Introduction:
Rhinitis medicamentosa is a case characterised by nasal congestion without rhinorrohea or sneezing. This condition is caused by the appliance of topical nasal decongestants for a prolonged phrase of time. Use of these consisting of topics decongestants for more than a week is able to cause this problem. This predicament should be differentiated from rhinitis caused the agency of use of drugs like oral contraceptives, antihypertensives and psychotrophic drugs.
History:
The denomination rhinitis medicamentosa was coined by Lake in 1946.
Synonyms:
Rebound rhinitis / chemical rhinitis
Pathophysiology:
The nasal gummy membrane is rich in resistance house vessels draining into capacitance venous sinusoids. These resistance blood vessels include small arteries, arterioles and arteriovenous inosculation. The capacitance vessels (venous sinusoids) are innervated dint of sympathetic fibers. Sympathetic stimulation causes activation of alpha 1 and alpha 2 receptors offering in the walls of the capacitance vessels which leads to decreased blood flow and compression of venous sinusoids causing nasal decongestion. Parasympathetic stimulation causes loose of acetyl choline which increases nasal secretions. Parasympathetic stimulation furthermore causes release of VIP (vasoactive of the intestines polypeptides) causing vasodilatation of the hindrance blood vessels leading on to expanding of sinusoids there by causing nasal repletion. In addition to sympathetic and parasympathetic innervation the nasal mucosa is richly endowed with sencory type c fibers. These sensory fibers put stimulation releases neurokinin A, calcitonin gene kin peptide and substance P. These substances object down regulation of sympathetic vasoconstriction causing nasal plethora. The exact pathophysiology of rhinitis medicamentosa is stifle not clear. Various hypothesis exist. Almost totality of them focus on dysregulation of sympathetic / parasympathetic tone by exogenous vasoconstriction molecules.
Possible mechanisms of rhinitis medicamentosa embody:
Secondary decrease in the production of endogenous norepinephrine from one side a negative feed back mechanism
Sympathomimetic amines used in the same proportion that topical decongestants have effects on the one and the other alpha and beta receptors. Their alpha goods predominate over beta effects causing nasal decongestion. This beneficial alpha truth is short lived while beta force is more prolonged. After cessation of alpha stimulation the sympathomimetic amines silent keep stimulating beta receptors causing reverberate nasal congestion.
Rebound increase in parasympathetic etc causing increased nasal secretion and nasal mucosal plethora
Types of topical nasal decongestants in exercise:
Two types of nasal decongestants are used.
Sympathomimetic amines - (pseudoephidrine, amphetamine, phenylephrine mescaline). These drugs activate sympathizing nerves by presynaptic release of endogenous norepinephrine, which binds to alpha receptors causing vasoconstriction capital on to nasal decongestion. Rebound vasodilatation may exist caused due to weak affinity of these drugs to beta receptors most important on to vasodilatation and nasal repletion.
Imidazolines - (zylometazoline, oxymetazoline, naphazoline). These drugs lead to vasoconstriction due to its effect without interrupti alpha 2 receptors. These drugs too cause a decrease in the endogenous secretion of norepinephrine via a negative feedback mechanism. This depression in the endogenous norepinephrine secretion causes fly back vasodilatation and nasal congestion.
Benzalkonium chloride the conservative commonly used in nasal drops receive been known to exacerbate rhinitis medicamentosa. The without the least error mechanism is still not known.
It should have existence borne in mind that use of nasal decongestants is fit to the presence of pre existing pathology in nasal mucosa causing nasal arrest. Pathologies can be infections, polypi, allergic rhinitis etc.
Symptoms:
Symptoms are usually confined to the nose.
Nasal shut up without significant rhinorrhoea and sneezing
These symptoms dont point out seasonal variations
Patient feels compelled to use nasal topical decongestants
Usage of these decongestants be suitable to more frequent
Physical examination of nose shows:
Nasal slimy membrane appears beefy red
Nasal mucosa is boggy, granular, friable and bleeds on touch
These patients snore and have sleep apnoea
Dry mouth and swallow are common findings
Histological features of rhinitis medicamentosa:
Nasal epithelium shows cruel hyperplasia
There is loss of cilia
Increase in the reckon of goblet cells and submucosal glands
Epidermal growing factor receptor:
This is a 70 kilodalton membrane glycoprotein what one is usually expressed in fetal airways. This receptor plays a essential role in epithelial cell proliferation, differentiation and airway arborescence in fetus. In healthy adult airways this receptor is usually not expressed. It is seen no other than in patients with malignancy involving airway. In patients by rhinitis medicamentosa this epidermal growth agent receptor is found to be expressed in generous quantities. They play a vital role in proliferation of goblet cells and mucous secretion by these glands.
Treatment:
The before anything else goal in management of these patients is material them discontinue the use of topical nasal decongestant. It should be borne in spirit that sudden cessation of use of consisting of topics nasal decongestants will cause more nasal congestion making patient's compliance that a great deal of difficult.
Oral prednisalone:
Patient with rhinitis medicamentosa is treated through oral prednisolone in doses of 15 mg thrice a day for 5 days, at the same time that the nasal decongestant is simultaneously withdrawn in a phased kinds. The patient is weaned from steroid through tapering the dose.
Use of intranasal steroids:
This is seemly popular because it causes fewer lateral effects than systemic steroids. It be possible to be safely administered for long durations. These patients may deduce significant benefit by using intranasal steroids because it helps in simultaneous control of nasal allergy and in like manner reduces the nasal mucosal inflammation and oedema.
Nasal briny douching:
Douching the nose with isotonic salt will help in clearing the nasal void of thick mucoid secretions thus enabling the steroid bough to permeate the nose fully.