Rhinitis medicamentosa is a condition characterised by nasal congestion without rhinorrohea or sneezing. This condition is caused by the use of topical nasal decongestants for a prolonged period of time. Use of these topical decongestants for more than a week is sufficient to cause this problem. This condition should be differentiated from rhinitis caused by use of drugs like oral contraceptives, antihypertensives and psychotrophic drugs.
The term rhinitis medicamentosa was coined by Lake in 1946.
Rebound rhinitis / chemical rhinitis
The nasal mucous membrane is rich in resistance blood vessels draining into capacitance venous sinusoids. These resistance blood vessels include small arteries, arterioles and arteriovenous anastomosis. The capacitance vessels (venous sinusoids) are innervated by sympathetic fibers. Sympathetic stimulation causes activation of alpha 1 and alpha 2 receptors present in the walls of the capacitance vessels which leads to decreased blood flow and constriction of venous sinusoids causing nasal decongestion. Parasympathetic stimulation causes release of acetyl choline which increases nasal secretions. Parasympathetic stimulation also causes release of VIP (vasoactive intestinal polypeptides) causing vasodilatation of the resistance blood vessels leading on to dilatation of sinusoids there by causing nasal congestion. In addition to sympathetic and parasympathetic innervation the nasal mucosa is richly endowed with sencory type c fibers. These sensory fibers on stimulation releases neurokinin A, calcitonin gene related peptide and substance P. These substances cause down regulation of sympathetic vasoconstriction causing nasal congestion. The exact pathophysiology of rhinitis medicamentosa is still not clear. Various hypothesis exist. Almost all of them focus on dysregulation of sympathetic / parasympathetic tone by exogenous vasoconstriction molecules.
Possible mechanisms of rhinitis medicamentosa include:
- Secondary decrease in the production of endogenous norepinephrine through a negative feed back mechanism
- Sympathomimetic amines used as topical decongestants have effects on both alpha and beta receptors. Their alpha effects predominate over beta effects causing nasal decongestion. This beneficial alpha effect is short lived while beta effect is more prolonged. After cessation of alpha stimulation the sympathomimetic amines still keep stimulating beta receptors causing rebound nasal congestion.
- Rebound increase in parasympathetic activity causing increased nasal secretion and nasal mucosal congestion
Get the whole article from here