Allergic Rhinitis

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Introduction and Terminology

The term "rhinitis" describes a symptom complex characterized by paroxysms of sneezing, nasal congestion, rhinorrhea, and itching of the nose. The different types of rhinitis are classified by pathogenic mechanism (eg, allergic rhinitis, infectious rhinitis). Although the term suggests inflammation, there are types of rhinitis where inflammation is not present (eg, vasomotor or atrophic rhinitis)[1]. The focus of this article is allergic rhinitis (AR), an IgE-mediated inflammatory condition. 


Atopic individuals respond to aeroallergen exposure by producing allergen-specific immunoglobulin E (IgE). These IgE antibodies attach to mast cells in the respiratory mucosa. Repeat allergen exposure causes IgE cross-linking at the mast cell surface which ultimately leads to the release of chemical mediators of inflammation. These mediators include histamine, leukotrienes, kinins, and prostaglandins. In some patients, this initial, immediate allergic response is followed by a late-phase reaction characterized by high levels of inflammatory mediators and invasion of the mucosa by inflammatory cells [2]. Continuous exposure to allergen over time may cause increased sensitivity (ie reaction to lower doses of allergen, known as priming) and hyper-reactivity (reaction to non-specific irritants such as smoke and strong odors) [3]. 


Allergic rhinitis affects as many as 40% of children in the US [1].

Risk Factors

  • Family history of AR or atopy
  • Personal history of asthma or eczema
  • Exposure to house dust mites
  • Maternal smoker during first post-natal year of life


The diagnosis of AR depends on the demonstration of a consistent symptomatic reaction to allergen. It is often made based on symptomatology, history, and supportive physical exam findings alone. Further evaluation is indicated if the symptoms prove difficult to manage or if the culprit allergen(s) is not identified.


Patients present with at least one of the following: sneezing, anterior or posterior rhinorrhea, congestion, itching of the nose. Rhinitis is often accompanied by symptoms affecting the eyes (conjunctivitis) and lower airways (cough). Children with perennial AR may endure significant impairment from their symptoms without awareness of the impact on quality of life. Untreated AR tends to negatively impact sleep, causing fatigue and day time sleepiness and is even associated with psychiatric and cognitive issues [3].


AR may be further sub-classified by temporal pattern of symptoms. Seasonal AR is caused by outdoor allergens such as tree, grass, and ragweed pollen that vary by region and time of year. Perennial AR is caused by year-round exposure, usually to indoor allergens (eg, dust mites, pet dander, and cockroaches). In subtropical and tropical climates, pollen may be present year-round, causing symptoms of perennial AR. Episodic AR is caused by exposure to allergens that are not present in the patient's usual environment, such as visiting a home with pets [1]. A good history might be enough to diagnose seasonal or episodic AR, while the culprit allergen in perennial AR is not often readily apparent.

Physical Exam

Suggestive findings on physical exam include:

  • Afebrile
  • Pale and boggy nasal mucosa, may be pale blue
  • Dark circles under the eyes thought to be secondary to venous congestion ("allergic shiners")
  • Horizontal crease on the nose due to allergic "salute"
  • "Rabbit nose"
  • Evidence of allergies such as eczema
  • Mouth breathing

Allergen-Specific Testing​

Allergy testing is discussed in more detail in a separate article. Skin and in-vitro allergy testing may be used to show sensitization to allergen. Sensitization is required for an allergic response, but not every patient who is sensitized to an allergen will manifest the symptoms of an allergic reaction upon exposure. Therefore, allergy testing is not entirely specific for the diagnosis of AR. It is also not entirely sensitive, as patients with a negative allergy test may have "local AR", in which the systemic response to allergen exposure is absent.   

Differential Diagnosis

  • Chronic nonallergic rhinitis
  • Chronic rhinosinusitis
  • Infectious rhinitis
  • Adenoidal hypertrophy
  • Choanal atresia
  • Unilateral rhinitis and nasal polyps
  • Foreign body
  • Rhinitis due to systemic medication

Because sensitization takes years to develop, AR should be lower on the differential for children under the age of 2 who present with rhinitis [3].


  1. Antihistamines- Competitive inhibitors for histamine at the mast cell H1 receptor sites. May also be related to anticholinergic affect. Should be given prior to exposure if possible. Peak levels at 5-7 hours after dose.
    1. First generation- Penetrate the central nervous system (CNS) and cause drowsiness, slow reaction time, and impair learning. (Benadryl, Brompheneramine, and Chlortrimeton)
    2. Second generation- Lipophobic and will not cross into the CNS. Less frequent dosing than first generation. (Claritin and Zyrtec)
    3. Intranasal
  2. Decongestants- Decrease blood flow to the tissues and improve patency of the nasal passages. May be combined with antihistamines. Topical decongestants may cause rhinitis medicamentosa which increases obstruction and should not be used for longer than 3 days.
  3. Intranasal Steroids- These are anti-inflamatory and decrease mucous production and edema. Should be used regularly rather than on an as-needed basis. Twice a day dosing. There are no associated systemic effects. Some believe intranasal steroids should be the first line of therapy (e.g. Vancenase, Beconase, Flonase, Nasacort).
  4. Cromolyn- Inhibits the release of histamine, and anti-inflammatory activity. Used as a maintenance prophylaxis. Very good safety record and well tolerated. Needs to be given initially four times a day, therefore compliance may be a problem.
  5. Leukotiene blockers- Can be useful especially in combination with first line therapies (e.g. Montelukast/Singulair).
  6. Immunotherapy- Alters the immune reactivity to antigens. May take up to 6-12 months to see results. Should be saved for selected patients that have failed medical management or have had intolerable side effects from medications. Should be skin tested and evaluated by a pediatric allergist. Make sure that positive skin test correlate with the symptoms.  Skin tests should not be performed on children <3 y.o.
  7. Environmental changes - Avoidance of allergens
    1. Eliminate dust and dust mites in the environment as best as possible
      1. Mattress covers
      2. Keep humidity down to decrease mold exposure.
      3. Eliminate carpeting and stuffed animals.
    2. Air conditioners and air purifiers
    3. Avoid pets if possible
    4. Keep windows closed at night and the early morning when the pollen counts are highest.
    5. Wash child's hair and pets frequently to eliminate the carriage of pollen and allergens
    6. Decrease mold exposure in the home.
    7. Avoid cigarette smoke
    8. Dust mite elimination.


1. Dykewicz MS, Wallace DV, Amrol DJ, et al. Rhinitis 2020: A practice parameter update. J Allergy Clin Immunol 2020; 146:721.

2. deShazo, RD and Kemp, SF. Pathogenesis of allergic rhinitis (rhinosinusitis). In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2021.

3. deShazo, RD and Kemp, SF. Allergic rhinitis: Clinical Manifestations, epidemiology, and diagnosis. In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2021.

4. Todd A. and Sheth K. Update on Allergic Rhinitis. Pediatrics in Review August 2005

5. Marks M: Physical Signs of Allergy of the Respiratory Tract in Children. New York, American College of Allergy, Asthma and Immunology, 1990

6. Fireman P. Therapeutic Approaches to Allergic Rhinitis.  Treating the child.  J. of Allergy and clinical Immunology 2000; 105 S 616-21.

7. Diagnosis and Management of Rhinitis: Updated Practice Parameter.  Journal of Allergy and Clinical Immunology.  2008;122 S1-84.

8. Rachelefsky,g. and Farrar JR. A Control Model to Evaluate Pharmocotherapy for Allergic Rhinitis in Children.  JAMA Pediatrics March 2013