Allergic Rhinitis

Etiology and Classification

Two factors necessary for expression of AR are sensitivity to an allergen and the presence of the allergen in the environment. AR classification as seasonal or perennial is giving way to the designations intermittent and persistent. The 2 sets of terms are based on different suppositions, but inhalant allergens are the main cause of all forms of AR irrespective of terminology. AR may also be categorized as mild-intermittent, moderate-severe intermittent, mild-persistent, and moderate-severe persistent ( Fig. 168.1 ). The symptoms of intermittent AR occur on <4 days per week or for <4 consecutive weeks. In persistent AR, symptoms occur on >4 days per week and/or for >4 consecutive weeks. The symptoms are considered mild when they are not troublesome, the sleep is normal, there is no impairment in daily activities, and there is no incapacity at work or school. Severe symptoms result in sleep disturbance and impairment in daily activities and school performance.

In temperate climates, airborne pollen responsible for exacerbation of intermittent AR appear in distinct phases: trees pollinate in the spring, grasses in the early summer, and weeds in the late summer. In temperate climates, mold spores persist outdoors only in the summer, but in warm climates they persist throughout the year. Symptoms of intermittent AR typically cease with the appearance of frost. Knowledge of the time of symptom occurrence, the regional patterns of pollination and mold sporulation, and the patient's allergen-specific IgE ( sIgE ) is necessary to recognize the cause of intermittent AR. Persistent AR is most often associated with the indoor allergens: house dust mites, animal danders, mice, and cockroaches. Cat and dog allergies are of major importance in the United States. The allergens from saliva and sebaceous secretions may remain airborne for a prolonged time. The ubiquitous major cat allergen, Fel d 1, may be carried on cat owners’ clothing into such “cat-free” settings as schools and hospitals.

Pathogenesis

The exposure of an atopic host to an allergen leads to the production of sIgE, which is strongly associated with eczema throughout childhood and with asthma and rhinitis after age 4 yr. The clinical reactions on reexposure to the allergen have been designated as early-phase and late-phase allergic responses. Bridging of the IgE molecules on the surface of mast cells by allergen initiates the early-phase allergic response, characterized by degranulation of mast cells and release of preformed and newly generated inflammatory mediators, including histamine, prostaglandin 2, and the cysteinyl leukotrienes. The late-phase allergic response appears 4-8 hr following allergen exposure. Inflammatory cells, including basophils, eosinophils, neutrophils, mast cells, and mononuclear cells, infiltrate the nasal mucosa. Eosinophils release proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and serve as a source of interleukin-3 (IL-3), IL-5, granulocyte-macrophage colony-stimulating factor, and IL-13. Repeated intranasal introduction of allergens causes “priming”—a more brisk response even with a lesser provocation. Over the course of an allergy season, a multifold increase in submucosal mast cells takes place. These cells, once thought to have a role exclusively in the early-phase allergic response, have an important function in sustaining chronic allergic disease.

Clinical Manifestations

Symptoms of AR may be ignored or mistakenly attributed to a respiratory infection. Older children blow their noses, but younger children tend to sniff and snort. Nasal itching brings on grimacing, twitching, and picking of the nose that may result in epistaxis. Children with AR often perform the allergic salute , an upward rubbing of the nose with an open palm or extended index finger. This maneuver relieves itching and briefly unblocks the nasal airway. It also gives rise to the nasal crease , a horizontal skin fold over the bridge of the nose. The diagnosis of AR is based on symptoms in the absence of an upper respiratory tract infection and structural abnormalities. Typical complaints include intermittent nasal congestion, itching, sneezing, clear rhinorrhea, and conjunctival irritation. Symptoms increase with greater exposure to the responsible allergen. The patients may lose their sense of smell and taste. Some experience headaches, wheezing, and coughing. Preschoolers with chronic wheezing and rhinitis experience more severe wheezing than children without rhinitis. Nasal congestion is often more severe at night, inducing mouth breathing and snoring, interfering with sleep, and rousing irritability.

Signs on physical examination include abnormalities of facial development, dental malocclusion, the allergic gape (continuous open-mouth breathing), chapped lips, allergic shiners (dark circles under the eyes; see Fig. 167.1 ), and the transverse nasal crease. Conjunctival edema, itching, tearing, and hyperemia are frequent findings. A nasal exam performed with a source of light and a speculum may reveal clear nasal secretions; edematous, boggy, and bluish mucus membranes with little or no erythema; and swollen turbinates that may block the nasal airway. It may be necessary to use a topical decongestant to perform an adequate examination. Thick, purulent nasal secretions indicate the presence of infection.

Differential Diagnosis

Evaluation of AR entails a thorough history, including details of the patient's environment and diet and a family history of allergic conditions (e.g., eczema, asthma, AR), physical examination, and laboratory evaluation. The history and laboratory findings provide clues to the provoking factors. Symptoms such as sneezing, rhinorrhea, nasal itching, and congestion and lab findings of elevated IgE, sIgE antibodies, and positive allergy skin test results typify AR. Intermittent AR differs from persistent AR by history and skin test results. Nonallergic rhinitides give rise to sporadic symptoms; their causes are often unknown. Nonallergic inflammatory rhinitis with eosinophils imitates AR in presentation and response to treatment, but without elevated IgE antibodies. Vasomotor rhinitis is characterized by excessive responsiveness of the nasal mucosa to physical stimuli. Other nonallergic conditions, such as infectious rhinitis, structural problems (e.g., nasal polyps, septal deviation), rhinitis medicamentosa (caused by overuse of topical vasoconstrictors), hormonal rhinitis associated with pregnancy or hypothyroidism, neoplasms, vasculitides, and granulomatous disorders may mimic AR ( Table 168.1 and Fig. 168.2 ). Occupational risks for rhinitis include exposure to allergens (grain dust, insects, latex, enzymes) and irritants (wood dust, paint, solvents, smoke, cold air).