Rhinitis is inflammation affecting the mucous membrane that lines the nose, which may lead to a feeling of stuffiness, with nasal discharge and sneezing.
Viral rhinitis is a feature of the common cold, and may sometimes lead to sinusitis.
Rhinitis due to allergy (see allergic rhinitis) may be seasonal (usually caused by pollens) or occur throughout the year (due to house dust, moulds, or pets). Allergic rhinitis commonly occurs with vasomotor rhinitis.
Vasomotor rhinitis may be intermittent or continual. The nose becomes over-responsive to stimuli such as pollutants, changes or extremes in temperature or humidity, certain foods or medicines, or certain emotions. Vasomotor rhinitis is common in pregnancy and in those taking combined oral contraceptives or other oestrogen drugs.
Hypertrophic rhinitis, which is characterized by thickening of the mucous membrane in the nose and chronic congestion of the nasal veins, can result from repeated nasal infections. The condition results in constant stuffiness and sometimes impairment of the sense of smell. In severe cases, treatment may involve surgical removal or shrinkage of part of the swollen tissue.
Atrophic rhinitis is characterized by wasting of the mucous membrane in the nose and can result from aging, chronic bacterial infections, or extensive nasal surgery. Features include persistent nasal infection, a nasal discharge, loss of smell, and an unpleasant odour.
Treatment may include antibiotic drugs and nose drops.
Rhinitis in detail - technical
Inflammation of the nasal mucosa.
The sinonasal mucosa is lined by pseudostratified columnar epithelium, with the exception of the olfactory clefts which are lined by olfactory epithelium. About 80% of the mucosa consists of ciliated columnar cells. The epithelial cells are also lined with hundreds of hairlike projections of actin filaments called microvilli that increase the total mucosal surface area. Goblet cells that produce mucus comprise approximately 20% of the sinonasal epithelium and progenitor basal cells comprise less than 5% (Wagenmann and Naclerio 1992).
A mucus blanket covers the sinonasal epithelium and is a critical component in sinonasal health. The mucus blanket is responsible for trapping debris. Through the beating action of the cilia on the epithelial cells, the mucus is propelled toward the pharynx, then swallowed. The mucus consists of an inner sol phase and an outer gel phase. The sol phase is composed mostly of water and electrolytes and has a lower viscosity when compared with the outer gel phase. In the normal state, the viscous outer gel phase is propelled by the cilia over the less viscous sol phase. This process of mucociliary clearance is essential in preventing stasis and in maintaining sinonasal health. Aside from its role in clearing debris, mucus itself is also immunologically active, being composed of carbohydrates, enzymes, proteins, immunoglobulins, and other active molecules.
The nasal mucosa is highly vascular and the underlying vessels are extremely porous allowing for rapid extravasation of fluid and absorption of drugs. Within the tissue of the turbinates and septal body, the nasal cavity contains erectile tissue composed of cavernous sinusoids that are under autonomic control. Below the epitheliumof the nasal cavity lies the lamina propria and submucosa, which contains the serous and mucinous glands, blood vessels, and a variety of immunologic cells including mast cells, plasma cells, and eosinophils.
The maintenance of nasal health is reliant upon the normal functioning and interplay of these multiple systems. Rhinitis, or inflammation of the lining of the nasal mucosa, can be the result of any number of dysfunctions or abnormalities, including immunologic dysfunction, mucociliary clearance dysfunction, autonomic dysfunction, infection, and a variety of other causes (see Table 1).
Table 1: Types of rhinitis
- Allergic Rhinitis
- Nonallergic Rhinitis
- Acute – usually viral
- E.g., Bacterial (Klebsiella rhinoscleroma), treponemal (syphilis, yaws), fungal
- Immune deficiency
- Mucociliary clearance abnormality
- Primary ciliary disorders (Kartagener’s, Young’s)
- Secondary – postinfectious including viral URI
- Autonomic imbalance (“vasomotor”)
- Nonallergic rhinitis with eosinophilia syndrome (NARES)
- E.g., Pregnancy, hypothyroidism
- E.g., growth hormone, estrogen replacement, oral contraceptives, antihypertensives, anti-migraine, erectile dysfunction medications
- Rhinitis medicamentosa
- Emotional (fight or flight)
- Food-induced (gustatory)
- Primary (etiology unknown but possibly infectious)
- Secondary (postsurgical)
- Manifestation of systemic disease
- E.g., Wegener’s, sarcoidosis
- Anatomical/mechanical factors
- Choanal atresia/stenosis
- Adenoid hypertrophy
- Septal deviation
- Turbinate hypertrophy (mucosal or bony)
- Pediatric: r/o cystic fibrosis
- Adult: +/ allergy, ASA triad
Rhinitis refers to the inflammation of the nasal cavity mucosa and typically includes symptoms of nasal congestion, sneezing, nasal pruritis, rhinorrhea, and postnasal drip. This condition is distinct from rhinosinusitis, which includes inflammation of the paranasal sinus mucosa. Rhinitis can be broadly divided into allergic and nonallergic, which can then be further subdivided as will be discussed later.
Allergic rhinitis (AR) is the most common form of rhinitis. It has been estimated to affect up to 15% of the US population and results in 2 to 5 billion dollars in health care costs spent annually. Studies have shown that AR impacts quality of life and sleep, emotional function, work performance, and the ability to perform daily activities (Reed et al. 2004).
Allergic Rhinitis: Etiology
AR is caused by an IgE-mediated allergy. After exposure to a particular allergen, mast cell degranulation releases several chemical mediators including histamine, prostaglandins, and leukotrienes resulting in mucous gland stimulation, increased vascular permeability, edema, and exudates. Clinically, these inflammatory effects manifest as the cardinal AR – nasal pruritis, sneezing, rhinorrhea, and nasal congestion. In addition to these immediate effects of mast cell degranulation, the released mediators also lead to the eventual migration of other inflammatory cells, including eosinophils, additional mast cells, and T cells. These inflammatory cells, along with a variety of cytokines, chemokines, neuropeptides, and adhesion molecules, prolong the mucosal inflammation and resultant nasal symptoms. With the destruction and remodeling of the nasal mucosa that occurs, including the destruction of sensory nerve fibers, allergic inflammation has a priming effect and leads to a state of nonspecific hyperresponsiveness, during which nonallergenic stimuli such as cold air and tobacco smoke can cause nasal symptoms. This inflammatory state also causes mucociliary dysfunction, which has been shown to correlate with the severity of AR (Kirtsreesakul et al. 2009). Mucosal swelling may also lead to sinus ostia obstruction and secondary rhinosinusitis.
AR can be subdivided into seasonal and perennial, although many affected individuals have components of both (e.g., perennial AR with seasonal exacerbations). Seasonal AR is caused by the pollens that arise during certain pollination seasons. In general, trees pollinate in the spring, grasses in the late spring and summer, and weeds in the fall, though there is often overlap. Molds may cause symptoms in the fall or all year round if growing indoors. Perennial AR is caused by indoor allergens such as mold, cockroaches, animal dander, or house dust mites. The development of AR is likely multifactorial, relying on both a genetic susceptibility as well as environmental factors.
Allergic Rhinitis: Evaluation and Management
The diagnosis of AR is based upon history, physical examination, and diagnostic testing. When a patient is suffering from two or more symptoms of AR (watery rhinorrhea, sneezing, nasal obstruction or nasal pruritis) for at least 1 h on most days, AR should be suspected. A thorough history of such patients will include a detailed description of his or her symptoms, onset, duration, severity, relationship to seasons, and exposures. A history of associated ocular, pharyngeal, otologic, and dermatologic symptoms should be elicited. Medications that have been used to treat symptoms, as well as the effectiveness on symptom control should be documented. A family history of allergies, eczema or asthma should be elicited as well, as a positive family history increases the probability of an allergic etiology. A social history should include occupational exposures, tobacco, and intranasal drug use.
Physical examinationmay reveal a variety of signs of AR; these may include a hyponasal voice, cobblestoning of the posterior pharynx, pale and boggy inferior turbinates, watery rhinorrhea, conjunctival injection and erythema, or a middle ear effusion. In children, one may find adenoid facies from adenoid hypertrophy, dark circles under the eyes from venous congestion (allergic shiners), and a supratip nasal crease from repetitively rubbing the nose (allergic salute). However, these findings are not specific for AR, as they can be found in other forms of chronic rhinitis, chronic rhinosinusitis, and adenoid hypertrophy.
Skin or in vitro testing is used to confirm the diagnosis of AR, as well as to determine the offending allergen(s). Both are valid forms of testing and are widely used. Skin testing is performed using a variety of techniques such as scratch, prick, intradermal, and patch tests. However, the results of these tests can be altered by medications (e.g., antihistamines) and dermatologic conditions (e.g., dermatographism). Serum tests are less invasive and are not affected by medications or dermatographism. Serum tests, including radioallergosorbent test (RAST) and multiple allergen simultaneous test (MAST), can detect serum-specific IgE toward a variety of allergens and correlate well with skin testing.
The main goal of treatment is to reduce the inflammation of the nasal mucosa and control the symptoms of AR. Treatment options include avoidance, pharmacotherapy, immunotherapy, and surgery. Though avoidance may be highly effective for certain allergens such as in occupational AR, it is much more difficult for indoor allergens and there is a lack of evidence for its effectiveness (Bousquet et al. 2008). Environmental controls that are frequently recommended include occlusive covers for mattresses, box springs, and pillows (+ washing all in hot water), high-efficiency particulate air (HEPA) filters, and removing reservoirs of allergens including carpeting and stuffed furniture. Intranasal corticosteroids are a first-line agent for both seasonal and perennial AR, and have been shown to have insignificant systemic levels of corticosteroid absorption and few adverse effects.
Intranasal corticosteroids have an anti-inflammatory effect through the reduction in IgE production, cytokine secretion, and eosinophilia. The maximal therapeutic effect of this drug occurs after 2 weeks of use. Oral antihistamines have also been found to be safe and effective for the treatment of symptoms of AR. Second generation antihistamines have fewer anticholinergic side effects and are less sedating than first generation antihistamines and are thus preferred. Topical intranasal antihistamines are a relatively new treatment available in the US for the treatment of seasonal allergic rhinitis. Leukotriene inhibitors competitively block the binding of cysteinyl leukotrienes to end-organ receptors. While not as effective as inhaled corticosteroids, this class of drugs has been shown to be effective in seasonal and perennial AR (Melvin and Patel 2011). Cromolyn sodium is a topical intranasal medication that stabilizes mast cells and prevents the degranulation of histamine, and is therefore useful as a preventative agent. This drug has a short half-life and requires frequent dosing (4–6 times per day).
These drugs are used alone or in combination for the treatment of AR, depending on symptom severity and the effectiveness of each drug for each patient. Treatment algorithms are available and help develop a stepwise approach to treating patients with AR that most effectively manages their symptoms.
Immunotherapy is the only therapeutic option that actually modifies the allergic mechanism through desensitization of the patient to the offending allergen( s). This treatment is indicated for seasonal and perennial AR. Subcutaneous immunotherapy uses extracts of the offending allergens, which are injected subcutaneously at increasing doses until a maintenance dose is reached. This results in a therapeutic benefit by inducing several immunologic changes including a rise in serum-specific IgG, a reduction in inflammatory cells in the nasal mucosa, suppression of the seasonal rise in IgE antibodies, and a shift from the TH2 to the TH1 cytokine profile (Robinson et al. 2004). Treatment duration generally lasts from 3 to 5 years. Given the risk of anaphylaxis associated with subcutaneous immunotherapy, other routes of administration of the allergen extract have been sought. Sublingual immunotherapy (SLIT) is now being utilized to a greater extent in this country because of its noninvasiveness, low incidence of adverse effects, and potential for self-administration. Studies have shown that SLIT is safe and reduces symptoms and frequency of medication use in patients with AR (Wilson et al. 2004).
While surgical therapy is not a first-line treatment in the management of AR, it may be useful as an adjunctive therapy when treating patients with symptoms refractory to medical management. Surgery does not eliminate the inflammatory state associated with AR, but it may be useful in alleviating symptoms of nasal obstruction as well as aiding in topical drug delivery. Septoplasty should be considered if the patient’s symptoms correlate with the finding of an ipsilateral septal deviation on physical examination. However, septoplasty should rarely be performed alone, given the central role of inferior turbinate hypertrophy in causing symptomatic nasal obstruction in allergic rhinitis. The goal of surgery of the inferior turbinates is to reduce their size and, thereby, increase the patency of the nasal cavity. A variety of techniques exist for a accomplishing this goal including lateralization outfracture, laser vaporization, submucous resection, submucous electrocautery, microdebrider turbinoplasty, radiofrequency ablation, coblation, and inferior turbinate resection. The last option should be used cautiously, and performed conservatively, as it can result in empty nose syndrome.
The term nonallergic rhinitis is applied to the same constellation of symptoms as allergic rhinitis when an allergic etiology has been excluded with negative allergy testing. There are a variety of types of nonallergic rhinitis (see Table 1), and the diagnosis is primarily based upon the patient’s history. Nonallergic rhinitis can be divided into infectious and noninfectious causes.
Infectious rhinitis can be further divided into acute or chronic etiologies. The most common acute form is the common cold, caused by a variety of viruses. Secondary bacterial infections and sinus involvement may occur. Acute forms of infectious rhinitis are often associated with systemic symptoms such as fevers, malaise, and myalgias. Chronic forms can either have a specific infectious agent such as in cases of tuberculosis (Mycobacterium tuberculosis), leprosy (Mycoplasma leprae), syphilis (Treponema pallidum), rhinoscleroma (Klebsiella rhinoscleromatis), fungal infections (e.g., Aspergillus), or they can be a manifestation of an underlying immune deficiency or genetic mucociliary clearance abnormality such as in primary ciliary dyskinesia and Young’s syndrome.
Non-allergic non-infectious rhinitis includes several heterogeneous disorders with symptoms identical to allergic rhinitis, but without evidence of being caused by a specific allergen or infectious pathogen. There is no strict diagnostic criteria for this group of disorders; however, it has been suggested that this condition persists for greater than 9 months each year and produces two or more symptoms, including rhinorrhea, nasal obstruction, sneezing, and postnasal drip (Bachert 2004). There are several types of nonallergic, noninfectious rhinitis.
Vasomotor rhinitis has been found to be the most common diagnosis among this group. No single pathogenesis has been discovered to cause vasomotor rhinitis, which is characterized by increased sensitivity to environmental factors. The typical age at onset is 30–40s with a female preponderance (ratio 2:1). Common environmental triggers include climate change, strong odors, perfumes, and pollution. Theories regarding the pathogenesis of vasomotor rhinitis include hypersensitive sensory receptors of the nasal mucosa to irritant stimuli and an imbalance between the parasympathetic and sympathetic nervous system. Treatment options include avoidance of noxious stimuli, intranasal anticholinergics (better for rhinorrhea), intranasal corticosteroids (better for obstructive symptoms), and intranasal antihistamines. Other adjunctive therapies include topical or oral decongestants, nasal saline spray or irrigation, and topical nasal capsaicin. (Ciprandi 2004).
Non-allergic rhinitis with eosinophilia syndrome
Non-allergic rhinitis with eosinophilia syndrome (NARES) refers to a symptom complex of sneezing, nasal pruritis, and watery rhinorrhea with associated nasal eosinophilia but without evidence of allergic disease on formal allergy testing. Patients generally present in middle age and nasal corticosteroids are often an effective treatment (Lund et al. 1994). The specific etiology is unclear; however, some view this syndrome as an early expression of Samter’s triad (nasal polyposis, intrinsic asthma, and intolerance to aspirin and other NSAIDs) because NARES patients frequently develop nasal polyps and asthma later in life.
Occupational rhinitis is caused by inhalant agents in the workplace such as latex, dander from laboratory animals, wood dusts, and a variety of chemical such as salts, glues, and solvents.
Hormonal rhinitis has a hormonal etiology and may occur during pregnancy, puberty, or in certain pathologic states involving hormonal imbalances including hypothyroidism and acromegaly.
Postinfectious rhinitis, characterized by nasal obstruction, watery secretions, postnasal drip, and sneezing, may occur following a persistent viral or bacterial infection. The symptoms are generally selflimiting, but do respond to topical steroids.
A variety of medications and illicit drugs can cause a drug-induced rhinitis. Medications that have been associated with nasal symptoms include ACE inhibitiors, beta-blockers, aspirin and other antiinflammatory agents, antidepressants, phosphodiesterase inhibitors (e.g., sildenafil, vardenafil, oral contraceptives, anti-migraine medications (Lund et al. 1994; Bachert 2004). Many of these medications act at receptors that are found throughout the body, including within the nasal mucosa. Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDS) are known to cause symptoms by increasing leukotriene production.
Rhinitis medicamentosa is a condition caused by the overuse of intranasal decongestants, such as oxymetazoline and phenylephrine. Withdrawal after extended use results in rebound nasal congestion. Overuse can also lead to erythematous, inflamed nasal mucosa. Intranasal cocaine use acts in a similar manner. Treatment of rhinitis medicamentosa involves weaning the patient off the offending agent while using an intranasal steroid and possibly a short course of oral steroids.
Foods may cause isolated nasal symptoms in the case of food-induced rhinitis. For example, hot and spicy foods can cause a gustatory rhinorrhea. Alcohol causes a physiologic vasodilation which may result in nasal congestion. A true food allergy will rarely if ever cause isolated rhinitis symptoms. Likely as a result of autonomic stimulation, emotional triggers such as stress and arousal have been shown to cause nasal symptoms (Lund et al. 1994).
Primary atrophic rhinitis
Primary atrophic rhinitis is a condition characterized by progressive atrophy of the nasal mucosa and underlying bone of the turbinates. Viscous secretions rapidly dry to form foul-smelling crusts. Though many would consider this an infectious rhinitis, the exact etiology is uncertain. Klebsiellae ozenae is often cultured, but it is unclear if bacterial colonization is a cause or a result of this condition. Several other bacterial infections associated with this condition have been cited including coccobacillus, diphtheroid bacilli, and pertussis. Other theories include nutritional deficiencies, endocrine imbalance, autonomic imbalance, and hereditary diseases. A secondary form of the disease can be caused by overzealous turbinate surgery, leading to increased patency of the nasal fossa. Treatments include antibiotics, nasal emmolients, vitamin supplementation, as well as cavity-narrowing operations.
Differential Diagnosis of Rhinitis
Anatomic and mechanical factors may play a role to varying degrees in the patient’s nasal symptoms. During the physical examination, identification of such factors should be sought. It is important to note and document the presence and extent of turbinate hypertrophy, septal deviations, gross polyps, and polypoid mucosa, adenoid hypertrophy, and any congenital abnormalities such as choanal atresia. These factors are taken into consideration when providing treatment options.
Rhinitis symptoms may also be a manifestation of numerous systemic diseases, including granulomatous diseases (Wegener’s granulomatosis, sarcoidosis, Churg–Strauss syndrome), autoimmune diseases (lupus, Sjogren syndrome), and cystic fibrosis. Signs on physical examination may suggest a systemic disease such as excessive crusting (Wegener), friable mucosa, excessive bleeding, submucosal cobblestoning (sarcoidosis), or polyps in a child (cystic fibrosis).
Rhinitis has numerous etiologies. All lead to the common endpoint of nasal inflammation and a similar constellation of symptoms. Treatment is aimed at the underlying cause and managing symptoms.
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