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Wise et al.

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In summary, systemic medications and intranasal illicit drugs affect the nasal mucosa. Increased mucosal edema, vasodilation, and inflammatory mediators are a consequence of systemic medications. Vasoconstriction and direct mucosal injury often accompanies illicit drug use. The physiologic response in drug-induced rhinitis differs from AR as it is not allergen-induced nor dependent on IgE mechanisms, although symptomatology may be similar. III.C.2. Rhinitis medicamentosa (RM)— RM, or rebound rhinitis, is a condition induced by prolonged use of topical intranasal decongestant (IND) 26,61 (Table III.C.2). Although no consensus diagnostic criteria exist, RM is classically associated with the triad of prolonged IND use, constant nasal obstruction, and poor shrinkage of the nasal mucosa 61 in the setting of nasal congestion, rhinorrhea, and decreased efficacy of further INDs. 55,62,63 Physical exam findings consist of mucosal edema, erythema, and hyperemia. The exact physiologic mechanism causing RM is unclear. Continuous IND use may decrease endogenous norepinephrine production and cause upregulation of the parasympathetic system, leading to rebound congestion once the decongestant is discontinued. 54,55 This may be further exacerbated by recurrent nasal tissue hypoxia and negative neural feedback with chronic decreased α -2 receptor responsiveness. 64 Mucosal changes include ciliary damage and loss, epithelial metaplasia and hyperplasia, dilated intercellular spaces, goblet cell hyperplasia, and edema. 65-67 Benzalkonium chloride (BKC), an antimicrobial preservative used in many nasal decongestants, has been implicated in the mechanism of RM. Studies have suggested that BKC is toxic to nasal epithelium and may propagate RM, although the data are inconclusive. 68-71 Neither duration, nor cumulative dose of IND needed to initiate RM is known. Rebound congestion has developed after 3 to 10 days of medication use, 55,66 but may not occur until after 30 days. 72,73 Other studies have demonstrated a lack of rebound after 8 weeks of continuous use. 72-75 Furthermore, doubling the dose of intranasal imidazoline did not increase the extent of rebound edema. 72 Although inconclusive, studies suggest that IND use should be discontinued after 3 days to avoid rebound congestion. 62,76,77 Treatment of RM involves discontinuation of INDs. Various medications have been used to improve nasal decongestion including nasal cromolyn, sedatives, nasal saline spray, oral antihistamines, oral decongestants, and intranasal corticosteroids (INCSs; sometimes used in conjunction with brief courses of systemic corticosteroids). 50,62,78-82 Only the use of INCSs has been demonstrated to mitigate rebound congestion after discontinuation of topical INDs. 67,81-83 Often there is an underlying rhinitis and/or anatomic issue that initiated the decongestant use. This underlying issue should be addressed to diminish the drive to continue to use INDs. Importantly, RM is typically associated with repeated exposure to INDs, with increasing symptoms at times when the medication is withheld. In contrast, AR is classically associated with an allergic trigger with similar symptoms increasing upon allergen exposure, and is dependent upon IgE-mediated inflammation.

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Int Forum Allergy Rhinol . Author manuscript; available in PMC 2020 June 10.