Rhinitis refers to the presence of inflammation of the mucosa of the nasal cavity (i.e., the lining of the nasal cavity). Rhinitis is distinct from rhinosinusitis. Often, noninflammatory conditions are grouped with rhinitis, but this is inappropriate, since the mechanisms are distinctly different. In fact, all nasal conditions with a cause that is not inflammatory should be considered to be in the category of rhinopathy.
Rhinitis may be further classified as follows:
Acute rhinitis is characterized by congestion, nasal discharge (watery-to-thick, mostly clear or gray), sore throat, malaise/fatigue and cough. Adults may experience 3 episodes per year and children can experience 4–6 episodes (or more) per year. Symptoms initially include some nasal congestion and thin nasal discharge, often with a scratchy or sore throat. Over several days, the nasal congestion typically worsens and the nasal discharge becomes more viscous, but within a week, symptoms spontaneously start to improve. Numerous viruses (including rhinovirus, parainfluenza, influenza, adenovirus, and others) cause this condition. Acute rhinitis is self-limiting, and treatment is usually supportive (rest; fluids; OTC medications, like ibuprofen, acetaminophen, decongestants, mucolytic agents, and nasal saline sprays). In a very small percentage of case (2–5% approximately), acute rhinitis is the precursor to acute bacterial rhinosinusitis.
Symptoms of allergic rhinitis include congestion, sneezing, itchy nose, and watery nasal discharge. In many patients, the sensation of itchy, watery eyes is a major issue. The mechanism for allergic rhinitis is an IgE-mediated hypersensitivity reaction against inhaled allergens. Allergic rhinitis may be classified as seasonal (if the allergens occur during specific seasons), perennial (if the allergens occur throughout the entire year), or mixed (if both seasonal and perennial allergens are involved). Diagnosis of allergic rhinitis is based upon clinical history, physical examination, and allergy testing. Treatment options include avoidance of relevant allergens, topical nasal steroids, systemic antihistamines, topical antihistamines, and decongestants. For more info on allergic rhinitis, click here.
Non-Allergic Rhinitis With Eosinophilia
Non-allergic rhinitis with eosinophilia (NARES) is characterized by symptoms of paroxysmal sneezing, watery rhinitis, and nasal itchiness. Symptoms are very similar to allergic rhinitis; however, detailed allergy evaluation of patients with NARES fails to identify a relevant inhaled allergen. In NARES, the secretions contain numerous eosinophils (a type of inflammatory cell), and the nasal lining demonstrates a dense infiltrate of eosinophils. NARES has been associated with ASA triad. Treatment with topical nasal steroids often produces a dramatic reduction in symptoms.
Nasal mastocytosis is a condition produced by an abundance of mast cells in the nasal mucosa; these mast cells show evidence of activation, and this activation produces release of pro-inflammatory mediators, which produce symptoms of congestion and rhinorrhea. Although symptoms are similar to allergic rhinitis in this relatively rare disorder, patients with nasal mastocytosis have negative allergy tests.
Granulomatous rhinitis is named for the specific type of inflammation, which is characterized granuloma formation within the nasal lining. Rhinoscleroma, tuberculosis, and syphilis all produce this relatively uncommon condition. Chronic granulomatous fungal sinusitis also may come to involve the nasal lining.
Numerous systemic vasculitis conditions (including Wegener’s granulomatosis (WG), Churg-Straus Syndrome (CSS), polyarteritis nodosa, hypersensitivity vasculitis, giant cell arteritis, Behçet’s disease, and others) can cause rhinitis. WG, known for the triad of respiratory tract granulomas, systemic vasculitis, and glomerulonephritis, commonly produces nasal symptoms of crusting, epistaxis, and rhinorrhea. Over time, WG produces a loss of intranasal structures, and in WG, the nasal mucosa loses its normal architecture. WG patients often develop septal perforation, which can lead to the external nasal deformity known as saddle-nose deformity.