Pathophysiology

The nose contains a large surface area where inhaled particles are trapped before they can flow into the lower respiratory structures. Most allergens are large and become trapped in the mucous membranes of the nasal tissue. In the mucous membranes, there is an initial reaction between the allergen and intraepithelial mast cells, which proceeds deeper to the perivenular mast cells, both of which are sensitized with specific IgE. In addition to IgE, the mucosal surface in the nose also contains IgA. The IgE attaches to the mucosal and submucosal mast cells, and the intensity of the symptoms is directly related to the allergen dose. When an allergen is inhaled, the IgE attached to the mast cells within the mucosa and submucosa stimulates the release of histamine and leukotrienes, causing local tissue edema and increased drainage.

Clinical Presentation

Allergic rhinitis should be suspected with seasonal or recurrent sneezing, disturbances of taste or smell, nasal congestion, dry mouth, postnasal discharge, and fatigue. Nasal discharge is thin and clear, and the patient may have nasal obstruction and facial discomfort. Watery, itchy, and puffy eyes commonly occur, but fever and chills are unusual. Typically the patient has a personal or family history of asthma, eczema, or other atopic disease.

A detailed environmental exposure history is essential. Dust mites, animal dander, and indoor allergens should be suspected when winter symptoms predominate because heating systems disseminate dust particles and aggravate symptoms during the winter months. Patients with seasonal symptoms are typically allergic to outdoor allergens such as pollen and ragweed. Symptoms that occur during late spring and early summer are generally triggered by grass pollens, whereas symptoms during late summer and early fall tend to be linked to weed pollens. Tree pollens tend to be associated with symptoms in late winter or early spring. These generalizations vary with geographic changes and daily fluctuations in allergen counts.

Because symptoms related to allergic rhinitis cause itching in the nose and throughout the upper respiratory tract, the pattern of symptoms is important. When is the patient asymptomatic? What medications has the patient been using? Where and when do symptoms occur? Is there associated itching, and if so, where?

The exact anatomic location of congestion should also be determined. Anatomic obstructions tend to cause unilateral nostril blockage, whereas nasal polyps generally cause bilateral obstruction.

Physical Examination

The physical examination can be performed with either a nasal speculum or an otoscope with an attached speculum. The nasal mucosa is typically pale (in contrast to viral or bacterial disease) because of chronic venous engorgement from the histamine and leukotrienes. The upper airway examination will also reveal swollen nasal turbinates with bleeding, mucus, crusting, and other signs of inflammation. Other common findings can include enlarged tonsils, postnasal drip, the well-recognized “allergic salute” (a crease across the nose from manipulating the tip of the nose), and conjunctival irritation.²

Diagnostics

Diagnosis of allergic rhinitis is primarily clinically based; patients report the hallmark symptoms of sneezing, rhinorrhea, and nasal and pharyngeal itching in the absence of infection. If there is a question about the cause of the symptoms, nasal cytologic studies (Wright stain) can demonstrate neutrophils or eosinophils and determine whether the symptoms are related to allergic rhinitis or infection. If further diagnostic tests are desired, the patient should be referred to an allergist for testing. Additional tests can include scratch or patch tests, which are used to test for skin response to suspected allergens. Radioallergosorbent tests (RASTs) determine serum levels of allergen-specific IgE titers, but skin testing is more sensitive and is the preferred diagnostic. However, RASTs are helpful in diagnosis of food-related allergies and can be used in patients with dermatographism or equivocal skin test results or in patients who cannot discontinue antihistamines.

Providers should exclude structural abnormalities within the nasopharynx, irritant exposure, pregnancy, hypothyroidism, idiopathic rhinitis, rhinitis medicamentosa, or prolonged use of topical alpha-adrenergic agents before making a diagnosis of allergic rhinitis. Many oral medications are also associated with rhinitis, including reserpine, methyldopa, nonsteroidal anti-inflammatory drugs (NSAIDs), and beta blockers.³ Infectious rhinitis tends to be associated with fever, purulent sinus drainage, and other signs of infectious sinusitis.

The most important way to control allergic rhinitis is through environmental control. Because the patient is typically allergic to several allergens, control of the indoor and outdoor environment is crucial.³ Nonspecific irritants (e.g., smoke) and indirect contact (e.g., secondary contact with animal dander) can cause symptoms that are indistinguishable from those of allergies.⁴ Although techniques to control environmental allergens are arduous, time-consuming, and sometimes expensive, they are often essential for symptom control. In general, it tends to be the time commitment involved, not the cost, that makes environmental control difficult for patients.

If the allergen is outdoors, minimizing both direct and indirect exposure is recommended. Long-sleeved clothing and a mask may also be necessary to minimize direct contact. However, it is often the indirect contact—when the allergen is brought into the house—that proves to be most bothersome. Keeping the windows closed and bathing and changing clothes immediately after entering the home should minimize exposure.

An indoor allergen is often the cause of complaints. House dust contains the waste products of dust mites that live in furniture, carpets, bedding, and mattresses. Stuffed animals are a significant problem for some patients. Pets, particularly cats and dogs, are also a major cause of allergic symptoms. Removal of the pet is not an effective means of environmental control because many people are not willing to give up their animal. Effective strategies include keeping the pet out of the bedroom at all times; keeping the pet outdoors as much as possible; washing the pet and pet bedding weekly; ventilating the home frequently to promote air exchange; having a friend or family member who is not allergic clean regularly with a high-efficiency particulate air (HEPA) or double-bag vacuum; and minimizing carpeting, drapes, and upholstered furniture. Attempts to eliminate cockroach proteins include storing foods in tightly sealed containers and having the pest eliminated.³ When possible, carpets should be eliminated, but if that is not an option, carpeting should be made of synthetic and short-napped fibers. Rugs should be washable; all loose or old rugs should be removed. Curtains (which should be cotton and, preferably, washable) and furniture should be cleaned and wiped regularly; dust-catching blinds should be avoided.

Other recommendations include keeping closet doors shut; covering machine-washable polyester pillows, mattresses, and comforters with allergy-free and zippered plastic covers; wet dusting; washing stuffed animals, sheets, and comforters in hot water (>54° C [130° F]) at least weekly; removing house plants and books; trimming bushes from the house; cleaning central heating and air-conditioning units; cleaning walls; using mold inhibitors when painting; reducing mold growth and humidity; and using a frost-free refrigerator. Although the efficacy of HEPA filters is unclear, HEPA furnace filters and room cleaners may also decrease allergen exposure.

Controlling environmental exposures is important in controlling symptoms, but the provider-patient relationship is also crucial. Environmental recommendations should be reasonable and made with compassion and clarity.

Medications

Pharmacologic interventions are appropriate if strict environmental control has not worked sufficiently, but they should be used only when allergies significantly affect quality of life. Because pharmacologic agents may be used for extended periods, the safety, side effect profile, and cost-effectiveness of each agent must be considered carefully. Pharmacologic therapy often combines several different medications to provide patients with optimum symptom relief.

Treatment of allergic rhinitis is multifaceted and includes a combination of medical therapies and behavior modifications. Intranasal steroids should be first-line treatment for allergic rhinitis⁵ because systemic treatments do not target the nasal mucosa as effectively.⁶ The benefit of intranasal steroids is that they provide a targeted dose of steroids, allowing maximal efficacy and sparing systemic steroid doses and side effects. Steroids exert their effects by reducing the inflammatory response and inhibiting cytokine release^5,6; they begin working as soon as 6 to 8 hours after the dose. However, patients often need 2 to 4 weeks of continued use to see maximum benefit.^5,6 Several intranasal steroids are available for use, and there is no demonstrable difference among the different steroids, so patients may start with any of the available preparations.⁵ If treating pregnant patients, the only intranasal steroid to receive a Category B rating from the U.S. Food and Drug Administration (FDA) is budesonide.⁵

Intranasal steroids have a good safety profile with few systemic side effects.⁵ No studies have shown any effects on the hypothalamic-pituitary axis.⁵ Most common side effects reported are nasal burning, stinging, and dryness.⁵ Patients may also report headaches, epistaxis, and pharyngitis.⁵

Oral antihistamines are another mainstay of treatment in allergic rhinitis because histamine is the primary mediator of the nasal allergic reaction and increases nasal secretion; blocking of the histamine can potentially interrupt the damaging chemical mediator cascade, producing symptoms from both the allergic and viral pathologic processes.⁵ Oral antihistamines can be effective in reducing sneezing, pruritus, and rhinorrhea, but overall are less effective than intranasal steroids in reducing the congestion associated with the allergic response.⁵ The second-generation antihistamines are preferable because they have far fewer central nervous system side effects, require only once-daily administration, and offer quick relief with a 1- to 2-hour onset of action.⁷ The second-generation antihistamines are effective throughout the allergic cycle. With the exception of cetirizine, the second-generation antihistamines do not produce significant sedation and should therefore be considered a first-line treatment of allergic rhinitis before use of first-generation antihistamines and for those who cannot tolerate inhaled nasal steroids or those with narrow-angle glaucoma or benign prostatic hyperplasia.^5,8 Initially more expensive than the first-generation agents, second-generation antihistamines, such as loratadine, cetirizine, and fexofenadine, are now available in generic formulations and can provide improved quality of life and work performance.

Although the second-generation antihistamines are very effective, they tend not to alleviate nasal congestion. Therefore, combination formulations with decongestants, such as fexofenadine and pseudoephedrine (Allegra-D) or loratadine and pseudoephedrine (Claritin-D), are useful. Unfortunately, the decongestant component can cause sleeplessness, tachycardia, tremors, and other side effects. Antihistamines and decongestants are contraindicated for patients with hypertension, prostate enlargement, or narrow-angle glaucoma.

First-generation antihistamines can also be considered as a treatment option for allergic rhinitis, but they are much more sedating than their newer counterparts. In addition to their sedating side effects, the first-generation antihistamines have poor selectivity for the H₁ receptors, and often have an effect on the muscarinic receptors as well, causing constipation, blurred vision, and urinary retention.¹ Several options are available over the counter, including diphenhydramine and chlorpheniramine, and there are also prescription agents including hydroxyzine or promethazine. Compliance with the first-generation antihistamines can be low, because they often need to be administered several times per day. Some studies have shown patients occasionally develop a tolerance to the sedating properties of these medications, but more study is needed.¹ Generally speaking, the first-generation antihistamines should be reserved for nighttime symptoms when patients may desire the sedating side effects of these medications.

Other intranasal agents that can be helpful in controlling allergic rhinitis include azelastine, cromolyn, and ipratropium bromide. Azelastine is an antihistamine spray, but it is expensive and can cause an unpleasant taste if it is not used correctly. One study has suggested that intranasal azelastine was superior to several second-generation antihistamines at relieving nasal symptoms.¹ Intranasal cromolyn affects the inhibition of mast cell degranulation; thus it affects local cytokine release. If it is taken regularly, cromolyn can prevent early- and late-phase allergic responses.¹ The major problem is the administration regimen, which is four times daily. Nevertheless, its safety profile makes it an appealing choice for some patients, and it is available over the counter.

Intranasal ipratropium bromide, an anticholinergic agent, is most effective for rhinorrhea and sneezing but is less useful for nasal congestion.¹ It is the treatment of choice for gustatory and vasomotor rhinitis and is often used to treat symptoms of the common cold.¹ It is generally safe and well tolerated. The most common drug-related problems are dryness and epistaxis.

Special consideration for patients who are pregnant includes use of chlorpheniramine and nasal cromolyn to alleviate symptoms. Intranasal beclomethasone may be used for intractable symptoms in place of oral therapy. Oral decongestants should be avoided during the first trimester and in breastfeeding mothers. As always, patients should inform their obstetrician/gynecologist of any medications they may be considering for treatment.

One nonpharmacologic intervention that has shown efficacy in allergic rhinitis is nasal saline irrigation. Patients can use a variety of devices, including a neti pot or plastic bottle to rinse the nares and potentially sinus cavities with isotonic saline. Few studies have examined the benefit of nasal saline irrigation, but one study has suggested that it is beneficial in pregnant women with allergic rhinitis.¹

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