Nasal congestion is experienced as reduced nasal airflow or a sensation of facial fullness and results from multiple interrelated mechanisms. It is primarily driven by mucosal inflammation, which leads to vasodilation, increased blood flow, and increased vascular permeability. This process triggers venous engorgement, excess nasal secretions, and tissue oedema, all of which narrow the nasal passages and impair airflow.¹

Nasal congestion may also arise from structural abnormalities within the nasal cavity. Conditions such as septal deviation, choanal atresia, concha bullosa, cleft palate, adenoid hypertrophy, and neoplasia can physically narrow or obstruct the nasal passages. The anterior nasal valve is the narrowest segment of the nasal airway, and airflow can be significantly compromised by its size and the overall shape and architecture of the nasal passages.¹

A nose for nuance in diagnosis

Initial assessment is largely subjective, relying on both patient and clinician interpretation of symptoms, making a detailed history and focused physical examination the cornerstone of diagnosis.²

A thorough history should characterise the nature of nasal blockage and associated rhinosinusitis symptoms, including postnasal drip, nasal itch, sneezing, and ocular symptoms. It should also explore related features such as facial pain, headache, and reduced olfaction, while documenting symptom duration, temporal pattern, and potential triggers.²

Diagnostic testing, such as endoscopy and allergy testing, fall beyond the scope of primary care practice, often requiring referral to specialists such as otolaryngologists and allergists. Features requiring urgent attention, including swollen or red eyelids, proptosis, diplopia, ophthalmoplegia, reduced visual acuity, severe frontal headache (unilateral or bilateral), frontal swelling, and any signs suggestive of meningitis or focal neurological deficit.²

Intranasal decongestants get the job done

Intranasal decongestants are among the most effective and widely used pharmacological options for relieving nasal congestion, largely due to their ease of use. They offer several advantages, including rapid onset of action, reduced drug degradation, and high absorption rates, as well as good patient compliance, ease of self-administration, non-invasive delivery, and the potential for direct nose-to-brain transport.³

Intranasal decongestants are broadly classified into beta-phenylethylamine derivatives and imidazoline derivatives, based on their adrenoreceptor activity. Beta-phenylethylamine derivatives act primarily via α1-adrenoreceptor stimulation to induce vasoconstriction but may be associated with rebound vasodilation due to weaker receptor affinity.⁴

Common intranasal decongestants include beta-phenylethylamine derivatives such as ephedrine hydrochloride (HCl, α1, α2, β1, β2 activity) and phenylephrine HCl (α1 activity), and imidazoline derivatives such as naphazoline HCl, oxymetazoline HCl, and xylometazoline HCl.⁴

Clinically, imidazoline derivatives demonstrate a more potent and longer-lasting effect. For example, studies show that oxymetazoline provides significant subjective and objective relief from nasal congestion for up to 12-hours. Subjective relief may be experienced as quickly as 25-seconds after application, while objective improvement occurs within five- to 10-minutes, with effects lasting up to 10-hours. In contrast, phenylephrine has a slower onset of action (15- to 20-minutes) and a shorter duration of effect (two- to four-hours).^4,5

Old but gold: An intranasal decongestant that still delivers

In South Africa, oxymetazoline HCI is indicated for the relief of nasal congestion associated with the common cold, sinusitis, and AR, and may also be used as adjunctive therapy in middle ear infections. It is approved for use in adults and children aged ≥6 years.

Oxymetazoline has a long history of safe use spanning >50-years when used as directed for short durations. When applied topically, it induces vasoconstriction within the nasal mucosa, reducing turbinate swelling, improving nasal patency, and providing effective relief of congestion from various causes. Use should remain limited to short durations (≤10-days) due to the risk of rhinitis medicamentosa (RM).⁶

When relief backfires: Understanding and managing rhinitis medicamentosa

RM, also known as rebound congestion, is a condition primarily caused by the prolonged use (>seven– to 10-days) of topical intranasal decongestants. Although the exact pathophysiology remains unclear, several mechanisms have been proposed.⁴

Clinically, patients typically present with recurrent nasal congestion without significant rhinorrhoea, usually in the setting of prolonged decongestant use. Severe cases may lead to mouth breathing, dry mouth, and snoring. Examination findings include swollen nasal mucosa with erythematous, granular, or pale and oedematous appearances, and in chronic cases, progression to atrophic, crusted mucosa.⁴

Several hypotheses have been proposed to explain the pathophysiology of RM. Chronic vasoconstriction may lead to mucosal ischaemia and subsequent interstitial oedema. Another hypothesis suggests fatigue of vasoconstrictive mechanisms, resulting in reactive hyperaemia, reduced responsiveness to endogenous catecholamines, and receptor desensitisation (tachyphylaxis), which drives escalating use.⁴

Altered vasomotor tone with increased vascular permeability and oedema has also been implicated, as well as a rebound effect where β-adrenergic activity outlasts α-adrenergic effects, resulting in vasodilation and worsening congestion.⁴

Management centres on immediate discontinuation of the topical decongestant. Patients should be counselled that symptoms may temporarily worsen after stopping therapy, to prevent premature discontinuation and perceived treatment failure.⁴

Conclusion

Nasal congestion is a common symptom in primary and specialist care, often associated with AR, rhinosinusitis, and other upper airway disorders, and may affect sleep and quality of life. It results from mucosal inflammation causing vascular changes, oedema, and airflow obstruction, although structural abnormalities may also contribute. Diagnosis relies on clinical history and examination, with attention to symptom patterns and red flag features. Nasal decongestants are effective and act quickly but should be used short term due to rebound congestion risk. RM may occur with prolonged use but is easily resolved with prompt discontinuation and counselling supportive care.

References

1. Naclerio RM, Bachert C, Baraniuk JN. Pathophysiology of nasal congestion. Int J Gen Med, 2010. [Internet]. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC2866558/

2.  Krouse J, Lund V, Fokkens W, Meltzer EO. Diagnostic strategies in nasal congestion. Int J Gen Med, 2010. [Internet]. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC2866556/

3.  Tai J, Han M, Lee D, Park IH, Lee SH, Kim TH. Different Methods and Formulations of Drugs and Vaccines for Nasal Administration. Pharmaceutics, 2022. [Internet]. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC9144811/

4.  Wahid NWB, Shermetaro C. Rhinitis Medicamentosa. [Updated 2023 Sep 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538318/

5. Stinson RJ and Sadofsky LR. Part 1 - imidazolines and the changing face of nasal decongestants. Front Pharmacol, 2025. [Internet]. Available at: https://pmc.ncbi.nlm.nih.gov/articles/PMC12698654/pdf/fphar-16-1655252.pdf

6.  Druce HM, Ramsey DL, Karnati S, Carr AN. Topical nasal decongestant oxymetazoline (0.05%) provides relief of nasal symptoms for 12-hours. Rhinology, 2018. [Internet]. Available at: https://pubmed.ncbi.nlm.nih.gov/29785414/

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