Allergic rhinitis is a chronic inflammatory disease of the upper airway caused by IgE sensitization to airborne allergens in genetically susceptible individuals. In the United States, symptoms of allergic rhinoconjunctivitis (ARC) affect between 20% to 30% of adults and as many as 40% of children. The clinical presentation characteristically is associated with frequent sneezing, nasal congestion, and nasal discharge. The vast majority of patients with allergic rhinitis complain or display ocular symptoms (ie, itchy/watery eyes), thus it is termed allergic rhinoconjunctivitis, for which it is better known. Involvement of the lower airway is frequent: up to 40% of patients with ARC also suffer from asthma, and most show evidence of bronchial hyperreactivity. Allergic rhinitis can affect the child’s quality of life and can be associated with conditions such as sleep disturbances and learning difficulties.
Allergic rhinitis has been subdivided into seasonal and perennial types based on time and duration of symptom occurrence. Seasonal symptoms that only occur in spring and summer are often referred to as classical hay fever (pollinosis), whereas perennial allergic rhinitis is caused by an allergic response to allergens such as dust mites and pet dander that are present throughout the year.
There is a wide variation in the prevalence of allergic rhinoconjunctivitis (ARC) worldwide.1 In the pediatric age, the numbers range from 0.8% to 14.9% in 6 to 7 year olds and from 1.4% to 39.7% in 13 to 14 year olds. The reasons behind these disparities are not completely understood, but both environmental and genetic factors are likely to play a role. Like other allergic diseases, the prevalence of ARC seems to be on the rise, particularly in industrialized countries, and as such, ARC has been named a “disease of civilization.” Risks factors for allergic rhinitis include family history of atopy, higher socienoconomic class, and evidence of sensitization.
Aeroallergen sensitization may occur within the first 2 years of life, especially in children with a family history of atopy, but classical symptoms of seasonal allergic rhinitis generally do not develop until 2 to 7 years of age.
In childhood, allergic rhinitis is more frequent in boys, but in adults it is more frequent in women. The prevalence of seasonal allergic rhinitis is higher in children and adolescents, whereas perennial allergic rhinitis has a higher prevalence in adults.
The pathogenesis of allergic rhinoconjunctivitis (ARC) responds to the same immune mechanisms as other allergic disorders. In this case, exposure to airborne allergens, in a genetically susceptible individual, initiates the series of events that lead to the local activation of allergen-specific T cells with a TH2 bias that direct the production of inflammatory cytokines, chemokines, and allergen-specific IgE.3 Upon reexposure to the same allergen, cross-liking of FceR-bound IgE on the surface of mast cells triggers the release of preformed mediators. Histamine released by mast cells is largely responsible for the immediate symptoms associated with ARC such as sneezing, itching, and rhinorrhea. Late responses are characterized by the recruitment of inflammatory cells (eosinophils, T cells, and basophils) to the nasal mucosa. Skin prick testing of the appropriate allergens gives a positive result, and nasal swabs and lavages or biopsy results of the mucosa reveals eosinophils, but neutrophils are usually also present.
A detailed clinical and environmental history is instrumental in determining whether allergies are the cause of the patient’s complaints.3 Questions should address not only the type and frequency of symptoms (sneezing, congestion, nasal discharge, itchy watery eyes) and any identified triggers but also the temporal relationship between perceived exposure and the development of symptoms consistent with an allergic reaction. In the patient with classical hay fever or cat allergies this may be clear-cut, but in the child with perennial nasal congestion and complaints of cough and/or malaise this relationship may not be readily apparent and the diagnosis of allergic rhinoconjunctivitis (ARC) may be missed. Noisy breathing and snoring is a common complaint referred by the parents of young children with ARC and in this age range, poor appetite may also be a manifestation of ARC. In the older child, headaches may be prominent; behavioral problems or poor school performance may be the result of sleep disturbances secondary to untreated respiratory allergies.4 Coexisting or past atopic conditions such as atopic dermatitis, food allergies, or asthma can be suggestive of an allergic etiology, as is a history of respiratory allergies in first-degree relatives. In contrast, a lack of response to conventional antiallergy medications usually points to nonallergic causes.
Atopic children do not have any particular habitus, and for those with seasonal ARC, the physical exam may be completely normal outside of the pollen season. Classical signs of respiratory allergies include the allergic shiners, allergic salute, and allergic crease. While these are often observed in atopic children, their presence neither confirms nor excludes the existence of allergies. The exam of the nasal cavity may be helpful in distinguishing allergic from nonallergic etiologies: Pale, enlarged turbinates and a clear rhinorrhea are usually a sign of ARC whereas an erythematous mucosa with crusty secretions suggests other causes. Nasal polyps, if present, should prompt the search for a different diagnosis, such as cystic fibrosis or, in the older child, aspirin sensitivity. Ocular itch, conjunctival redness or swelling, and tearing are common symptoms of allergic conjunctivitis as part of ARC. In children, findings of dental malocclusion, a high-arched palate, and upper lip elevation may suggest early-onset and/or longstanding disease. A cobblestone-like appearance of the posterior pharynx is usually found in patients with ARC.
Determination of specific IgE is indicated to (1) provide evidence of an allergic basis for the patient’s symptoms, (2) confirm suspected causes of the patient’s symptoms, or (3) assess the sensitivity to a specific allergen for avoidance measures and/or allergen immunotherapy. The number of skin tests and the allergens selected for skin testing should be determined on the basis of the patient’s age, history, and environmental exposures. The percutaneous skin prick technique is preferred due to its simplicity, low cost, and rapid results. Comparable results can be obtained through the determination of levels of specific IgE in serum. When correctly performed, both techniques display a high degree of sensitivity and specificity for the detection of allergic sensitization. However, the findings should be interpreted in the context of the clinical history, because allergic sensitization does not always correlate with clinical allergy. In certain cases, radiological exams could be indicated in order to exclude other causes of nasal congestion, such as adenoid hypertrophy or sinusitis. A polysomnographic test may be necessary to confirm the diagnosis of obstructive sleep apnea (see Chapter 509).
Even if the coexistence of chronic or recurrent nasal and eye symptoms strongly suggests an allergic etiology, the differential diagnosis of chronic rhinitis is vast and depends on the age of the patient. Irritants or toxins can directly influence the nasal mucosa through non–IgE-dependent mechanisms and induce nasal symptoms that are similar to allergic rhinitis and occur after exposure. Other examples of nonallergic rhinitis are infectious rhinitis (usually virally induced and responsible for more than 90% of cases in infants and toddlers), vasomotor rhinitis, and the nonallergic rhinitis with eosinophilia syndrome (NARES). This syndrome is characterized by rhinitis in the absence of atopy shown by allergy skin testing, and > 20% eosinophils on nasal cytology.5 Nasal congestion and discharge that occurs after ingestion of foods or alcoholic products is vagally mediated and usually not a manifestation of food allergy. Chronic nasal congestion can present in patients who take angiotensin-converting enzyme inhibitors, NSAIDS, and other medications, and hormonal rhinitis should be considered in female adolescents. Aside from rhinitis, other conditions may mimic allergic rhinoconjunctivitis, such as nasal polyps and adenoidal hypertrophy, as well as anatomic abnormalities of the nasal or facial structures that may result in the narrowing of the upper airway.
Optimal management of allergic rhinoconjunctivitis in children requires preventive measures to minimize allergen exposure together with the judicious use of pharmacological agents to curtail symptoms, improve the quality of life of the child, and, ideally, prevent the development of long-term complications.6 Because allergic rhinoconjunctivitis is a chronic disease, patient education is a key element in promoting adherence and optimizing treatment outcome.
While allergen avoidance is effective in the control of allergic rhinoconjunctivitis, complete avoidance may not be possible or even practical. Dust mite exposure can be reduced through measures that kill the mites or degrade or prevent their fecal pellets from becoming airborne. When pet dander is the trigger, removal of the pet from the home is the safest option, but patients should be aware that several weeks may be required before the allergen concentration reaches levels found in the animal-free home. Alternatively, confining the cat to an uncarpeted room with HEPA filtration may reduce airborne allergen dissemination to the rest of the house by 90%.
Intranasal corticosteroids (INC) are the quintessential anti-inflammatory drugs used for treating allergic rhinoconjunctivitis (ARC). As monotherapy, INC are more efficacious than antihistamines, leukotriene receptor antagonists, or their combination in the management of the major symptoms of allergic rhinoconjunctivitis. INC provide substantial relief even when used on an as-needed schedule.7,8 Local side effects (burning or stinging) are usually mild. When used at the recommended doses, intranasal corticosteroids are not generally associated with clinically significant effects on the hypothalamic-pituitary-adrenal axis, ocular pressure or cataract formation, or bone density.
Second-generation oral antihistamines (eg, loratadine, desloratadine, fexofenadine, cetirizine, levocetirizine, and others) are preferred over first-generation medications for the treatment of allergic rhinoconjunctivitis because of their reduced tendency to cause sedation and/or anticholinergic effects. These drugs are particularly effective in the management of the ocular and nasal symptoms associated with seasonal allergies. Because of their fast onset of action, they can be used on as-needed basis, although maximal benefit has been reported with long-term use.
The effectiveness of leukotriene receptor antagonists in the treatment of allergic rhinoconjunctivitis is comparable to that of oral antihistamines. As single agents, they are less effective than intranasal corticosteroids for the treatment of allergic rhinoconjunctivitis, but they should be considered in those patients with concomitant asthma or in those in whom corticosteroids are contraindicated or unwelcome. Combination of a leukotriene receptor antagonists and an antihistaminic does not provide added benefit and, in general, should not be recommended.
Isotonic and hypertonic saline solutions, used as either single or adjunctive agents, are of benefit for reducing symptoms in patients with allergic rhinoconjunctivitis or rhinosinusitis. The topical decongestants that work by constricting the blood vessels lining the nose (eg, oxymetazo-line, phenylephrine, xylometazoline and naphazoline nasal sprays) may provide temporary relief, but their longer-term use is discouraged due to the risk of rebound nasal congestion (rhinitis medicamentosa) that sets in within 5 to 7 days of repeated use. Oral decongestants are also not recommended in children due to their well-recognized cardiovascular and CNS side effects.9
Allergen-specific subcutaneous immunotherapy is a clearly effective therapy for allergic rhinitis, specially in those patients with pollinosis and/or house dust mite allergy. Subcutaneous immunotherapy is currently the only treatment that modifies the course of allergic rhinoconjunctivitis by redirecting the immune response toward a tolerant state, and its clinical benefits may be sustained years after discontinuation of treatment. Allergen immunotherapy for allergic rhinitis may prevent the development of new allergen sensitization and has been shown to reduce the risk of asthma in children and adolescents with allergic rhinitis.