Allergic diseases are the most common chronic disease in children in the United States and will present frequently to the ED. At least one-quarter of children will be affected at some point during childhood.¹ Pediatric allergic disease is more common in developed countries and the incidence has been shown to be rising dramatically.² Pediatric allergic disease comprises a spectrum of disorders, with the most common being asthma (see Chapter 35), urticaria, allergic rhinitis (AR), and allergic conjunctivitis (AC). The focus of this chapter is allergic rhinitis, allergic conjunctivitis, and urticaria.

In general, allergic reactions are due to heightened responses of the immune system to antigens encountered in everyday life. The most severe of these reactions is anaphylaxis, which involves multiple organ systems and can be life-threatening (see Chapter 69). Allergens are antigens that trigger the allergic response and are most commonly proteins, although carbohydrates and drugs can also serve as allergens. Allergens stimulate production of specific IgE antibodies in the sensitive individual and bind to the surface of the mast cells which usually reside near mucosal surfaces, in submucosal surfaces near venules, and in cutaneous tissue.³ The allergic reaction is triggered when specific IgE antibodies are bridged by the offending allergen which causes degranulation of the mast cell and releases histamine, prostaglandins, leukotrienes, and other inflammatory mediators (Fig. 68-1).³ At the tissue level, this results in increased capillary permeability, vasodilatation, mucosal edema, mucus secretion, and sensory nerve stimulation.³

In first-world countries, AR affects from 20% to 40% of children, making it the most common of the pediatric allergic conditions.⁴ Because it is so common, the economic burden of this seemingly benign disease is quite staggering. AR is a chronic IgE-mediated disease, but there is also a late-phase reaction with tissue eosinophilia, resulting predominantly in nasal congestion.⁴ AR is uncommon in children under the age of 2 years, because it is felt that several years of repeated antigen exposure is required to develop symptoms. AR is frequently associated with other conditions, most commonly allergic conjunctivitis, sinusitis, asthma, and otitis media.⁵ Children with moderate to severe AR may suffer from sleep disturbance and significant impairment of daily activities and performance in school.⁵ Asthma and AR are closely linked as well, particularly in atopic individuals.⁵ Treatment of AR has been shown to reduce bronchospasm, ED visits for asthma, and hospitalization.⁵

The diagnosis of AR in the ED is chiefly clinical, with the main symptoms being nasal congestion or blockage, watery discharge, sneezing, and itching.⁵ These symptoms are often seen during viral upper respiratory infections as well, but with a shorter duration. If symptoms last more than 10 days or recur frequently, then the child most likely has AR. Other causes of chronic nasal symptoms include foreign body, adenoidal hypertrophy, or polyps. Physical findings include “allergic shiners” (darkening of lower eyelids), the “allergic salute” (frequently pushing on the nose with the palm of hand to open the nasal passages) (Fig. 68-2), and the “allergic crease” (a transverse line across the bridge of the nose). Children with AR will frequently be “mouth breathers” due to nasal congestion.

The initial phase of treatment for AR involves removing causative allergens from the patient’s environment, which may be very difficult for environmental allergens, such as pollen. Antihistamines are the first line of therapy for mild, intermittent symptoms and are effective in controlling the rhinorrhea, sneezing, and pruritus seen with AR. Second-generation antihistamines are preferred, because they are less sedating, have a faster onset, and are longer lasting.⁶ Intranasal antihistamine use can be helpful, but have a bitter taste and are less effective than intranasal corticosteroids. Intranasal anticholinergic sprays offer symptomatic relief of rhinorrhea, but no relief for pruritus or congestion.⁵ Intranasal corticosteroids are the most effective medication for AR, and along with oral antihistamines are the mainstay of therapy for patients with severe, persistent symptoms.⁶ Other therapies include short courses of intranasal decongestants, leukotriene-modifying agents, and allergen immunotherapy.⁵ Systemic corticosteroids should rarely if ever be required for treating children with AR.⁵

AC is a common pediatric condition as well, affecting up to 30% of atopic children.⁷ The eyes may be affected alone, due to their high vascularity and direct contact with environmental allergens, or more frequently in conjunction with nasal allergies. The majority of patients with AR have coexistent AC and for many of these patients, the ocular symptoms are as severe as the rhinitis symptoms.⁸ AC (Fig. 68-3) occurs in two forms, seasonal allergic conjunctivitis (SAC), which is usually associated with AR and perennial allergic conjunctivitis (PAC).⁷ SAC, or “hay fever” conjunctivitis, is most commonly triggered by pollens, but can be caused by mold spores as well. SAC is the most common allergic disease of the eye.⁹ PAC is caused by allergens that are present year-round. AC is rarely caused by food allergens. Less common forms of AC include vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), and giant papillary conjunctivitis (GPC).⁹ VKC is not IgE mediated, but occurs more frequently in children with seasonal allergies, atopic dermatitis, and asthma.⁷ It is more common in boys and may threaten eyesight if the cornea is involved. Clinically, there is severe itching, and giant papillae are seen on the upper tarsal plate (Fig. 68-4).¹⁰ AKC more frequently involves the lower tarsal plate and is seen in children with atopic dermatitis. Patients may have eyelid eczema, and eyesight may be threatened if the cornea is involved. GPC is most frequently seen in patients who use extended-wear contact lenses, especially if worn at night. Symptoms include itching, mucoid discharge, and giant papillae on the upper tarsal conjunctiva (Fig. 68-5).¹⁰