Pediatric Allergic Rhinitis

http://emedicine.medscape.com/article/889259-overview#showall Author Jack M Becker, MD Clinical Associate Professor of Pediatrics, Drexel University School of Medicine Jack M Becker, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, and American College of Allergy, Asthma and Immunology Disclosure: Ivax Honoraria Speaking and teaching; teva Honoraria Speaking and teaching Specialty Editor Board C Lucy Park, MD Head, Division of Allergy, Immunology, and Pulmonology, Associate Professor, Department of Pediatrics, University of Illinois at Chicago College of Medicine C Lucy Park, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Medical Association, Chicago Medical Society, Clinical Immunology Society, and Illinois State Medical Society Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference John Wilson Georgitis, MD Consulting Staff, Lafayette Allergy Services ohn Wilson Georgitis, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association for the Advancement of Science, American College of Chest Physicians, American Lung Association, American Medical Writers Association, and American Thoracic Society David Pallares, MD Clinical Assistant Professor, Department of Pediatrics, Division of Allergy and Immunology, University of Louisville School of Medicine David Pallares, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology Chief Editor Harumi Jyonouchi, MD Associate Professor, Division of Pulmonary, Allergy/Immunology, and Infectious Diseases, Department of Pediatrics, University of Medicine and Dentistry of New Jersey-New Jersey Medical School Harumi Jyonouchi, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American Association of Immunologists, American Medical Association, Clinical Immunology Society, New York Academy of Sciences, Society for Experimental Biology and Medicine, Society for Mucosal Immunology, and Society for Pediatric Research Practice Essentials Allergic rhinitis usually presents in early childhood and is caused by an immunoglobulin Emediated reaction to various allergens in the nasal mucosa. Sensitization to outdoor allergens can occur in allergic rhinitis in children older than 2 years; however, sensitization in children aged 4-6 years is more common. Clinically significant sensitization to indoor allergens may

occur in children younger than 2 years. The most common allergens include dust mites, pet danders, cockroaches, molds, and pollens. Essential update: FDA approves carbinoxamine ER oral suspension for pediatric allergic rhinitis In spring 2013, the FDA approved carbinoxamine maleate extended-release, the first liquid, sustained-release histamine-H1 receptor blocker, for the treatment of seasonal and perennial allergic rhinitis in children aged 2 years and older.[1, 2] This formulation will be available in a 4 mg/5 mL suspension and is dosed once every 12 hours. Other indications for carbinoxamine maleate extended release include symptomatic management of[1, 2] : vasomotor rhinitis; allergic conjunctivitis due to inhalant allergens and foods; mild, uncomplicated allergic skin manifestations of urticaria and angioedema; dermatographism; anaphylactic reactions adjunctive to epinephrine and other standard measures after the acute manifestations have been controlled; and amelioration of the severity of allergic reactions to blood or plasma. Signs and symptoms The history of the patient with allergic rhinitis 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. Signs and symptoms of pediatric allergic rhinitis include the following: Rhinorrhea, nasal congestion, postnasal drainage Repetitive sneezing Itching of the palate, nose, or eyes Snoring Frequent sore throats Constant clearing of the throat, cough Headaches See Clinical Presentation for more detail. Diagnosis Perform a full examination to detect other diseases, such as asthma, eczema, and cystic fibrosis, which occur in children in connection with allergic rhinitis. 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 allergic salute Eyes: Marked erythema of palpebral conjunctivae and papillary hypertrophy of tarsal conjunctivae; chemosis of the conjunctivae, usually with a watery discharge; 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:

Nasal smear Complete blood count with differential Serum IgE: An elevated IgE value is suggestive of the diagnosis. Allergen-specific IgE testing (radioallergosorbent test [RAST]): Can be helpful if a specific allergen is suspected Skin prick testing: Highly sensitive and specific for aeroallergens 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 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 (allergy shots) 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 dont 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: 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 allergic rhinitis 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 allergic rhinitis were only 3% less productive.[3] This suggests that effective medications may reduce the overall cost of decreased productivity. Allergic rhinitis 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 Fce 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 feel as allergic rhinitis, 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 allergic rhinitis 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. Studies have shown that most patients with asthma also have allergic rhinitis. Guidelines regarding the impact of allergic rhinitis on asthma have been established.[4] Allergic reactions of the upper airway can trigger lower airway symptoms and vice versa. One study showed that patients with untreated allergic rhinitis 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.[5] 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. How patient feel when they have allergy symptoms.

Nasal symptoms and affect on work performance. Pathophysiology Understanding the function of the nose is important in order to understand allergic rhinitis. 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 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 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 Fc 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 plateletactivating 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 predominated by 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%.[6] 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, 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.[7] Comorbidity of other atopic diseases (asthma, atopic dermatitis) or upper airway inflammation (sinusitis, otitis media) is significant in allergic rhinitis. Individuals with allergic rhinitis have a higher frequency of these conditions than individuals without allergic rhinitis. Quality-of-life surveys have revealed that patients with significant allergic rhinitis found symptoms to be just as debilitating as symptoms in patients with moderate-to-severe asthma. Patients with allergic rhinitis 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 allergic rhinitis 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. Race Allergic rhinitis has no race predilection; however, individuals from nonwhite backgrounds seek out medical attention less often than whites. Sex Allergic rhinitis has no sex predilection. Age Allergic rhinitis usually presents in early childhood. Allergic rhinitis caused by sensitization to outdoor allergens can occur in children older than 2 years; however, sensitization in children aged 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. Allergic rhinitislike 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.[8] 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. Few patients present soon after the onset of allergic rhinitis symptoms. Usually, allergic rhinitis 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. 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 not experiencing allergic symptoms. Sudden onset of nasal symptoms is often associated with 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 o Symptoms of rhinitis consist of rhinorrhea, nasal congestion, postnasal drainage, repetitive sneezing, and itching of the palate, nose, or eyes. Snoring, frequent sore throats, constant clearing of the throat, cough, itchy eyes, and headaches are symptoms often associated with rhinitis. o When obtaining the history, ascertain the following: Determine which symptoms are reported by the patient or parent. 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. Timing of symptoms o 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, or school, or when the patient is around animals. o Determine when symptoms occur and whether they occur primarily at night, in school, outdoors, or at a relative's or friend's home. o 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. o 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, allergic rhinitis should be suspected; however, a negative response does not eliminate the possibility of allergic rhinitis. 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. o 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 o Determine whether symptoms last for weeks, months, or hours. o 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 allergic rhinitis unless concomitant exposure occurs. o In winter in the northern regions, virtually all pollens are absent; therefore, any allergic rhinitislike 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, allergic rhinitis 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.) Family history o 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 allergic rhinitis. This increases to 50-70% if both parents have allergies or atopic asthma. Related medical history o Patients with a history of infantile eczema (atopic dermatitis) have a 70% chance of having allergic rhinitis, asthma, or both. o Patients with a history of asthma also have higher incidence of allergic rhinitis. Social and environmental history o 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). o 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). o 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 of the plastic covers, but standard bedding (bed mattress) can harbor dust mites.
o

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

Head
o

o o

Allergic shiners (dark, puffy, lower eyelids) may be present (see image below). 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, which is the upward rubbing of the nose, is commonly seen in parents as well. 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.

Eyes
o

Ears

o o

Tympanic membranes should be examined for the presence of chronic infection or middle ear effusion. The role of allergic rhinitis in chronic otitis media is not clear, but decreased numbers of infections have been noted in children with allergic rhinitis once therapy was instituted. 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. 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 can mimic the signs and symptoms of allergic rhinitis. Chronic nasal congestion due to adenoid hypertrophy is frequently seen in young children with recurrent otitis media and sinusitis.

Nose
o o o

o o

Throat
o

Causes

Perennial symptoms are usually caused by indoor allergens, including the following: o Dust mites o Cat dander o Dog dander o Indoor molds o Cockroaches o 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 miteproof encasings. o Other furry animals Seasonal symptoms are usually caused by airborne pollen and outdoor molds, including the following: o Tree pollen o Grass pollen o Outdoor mold spores o Weed pollen: Flowers do not cause allergic rhinitis because they do not use wind-borne pollination.

Differential Diagnoses Adenoidal hyperplasia Agammaglobulinemia Aspergillosis Cystic Fibrosis Gastroesophageal Reflux Nasal Polyps Sinusitis 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: Nasal smear: Eosinophils usually indicate allergy. Neutrophils are more indicative of an infectious process, such as sinusitis. CBC count with differential: A CBC count may reveal an increased number of eosinophils. An eosinophil count within the reference range does not exclude allergic rhinitis; 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 allergic rhinitis; however, an elevated IgE value is suggestive of the diagnosis. Allergenspecific IgE testing, also known as radioallergosorbent test (RAST), can be helpful if a specific allergen is suspected. 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 age 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.[9] Patients may be sensitive on a molecular level before IgE response is clinically seen on standard skin testing. This may be a first step toward better customization of immunotherapy in the future.[10] Skin prick testing: This test is highly sensitive and specific for aeroallergens. Imaging studies are not needed unless sinusitis is suspected, in which case, a limited CT scan of the sinuses (without contrast) is indicated

RAST 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, and tests for food allergies are not indicated in patients with allergic rhinitis. RAST testing for allergens, such as dust mites, cat dander, and dog dander, is almost as sensitive and specific as allergen skin testing. Skin testing to identify the triggering agent o Skin testing has high sensitivity and specificity and is the preferred method of quick allergen identification for aeroallergens. o Skin testing is helpful if the allergens can be eliminated from the patient's environment or if the patient can avoid them. o Skin testing 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. o Skin testing is required if the patient is interested in allergen immunotherapy.

Rhinoscopy: This 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.

Medical Care Treatment of allergic rhinitis (AR) can be divided into 3 categories: avoidance of allergens or environmental controls, medications, and allergen-specific immunotherapy (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 to attenuate symptoms. Identification and elimination is easiest for dust mite allergens. o Feathered bedding should be removed and replaced with a fiber-filled product encased by dust miteproof 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. o A bed pad that is placed on top is not helpful and may be another source of dust mite infestation. o Less expensive plastic encasings may leak allergens through needle holes or between zipper teeth; therefore, more expensive dust miteproof covers are preferable. o 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. o Care should be taken to be sure the encasings are dust miteproof. 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 miteproof. Pollen is more difficult to avoid because daily activities must be altered to do so. o 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. o 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. o Another intervention is to obtain a window filter or filter fan, which allows air, but not pollen, to enter the room. o 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. See Medication for a discussion of medications and allergen-specific immunotherapy (ie, allergy shots). A recent study concluded that specific immunotherapy can be recommended for treatment because it is effective in reducing symptoms.[11] 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. 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. If medical therapies do not produce an adequate result, referral to an ENT specialist should be indicated for possible surgical intervention. Dietary restrictions do not help because allergic rhinitis is not triggered by foods.

Diet

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. Medication Summary Many groups of medications are used for allergic rhinitis (AR), including antihistamines, corticosteroids, decongestants, saline, sodium cromolyn, and antileukotrienes. 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 immunotherapy is also available in some parts of the United States as well as other countries of the world.[12] In this form of therapy, small amounts of the allergen are placed under the tongue on a daily basis. The 2 main advantages are that no injections are necessary and treatment can be administered at home. Currently, the formula is not approved by the FDA as it has not been shown to be effective in the United States. However, it has been shown to be effective for certain allergens in several European studies. This is probably

due to different allergens and preparations used in the different countries. Also, grass pollen is not a major allergen in many places in the United States, so its use may not be as great there as in Europe.[13] The formulations that have been tested in other countries are not available in the United States. 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), which require a prescription. View full drug information 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. View full drug information 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 View full drug information Loratadine (Claritin) Nonsedating second-generation antihistamine. Fewer adverse effects than with firstgeneration medications. Selectively inhibits peripheral histamine H1 receptors. Available as tab, disintegrating tab (Reditab), syr (5 mg/5 mL), or combined with pseudoephedrine in 12or 24-h preparations. The only one that is presently available without a prescription View full drug information Desloratadine (Clarinex, Clarinex RediTabs) Nonsedating second-generation antihistamine. Fewer adverse effects than with firstgeneration 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). View full drug information 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. Intranasal Antihistamines 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. View full drug information 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. View full drug information Olopatadine intranasal (Patanase) Intranasal antihistamine indicated 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 antiinflammatory 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. A longer study began in late 2007. View full drug information Beclomethasone, intranasal (Beconase AQ, QNASL) May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation. QNASL available as intranasal dry powder. View full drug information

Budesonide intranasal (Rhinocort Aqua) May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation. View full drug information 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. View full drug information Flunisolide intranasal (Nasarel) May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation. View full drug information Fluticasone intranasal (Flonase, Veramyst) May decrease number and activity of inflammatory cells, resulting in decreased nasal inflammation. View full drug information 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). View full drug information 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.

View full drug information Azelastine/fluticasone intranasal (Dymista) This combination product elicits histamine H1-receptor antagonist activity and antiinflammatory 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 an addictive medication that is effective in shrinking nasal membranes and is not recommended for long-term use. Use of oxymetazoline hydrochloride for more than 7-10 d is habit forming. Patients can be addicted for years at a time. Addiction is termed rhinitis medicamentosa. Ipratropium bromide can be used for a prolonged period of time. View full drug information Ipratropium intranasal (Atrovent Nasal Spray) Anticholinergic used for reducing rhinorrhea in patients with AR or vasomotor rhinitis. An excellent medication for decreasing rhinitis. Nonaddictive 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. Intranasal mast cell stabilizers 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. View full drug information 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. Leukotriene Receptor Antagonists 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. View full drug information 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. Further Outpatient Care Patients with allergic rhinitis (AR) need continuous follow-up care because allergic rhinitis 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. 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. Deterrence/Prevention The best deterrent is to avoid allergens that trigger symptoms. This means diligent environmental controls and patient compliance with medication use. Complications Primary complications of allergic rhinitis 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. Allergic rhinitis can lead to rhinitis medicamentosa when topical nasal decongestants are used in excess. Allergic rhinitis 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. Prognosis Most patients are able to live normal lives with the symptoms. Only patients who receive allergen-specific immunotherapy are cured of the disease; however, many patients do very well with intermittent symptomatic care. Allergic rhinitis symptoms may recur 2-3 years after discontinuation of allergen immunotherapy. 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.

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