Rhinitis is inflammation of the nasal mucous membrane, with resultant nasal congestion, rhinorrhea, and variable associated symptoms depending on etiology (eg, itching, sneezing, watery or purulent rhinorrhea, postnasal drip, anosmia). Rhinitis is classified as allergic or nonallergic. The cause of nonallergic rhinitis is usually viral, although irritants can cause it. Diagnosis is usually clinical. Treatment includes humidification of room air, sympathomimetic amines, and antihistamines. Bacterial superinfection requires appropriate antibiotic treatment.
There are several forms of nonallergic rhinitis. (Also see Allergic Rhinitis.)
Acute rhinitis
Acute rhinitis, manifesting with edema and vasodilation of the nasal mucous membrane, rhinorrhea, and obstruction, is usually the result of a common cold (which is viral); other causes include streptococcal, pneumococcal, and staphylococcal infections.
Chronic rhinitis
Chronic rhinitis is generally a prolongation of subacute (resolved in 30 to 90 days) inflammatory or infectious rhinitis. It may also rarely occur in syphilis, tuberculosis, leishmaniasis, blastomycosis, histoplasmosis, and leprosy—all of which are infections characterized by granuloma formation and destruction of soft tissue, cartilage, and bone. Rhinoscleroma is an infection caused by Klebsiella rhinoscleromatis that can cause progressive nasal obstruction from indurated inflammatory tissue in the lamina propria. Rhinosporidiosis is a fungal infection caused by Rhinosporidium seeberi and can lead to chronic rhinitis characterized by bleeding polyps. Both low humidity and airborne irritants can also result in chronic rhinitis.
Patients with chronic rhinitis often develop nasal obstruction, purulent rhinorrhea, and frequent bleeding.
Atrophic rhinitis
Atrophic rhinitis, a form of chronic rhinitis, results in atrophy and sclerosis of mucous membrane; the mucous membrane changes from ciliated pseudostratified columnar epithelium to stratified squamous epithelium, and the lamina propria is reduced in amount and vascularity. Atrophic rhinitis is associated with advanced age, granulomatosis with polyangiitis (GPA), and iatrogenically induced excessive nasal tissue extirpation, usually during sinus surgery. Although the exact etiology is unknown, chronic bacterial infection frequently plays a role. Nasal mucosal atrophy often occurs in older patients.
Vasomotor rhinitis
Vasomotor rhinitis is the most common subtype of nonallergic rhinitis. It accounts for approximately 80% of cases of allergic rhinitis (1). Vasomotor rhinitis is a chronic condition in which intermittent vascular engorgement of the nasal mucous membrane leads to watery rhinorrhea and sneezing. The etiology is typically mucosal hyperresponsiveness to environmental factors such as temperature, pressure, and humidity; no allergy can usually be identified. Cold air and a dry atmosphere are particular triggers.
Reference
1. Baroody FM, Gevaert P, Smith PK, et al. Nonallergic Rhinopathy: A Comprehensive Review of Classification, Diagnosis, and Treatment. J Allergy Clin Immunol Pract. 2024;12(6):1436-1447. doi:10.1016/j.jaip.2024.03.009
Pathophysiology of Nonallergic Rhinitis
Sensory nerve endings in the nasal mucosa of patients with nonallergic rhinitis respond to various stimuli, including viral antigens, chemical irritants, temperature changes, and strong odors, through transient receptor potential (TRP) channels, particularly transient receptor potential vanilloid 1 (TRPV1) channels, historically known as a capsaicin receptor. Activation of these channels leads to the release of neuropeptides like substance P and calcitonin gene-related peptide (CGRP), which cause vasodilation and increased vascular permeability, resulting in nasal congestion and rhinorrhea (Sensory nerve endings in the nasal mucosa of patients with nonallergic rhinitis respond to various stimuli, including viral antigens, chemical irritants, temperature changes, and strong odors, through transient receptor potential (TRP) channels, particularly transient receptor potential vanilloid 1 (TRPV1) channels, historically known as a capsaicin receptor. Activation of these channels leads to the release of neuropeptides like substance P and calcitonin gene-related peptide (CGRP), which cause vasodilation and increased vascular permeability, resulting in nasal congestion and rhinorrhea (1).
Autonomic dysfunction with increased parasympathetic activity is often seen.
Pathophysiology reference
1. Baroody FM, Gevaert P, Smith PK, et al. Nonallergic Rhinopathy: A Comprehensive Review of Classification, Diagnosis, and Treatment. J Allergy Clin Immunol Pract. 2024;12(6):1436-1447. doi:10.1016/j.jaip.2024.03.009
Symptoms and Signs of Nonallergic Rhinitis
Acute rhinitis results in cough; low-grade fever; nasal congestion and itching; rhinorrhea with post-nasal drip; and sneezing.
Chronic rhinitis manifestations are similar to those of acute rhinitis, but in prolonged or severe cases, patients may also have thick, foul-smelling, mucopurulent drainage; mucosal crusting; and/or bleeding. Sneezing and nasal itching are less common.
Atrophic rhinitis results in enlargement of the nasal cavities and epistaxis that may be recurrent and severe. It is differentiated from the other types of rhinitis by the presence of crust formation, malodorous bacterial colonization, nasal congestion, and anosmia.
Vasomotor rhinitis results in watery rhinorrhea and postnasal drip. The turgescent (highly vascularized) nasal mucous membrane varies from bright red to purple. The condition is marked by periods of remission and exacerbation. Sneezing and nasal itching can occur but are less common than other nasal symptoms.
Diagnosis of Nonallergic Rhinitis
The different forms of rhinitis are diagnosed clinically. Testing is usually unnecessary. It is differentiated from allergic rhinitis by the absence of an identifiable allergen, a hallmark feature of allergic rhinitis.
Vasomotor rhinitis is differentiated from specific viral and bacterial infections of the nose by the lack of purulent exudate and crusting.
Treatment of Nonallergic Rhinitis
For acute (viral) rhinitis, analgesics, antihistamines, and/or decongestants
For atrophic rhinitis, topical treatment with antibiotics, estrogens, and vitamin A and DFor atrophic rhinitis, topical treatment with antibiotics, estrogens, and vitamin A and D
For vasomotor rhinitis, humidification and sometimes topical glucocorticoids and oral pseudoephedrineFor vasomotor rhinitis, humidification and sometimes topical glucocorticoids and oral pseudoephedrine
Acute (viral) rhinitis is often self-limited, and the treatment is generally symptomatic (1). Symptomatic therapy consists of analgesics (eg, acetaminophen and nonsteroidal anti-inflammatory drugs [NSAIDs]), antihistamines, and/or decongestants. Analgesics may be used for relief of pain and/or fever. Second-generation antihistamines (eg, cetirizine, fexofenadine) are preferred compared to first-generation anti-histamines because first-generation agents have greater anticholinergic activity, which can cause excessive drying of the mucous membranes and increased irritation. First-generation antihistamines may also increase the risk of sedation and falls in older adults, and chronic use has been increasingly associated with dementia. Topical decongestants may provide some relief, but should not be used for more than 3 days to avoid rebound nasal mucosal congestion. (See also ). Symptomatic therapy consists of analgesics (eg, acetaminophen and nonsteroidal anti-inflammatory drugs [NSAIDs]), antihistamines, and/or decongestants. Analgesics may be used for relief of pain and/or fever. Second-generation antihistamines (eg, cetirizine, fexofenadine) are preferred compared to first-generation anti-histamines because first-generation agents have greater anticholinergic activity, which can cause excessive drying of the mucous membranes and increased irritation. First-generation antihistamines may also increase the risk of sedation and falls in older adults, and chronic use has been increasingly associated with dementia. Topical decongestants may provide some relief, but should not be used for more than 3 days to avoid rebound nasal mucosal congestion. (See alsoCommon Cold). Intranasal mast cell stabilizers (eg, cromolyn) or dual-action mast-cell stabilizers/antihistamines (eg, azelastine, olopatadine) are alternative options (see table ). Intranasal mast cell stabilizers (eg, cromolyn) or dual-action mast-cell stabilizers/antihistamines (eg, azelastine, olopatadine) are alternative options (see tableIntranasal Mast Cell Stabilizers). If symptoms persist, biopsy may be necessary to exclude cancer.
Treatment of atrophic rhinitis is directed at reducing the crusting and eliminating the odor with nasal irrigation, topical antibiotics (eg, mupirocin), topical or systemic estrogens, and vitamins A and D. Occluding or reducing the patency of the nasal cavities surgically decreases the crusting caused by the drying effect of air flowing over the atrophic mucous membrane. Surgical interventions, such as occluding or reducing the patency of the nasal cavities, may be performed to decrease crusting (by reducing the drying effect of air flowing over the atrophic mucous membrane), increase lubrication, and possibly improve vascularization (is directed at reducing the crusting and eliminating the odor with nasal irrigation, topical antibiotics (eg, mupirocin), topical or systemic estrogens, and vitamins A and D. Occluding or reducing the patency of the nasal cavities surgically decreases the crusting caused by the drying effect of air flowing over the atrophic mucous membrane. Surgical interventions, such as occluding or reducing the patency of the nasal cavities, may be performed to decrease crusting (by reducing the drying effect of air flowing over the atrophic mucous membrane), increase lubrication, and possibly improve vascularization (2).
Treatment of vasomotor rhinitis is by trial and error and may not always be satisfactory. Patients benefit from humidified air, which may be provided by a humidified central heating system or a vaporizer in the workroom or bedroom. Topical anticholinergics (eg, ipratropium) can be helpful in drying excessive secretions and reducing rhinorrhea and postnasal drip. Topical glucocorticoids (eg, mometasone 2 sprays twice a day) and nasal antihistamines (eg, olopatadine and azelastine 1 spray twice a day) can also be of some benefit.is by trial and error and may not always be satisfactory. Patients benefit from humidified air, which may be provided by a humidified central heating system or a vaporizer in the workroom or bedroom. Topical anticholinergics (eg, ipratropium) can be helpful in drying excessive secretions and reducing rhinorrhea and postnasal drip. Topical glucocorticoids (eg, mometasone 2 sprays twice a day) and nasal antihistamines (eg, olopatadine and azelastine 1 spray twice a day) can also be of some benefit.
Topical decongestants (eg, intranasal oxymetazoline) should be avoided for the treatment of rhinitis in general because they cause the vasculature of the nasal mucous membrane to lose its sensitivity to other vasoconstrictive stimuli—eg, the humidity and temperature of inspired air. Rebound congestion can result after 3 days of continuous use; chronic use and dependence is known as rhinitis medicamentosa (Topical decongestants (eg, intranasal oxymetazoline) should be avoided for the treatment of rhinitis in general because they cause the vasculature of the nasal mucous membrane to lose its sensitivity to other vasoconstrictive stimuli—eg, the humidity and temperature of inspired air. Rebound congestion can result after 3 days of continuous use; chronic use and dependence is known as rhinitis medicamentosa (1). Leukotriene receptor antagonists (LTRAs, eg, montelukast) should not be used in the treatment of nonallergic rhinitis due to a lack of data supporting its efficacy and deleterious psychiatric adverse effects.). Leukotriene receptor antagonists (LTRAs, eg, montelukast) should not be used in the treatment of nonallergic rhinitis due to a lack of data supporting its efficacy and deleterious psychiatric adverse effects.
Treatment references
1. Dykewicz MS, Wallace DV, Amrol DJ, et al. Rhinitis 2020: A practice parameter update. J Allergy Clin Immunol. 2020;146(4):721-767. doi:10.1016/j.jaci.2020.07.007
2. Mishra A, Kawatra R, Gola M. Interventions for atrophic rhinitis. Cochrane Database Syst Rev. 2012;2012(2):CD008280. Published 2012 Feb 15. doi:10.1002/14651858.CD008280.pub2
