Pediatric Allergic Rhinitis 

Updated: Jun 04, 2021
Author: Jack M Becker, MD; Chief Editor: Harumi Jyonouchi, MD 

Overview

Practice Essentials

Allergic rhinitis usually presents in early childhood and is caused by an immunoglobulin E (IgE)-mediated reaction to various indoor and outdoor allergens. An IgE-mediated reaction is when an allergen, that the body has previously recognized and processed to create IgE, is reintroduced. The previously made IgE is attached to a MAST cell and when 2 IgEs on that mast cell attach to the same antigen, it triggers the mast cell to degranulate and trigger the reaction. The degranulation releases mediators such as histamines and leukotrienes. In the case of allergic rhinitis, the reaction takes place in the nasal passages. The reaction is the same for all allergic reactions. Sensitization to indoor allergens can occur in allergic rhinitis in children older than 2 years; however, sensitization to outdoor allergens is more common in children older than 4–6 years. Clinically significant sensitization to indoor allergens may occur in children younger than 2 years, but this is unusual. In the very young, there is a significant chance of a false-positive test, commonly secondary to atopic dermatitis. The most common indoor allergens include dust mites, pet danders, cockroaches, molds, and pollens.

Signs and symptoms

The history of the patient with allergic rhinitis is usually straightforward, but at times may have a complex set of symptoms. The diagnosis is easy to make in a patient with a new pet or with symptoms that have distinct seasonal variation. Alternatively, younger patients may present with varying signs or symptoms, the family may not appreciate the nasal stuffiness, but may note the chronic nasal congestion. At times, a young child presents with what appears as seasonal allergies, when in fact it is a pet allergy, since the dander is shed in the spring and reaccumulates in the fall. In older children, symptoms may have been present for years and, therefore, appear to be less severe, because the child has accommodated them. Also making diagnosis challenging is that symptoms of an upper respirtory illness can mimic allergies, convincing  patients that they have an allergy. This is especially true in the fall season with rhinovirus.

Signs and symptoms of pediatric allergic rhinitis include the following:

  • Rhinorrhea, nasal congestion, postnasal drainage

  • Pale nasal turbinates, with or without clear nasal discharge

  • Repetitive sneezing

  • Itching of the palate, nose, ears, or eyes

  • Snoring

  • Frequent sore throats

  • Constant clearing of the throat, cough

  • Headaches

See Clinical Presentation for more detail.

Diagnosis

A full examination to detect other diseases should be performed. Other diagnoses such as adenoidal hypertrophy, asthma, eczema, gastroesphogeal reflux, and cystic fibrosis, which occur in children in connection with allergic rhinitis, should be suspected. Evaluation of the child involves the head, eyes, ears, nose, and throat, and can include the following:

  • Head: Allergic shiners (dark, puffy, lower eyelids), Morgan-Dennie lines (lines under the lower eyelid), transverse crease at lower third of nose secondary to nose rubbing as in the allergic salute

  • Eyes: Marked erythema of palpebral conjunctivae and papillary hypertrophy of tarsal conjunctivae; chemosis of the conjunctivae, usually with a watery discharge; in severe cases, cataracts from severe rubbing secondary to itching

  • Ears: Chronic infection or middle ear effusion

  • Nose: Enlarged turbinates with pale-bluish mucosa due to edema; clear or white nasal discharge (rarely yellow or green); dried blood secondary to trauma from nose rubbing; rarely, polyps (if polyps detected on rhinoscopy, mandatory workup for cystic fibrosis in children)

  • Throat: Discoloration of frontal incisors, high arched palate, and malocclusion associated with chronic mouth breathing; cobblestoning in the posterior pharynx secondary to chronic nasal congestion and postnasal drainage

Testing

No laboratory studies are needed in allergic rhinitis if the patient has a straightforward history. When the history is confusing, various studies are helpful, including the following:

  • Skin testing: highly sensitive and specific for aeroallergens

  • Allergen-specific IgE: can be helpful if a specific allergen is suspected

  • Serum IgE: elevated IgE value is suggestive of allergic rhinitis; it is not as sensitive as skin-prick testing and thus is rarely used today due to its limited utilty

  • Nasal smear: commonly used in the past, but with present lab regulations it is now rarely performed

Imaging studies

In general, imaging studies are not needed in pediatric allergic rhinitis unless sinusitis is suspected. In such cases, a limited computed tomography scan of the sinuses (without contrast) is indicated.

Procedures

Allergy skin testing is useful to identify suspected allergens. Testing can be done by both skin-prick or intradermal skin testing.

Spirometry maybe considered because as many as 70% of children with asthma have concomitant allergic rhinitis.

Rhinoscopy can be helpful in direct examination of the upper airway for identification of an obstructive versus infectious etiology of the rhinitis and for evaluation of nasal polyposis.

See Workup for more detail.

Management

Treatment of allergic rhinitis can be divided into 3 categories:

  • Avoidance of allergens or environmental controls

  • Medications

  • Allergen-specific immunotherapy (subcutaneous injection or sublingual tablet)

Pharmacotherapy

Many groups of medications are used for allergic rhinitis, including antihistamines, corticosteroids, decongestants, saline, sodium cromolyn, and antileukotrienes. These can be further subdivided into intranasal and oral therapies.

The following medications are used in pediatric patients with allergic rhinitis:

  • Second-generation antihistamines (eg, cetirizine, levocetirizine, loratadine, desloratadine, fexofenadine)

  • Intranasal antihistamines (eg, azelastine, intranasal olopatadine)

  • Intranasal corticosteroids (eg, intranasal beclomethasone, intranasal budesonide, intranasal ciclesonide, intranasal flunisolide, intranasal fluticasone, intranasal mometasone, intranasal triamcinolone)

  • Intranasal antihistamine/corticosteroid (eg, azelastine/fluticasone intranasal)

  • Intranasal decongestants (eg, ipratropium intranasal)

  • Intranasal mast cell stabilizers (eg, intranasal cromolyn sodium)

  • Leukotriene receptor antagonists (eg, montelukast)

Nonpharmacotherapy

The following are management options in allergic rhinitis that don’t involve medications:

  • Allergen-specific immunotherapy: The only form of therapy that can cure allergy symptoms; must be customized to the patient's individual allergies

  • Saline nasal irrigation: Effective in approximately 50% of patients with allergic rhinitis

  • Removal of the trigger, if identified

Surgical option

No routine surgical care is needed for pediatric allergic rhinitis. However, in selected patients, the following surgical intervention may be performed to provide some relief:

  • Adeniodectomy

  • Turbinectomies

  • Nasal polypectomy

See Treatment and Medication for more detail.

Background

Although allergic rhinitis (AR) is a common disease, the impact on daily life cannot be underestimated. Some patients find AR to be just as debilitating and intrusive as severe asthma. Employees with untreated allergies are reportedly 10% less productive than coworkers without allergies, whereas those using allergy medications to treat AR were only 3% less productive.[1] This suggests that effective medications may reduce the overall cost of decreased productivity.

AR is caused by an immunoglobulin E (IgE)–mediated reaction to various allergens in the nasal mucosa. The most common allergens include dust mites, pet danders, cockroaches, molds, and pollens. For example, tree pollen allergen binds to IgE antibodies that are attached to a mast cell via Fcε receptor. When 2 IgE molecules bind to the same tree pollen allergen, they cause the mast cell to fire off (degranurate), leading to release of various inflammatory mediators that cause the symptoms we recognize as AR, including sneezing; nasal congestion; stuffiness; rhinorrhea (runny nose); cough; itching of the nose, eyes, and throat; sinus pressure; headache; and epistaxis (bloody nose).

The allergens present in the outdoor environment vary with the time of year and location. Knowing what allergens are in the environment at a specific time of year helps in diagnosing and treating AR and helps in excluding allergy as a cause of the patient's symptoms. For example, a patient who presents with nasal congestion in November in Boston, Massachusetts cannot have allergic rhinitis attributed to tree pollen allergy, which is prevalent in spring.

Allergen exposure likely causes both upper and lower airway inflammation, meaning that both the nose and the lungs may be involved. Many experts believe that a patient's airway needs to be evaluated as a total entity, not as individual parts. It is referred to as the one airway hypothesis. Studies have shown that most pediatric patients with asthma also have AR. Guidelines regarding the impact of AR on asthma have been established.[2] Allergic reactions of the upper airway can trigger lower airway symptoms and vice versa. One study showed that patients with untreated AR and asthma have an almost 2-fold greater risk of having an emergency department visit and almost a 3-fold greater risk of being hospitalized for an asthma exacerbation, respectively.[3] Similarly there are studies that reveal treatment of one disease entity improves the other.

The graphs below detail the significant impact of nasal allergies.

Impact of nasal allergies. Impact of nasal allergies.
How patient feel when they have allergy symptoms. How patient feel when they have allergy symptoms.
Nasal symptoms and affect on work performance. Nasal symptoms and affect on work performance.

Pathophysiology

Understanding the function of the nose is important in order to understand allergic rhinitis (AR). The purpose of the nose is to filter, humidify, and regulate the temperature of inspired air. This is accomplished on a large surface area spread over 3 turbinates in each nostril. A triad of physical elements (ie, a thin layer of mucus, cilia, and vibrissae [hairs] that trap particles in the air) accomplishes temperature regulation. The amount of blood flow to each nostril regulates the size of the turbinates and affects airflow resistance. The nature of the filtered particles can affect the nose. Irritants (eg, cigarette smoke, cold air) cause short-term rhinitis; however, allergens cause a cascade of events that can lead to more significant, prolonged inflammatory reactions.

In short, rhinitis results from a local defense mechanism in the nasal airways that attempts to prevent irritants and allergens from entering the lungs.

Allergic reactions require exposure and then sensitization to allergens. To be sensitized, the patient must be exposed to allergens for a period of time. Sensitization to highly allergenic indoor allergens can rarely occur in children younger than 2 years. Sensitization to outdoor allergens usually occurs when a child is older than 3–5 years, and the average age at presentation is 9–10 years. The allergic reaction begins with the cross-linking of the allergen to 2 adjacent IgE molecules that are bound to high-affinity Fcε receptors on the surface of a mast cell. This cross-linking causes mast cells to degranulate, releasing various mediators. The best-known mediators are histamine, prostaglandin D2, tryptase, heparin, and platelet-activating factor, as well as leukotrienes and other cytokines.

These substances produce 2 types of reactions: immediate and late-phase. The immediate reactions in the nasal mucosa induce acute allergy symptoms (eg, nasal itch, clear nasal discharge, sneezing, congestion). The late-phase reaction occurs hours later, secondary to the recruitment of inflammatory cells into the tissue by the action of mediators (termed chemokines) released by the mast cell. Recruited cells are predominately the eosinophils and basophils, which, in turn, release their inflammatory mediators, leading to continuation of the cascade. In very sensitive individuals, this allergen-induced nasal inflammation causes priming of the nasal mucosa. Primed nasal mucosa becomes hyperresponsive, at which point even nonspecific triggers or small amounts of the antigen can cause significant symptoms.

Frequency

United States

Prevalence in the United States is 10–20%.[4] One survey demonstrated rates as high as 38.2% when patients were asked if they experienced fewer than 7 days of symptoms. When allergic rhinitis was defined as symptoms lasting more than 31 days, prevalence dropped to 17%.

International

In temperate areas of Europe and Asia, frequency is similar to that in the United States.

Mortality/Morbidity

Mortality is not associated with allergic rhinitis (AR), but significant morbidity occurs. Morbidity is manifested in several ways. Annually, an estimated 824,000 school days are missed, and an estimated 4,230,000 days of reduced quality-of-life functions are reported.[5] Comorbidity of other atopic diseases (asthma, atopic dermatitis) or upper airway inflammation (sinusitis, otitis media) is significant in AR. Individuals with AR have a higher frequency of these conditions than individuals without AR.

Quality-of-life surveys have revealed that patients with significant AR found symptoms to be just as debilitating as symptoms in patients with moderate-to-severe asthma. Patients with AR felt they were equally impaired and unable to participate in the activities of normal living similar to those with the moderate-to-severe asthma. They felt that chronic congestion, sneezing, the need to wipe the nose, and a decrease in restful sleep compromised levels of their daily activity.

The financial cost of AR is difficult to estimate. Self-treating patients are estimated to spend an average of 56 dollars per year. The direct cost of prescription medication exceeds 6 billion dollars per year worldwide, and lost productivity is estimated at 1.5 billion dollars per year.

Epidemiology

Race-, sex-, and age-related demographics

Allergic rhinitis (AR) has no race predilection; however, individuals from nonwhite backgrounds seek out medical attention less often than whites. The incidence is higher in urban and suburban areas versus more rural ones.

AR has no sex predilection.

AR usually presents in early childhood. AR caused by sensitization to outdoor allergens can occur in children older than 2 years; however, sensitization in children older than 4-6 years is more common. Clinically significant sensitization to indoor allergens may occur in children younger than 2 years. This is typically associated with significant exposures to indoor allergens (eg, molds, furry animals, cockroaches, dust mites). Some children may be sensitized to outdoor allergens at this young age if they have significant exposure. Incidence continues to increase until the fourth decade of life, when symptoms begin to fade; however, individuals can develop symptoms at any age.

AR-like symptoms (runny nose, blocked nose, or sneezing apart from a cold) may begin as early as age 18 months. In a report from the Pollution and Asthma Risk: an Infant Study (PARIS), 9.1% of the 1859 toddlers in the study cohort reported allergic rhinitis-like symptoms at age 18 months.[6]

Prognosis

Most patients are able to live normal lives with the symptoms.

Only patients who receive allergen-specific immunotherapy have resolution of allergic rhinitis (AR) symptoms; however, many patients do very well with intermittent symptomatic care with medication. AR symptoms may recur 2–3 years after discontinuation of allergen immunotherapy, but are usually less severe than the original presentation.

A small percentage of patients improve during the teenage years, but in most, symptoms recur in the early twenties or later. Symptoms begin to wane when patients reach the fifth decade of life.

Patient Education

An abundance of educational material is available from many resources such as medical associations, professional societies (eg, American Academy of Allergy, Asthma, and Immunology, American College of Allergy, Asthma, and Immunology), and pharmaceutical companies. All basically instruct the patient to avoid triggers, use medications, and see a specialist if symptoms persist. Some educational materials are very sophisticated, and several pharmaceutical companies provide extensive web sites to assist patients.

For patient education resources, see the Allergy Center, as well as Hay Fever, Indoor Allergies, and Allergy Shots.

 

Presentation

History

The history of the patient with allergic rhinitis (AR) may be straightforward or may include a complex set of symptoms. The diagnosis is easy to make in a patient with a new pet or with symptoms that have distinct seasonal variation. Alternatively, younger patients may present with varying signs or symptoms, the family may not appreciate the nasal stuffiness but may note the chronic nasal congestion. In older children, symptoms may have been present for years and, therefore, appear to be less severe because the child has accommodated them.

Physicians should try to identify seasonal variations, provocative elements in the environment, and the timing of events that lead to symptoms. For example, if the patient only has issues during the week, this may lead to investigating the environment of the child's classroom or daycare for allergens like pets or molds. Few patients present soon after the onset of AR symptoms. Usually, AR symptoms have been present for years and have been slowly worsening during each allergy season.

This is especially true for patients with pet allergies. The symptoms appear slowly, over years. They can worsen in the spring and fall and be confused with pollen allergy. This occurs for pets usually shed more in the warmer weather and then in the fall when more time is spent indoors with worsening symptoms. Also, many families believe that the fact that the pet was present before the onset of the child's symptoms exclude the possibility of allergy to the family pet, but this is not true. The family often believe that the family pet is hypoallergenic. No cats or dogs are truly hypoallergenic. Some pets trigger less allergic symptoms in some individuals. In addition, dander exposure is crucial in triggering symptoms. Therefore, a large home without carpeting and a small pet will probably trigger less severe symptoms than a large pet in a small house. An interesting phenomenon is what is referred to as the "Thanksgiving effect," which is when a child goes off to college and returns home for Thanksgiving to discover that their family pet, which  did not previously trigger allergy symptoms, now does in fact trigger them. This is because the individual's mast cells have had a chance to no longer be saturated with pet dander and can now degranulate. This situation may also occur when a child is away from a pet for a shorter period of time (several days).

Unless a new exposure to large amounts of allergens is reported (eg, pet, feather pillow), a patient who describes a sudden onset of nasal allergy symptoms is probably not experiencing allergic symptoms. Sudden onset of nasal symptoms is often associated with either an upper respiratory tract infection or acute sinusitis or acute bacterial sinusitis superimposed on chronic sinusitis. In children younger than 5 years, differentiating allergy symptoms from recurrent upper respiratory viral infection is even more difficult, especially in those who attend daycare and experience frequent rhinitis symptoms.

Nature of symptoms

Symptoms of rhinitis consist of rhinorrhea, nasal congestion, postnasal drainage, repetitive sneezing, and itching of the palate, ears, nose, or eyes. Snoring, frequent sore throats, constant clearing of the throat, cough, itchy eyes, and headaches are symptoms often associated with rhinitis.

When obtaining the history, ascertain the following:

  • Determine which symptoms are reported by the patient or parent

  • Ask if symptoms occur in different locations

  • Determine whether the patient has rhinorrhea, sniffling, nasal itching, sneezing, cough, congestion, or nasal discharge. Determine the color of the nasal discharge

  • Determine whether any associated ocular or respiratory symptoms are present

  • Ask about snoring, which may worsen in pollen season or be related to adenoidal hypertrophe

Timing of symptoms

Identify whether symptoms are present or worsen during certain seasons, such as the spring or fall. In addition, try to identify whether symptoms are worse in specific places, such as home, work, school, or on vacation or when the patient is around animals.

Determine when symptoms occur and whether they occur primarily at night, in school, outdoors, or at a relative's or friend's home.

Determine whether symptoms occur only at a certain time of the year or throughout the year. Remember that symptoms in the fall and spring may still indicate a pet allergy.

Determine whether symptoms ever improve and, if so, what actions help alleviate symptoms. Most patients have tried over-the-counter antihistamine medication. If these medications help, AR should be suspected; however, a negative response does not eliminate the possibility of AR. Ask if the patient's symptoms improve when they are away from certain locations. For example, a child who has less symptoms at college or camp may have an allergy to the family pet, feather pillows, or dust mites in their bedding.

Determine whether symptoms improve when the patient is taking antibiotics. Most patients receive antibiotics for various reasons unrelated to nasal symptoms. If symptoms respond to antibiotic therapy, the clinical diagnosis may be sinusitis, which may have been either primary sinusitis or secondary sinusitis caused by allergic rhinitis.

Duration of symptoms

Determine whether symptoms last for weeks, months, or hours.

Most pollen seasons are at least 6 weeks long in more moderate climates. In the south and far north, the season can be longer or shorter, respectively. Symptoms that last less than 2 weeks rarely indicate AR, unless concomitant exposure occurs. For example, a child only allergic to one type of tree could have 2 weeks of exposure, but this is less common.

In winter in the northern regions, virtually all outdoor pollens are absent; therefore, any AR–like symptoms are the result of indoor allergen exposure or are associated with nonallergic causes. Although patients are usually exposed to the same allergens throughout the year, AR symptoms triggered by indoor allergens can worsen in winter secondary to longer hours spent indoors during the cold months. This may also be associated with closed windows and doors in winter, resulting in increased recirculation of indoor allergens. An example of winter-only exposure is a person who is allergic to dust mites who uses a down comforter only during the winter (dust mites are highly infested in a down comforter.), also a patient with adenoidal hypertrophy may be worse in the winter due to lower ambient humidity leading to more nasal irritation. Nasal symptoms can also be worse in the winter due the dryness of the air that is found in forced air heat. Now, with most homes being more tightly sealed and kept at warmer temperatures, the use of a fan in the winter is more common. The use of a fan increases overall dryness for it blows warm, dry air.

Family history

Children with parents who have allergies or asthma are more likely to be affected.

If a child has one parent with allergies, chances are 30% that a child will have AR. This increases to 50–70% if both parents have allergies or atopic asthma.

Related medical history

Patients with a history of infantile eczema (atopic dermatitis) have a 70% chance of having AR, asthma, or both. Patients with a history of asthma also have higher incidence of AR.

Social and environmental history

The patient's environment is very important. Ask about the presence of a pet or beddings (eg, pillow, bedspread, comforter [especially containing feathers]) and other home items likely infested by dust mites (eg, carpeted floor, stuffed animals, dusty closet, nonleather furniture) as well as the timing of initial exposure. Many times, exposure to dust, feathers, or pets coincides with the onset of symptoms, making diagnosis and treatment easier. However, patients could become sensitized to indoor allergens by exposure in places other than the home where they spend a fair numbers of hours (eg, schools, daycare center, baby sitters' and relatives' homes). Cigarette smoke can also be an irritant and trigger symptoms, so the presence of a smoker in the home can also play a part in the child's symptoms.

Questions must be raised regarding any environment in which the patient spends more than a few hours per week. This includes baby-sitters' and relatives' homes, daycare facilities, and schools (classroom pets).

For children younger than 3 years, ask about the child's bed. Cribs or toddler beds that use crib mattresses do not have dust mites because these mattresses rountinely have plastic covers, but standard bedding (bed mattress) can harbor dust mites.

Physical

A full examination should always be performed to detect other diseases, such as asthma, eczema, adenoidal hypertrophy, and cystic fibrosis, which occur in connection with allergic rhinitis (AR). Evaluation involves the head, eyes, ears, nose, and throat. Upon inspection, signs described below can be noted.

Head

Allergic shiners (dark, puffy, lower eyelids) may be present (see image below).

Photo demonstrates allergic shiners. Note the peri Photo demonstrates allergic shiners. Note the periorbital edema and bluish discoloration seen in allergic rhinitis and sinusitis.

Morgan-Dennie lines (lines under the lower eyelid) may be observed.

Transverse crease at the lower third of the nose secondary to the allergic salute (shown below), which is the upward rubbing of the nose, is commonly seen in parents as well.

Photo demonstrates the allergic salute, which is t Photo demonstrates the allergic salute, which is the action performed when a patient rubs the nose using a motion across the nose.

Eyes

Marked erythema of palpebral conjunctivae and papillary hypertrophy of tarsal conjunctivae are observed. Chemosis of the conjunctivae may be present. Patients usually have a watery discharge.

Cataracts have occurred from severe rubbing secondary to itching.

Ears

Tympanic membranes should be examined for the presence of chronic infection or middle ear effusion.

The role of AR in chronic otitis media is not clear, but decreased numbers of infections have been noted in AR children once therapy was instituted.

Nose

Nasal examination is often helpful in the diagnosis.

Turbinates are enlarged and have a pale-bluish mucosa due to edema.

Discharge is usually clear but can be white. The discharge is rarely yellow or green. If colored discharge is observed, a diagnosis of viral infection or sinusitis should be considered.

Dried blood is commonly observed secondary to trauma from rubbing the nose.

Polyps are rarely observed in children. If polyps are noted or suspected, perform rhinoscopy. If polyps are detected, a workup for cystic fibrosis is mandatory in children. Also consider the diagnosis of aspirin sensitivity in adults.

Throat

Inspection of the dentition can be informative. Discoloration of frontal incisors and a high arched palate are associated with chronic mouth breathing. Malocclusion is commonly associated with chronic mouth breathing.

Cobblestoning in the posterior pharynx is also a sign of follicular hypertrophy of mucosal lymphoid tissue secondary to chronic nasal congestion and postnasal drainage.

Note the size of tonsillar tissue, which may provide a clue to the size of the adenoids; large adenoids (adenoidal hypertrophy) can mimic the signs and symptoms of AR. Chronic nasal congestion due to adenoid hypertrophy is frequently seen in young children with recurrent otitis media and sinusitis.

Causes

Perennial symptoms are usually caused by indoor allergens, including the following:

  • Dust mites

  • Cat dander

  • Dog dander

  • Indoor molds

  • Cockroaches

  • Feathers: In most occasions, feather pillows and comforters are highly allergenic, secondary to dust mite infestation. Nonfeathered bedding usually has less dust mite infestation but does have progressively more dust mites over time; dust mites lay eggs every 3 weeks and accumulate where human dander accumulates. Thus nonwashable beddings (eg, pillows, bed mattress) should be encased by dust mite–proof encasings.

  • Other furry animals

Seasonal symptoms are usually caused by airborne pollen and outdoor molds, which are usually highest in late afternoon and early morning hours. These allergens include the following:

  • Tree pollen

  • Grass pollen

  • Outdoor mold spores

  • Weed pollen: Flowers do not cause allergic rhinitis because they do not use wind-borne pollination.

Complications

See the list below:

  • Primary complications of allergic rhinitis (AR) are associated diseases.

  • Sinusitis is a common complication occurring secondary to the inflamed nasal turbinates that block the ostiomeatal complex of the sinuses and other sinus passages.

  • Recurrent or chronic otitis media can also be a secondary complication. It is thought to occur as a result of an inflamed nasal passages that adversely affect the drainage of the auditory tube.

  • AR can lead to rhinitis medicamentosa when topical nasal decongestants are used in excess.

  • AR can cause other conditions, such as insomnia, irritability, headache, chronic fatigue, and pharyngitis. These occur secondary to chronic nasal congestion and discharge, mouth breathing, and sleep disturbance.  It was reported that uncontrolled allergic rhinitis can exacerbate symptoms of ADHD, tic disorder, anxiety and OCD.

 

DDx

Diagnostic Considerations

Inflammatory causes

Bottle feeding (children >18 mo)

Vasomotor rhinitis

Viral infection

Obstructive causes

Adenoid hyperplasia

Choanal atresia

Foreign body

Deviated septum

Nasal polyps

Neoplasm

Oral allergy syndrome

Oral allergy syndrome (OAS), also known as pollen-food syndrome, occurs when the body perceives certain foods, primarily fruits and vegetables, as an allergen and causes a contact dermatitis reaction in the mouth. This is often due to cross-reactivity between pollens and fruit/vegetable allergens. These food allergens are heat labile and easily lose their allergenicity with heating. Thus, patients with this condition report an itchy mouth when eating certain fruits or vegetables in their natural form. For example, eating a whole fresh apple causes a reaction, but eating apple pie or apple sauce or drinking apple juice does not.

The most common pollens associated with OAS include birch and ragweed pollens. Birch tree pollen cross-reacts with apple, pear, peach, celery, and carrots. Ragweed cross-reacts with melon, watermelon, cantaloupe, honeydew, zucchini, and cucumber.

Making the proper diagnosis is important because OAS can be confused with a potentially life-threatening anaphylactic reaction to food allergens. Studies have shown that use of allergen immunotherapy to cross-reactive pollens decreases or eliminates this reaction.

Differential Diagnoses

 

Workup

Laboratory Studies

No studies are needed in allergic rhinitis (AR) if the patient has a straightforward history. When the history is confusing, various studies are helpful, including the following:

  • Skin-prick testing: This test is highly sensitive and specific for aeroallergens. However, a false positive reaction can occur without corresponding clinical features, especially when skin mast cells are easily activated by pressure or other physical stimuli.

  • Serum allergen-specific IgE testing: The main limitations are that patients may be sensitive on a molecular level before IgE response is clinically seen on standard skin testing. This may lead to positive results on laboratory tests that are not triggering clinical symptoms. A future advantage is that this may be a first step toward better customization of immunotherapy in the future.[7]

  • Nasal smear: Eosinophils usually indicate allergy. Neutrophils are more indicative of an infectious process, such as sinusitis. This is not used often anymore because of the difficulty in having the test performed. It was used commonly when office laboratories were common.

  • CBC count with differential: A CBC count may reveal an increased number of eosinophils. An eosinophil count within the reference range does not exclude AR; however, an elevated eosinophil count is suggestive of the diagnosis.

  • Immunoglobulin E (IgE): Serum IgE values are not routinely recommended to evaluate atopy. An IgE value within the reference range does not exclude AR; however, an elevated IgE value is suggestive of the diagnosis. Allergen-specific IgE testing, also known as ImmunoCAP testing, is a blood test that can identify if a patient has specfic IgE to an allergen. This test replaced the older RAST test that is no longer in use.  ImmunoCAP can be helpful if a specific allergen is suspected. Newer ImmunoCAP tests can now detect different parts of allergens; this is called component testing. For example, component testing can inform the patient if they are allergic to not only dogs but also a cross-reactive antigen to cats and horses. In addition, it can tell if a patient is allergic to all dogs or just the male ones, as some patients are postive or negative to a prostate antigen in dogs. Screening of a large number of allergens can cause confusion because of the possibility of false positives. This is especially true for IgE food allergy testing. The results of one explorative study found that low levels of serum IgE can be detected from the age of 6 months. The study suggests that detectable levels of IgE sensitization are associated with present symptoms of eczema, rhinitis, asthma, and food and inhalant allergens, and may also be predictive of future allergic symptoms.[8]

Imaging Studies

Imaging studies are not needed unless sinusitis is suspected, in which case, a limited CT scan of the sinuses (without contrast) is indicated.

Other Tests

See the list below:

  • Allergen-specific serum IgE for common allergens can be used to identify the patient's triggers. These might include dust mites, cat dander, dog dander, grass pollens, tree pollens, weed pollens, and molds.

  • Foods rarely cause allergic rhinitis (AR), and tests for food allergies are not indicated in patients with AR.

  • Allergen-specific IgE testing for aeroallergens, such as dust mites, cat dander, and dog dander, is almost as sensitive and specific as allergen skin testing.

Procedures

Skin testing

Skin testing is used to identify the triggering agent. It has high sensitivity and specificity and is the preferred method of quick allergen identification for aeroallergens.

Skin testing is helpful if the allergens can be eliminated from the patient's environment or if the patient can avoid them. It is extremely helpful when patients are unresponsive to standard therapy or are unwilling to acknowledge the trigger, which is especially true if the family pet is a possible trigger.

Skin testing is required if the patient is interested in allergen immunotherapy.

Rhinoscopy

Rhinoscopy is helpful in direct examination of the upper airway in identifying whether the etiology of rhinitis is obstructive or infectious and for evaluation of nasal polyposis.

 

Treatment

Approach Considerations

Patients with allergic rhinitis (AR) need continuous follow-up care because AR is a chronic disease that waxes and wanes with seasons and age. The fluctuation of symptoms requires adjustment of medications.

Patients rarely outgrow allergic rhinitis in childhood.

Medical Care

Treatment of allergic rhinitis (AR) can be divided into 3 categories: avoidance of allergens or environmental controls, medications, and allergen-specific immunotherapy (sublingual or allergy shots).

  • Use of environmental controls is not adequately explored in most patients. For many patients, the removal of the trigger can have a dramatic effect. Difficulty arises when the trigger needs to be identified and eliminated. Eliminating the trigger may be simple if removal of a feather pillow or blanket is involved; however, it can be very difficult if a family pet needs to be removed. Although avoiding outdoor pollens is impossible, the patient can reduce exposure to pollens for attenuating symptoms. This sometimes is as simple as closing a bedroom window, using an air conditioner, or installing a pollen filter.

  • Identification and elimination is easiest for dust mite allergens.

    • Feathered bedding should be removed and replaced with a fiber-filled product encased by dust mite–proof encasings. Such encasings can be purchased at the local stores or via mail orders. These encasings should be zip-locked and cover all surface areas.

    • A bed pad that is placed on top is not helpful and may be another source of dust mite infestation.

    • Less expensive plastic encasings may leak allergens through needle holes or between zipper teeth; therefore, more expensive dust mite–proof covers are preferable.

    • The pillow must be covered; this is even more crucial than covering the bed mattress itself because the pillow is where the patient's head usually spends most of the night. Box springs usually do not need to be covered.

    • Care should be taken to be sure the encasings are dust mite–proof. Some products may claim to be an allergy cover but may not provide the proper protection for dust mite. Also hypoallergenic bedding usually refers to the fact that the bedding is not made of feathers and does not necessarily mean that it is dust mite–proof.

  • Pollen is more difficult to avoid because daily activities must be altered to do so.

    • The patient is best advised to remain indoors with air-conditioning during the period of the highest pollen counts of the day. Commonly, remaining indoors is not possible because of activities, and many schools are not air-conditioned. If it is a room unit air-conditioner, then it must be set to indoor air, not to draw in the outdoor pollens.

    • An easy intervention is to keep the windows closed, which is easily accomplished in air-conditioned homes, and must be done throughout the year. Windows tend to be opened most frequently during fall and spring in moderate climates, but these seasons are the worst possible times for open windows for patients with pollen allergy. If windows must be open, open them during the day and close them at night. Many pollen counts are highest during the night, especially for molds and trees.

    • Another intervention is to obtain a window filter or filter fan, which allows air, but not pollen, to enter the room.

    • Advise patients to wash head to toe and to change clothing upon coming in from the outdoors during high pollen season. Avoid hanging cloths outdoors to dry.

  • The most difficult trigger to avoid is the family pet. Ideally, the pet should be removed from the home, but removal is the option, not the rule. Some helpful manipulations include removing the pet from the patient's bedroom and play area, using air cleaners in these areas and, occasionally, frequently sponge-bathing the pet (once per week). Even when these interventions are performed, many patients continue to experience symptoms. Other therapies are necessary in these patients; however, some patients choose to live with the source of offending allergens.

  • A new intervention for cats is use of a specific cat food that has anti-Fel D 1 antibodies in it. The cat is eating the antibodies, which causes the cat to shed less Fel D 1. Since Fel D1 is the main cat allergen, some patients may experience less symptoms around the cat. This is a relatively new product, so long-term information is not yet available.

  • See Medication for a discussion of medications and allergen-specific immunotherapy (ie, allergy shots and sublingual[9] ). A 2009 study concluded that specific immunotherapy can be recommended for treatment because it is effective in reducing symptoms.[10] The US Food and Drug Administration (FDA) has approved several products for sublingual immunotherapy in patients with grass, dust mite, or ragweed allergy[11, 12, 13]

Surgical Care

No routine surgical care is needed.

Some patients may be seen by ear, nose, and throat (ENT) specialists, and turbinectomies may be performed to provide some relief. This is an extreme measure and is reserved for patients in whom all other therapies have failed.

Rarely, in adults, if nasal polyps do not respond to topical nasal steroids, surgical removal may be necessary, although the polyps often grow back.

Consultations

Primary care physicians can attend to most patients.

Patients in whom diagnosis or treatment is more difficult may require consultation with a specialist. This usually starts with an allergist, who performs a complete allergy evaluation, including diagnostic tests. Therapy is instituted, which is a combination of environmental manipulations, medications and, in some patients, allergen-specific immunotherapy.

Refer patients in whom allergic rhinitis becomes hard to manage or diagnose to an allergist for complete evaluation and advanced treatment, including institution of allergen-specific immunotherapy.

If medical therapies do not produce an adequate result, referral to an ENT specialist should be indicated for possible surgical intervention.

Diet

Dietary restrictions do not help because allergic rhinitis is not triggered by foods.

Activity

No limitations are placed on activity.

For some pollens, patients with allergic rhinitis benefit from avoiding the outdoors during peak pollen periods of the day. This time varies according to pollens and location. Geographic location and distance from the source have an impact. Patients who are miles away from the source have different peak pollen times than patients near the source.

Prevention

The best deterrent is to avoid allergens that trigger symptoms. This means diligent environmental controls and patient compliance with medication use.

Exposure to allergens in first year may reduce subsequent wheezing and atopy.

In the Urban Environment and Childhood Asthma (URECA) study of 467 urban children who had at least 1 parent with an allergic disease or asthma, researchers found that exposure during the first year of life to specific allergens and bacteria reduced recurrent wheeze and atopy at age 3 years.[14, 15]

Newer studies suggest that infants who are moisturized daily in the first two years may have less food allergies and possibly allergic rhinitis.

 

Guidelines

Guidelines Summary

Joint Task Force on Practice Parameters (JTFPP)

In 2017, the Joint Task Force on Practice Parameters (JTFPP) released updated recommendations for the treatment of seasonal allergic rhinitis (SAR) in adolescents and adults.[16]

Updated guidelines include the following:

  • In patients aged 12 years or older, nasal symptoms of SAR should be treated at least initially with an intranasal corticosteroid (INCS) alone rather than an INCS–oral antihistamine combination.

  • In patients aged 15 years or older, moderate to severe SAR should be treated with an INCS over a leukotriene receptor antagonist (LTRA).

  • Clinicians may recommend combination therapy with an INCS and an intranasal antihistamine (INAH) over either agent alone.

American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNS)

In 2015, the American Academy of Otolaryngology-Head and Neck Surgery Foundation (AAO-HNS) released guidelines for treating patients ages 2 and up who suffer from allergic rhinitis.[17]

Key recommendations include the following:

  • For patients with a stuffy nose, nasal passage discoloration, and/or red and watery eyes, doctors should forgo sinus imaging process in favor of specific immunoglobulin E screening. Sinonasal imaging exposes patients to unnecessary radiation.
  • Intranasal steroids and oral antihistamines are recommended as first lines of treatment. Oral leukotriene receptor antagonists are not.
  • Sublingual or subcutaneous immunotherapy should be offered to patients who do not respond to pharmacologic therapy.
 

Medication

Medication Summary

Many classes of medications are used for allergic rhinitis (AR), including antihistamines, corticosteroids, decongestants, saline, sodium cromolyn, and leukotriene receptor antagonists. These can be further subdivided into intranasal and oral therapies. Intranasal administration has the advantage of directly affecting the site of action, and, in general, intranasal medications have fewer adverse effects and no systemic effects. The main advantage of oral therapy is ease of use. Some patients resist using intranasal medications.

Allergen-specific immunotherapy is an alternative form of therapy that has several advantages. Most importantly, it is the only form of therapy that can cure allergy symptoms. Allergen-specific immunotherapy must be customized to the patient's individual allergies and involves weekly injections of increasing concentrations of an allergen until the maintenance dose is reached and a monthly injection of the maintenance dose for several years. The process usually does not produce clinical results in the first 6 months but results are seen afterwards. The recommended course is usually 4–5 years. Allergen-specific immunotherapy has been demonstrated to be more cost effective and improves the patient's quality of life more efficiently than standard allergy medications.

Sublingual (SL) immunotherapy (SLIT) has been available in other countries of the world.[9] In this form of therapy, small amounts of the allergen are placed under the tongue on a daily basis. The two main advantages are that no injections are necessary and treatment can be administered at home. In spite of the safety record of sublingual therapy, which has very few serious reactions, the FDA recommendations are that the first dose be given in a physician's office and an epinephrine autoinjector is to be prescribed.

In April 2014, the FDA approved three SL tablets. Two are for grass allergies and the third is for ragweed. Oralair consists of five calibrated grass pollen extracts (Oralair). It contains Perennial Ryegrass (Lolium perenne), Kentucky bluegrass (Poa pratensis), Timothy grass (Phleum pratense), Orchard grass (Dactylis glomerata), and Sweet Vernal grass (Anthoxanthum odoratum).[11] The Oralair SL tablet needs to be initiated 4 months prior to the season for the specific allergen. It is approved for adults and children aged 5-65 years.

The second SL immunotherapy for grass is only one type of grass. Timothy grass (Grastek) was also approved in April 2014. It should be initiated at least 12 weeks before the start of the grass pollen season.[12] Efficacy and safety in North America was established in a large study (n=1500) of adults and children aged 5-65 years. Results showed a 23% improvement of symptoms in the entire grass pollen season.[13] Timothy grass cross-reacts with the following grasses, including sweet vernal, orchard (also known as cocksfoot), perennial rye, Kentucky blue (also known as June grass), meadow fescue, and redtop. This high cross-reactivity allows for Grastek to be effective for a patient with grass pollen allergies.

The third one is Ragwitek. Like the other two, it needs to be started prior to the onset of the season. It is a short ragweed extract (Ambrosia artemisiifolia) for adults and children aged 5–65 years.

A fourth one, called Odactra, was released in 2017.  It is sublingual therapy for dust mite allergies in individuals aged 18–65 years.

Saline nasal irrigation is effective in approximately 50% of patients with allergic rhinitis. Irrigation assists the body's natural function of rinsing allergens out of nasal passages. Tap water cannot be used because it is hypotonic and causes edema, leading to greater congestion.

Antihistamines, 2nd Generation

Class Summary

Antihistamines are classified in several ways, including sedating and nonsedating, newer and older, and first- and second-generation antihistamines (most widely accepted classification). First-generation antihistamines are primarily over-the-counter OTC) and are included in many combination products for cough, colds, and allergies. These include brompheniramine, chlorpheniramine (Chlor-Trimeton), and diphenhydramine (Benadryl). Some 2nd generation antihistamines, such as fexofenadine (Allegra), loratadine (Claritin), and cetirizine (Zyrtec) are now available OTC without a prescription. Second-generation antihistamines include desloratadine (Clarinex), and levocetirizine dihydrochloride (XYZAL), are also available without a prescription.

Cetirizine (Zyrtec, Zyrtec Allergy, Children's Zyrtec Allergy)

Low-sedating second-generation medication with fewer adverse effects than first-generation medications. Selectively inhibits peripheral histamine H1 receptors. Available as syr (5 mg/5 mL) and 5- or 10-mg tab.

Levocetirizine (Xyzal)

Histamine H1-receptor antagonist. Active enantiomer of cetirizine. Peak plasma levels are reached within 1 h, and half-life is about 8 h. Available as a 5-mg breakable (scored) tab. Indicated for seasonal and perennial AR

Loratadine (Claritin)

Nonsedating second-generation antihistamine. Fewer adverse effects than with first-generation medications. Selectively inhibits peripheral histamine H1 receptors. Available as tab, disintegrating tab (Reditab), syr (5 mg/5 mL), or combined with pseudoephedrine in 12- or 24-h preparations. 

Desloratadine (Clarinex, Clarinex RediTabs)

Nonsedating second-generation antihistamine. Fewer adverse effects than with first-generation antihistamines. Selectively inhibits peripheral histamine H1 receptors. Relieves nasal congestion and systemic effects of seasonal allergies. Long-acting tricyclic histamine antagonist selective for H1-receptor. Major metabolite of loratadine, which, after ingestion, is extensively metabolized to active metabolite 3-hydroxydesloratadine. Available as tabs, syr (0.5 mg/mL), or PO disintegrating Reditabs (2.5 and 5 mg).

Fexofenadine (Allegra, Allegra Allergy 12 Hour, Allegra Allergy 24 Hour, Children's Allegra Allergy)

Nonsedating second-generation medication with fewer adverse effects than first-generation medications. Competes with histamine for H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Available OTC in qd and bid preparations. Also OTC available combined with pseudoephedrine.

Antihistamines, Intranasal

Class Summary

These agents are an alternative to oral antihistamines to treat allergic rhinitis. Currently, azelastine and olopatadine are the only agents available in the United States and require a prescription.

Azelastine (Astelin Nasal Spray, Astepro)

An effective antihistamine delivered via the intranasal route. Mechanism is similar to PO antihistamines. Systemic absorption occurs and may cause sedation, headache, and nasal burning.

Olopatadine intranasal (Patanase)

Intranasal antihistamine spray for seasonal allergic rhinitis. Available as 6% intranasal solution (delivers 665 mcg/spray).

Corticosteroids, Intranasal

Class Summary

This class of medications is most effective. Intranasal corticosteroids are potent anti-inflammatory agents shown to decrease allergic rhinitis symptoms in more than 90% of patients. Presently, 9 medications are available in this class, and all are essentially equivalent in efficacy, although few head-to-head studies have been performed. Mometasone (Nasonex) and fluticasone furoate (Veramyst) have been demonstrated to have a somewhat faster onset of action; however, after one week, no difference is found between medications. Most can be used on a once-daily basis, and all have a similar safety profile. Nasonex is the only medication that did not show an effect on growth at one year. Veramyst did not show a growth effect in a 2-week study that is designed to evaluate for growth affects.

There are 2 nasal inhalers, Qnasl and Zetonna. They are a spray form and allow for better nasal deposition for some patients who like a spray-type inhaler. They have shown to help decrease ocular symptoms. In the spring of 2014, Nasacort (triamcinolone) . Only Qnasl, Zetonna and Nasonex are presently available by prescription. The other are over the counter

Beclomethasone, intranasal (Beconase AQ, QNASL)

Corticosteroid with potent anti-inflammatory properties. Elicits effects on various cells, including mast cells and eosinophils. It also elicits effects on inflammatory mediators (eg, histamine, eicosanoids, leukotrienes, cytokines). Available in solution or suspension forms and delivered as a metered-dose nasal sprays. Beconase AQ is approved for children aged 6 y or older. QNASL is indicated for children aged 4 y or older.

Budesonide intranasal (Rhinocort Aqua)

May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation.

Ciclesonide intranasal (Omnaris, Zetonna)

Corticosteroid nasal spray indicated for AR. Prodrug that is enzymatically hydrolyzed to pharmacologic active metabolite C21-desisobutyryl-ciclesonide following intranasal application. Corticosteroids have a wide range of effects on multiple cell types (eg, mast cells, eosinophils, neutrophils, macrophages, lymphocytes) and mediators (eg, histamines, eicosanoids, leukotrienes, cytokines) involved in allergic inflammation. Each spray delivers 50 mcg.

Flunisolide intranasal (Nasarel)

May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation.

Fluticasone intranasal (Flonase, Veramyst)

May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation.  Veramyst is now available as OTC (Brand name: Flonase sensimist)

Mometasone, intranasal (Nasonex)

May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation. Demonstrated no mineralocorticoid, androgenic, antiandrogenic, or estrogenic activity in preclinical trials. Decreases rhinovirus-induced up-regulation in respiratory epithelial cells and modulate pretranscriptional mechanisms. Reduces intraepithelial eosinophilia and inflammatory cell infiltration (eg, eosinophils, lymphocytes, monocytes, neutrophils, plasma cells).

Triamcinolone, intranasal (Nasacort AQ)

May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation.

Antihistamine/Corticosteroid, Intranasal

Class Summary

Combination products are emerging on the market for patients who require an intranasal antihistamine and corticosteroids.

Azelastine/fluticasone intranasal (Dymista)

This combination product elicits histamine H1-receptor antagonist activity and anti-inflammatory effects. It is indicated for seasonal allergic rhinitis in adults and children aged 12 years or older.

Intranasal decongestants

Class Summary

Decongestants are effective for short-term symptom control. They decrease nasal discharge and congestion and are available without a prescription. The 2 medications in this group are oxymetazoline hydrochloride (Afrin) and ipratropium bromide (Atrovent). Oxymetazoline hydrochloride is effective in shrinking nasal membranes and is not recommended for long-term use. Use of oxymetazoline hydrochloride for more than 7-10 days can cause rebound congestion. When used for >4-6 days nasal vasoconstrictive medications, that are used topically, can cause rhinitis medicamentosa, a condition characterized by nasal congestion in the absence of rhinorrhea or sneezing. Ipratropium bromide can be used for a prolonged period of time.

Ipratropium intranasal (Atrovent Nasal Spray)

Anticholinergic used for reducing rhinorrhea in patients with AR or vasomotor rhinitis. An excellent medication for decreasing rhinitis. Does not cause rebound congestion and lasts for 12 hours. Does not shrink the nasal mucosa, but inhibits secretion that causes rhinitis. Used alone or in conjunction with other medications.

Oxymetazoline (Afrin 12 Hour, Afrin Sinus, Mucinex Nasal Spray Full Force, Sinus Nasal Spray, Dristan Spray)

A representative topical decongestant applied directly to mucous membranes, where it stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in BP, vascular redistribution, and cardiac stimulation. Use not recommended for >3 days.

Leukotriene Receptor Antagonists

Class Summary

Montelukast has been approved as monotherapy for allergic rhinitis. It has been shown to be most effective in patients in whom significant congestion is a primary complaint. It has also been shown to work as adjunctive therapy with present second-generation antihistamines to provide greater relief of symptoms than antihistamines alone. It is beneficial in patients with symptoms in whom present antihistamines are not adequate. A study has shown a combination with cetirizine is as effective as an intranasal corticosteroid. Antileukotriene can also be added to the treatment plan in patients receiving antihistamines and intranasal therapy.

Montelukast (Singulair)

Inhibits airway cysteinyl leukotriene receptors. Because these receptors are found throughout the airway, the medication can mediate the effect in the upper and lower airway.

Allergen Immunotherapy

Class Summary

Immunotherapy with daily sublingual (SL) tablets may be able to replace weekly injections in some individuals, depending on the offending allergens. Depending on the particular SL tablet, therapy must be initiated at least 3-4 months before the allergen season that is being treated.

Grass pollens allergen extract (Oralair)

SL immunotherapy indicated for grass pollen–induced allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for grass pollen–specific immunoglobulin E antibodies for any of the 5 grass species contained in the product. It consists of 5 purified and calibrated pollen extracts: Perennial Ryegrass (Lolium perenne Poa pratensis), Timothy grass (Phleum pretense), Orchard grass (Dactylis glomerata), and Sweet Vernal grass (Anthoxanthum odoratum). It is approved for adults and children aged 5-65 years.

Timothy grass pollen allergen extract (Grastek)

SL immunotherapy indicated for allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for Timothy grass pollen-specific IgE antibodies. It is approved for adults and children aged 5-65 years.

Ragweed allergen extract (Ragwitek)

SL immunotherapy indicated for short ragweed (Ambrosia artemisiifolia) pollen-induced allergic rhinitis (with or without conjunctivitis) confirmed by positive skin test or in vitro testing for ragweed-specific IgE antibodies. It is approved for adults and children aged 5-65 years.

House dust mite immunotherapy (Odactra)

SL indicated for dust mite-induced allergic rhinitis with or without conjunctivitis, confirmed by in vitro testing for IgE antibodies to Dermatophagoides farinae or Dermatophagoides pteronyssinus house dust mites, or skin testing to licensed house dust mite allergen extracts, in people aged 18-65 years. 

Mast Cell Stabilizers, Intranasal

Class Summary

These are effective therapy for AR in approximately 70-80% of patients. They produce mast cell stabilization and antiallergic effects by inhibiting mast cell degranulation. They have no direct anti-inflammatory or antihistaminic effects and minimal bronchodilator effects. They are effective for prophylaxis. They also clean out antigens mechanically, similar to saline. These products are now available over the counter.

Cromolyn sodium, intranasal (NasalCrom)

Used on a daily basis for seasonal or perennial AR. Significant effect may not be seen for 4-7 d. Administer just before exposure in patients with isolated and predictable periods of exposure (eg, animal allergy, occupational allergy). Generally less effective than nasal corticosteroids. Protective effect lasts 4-8 h; thus, frequent dosing is necessary. If desired, may be used with other medicines, including other allergy medicines.

 

Questions & Answers

Overview

How is pediatric allergic rhinitis characterized?

What are the history findings of pediatric allergic rhinitis?

What are the signs and symptoms of pediatric allergic rhinitis?

What is involved in the diagnosis of pediatric allergic rhinitis?

Which studies are indicated in the workup of pediatric allergic rhinitis?

When are imaging studies indicated in pediatric allergic rhinitis?

Which procedures are indicated in the workup of pediatric allergic rhinitis?

What are the categories of pediatric allergic rhinitis treatment?

Which medications are used in the treatment of pediatric allergic rhinitis?

Which management options for pediatric allergic rhinitis do not involve medications?

Which surgical interventions may be indicated in the treatment of pediatric allergic rhinitis?

How does pediatric allergic rhinitis affect daily life?

What causes pediatric allergic rhinitis?

How do nasal allergies affect pediatric allergic rhinitis?

What is the pathophysiology of pediatric allergic rhinitis?

What is the role of allergic reactions in the pathophysiology of pediatric allergic rhinitis?

How common is pediatric allergic rhinitis in the US?

How common is pediatric allergic rhinitis in Europe and Asia?

What mortality and morbidity are associated with pediatric allergic rhinitis?

What are the race and sex predilections of pediatric allergic rhinitis?

What are the age-related demographics of pediatric allergic rhinitis?

What is the prognosis of pediatric allergic rhinitis?

What is involved in patient education for pediatric allergic rhinitis?

Presentation

What social and environmental history is associated with pediatric allergic rhinitis?

What is the clinical history of pediatric allergic rhinitis?

What information should be collected in the clinical history of pediatric allergic rhinitis?

How are nonallergic symptoms distinguished from pediatric allergic rhinitis?

What information should be obtained about the nature of symptoms in pediatric allergic rhinitis?

What information should be obtained about the timing of symptoms in pediatric allergic rhinitis?

What information should be obtained about the duration of symptoms in pediatric allergic rhinitis?

What family history is associated with pediatric allergic rhinitis?

What related medical history is associated with pediatric allergic rhinitis?

What is involved in the physical exam for pediatric allergic rhinitis?

What physical findings of pediatric allergic rhinitis are noted on the head?

What physical findings of pediatric allergic rhinitis are noted about the eyes?

What physical findings of pediatric allergic rhinitis are noted in the ears?

What physical findings of pediatric allergic rhinitis are noted in the nose?

What physical findings of pediatric allergic rhinitis are noted in the throat?

What causes perennial symptoms of pediatric allergic rhinitis?

What causes seasonal symptoms of pediatric allergic rhinitis?

What are the potential complications of pediatric allergic rhinitis?

DDX

What are the diagnostic considerations in pediatric allergic rhinitis?

What are the differential diagnoses for Pediatric Allergic Rhinitis?

Workup

Which lab studies are indicated in the workup of pediatric allergic rhinitis?

Which imaging studies are indicated in the workup of pediatric allergic rhinitis?

What other tests are indicated in the workup of pediatric allergic rhinitis?

What is the role of rhinoscopy in the workup of pediatric allergic rhinitis?

What is the role of skin testing in the workup of pediatric allergic rhinitis?

Treatment

What are the approach considerations regarding the treatment of pediatric allergic rhinitis?

What are the categories of treatment for pediatric allergic rhinitis?

What is the role of environmental controls in the treatment of pediatric allergic rhinitis?

What is the role of eliminating dust mite allergens in the treatment of pediatric allergic rhinitis?

How can pollen be avoided by patients with pediatric allergic rhinitis?

What is the most difficult trigger of pediatric allergic rhinitis to avoid?

When is surgical indicated in the treatment of pediatric allergic rhinitis?

Which specialist consultations are indicated in the treatment of pediatric allergic rhinitis?

What dietary restrictions are indicated in the treatment of pediatric allergic rhinitis?

What activity restrictions are indicated in the treatment of pediatric allergic rhinitis?

What is the most effective approach to avoiding symptoms in pediatric allergic rhinitis?

Guidelines

What are the recommendations for the treatment of seasonal allergic rhinitis (SAR) in adolescents and adults?

What are the treatment guidelines for pediatric allergic rhinitis?

Medications

Which medications are used in the treatment of allergic rhinitis (AR)?

What are the advantages of allergen-specific immunotherapy for the treatment of pediatric allergic rhinitis?

What are the advantages of sublingual (SL) immunotherapy in the treatment of pediatric allergic rhinitis?

Which sublingual (SL) tablets have been approved for use in the treatment of pediatric allergic rhinitis?

How effective is saline nasal irrigation in the treatment of pediatric allergic rhinitis?

Which medications in the drug class Mast Cell Stabilizers, Intranasal are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Allergen Immunotherapy are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Leukotriene Receptor Antagonists are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Intranasal decongestants are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Antihistamine/Corticosteroid, Intranasal are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Corticosteroids, Intranasal are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Antihistamines, Intranasal are used in the treatment of Pediatric Allergic Rhinitis?

Which medications in the drug class Antihistamines, 2nd Generation are used in the treatment of Pediatric Allergic Rhinitis?