Paul J. Eakin
HIGH YIELD FACTS
• Allergy related disease is extremely common and will present frequently to the emergency department (ED).
• The diagnosis of allergic conjunctivitis/rhinitis is often missed or delayed.
• Complications of allergic conjunctivitis/rhinitis include exacerbation of asthma, sinusitis, middle ear infections and effusions, and sleep disturbances.
BACKGROUND
Allergic disease is extremely common in the United States and presents frequently to the ED. Forty percent 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.2,3 Pediatric allergic disease comprises a spectrum of disorders, with the most common being asthma (see Chapter 34), urticaria, allergic rhinitis (AR), and allergic conjunctivitis (AC). The focus of this chapter will be allergic rhinitis, allergic conjunctivitis, and urticaria.
PATHOPHYSIOLOGY
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 (see Chapter 68). 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 cell which usually reside near mucosal surfaces, in submucosal surfaces near venules, and in cutaneous tissue.4 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. 67-1).4 At the tissue level, this results in increased capillary permeability, vasodilatation, mucosal edema, mucus secretion, and sensory nerve stimulation.4
FIGURE 67-1. Release of histamine, cytokines, prostaglandins, and other inflammatory mediators.
ALLERGIC RHINITIS
AR affects up to 40% of children in the United States, making it the most common chronic disease in children.5 Because it is so common, the economic burden of this seemingly benign disease is quite staggering.6,7 AR is an IgE mediated disease, but there is also a late phase reaction with tissue eosinophilia, resulting predominantly in nasal congestion.8 AR is frequently associated with other conditions, most commonly allergic conjunctivitis, sinusitis, asthma, and otitis media.9 Children with moderate-to-severe AR may suffer from sleep disturbance and significant impairment of daily activities and performance in school.9 Asthma and AR are closely linked as well, particularly in atopic individuals.8 Treatment of AR has been shown to reduce bronchospasm, ED visits for asthma, and hospitalization.8
DIAGNOSIS
The diagnosis of AR in the ED is chiefly clinical, with the main symptoms being nasal congestion or blockage, watery discharge, sneezing, and itching.9 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.9 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. 67-2), and the “allergic crease” (a transverse line across the bridge of the nose). Children commonly mouth breathe due to nasal congestion.
FIGURE 67-2. The allergic salute.
TREATMENT
The initial phase of treatment for AR involves removing causative allergens from the patient’s environment which can be close to impossible for environmental allergens, such as pollen.8 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.8 Intranasal antihistamines use can be helpful, but have a bitter taste and are less effective than intranasal steroids. Intranasal anticholinergic sprays offers symptomatic relief of rhinorrhea.10 Intranasal steroids are the most effective medication for AR and along with oral antihistamines they are the mainstay of therapy for patients with severe, persistent symptoms.10 Other therapies include short courses of intranasal decongestants and leukotriene-modifying agents.8
ALLERGIC CONJUNCTIVITIS
AC is a common pediatric condition as well, affecting up to 30% of atopic children.11 The eyes may be affected alone, due to its high vascularity and direct contact with environmental allergens, or more frequently in conjunction with nasal allergies. Research has shown more than 75% of patients with AR had coexistent AC and for many of these patients, the ocular symptoms are as severe as the rhinitis symptoms.12 AC (Fig. 67-3) occurs in two forms, seasonal allergic conjunctivitis (SAC), which is usually associated with AR and perennial allergic conjunctivitis (PAC).11 SAC is most commonly triggered by pollens, but can be caused by mold spores as well. PAC is caused by allergens that are present year round. AC is rarely caused by food allergens.9 Less common forms of AC include vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), and giant papillary conjunctivitis (GPC).11,13VKC is not IgE mediated, but occurs more frequently in children with seasonal allergies, atopic dermatitis, and asthma.11 It is more common in boys and may threaten eyesight if the corneal is involved. Clinically, there is severe itching and giant papillae are seen on the upper tarsal plate (Fig. 67-4).13AKC 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. 67-5).13
FIGURE 67-3. Allergic conjunctivitis. Arrow indicates chemosis. (Reproduced with permission from Adkinson NF, Busse WW, Bochner BS, et al: Middleton’s Allergy: Principals and Practice. 7th ed. Mosby/Elsevier; 2008.)
FIGURE 67-4. Vernal Keratoconjunctivitis. (Reproduced with permission from Adkinson NF, Busse WW, Bochner BS, et al: Middleton’s Allergy: Principals and Practice. 7th ed. Mosby/Elsevier; 2008.)
FIGURE 67-5. Giant papillary conjunctivitis. (Reproduced with permission from Adkinson NF, Busse WW, Bochner BS, et al: Middleton’s Allergy: Principals and Practice. 7th ed. Mosby/Elsevier; 2008.)
DIAGNOSIS
The differential diagnosis of AC includes nonallergic conjunctivitis, foreign body, nasolacrimal duct obstruction, corneal abrasion, and uveitis.11 Nonallergic conjunctivitis can have viral or bacterial etiologies with symptoms usually starting unilaterally. There is more frequent stinging, foreign body sensation, or irritation; whereas the main symptoms for AC include bilateral itching, watery discharge, and nasal involvement.14 The diagnosis of ocular allergy is made clinically.
TREATMENT
The primary treatment of ocular allergy involves avoidance of allergens and cold compresses. Patients who wear contact lenses should discontinue use while on treatment for ocular allergy. Secondary treatment includes antihistamines, mast cell stabilizers, anti-inflammatory agents, and topical corticosteroids. Oral antihistamines may help with some symptoms, but they often exacerbate eye dryness.11 Dual-acting antihistamine and mast cell stabilizing drugs are the most commonly prescribed drugs for ocular allergies. Table 67-1 has a partial listing of ophthalmic agents for allergic conjunctivitis.11 In patients with rhinoconjunctivitis, the use of intranasal corticosteroids will reduce ocular symptoms as well. Topical corticosteroids are highly effective, but should be prescribed by ophthalmologists.14 Allergen immunotherapy can be very effective for patients with severe, persistent SAC or PAC.13
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TABLE 67-1 |
Ophthalmic Agents for Allergic Conjunctivitis |
URTICARIA
Urticaria (hives) and angioedema are very common, affecting more than 20% of people during their lifetime.15 They are classified as acute if lasting less than 6 weeks or chronic if lasting for more than 6 weeks.15 Acute urticaria describes raised and slightly erythematous wheals or papules that are pruritic and edematous (Figs. 67-6 and 67-7). Acute urticaria favors the trunk and extremities and is a transient process with new crops of hives appearing and resolving over several hours. Angioedema results from the same IgE-mediated process as urticaria, but involves deeper dermal and subcutaneous tissues.15Angioedema favors the face, lips, tongue, mouth, genitalia, and extremities.16 In children, the most common triggering agents for acute urticaria include infections, medications, and foods.15 For younger children, the most common foods that cause urticaria are egg, milk, soy, peanut, and wheat. For older children, common triggering foods are fish, seafood, nuts, and peanuts.15 Viral infections can commonly cause pediatric urticaria.17 Frequently, chronic urticaria is accompanied by angioedema and is most often idiopathic. Less frequently, children may suffer from physical urticaria, which can be brought on by pressure, exercise, contact with water, cold exposure, or less commonly sun exposure.16
FIGURE 67-6. Hives on trunk with excoriation from scratching.
FIGURE 67-7. Focal hives to knee on patient with respiratory infection.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis for acute pruritic rash includes atopic dermatitis, contact dermatitis, insect bites, or drug eruptions. Chronic urticaria is less common in children than adults.15 The differential diagnosis of chronic urticaria includes thyroid disease, mastocytosis, malignancy, systemic lupus erythematosus, and juvenile rheumatoid arthritis.16 Hereditary angioedema causes chronic intermittent angioedema, but is beyond the scope of this chapter.
DIAGNOSIS
The diagnosis of acute urticaria is made clinically, but laboratory testing may be considered for chronic urticaria. This would include complete blood count, ESR, urine testing, thyroid antibody testing, and liver function tests.15
TREATMENT
Acute urticaria is usually a self-limited process which will resolve with antihistamines and avoidance of the provoking allergen, if known. First or second generation antihistamines can be used.18,19 If symptoms continue while on a second-generation H1 antagonist, addition of an H2 antagonist such as ranitidine may be helpful. Physical urticaria can generally be treated by avoidance of the provoking stimuli along with antihistamines. Chronic urticaria is treated with nonsedating antihistamines and may require higher doses than other conditions. Antileukotriene agents used in conjunction with antihistamines may be helpful. If urticaria persists after this, a short course of oral corticosteroids may be considered. Referral to an allergist may be necessary for refractory cases and immunomodulatory therapy may be required.15
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