Rhinitis medicamentosa

Rhinitis medicamentosa
Classification and external resources
ICD-9-CM 472.0
DiseasesDB 11545
eMedicine article/995056

Rhinitis medicamentosa (or RM) is a condition of rebound nasal congestion brought on by extended use of topical decongestants (e.g., oxymetazoline, phenylephrine, xylometazoline, and naphazoline nasal sprays) and certain oral medications (e.g., sympathomimetic amines and various 2-imidazolines) that constrict blood vessels in the lining of the nose.[1]

Presentation

The characteristic presentation of RM involves nasal congestion without rhinorrhea, postnasal drip, or sneezing following several days of decongestant use.[1] This condition typically occurs after 5–7 days of use of topical decongestants. Patients often try increasing both the dose and the frequency of nasal sprays upon the onset of RM, worsening the condition. The swelling of the nasal passages caused by rebound congestion may eventually result in permanent turbinate hyperplasia, which may block nasal breathing until surgically removed.[2]

Commercial introduction of Oxymetazoline brand Afrin. The prolonged use of nasal vasoconstrictors cause rhinitis medicamentosa

Pathophysiology

The pathophysiology of RM is unclear, although several mechanisms involving norepinephrine signaling have been proposed.[1] RM is associated with histological changes that include: an increase in the number of lymphocytes and fibroblasts, epithelial cell denudation, epithelial edema, goblet cell hyperplasia, increased expression of the epidermal growth factor receptor, increased mucus production, nasociliary loss, inflammatory cell infiltration, and squamous cell metaplasia.[1]

Direct acting sympathomimetic amines, such as phenylephrine stimulate alpha adrenergic receptors, while mixed-acting agents, such as pseudoephedrine can stimulate both alpha and beta adrenergic receptors directly and indirectly by releasing norepinephrine from sympathetic nerve terminals.[3] At first, the vasoconstrictive effect of alpha-receptors dominates, but with continued use of an alpha agonist, this effect fades first, allowing the vasodilation due to beta-receptor stimulation to emerge.[4]

2-Imidazoline derivatives, such as oxymetazoline, may participate in negative feedback on endogenous norepinephrine production. Therefore, after cessation of prolonged use, there will be inadequate sympathetic vasoconstriction in the nasal mucosa, and domination of parasympathetic activity can result in increased secretions and nasal edema.[5][6] However, if oxymetazoline is used only nightly for allergic rhinitis, it can be used longer than one week without risk of rhinitis medicamentosa.[7]

Treatment

The treatment of RM involves withdrawal of the offending nasal spray or oral medication. Both a "cold turkey" and a "weaning" approach can be used. Cold turkey is the most effective treatment method, as it directly removes the cause of the condition, yet the time period between the discontinuation of the drug and the relief of symptoms may be too long for some individuals (particularly when trying to go to sleep when they are unable to breathe through their nose). The use of over-the-counter (OTC) saline nasal sprays may help open the nose without causing RM if the spray does not contain a decongestant.[8] Symptoms of congestion and runny nose can often be treated with corticosteroid nasal sprays under the supervision of a physician. For very severe cases, oral steroids or nasal surgery may be necessary.

For RM caused by topical decongestants, there are anecdotal reports of persons having success by withdrawing treatment from one nostril at a time.[1][9]

A study has shown that the anti-infective agent benzalkonium chloride, which is frequently added to topical nasal sprays as a preservative, aggravates the condition by further increasing the rebound swelling.[10]

Causes

Common issues that lead to overuse of topical decongestants:

See also

References

  1. 1 2 3 4 5 Ramey JT, Bailen E, Lockey RF (2006). "Rhinitis medicamentosa" (PDF). J. Investig. Allergol. Clin. Immunol. 16 (3): 148–155. PMID 16784007. Retrieved 29 April 2015.
  2. ↑ Rhinitis Medicamentosa, > Epidemiology, > Morbidity
  3. ↑ Brunton L, Parker K, Blumenthal D, Buxton I (2008) Goodman & Gilman's Manuel of Pharmacology and Therapeutics, Chapter 10, Adrenergic Agonists and Antagonists, McGraw-Hill, New York.
  4. ↑ Passali D, Salerni L, Passali G, Passali F, Bellussi L (2006) Nasal decongestants in the treatment of chronic nasal obstruction: efficacy and safety of use. Expert Opin Drug Saf 5(6):783–790.
  5. ↑ Lacroix J (1989) Adrenergic and nonadrenergic mechanisms in sympathetic vascular control of the nasal mucosa. Acta Physiol Scand Suppl 581:1–63
  6. ↑ Elwany S, Stephanos W (1983) Rhinitis medicamentosa—an experimental histopathological and biochemical study. ORL J Otorhinolaryngol Relat Spec 45(4):187–194
  7. ↑ Baroody FM, Brown D, Gavanescu L, Detineo M, Naclerio RM (2011). "Oxymetazoline adds to the effectiveness of fluticasone furoate in the treatment of perennial allergic rhinitis.". J Allergy Clin Immunol. 127 (4): 927–34. doi:10.1016/j.jaci.2011.01.037. PMID 21377716.
  8. ↑ Graf, P (2005). "Rhinitis medicamentosa: a review of causes and treatment.". Treatments in respiratory medicine. 4 (1): 21–9. doi:10.2165/00151829-200504010-00003. PMID 15725047.
  9. ↑ Saltus, Richard (March 14, 2006), "Nasal Sprays Can Bring on Vicious Cycle", New York Times
  10. ↑ Graf, P.; Hallén, H.; Juto, J. E. (1995). "Benzalkonium chloride in a decongestant nasal spray aggravates rhinitis medicamentosa in healthy volunteers". Clinical and Experimental Allergy. 25 (5): 395–400. PMID 7553241.

Further reading

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