Rhinitis Medicamentosa

Updated: Jan 02, 2018
Author: Mark S Dykewicz, MD; Chief Editor: Michael A Kaliner, MD 



Rhinitis medicamentosa (RM), also known as rebound rhinitis, is a condition characterized by nasal congestion that is triggered by the overuse of topical vasoconstrictive medications, most notably intranasal decongestants; recreational use of intranasal cocaine may also cause a similar condition.[1, 2, 3] Underlying reasons for intranasal decongestant use can usually be identified, such as allergic or nonallergic rhinitis, acute or chronic rhinosinusitis, nasal polyps, night-time use of continuous positive airway pressure (CPAP), or upper respiratory tract infection. With regular daily use, some patients may develop rhinitis medicamentosa in 3 days, whereas others may not have evidence of rebound congestion after 4 to 6 weeks of use.[2] Management of rhinitis medicamentosa is focused on withdrawal of intranasal decongestants and treatment of congestion and underlying conditions with appropriate interventions.

Rhinitis medicamentosa is now generally considered a subset of drug-induced rhinitis that may include the development of congestion and other nasal symptoms from medications that are not administered by the intranasal route.[2] Examples of orally administered agents that may cause drug-induced rhinitis include ACE inhibitors, beta blockers, alpha adrenergic receptor antagonists used in the treatment of benign prostatic hypertrophy, and phosphodiesterase-5 selective inhibitors used to treat erectile dysfunction.[2, 4] Aspirin and other NSAIDs may also produce nasal symptoms in sensitive individuals, sometimes as part of a broader presentation of aspirin-exacerbated respiratory disease (AERD), formerly known as Samter’s Triad, that may include chronic rhinosinusitis with nasal polyps, asthma and aspirin/NSAID sensitivity.


The pathophysiology of rhinitis medicamentosa is not well understood.[1] Based on knowledge of the physiology of the nasal mucosa, various hypotheses exist; they mainly focus on dysregulation of sympathetic/parasympathetic tone by exogenous vasoconstricting molecules. Proposed mechanisms describe secondary decrease in production of endogenous norepinephrine through a negative feedback mechanism;[5]  a beta effect of sympathomimetic amines that outlasts the alpha effect and causes rebound swelling;[6] increased parasympathetic activity, vascular permeability, and edema formation by altering vasomotor tone, thus creating the rebound congestion.[7]  There is also evidence that intranasal cationic adrenergic decongestant drugs may be trapped into cellular endomembrane compartments caused by V-ATPase-dependent sequestration that results in a tissue reservoir of these drugs, influencing the toxicity and pharmacology of these agents.[8]

Nasal decongestants

Nasal decongestants (either administered intranasally or orally) can be classified as either sympathomimetic amines or imidazolines. Sympathomimetic amines (eg, pseudoephedrine, amphetamine, benzedrine, mescaline, phenylephrine, ephedrine) activate sympathetic nerves through presynaptic release of endogenous norepinephrine, which subsequently binds to alpha-receptors and causes vasoconstriction. Rebound vasodilation may be induced through weak affinity toward beta-adrenoreceptors. Imidazolines (eg, oxymetazoline[9] , xylometazoline, naphazoline, clonidine) cause vasoconstriction primarily through alpha2-adrenergic receptors, but may also decrease endogenous norepinephrine though a negative feedback mechanism.

Benzalkonium chloride

Benzalkonium chloride (BKC) is an antimicrobial preservative commonly used in aqueous nasal, ophthalmic, and ocular products, and has long been used at concentrations ≤0.1%.[10] While there are conflicting reports of damage to human nasal epithelia or aggravation of rhinitis medicamentosa associated with intranasal products that contain BKC[11, 12, 13, 14, 15] , intranasal products with BKC are generally safe and well tolerated for short-term and long-term use.[10]



The incidence of rhinitis medicamentosa is uncertain and may be underreported because of over-the-counter availability of intranasal decongestants. In a survey of 119 allergists, 6.7% had rhinitis medicamentosa. In a study conducted over 10 years in an otolaryngology (ENT) office, the incidence of rhinitis medicamentosa was 1%.[16] In another study, an ENT practitioner diagnosed rhinitis medicamentosa in 52 out of 100 consecutive noninfectious patients who presented with nasal obstruction.


Rhinitis medicamentosa can lead to chronic rhinosinusitis, atrophic rhinitis, turbinate hyperplasia, psychological dependence, and an abstinence syndrome upon intranasal decongestant withdrawal that may include headaches, sleep disturbances, restlessness, irritability, and anxiety. A case of neonatal respiratory distress syndrome from topical phenylephrine has been reported.[17]


Rhinitis medicamentosa occurs at a similar rate in men and women.


Peak incidence occurs in young and middle-aged adults.


Prognosis of rhinitis medicamentosa is favorable if underlying factors that led to overuse of intranasal decongestants are addressed and treated or have resolved, and patients adhere to recommendations to limit intranasal decongestants to short-term use.

Studies showed that nearly all patients were able to eventually stop using the offending medication.[18]

Those who used topical preparations again, even 1 year later, had rapid rebound congestion within a few days.[19]

Patient Education

Because rhinitis medicamentosa may occasionally develop after 3 days of intranasal decongestant administration, patients whould be instructed to generally limit intranasal decongestants to short-term use.

The key to treatment and prevention of rhinitis medicamentosa lies in educating the patient about the consequences of using intranasal decongestants for longer than 5–7 days, and often applicable, the need to treat the underlying cause for chronic nasal congestion that led to over use of intranasal decongestants.




Symptoms are confined to the nose and consist of chronic nasal congestion as the most prominent symptom.

Symptoms do not change based on the season or whether the patient is spending time indoors or outdoors.

Because use of intranasal decongestants may not be volunteered by patients, the clinicla must directly ask about all nose spray usage to diagnose rhinitis medicamentosa.[20]

A history of more frequent or prolonged duration of use of intranasal decongestant sprays makes rhinitis medicamentosa more likely.

A common clinical history is a patient with nasal congestion from a cold or rhinitis who uses an over-the-counter intranasal decongestant for relief, and then continues to use the decongestant for weeks, months, or years. Cessation of the intranasal decongestant is followed by rebound congestion that is quite profound, leading to more use of the decongestant.

Patients with rhinitis medicamentosa often snore, have sleep apnea, or breathe mostly through their mouths. This can result in sore throat and dry mouth.

Physical Examination

The classic presentation is that the nasal mucous membranes appear "beefy-red," inflamed, and may show areas of punctate bleeding and scant mucus. There may be areas of increased tissue friability and profuse stringy mucoid discharge. Occasionally, however, the mucosa may appear pale.


Overuse of topical nasal vasoconstrictive medications (intranasal decongestants or cocaine) is the only cause of rhinitis medicamentosa.

Factors that cause nasal congestion that may lead to overusage of intranasal decongestants include the following:

  • Allergic rhinitis, nonallergic rhinitis

  • Deviated nasal septum

  • Nasal polyps, AERD (ie, nasal polyps, asthma, and aspiring intolerance)

  • Use of CPAP machine at night for sleep apnea

  • Upper respiratory infection

  • Rhinosinusitis

  • Pregnancy[21]



Differential Diagnoses

  • Allergic Rhinitis

  • Continuous Positive Airway Pressure (CPAP) Rhinitis

  • Rhinitis, Nonallergic

  • Rhinosinusitis



Approach Considerations

Carefully collected medical history (see History and Physical Examination) usually determines the diagnosis.

Laboratory Studies

There are no definitive laboratory studies for diagnosis of rhinitis medicamentosa per se, but other tests (see Other Tests) may be useful for identifying an underlying cause for nasal congestion that led to overuse of intranasal decongestants.

Imaging Studies

Sinus imaging studies may be helpful to rule out rhinosinusitis, nasal polyps, deviated septum, or other anatomic causes for nasal obstruction.

Other Tests

Rhinitis medicamentosa usually coexists with other medical conditions that originally trigger decongestant use. It is important to identify any condition that can be potentially treated.

  • Allergy skin testing or in vitro IgE tests for specific IgE to aeroallergens generally are indicated to determine if the underlying cause of nasal congestion is allergic rhinitis or not.

  • Rhinoscopy (rigid or fiberoptic) is useful in identification of nasal septal deviation, other anatomic abnormalities, and nasal polyps.

  • Patients who are suspected to hae AERD may be considered for aspirin challenge.

Histologic Findings

The following findings have been reported in rhinitis medicamentosa, but most findings may occur in some other types of rhinitis, and therefore are not diagnostic.

  • Increased vascularity, edema of the nasal mucosa

  • Squamous cell metaplasia; change from ciliated columnar to nonciliated stratified squamous epithelium

  • Mononuclear infiltration

  • Glandular and Goblet cell hyperplasia

  • Increased secretory activity

  • Abnormal cilia structure and function

  • Increase in plasma cells, fibroblasts, and lymphocytes



Medical Care

Once rhinitis medicamentosa is identified, topical decongestant use must be discouraged and discontinued as soon as possible. Patients need to be educated on their condition and offered other methods of treatment that will help them with the medical conditions that originally triggered the intranasal decongestant use. For allergic rhinitis, for example, this might include allergen reduction/avoidance, pharmacotherapy, and/or allergen immunotherapy. For those patients unable or unwilling to immediately stop intranasal decongestants, several strategies may ease the withdrawal process.

The first week is often the most difficult for weaning or withdrawal. Several studies confirm efficacy of nasal corticosteroids in the treatment and prevention of rhinitis medicamentosa. Although not always necessary, short-course oral corticosteroids, as described below, are the most effective way to break the cyclic use of topical vasoconstrictors. The oral corticosteroids are often used for 5-10 days, with nasal corticosteroids started at the same time and continued until the process is corrected.

Nasal irrigation with saline solutions delivered by devices such as NeilMed may be useful.

Intranasal decongestants can be weaned gradually, allowing patients to use sprays at night in one nostril only and alternating the left and right nostril until congestion is decreased.

Pain relief from analgesics should be offered to patients who experience headaches during withdrawal from intranasal decongestants.

Oral systemic decongestants may be helpful in relieving nasal congestion as intranasal decongestants are withdrawn.


Rhinitis of pregnancy affects as many as 20% of expecting mothers, although the most common causes of nasal symptoms in pregnant women are the same as in men and nonpregnant women.

Therapy for a pregnant patient with rhinitis medicamentosa generally is the same as outlined above, although oral decongestants should be avoided in the first trimester because of risk of gastroschisis.[2]

Continuous positive airway pressure (CPAP)-induced rhinitis

CPAP prescribed for sleep apnea, can cause increased air flow through the nasal cavity, which, in turn, causes dry mucous membrane, overproduction of the mucus, and congestion.

Appropriate use of such machines should be ensured, including evaluation of pressure used, regular maintenance, and humidification of the air delivered. Nasal gel is recommended to prevent drying of the mucous membranes of the nasal cavity.

Surgical Care

Surgical treatment generally is not recommended unless polyps or significantly deviated nasal septum are present and causing nasal congestion. However, when inferior turbinate hypertrophy is present with nasal obstruction and patients have failed medical management, partial inferior turbinate reduction is an option.[22]


Consult an allergist, immunologist, or otorhinolaryngologist if a patient's case is complicated and refractory to treatment or if the primary care physician is unsure of diagnosis.



Further Outpatient Care

Short-term follow-up may be needed to assess whether additional medical intervention is required.


Patients should be instructed to avoid topical vasoconstrictors in the future. Studies showed that those with a history of rhinitis medicamentosa who successfully stop using the offending medication have a rapid onset of rebound congestion upon repeat use of topical vasoconstrictor medication, even if used for only a few days.[19]  

Placebo-controlled studies of perennial and seasonal allergic rhinitis demonstrate that concurrent administration of intranasal corticosteroids and intranasal decongestants provide additional benefit in relief of nasal congestion. When an intranasal decongestant was given along with the intranasal steroid once a day for up to 4 weeks, the development of rhinitis medicamentosa did not occur.[23, 24]  One study reported that rebound congestion from the intranasal decongestant oxymetazoline was reversed by intranasal corticosteroid use.[25]

Further long-term studies are needed to determine how effective concomitant administration of intranasal decongestant and intranasal corticosteroid is as a strategy to avoid development of rhinitis medicamentosa.