Rhinitis medicamentosa - a consequence of using vasoconstrictor medications

The main symptom of rhinitis medicamentosa is persistent or rapidly recurring nasal congestion, which forces a person to use vasoconstrictor drops or sprays more and more often. After each application, nasal breathing temporarily improves, but the swelling then returns, often becoming more severe than it was initially, while the duration of the medication’s effect gradually shortens. Secondary manifestations include mouth breathing, dryness of the mouth and throat, snoring, sleep disturbance, feeling unrefreshed in the morning, headache, reduced sense of smell, dryness and burning in the nose, crust formation, and sometimes nosebleeds. Profuse nasal discharge, itching, sneezing attacks, and tearing are less characteristic of isolated rhinitis medicamentosa and more often indicate a persistent allergic, infectious, or vasomotor component.

The condition is not an infection and cannot be transmitted to other people. It develops primarily with prolonged or excessively frequent use of topical α-adrenergic agonists such as oxymetazoline, xylometazoline, naphazoline, phenylephrine, and other vasoconstrictor agents. Initially, they constrict blood vessels in the nasal mucosa and rapidly reduce swelling. With repeated use, adrenergic receptor sensitivity decreases, tachyphylaxis develops, the body’s own regulation of vascular tone becomes impaired, and periods of ischemia are followed by reactive vasodilation and increased swelling. The main target tissues are the mucosa of the nasal cavity and the vascular plexuses of the inferior turbinates. With a prolonged process, epithelial damage, impaired mucociliary clearance, and persistent turbinate hypertrophy may develop.

Rhinitis medicamentosa is more common in adults who self-administer decongestants for colds, allergic or vasomotor rhinitis, a deviated nasal septum, and other causes of difficult nasal breathing. It occurs less often in children, but is particularly dangerous because of the risk of systemic effects and overdose from vasoconstrictor agents. In older patients, coexisting hypertension, arrhythmias, ischemic heart disease, glaucoma, and prostate disorders must be taken into account. Rebound congestion may develop after only a few days of regular use, although the exact safe duration depends on the active substance and the dosing regimen. Without discontinuation of the vasoconstrictor medication, the condition may persist for months or years. After withdrawal, the most pronounced swelling usually decreases within several days or weeks, but recovery of the nasal mucosa after many years of use may take considerably longer. No single average duration of the condition has been established.

How to determine whether you have rhinitis medicamentosa

The most characteristic combination of signs is regular use of vasoconstrictor drops or sprays, an increasingly shorter period of free nasal breathing after each dose, and a sharp increase in congestion when the next dose is missed. A person gradually begins carrying the bottle everywhere, using the medication at night, applying it more frequently, or switching to a higher concentration. Congestion is usually bilateral, although one side of the nose may swell more than the other depending on body position. Nasal discharge, itching, frequent sneezing, and tearing are either absent or much less pronounced than in allergic rhinitis.

For an initial self-assessment, record the name of the active ingredient, its concentration, how frequently it is used, and for how long it has been used. If the medication is being used every day for longer than the period specified in the instructions and the nose barely breathes without it, the likelihood of rhinitis medicamentosa is high. At the same time, however, it is necessary to identify the original reason that prompted the use of a vasoconstrictor agent: allergic or vasomotor rhinitis, a viral infection, chronic rhinosinusitis, polyps, a deviated nasal septum, turbinate hypertrophy, pregnancy, or exposure to dust, smoke, or chemicals.

The diagnosis is usually made by an otorhinolaryngologist based on the medical history and examination of the nasal cavity. Anterior rhinoscopy or endoscopy may reveal marked swelling of the inferior turbinates, redness, pallor or bluish discoloration of the mucosa, dryness, crusting, and areas of bleeding. Objective assessment of nasal airflow may include anterior active rhinomanometry, acoustic rhinometry, and measurement of peak nasal inspiratory flow. If allergy is suspected, allergy testing is performed. If chronic rhinosinusitis or polyps are suspected, endoscopy and, when indicated, computed tomography of the paranasal sinuses may be required. There is no specific laboratory test for rhinitis medicamentosa.

Red flags

Rhinitis medicamentosa itself rarely requires emergency care, but other diseases or systemic complications from vasoconstrictor medications may be hidden behind what appears to be familiar nasal congestion.

Immediate medical attention is required if breathing becomes difficult not only through the nose but also through the mouth, or if there is a sensation of choking, wheezing, swelling of the tongue or larynx, or bluish discoloration of the lips. These may be manifestations of bronchospasm, angioedema, or another acute condition.

Chest pain or pressure, severe palpitations, irregular heartbeat, a sudden rise in blood pressure, fainting, or pronounced weakness require urgent cardiovascular assessment. Topical α-adrenergic agonists may be partially absorbed into the bloodstream, especially when they are used too frequently, when the mucosa is damaged, or when the medication is swallowed.

Severe headache, visual or speech disturbances, impaired coordination, numbness or weakness of a limb, or confusion are reasons to call emergency medical services. These symptoms must not automatically be attributed to a “blocked nose.”

High fever, increasing one-sided facial pain, purulent or foul-smelling discharge, eyelid swelling, pain with eye movement, double vision, or deterioration in vision require urgent examination by an ENT specialist and, when ocular symptoms are present, by an ophthalmologist as well. These manifestations are not characteristic of isolated rhinitis medicamentosa and may indicate complicated rhinosinusitis.

Persistent one-sided nasal obstruction, recurrent bleeding from one side of the nose, bloody discharge, an unpleasant odor, or progressive deformity require endoscopic evaluation to exclude a foreign body, polyp, vascular lesion, or neoplastic process.

Accidental swallowing of vasoconstrictor drops by a child, unusual drowsiness, lethargy, cold skin, slow breathing, bradycardia, or unstable blood pressure are particularly dangerous. In such a situation, emergency medical services should be called immediately and the medication packaging should be shown to the medical team. Pregnant women, older patients, and people with hypertension, arrhythmias, ischemic heart disease, glaucoma, or hyperthyroidism require medical assessment at the first signs of systemic reactions.

Initial self-care methods for rhinitis medicamentosa

The main rule is not to increase the frequency, amount, or concentration of the vasoconstrictor medication and not to replace it with another medication from the same class. Using oxymetazoline instead of xylometazoline or naphazoline does not interrupt the pathological mechanism. Before seeing a doctor, it is useful to record the actual frequency of use, including nighttime doses. This will help the physician choose a withdrawal strategy, either abrupt or gradual. After many years of use and in cases of severe congestion, it is preferable to develop the withdrawal plan together with an ENT specialist.

A ready-made sterile 0.9% isotonic sodium chloride solution may be used to cleanse and moisturize the nasal mucosa. For high-volume nasal irrigation, only sterile, distilled, or previously boiled and cooled water should be used. A homemade isotonic solution can be prepared using 9 g of pure table salt per 1 liter of water. The solution should be warm, approximately at body temperature. Usually, 100–200 ml for the entire procedure once or twice daily is sufficient. The fluid should be introduced without strong pressure while leaning over a sink and turning the head slightly to one side. Irrigation should be stopped if pain, pronounced pressure in the ears, or bleeding occurs. It should not be performed when a nasal passage is completely obstructed, in acute otitis, with frequent nosebleeds, or after surgery without the physician’s permission.

It is advisable to maintain a room temperature of approximately 18–22 °C and humidity of 40–60%, ventilate the room regularly, and avoid a direct stream of cold air toward the face. Excessively dry air promotes crust formation, while excessive humidity encourages mold growth. Tobacco smoke, scented candles, aerosol air fresheners, strong perfumes, construction dust, and aggressive household chemicals should be avoided.

Sleeping with the head of the bed moderately elevated by 10–15 cm may help. This can partially reduce nighttime venous engorgement of the nasal mucosa. Several high pillows that sharply bend the neck should not be used. Moderate physical activity is acceptable, but intense exercise should temporarily be limited if vasoconstrictor medications cause palpitations, headache, or fluctuations in blood pressure.

There is no special diet that treats rhinitis medicamentosa. It may be useful to temporarily limit alcohol, very hot foods, excessive amounts of spicy seasonings, and foods that individually worsen nasal congestion. Fluid intake should remain normal, approximately 25–30 ml of fluid per kilogram of body weight per day, taking food intake and climate into account. In heart or kidney failure, edema, or when fluid restriction has been prescribed, this amount must not be increased independently. Water and warm unsweetened beverages are preferable. Forcing excessive fluid intake does not relieve turbinate swelling.

Onion juice, garlic juice, lemon juice, concentrated essential oils, alcohol tinctures, hydrogen peroxide, and other irritating substances must not be instilled into the nose. They may cause chemical burns and further damage the mucociliary epithelium. Steam inhalation over boiling water does not restore vascular regulation and carries a risk of burns. Vasoconstrictor drops must not be diluted “by eye,” transferred into unlabelled bottles, or used simultaneously with other products containing a decongestant.

The frequency of spray use, duration of its effect, nighttime awakenings, nosebleeds, headache, pulse, and blood pressure should be monitored. If congestion does not begin to decrease after withdrawal from the decongestant is started, if significant sleep disturbance persists, or if unilateral symptoms develop, examination by an ENT specialist is necessary.

Stages and possible progression of rhinitis medicamentosa

There is no official universal staging system for rhinitis medicamentosa. For practical purposes, it is possible to distinguish an initial period of use, a phase of reduced sensitivity to the medication, and a chronic phase involving structural and functional damage to the mucosa.

Initially, the vasoconstrictor restores nasal breathing rapidly and for a prolonged period. Later, the duration of its effect shortens, the need for more frequent use develops, and rebound swelling occurs after the medication wears off. In the chronic stage, congestion is present almost constantly, sleep becomes disturbed, the sense of smell declines, and the mucosa becomes dry and fragile or, conversely, swollen and hypertrophic.

Factors that contribute to chronic disease include prolonged self-treatment, frequent dosing, exceeding the recommended concentration, simultaneous use of several decongestants, failure to treat the underlying allergic or vasomotor rhinitis, a deviated nasal septum, polyps, chronic rhinosinusitis, smoking, and constant exposure to irritants.

Without discontinuing the vasoconstrictor medication, the pathological cycle continues. Possible consequences include chronic impairment of nasal breathing, hypertrophy of the inferior turbinates, epithelial damage, crust formation, recurrent bleeding, reduced sense of smell, sleep disturbance, snoring, and deterioration in quality of life. Persistent swelling may interfere with ventilation of the paranasal sinuses and auditory tubes. Rhinitis medicamentosa does not necessarily progress directly into bacterial sinusitis, but impaired mucosal clearance creates an unfavorable background.

After withdrawal of the medication, the prognosis is usually favorable, although congestion may temporarily worsen during the first few days. After prolonged misuse, restoration of vascular reactivity and mucosal structure takes considerably longer. Returning to uncontrolled decongestant use may rapidly trigger a relapse.

Integrative treatment methods for rhinitis medicamentosa

In rhinitis medicamentosa, the main goal is not merely to temporarily reduce congestion but to completely discontinue vasoconstrictor drops. Prolonged use of naphazoline, xylometazoline, oxymetazoline, and other α-adrenergic agonists disrupts regulation of vascular tone, decreases adrenergic receptor sensitivity, maintains epithelial ischemia, and promotes subsequent reactive engorgement of the mucosa.

After the decongestant effect ends, the venous plexuses of the turbinates become engorged with blood, capillary permeability increases, and pronounced swelling develops. Repeated instillation temporarily constricts the vessels but maintains the pathological cycle. Therefore, an integrative regimen should simultaneously make discontinuation of the medication easier, reduce venous engorgement and exudation, control inflammation, and create conditions for restoration of the epithelial barrier.

The central topical component is the ABP-153 oil infusion, administered intranasally. The basic version without DMSO is suitable for processes involving the superficial mucosa and the nasal cavity. Its clinical objectives are to reduce reactive inflammation and swelling, protect damaged epithelium, normalize secretion, and create conditions for restoration of the mucosa’s own vascular regulation.

According to accumulated clinical observations, patients who had used “Naphthyzin” and “Otrivin” for prolonged periods gradually reduced their need for vasoconstrictor drops while using ABP-153 and discontinued them within 14 days. These observations come from real-world clinical practice and do not represent an established universal efficacy rate. For objective assessment, they need to be systematized with consideration of the duration of dependence, baseline frequency of instillation, withdrawal method, changes in nasal breathing, and condition of the mucosa.

Menthol, camphor, borneol, eucalyptus, clove, and other biologically active components of ABP-153 may cause burning, sneezing, or a temporary increase in rebound congestion during the first applications. If pronounced irritation, bleeding, increasing swelling, or rhinorrhea occurs, use should be discontinued.

ABP-153 should not be administered at the same time as water-based nasal medications. Saline cleansing and the prescribed water-based spray should be used first, while the oil infusion should be administered in a separate time window. The penetrating version ABP-153D is not required for rhinitis medicamentosa because the primary target consists of the superficial mucosa, epithelium, and vascular plexuses of the turbinates rather than deep tissues.

A second important approach is correction of venous engorgement in the nasal turbinates. For this purpose, a standardized extract of butcher’s broom Ruscus aculeatus is used. Ruscogenins increase the tone of venous and lymphatic vessels, reduce capillary permeability, reduce fluid leakage into tissues, and decrease blood stasis in the cavernous plexuses. Butcher’s broom is not an adrenergic agonist and does not cause ischemic damage to the mucosa or rhinitis medicamentosa. It does not replace the topical effect of ABP-153, but complements it through systemic correction of the vascular and lymphatic component of swelling. In patients with arterial hypertension and in those simultaneously using decongestants, sympathomimetics, antihypertensive medications, or other agents affecting vascular tone, blood pressure monitoring is required. Possible adverse effects include dyspepsia, headache, changes in blood pressure, and allergic reactions.

An oral dry extract of heartleaf Houttuynia Houttuynia cordata is used to address mucosal inflammation, pathological secretion, and the exudative component. Prolonged exposure to decongestants is accompanied by epithelial damage, impaired mucociliary clearance, and increased mucosal reactivity. The small amount of Houttuynia cordata present in ABP-153 does not provide comparable systemic exposure, so the oral extract is considered a separate component. Its inclusion is particularly justified in pronounced rhinorrhea, postnasal drip, frequent inflammatory exacerbations, and when rhinitis medicamentosa is combined with chronic rhinopharyngitis or rhinosinusitis. Houttuynia may cause dyspepsia, increased urination, and allergic reactions. Caution is required in severe decompensated liver or kidney disease, active autoimmune processes, and simultaneous use of diuretics or immunosuppressants.

Murdannia loriformis complements the regimen at the level of immunoinflammatory and lymphatic regulation. Its use is intended to reduce persistent inflammatory activity, exudate formation, and tissue overload that may remain after prolonged use of vasoconstrictor medications. Murdannia loriformis is not a direct decongestant and should not be regarded as a herbal substitute for “Naphthyzin,” “Otrivin,” or other α-adrenergic agonists. Its role is to support systemic mechanisms responsible for resolution of inflammation and restoration of interstitial exchange. In people prone to arterial hypotension and in cases of acute nephritis, pancreatitis, cholangitis, pregnancy, or breastfeeding, individual safety assessment is necessary. Possible adverse effects include dyspepsia, weakness, reduced blood pressure, and allergic reactions.

Squalene is included as an additional membrane-repairing and antioxidant component. After intestinal absorption, it enters lipid transport pathways and participates in maintaining cell membranes. Its role is to reduce the consequences of oxidative damage and provide an additional metabolic background for epithelial recovery. Squalene does not have a direct vasoconstrictor or independent lymphatic drainage effect and does not replace butcher’s broom. It has a supportive role: ABP-153 provides the primary topical effect, butcher’s broom regulates the venous and lymphatic component, Houttuynia cordata and Murdannia loriformis act on inflammation and exudation, while squalene supports membrane recovery. Squalene is contraindicated in individuals with intolerance to fish, seafood, or sulfites. Nausea, abdominal discomfort, loose stools, and allergic reactions may occur.

A rationally selected combination does not cause tachyphylaxis, mucosal ischemia, rhinitis medicamentosa, or pronounced rebound swelling characteristic of prolonged use of α-adrenergic agonists. It does not contain systemic glucocorticosteroids and therefore does not create their typical risks of hyperglycemia, adrenal suppression, osteoporosis, glaucoma, and systemic immune suppression. Herbal origin does not exclude individual allergy, mucosal irritation, dyspepsia, changes in blood pressure, or drug interactions. The final combination is determined by the duration of decongestant dependence, severity of mucosal damage, predominance of congestion or rhinorrhea, liver, kidney, and cardiovascular status, and medications already being used.

What you need to know about standard protocols in modern medicine

Complete discontinuation of the topical vasoconstrictor medication is the basis of treatment for rhinitis medicamentosa. Without stopping naphazoline, xylometazoline, oxymetazoline, and other α-adrenergic agonists, other treatments primarily provide only temporary masking of nasal congestion. There is no single approach requiring exclusively abrupt or exclusively gradual withdrawal. Clinical practice includes immediate discontinuation, sequential withdrawal first from one nostril and then the other, or gradual reduction in frequency of use. The method is selected according to the duration of dependence, severity of swelling, cardiovascular and other comorbidities, and the patient’s ability to tolerate temporary worsening of nasal breathing.

After discontinuation of the decongestant, congestion often increases sharply because of reactive vasodilation and engorgement of the cavernous tissue of the turbinates. This does not mean that the medication should be restarted. Repeated instillation once again initiates the cycle of short-term vasoconstriction, subsequent ischemia, reduced sensitivity of α-adrenergic receptors, and even more pronounced rebound swelling. Continued use maintains damage to the ciliated epithelium, dryness, crust formation, bleeding, and chronic vascular dysregulation.

Intranasal glucocorticosteroids such as fluticasone, mometasone, budesonide, and beclomethasone reduce inflammatory reactions and mucosal swelling and may make the decongestant withdrawal period easier. Their efficacy in rhinitis medicamentosa has been supported by only a limited number of small studies, so they do not guarantee recovery and do not eliminate the original cause of congestion, such as allergic rhinitis, vasomotor dysregulation, a deviated nasal septum, polyps, or turbinate hypertrophy.

The most common adverse reactions to intranasal corticosteroids are dryness, burning, soreness, irritation, unpleasant taste, crusting, and nosebleeds. Directing the spray toward the septum increases the risk of chronic trauma, ulceration, and, rarely, perforation. Prolonged suppression of local immunity may promote nasopharyngeal candidiasis, mask bacterial or fungal infection, and delay mucosal recovery after trauma or surgery.

With prolonged use of high doses, simultaneous use of several steroid medications, or damaged mucosa, systemic absorption may occur. Possible consequences include suppression of the hypothalamic-pituitary-adrenal axis, reduced endogenous cortisol production, manifestations of hypercortisolism, growth retardation in children, increased intraocular pressure, glaucoma, and cataracts. Abrupt discontinuation after substantial systemic steroid exposure may be accompanied by manifestations of adrenal insufficiency.

The combination of fluticasone with ritonavir or cobicistat is particularly dangerous. Strong inhibition of CYP3A4 markedly increases systemic exposure to the corticosteroid and may lead to Cushing syndrome and secondary adrenal insufficiency. Caution is also required with ketoconazole and other strong CYP3A4 inhibitors. Intranasal corticosteroids should not be started independently in the presence of an unhealed nasal injury or postoperative wound, mucosal ulcers, active untreated infection, frequent bleeding, glaucoma, or cataracts.

Systemic glucocorticosteroids such as prednisolone, prednisone, and similar medications are sometimes prescribed by a physician in cases of extremely severe swelling when the patient is unable to discontinue the decongestant by another method. This is not mandatory therapy for rhinitis medicamentosa, and the evidence supporting this use is limited.

Even a short course of systemic corticosteroids may cause insomnia, anxiety, irritability, depressive or manic reactions, increased appetite, elevated blood pressure and glucose levels, sodium and fluid retention, edema, dyspepsia, and reduced resistance to infection. Exacerbation of gastritis, erosive gastric injury, cardiac rhythm disturbances, and decompensation of diabetes mellitus may occur.

Repeated or prolonged courses increase the risk of peptic ulcer bleeding, steroid-induced diabetes, pronounced muscle weakness and atrophy, osteoporosis, fractures, aseptic bone necrosis, cataracts, glaucoma, immune suppression, and reactivation of latent infections. Adrenal suppression creates a risk of acute insufficiency if treatment is stopped abruptly or during infection, surgery, or other physiological stress.

Systemic glucocorticosteroids should not be started independently in uncontrolled diabetes or arterial hypertension, active infection, peptic ulcer disease or gastrointestinal bleeding, severe psychiatric reactions to steroids, or glaucoma. Combination with NSAIDs and anticoagulants sharply increases the risk of bleeding, while certain antifungal and antiviral medications may increase systemic corticosteroid concentrations.

Intranasal antihistamines, for example azelastine, may be used when rhinitis medicamentosa is combined with allergic or mixed inflammation. In isolated rebound swelling after decongestant use, they do not eliminate the underlying vascular dependence. Possible adverse effects include a bitter taste, dryness, burning, irritation, nosebleeds, headache, dizziness, fatigue, and drowsiness.

Azelastine may slow reaction time and impair concentration. Combining it with alcohol, benzodiazepines, sleeping medications, opioids, and other sedatives increases central nervous system depression. Until individual tolerance has been assessed, driving and operating machinery may be unsafe.

Oral antihistamines are primarily effective when an allergic component is present, such as itching, sneezing, watery rhinorrhea, and tearing. They do not eliminate dependence on the decongestant itself. First-generation medications may cause drowsiness, impaired memory and reaction time, mucosal dryness, thickening of secretions, constipation, tachycardia, impaired accommodation, and urinary retention.

In older patients, sedating antihistamines increase the risk of confusion, delirium, falls, and fractures. Some medications prolong the QT interval and may provoke dangerous arrhythmias. Second-generation agents are usually better tolerated, but they may cause drowsiness, headache, palpitations, and may accumulate when liver or kidney function is impaired.

Oral sympathomimetics, including pseudoephedrine, are sometimes used for temporary relief of congestion, but they do not restore damaged mucosa and effectively replace one adrenergic agonist with another. Pseudoephedrine may cause tachycardia, increased blood pressure, arrhythmia, tremor, anxiety, insomnia, psychomotor agitation, and urinary retention.

In predisposed patients, hypertensive crisis, myocardial ischemia, and cerebrovascular events may occur. Pseudoephedrine should not be started independently in uncontrolled hypertension, severe cardiovascular disease, cardiac rhythm disorders, hyperthyroidism, angle-closure glaucoma, prostatic hyperplasia, pregnancy, or during simultaneous treatment with monoamine oxidase inhibitors or within two weeks after they have been discontinued.

Antibiotics do not treat rhinitis medicamentosa. They are prescribed only when a separate bacterial process has been confirmed. Unjustified use may cause diarrhea, candidiasis, allergic reactions, drug-induced liver or kidney injury, antibiotic-associated colitis, and selection of resistant microorganisms. Using an antibiotic instead of withdrawing the decongestant does not affect the mechanism of the condition.

If pronounced hypertrophy of the inferior turbinates persists after withdrawal of the vasoconstrictor and conservative treatment, radiofrequency reduction, coblation, submucosal vasotomy, or other procedures may be considered. In cases of significant deviation of the nasal septum, septoplasty may be considered separately. Surgery does not eliminate the need to stop decongestant misuse and to treat the underlying allergic or vasomotor rhinitis.

Surgical procedures may cause bleeding, infection, pain, prolonged crust formation, scarring, adhesions, sensory disturbances, deterioration of the sense of smell, and recurrent enlargement of the turbinates. Excessive tissue removal may lead to empty nose syndrome, in which a wide nasal passage is paradoxically accompanied by a sensation of suffocation, severe dryness, sleep disturbance, anxiety, and a profound reduction in quality of life.

A reliable rate of complete mucosal recovery and absence of recurrence over two years has not been established for any single rhinitis medicamentosa protocol. The prognosis depends on the duration and frequency of decongestant use, severity of epithelial damage, presence of turbinate hypertrophy, structural obstruction, and adequate treatment of the original cause of congestion.

Combined use of intranasal and systemic glucocorticosteroids, antihistamines, oral sympathomimetics, and repeated return to vasoconstrictor drops may worsen mucosal damage and dryness and provoke bleeding, hormonal disturbances, increased blood pressure, arrhythmia, insomnia, urinary retention, and continuation of medication dependence. Alternative integrative approaches based on individually selected herbal formulations may act on inflammation, venous engorgement, capillary permeability, and epithelial recovery and generally do not produce the same degree of aggressive local and systemic effects as prolonged combined use of chemically synthesized medications.

Why dosages and duration of treatment are not specified in the article

Rhinitis medicamentosa develops differently in different patients. One person may use vasoconstrictor drops for several months, while another may use them for many years. The substance used, frequency of instillation, severity of nighttime congestion, condition of the nasal mucosa, and degree of turbinate enlargement also differ. In some patients, medication dependence coexists with allergic or vasomotor rhinitis, chronic rhinosinusitis, a deviated nasal septum, polyps, or mucosal hypertrophy. Therefore, the same decongestant withdrawal regimen and the same dosages of restorative agents are not suitable for everyone.

To develop an individualized program, it is necessary to assess the duration of naphazoline, xylometazoline, oxymetazoline, or other decongestant use, daily frequency of use, the feasibility of gradual or abrupt discontinuation, severity of rebound swelling, and preservation of nasal breathing. Age, body weight, blood pressure, liver, kidney, and cardiovascular status, allergy history, comorbidities, and medications already being taken are also considered. A universal dosage may be insufficient in long-standing dependence or excessive in the early stages of rhinitis medicamentosa.

For this reason, the article describes treatment approaches and the sequence of mucosal recovery but does not replace an individualized clinical and pharmacological assessment. A short question can be asked in the comments section of the article, while an individualized program for withdrawal from vasoconstrictor medications and restorative therapy can be developed by booking a consultation with a clinical pharmacologist specializing in integrative medicine.