Nasal congestion: A review of its etiology, evaluation, and treatment.

Abstract

The most common clinical syndromes that cause nasal congestion are allergic rhinitis, vasomotor rhinitis, chronic sinusitis, and upper respiratory viral infections (common colds). Nasal congestion, in turn, can lead to sequelae such as sinusitis, otitis media, and the onset or worsening of mild to severe sleep disturbances, including obstructive sleep apnea. There is a host of conservative treatments, including decongestant pharmacotherapy, antiallergy measures, and nasal dilation devices. Several surgical procedures are also available. This article reviews the current guidelines for the workup and diagnosis of nasal congestion and briefly describes the many and varied approaches to treatment.

Introduction

Nasal congestion is a key component of rhinitis. Rhinitis is defined as an inflammation of the lining of the nose that is characterized by nasal congestion, rhinorrhea, sneezing, andlor itching. [1]

Nasal congestion causes nasal obstruction, but not all nasal obstruction is caused by congestion. Nasal congestion involves the cavernous tissues in the turbinates. The focus of this article is on the phenomenon of nasal congestion rather than on the broader problem of nasal obstruction. Nasal obstruction was reviewed by Kimmelman, who in 1989 published a practical outline to guide the treatment of the most common etiologies, including allergic rhinitis, infectious rhinitis, and vasomotor rhinitis. [2] Kimmelman estimated that in the United States alone at that time, an estimated $5 billion was being spent annually on medications to relieve nasal obstruction. An additional $60 million was being spent on surgical remedies, and another $10 billion on the treatment of associated disorders, such as recurrent rhinosinusitis, otitis media, bronchitis, and asthma. Further adding to the condition's economic impact are less tangible factors, such as absenteeism and decreased productivity. [3]

The most common clinical syndromes that cause nasal congestion are allergic rhinitis, vasomotor rhinitis, chronic sinusitis, and upper respiratory viral infections (common colds). Nasal congestion, in turn, can lead to sequelae such as sinusitis, otitis media, and the onset or worsening of mild to severe sleep disturbances, including obstructive sleep apnea.

Diagnosis

History. As is the case with any medical problem, a complete history is essential to obtain clues about the etiology of the nasal congestion. It is important to elicit details such as frequency, duration, temporal pattern of the obstruction, precipitating factors, and the presence and character of allergic symptoms, such as sneezing, nasal itching, and rhinorrhea. A patient might describe symptoms of secondary middle ear effusion, including ear popping, poor speech perception, ear pain, or tinnitus. Symptoms related to quality of life--such as poor sleep, associated daytime somnolence, and snoring that disturbs a bed partner's sleep--might indicate nocturnal nasal congestion.

Associated headache, nasal pain, and purulent discharge suggest that an infection might be present. A history of previous consultations and medication use might give an indication of the extent of the problem. A history of previous or current illnesses and associated medication use can provide clues to the etiology of nasal congestion and help identify possible aggravating factors. A history of smoking, alcohol consumption, or other drug intake could also be important-for example, in diagnosing cocaine-induced septal perforation.

Any history of nasal surgery or trauma to the nose is pertinent. A history of inhalant, food, and drug allergies is important because allergic rhinitis is a significant cause of nasal congestion. [4] A history of asthma, especially seasonal asthma, is an important clue because of the high incidence of its concurrence with rhinitis.

Pregnancy must be ruled out. The estrogen that is produced during pregnancy tends to inhibit acetyicholinesterase activity, leading to edema of the nasal mucosa and resultant congestion. [5]

Physical examination. The physical examination should begin during the interview. The physician should determine the presence or absence of hyponasal speech, which suggests that sinus and nasal congestion is fairly severe. During the interview, one might also detect signs of allergy, such as "allergic shiners" (periorbital edema), the "allergic salute," and urticaria. Although the examination should concentrate on the nose, it should also encompass the entire head and neck. A complete head and neck examination should always be performed, and note should be taken of any changes in the eyes, eyelids, ears, and throat. Such changes can include the presence of chemosis, epiphora, middle ear effusion, inflammation in the pharynx, and lymphadenopathy.

The presence of wheezing might indicate concomitant asthma. Ideally, the nose should be examined before and after decongestion via anterior rhinoscopy. Sometimes a more detailed examination of the turbinates, meatus, septum, and nasopharynx by rigid and/or flexible endoscopy is required.

Measurement of nasal resistance. Since the early 20th century, researchers have tried to measure nasal resistance and nasal patency. Initially, a simple mirror was placed under the nostrils to detect airflow. In time, rhinomanometric techniques evolved that simultaneously measured pressure and flow. Calculations of transnasal resistance were made according to Ohm's law.

In recent years, we have seen the development of acoustic rhinometry, which makes use of reflected sound waves to estimate nasal geometry and area. This method has great clinical potential because it is noninvasive, rapid, and performed quite easily. [6] Several centers have shown that acoustic rhinometry can quantify the effect of septoplasty and the medical treatment of nasal polyposis. Acoustic rhinometry has also been used to examine patients before and after functional endoscopic sinus surgery in order to measure the size of the surgically produced cavity. [7,8]

Porter et al reported on the use of manometric rhinometry. [9] In this procedure, a volume of air that has been removed from a closed nasal space is measured, and the pressure change in the cavity is recorded. The original volume is then calculated by measuring the change in pressure.

All these methods have been useful from a research perspective, and acoustic rhinometry is gaining popularity as a clinical tool as well.

Other methods of evaluation. Various laboratory examinations and radiologic studies can aid in identifying the cause of congestion and in estimating its extent. Laboratory tests include measurements of the complete blood count with differential, the erythrocyte sedimentation rate, and serum total and allergen-specific immunoglobulin E levels as well as analyses of nasal cytology and allergic skin reactions.

Radiologic studies can also provide useful information. Computed tomography (CT) of the sinuses provides a good distinction between bone and soft tissue, and magnetic resonance imaging differentiates soft tissue masses.

Common differential diagnoses

Among the differential diagnoses for patients with nasal congestion are rhinitis, structural defects, neoplasms, drug reactions, endocrine or metabolic conditions, and systemic inflammatory and granulomatous conditions (table 1).

Rhinitis. Allergic rhinitis might be the most common cause of nasal congestion. Patients are typically young, otherwise healthy adults who have a history of sneezing and itchy and runny nose and eyes, with or without previous nasal congestion. Patients whose rhinitis is perennial generally report that their symptoms worsen during the spring or fall. Usually, these patients have tried over-the-counter (OTC) allergy medications, which provided only a partial relief of symptoms. Symptoms have usually been present for several years before patients seek medical attention, and the onset of symptoms might have occurred during adolescence. Patients might have a history of occasional wheezing or bronchospasm, and some have a family history of asthma, allergies, or atopic eczema.

Infectious rhinitis can be of viral, bacterial, or fungal etiology. (Because both the sinuses and nasal passages are usually involved, a better term might be infectious rhinosinusitis.) The condition can be acute or chronic. Young children experience an average of six to eight colds a year. The associated rhinorrhea is usually copious. Viral rhinitis (colds) normally resolves spontaneously within 7 days, while bacterial rhinosinusitis persists longer and features more intense symptoms. Endoscopy to visualize the nasal cavity, including the ostiomeatal unit, helps make the diagnosis. Under endoscopic guidance, any purulent material seen can be sampled and cultured to direct antibiotic therapy. [10] CT of the sinuses can assist in the evaluation of chronic disease.

Structural causes. The most common structural abnormality is a deviated nasal septum, which can cause a sensation of chronic unilateral nasal congestion or congestion that fluctuates with the nasal cycle. The patient might report a history of nasal trauma. The physical examination usually reveals an anterior septal deflection. The turbinates can exhibit a compensatory hypertrophy on the side away from the deviation. Nasal valve disorders can also cause nasal obstruction.

Lesional causes. Obstruction and congestion can be caused by idiopathic nasal or nasopharyngeal polpys or polyps that occur in association with cystic fibrosis, asthma, aspirin sensitivity, chronic rhinosinusitis, and allergic rhinitis. Nasal polyps appear as bluish, water-filled "bags." Other neoplasms that can appear in the nose are angiofibromas, adenocarcinomas, melanomas, esthesioneuroblastomas, and neuroendocrine carcinomas.

Drug-induced causes. Rhinitis medicamentosa is the most commonly recognized type of drug-induced congestion. It is a rebound congestion that is caused by the overuse of topical nasal decongestants. Other common drugs that can provoke similar symptoms are aspirin, nonsteroidal anti-inflammatory drugs, beta blockers (oral and ophthalmic), bromocriptine, estrogens, oral contraceptives, prazosin, methyladopa, phentolamine, guanethidine, reserpine, and tricyclic antidepressants. [11] There seems to be no correlation between the severity of rhinitis medicamentosa and the frequency of topical decongestant use. [12-14] Some studies have shown that in addition to the vasoconstrictor in decongestants, the preservative (usually benzalkonium) might also contribute to, and even accentuate, rhinitis medicamentosa. [15]

Endocrine and metabolic causes. States of hormonal flux (e.g., pregnancy and puberty) are associated with nasal mucosal engorgement and obstruction. The presence of hypothyroidism might also be related to rhinitic symptoms.

Systemic inflammatory and granulomatous causes. Vasomotor and idiopathic rhinitis are relatively common forms of rhinitis and are characterized by symptoms of nasal obstruction, postnasal drainage, anterior rhinorrhea, and sneezing of unknown etiology. Symptoms manifest in response to environmental triggers, such as smoke, dust, fumes, exhaust, changes in temperature and humidity, and strong perfumes, bleaches, and solvents. It is necessary to exclude other causes of rhinitis before a patient' s condition can be diagnosed as idiopathic rhinitis.

The symptoms of nonallergic rhinitis with eosinophilia syndrome (NARES) are similar to those of perennial allergic rhinitis--sneezing, itching, rhinorrhea, and nasal congestion. Allergy tests are negative, but nasal smears are positive for eosinophils. NARES might represent an allergy to an unknown agent or an overlap syndrome with vasomotor rhinitis, in which eosinophilia is absent. [11]

Symptoms can also be caused by numerous uncommon inflammatory conditions, including sarcoidosis, Wegener's granulomatosis, Churg-Strauss syndrome, lupus, other collagen diseases, and Sjogren's s syndrome. Rhinitis is just one part of a constellation of systemic symptoms in these cases.

Nasal obstruction and sleep disturbance

The part that nasal obstruction plays in sleep disturbance is controversial. Some authors believe nasal obstruction can cause frank obstructive sleep apnea syndrome, while others minimize its role.

In the normal awake state, nasal airway resistance markedly exceeds that of oral airway resistance. During sleep, the relaxation of the oral and pharyngeal musculature leads to a reversal of the resistance patterns of the nose and oral cavity, and oral airway resistance increases. Breathing through an inefficient oral cavity requires increased effort, which leads to greater negative pressures in the pharynx and a higher risk of collapse. The resistance in the nasal cavity, which has a more rigid frame, is more constant during both the awake and asleep states. The pharynx still connects the nose to the trachea, but the lower resistance to airflow makes a collapse of the pharynx less likely. The nose appears to be the more efficient route of breathing during sleep. [16]

Although the effects of sleep on the nose are less than its effects on the oral cavity, changes in nasal patency do occur. Nasal resistance is known to increase during recumbency, as mucosal congestion takes place. [17] An underlying limitation of nasal airflow, which can be subclinical during the daytime while the patient is upright, can manifest at night shortly after the patient becomes recumbent. Any process that produces nasal congestion while the patient is awake will have an additive effect on nasal airflow during sleep.

Studies have demonstrated a significant correlation between nasal resistance and snoring. [16, 18] Patients who snore habitually are more likely to complain of nighttime nasal congestion, nasal discharge, and congestion caused by allergic rhinitis.

Upper airway resistance syndrome (UARS) is characterized by an increase in the amount of work that is required to breathe during sleep in order to overcome the elevated airway resistance. UARS causes numerous microarousals that fragment sleep and diminish its quality. Sleep fragmentation has been shown to lower patients' subjective assessments of wakefulness, mood, and attention. [19] Patients with UARS often complain of daytime somnolence, which can be assessed objectively with instruments such as the multiple sleep latency test.

It appears that the nose might play a significant role in the development of UARS. The nasal obstruction associated with allergic rhinitis has been found to fragment sleep and significantly increase the incidence of microarousals. [20] The effects of allergic rhinitis can be alleviated with medical therapy to reduce allergic inflammation. Intranasal topical corticosteroids significantly reduce nasal congestion in patients with allergic rhinitis, which improves the quality of their sleep and alleviates daytime sleepiness . [21]

Patients with UARS do not have frequent enough apneic episodes to meet the criteria for obstructive sleep apnea syndrome (OSAS). Some authors believe that UARS might be a precursor to OSAS and suggest that a continuum exists between normal nocturnal breathing, occasional snoring, habitual snoring, UARS, and OSAS. For example, patients might progress from one point to another on the continuum as their weight fluctuates. Similarly, nasal obstruction might move a patient up or down the continuum.

A direct linear correlation between nasal resistance and the respiratory disturbance index (RDI) has not been observed, although the two indices do seem to have an association. [16,18] Complete obstruction from nasal packing has long been suspected of causing apneic episodes. Studies that provide evidence both for and against packing as a cause of OSAS have been published. [22-25] It might be that patients who undergo nasal packing in addition to having other risk factors make up the primary population of those who experience apneic episodes. [26]

Patients who are allergic to ragweed have longer and more frequent episodes of obstructive apnea during their acute season than they do during their off season, which might be attributable to increased nasal resistance. [27] Fixed anatomic obstructions, such as a deviated nasal septum, might contribute to OSAS. Surgical repair can improve the RDI. [28] Nasal obstruction can be at least partly responsible for the development of OSAS.

Conservative management

Effective conservative treatments include decongestant drugs, antiallergy measures, and nasal dilation devices (table 2).

Decongestants. Decongestants generally serve as the first-line treatment for nasal congestion (table 3). They are marketed as topical and oral formulations.

Topical. Topical vasoconstrictors are divided into two categories: the sympathomimetic amines and their imidazoline derivatives. The sympathomimetic amines include ephedrine and phenylephrine, and the imidazolines include naphazoline, oxymetazoline, tetrahydrozoline, and xylometazoline. Both categories of drugs produce local vasoconstriction by stimulating the adrenergic receptors on the lamina propria of vessels. The imidazolines have a lesser myocardial and bronchiolar effect, whereas the amines produce more rapid tachyphylaxis and are less toxic to the nasal cilia.

Patients who experience rhinitis medicamentosa can be treated by slowly weaning them from the topical agent. The patient should be informed that congestion might last for as long as 2 to 4 weeks after their medication is stopped. Sleeping with the open nostril upward can help alleviate the congestion. The addition of steroids can be helpful in more difficult cases."

Oral. The oral decongestants ephedrine, pseudoephedrine, and phenylpropanolamine all have alpha-adrenoceptor agonist activity. Ephedrine also has an effect on beta-adrenoceptors. Alpha-adrenergic vasoconstrictors diminish nasal obstruction, but they have no influence on itching, sneezing, and nasal secretion. [1]

All decongestants can interact adversely with monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants, indomethacin, beta blockers, methyldopa, some general anesthetics, digitalis, antihypertensives, rauwolfia alkaloids, other central nervous system (CNS) stimulants, and possibly theophylline. Possible side effects include restlessness, nervousness, insomnia, headache, angina pectoris, tachycardia, and hypertension. Because decongestants produce generalized peripheral vasoconstriction, they must be used cautiously at all times and should be avoided by patients who have cardiovascular disease, hypertension, diabetes mellitus, glaucoma, thyroid disease, hepatic disease, renal disease, peptic ulcer, and possibly duodenal ulcers. Decongestants can also precipitate urinary retention in patients with prostatic hypertrophy. [29]

Antiallergy measures. For patients who have allergic causes of nasal congestion, there are two general treatment options: (1) avoidance and environmental control and (2) pharmacotherapy with antihistamines, antihistamine/decongestant combinations, corticosteroids, mast cell stabilizers, and immunotherapy. These modalities can be used singly or in combination, depending on the severity of the disease.

Avoidance and environmental control. Avoidance is a mainstay of allergy treatment. Indoor and outdoor allergens must be identified and avoided. The most common allergens are pollen (seasonal allergic rhinitis), house dust mites, animal dander, and molds (perennial allergic rhinitis).

Antihistamines. [H.sub.1] antihistamines represent one of the basic treatment options for allergic rhinitis (table 4). Their primary activity involves a dose-related competitive binding of the [H.sub.1] receptors on target cells.

The first-generation, or "classic," antihistamines are chlorpheniramine, diphenhydramine, hydroxyzine, and triprolidine. These drugs are lipophilic and thus cross the blood-brain barrier and attach to [H.sub.1] receptors on brain cells. Therefore, they typically cause sedation. They can also have anticholinergic effects, such as mucous membrane dryness, cardiac stimulation, blurred vision, decreased gastrointestinal motility, and urinary retention. The classic antihistamines can increase the CNS-depressant effects of various other drugs, such as MAOIs, tricyclic antidepressants, alcohol, antiparkinson drugs, barbiturates, tranquilizers, and narcotics. [29]

The second-generation antihistamines include acrivastine, cetirizine, fexofenadine, and loratadine. Fexofenadine and loratadine are nonsedating agents, and acrivastine and cetirizine have low sedative properties. [30] There have been reports that patients who used astemizole and terfenadine (both of which have been withdrawn from the U.S. market) experienced serious cardiac side effects (torsade de pointes) when these drugs were taken with a macrolide antibiotic or an imidazole antifungal, as well as when taken in overdose. Cetirizine, fexofenadine, and loratadine do not cause these drug interactions, nor do they produce torsade de pointes, even at high doses; extensive data on acrivastine are not yet available, but it appears to lack this effect also.

Three of the newer antihistamines available for topical use are azelastine, levocabastine, and olopatadine. Azelastine inhibits the production of histamine and other inflammatory mediators and seems to demonstrate decongestant properties. It is mildly sedating and can cause a dose-related taste alteration. Although an oral form is available elsewhere, this drug is available only as a topical nasal agent in the United States. Levocabastine is applied topically to the eyes. It is highly selective and has a very rapid onset of action and prolonged activity. Levocabastine appears to produce no sedative or psychomotor alterations. [29]

Antihistamine/decongestant combinations. Combined antihistamine/decongestant preparations are prevalent in the market (table 5). Together they not only relieve nasal congestion but control rhinorrhea, sneezing, tearing, and nasal and ocular itching. The entire symptom complex is often present in allergic rhinitis. Many studies have shown that the two classes of drugs are more effective in combination than either individual agent plus placebo. [31,32]

Corticosteroids. Steroids reduce inflammation by decreasing the infiltration of inflammatory cells, especially mast cells and eosinophils. They also diminish the hyper-reactivity and vascular permeability of the nasal mucosa, and they might decrease the release of mediators from mast cells. [1] Steroids can be taken orally, parenterally, topically, and, by some, intramuscularly. For nasal congestion, topical nasal administration is preferred because it enhances the drug's therapeutic value while minimizing its systemic effects (table 6). Hilberg showed that the topical steroid budesonide was superior to the antihistamine terfenadine in relieving nasal congestion, although this might not be a good comparison because terfenadine would not be expected to decrease congestion. [33] The steroid fluticasone has been shown to be significantly more effective than the antihistamine loratadine in treating seasonal allergic rhinitis. [34] Other topical steroids include beclomethasone, flunisolide, mometasone, and triamci nolone.

The improper use of topical steroids can cause local burning and irritation, candidiasis, and septal perforations. Their role in inducing glaucoma, cataracts, and growth suppression in children has been hotly debated, although most studies suggest that topical intranasal (as opposed to orally inhaled) steroids do not increase the incidence of these side effects.

Barnes and Pedersen, in their extensive review, concluded that the dose of inhaled steroids that is used for asthma is safe for most adults and children. [35] These doses are similar to or greater than the doses used for chronic rhinitis.

Mast cell stabilizers. Cromolyn and the more potent nedocromil prevent the dissolution of the mast cell wall and thereby prevent degranulation. They inhibit the calcium-dependent degranulation that occurs with the accumulation of cyclic AMP. As a result, these agents reduce nasal itching, sneezing, rhinorrhea, and nasal obstruction in allergic rhinitis. Both cromolyn and nedocromil can be used topically with minimal side effects. However, because their duration of effect is quite short, they must be applied several times a day. [36] Cromolyn is available as an OTC product in the United States; nedocromil is not yet available in topical nasal form. Cromolyn has been shown to be less effective than nasal steroids in controlling allergic symptoms. [37]

Immunotherapy. Immunotherapy (desensitization) is not necessary for all allergic patients. It is usually considered only for patients with moderate to severe symptoms who have experienced insufficient allergy control with pharmacotherapy and avoidance techniques. Although the exact mechanisms of immunotherapy are not completely understood, we do know that they involve the development of immunoglobulin G-blocking antibodies and the alteration of T cell interactions. [38]

Anticholinergics, such as ipratropium and oxitropium, decrease the amount of nasal secretions, but they have no effect on nasal obstruction. Anticholinergics inhibit muscarinic cholinergic receptors. They have no role in treating nasal congestion. [39]

Nasal dilation devices. External nasal dilators (e.g., Breathe Right nasal strips) have been reported to improve breathing for patients with anterior nasal obstruction as well as for pregnant women. They have even been reported to reduce the number of obstructive respiratory events in infants. These devices decrease upper airway resistance by enlarging the area in the nasal valve. [40] Another helpful tool is the nasal continuous positive-airway pressure (CPAP) device, which exerts a pneumatic splinting effect. [41] It works primarily on the elastic upper airway, preventing airway collapse and eliminating snoring and its clinical complications.

Surgical management

Among the many surgical procedures that have been used for the treatment of nasal obstruction are the trimming of the inferior turbinates, laser therapy, linear cautery, submucosal diathermy, and turbinate cryotherapy. All of them have been reported to be effective over the short term, but they provide no sustained benefit. [42] Radiofrequency ablation (somnoplasty) and microdebridement of the turbinates are two of the newer techniques, but long-term data on their effectiveness are not yet available. Various authors have reported that acoustic rhinometry has been documented to increase cross-sectional areas in nostrils that have undergone procedures such as inferior turbinectomy or turbinoplasty with or without septoplasty. [43,44]

As noted earlier, not all nasal obstruction is the result of nasal congestion. Obstructive symptoms can also be caused by nasal valve problems, which can often be corrected surgically. In a series of 500 patients, Elwany and Thabet found obstructions at the level of the nasal valve in 65 (13%), all of whom had their defects successfully corrected with surgery. [45] The septum is a key area; significant septal deviations can be corrected with septoplasty with good long-term results [43,44,46] Corrective septorhinoplasty, on the other hand, resulted in unsatisfactory outcomes for patients with severe, gross airflow asymmetry preoperatively, according to McKee et al. [47] They suggested that patients with severely deformed airways are not likely to achieve a satisfactory correction with only a single procedure.

Acknowledgment

The authors extend many thanks to Rizwan Moinuddin, Mohammed Ahmed, and Anna Lisa Somera for their assistance.

From the Section of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of Chicago.

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Differential diagnoses for patients with nasal congestion

Rhinitis

Allergic rhinitis

Infectious rhinitis (viral or bacterial)

Structural

Deviated nasal septum

Hypertrophic turbinates

Nasal valve disorder

Lesional

Nasal polyps

Other neoplasms (e.g., angiofibromas, adenocarcinomas, etc.)

Drug-induced

Rhinitis medicamentosa

Reaction to beta blockers, aspirin, nonsteroidal anti-inflammatory drugs, etc.

Endocrine and metabolic

Pregnancy

Puberty

Hypothyroidism

Systemic inflammatory and granulomatous

Vasomotor and idiopathic rhinitis

Sarcoidosis, Wegener's granulomatosis, or Churg-Strauss syndrome

Collagen vascular diseases 

Conservative management options

Decongestants

Topical

Oral

Antiallergy measures

Avoidance and environmental control

Antihistamines

Antihistamine/decongestant combinations

Corticosteroids

Mast cell stabilizers

Immunotherapy

Nasal dilation devices

Patency strips or springs

CPAP

Decongestants

Topical

Ephedrine

Naphazolline

Oxymetazoline

Phenylephrine

Tetrahyrdrozoline

Xylometazoline

Oral

Ephedrine

Phenylpropanolamine

Pseudoephedrine

Antihistamines

First generation

Chlorpheniramine

Diphenhydramine

Hydroxyzine

Triprolidine

Second generation

Acrivastine

Cetirizine

Fexofenadine

Loratadine

Topical

Azelastine (nasal)

Levocabastine (ophthalmic)

Olopatadine (ophthalmic)

Antihistamine/decongestant combinations

Acrivastine and pseudoephedrine

Azatadine and pseudoephedrine

Brompheniramine and phenylpropanolamine

Chlorpheniramine and phenylpropanolamine 

Cinnarizine and phenylpropanolamine

Fexofenadine and pseudoephedrine

Loratadine and pseudoephedrine

Triprolidine and pseudoephedrine

Topical intranasal steroids

Beclomethasone

Budesonide

Flunisolide

Fluticasone

Mometasone

Triamcinolone