Nonallergic & Allergic Rhinitis: Introduction
Rhinitis is defined as an inflammatory condition that affects the nasal mucosa. The symptoms of rhinitis include nasal obstruction, hyperirritability, and hypersecretion. Rhinitis can be caused by a variety of different allergic and nonallergic conditions (Table 14–1). The incidence of rhinitis seems to have increased since the industrial revolution. One in five Americans is estimated to be afflicted with rhinitis.
| Allergic Rhinitis | Infectious Rhinitis | Nonallergic, Noninfectious Rhinitis | Miscellaneous |
|---|---|---|---|
|
| Eosinophilic syndromes
|
|
Noneosinophilic syndromes
|
Allergic rhinitis is one of the most common chronic conditions in the United States. Of the approximately 50 million US individuals who have rhinitis, many do not have an allergic cause to their rhinitis. The symptoms of nonallergic rhinitis include nasal obstruction, hypersecretion, and irritability, none of which is due to allergy.
Anatomy & Physiology
Airflow through the nose is more efficient in gas exchange and requires less energy than mouth breathing. The nose serves as the initial conduit into the airway. As such, it has important functions of warming, humidifying, and cleansing the air that we breathe. The nasal cycle consists of simultaneous sympathetic and parasympathetic modulation in opposite directions on opposite sides of the nose. The nasal cycle can alter airflow in one nostril by up to 80%, while maintaining total airflow.
From anterior to posterior, the different structural elements of the nose act together to achieve these functions. The nasal vestibule is lined by vibrissae that filter large particulates as they enter the nose. The vestibule then communicates with the nasal valve region, where the nasal mucosa becomes a ciliated, pseudostratified, columnar epithelium. This type of epithelium permeates the entire sinonasal cavity; its importance is underscored when considering conditions such as Kartagener syndrome in which immotile cilia lead to chronic crusting from mucus stasis. Under the mucosa lie stromal cells, inflammatory cells, nerves, blood vessels, and seromucous glands. Each of these elements may play a role in nasal inflammation.
The nose is divided into left and right chambers by a septum comprised of cartilage and bone. Laterally, three bony projections—superior, middle, and inferior turbinates—project into the nasal cavity. These turbinate bones are lined by mucosa, thereby increasing the nasal surface area and covering important sinus ostia. The nasolacrimal duct drains into the inferior meatus. The frontal, maxillary, and anterior ethmoid sinuses drain into the middle meatus; the posterior ethmoid sinuses drain into the superior meatus. Finally, the sphenoid sinus ostia are superior to the choana and drain medially to the superior turbinate. Inflammation in these critical drainage sites can lead to epiphora or sinus disease.
Nasal vascularity includes the internal and external carotid arteries, which feed the nose. The anterior and posterior ethmoid arteries are terminal branches of the ophthalmic artery, a branch of the internal carotid artery. The external carotid artery supplies the sphenopalatine artery. The venous drainage of the nose is primarily through the pterygoid and ophthalmic plexuses.
Finally, the character of the nasal mucus itself is significant. Nasal and sinus mucus typically exists in two layers on the epithelial surface. The deeper layer is thinner and less viscous than the outer layer and therefore allows the cilia to beat with less resistance. The outer layer traps inhaled particulates and has a greater density of inflammatory mediators and leukocytes to protect against infectious agents and foreign substances.
Nonallergic Rhinitis
Nonallergic rhinitis typically presents with clear rhinorrhea and nasal obstruction. Sneezing and itchy, watery eyes do not typically present with nonallergic rhinitis. There is an increasing incidence of nonallergic rhinitis with advancing age. Patients with nonallergic rhinitis should always be questioned about the use of over-the-counter nasal sprays, previous trauma, work or chemical exposure, and previous intranasal drug use. Epistaxis, pain, and unilateral symptoms may be harbingers of a neoplasm and should be noted.
Viral rhinitis is very common and often associated with other manifestations of viral illness, which can include headache, malaise, body aches, and cough. Nasal drainage in viral rhinitis is most often clear or white and can be accompanied by nasal congestion and sneezing.
A number of different indoor and outdoor pollutants may affect the nose. These agents include dust, ozone, sulfur dioxide, cigarette smoke, garden sprays, and ammonia. Irritant agents can be found in a variety of work environments. Typically, these agents cause nasal dryness, reduced airflow, rhinorrhea, and sneezing. Decreased ciliary movements within the nose have been seen in chronic cigarette smoke exposure and in exposure to wood particles. Environmental control is critical in these patients. Limiting exposure through removal of the causal agent, avoidance, improving ventilation, and the use of protective particulate respirator masks are all helpful.
Patients with vasomotor rhinitis present with symptoms of nasal obstruction and clear nasal drainage. The symptoms are often associated with changes in temperature, eating, exposure to odors and chemicals, or alcohol use. Some clinicians suggest that abnormal autonomic regulation of nasal function leads to vasomotor rhinitis.
Nonallergic rhinitis with eosinophilia (NARES) is a recently described syndrome in which patients present with nasal obstruction and congestion; these patients frequently experience more severe exacerbations, including the development of sinusitis and polyposis. These patients also display marked eosinophilia on nasal smears (> 25%) but are not allergic to any inhalant allergens by skin testing or in vitro testing. The cause of NARES remains unknown.
Patients with rhinitis medicamentosa often present with nasal obstruction that has worsened over a number of years. They typically have been using over-the-counter topical vasoconstrictive nasal sprays. Many times these patients need increasing doses of these sprays as tachyphylaxis occurs. The use of these sprays for prolonged periods leads to rebound rhinitis in which the patient experiences severe obstruction as the effects of the topical agents subside.
Another common presentation of nonallergic rhinitis is rhinitis associated with pregnancy. The systemic concentration of estrogen rises throughout pregnancy. This rise in estrogen leads to a rise in hyaluronic acid in the nasal tissue, which can result in increasing nasal edema and congestion. Moreover, there is an increase in mucous glands and a decrease in nasal cilia during pregnancy, both of which heighten nasal congestion decreasing mucus clearance. Rhinitis is usually most severe during the second and third trimesters of pregnancy.
The physical examination of a patient with rhinitis should include a thorough head and neck exam. Externally, the nose is evaluated for evidence of previous trauma or saddling, which can be indicative of septal deficiency. Internally, the nasal septal position and character are examined. Signs of chronic inflammation, vasculitis, and septal perforation can be indicative of a variety of systemic problems ranging from Wegener granulomatosis to cocaine abuse. The size and character of the turbinates are also important to note, as is the character of any rhinorrhea. Moreover, the physician should examine the patient for nasal polyposis or other intranasal masses or tumors.
A more in-depth examination of the nasal cavity can be accomplished—after applying topical anesthesia—with the use of either a rigid or flexible nasal endoscope. A 4.0-mm rigid nasal endoscope may be used for adults and a 2.7-mm nasal endoscope for children. This affords visualization of the middle meatus, sphenoethmoidal recess, and nasopharynx regions otherwise not seen with anterior rhinoscopy. In addition, nasal cytology can be helpful to determine both cell types and the presence of ciliary motility.
The treatment of nonallergic rhinitis includes the avoidance of offending agents such as chemicals, perfumes, cigarette smoke, and other fumes. In addition, for patients with workplace exposure, a particulate mask can be useful in limiting irritants.
Saline irrigation is an important adjunctive treatment to help avert intranasal stasis and reduce crusting. The use of saline not only increases the efficacy of intranasal topical medications but also improves ciliary function.
Topical intranasal steroids work in the nasal mucosa to reduce eosinophil and neutrophil chemotaxis; they also reduce inflammation, suppress mast cell-related reactions, and decrease intracellular edema. Although primarily used for allergic rhinitis, some nonallergic patients respond to topical intranasal steroids
Other treatments for nonallergic rhinitis include the adrenergic agents. There are two main families of adrenergic drugs: (1) phenylamines (eg, ephedrine, pseudoephedrine, phenylephrine, and phenylpropanolamine) and (2) imidazolines (eg, xylometazoline, oxymetazoline, and naphazoline). Phenylamines are oral agents, whereas imidazolines are topical agents. The primary role of phenylamines is to decrease mucosal capacitance vessels by agonizing α-adrenergic receptors; this leads to a decongestant effect. Phenylamines can cause dose-related adverse effects such as tremulousness, irritability, tachycardia, hypertension, and urinary retention. They are contraindicated in patients with hypertension, severe coronary artery disease, and in patients on monoamine oxidase inhibitors. Topical imidazolines decrease nasal blood flow by affecting α1– and α2-adrenergic receptors. Potent vasoconstriction can cause rebound congestion upon withdrawal of the drug (rhinitis medicamentosa) if used for more than 5 days. In light of this, patients should be cautioned when using these sprays for prolonged periods (rhinitis medicamentosa).
Anticholinergic agents such as ipratropium bromide can be used topically to block parasympathetic input and thereby decrease rhinorrhea. Ipratropium bromide is available in a 0.03% formulation for noninfectious rhinitis and a 0.06% concentration for viral rhinitis. Anticholinergic agents can be used in combination with intranasal steroids. They should be avoided in patients with narrow-angle glaucoma, prostatic hypertrophy, or bladder neck obstruction.
Newer therapies that have been tried for vasomotor rhinitis include the use of intranasal antihistamine sprays. Azelastine spray (eg, Astepro 0.15%) and olopatadine (eg, Patanase) are new, once-a-day intranasal antihistamines that may relieve vasomotor rhinitis.
Some over-the-counter sprays, such as cromolyn sodium, are safe to be used repetitively. These intranasal sprays act to stabilize mast cell membranes. They must be given prior to mast cell degranulation to be effective and have relatively short half-lives, so their administration must be frequent. Finally, some clinicians are using leukotriene inhibitors as adjuvant treatments in the treatment of nonallergic rhinitis. However, more studies on the efficacy of these agents in nonallergic rhinitis are warranted.
The surgical treatment for nonallergic rhinitis is focused on correcting structural abnormalities that may contribute to patient symptoms. Septal deviation is a common defect that can contribute to nasal obstruction. Septoplasty or nasoseptal reconstruction is used to correct cartilaginous or bony abnormalities of the septum. Septal perforations can contribute to crusting or epistaxis. The surgical correction of septal perforations may include the placement of septal buttons, advancement flap closures of perforations, and, more recently, free-tissue transfers for large perforations.
Inferior turbinate surgery is also commonly used to counteract nonallergic rhinitis. The type and extent of surgery on the inferior turbinate continues to be a source of debate. Various techniques for turbinate surgery exist and include outfracture, cauterization, radiofrequency ablation, submucous resection, submucosal reduction via a microdebrider, and partial or complete turbinate resection. In general, the current trend is to preserve as much turbinate mucosa as possible to allow normal physiologic function to continue.
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