This is the most common allergic disease, affecting 10% to 20% of US children. Symptoms include:

Signs on physical exam include:

A transverse nasal crease is often present. Multiple infraorbital folds (Dennie-Morgan lines) may also be present.

Allergic rhinoconjunctivitis (AR) can have either perennial or seasonal symptoms or elements of both. Perennial AR is characterized by year-round symptoms, usually because of chronic exposure to indoor allergens such as dust mite, animal danders, and mold spores. Chronic congestion is often the most prominent symptom. Reduction of exposure is vital to effective treatment. Dust mites reside in cloth items that are not laundered frequently, such as mattresses, carpeting, and stuffed animals. Plastic mattress encasing and bedroom carpet removal are the two most effective avoidance measures. For animals, pet elimination is greatly preferred, but frequent cat and dog washing may reduce pet allergenicity. Dehumidification and chlorine bleach cleaning are effective for indoor mold reduction.

Seasonal AR is usually caused by sensitivity to outdoor allergens such as pollens and mold spores. Allergy seasons and offending allergens are region and climate dependent. Throughout most of the United States, tree pollens cause signs and symptoms of intense nasal and eye itching, mucosal swelling, sneezing, eye redness, rhinorrhea, and tearing in the early spring (March through May). In the Northeast and Midwest, oak and birch are prevalent. In the Southeast, hickory and pecan are most prevalent. In the Southwest, red cedar is a particularly allergenic tree. Pine pollen rarely causes allergy. In the late spring (May through June) grass pollen allergy predominates. In the early fall (late August through October) ragweed is the major allergen.

AR is treated with avoidance, medical management, and allergen immunotherapy. Avoidance is best for indoor allergens. Mild or intermittent symptoms usually respond well to oral antihistamine given as needed with or without decongestant. Chronic perennial or seasonal AR is best treated with ongoing therapy, which can include:

More severe cases may require topical ocular steroids or occasional courses of oral steroids. Prolonged use of topical decongestants, which can cause rhinitis medicamentosa, should be avoided. Allergen immunotherapy involves administration of the offending allergen, in escalating doses until the patient develops sufficient tolerance.

Anaphylaxis usually results from severe IgE mediated sensitization to substances that are either ingested or encountered systemically such as foods, medications, allergenic extracts, latex, and bee venom. Rapid onset of breathing difficulty and/or cardiovascular collapse can ensue, and this requires quick and decisive action for successful treatment and prevention of death. Early and frequent administration of epinephrine 1:1000, 0.01 mL/kg SQ up to 0.3 mL per dose, is the cornerstone of therapy. Use of an antihistamine, such as diphenhydramine 1 mg/kg given parenterally up to every 4 to 6 hours is also important. Many experts recommend adding a histamine 2 (H2) blockade, such as cimetidine (4 mg/kg parenterally). A corticosteroid (methylprednisolone 1-2 mg/kg) can be helpful in preventing a late-phase reaction and is also recommended. Supportive therapy with supplemental oxygen, aerosolized bronchodilators, supine positioning with elevation of the lower extremities, compression trousers, and intravenous fluid administration may be required if more severe or protracted signs and symptoms develop. In rapidly progressive severe reactions, intravenous vasopressors, intravascular colloidal solutions, intravenous aminophylline, and mechanical ventilation should be considered.

Anaphylactoid reactions, which are not IgE mediated, resemble anaphylaxis caused by direct mast cell degranulation. These have been observed most commonly with radiocontrast media and opiates. These reactions should be treated with similar medical management. Pretreatment with antihistamine and corticosteroid is effective in reducing severity for most cases of anaphylactoid reactions, but is not effective for IgE-mediated anaphylaxis as with latex or penicillin. Use of lower osmolality radiocontrast can reduce the risk of reaction in patients with a past history of reaction. There is no allergic cross- reaction between radiocontrast media and seafood.

Penicillin is the most frequently implicated medication and reactions are often caused by allergy to metabolites of the parent compound. There exists extensive cross-reactivity among the penicillins. Cephalosporins usually show about 20% cross-reactivity with penicillins, but this percentage is probably higher for true anaphylaxis. If penicillin is required, allergy skin testing cannot currently be performed, as the test reagent for the major metabolite was recalled and has been unavailable for several years. For patients with histories of anaphylaxis or other severe reactions, successful desensitization can be undertaken in intensive care settings if penicillin is needed. For those with milder histories, a closely supervised test dose challenge can be considered. Reliable testing is not yet available for other antibiotics.

High molecular weight biological medications are also frequent causes of anaphylaxis and include allergenic extracts for immunotherapy, insulin, chymopapain, and horse serum (snake bite antivenin). Latex allergy appears
to be a frequent cause of intraoperative anaphylaxis in patients with spina bifida and congenital urogenital anomalies. Among cancer chemotherapeutic agents, cisplatinum is a frequent cause of anaphylaxis. Beta-blockers can make anaphylaxis extremely difficult to treat and may increase the likelihood of anaphylaxis.

Food anaphylaxis is more common in children than adults, and can be fatal, especially with severe peanut allergy. The most common allergenic foods in children are peanut, milk, egg, soybean, fish, and wheat. Shellfish and nuts are also common offenders. Keep in mind peanuts are legumes, not nuts. Complete dietary avoidance is necessary for true food allergy. Injectable epinephrine should be kept on hand at all times for emergency use.

Allergenic reactions to insect stings affect approximately 1% to 5% of children with most manifesting as large local swelling, redness, pain, and itch at the site of the sting. Extremely large local reactions, distant cutaneous reactions, and systemic reactions with respiratory and/or cardiovascular compromise are much more serious problems that usually require some medical intervention.

Stinging insects include honeybees (Apis), Vespids (yellow jacket, white-faced hornet, yellow hornet), wasps (Polistes), and imported fire ants (Solenopsis). Bee venom contains many proteins that can act as potential allergens such as Phospholipase A, hyaluronidase, mellitin (Apis), and acid phosphatase (Vespids). There is extensive crossreactivity of allergy among the Vespids, about 50% crossreactivity between Vespids and wasps, and much less cross-reactivity between Vespids and honeybees. Yellow jackets are the most frequent cause of stings and reactions because of their aggressive nature. Allergy to stings is more likely with multiple sting exposures and very frequent stings. Progression from milder to more serious reactions is the exception rather than the rule in individual children with large local or distant cutaneous reactions without respiratory or cardiovascular involvement. Therefore, skin testing and immunotherapy are only recommended for children with histories of respiratory or cardiovascular reactions to stings. These children should have injectable epinephrine available at all times during the seasons at risk for stings. Immunotherapy is effective in the majority of cases and represents the only viable preventive treatment for bee sting allergy. Use of insect repellant, avoidance of bright clothing, perfumes, garbage cans, and careful examination of all outdoor food items are also important preventive measures.