Nasal congestion: a review of its etiology, evaluation, treatment

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

Jacquelynne P. Corey, MD , FACS , FAAOA Steven M. Houser, MD

Bernard A. Ng, MD, FPSOHNS

Abstract

The most common clin ical syndro mes that cause nasal congestion are allergic rhinitis, vasomotorrhinitis, chronic sinusitis, and upper respiratory vira l inf ections (common colds). Nasa l congestion, in turn , can lead to sequelae such as sinusitis, otitis media, and the onse t or worsening of mild to severe sleep disturbances, including obs truc- tive sleep apnea. There is a host of conservative treat- ments, inc luding decongestan t pharmacotherapy, antiallergy measures, and nasal dilation dev ices. Several surgical procedu res are also available. This article re- views the current guidelinesfor the workup and diagnosis of nasa l congestion and briefly describes the many and varied approaches to treatment.

Introduction

Nasal co nges tion is a key component of rhinitis. Rhinitis is defined as an infl amm ation of the lining ofthe nose that is characterized by nasal congestion, rhinorrhea, sneez- ing, and/or itching.'

Nasal congestion cau ses nasal obstruction, but not all nasal obstru ction is caused by congestion . Nasal con ges- tion involves the cavernous tissues in the turbinates. Th e focus of this artiele is on the phenomenon of nasal conges - tion rather than on the broader problem of nasal obstruc- tion. Nasal ob struction was reviewe d by Kim melma n, who in 1989 published a practical outline to guide the treatment of the most co mmon etiologies, including aller- gic rhinitis, infectious rhinitis, and vaso motor rhinitis.' Kimmelman estimated that in the United States alone at that time, an estimated $5 billi on was being spent annu- ally on medications to relieve nasal obstruction. An addi- tional $60 mill ion was being spent on surg ical reme dies, and another $ 10 billion on the treatment of associated

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

Reprint reques ts: J.P. Corey, MO, Section of Otolaryngology-Head and Neck Surgery, University of Chicago . 584 1 S. Maryla nd Ave., MC I03 5, Chicago , IL 60637 . Phone: (773) 702-0382 ; fax:

(773) 702-6809; e-mail: jcorey@surgery .bsd.uchicago.edu Research support for this article was provided by Schering Corp.

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disorders, such as recurrent rhino sinu sitis, otitis medi a, bronchit is, and asthma. Furth er adding to the condition ' s eco nomic impact are less tangible factors, such as absen- teeism and decreased producti vity.'

The most common e1inical syndromes that cause nasal congestion are allergic rhinitis, vasomotorrhinitis, chronic sinusitis, and upper res piratory viral infections (common colds) . Nasa l co ngestion, in turn, can lead to sequelae such as sinusitis, otitis media, and the onset

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worsening of mild to severe slee p dist urbances , ineluding obstruc- tive sleep apnea.

Diagnosis

Hi story. As is the case with any medic al problem, a co mplete history is essential to obtain clues about the etiology of the nasal co ngestion. It is imp ortant to elieit details such as frequ ency, duration , temporai pattern of the obstruction, precipitatin g factors, and the pre sence and character of allergic symptoms, such as sneezing, nasal itchin g, and rhin orrhea. A patient might describe symptoms of secondary middle eal' effusion, ineluding eal' poppin g, poor speech percepti on, eal'pain,

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tinnitu s.

Sympt oms related to quality of life-such as poor sleep, associated daytime somnolence, and snor ing that disturb s a bed partner ' s sleep- might indicate nocturnal nasal congestion.

Associated headache, nasal pain, and purul ent dis- cha rge suggest that an infection might be present. A history of previous cons ultations and medication use might give an ind ication of the extent of the problem. A history of previous or curre nt iIInesses and associated medication use can provide e1 ues to the etiology of nasal co ngestion and help ide ntify poss ible aggravating factors.

A history of smo king, aIcohol consumption,

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other drug intake could also be importa nt-for exa mple, in diagnos- ing cocai ne-induced septal perforation .

Any history of nasal surgery

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traum a to the nose is pertinent. A history of inhalant, food , and drug allergies is important because allergic rhinitis is a sig nificant cause of nasal congestion.' A history of asthma, especially sea-

ENT-Ear, Nose&Throat JournalsSeptember 2000

COR EY, HOUSER, NG

sonal asthma, is an important clue beca use of the high incidenee of its eoncurrence with rhinitis.

Pregnaney must be ruled out. The estrogen that is produeed during pregnancy tends to inhibit acety lcho- linesteraseaetivity, leading to edema of the nasa l mueosa and resultant congestion.'

Physicalexamination. The physical exam ination should begin during the interview. The physician should deter- minethe presenee or absence of hyponasal speeeh, which suggests that sinus and nasa l eongestion is fairly severe.

During the interview, one might also deteet signs of alIergy, such as "allergic shiners" (periorbital edema), the

"allergic salute," and urticaria. AIthough the exam ination shouldconcentrate on the nose, it should also encompass the entire head and neck. A complete head and neck examination should always be performed, and note shou ld be taken of any changes in the eyes , eyelids, ears, and throat.Such changes can include the presence of chemo- sis, epiphora, middle ear effusion, inflammation in the pharynx, and lymphadenopathy.

The presence of wheezing might indieate concomitant asthma. Ideally, the nose should be examined before and afterdeeongestion via anterior rhi noscopy. Sometimes a mare detailed examination of the turbinates, meatus, septum. and nasopharynx by rigid and/or flexib le endos- eopy is required.

Measurement ofnasal resistance. Since the early 20th eentury, researchers have tried to measure nasal resis- tance and nasal patency. Initially, a simple mirror was plaeed under the nostri ls to de teet airflow. In time, rhinomanometric techniques evolved that simultaneously measured pressure and flow . Caleulations of transnasal resistanee were made according to Ohm's law.

In reeent years, we have seen the development of aeoustierhinometry, which makes use of reflected sound wavesto estimate nasal geometry and area. Thi s method has great clinical potential because it is noninvasive, rapid, and performed quite easily." Several centers have shown that acoustic rhinometry can quantify the effect of septoplasty and the medical trea tment of nasal polyposis.

Aeoustie rhinometry has also been used to examine pa- tients before and afte r functional endoscopic sinus sur- gery in order to measure the size of the surgically pro - dueed eavity.

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Porter et al reported on the use of manometrie rhinometry.9 In this procedure, avolume of air that has beenremovedfrom a closed nasal space is measured, and thepressurechange in the cavity is recorded. The original volume is then caleulated by measuring the change in pressure.

All these method s have been useful from aresearch perspeetive, and acoustic rhinometry is gaining popular- ity as a clinical tool as weIl.

Other metlzods of evaluation . Various laboratory ex-

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aminations and radiologic studies can aid in identifying the cause of congestion and in estimating its extent.

Laboratory tests include measurements of the complete blood cou nt with differential, the erythrocyte sedimenta- tion rate, and serum total and allergen-specific immuno- globu lin E levels as weIl as analyses of nasal cyto logy and aIlergic skin reactions.

Radiologic studies can also provi de useful information.

Computed tomography (CT) of the sinuses provides a good disti nction between bone and soft tissue, and mag- netic resonance imaging differentiates soft tissue masses.

Common differen tial diagnoses

Among the differentia l diag noses for patients with nasal congestion are rhinitis, structura l defects, neoplasms, drug reactions, endocrine or metabolic conditions, and systemic inflammatory and granulomatous conditions (table 1).

Rhinitis. AIlergic rhinitis might be the most common cause of nasal congestion. Patients are typicaIly young, otherwise hea Ithy adu lts who have a history of sneezing and itchy and runny nose and eyes, with or without previous nasa l congestion. Patients whose rhini tis is per- Table 1. Differential diagnoses for patients with nasal eongestian

Rhinitis Allergic rhinitis

Infectious rhinitis (viral or bacterial) Struetural

Deviated nasal septum Hypertrophic turbinates Nasal valve disord er Lesional

Nasal polyps

Oth er neoplasms (e.g., angiofibromas, adenocarci nomas, etc.)

Drug-indueed

Rhinitis medica mentosa

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

Endoerine and metabolie Pregnancy

Puberty Hypothyroidism

Systemie inflamm atory and granulomatous Vasomotor and idiop athic rhinitis

Sarcoidosis, W egener's granulomatosis, or Churg-Strauss syndrome

Collagen vascular diseases

ENT-Ear, Nose&Throat Journal· September 2000

ennial 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 parti al re!ief of symptoms. Symptoms have usually been present for several years before patients seek medi- cal attention, and the onset of symptoms might have occurred during adolescence. Patients might have a his- tory 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.y 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 visu- alize the nasal cavity, including the ostiomeatal unit, helps make the diagnosis. Under endoscopic guidance, any purulent material seen can be sampled and cultured to direet antibiotic therapy.

¹⁰

CT of the sinuses can assist in the evaluation of chronic disease.

Structural causes. The most common structural abnor- mality is a deviated nasal septum, which can cause a sensation of chronic unilateral nasal congestion or con- gestion 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 polyps 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 conges- tion. It is a rebound congestion that is caused by the overuse of topieal nasal decongestants. Other common drugs that can provoke similar symptoms are aspirin, nonsteroidal anti-inflammatory drugs, beta blockers (oral and ophthalmic), bromocriptine, estrogens, oral contra- ceptives, prazosin, methyldopa, phentolamine, guanethi- dine, reserpine, and tricyclic antidepressants.' There seems to be no correlation between the severity of rhinitis medicamentosa and the frequency of topieal deconges- tant use.

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Some studies have shown that in addition to the vasoconstrictor in decongestants, the preservative

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(usually benzalkonium) might also contribute to, and even accentuate, rhinitis medicamentosa."

Endocrine and tnetabolic causes. States of hormonai flux (e.g., pregnancy and puberty) are associated with nasal mucosal engorgement and obstruction. The pres- ence 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 rhinor- rhea, and sneezing ofunknown etiology. Symptoms mani- fest in response to environmental triggers, such as smoke, dust, fumes, exhaust, changes in temperature and humid- ity, and strong perfumes, bleaches, and solvents. It is nee- essary to exclude othercauses 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.'

Symptoms can also be caused by numerous uncom- mon inflammatory conditions, including sarcoidosis, Wegener's granulomatosis, Churg-Strauss syndrome, lu- pus, other collagen diseases, and Sjögren'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 norrnai awake state, nasal airway resistance markedly exceeds that of oral airway resistance. During sleep, the relaxation of the oral and pharyngeal muscula- ture 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 in- creased effart, which leads to greater negative pressures in the pharynx and a higher risk of collapse. The resistance in the nasal cavity, which has a mare 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 phar- ynx less !ikely. The nose appears to be the more efficient route of breathing during sleep."

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 re- cumbency, as mucosal congestion takes place.'? An un-

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COREY, HOUSER, NG

derlying limitation of nasal airflow, which can be subelinical during the daytime while the patient is upright, can manifest at night shortly after the patient becomes reeumbent. 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.":" 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 charac- terized 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 qual- ity. Sleep fragmentation has been shown to lower pa- tients' subjective assessments ofwakefulness, mood, and attention.'? Patients with UARS often complain of day- time 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 associ- ated with allergic rhinitis has been found to fragment sleep and significantly increase the incidenee of microarousals." The effects of allergic rhinitis can be alleviated with medical therapy to reduce allergic inflam- mation . Intranasai topieal corticosteroids significantly reduce nasal congestion in patients with allergic rhinitis, which improves the quality of their sleep and alleviates daytime sleepiness."

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 con- tinuum exists between normal nocturnal breathing, occa- sionai snoring, habitual snoring, UARS, and OSAS. For example, patients might progress from one point to an- other on the continuum as their weight fluctuates. Simi- larly, nasal obstruction might move a patient up or down the continuum.

Adireet linear correlation between nasal resistance and the respiratory disturbance index (RDI) has not been observed, although the two indiees do seem to have an association. 16,18Complete obstruction from nasal paeking has long been suspected of causing apneic episodes.

Studies that provide evidence both for and against pack- ing as a cause of OSAS have been published.P:" It might be that patients who undergo nasal paeking in addition to having other risk factors make up the primary population of those who experience apneic episodes."

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

696

might be attributable to increased nasal resistance." Fixed anatomic obstructions, such as a deviated nasal septum, might contribute to OSAS. Surgical repair can improve the RDF8Nasal obstruction can be at least partly respon- sible for the development of OSAS.

Conservative management

Effective conservative treatments inelude 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 topieal and oral formulations.

Topieal. Topieal vasoconstrictors are divided into two categories: the sympathomimetic amines and their imidazoline derivatives. The sympathomimetic amines inelude ephedrine and phenylephrine, and the imidazolines inelude naphazoline, oxymetazoline, tetrahydrozoline, and xylometazoline. Both categories of drugs produce local vasoconstriction by stimulating the adrenergic re- ceptors on the lamina propria ofvessels. 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 topieal agent.

The patient should be informed that congestion might last for as long as 2 to 4 weeks after their medieation 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, pseudoephe- drine, and phenylpropanolamine all have alpha- adrenoceptor agonist activity. Ephedrine also has an ef- fect on beta-adrenoceptors. Alpha-adrenergic vasocon- strictors diminish nasal obstruction, but they have no influence on itching, sneezing, and nasal secretion.'

Table 2. Conservative management options Decongestants

Topieal Oral

Antiallergy measures

Avoidanee and environmental control Antihistamines

Antihistamine/decongestant combinations Corticosteroids

Mast eeli stabilizers Immunotherapy

Nasal dilation devices

Patency strips or springs CPAP

ENT-Ear, Nose & ThroatJournalsSeptember 2000

Table 3. Decongestants Topieal

Ephedrine Naphazoline Oxymetazoline Phenylephrine Tetrahyrdrozoline Xylometazoline

Oral

Ephedrine

Phenylpropanolamine Pseudoephedrine

All deeongestants ean interaet adversely with monoam- ine oxidase inhibitors (MAOIs), tricyclie antidepressants, indomethaein, beta bloekers, methyldopa, some general anestheties, digitalis, antihypertensives, rauwolfia alka- loids, othereentral nervous system (CNS) stimulants, and possibly theophylline. Possible side effeets include rest- lessness, nervousness, insomnia, headaehe, angina peeto- ris, taehyeardia, and hypertension. Beeause deeonges- tants produee generalized peripheral vasoeonstrietion, they must be used eautiously at all times and should be avoided by patients who have eardiovaseular disease, hy- pertension, diabetes mellitus, glaueoma, thyroid disease, hepatic disease, renal disease, peptie ulcer, and possibly duodenal ulcers. Deeongestants ean also preeipitate uri- nary retention in patients with prostatic hypertrophy."

Antiallergy measures. For patients who have allergie causes of nasal eongestion, there are two general treat- ment options: (1) avoidanee and environmental eontrol and (2) pharmaeotherapy with antihistamines, antihista-

Table 4. Antihistamines First generation

Chlorpheniramine Diphenhydramine Hydroxyzine Triprolidine

Second generation

Acrivastine

Cetirizine Fexofenadine Loratadine

Topieal

Azelastine (nasal)

Levocabastine (ophthalmic) Olopatadine (ophthalmic)

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mine/deeongestant eombinations, eortieosteroids, mast eelI stabilizers, and immunotherapy. These modalities ean be used singly or in eombination, depending on the severity of the disease.

Avoidanee and environmental contro!. Avoidanee is a mainstay of allergy treat ment. Indoor and outdoor aller- gens must be identified and avoided. The most common allergens are pollen (seasonal allergic rhinitis), house dust mites, animal dander, and molds (perennial allergie rhinitis).

Antihistamines. H

₁

antihistamines represent one of the basic treatment options for allergic rhinitis (table 4). Their primary aetivity involves adose-related competitive bind- ing of the H

₁

reeeptors on target eelIs.

The first-generation, or "classic," antihistamines are ehlorpheniramine, diphenhydramine, hydroxyzine, and triprolidine. These drugs are lipophilic and thus cross the blood-brain barrier and attach to H

₁

reeeptors on brain eelIs. Therefore, they typieally eause sedation. They ean also have antieholinergie effeets, such as mucous mem- brane dryness , eardiae stimulation, blurred vision, de- ereased gastrointestinal motility, and urinary retention.

The elassie antihistamines ean inerease the CNS-depres- sant effeets of various other drugs , such as MAOIs, trieyclie antidepressants, alcohol, antiparkinson drugs, barbiturates, tranquilizers, and narcotics ."

The second-generation antihistamines include aerivastine, eetirizine, fexofenadine, and loratadine.

Fexofenadine and loratadine are nonsedating agents, and aerivastine and eetirizine have low sedative properties."

There have been reports that patients who used astemizole and terfenadine (both ofwhieh have been withdrawn from the U.S. market) experieneed serious cardiac side effeets (torsade de pointes) when these drugs were taken with a maerolide antibiotie

of

an imidazole antifungal, as well as when take n in overdose. Cetirizine, fexofenadine, and loratadine do not eause these drug interaetions, nor do they produee torsade de pointes, even at high doses;

extensive data on aerivastine are not yet available, but it appears to lack this effeet also.

Three of the newer antihistamines available for topieal use are azelastine, levoeabastine, and olopatadine.

Azelastine inhibits the produetion ofhistamine and other inflammatory mediators and seems to demonstrate de- eongestant properties. It is mildly sedating and ean eause a dose-related taste alteration. Although an oral form is available elsewhere, this drug is available only as a topieal nasal agent in the United States. Levoeabastine is applied topieally to the eyes . It is highly seleetive and has a very rapid onset of action and prolonged aetivity.

Levoeabastine appears to produee no sedati ve or psyeho- motor alterations ."

Antihistamine/decongestant combinations. Combined antihistamine/deeongestant preparations are prevalent in the market (table 5). Together they not only relieve nasal

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COREY, HOUSER, NG

congestion but contral 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 elasses of drugs are mare effective in combi- nation than either individual agent pIus placebo." :"

Cortieosteroids. Steraids reduce inflammation by de- creasing 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 fram mast cells.' Steraids can be taken orally , parenterally, topically, and, by some , intramuscularly. For nasal con- gestion , topieal nasal administration is preferred because it enhances the drug ' s therapeutic value while minimizing its systemic effects (table 6). Hilberg showed that the topieal steraid budesonide was superior to the antihista- mine terfenadine in relieving nasal congestion, although this might not be a good camparisan because terfenadine would not be expected to decrease congestion." The steraid fluticasone has been shown to be significantly mare effective than the antihistamine loratadine in treat- ing seasonal allergic rhinitis." Other topieal steroids inelude beelomethasone , flunisolide, mometasane, and triamcinolone.

The impraper use of topieal steraids can cause local burning and irritation, candidiasis, and septal perfora- tions. Their raIe in inducing glaucoma, cataracts, and grawth suppres sian in children has been hotly debated, although most studies suggest that topieal intrana sal (as opposed to orall y inhaled ) steraids do not increase the incidenee of these side effects.

Barnes and Pedersen, in their extensive review, con- cluded that the dose of inhaled steroid s that is used for asthma is safe for most adults and children." These doses are similar to or greater than the doses used for chranic rhinitis .

Mast eel! stabilizers. Cromolyn and the mare patent nedocramil prevent the dissolution of the mast cell wall and thereby prevent degranulation. They inhibit the eal- cium-dependent degranulation that occurs with the accu- mulation of cyelic AMP. As aresult, these agents reduce nasal itching, sneezing, rhinorrhea, and nasal obstruction in allergic rhinitis. Both cramolyn and nedocramil can be used topically with minimaI side effects. However, be- cause their duration of effect is quite short, they must be applied several times a day." Cramolyn is available as an OTC praduct in the United States ; nedocramil is not yet available in topie al nasal form. Cramolyn has been shown to be less effective than nasal steroids in contralling allergic symptorns."

Itnmunotherapy. Immunotherapy (desensitization) is not necessary for all allergic patients. It is usually consid- ered only for patient s with moderate to severe symptoms who have experienced insufficient allergy contral with

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Table 5. Antihistamine/deeongestant eombinations

Acrivastine and pseudoephedrine

Azatadine and pseudoephedrine

Brompheniramine and phenylpropanolamine Chlorpheniramine and phenylpropanolamine Cinnarizine and phenylpropanolamine Fexofenadine and pseudoephedrine Loratadine and pseudoephedrine Triprolidine and pseudoephedrine

pharmacotherapy and avoidanee techniques. Although the exact mechani sms of immunotherapy are not com- pletely understood, we do know that they involve the development of immunoglobulin G-blocking antibodies and the alteratian of T cell interactions ."

Anticholinergics, such as ipratropium and oxitrapium, decrease the amount ofnasal secretions, but they have no effect on nasal obstruction. Anticholinergics inhibit mus- carinic cholinergic receptors. They have no raIe in treat- ing nasal congestion."

Nasal dilation devices. External nasal dilators (e.g., Breathe Right nasal strips) have been reported to imprave breathing for patients with anterior nasal obstruction as weIl as for pregnant women. They have even been re- ported to reduce the number of obstructive respiratory events in infants. These devices decrease upper airway resistance by enlarging the area in the nasal valve."

Another helpful tool is the nasal continuous positive- airway pressure (CPAP) device, which exerts a pneu- matic splinting effect." It works primarily on the elastic upper airway, preventing airway collapse and eliminating snoring and its elinical 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 , sub- mucosal diathermy, and turbinate cryotherapy. All of them have been reported to be effective over the short term, but they provide no sustained benefit.?

Radiofrequency ablation (somnoplasty) and micrade- bridement of the turbinates are two of the newer tech-

Table 6. Topieal intranasal steroids

Beclomethasone

Budesonide Flunisolide Fluticasone Mometasone Triamcinolone

ENT·Ear, Nose&ThroatJournalsSeptember 2000

niques , but long-term data on their effectiveness are not yet avail able. Various authors have reported that acoustic rhinometry has been documented to increase cross-sec- tional areas in nostrils that have undergone procedures such as inferior turbine ctomy or turbinoplasty with or without septoplasty.":"

As noted earlier, not all nasal obstruction is the result of nasal congestion.Obstructive symptoms can also bec aused by nasal valve probIems, 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 cor- rected with surgery

^.45

The septum is a key area; significant septal deviations can be corrected with septoplasty with good long-term result s.

^43,44,46

Corrective septorhinoplasty, on the other hand, resulted in unsatisfactory outcomes for patient s with severe, gross airflow asymmetry preopera- tively, accord ing to McKee et al." They suggested that patients with severely deformed airways are not likel y to achieve a satisfactory correction with only a single pro- cedure.

Acknowledgment

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

References

I . Internati onal Consens us Report on the diagnosis and management of rhinitis. International Rhinitis Management Working Group . Allergy 1994;49(19 Suppl):1-34.

2. Kimmelman CP. The proble m of nasal obstruetion. Otolaryngol Clin North Am 1989;22:253-64.

3. Hadley JA. Overview of otolaryng ie allergy management. An eeleetic and cost-effective approae h. Otolaryngol Clin North Am 1998;31:

69-8 2.

4. Mabry RL. Rhinitis medieamentosa: The forgotteri faetor in nasal obstruetion. South Med J 1982;75:817-9.

5. Turnbull GL, Rundell OH, Rayburn WF, et al. Managing pregnancy- related nocturn al nasal eongestion. The external nasal dilat or. J Reprod Med 1996;41 :897-902.

6. Roithmann R, Cole P, Chapnik J, et al. Aeo ustie rhinometry in the evaluation of nasal obstrue tion. Laryngoseope 1995;105:275-81.

7. Szues E, Clemen t PA. Aeo ustie rhinome try and rhinomanometry in the evaluation ofnasal pateney of patients with nasal septal deviation.

Am J Rhinol 1998;12:345-52.

8. Lund VJ, Flood J, Sykes AP, Riehards DH . Effeet of flutic asone in severe polyposis. Areh Otolaryngol Head Neek Surg 1998;124:

513-8.

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For mare inforrnationCircle 110 an Reader Service Card

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COREY , HOUSER, NG

9. Porter M, Willi amsan I, Kerridge D, Maw R. Manometric rhinometry:

A new method of measurin g nasal volume. Rhinology 1995;33:86-8.

10. Nadel DM, Lanza DC, Kennedy DW. Endoscopically guided cultures in chronic sinusitis. Am J Rhinol 1998;12:233-4 1.

II. Corey JP. Chroni c rhiniti s: The differential diagnosis. Hosp Med 1996;32(3 Suppl ):3-8.

12. Graf P, Halle n H, Juta JE. Four-week use of oxy metazoline nasal spray (Nezer il) once daily at night induees rebound swelling and nasal hyperreactivity. Acta Otolaryngol 1995;115:71-5.

13. Talaat M, Belal A, Aziz T, et al. Rhinitis medicamentosa: Electro n microscopic study. J Laryngol Otol 1981;95:125-3I.

14. Petru son B, Hanssan HA. Function and structure of the nasa! mucosa after 6 weeks' use of nose-drops. Acta Otolaryngol 1982;94:563-9.

15. Graf P, Halle n H. Effect on the nasal mucosa of long-term treatment with oxymetazoline, benzalkonium chloride, and placebo nasal sprays . Laryngoscope 1996;106:605-9.

16. Olsen KD, Kern EB. Nasal influences on snoring and obstructive sleep apnea. Mayo Clin Proc 1990;65:1095-105 .

17. Rundcrantz H. Posturai variations of nasa l patency. Acta Otolaryngol 1969;69:435-43 .

18. Young T, Finn L, Kim H. Nasal obstruction as a risk factor for sleep- disordered breathin g. The University of Wisconsin Sleep and Respi- ratory Research Group. J AlIergy Clin Immunol 1997;99 :S757-62.

19. Martin SE, Engleman HM, Deary JJ, Douglas NJ. The effect of sleep fragmentatia n on daytime function. Am J Respir Crit Care Med 1996;153:1328-32.

20. Lavie P, Gertner R, Zomer J, PodoshinL.Breathin g disorders in sleep associated with "rnicroarousals" in patients with allergic rhinitis. Acta Otolaryngol 1981;92:529-3 3.

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2 1. Craig

n ,

Teets S, Lehman EB, et al. Nasa l congestion secondary to allergic rhinitis as a cause of sleep disturbance and dayt ime fatigue and the response to topieal nasal corticosteroid s. J AlIergy Clin Immunol 1998;10I:633-7.

22. Carskadon MA, Bearpark HM, Sharkey KM, et al. Effect s of meno- pause and nasal occlu sion on breath ing durin g sleep. Am J Respir Crit Care Med 1997;155 :205-10 .

23. Serpell MG, Padgham N, McQueen F, et al. The influ ence of nasal obstruction and its relief on oxygen saturation dur ing sleep and the early postoperative period . Anaesthesia 1994;4 9:538-40.

24. Buckley JG, Hickey SA, Fitzgerald O'Connor AF. Does post-opera- tive nasal paekin g cause nocturnal oxygen desaturati on? J Laryngol OtoI1 991;105:109- 11.

25. Wetmore SJ, Scrima L, Hiller FC. Sleep apnea in epistaxis patients treated with nasal packs. Otolaryngol Head Neck Surg 1988;98:

596-9.

26. Loftus BC, Blitzer A, Cozine K. Epistaxis, medical history , and the nasopulm onary refle x: What is clinically relevant ? Otolaryngol Head Neck Surg 1994;110:363-9.

27. McNicholas WT , Tarl o S, Cole P, et al. Obstru ctive apneas durin g sleep in patients with seas onal allergic rhinitis. Am Rev Respir Dis 1982;126:625-8 .

28. Heimer D, Scharf SM, Lieber man A, Lavie P. Sleep apnea syndrome treated by repair of deviated nasal septum oChest 1983;84:184-5.

29. Krause HF. Antihistamine s and decon gestants. Otolar yngol Head Neck Surg 1992; 107:835-40 .

30. Fireman P. Treatment strategies designed to minimi ze medical com- plications of allergic rhinitis. Am J Rhinol 1997; Il :95-102.

31. Connell JT. A novel method to assess antihistamine and decongestant efficacy. Ann Alle rgy 1979;42:278-85.

32. Falliers CJ, Redding MA. Controlled comp arison of a new antihista- mine-decongestant comb ination to its indiv idual components. Ann AlIergy 1980;45 :75- 80.

33. Hilberg O. Effect of terfen adine and budesonide on nasal symptoms, olfaction, and nasal airway patency follow ing alle rgen challenge.

AlIergy 1995;50:683-8.

34. Ratner PH, van Bavel JH, Martin BG, et al. A comp arison of the efficacy of fluticaso ne propion ate aqueous nasal spray and loratadine, alone and in comb ination, for the treatment of seasonal allergic rhinit is. J Fam Pract 1998;47:118-25 .

35. Barnes PJ, Peder sen S. Efficacy and safety of inhaled corticosteroids in asthma. Report of a workshop heid in Eze, France , October 1992.

Am Rev Respir Dis 1993;148 :SI-S26.

36. King HC. Mast cell stabilizers . Otol aryngol Head Neck Surg 1992;107:841-4.

37. Meltzer EO. An overview of current pharm acotherapy in perenn ial rhinitis. J AlIergy Clin Immunol 1995;95:1097-110 .

38. Fornadley J. AlIergy immunotherapy. Otola ryngol CHn North Am 1998;31:111-27.

39. Bronsky EA, Druce H, Findl ay SR, et al. A clinical trial ofipratropium bromide nasal spray in patients with perennial nonallergic rhinitis. J AlIergy Clin Immunol 1995;95:1117-22.

40. Chaudhry MR, Akht ar S, Dwalsaint F. Rhino manometric evaluation of the impro ved meeh anieal therapeuti c nasa! dilator in patients with anterior nasal obstruction. Rhinology 1996 ;34:32-4.

41. Wang CH, Lin HC, Huang

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et al. Different ial effects of nasal continuous positiv e airw ay pressure on reversible or fixed upper and

!ower airway obstructio n. Eur Respir J 1996;9:952-9.

42. Warwick-Brown NP, Mark s NJ. Turb inate surgery: How effective is it? A long-term assessmeel. ORL J Otorhinol aryngol Relat Spec 1987;49:314-20.

43. Grymer LF, Illum P, Hilberg O. Septoplasty and comp ensatory inferior turbinate hypertrophy: A randomized study evaluated by acoustic rhinomet ry. J Laryngol OtoI1 993 ;107:413-7 .

44. Marais J, Murray JA, Marshall I, et al. Minimal cross-sectional areas, nasa! peak flow and patients' satisfaction in septop!asty and inferior turbinect omy. Rhinol ogy 1994;32:145-7.

45. Elwany S, Thab et H. Obstruction of the nasal valve. J Laryngol Otol 1996:110:221-4.

46. Bohlin L, Dahlqvist A. Nasal airway resistance and complicati ons following functional septoplasty: A ten-year follow-up study. Rhinol- ogy 1994;32:195-7.

47. McKee GJ, O'Neill G, Roberts C, Lesser TH. Nasal airflow after septorhinoplasty. Clin Otolaryngol 1994;19:254-7.

ENT-Ear, Nose & Throat JournalsSeptember 2000