In contrast to drug-induced rhinitis caused by oral medications, which resolves promptly with cessation of the offending agent, rhinitis medicamentosa can persist for prolonged periods and usually requires treatment with a burst of oral corticosteroids for 7 to 14 days for resolution.17 Patients with rhinitis medicamentosa should be evaluated and treated for potential associated allergic or vasomotor rhinitis. Chronic sinusitis is another common complicating factor in such cases.
COMPLICATING FACTORS AND ASSOCIATED CONDITIONS
Other conditions can mimic or aggravate symptoms of rhinitis. These are often associated with structural issues, such as nasal septal deviation, nasal polyps or, rarely, nasopharyngeal tumors.1,10 Cerebrospinal fluid leak presents as clear rhinorrhea in the setting of recent regional trauma or surgery. Chronic sinusitis with or without nasal polyps usually presents in adulthood; it may occur in conjunction with allergic or nonallergic rhinitis. Consider the possibility of complicating sinusitis in patients who do not respond to standard rhinitis therapy.
Aspirin-exacerbated respiratory disease (AERD) consists of the triad of aspirin(Drug information on aspirin) intolerance, chronic sinusitis with nasal polyps, and persistent asthma. Treatment of nasal polyps with nasal corticosteroids (with or without a brief initial course of oral corticosteroids), or alternately in the case of AERD, treatment by an allergist with aspirin desensitization followed by daily maintenance aspirin therapy, often will decrease the size of polyps and reduce the need for surgery.10
The clinical history typically focuses on symptoms compatible with allergic rhinitis in the nose (congestion, rhinorrhea, pruritus), eyes (itching, redness), and ears (congestion). Pruritus and sneezing are more common in allergic rhinitis, particularly in seasonal allergic rhinitis,11 whereas congestion and rhinorrhea are the most salient features of nonallergic rhinitis.18 Among the types of nonallergic rhinitis, vasomotor rhinitis may have irritant triggers (scents, tobacco smoke), but it should be pointed out that this is frequently reported by patients with allergic rhinitis as well.18 Patients with long-term use of intranasal decongestants or cocaine may have rhinitis medicamentosa.
In addition, the history focuses on symptoms that raise suspicion of other diagnoses, such as pain, bloody or purulent discharge, fever, headache, and unilateral symptoms. Include questions to detect comorbid conditions (sinusitis, obstructive sleep apnea, asthma, eczema, otitis media).19
Gendo and Larson20 calculated likelihood ratios for previous studies, looking at the clinical performance of various aspects of the allergic rhinitis history. Particularly helpful were questions about triggers (pollen and animals), which had high positive likelihood ratios, and to a lesser extent, questions about particular symptoms in the nose or eyes, seasonality of symptoms, and patient or family history of atopic disease. Overall, none of the history items that they examined had low negative likelihood ratios, so while the patient history can build a good case for allergic rhinitis, the lack of individual items in the history is not as helpful for ruling out allergic rhinitis.
The targeted physical examination for patients with suspected allergic rhinitis typically includes examination of the eyes for conjunctival swelling and erythema, eyelid swelling, or lower eyelid venous stasis (“allergic shiners”). The nose may have a lateral crease (“allergic crease”) from rubbing it in an upward direction because of itching. Nasal turbinates are typically swollen; additional findings to be ruled out by nasal speculum examination include septal deviation, granulomas, polyps, or tumors. Examination of the ear may reveal a middle ear effusion, with clouding of the tympanic membrane or a visible air fluid level.
Given the relatively high pretest probability of allergic rhinitis in patients with rhinitis-type complaints, the even higher post-test probability when factoring in a compatible history and physical findings, and the minimal adverse effects of current allergic rhinitis medications, initial empiric therapy is recommended. In patients who do not respond well to empiric therapy, testing for specific allergens provides greater diagnostic certainty and helps identify allergic rhinitis triggers for avoidance and/or for consideration for allergen immunotherapy.
Skin testing can be either puncture or intradermal. Puncture skin testing is performed by placing a drop of each of a number of standardized allergen extracts on the skin and then puncturing the skin with a needle at each drop, to insert the allergen into the epidermis.21 False-negative results can be seen in patients who are currently taking antihistamines, which should be discontinued for approximately 5 days before testing.22 False-positives can be seen in patients with dermatographism; thus, drops of saline (negative control) and histamine solution (positive control) are included in the panel. Wheal and flare diameter is read at 15 to 20 minutes.21
Intradermal skin testing has higher sensitivity than puncture skin testing (a 1000-fold lower concentration of allergen will produce the same size wheal in intradermal compared with puncture skin testing),21 so intradermal skin testing is often performed to gain additional sensitivity in the case of negative puncture tests that are thought to be falsely negative based on a convincing history.22 Positive puncture tests do not require further confirmation by intradermal testing.
Intradermal tests are performed by injecting extract directly into the dermis with a 26- to 27-gauge needle to form a 2- to 3-mm bleb. Wheal and flare results are measured at 15 to 20 minutes.21 Although both types of skin tests rarely cause systemic reactions, physicians who perform them need to be able to treat anaphylaxis emergently should it occur.22
In vitro detection of allergen-specific IgE antibody is an alternate method of allergy testing. These tests expose patient sera to bound allergen and then use radiolabeled anti-IgE antibody to detect specific IgE from patient sera, and radioactivity is quantified to give the test result.23 Given that specific IgE immunoassays are only 70% to 75% sensitive compared with puncture or intradermal skin testing,10 and given the ease and lower cost of skin tests,22 skin tests are preferred over IgE immunoassays. Reasons for obtaining specific IgE immunoassays include greater ease for physician and patient, current antihistamine use or dermatographism, and lack of patient cooperation with skin testing (eg, in young children).22
A positive puncture or intradermal skin test or a positive immunoassay test indicates sensitization, which must be considered in clinical context.21,22 For example, a patient with perennial symptoms whose tests are negative for indoor and perennial aeroallergens (mite, roach, pet dander, and so forth) and positive for grass pollen in an area where grass pollen is seasonal does not have confirmatory evidence of seasonal allergic rhinitis; the patient may have nonallergic rhinitis.
In a patient whose history and examination findings—and possibly confirmatory allergen test results—have helped clarify the type of rhinitis present, appropriate therapy can be undertaken. This will be discussed in Part 2 of this article, which will appear in a coming issue.