Learning Outcome

1. List causes of allergic rhinitis
2. Describe the management of allergic rhinitis
3. Summarize the role of the nurse in managing allergic rhinitis
4. Describe ways to reduce the risk of allergic rhinitis

Introduction

Allergic rhinitis (AR) is an atopic disease characterized by symptoms of nasal congestion, clear rhinorrhea, sneezing, and nasal pruritis. It can affect one in every six individuals and has associations with significant morbidity, loss of productivity, and health-care costs. Historically, the belief was that AR was a condition of the nasal passages only. Still, the treatment of AR is now a systemic disease due to its close association with asthma and atopic dermatitis.[1] AR can be classified as seasonal (intermittent) or perennial (chronic), with approximately 20% of cases being seasonal, 40% perennial, and 40% with both features.[2] Outside of nasal symptoms, patients suffering from untreated AR can also have allergic conjunctivitis, post-nasal drip, non-productive cough, Eustachian tube dysfunction, and chronic sinusitis. Once diagnosed, AR is treatable with a variety of modalities, with intra-nasal glucocorticoids being first-line therapy.[1]

Nursing Diagnosis

• Runny nose
• Congested nose
• Postnasal drip
• Sneezing
• Itching

Causes

Allergic rhinitis is an immunoglobulin (Ig)E-mediated response against inhaled allergens that cause inflammation driven by type 2 helper (Th2) cells. There is a considerable genetic component to the allergic reaction, classified into early and late phase reactions.[2] The initial response occurs within minutes of exposure to allergens and characteristically manifests degranulation of host mast cells. This releases a variety of pre-formed and newly synthesized mediators, with histamine (H) being one of the primary mediators of allergic rhinitis. Histamine induces sneezing via the trigeminal nerve and also plays a role in rhinorrhea by stimulating mucous glands. Other immune mediators such as leukotrienes and prostaglandins are also implicated as they act on blood vessels to cause nasal congestion. Four to six hours after the initial response, an influx of cytokines, such as interleukins (IL)-4 and IL-13, from mast cells occurs, signifying the development of the late phase response. These cytokines, in turn, facilitate infiltration of eosinophils, T-lymphocytes, and basophils into the nasal mucosa and produce nasal congestion.[3]

In long-standing AR, due to eosinophilic infiltration and nasal mucosa obliteration, a non-IgE mediated hyperresponsiveness develops. The nasal mucosa now becomes hyperreactive to normal stimuli (such as tobacco smoke, cold air) and causes symptoms of sneezing, rhinorrhea, and nasal pruritis.[4]

There are data to suggest there may be a genetic component to the development of allergic rhinitis, but studies are generally lacking. Monozygotic twins show 45% to 60% concordance, and dizygotic twins have a concordance rate of approximately 25% in the development of AR. Specific regions on chromosomes 3 and 4 also correlate with allergic responses.[5]

Risk Factors

The prevalence of allergic rhinitis based on physician diagnosis is approximately 15%; however, the prevalence is estimated to be as high as 30% based on patients with nasal symptoms. AR is known to peak in the second to fourth decades of life and then gradually decline.[6] The incidence of AR in the pediatric population is also quite high, making it one of the most common chronic pediatric disorders. According to data from the International Study for Asthma and Allergies in Childhood, 14.6% in the 13 to 14 year age group and 8.5% in the 6 to 7 year age group display symptoms of rhinoconjunctivitis linked to allergic rhinitis.[7] Seasonal allergic rhinitis seems to be more common in the pediatric age group, whereas chronic rhinitis is more prevalent in adults.[8]

A systematic review from 2018 estimated that 3.6% of adults had missed work and 36% had impaired work performance due to allergic rhinitis. Economic evaluations have shown that indirect costs associated with lost work productivity account for the majority of the cost-burden for AR.[9] 

Risk factors for developing AR include a family history of atopy, male sex, a presence of allergen-specific IgE, a serum IgE greater than 100 IU/mL before age 6, and/or higher socioeconomic status.[5] Studies in young children have shown a higher risk of AR in those with early introduction of foods or formula and/or heavy exposure to cigarette smoking in the first year of life.[2] Although many recent studies have evaluated the link between pollution and the development of AR, no significant correlation yet exists definitively. Interestingly, there are several factors identified that may have a protective effect on the development of AR. The role of breastfeeding in the development of AR is often debated, but it is still recommended due to its many other known benefits and no associated harms. There is no evidence that pet avoidance in childhood prevents AR; however, it is hypothesized that early pet exposure may induce immune tolerance. There is growing interest in the "farm effect" on the development of allergies, and a metanalysis of 8 studies showed a 40% lower risk in subjects who had lived on a farm during their first year of life.[10]

Assessment

Taking a thorough, detailed history is an essential part of AR evaluation, so questions should focus on the types of symptoms, the time, duration, and frequency of symptoms, suspected exposures, and exacerbating factors.[10] Patients with intermittent or seasonal allergic rhinitis have symptoms of sneezing, rhinorrhea, and watery eyes. On the other hand, patients with persistent, chronic AR complain of postnasal drip and chronic nasal congestion and obstruction.[8] These patients will often have a family history of allergic rhinitis or a personal history of asthma. Patients with intermittent rhinitis may report triggers such as pollens, animal dander, flooring/upholstery, mold, humidity, and/or tobacco smoke.[11]

On physical examination, clinicians may notice mouth breathing, frequent sniffling and/or throat clearing, transverse supra-tip nasal crease, and dark circles under the eyes (allergic shiners). Otoscopic examination of the nose typically reveals swelling of the nasal mucosa and thin, clear secretions. Whenever possible, an internal endoscopic examination of the nasal cavity should be conducted to assess nasal polyps and structural abnormalities. Pneumatic otoscopy can be used to assess for eustachian tube dysfunction, which can be a common finding in patients with allergic rhinitis. Palpation of sinuses may elicit tenderness in patients with chronic symptoms. These patients should also undergo careful examination for signs of asthma or dermatitis.[11]

Evaluation

Allergic rhinitis is largely a clinical diagnosis made based on a thorough history and physical. A positive response to empiric treatment with a nasal glucocorticoid can help clinch the diagnosis. A formal diagnosis is possible with either serum testing for allergen-specific IgE or allergy skin testing.[6] As stated by the American Academy of Otolaryngology guidelines, allergy testing should be reserved for patients who are unresponsive to empiric treatment or require identification of a specific allergen to target therapy.[1] Serum testing does not require trained technicians, and the patient does not need to stop taking antihistamines in advance. On the other hand, skin allergy testing requires a trained professional to perform testing, and results are available immediately. In patients with seasonal symptoms, testing should is preferable when symptoms are present to be able to best identify the triggers.[6] Skin testing is known to have slightly better sensitivity than serum testing and is more cost-effective. Contraindications to skin allergy testing include patients with uncontrolled or severe asthma, unstable cardiovascular disease, pregnancy, and/or concurrent beta-blocker therapy. H2-receptor antagonists, tricyclic antidepressants, and anti-IgE monoclonal antibody omalizumab can interfere with allergy skin test response; therefore, cessation is advisable before testing.[10]

Radiographic imaging is not routinely recommended for the diagnosis of AR and is mostly used to rule out other conditions such as rhinosinusitis.[10]

Medical Management

Avoidance of triggers, especially in those with seasonal symptoms, is encouraged, although it is not always practical, such as in the case of allergy to pollens. Precautions can be taken to avoid dust mites, animal dander, and upholstery. If removal of a pet from home is not feasible, isolating the pet to a single room in the house may be an option. It is important to note that it may take up to 20 weeks to completely eliminate cat dander from home even after removal.  It is also recommended to use allergen-impermeable bedding covers, wash sheets in hot water, and use a vacuum cleaner with high-efficiency particulate air (HEPA) filters.[5] 

Pharmacological options include antihistamines, intranasal steroids, leukotriene receptor antagonists (LTRAs), and immunotherapy. First-generation antihistamines include diphenhydramine, chlorpheniramine, and hydroxyzine; whereas, fexofenadine, loratadine, desloratadine, and cetirizine are examples of second-generation antihistamines. Both first- and second-generation antihistamines are effective at controlling symptoms of AR, but first-generation antihistamines can be quite sedating due to their ability to cross the blood-brain barrier. These agents also act on muscarinic receptors, causing side effects of dry mouth, urinary retention, constipation, and/or tachycardia. Second-generation antihistamines have improved H1 selectivity, are less sedating, and have longer half-lives (12 to 24 hours) compared to those of the first-generation. Fexofenadine has no sedating effects, but loratadine and desloratadine may be sedating at higher doses. Cetirizine has the most potential for sedation of all second-generation antihistamines. In terms of symptom relief, there is no one agent recommended over others.[5] Intranasal antihistamines, such as azelastine, have a rapid onset and are more efficacious than oral antihistamines in relieving nasal symptoms. They are recommended as first or second-line therapies for AR.[10]

Intranasal corticosteroid therapy can be as monotherapy or in combination with oral antihistamines in patients in patients with mild, moderate, or severe symptoms. Studies have shown intranasal corticosteroids are superior to antihistamines in effectively reducing nasal inflammation and improving mucosal pathology.[12] Commonly available nasal sprays in the United States include beclomethasone, budesonide, fluticasone propionate, mometasone furoate, and triamcinolone acetonide. Proper administration of nasal spray is critical in achieving an optimal clinical response; therefore, patients should always receive counsel on the appropriate use of devices. They should be used regularly, as their peak effect may take multiple days to develop. The most common side effect reported is nasal irritation, which can be prevented by spraying away from the nasal septum.[11] Oral and injectable steroids have been shown to alleviate symptoms of AR but are not recommended for routine use due to their significant side-effect profile.[10]

Leukotriene receptor antagonists (LTRAs) such as montelukast and zafirlukast can be beneficial in patients with AR, but they are not as efficacious as intranasal corticosteroids.[13] Their use is often in combination therapy with other agents. For patients in whom avoidance measures and combination pharmacotherapy are not effective, allergen immunotherapy should be considered.  Subcutaneous immunotherapy (SCIT) or sublingual immunotherapy (SLIT) are commonly used therapies. Weekly incremental doses are given for 6 to 8 months, followed by maintenance doses for 3 to 5 years. Typically, patients experience a prolonged, protective effect, and therapy can be ceased.[1]

Oral decongestants such as pseudoephedrine are useful in relieving symptoms but are not recommended for extended daily use due to their side-effect profile. Intranasal decongestants such as xylometazoline are alpha-agonists that are delivered directly to nasal tissue to produce vasoconstriction. Prolonged use of intranasal decongestants have a risk of causing rebound nasal congestion (rhinitis medicamentosa) and, therefore, should not be used for more than a week.[10] Sodium cromoglycate (Cromolyn) is effective in reducing sneezing, rhinorrhea, and nasal pruritis, so it is a reasonable option. Surgical treatment is reserved for patients with rhinitis, polyposis, or chronic sinus disease refractory to medical treatment.[5] Budesonide is the only FDA-approved agent for pregnant patients experiencing symptoms of allergic rhinitis.[1] Omalizumab, a monoclonal antibody, has been shown to be beneficial in patients with AR, although the cost associated with therapy is a limiting factor in its use.[14] Nasal saline can be another option in conjunction with other treatment modalities. Isotonic solutions have shown to be more beneficial in adults, whereas hypertonic solutions may be more effective in children.[10]

Nursing Management

• Obtain a thorough history of allergy and seasonal variation
• Understand the triggers
• Teach the patient how to use a nasal spray
• Encourage medication compliance
• Encourage avoiding triggers
• Counsel about how to quit smoking

When To Seek Help

• Fever
• Headache
• Mental status changes
• Productive cough
• Dyspnea

Outcome Identification

• Able to breathe through the nose
• No nasal discharge
• Able to sleep

Monitoring

• Environmental control
• Education about avoiding allergens
• Medication compliance

Coordination of Care

According to the "ecology of medical care" model, only a minority of patients seek medical care for their symptoms; and most of these are managed by their primary care physician/provider (PCP). Therefore, it is crucial to provide patients with information on self-management and when to contact their PCP. The involvement of community pharmacists and nurse practitioners can play a vital role in achieving these goals. PCPs and allergy specialists often work closely in co-managing patients with AR. Access to healthcare and specialists varies globally, but PCPs, pediatricians, allergists, and/or ENT specialists may be involved in caring for these patients when available.[15]

Health Teaching and Health Promotion

Patients often underestimate the severity of this condition and fail to seek medical therapy. It is important to get rhinitis under control, especially due to the link between AR and asthma, and poor control of rhinitis typically predicts poor control of asthma.[16] Patient compliance with the treatment regimen is key in proper management and alleviation of symptoms. Patients should receive educational materials with information about allergic rhinitis and its implications. Moreover, patient education on the proper administration of nasal sprays also plays an essential role in a patient's response to therapy.[17] Patients should be advised to look down and squirt nasal spray just inside the nostril, aiming toward both sides' outer walls. It should be stressed that the patient should not take a deep breath or sniff hard after spraying.[18] Counseling patients on avoidance of known allergens is a necessary but time-consuming task.[17]

Discharge Planning

Avoid triggers

Do not smoke

Follow up if symptoms worsen

The of as-needed inhalers

Pearls and Other issues

• Avoidance of triggers, especially in those with seasonal symptoms, is encouraged, although it is not always practical, such as in the case of allergy to pollens.
• Precautions can be taken to avoid dust mites, animal dander, and upholstery.
• If removal of a pet from the home is not feasible, isolating the pet to a single room in the house may be an option. It is important to note that it may take up to 20 weeks to completely eliminate cat dander from a home even after removal.  
• It is also recommended to use allergen-impermeable bedding covers, wash sheets in hot water, and use a vacuum cleaner with high-efficiency particulate air (HEPA) filters.[5]