Rhinitis medicamentosa

Rhinitis medicamentosa (RM), also known as rebound rhinitis This is an acquired

sensitivity of the nasal lining
Essential ENT by Rogan J Corbridge MB BS, BSC, 2nd ed 2011 137

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] 
[1
Black MJ, Remsen KA. Rhinitis medicamentosa. Can Med Assoc J. 1980 Apr 19. 122(8):881-
4. [Medline].

, 2

[Guideline] Wallace DV, Dykewicz MS, Bernstein DI, et al. The diagnosis and management of
rhinitis: an updated practice parameter. J Allergy Clin Immunol. 2008 Aug. 122(2 Suppl):S1-84.
[Medline]. [Full Text].

, 3], 

Doshi J. Rhinitis medicamentosa: what an otolaryngologist needs to know. Eur Arch

Otorhinolaryngol. 2009 May. 266(5):623-5. [Medline].

Pathophysiology
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]
https://emedicine.medscape.com/article/995056-overview#showall

[8
Morissette G, Bouthillier J, Marceau F. Trapping of adrenergic decongestant drugs into cellular
endomembrane compartments: toxicological and pharmacological consequences. Int
Immunopharmacol. 2007 Dec 20. 7(14):1869-79. [Medline].

]
cause

The cause of this condition is primarily by the prolonged use (more than 7 to 10 days) of topical
nasal decongestant. However, intranasal cocaine use has also been reported to cause a similar
condition. 
Physiology of nasal congestion 
The nasal mucosa vascular system can divide into resistance vessels (arterioles) which are
predominantly regulated by alpha-2 adrenoreceptors, and capacitance vessels (venous plexus)
regulated by both alpha-1 and alpha-2 adrenoreceptors. Stimulation of these receptors leads to
the decongestants effect;  where there is vasoconstriction of the large venous sinusoids and
collecting veins, leading to decreased blood flow and subsequently decreased nasal edema and
rhinorrhoea.
Contributing factors of nasal congestion include parasympathetic nervous system stimulation, the
release of local mediators including mast cells, eosinophils, basophils; which subsequently
stimulates the release of histamine, tryptase, kinins, prostaglandins, and leukotrienes, inducing an
overall change in nasal resistance and capacitance vessels.[2] There is exudation of plasma
through superficial capillaries, and increase mucin production by goblet cells. 
Topical nasal decongestants 
Topical nasal decongestants can classify as either beta-phenylethylamine derivatives or
imidazoline derivatives. Beta-phenylethylamine derivatives mimic the effects of the sympathetic
nervous system stimulation by producing vasoconstriction via the activation of alpha-1
adrenoreceptors. Rebound vasodilation may occur due to weak affinity towards beta–
adrenoreceptors. Imidazolines, on the other hand, produces its effect mainly via alpha-2 
adrenoreceptors. This difference in adrenoreceptor sensitivity makes the imidazoline agents more
effective at decreasing mucosal blood flow due to its vasoconstrictive effect to both capacitance
and resistance vessels in the nasal mucosa.
Comparatively, imidazole group demonstrates a more potent and longer-acting effect. For
example, 0.1% xylometazoline hydrochloride works within a few minutes and lasts up to 10
hours, while 1% phenylephrine works within 15 to 20 minutes with effects lasting 2 to 4 hours.
Types of intranasal decongestant (adrenoreceptor activity)
 Beta-phenylethylamine derivatives
o Ephedrine HCl (alpha-1, alpha-2, beta-1, beta-2) 
o Phenylephrine HCl (alpha-1) 

 Imidazoline derivatives (primarily alpha-2 agonists) 

o Naphazoline HCl  
o Oxymetazoline HCl 
 o Xylometazoline HCl 
Benzalkonium chloride (BKC)
A common antimicrobial preservative benzalkonium chloride (BKC) used in the topical nasal
preparations has correlations with exacerbation of RM, as it may increase the risk of
developing RM by inducing mucosal swelling.[3][4][5]. However, this is arguably open to
debate as there is no evidence of worsening congestion in those who use intranasal
corticosteroids containing BKC.[6][7][8]
https://www.ncbi.nlm.nih.gov/books/NBK538318/

Causes
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]
https://www.healthline.com/health/nasal-congestion#causes

Symptoms
 Nasal congestion that won't go away and there are no other allergy symptoms
occurring
 Nasal congestion that doesn't change in relation to seasonal or other types of
allergy triggers
 Nasal congestion that gets worse with the increase in frequency and dosage of
nasal spray
https://theallergygroup.com/Resources/Blog/ArticleID/2149/Rhinitis-Medicamentosa-Symptoms-
Causes-Treatment

History and Physical

The patient typically reports a recurrence of nasal congestion, particularly without rhinorrhea on
a background of prolonged use of an intranasal decongestant.  Severe nasal congestion may lead
to oral breathing, dry mouth, and snoring. Clinical examination will reveal nasal mucosa
swelling, erythematous and granular appearances. Pale and edematous appearances have also
been noted.[12] As the disease progresses, the nasal membrane becomes atrophic and crusty.[13]
12 Blue JA. Rhinitis medicamentosa. Ann Allergy. 1968 Aug;26(8):425-9. [PubMed] [Reference list]

13 Baldwin RL. Rhinitis medicamentosa (an approach to treatment). J Med Assoc State Ala. 1975
Aug;47(2):33-5. [PubMed] [Reference list]

The determination of RM on clinical grounds and there are no definitive biochemical tests or imaging
studies that can confirm this. Therefore, careful assessment of symptoms, history, and examination is
imperative in formulating an accurate diagnosis. It is also vital to acknowledge that other sinonasal
conditions may co-exist with RM.

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.
https://emedicine.medscape.com/article/995056-treatment#d7
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]
 [22

Seidman MD, Gurgel RK, Lin SY, Schwartz SR, Baroody FM, Bonner JR, et al. Clinical practice
guideline: allergic rhinitis executive summary. Otolaryngol Head Neck Surg. 2015 Feb. 152 (2):197-
206. [Medline].
]

Prognosis
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]
 [18
Graf PM, Hallen H. One year follow-up of patients with rhinitis medicamentosa after vasoconstrictor
withdrawal. Am J Rhinol. 1997 Jan-Feb. 11(1):67-72. [Medline].

] [19
Graf P, Hallen H. One-week use of oxymetazoline nasal spray in patients with rhinitis medicamentosa 1 year after treatment. ORL J Otorhinolaryngol
Relat Spec. 1997 Jan-Feb. 59(1):39-44. [Medline].

Prognosis
It takes approximately one year for complete recovery in cases of long-term overuse.[14]
14 Hallén H, Enerdal J, Graf P. Fluticasone propionate nasal spray is more effective and has a faster onset
of action than placebo in treatment of rhinitis medicamentosa. Clin. Exp. Allergy. 1997 May;27(5):552-
8. [PubMed] [Reference list]

Conclusion
Very few studies have been published on rebound congestion
and rhinitis medicamentosa and some of them report contradictory results.
Studies precisely analysing the consequences of prolonged use of nasal
decongestants were conducted on animal models or healthy subjects. Various
pathophysiological hypotheses have been proposed to explain the
accentuation of congestion induced by nasal decongestants, but they cannot be
extrapolated to the clinical setting. Other studies are therefore necessary to
specifically compare patients with rhinitis or rhinosinusitis treated by various
modalities.
The analysis conducted by the task force tends to refute the concepts of
rebound congestion and rhinitis medicamentosa. Nasal decongestants must
nevertheless be used in a controlled medical setting, in compliance with
prescription guidelines in view of the potentially serious systemic effects. In
patients with persistent nasal congestion despite the use of nasal
decongestants or accentuation of nasal congestion after stopping nasal
decongestants, the physician must review the aetiological work-up of an often
poorly defined nasal sinus disease. Alternative medical and/or surgical
treatments must then be proposed.