General Medical Information

Drug-induced Rhinitis

Shawn D. Newlands

Drug-induced rhinitis can be caused by systemic drugs that have effects on the nasal mucosa or by topical drugs. Antihypertensive drugs are the most often implicated systemic medications. Drugs believed to induce rhinitis include reserpine, guanethidine, phentolamine, methyldopa, prazosin, chlorpromazine, and drugs in the b-blocker and angiotensin-converting enzyme classes (2). These drugs can cause fairly mild symptoms of isolated congestion or rhinorrhea or can be part of a complex of symptoms that includes rhinosinusitis, nasal polyposis, and asthma.

Of the topical drugs, cocaine and over-the-counter nasal decongestants commonly cause drug-induced rhinitis. Rhinitis medicamentosa is caused by prolonged use of topical vasoconstricting agents such as cocaine, oxymetazoline hydrochloride, and phenylephrine hydrochloride, as well as others derived from sympathomimetic amines and imidazoles. Patients with chronic nasal obstruction due to anatomic abnormalities such as deviated septum or due to use of medications may be tempted to use these fast-acting topical sprays or drops for longer than is recommended by the manufacturer, usually 3 days. Tachyphylaxis—the rapid reduction in drug effect after administration of several doses—may prompt the patient to use vasoconstricting agents for extended periods. This causes further rebound effects due to down-regulation of nasal mucosal a-adrenergic receptors. Rhinitis medicamentosa is caused by refractory vasodilatation of mucosal blood vessels or excessive mucosal edema. With prolonged vasoconstriction, mucosal arterioles and vessels become fatigued and hypoxic, subsequently vasodilating to resupply nutrients to the highly vascular mucosa. However, as vascular cells vasodilate, they become increasingly permeable and allow an excessive amount of water to off-load into the hypertonic nasal mucosa. Mucosal injury, such as loss of cilia, metaplasia, or fibrosis, can occur as a more serious consequence of prolonged hypoxia owing to the use of vasoconstrictors. Abuse of cocaine also irritates and inflames the mucosa and can lead to septal perforation.

Rhinitis medicamentosa can overlie the original pathologic condition for which the decongestant abuse was started, which can cause a diagnostic dilemma. This diagnosis must be considered for any patient using the causative medicines for more than 7 days. One diagnostic technique is to ask patients to show the physician any over-the-counter sprays they are taking. Patients with rhinitis medicamentosa rarely travel without a spray, so strong is their reliance on nasal decongestants.

The objective of therapy for rhinitis medicamentosa is to eliminate this secondary refractory condition so that the primary condition, such as allergic rhinitis, turbinate hypertrophy, deviated nasal septum, or sinusitis, can be managed effectively. Therapy for rhinitis medicamentosa begins with cessation of topical administration of a vasoconstrictor. The physician must explain the importance of this first crucial step to secure full compliance. Replacement of the vasoconstrictive spray with saline nasal spray helps both patients with and without allergies. Saline nasal spray mobilizes and loosens secretions and keeps the recovering mucosa hydrated.

For patients with acute nasal obstruction after nasal spray withdrawal, some physicians administer a high burst of prednisone with a rapid taper to reduce mucosal edema. Patients with allergic rhinitis should take a daytime course of oral vasoconstrictors or oral antihistamines and an oral antihistamine at night. Patients with concurrent allergy may find additional relief with the use of a corticosteroid nasal spray during the previous oral regimen. Although corticosteroid sprays or anticholinergic agents provide some symptomatic relief from rhinitis medicamentosa to persons who do not have allergies, few studies have been performed to investigate the efficacy of managing rhinitis medicamentosa with these products.