Rhinitis medicamentosa (RM) is a condition of rebound nasal congestion brought on by overuse of intranasal vasoconstrictive medications. This disorder typically occurs after 5-7 days of medication use. Many reasons for the initial use of the medication are possible, and eliciting the reason for use of vasoconstrictive medications is important. As the patient continues using medication, tachyphylaxis occurs, resulting in increased frequency and shorter duration of action for the offending medication.
Debate exists about how decongestant nasal sprays cause the classic rebound swelling of RM. Because prolonged topical nasal decongestants bring on the disorder, understanding how these medications affect the nasal mucosa is helpful.
Topical nasal decongestants fall into 2 general classes, as follows:
Sympathomimetic amines, including ephedrine and phenylephrine
Imidazoles, including oxymetazoline and xylometazoline
All sympathomimetic amines act on both alpha-receptors and some beta-receptors. Imidazoles act on the more selective alpha2 receptors. Sympathomimetic drugs contract the smooth muscle of the venous erectile tissue causing mucosal shrinkage and decreasing airway resistance. The venous erectile tissue is sensitive to both alpha and alpha2 stimulation, but the imidazole action on alpha2 receptors is probably responsible for the decrease in mucosal blood flow because resistance vessels are most sensitive to alpha2 agonists. With prolonged vasoconstriction, the mucosa become less responsive to the drug and a reversal to vasodilatation occurs. Patients may develop tachyphylaxis— a rapidly decreasing response to a drug following administration of the initial doses— resulting from the need for more frequent doses to provide adequate decongestion.
The secondary vasodilatation is not well understood. One theory suggests that the sympathomimetic amines, which have activity at both alpha and beta sites, have a longer beta effect that outlasts the alpha effect and causes rebound swelling. A second theory postulates that prolonged vasoconstriction causes tissue hypoxia with a resulting reactive hyperemia, rebound swelling, and vasodilatation. A third theory postulates that alpha2 agonists stimulate a negative feedback loop that involves the presynaptic nerve endings. With prolonged use of these agonists, a decrease in endogenous noradrenaline would occur, and, once the exogenous drug disappears, a rebound congestion develops. A fourth theory suggests that the medication causes increased parasympathetic activity, vascular permeability, and edema formation by altering vasomotor tone, thus creating the rebound congestion.
Nasal medications containing the quaternary ammonium benzalkonium chloride (BKC), a preservative that prevents the growth of microorganisms, cause more rebound congestion than the same decongestant administered preservative-free. BKC, therefore, may aggravate RM.
In a study conducted over 10 years in an otolaryngology (ENT) office, the incidence of RM was 1%. In another study, an ENT practitioner diagnosed RM in 52 out of 100 consecutive noninfectious patients presenting with nasal obstruction.
Similar frequency ranges occur in Europe.
With continued usage, RM leads to chronic sinusitis, atrophic rhinitis, and permanent turbinate hyperplasia. However, in neonates, who are obligate nose breathers, prolonged use of topical vasoconstrictor causes RM and consequent apnea and cyanosis. After the withdrawal of the offending medication, patients recover. No deaths are reported.
Peak incidence occurs in young and middle-aged adults.
Symptoms are confined to the nose and consist of chronic nasal congestion.
Physician must ask about nose spray usage to diagnose RM, as patients frequently neglect to mention these over-the-counter medications.
The frequency and duration of nasal spray use is also important.
Patients often try to increase both the dose and the frequency of topical decongestants.
Physical findings are confined to the nose.
The nasal mucous membranes may appear hyperemic, granular, and boggy with areas of increased tissue friability and punctate bleeding.
The mucus is usually clear and minimal unless an accompanying sinus infection is present. However, reports exist of the mucosa appearing pale and anemic with nasal of discharge that is stringy, profuse, and mucoid.
The use of topical 4% cocaine to induce local vasoconstriction and shrinkage is usually ineffective in RM.
Topical nasal vasoconstrictive medication
Sympathomimetic amines include ephedrine and phenylephrine
Imidazoline derivatives include oxymetazoline and xylometazoline
BKC, a preservative used in nasal preparations, is thought to worsen RM, though debate is taking place in the literature
Medications that cause stuffy nose and may cause an increase in vasoconstrictor use
Antihypertensives, such as reserpine, hydralazine, guanethidine, methyldopa, and prazosin
Beta-blockers, such as propranolol and nadolol
Antidepressants and antipsychotics, including thioridazine, chlordiazepoxide-amitriptyline, and perphenazine
Associated factors that cause nasal stuffiness
Deviated nasal septum
Upper respiratory infection (URI)
Pregnancy or other conditions with high levels of estrogen, such as puberty in boys and girls, menarche, estrogen replacement therapy, and oral contraceptive use