Vasomotor Rhinitis Essay, Research Paper

Enos Stevenson

Health- Ms. Baker

Vasomotor Rhinitis

Introduction

Rhinitis is defined as an inflammation of the nasal mucosa and it is characterized by nasal obstruction, rhinorrhea, sneezing, and pruritits . The etiologies of rhinitis can be broadly classified into 4 main categories: allergic, infectious, and non-allergic, non-infectious (vasomotor rhinitis). Allergic rhinitis is a mediated reaction to certain environmental agents, often a type of pollen. As the name describes, some type of pathogen is evident in infectious rhinitis. Most commonly, viruses are the culprit, which then may allow a secondary bacterial infection to flourish. Fungal infections are more commonly seen in immunocompromised patients. Non-allergic, non-infectious rhinitis is a broad category which encompasses all other forms of rhinitis, including ones of an idiopathic etiology. In this category, certain elements illicit a hyperactive response from the sympathetic and parasympathetic nervous system and/or a non-IgE mediated release of vasoactive mediators. These elements include drugs, hormones, and irritants, even cold air. Other causes of these responses can also be due to an eosinophilia or mastocytosis in the nasal mucosa or physical or mental stress. In the majority of cases, 60-70%, the cause of non-allergic, non-infectious rhinitis is unknown.. In the following text, the topic of vasomotor rhinitis will be explored further including the pathophysiology, prevention, and treatment of this condition.

Pathology

There are a number of mechanisms which interact in the nose to allow it to function appropriately in a variety of environments. The autonomic nervous system controls the blood supply into the nasal mucosa and the secretion of mucus. The diameter of the resistance vessels in the nose is mediated by the sympathetic nervous system while the parasympathetic nervous system controls glandular secretion and to a lesser extent, exerts an effect on the capacitance vessels. Either a hypoactive sympathetic nervous system or a hyperactive parasympathetic nervous system can engorge these vessels, creating a increased interstitial edema and thus congestion. Activation of the parasympathetic nervous system can also increase mucosal secretions leading to excess rhinorrhea.

Other theories state that there is an increase in vasoactive peptides released from cells such as mast cells. These peptides include histamine, leukotrienes, prostaglandins, vasoactive intestinal polypeptide, and kinins. Not only do these elements control the diameter of vessels, thus enhancing congestion but some also may enhance the effects of acetylcholine from the parasympathetic nervous system on nasal secretions, increasing rhinorrhea. Keep in mind that the release of these peptides is non-IgE mediated, as it is in allergic rhinitis. In some cases of Vasomotor Rhinitis, eosinophils or mast cells may be increased in the nasal mucosa.

Overactive irritant receptors may also play a role in Vasomotor Rhinitis. Many cases are associated with a specific agent or condition. Examples of such agents/conditions are: changes in temperature or barometric pressure, turbulent air, perfumes, strong cooking odors, smoke, inorganic dust, air pollution, and stress (emotional or physical). Therefore the pathophysiology dictates the management of Vasomotor Rhinitis: 1) upregulate the sympathetic nervous system, 2) downregulate the parasympathetic nervous system, 3) decrease vasoactive peptides, and 4) identify and avoid irritants. Treatments also will vary depending on the type of Vasomotor Rhinitis. Some patients will have all or just one of the aforementioned problems. Others may have Vasomotor Rhinitis in combination with other types of rhinitis, such as allergic rhinitits. Therefore, the treatment plan must be tailored to the patient and many types of treatment may need to be tried before the problem is under control. Unfortunately, most treatments achieve only symptomatic control.

The Patient

Vasomotor Rhinitis can have a variable presentation. Most patients seem to be older and it sometimes can present with a seasonal pattern. Patients present with rhinorrhea (thick or scanty), frontal headaches, and congested turbinates but usually no pruritis. There is usually no history of allergies and an irritant may or may not be identified by the patient . Some patients may have a history of other autonomic dysfunction states. Other conditions which must be considered in the differential diagnosis are: allergic rhinitis, infectious rhinitis, cystic fibrosis, HIV, pregnancy, trauma, structural abnormalities, hypothyroidism, nasal polyps and Rhinitis Medicamentosa.

Treatment

Non-surgical, Non-pharmacological. If the irritant is known, the best treatment is prevention, just avoid it. If it is not known, cleaning out the nasal mucosa periodically may help. This can be accomplished by the use of over-the-counter saline sprays or with an irrigator such as the Grossan irrigator which attaches to a Waterpik.

Pharmacological. Antihistamines have a variable response. They seem to help patients whose main symptom is rhinorrhea. The antihistamines are separated into 2 generations, 1st and 2nd. The 1st generation drugs, unlike the 2nd generation, cross the blood brain barrier and produce effects there and are also very inexpensive. Not only do they antagonize histamine but they are also anticholinergic and some prevent mediator release from mast cells. However, the anti-cholinergic effect is mostly seen in the 1st generation antihistamines. The plasma half-life is 4-6 hours and they have high bioavailability. Most are transformed in the liver and are excreted by the kidney. The adverse effects are produced by both the antihistamine and anticholinergic activity and include: drowsiness, dizziness, tremors, dry mouth, irritability, urinary retention, constipation, and blurred visions. Delirium, hallucinations, convulsions and death can occur in large enough quantities. The use of other CNS depressants and MAO inhibitors are contraindicated with antihistamines, as well as the use of Clarythromycin and Erythromycin with some 2nd generation drugs.

Ant-cholinergic agents are also effective in patients who have rhinorrhea as their main symptom. These drugs are muscarinic antagonists. The systemic adverse effects are blurred vision, confusion mydriasis, constipation, and urinary retention. The suggested drug is Ipratroprium bromide, which in its topical formulation, Atrovent, should have less systemic adverse effects. They should be avoided in patients with tachycardias, obstructive uropathy, and narrow-angle glaucoma .

Topical steroids help with congestion, rhinorrhea, and sneezing. They suppress the local inflammatory response caused by vasoactive mediators by inhibiting Phospholipase A2, reduce the activity of acetylcholine receptors, and decrease basophil, mast cell, and eosinophil counts . However, they cannot be used acutely. They must be used at least one to two weeks before the desired results are achieved. Topical steroids such as Beclomethasone, Flunisolide, and Fluticasone are recommended. Most steroids have extensive first pass metabolism. The byproducts are conjugated to glucuronic acid, which are then excreted by the kidney. These topical preparations taken in recommended doses do not influence adrenal function. Some adverse effects are mucosal edema, mild erythema, burning or stinging upon application, drying of the mucosa, epistaxis, and nasopharyngeal candidiasis.

Decongestants, or sympathomimetic agents, are used mostly for congestion. For multiple symptoms, decongestants which are formulated with antihistamines can be used. Suggested drugs are Pseudoephedrine, Phenylpropanolamine (both oral) and Phenylephrine, and Oxymetazoline (nasal sprays). These drugs are alpha receptor agonists. Pseudoephedrine also induces the release of norepinephrine. These are good drugs for acute relief. Systemic adverse effects include nervousness, insomnia, irritability, and difficulty urinating in elderly males . Topically, these drugs can cause Rhinitis Medicamentosa (a rebound congestion which occurs after taking topical formulations of these drugs for more than five days). They are contraindicated in persons with labile or overt hypertension or in patients taking MAO inhibitors. Decongestants have not been shown to have an effect on blood pressure in normotensive patients.

Surgical. If the rhinitis does not respond to the above therapy, surgical procedures can be performed. Cryosurgery affects the mucosa and submucosa, making it a quite successful procedure for congestion. However, there is sometimes prolonged post-operative nasal congestion and the possibility of damage to the nasal septum. Vidian neurectomy disrupts both sympathetic and parasympathetic fibers to the mucosa and it mainly diminishes rhinorrhea. If chronic hypertrophic changes appear in the mucosa, a number of surgical procedures can be tried. They will be mentioned briefly. Intraturbinate steroid injections give variable results but have detrimental complications (blindness, due to retinal spasm or embolism). Turbinate outfracture is usually not very successful and the turbinate usually drifts back. Cauterization can be accomplished via silver nitrate or electrical current, however it only affects the mucosa. Cryosurgery is considered superior to cauterization because it also affects the submucosa. Submucosal resection of the conchal bone is a difficult procedure with much post-operative bleeding. Partial or total inferior turbinate resection works well for nasal congestion but can give post-operative bleeding and crusting

References

1. Gluckman, Jack L. and Stegmoyer, Robert. Nonallergic Rhinitis. In: Paparella, Michael M., Shumrick, Donald A., Meyerhoff, William, eds., Otolaryngology, Volume III, Head and Neck. W. B. Saunders Co., 1991, pp.1889-1898.

2. Kimmelman, Charles P. and Ali, G. H. A. Vasomotor Rhinitis. In: Sataloff, Robert T., ed., The Otolaryngologic Clinics of North America – Volume 19, Number 1. W. B. Saunders Co., Feb. 1986, pp65-71.

3. Connell, John T. Nasal Disease. In: Settipane, Guy A., ed., Rhinitis. Providence, Rhode Island. Oceanside Publications Inc., 1991, pp161-164.

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