An estimated 35 million persons in the United States have allergic disease. Allergy is defined as a hypersensitive or pathologic reaction to environmental factors or substances such as pollens, food, and dust in amounts that do not affect most people. A large proportion of allergic diseases result from inhalant exposure of the upper respiratory tract. Allergic rhinitis alone has been estimated to affect 20% of the U.S. population.
Gell and Coombs classified hypersensitivity reactions into four types (Table 19-1). Otolaryngologists deal mostly with type I (IgE mediated) allergic reactions, which are clinically found in bronchial asthma, allergic rhinitis, urticaria, drug and food allergies, and reactions to insect stings. These allergies can be classified as atopic (immunoglobulin E [IgE] mediated) versus nonatopic (non-IgE mediated).
Allergic diseases affect persons 3 to 5 years of age and older. Children younger than this have not developed sufficient IgE levels to cause allergic reactions. However, even infants may develop non-IgE mediated food intolerance (especially to milk protein). Inhalant antigens include pollens, house dust, animal dander, molds, and insect materials. Exposure to these antigens results in a type I IgE-mediated hypersensitivity reaction with mast cell degranulation and release of histamine and other vasoactive mediators. There are several otolaryngologic manifestations of allergic reactions. These are discussed below and are summarized in Table 19-2. Management of each of these sequelae is discussed in the specific chapters on these topics.
ALLERGIC RHINITIS
Allergic rhinitis is the most common manifestation of upper respiratory tract allergy, and may be seasonal or perennial. Seasonal allergic rhinitis often is caused by pollen and insects, whereas perennial allergic rhinitis often is caused by dust and animal dander. Molds can cause either type. Maximal symptoms of seasonal allergic rhinitis depend on geographic location, but they occur between late spring and early fall.
On physical examination, the nasal turbinates are classically described as pale, blue, and edematous with a thin, clear mucous covering. The turbinates may be erythematous and swollen. Patients may have “allergic shiners,” dark discolorations under the eyes that result from venous stasis in the thin tissues of the eyelids caused by nasal congestion. Children may have a horizontal crease across the lower nose caused by repeated rubbing and subsequent scarring in this area. Chronic childhood nasal obstruction eventually leads to mouth breathing and typical “adenoid facies,” with a raised upper lip, mandible maintained open, and small poorly developed nostrils.
Symptoms of allergic rhinitis include nasal congestion, watery rhinorrhea, sneezing, nasal pruritus, conjunctivitis, tearing, itchy palate, and postnasal drip. The differential diagnosis includes vasomotor rhinitis, rhinitis medicamentosa, hormonal rhinitis, the common cold, sinusitis, and structural lesions that lead to nasal obstruction, such as nasal septal deviation, adenoid hyperplasia, nasal foreign body, and tumors of the nose and nasopharynx. Complications and sequelae of allergic rhinitis include serous otitis media, sinusitis, adenotonsillar hyperplasia, lingual tonsillar hyperplasia, sore throat, and paranasal sinus polyps and mucoceles (Table 19-3).
TABLE 19-1. Gell and Coombs hypersensitivity reactions
Type of reaction
Mediator
Mechanism
Example
I (Anaphylactic)
IgE
IgE binds to membranes of mast cells and basophils causing release of vasoactive mediators
Allergic reactions are responsible for some diseases of the outer, middle, and inner ears. The external ear is susceptible to allergic eczema. This may be caused by a food allergy or an allergic reaction to a fungal infection of the external ear. In both instances, eczema leads to loss of normal skin integrity, which may lead to bacterial invasion and otitis externa. Otitis media caused by allergic eustachian tube obstruction often is a complication of allergic rhinitis. This is believed to result from loss of normal ear aeration and loss of equalization with atmospheric pressure. This effusion, which leads to a conductive hearing loss, may become infected, and purulent otitis media may develop. Allergy will also have a direct effect on middle ear mucosa. Mucosa previously sensitized to an allergen will respond with a full immune response. Mediators present in the middle ear with activate-primed neutrophils and eosinophils to chronically release allergy-related extracellular proteins, which also lead to effusion and inflammation.
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