all acute symptoms. Other mediators such as prostaglandins, leukotrienes, platelet-activating factor, and bradykinin are affect some symptoms.

Cellular infiltration
Mast cell degranulation continues to amplify reactions including recruitment of eosinophils. Eosinophils further promote IgE production, mast cell growth, and inflammation.

Eosinophils also release oxygen radicals and proteins which cause epithelial injury and desquamation, subepithelial fibrosis, and hyperresponsiveness.

Clinical Presentation

Signs & Symptoms

Classic manifestation consist of paroxysms of:

  • Sneezing
  • Rhinorrhea
  • Nasal obstruction
  • Nasal itching

Other common symptoms include:

  • Postnasal drip
  • Cough
  • Irritability
  • Fatigue
  • Itching of palate and/or inner ear

Symptoms may coexist with allergic conjunctivitis which would present with bilateral itching, tearing, and/or burning of the eye.

Children may repeatedly snort, sniff, cough, and clear their throat as typically do not blow their nose. In some patients, sleep may be disturbed.

Physical findings may be present:

  • Infraorbital edema and darkening due to subcutaneous venodilation
  • Accentuated lines or folds below lower lids (Dennie-Morgan lines) - suggests concomitant allergic conjunctivitis
  • Transverse nasal crease from pushing tip of nose up
  • Allergic facies (seen in children) - highly arched palate, open mouth breathing, dental malocclusion
  • Pale blue/pallar with turbinate edema in nasal mucosa
  • Clear rhinorrhea
  • Hyperplastic lymphoid tissue in posterior pharynx (“cobblestoning”)
  • Tympanic membrane retract or serous fluid behind TM

History & Physical Exam

A detailed history may be sufficient for diagnoses alone, especially some forms of seasonal allergic rhinitis or if there is an obvious connection between exposure and onset of symptoms.

Questions that may elucidate cause include:

  • Personal past history
  • Family history of allergy
  • Variability based on setting (eg. on vacation)
  • Notable triggers of symptoms

Physical exam should include an HEENT exam.

Risk factors

Risk factors for allergic rhinitis include:

  • Presence of allergen-specific IgE
  • Personal or family history of atopy
  • Male sex
  • Birth during the pollen season
  • Firstborn status
  • Early use of antibiotics
  • Maternal smoking exposure in the first year of life
  • Exposure to indoor allergens, such as dust mite and molds
  • Serum IgE >100 international units/mL before age six years
  • Frequent respiratory tract infections or long-lasting infections
  • Tonsillectomy
  • Heavy traffic near the home
  • Consumption of drinks with preservatives/colorants
  • Living near a weedy area, an air-polluting factory, or a mine

Diagnosis

Criteria

Diagnosis is made clinically based on paroxysmal characteristic symptoms.

It should be noted that response to treatment is not definitive confirmation as common therapies are also effective for nonallergic rhinitis.

Classification of allergic rhinitis can be made to guide treatment:

  • Intermittent: <4 days/week or <4 weeks
  • Persistent: >4 days/week and >4 weeks
  • Mild: there is no sleep disturbance, impairment of activities, school, or work, or troublesome symptoms
  • Moderate-severe: there is sleep disturbance, impairment, and/or troublesome symptoms

Work-up

While a work-up is not required for presumptive diagnosis and treatment, allergy testing can aid in finding triggers when history alone is insufficient. Further evaluation may be indicated if symptoms prove difficult to manage as well.

This primarily consist of skin testing through allergist referral. In rare cases, serum IgE immunoassays and nasal cytology can be performed.

Differential

For children under 2 years of age, the differential diagnoses should be considered seriously as allergic sensitization takes a few years to develop:

  • Adenoidal hypertrophy
  • Acute or chronic sinusitis
  • Congenital abnormalities (choanal atresia)
  • Foreign bodies
  • Nasal polyps

For older children and adults, rhinitis can result from inflammatory or noninflammatory causes:

  • Acute infectious rhinitis (ie. common cold) - nasal symptoms, sore throat, then cough over course of few days
  • Chronic nonallergic rhinitis - perennial symptoms with mild/absent nasal itching and sneezing
  • Chronic rhinosinusitis - lasts >12 weeks and criteria involving the paranasal sinuses
  • Rhinitis medicamentosa - complication of vasoconstrictor nasal sprays or intranasal cocaine use
  • Rhinitis due to systemic medications - meds include birth control pills, antihypertensives, erectile dysfunction drugs, and NSAIDs
  • Atrophic rhinitis - progressive atrophy of nasal mucosa in older adults
  • Rhinitis associated with hormone changes - pregnancy or hypothyroidism related
  • Unilateral rhinitis or nasal polyps - nasal obstruction
  • Rhinitis with immunologic disorders - systemic autoimmune disorders may have rhinitis manifestations

Red Flags / Complications

Allergic rhinitis may develop into chronic rhinosinusitis where nasal inflammation with congestion and discharge persist for >3 months. Chronic inflammation can result in nasal polyps, which are typically benign (bilateral) but can be concerning if unilateral (malignancy).

Sensitization to allergens can cause adenoid hypertrophy and eustachian tube dysfunction. Allergic rhinitis can also be a risk factor for asthma.

Other complications include:

  • Otitis media with effusion
  • Persistent cough
  • Eosinophilic esophagitis

Management

Non-pharmacological

Non-pharmacological strategies are recommended for all patients regardless of use of pharmacologic treatments. This consist of:

  • Allergen avoidance
  • Nasal saline

Nasal saline may be sufficient in improving mild symptoms. They can also be administered prior to use of pharmacologic nasal sprays for improved efficacy. Patients should be educated on proper nasal saline use.

Pharmacological / Interventional

Pharmacotherapy is available for adults and children ≥2 years of age. The choice of therapy is based on severity and persistence (as defined above).

It should be noted that patients who self-treat tend to use non-optimal agents (eg. sedating antihistamines) and thus clinicians should focus on education on efficacy of various treatments.

Optimal nasal spray technique should be taught. For nonaerosol sprays:

  • Positioning the head to prevent spray from draining down throat by pointing head slightly downwards
  • Avoiding pointing the spray at the septum (to prevent irritation)
    For aerosol sprays:
  • Tilt head slightly back
  • Hold breath for few second after dispensing spray and exhaling through the mouth after
  • Avoid blowing nose for 15 minutes after use

Pre-treatment with nasal saline or decongestant spray can be considered.

Mild or intermittent symptoms
While treatment if best when taken regularly, mild or intermittent symptoms such as those to predictable allergen exposures (eg. relative’s pet), as needed use may be sufficient.

For patients with predictable seasonal allergies, initiating regular treatment a week or more prior to pollen season may be more effective.

Persistent or moderate-to-severe symptoms
Options are similar to mild/intermittent symptoms. Additionally, intranasal corticosteroids or antimuscarinics (or a combination of them) can be used as an adjunct.

Immunotherapy consisting of regular allergy injections are rare as they can be costly. Types include:

  • Subcutaneous immunotherapy (injection; generates more pronouced allergen-specific IgG4 responses)
  • Sublingual immunotherapy (oral induction)

References

Tools / Guidelines

Additional Reading