A sleep clinician’s guide to runny noses: evaluation and management of chronic rhinosinusitis to improve sleep apnea care in adults

Abstract

Study Objectives:

The treatment of obstructive sleep apnea is often impeded by intolerance of positive airway pressure therapy, which is frequently attributed to the inability to breathe through the nose. Providers caring for patients with sleep apnea need a working knowledge of nasal passage disease and available treatments to better manage this common comorbidity.

Methods:

This review examines the literature connecting rhinosinusitis to adverse sleep and sleep apnea outcomes. It explores the different types of nasal and sinus diseases a sleep apnea provider might encounter, focusing on the medications used to treat them and indications for referral to otolaryngology.

Results:

Chronic rhinosinusitis can be either allergic or nonallergic. Both types can interfere with sleep and sleep apnea therapy. The successful management of chronic rhinosinusitis can improve positive airway pressure tolerance and adherence. A wide range of over-the-counter and prescription pharmacotherapy is available, with data supporting intranasal over oral treatment. Surgical treatment for chronic rhinosinusitis in obstructive sleep apnea addresses nasal obstruction, often with inferior turbinate reduction and septoplasty.

Conclusions:

Sleep specialists should have a working knowledge of the available options to treat chronic rhinosinusitis. These options are often safe, effective, and readily accessible. Otolaryngologists and allergists/immunologists provide additional treatment options for more complicated patients. Providing treatment for chronic rhinosinusitis should be included as part of comprehensive sleep apnea care.

Citation:

Ali MM, Ellison M, Iweala OI, Spector AR. A sleep clinician’s guide to runny noses: evaluation and management of chronic rhinosinusitis to improve sleep apnea care in adults. J Clin Sleep Med. 2023;19(8):1545–1552.

INTRODUCTION

Obstructive sleep apnea (OSA) is a highly prevalent condition that affects approximately 15–30% of males and 10–15% of females in North America when OSA is defined as an apnea-hypopnea index (AHI) of at least 5 events per hour.¹ The prevalence only increases with population age. Patients with OSA are at increased risk of drowsy driving and car crashes,² neuropsychiatric dysfunction,³ cardiovascular and cerebrovascular morbidity,⁴ and multiple other complications.^5–7 Thus, successful treatment of OSA is considered to be critically important to good health.

While several options exist to treat OSA, the mainstay of therapy is positive airway pressure (PAP), which is administered as either continuous PAP (CPAP) or bilevel PAP (BPAP). PAP therapy is administered through a mask applied to the nose or to the nose and mouth. In either case, patients experience air pressure applied to the nasal passages. This can be especially difficult to tolerate for patients with nasal congestion or sinus disease. Indeed, difficulty breathing through the nose is predictive of PAP nonadherence.⁸ Excess nasal drainage or “postnasal drainage” is frequently cited by patients as a reason that they cannot tolerate PAP therapy.

Like OSA, rhinosinusitis, a broad term that indicates inflammation of the nasal cavity and paranasal sinuses, is highly prevalent, affecting approximately 16% of American adults.⁹ As a result, it would be expected that a sizable percentage of the population would have both conditions even if they were unrelated. However, there is evidence that the presence of rhinosinusitis increases the risk for OSA.¹⁰ Rhinosinusitis can be considered partially responsible for both causing OSA and preventing its adequate treatment.

In this context, the proper management of rhinosinusitis becomes critically important to providers who treat sleep disorders. This review will discuss the evidence linking rhinosinusitis to sleep disorders, particularly OSA, and provide a summary of treatment options for the management of rhinosinusitis.

RHINOSINUSITIS: THE BASICS

Rhinosinusitis and its component conditions, rhinitis and sinusitis, can be either allergic or nonallergic. Allergic rhinitis affects 10–20% of adults in North America.¹¹ After repeated exposures to an allergen, atopic individuals will produce an allergen-specific immunoglobulin E (sIgE). sIgE is bound to IgE receptors on mast cells in the nasal mucosa and to basophils in the peripheral blood. On subsequent exposure to the allergen, the allergen will bind to the corresponding sIgE on the mast or basophil cell. These cells are activated, and chemical mediators (cytokines, interleukins, histamines, leukotrienes) are released, leading to the immediate and delayed symptoms of allergic rhinitis, such as sneezing, itchy and runny nose, and congestion.¹²

Nonallergic rhinosinusitis, on the other hand, is non-IgE dependent. There are numerous etiologies for nonallergic rhinitis, both inflammatory and noninflammatory.¹³ Among the inflammatory subtypes are infectious, irritant, and nonallergic rhinitis with eosinophilia syndrome. The noninflammatory subtypes include atrophic, gustatory, drug- or hormone-induced, senile, postsurgical, and vasomotor.¹³ Many commonly prescribed medications can contribute to nasal congestion (Table 1).¹⁴

Table 1.

Drug-induced rhinitis.

Drug Name	Drug Class	Common Indication
Lisinopril	ACE inhibitor	Hypertension
Clonidine	α-2 Receptor agonist	Hypertension
Quetiapine	Atypical antipsychotic	Psychosis
Haloperidol	Typical antipsychotic	Psychosis
Tamsulosin	α-1 Receptor antagonist	Prostatic hypertrophy
Terazosin	α-1 Receptor antagonist	Prostatic hypertrophy
Finasteride	5α-Reductase inhibitor	Prostatic hypertrophy
Sildenafil	Phosphodiesterase type 5 inhibitor	Erectile dysfunction
Estradiol	Sex hormone	Contraception

Common medications that can cause nonallergic rhinitis (data from reference ⁶⁹).

Based on the duration of symptoms, rhinosinusitis can also be classified as acute (symptoms for < 4 weeks), subacute (4–12 weeks), or chronic (> 12 weeks). Recurrent sinusitis is defined as 4 or more acute, nonoverlapping episodes of sinusitis per year.

Rhinosinusitis must also be differentiated from nasal obstruction for other reasons. For instance, anatomical deformities, such as a deviated nasal septum, nasal polyps, or the rare nasal mass or neoplasm, can mimic rhinosinusitis by making nasal breathing difficult.¹⁵

RHINOSINUSITIS AND SLEEP

The sleep symptoms that result from rhinosinusitis can also be significant. Sleep disruption is markedly more common in those with chronic rhinosinusitis (CRS), with rates of sleep trouble as high as 60–75% compared to 8–18% in the general population.¹⁶ Snoring, difficulty falling asleep, difficulty staying asleep, early morning awakenings, and excessive daytime sleepiness are all more common in patients with CRS.¹⁷ Given the overlap of these symptoms with the symptoms of OSA, however, it is not known if rhinosinusitis disturbs sleep directly or if it increases the risk for OSA, which then causes the sleep dysfunction. Intriguingly, it has also been shown that the presence of insomnia is a risk factor for the subsequent development of CRS, although why this might be the case is uncertain.¹⁸

One possible explanation for the difficulty falling and staying asleep in the setting of CRS is elevated histamine. Histamine is an allergic mediator but also a neurotransmitter that increases wakefulness.¹⁹ However, there is currently no evidence to suggest that local increases in histamine in the nasal tissues translate to increased brain histamine. Additionally, the sleep disruption in nonallergic rhinitis might exceed that of allergic rhinitis²⁰ or be the same as allergic rhinitis,²¹ making it unlikely that histamine is the primary culprit.

RHINOSINUSITIS AND OSA

The relationship between CRS and OSA appears to be bidirectional. In a Taiwanese population, the risk of developing CRS was three times higher among patients with OSA.²² And in an American population, patients being diagnosed with CRS had a higher likelihood of having already been diagnosed with OSA than a control population without CRS.²³

There is less evidence supporting CRS as a risk factor for OSA, but one small study did demonstrate this to be the case.²⁰ There are theoretical mechanisms why this might occur. It is possible that CRS increases the risk of OSA by increasing nasal resistance, thereby causing more oral breathing; oral, compared with nasal breathing, can lead to a significantly higher AHI.¹⁰ We suggest that life-long difficulty with nasal breathing can contribute to craniofacial growth patterns (eg, retrognathia), which make OSA more likely.

Oral breathing might predispose to OSA via several mechanisms. First, upper airway resistance during sleep is significantly lower during nasal breathing than during oral breathing.¹⁰ Additionally, in nonobese patients, it was demonstrated that the jaw and tongue positioning with open-mouth breathing led to higher AHIs.²⁴ Finally, the nasal-ventilatory reflex involves increased ventilation, breathing rate, and minute ventilation via stimulation of nasal receptors; oral breathing bypasses these receptors.²⁵

CRS might also be a factor that contributes to the higher prevalence of OSA in Black patients. Among patients with CRS, those who were identified as African-American were twice as likely as White patients to have OSA.²⁶ This finding was not related to body mass index, sex, or age, and it is a larger disparity than is seen in the general population.^27,28 The reason that CRS appears to exacerbate the known disparity in OSA prevalence is unknown. Environmental factors, such as exposure to air pollution, might explain this association.²⁹

While CRS and OSA are highly comorbid, it is premature to conclude that either causes the other. Their comorbidity, however, still has important clinical implications. For instance, nocturnal nasal congestion in patients with hypertension and comorbid OSA was associated with more poorly controlled blood pressure.³⁰ Furthermore, the presence of CRS can affect the treatment of OSA.

RHINOSINUSITIS AND PAP THERAPY

For patients with CRS, PAP therapy can be difficult to tolerate. Among patients who discontinued use within the first 2 months of treatment, there was a significantly higher proportion of patients with high nasal resistance.⁸ This is particularly problematic as early success with PAP therapy is a strong predictor of long-term success with PAP therapy.^8,31

Moreover, severe rhinosinusitis need not be present prior to PAP therapy to interfere with treatment. PAP therapy might induce or exacerbate pre-existing mild rhinitis.³² This has been termed “CPAP rhinitis.”³³ The presumed mechanism for this is the exposure to cold or dry pressurized air. CPAP has also been shown to induce nasal inflammation³⁴ with upregulation of proinflammatory macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor α (TNF-α) in rats exposed to CPAP.³⁵ In humans, increases in nasal neutrophils were observed after CPAP treatment in both allergic and nonallergic rhinitis.³⁶ Heated humidification is often added to PAP therapy to mitigate CPAP rhinitis, but it not always adequate.

On the other hand, CPAP also has the potential to improve congestion in patients with allergic rhinitis.³⁷ Even without the mitigation of humidification or antihistamines, patients with allergic rhinitis had improved nasal symptoms after starting CPAP, while those with nonallergic rhinitis clinically worsened.³⁶ One might speculate that the filtration built into PAP devices reduces exposure to allergens overnight as the mechanism for this improvement, but this has not been established.

EVALUATION OF RHINOSINUSITIS

Prior to starting PAP therapy, the prescribing provider can screen for nasal congestion and rhinorrhea and recommend treatment with the goal of improving early PAP tolerance. Patients should be asked about the timing of symptoms (eg, do they only occur while in bed, suggesting an allergen is present in the bedroom), presence and quality of drainage (eg, postnasal only, thin, thick, purulent), and laterality. A complaint of an itchy nose often points to an allergic etiology. Thicker, green discharge could indicate an infection. And consistent symptoms on only one side might point to an anatomical etiology (eg, septal deviation, neoplasm).

Guidelines from the American Academy of Otolaryngology–Head and Neck Surgery define CRS as the presence of at least two out of four cardinal symptoms (facial pain/pressure, hyposmia/anosmia, nasal obstruction, and nasal drainage) for at least 12 consecutive weeks, in addition to objective evidence on physical examination (anterior rhinoscopy or endoscopy) or radiography such as computed tomography.³⁸ Additional relevant history includes a history of prior nasal or sinus surgery, known environmental (perennial) allergies or seasonality of symptoms, prior allergy testing, or allergy immunotherapy. For patients suspected of having allergic rhinitis, a referral for allergy testing can be considered to help the patient identify the triggering allergen(s). Although there is significant overlap in the treatment for allergic and nonallergic rhinosinusitis, determining which patients have an allergic etiology can help with more targeted management, including avoidance of the allergen or desensitization therapy (allergy immunotherapy).

While anterior rhinoscopy can reveal both anatomic causes and mucosal changes that contribute to nasal obstruction, many sleep doctors are not adequately trained in this procedure. If needed, providers can request examination by an otolaryngologist or an allergist/immunologist. If there is a strong history of nasal obstruction, especially one that is constant, noncontrast enhanced computed tomography of the sinuses is the imaging of choice.³⁹ Imaging studies should be performed only if at least two of four self-reported criteria for CRS are present because there is a high false-positive rate for sinus abnormalities.⁴⁰ Plain sinus X-rays are not recommended.

MANAGEMENT OF CHRONIC RHINITIS

Nonprescription remedies

Rhinitis, compared with sinusitis, tends to be the larger impediment to CPAP. Initial management of rhinitis includes several over-the-counter remedies. Nasal lavage using saline should typically be performed first before applying any topical medications. This procedure can be done on a regular basis and could be sufficient therapy for patients with mild symptoms.⁴¹ For those who need additional therapy, lavage can better expose the intranasal surface to topical medications. Eucalyptol, capsaicin, wintergreen, and horseradish are all used to improve congestion. If the primary complaint is dryness, personal lubricants or small quantities of petrolatum could be considered. Saline sprays with sorbitol are available. Some patients will find relief with externally applied adherent nasal strips, which can be worn under PAP therapy masks if needed. These widen and stabilize the nasal valve, which can be anatomically narrow or overly compliant (especially with older patients), and which CPAP masks can compress.

Intranasal steroids

To reduce the mucosal inflammation that often drives rhinitis, topical steroids are a mainstay of therapy. Intranasal corticosteroids are the most effective medication class for controlling symptoms of allergic rhinitis.⁴² They reduce inflammation through several mechanisms, including inhibiting cytokine release. The onset of action is up to 30 minutes, but maximum effectiveness is usually noted after 2–4 weeks of daily use.⁴³ One common adverse effect is epistaxis, the risk of which can be mitigated by using a proper administration technique. Patients should be advised to direct the spray with the contralateral hand slightly toward the lateral wall of the nares, and not toward the nasal septum, pointing the nozzle toward the back of the eyeball on the same side being sprayed.

There are several intranasal steroids on the market, and no evidence indicates that any is superior. The theoretical concern of hypothalamic-pituitary axis suppression has not been shown with current intranasal corticosteroids.⁴⁴ In a small study of patients with allergic rhinitis, patients treated with intranasal steroids self-reported improved sleep compared with the placebo therapy group, although no improvement in daytime sleepiness was observed.⁴⁵

Intranasal steroids have demonstrated efficacy in reducing the severity of OSA. After 4 weeks of treatment with intranasal fluticasone, patients with comorbid OSA and rhinitis showed significantly lower AHIs compared with the placebo group, although the magnitude of the effect was modest (AHI reductions of 3 events/h).⁴⁶ Similarly, patients with OSA with allergic rhinitis had significantly improved lowest oxygen saturation and supine AHI after 10 to 12 weeks’ treatment with intranasal steroids.⁴⁷ Those with allergic rhinitis had a nearly 2% improvement in minimum oxygen saturations, with reductions in AHI of 11 events/h after intranasal steroid treatment compared with no meaningful change in oxygen saturations and an AHI reduction of only 3 events/h in the control group.

Although intranasal steroids alone are not going to adequately treat OSA, their use might allow patients to tolerate PAP therapy, which would lead to more effective treatment of OSA. In a randomized study of fluticasone furoate nasal spray, there was improvement in rhinorrhea and congestion as well as increased CPAP usage at 90 days.⁴⁸ The difference in CPAP usage at 30 days was not significant, indicating that treatment might need to be extended for several months to observe the benefit. In this study, those treated with intranasal steroids used CPAP 6 more days out of the 90 days than the control group. And on the nights that CPAP was used, the patients were able to maintain CPAP for 60 minutes longer per night (348 minutes vs 288 minutes) in the intranasal steroid group than the control group. While other studies have not shown this benefit, they had an observation window of only 4 weeks.^49,50 To date, studies on the effect of intranasal steroids on CPAP usage include undifferentiated patients with OSA who are starting CPAP therapy. No study could be identified that targets a population of patients specifically with chronic rhinitis and OSA who are starting CPAP therapy, but it is possible that treating the rhinitis population with nasal steroids while introducing CPAP therapy would show an even greater effect on device usage.

Both over-the-counter and prescription intranasal steroids are available. Those that require prescriptions tend to be higher potency steroids, which should be reserved for those who are unresponsive to the lower potency, over-the-counter options. Table 2 lists the intranasal steroids available in the United States and their availability.

Table 2.

Intranasal corticosteroids.

Generic Name	Common Brand Name	Availability
Beclomethasone dipropionate	Beconase AQ, Alanase, Vancenase AQ, Qnasl	Prescription
Budesonide	Rhinocort	Over-the-counter
Ciclesonide	Omnaris, Zetonna	Prescription
Flunisolide	Aerospan	Prescription
Fluticasone furoate	Veramyst	Over-the-counter
Fluticasone propionate	Flonase	Over-the-counter
Mometasone furoate	Nasonex	Over-the-counter
Triamcinalone acetonide	Nasocort	Over-the-counter

Availability of intranasal corticosteroids that are sold in the United States by generic and brand name.

Intranasal antihistamines

Antihistamine nasal sprays are second-line agents after intranasal steroids for the management of chronic rhinitis. Nasal antihistamines are effective even in nonallergic rhinitis.⁵¹ There are two nasal antihistamines available in the United States: azelastine, which, until recently, was available by prescription only and is now available at a higher dose over-the-counter, and olopatadine (prescription). Both drugs are peripheral H-1 receptor antagonists. Compared with oral administration, nasal antihistamines deliver a higher concentration of medicine to the nasal cavity and have fewer side effects, with similar or superior benefits in treating chronic rhinitis.⁵² Common adverse effects include a strong, bad aftertaste and drying, which may result in crusting. Like the intranasal steroids, avoiding direct administration to the nasal septum can help prevent local side effects.

Intranasal steroids and intranasal antihistamines can be used together for patients who have an inadequate response to the individual therapies. Products may be administered separately or as a combination. The antihistamine/steroid sprays are azelastine and fluticasone and olopatadine and mometasone. The combination products have side effects similar to each individual medication. The advantage of the combination is ease of administration and half the overall volume of spray.

Oral antihistamines

Oral antihistamines are commonly used to treat environmental allergies and chronic rhinitis. However, oral antihistamines without an intranasal steroid or intranasal antihistamine are unlikely to be sufficient in the treatment of rhinitis.⁵³ They could be used for excess rhinorrhea or postnasal drip if those symptoms interfere with PAP usage. It is important for providers caring for patients with OSA to be familiar with their uses, limitations, and potential side effects.

Antihistamines can target H-1, H-2, or H-3 histamine receptors. H-1 antihistamines work by blocking histamine-related smooth muscle constriction, mucus secretion, and vascular permeability, thus reducing swelling in the nasal passages and allowing improved airflow.⁵⁴ H-1 antihistamines are further categorized as first generation (sedating) or second generation (nonsedating), which is determined by their lipid solubility and ability to cross the blood–brain barrier. Second-generation antihistamines are more lipophobic, thus reducing central nervous system side effects.⁵⁵ As a result, first-generation—not second-generation—antihistamines are those that are included in nighttime cold medicines and sleep aids. Table 3 provides a list of H-1 receptor antagonists that are available in the United States. The H-2 receptor antagonists, which are predominantly used for gastrointestinal disorders, and the H-3 receptor inverse agonist/antagonist, pitolisant, which is indicated for narcolepsy, will not be discussed here.

Table 3.

Oral H-1 antihistamines.

Generic Name	Common Brand Name	Generation
Brompheniramine	Dimetapp	First
Carbinoxamine	Arbinoxa, Karbinal ER, Palgic, Ryvent	First
Cetirizine	Zyrtec	Second*
Chlorpheniramine	Allerest, Contac, Triaminic	First
Clemastine	Tavegyl	First
Cyproheptadine	Periactin	First
Desloratadine	Clarinex	Second
Dimenhydrinate	Dramamine	First
Diphenhydramine	Benadryl, Simply Sleep, Sominex, Unisom, ZZZQuil	First
Doxylamine	Unisom	First
Fexofenadine	Allegra	Second
Hydroxyzine	Atarax	First
Levocetirizine	Xyzal	Second
Loratadine	Alavert, Claritin	Second
Meclizine	Antivert, Bonine	First
Promethazine	Phenergan	First
Triplodine	Histex	First

Oral H-1 antihistamines that are available in the United States by classification as first (crosses blood–brain barrier) or second (does not significantly cross blood–brain barrier) generation. *While categorized as a second-generation antihistamine, cetirizine does cross the blood–brain barrier and can cause sedation in some patients, although less than would be expected for a true first-generation antihistamine.⁷⁰

Decongestants

Intranasal and oral decongestants cause vasoconstriction by stimulating adrenergic receptors, thereby decreasing inflammation and congestion.⁵⁶ Oxymetazoline is the commonly available intranasal decongestant. While highly effective in the very short term, it can lead to rebound congestion known as rhinitis medicamentosa if used consistently for more than just 3–5 consecutive days.¹⁴ Oxymetazoline is stronger and longer acting than the oral decongestants, although the effect of the oral decongestants can be prolonged with extended-release formulations.¹⁴ Common side effects include nasal dryness and sneezing.

Pseudoephedrine and phenylephrine are the oral decongestants in common use in the United States. Pseudoephedrine is a potent stimulant with effects on heart rate, appetite, and wakefulness, among others.⁵⁷ Attendant with these effects is its abuse potential. Phenylephrine is thought to have less abuse potential, as it has a less powerful stimulant effect when administered orally than pseudoephedrine, which also makes it less effective as a decongestant.⁵⁸ Oral decongestants may cause headache, hypertension, elevated intraocular pressure, tachycardia, insomnia, and urinary retention.⁵⁸

Although effective in reducing nasal congestion, decongestants are not effective treatments for OSA when used alone. The use of the intranasal decongestants xylometazoline and oxymetazoline resulted in small and clinically insignificant reductions in AHI.^59,60 The value of these medications, when used safely and intermittently, would be to improve tolerance of PAP therapy. However, no study has directly examined improvement in PAP tolerance or adherence due to intranasal decongestants. Some otolaryngologists use an oxymetazoline “trial” to help decide if surgical intervention would be helpful in improving PAP tolerance. The thought is that if pharmacologically reduced nasal erectile tissues improve PAP tolerance in the short term, surgical intervention could help in the long term.

Other pharmacologic options

Given the risks of decongestant use or overuse, providers may choose options with less risk, although with likely less immediate benefit as well. Intranasal cromolyn is a mast cell stabilizer. The reduction in histamine release from mast cell degranulation can reduce the congestion associated with allergic rhinitis. Cromolyn nasal sprays are available over-the-counter and have few side effects.⁶¹ Intranasal ipratropium is an anticholinergic nasal spray that is available by prescription. The efficacy and safety profile stacks up favorably with intranasal steroids.⁶² Ipratropium does not reduce nasal resistance (nasal congestion), but by reducing rhinorrhea it may improve CPAP tolerance. Finally, the oral leukotriene receptor antagonist montelukast has shown efficacy in reducing the symptoms of allergic rhinitis comparable to intranasal steroids.⁶³ Montelukast works by blocking type 1 cysteinyl-leukotriene receptors, thereby reducing bronchoconstriction, mucus production, and airway inflammation.⁶³ Each of these options could be attempted by sleep providers given their favorable safety profiles, but the impact of these medications on sleep has not been established.

Surgical options

Patients who fail to respond to conservative measures for chronic rhinitis with or without sinusitis within 6–12 weeks should be referred to otolaryngology for further evaluation.⁶⁴ However, if a nasal obstruction is identified that is not likely to be amenable to medical intervention, an earlier referral for a surgical evaluation would be indicated. Surgery is one of the pillars of CRS treatment, along with avoidance of triggers, medication, and allergy immunotherapy. Nasal obstruction is a common symptom of CRS and probably the factor that most contributes to difficulty with CPAP treatment. For example, nasal obstructions lead to struggles to use nasal CPAP due to mouth breathing, which causes oral leak with dry mouth and sore throat. For the patient with nasal obstruction and OSA, the primary goal of surgery is to change the physical structure of the nasal passage. The boundaries of the nasal passage are the nasal septum, the several nasal turbinates, the nasal floor, and the olfactory recess. Surgery addresses the nasal septum and the nasal turbinates—most commonly, the inferior turbinates. The inferior turbinate, shaped somewhat like the thumb, fluctuates in size dramatically. Its submucosal tissue is erectile tissue. The size normally varies during the day (referred to as the nasal cycle), but the inferior turbinates can enlarge enough to block the passage completely and bilaterally when triggered by allergic response and/or vasomotor autonomic dysregulation. Nasal septoplasty straightens and thins the nasal septum. Typically done under general anesthesia, the procedure is entirely intranasal, is well tolerated, and is low risk. Patients typically go home on the same day.

Inferior turbinate reduction has several techniques.⁶⁵ In-office techniques involve applying heat (radiofrequency energy) to the thumb-shaped structure’s submucosal tissue. Advantages include being office-based and requiring just topical and local anesthesia. Disadvantages include potential for prolonged healing (burn injury) and very unpredictable (poor) long-term success. Operating room techniques involve repositioning or removing part of the inferior turbinate, often using an instrument called a microdebrider, which is akin to a liposuction device. The submucosal erectile tissue is reduced through controlled volume reduction, leaving the thin bone intact and preserving the surface mucosa. Advantages include much more predictable long-term success, less risk of healing complication, and better reduction in nonobstructive symptoms. Disadvantages include the need for general anesthesia and a more challenging recovery due to silastic nasal splints that are often placed for 4–5 days after surgery. In certain cases, microdebrider turbinate reduction can be performed under local anesthesia as an outpatient procedure.

Surgery would also be needed for other fixed anatomic or structural problems, such as obstructive nasal polyps, intranasal synechiae or scar, or widened turbinates (eg, concha bullosa, medial inferior turbinate bone position). If such problems are found via anterior rhinoscopy or sinus computed tomography, an otolaryngologist can address these.

Inherent in CRS is sinus disease. Unlike surgical treatment of nasal obstruction, endoscopic sinus surgery, which can improve the symptoms of CRS, has not been shown to have a significant impact on the severity of OSA or on the sleep of patients with OSA and CRS.^66–68

Treatment summary

Sleep providers can provide initial care for CRS for patients on PAP therapy, particularly those who have prominent rhinitis, with the goal of improving PAP adherence and tolerability. Nasal saline lavage, intranasal steroids, and intranasal antihistamines are the foundations of therapy, with a much smaller role for oral antihistamines than might be assumed. There is limited evidence for improving PAP tolerance with intranasal mast cell stabilizers, intranasal anticholinergics, and oral leukotriene receptor antagonists as either adjunctive or single-agent therapies. With a very favorable safety profile for nasal steroids and nasal antihistamines, symptoms may be controlled without the need for further testing or more specialized care. However, some patients will not respond to any of the above therapies. At that time, a referral to an otolaryngologist or allergist/immunologist would be indicated to perform additional workup.

CONCLUSIONS

Chronic rhinosinusitis is a potential impediment to PAP therapy and possibly contributes to the development of OSA in the first place. The proper identification and management of CRS can improve PAP tolerance and adherence. There are many options for therapy, most of which are both safe and effective, and many of which are available over-the-counter. Sleep clinicians caring for patients with OSA should be familiar with these options to provide comprehensive care to their patients. They should not hesitate to refer to otolaryngologists or allergists/immunologists when screening questions or physical examination findings indicate or when initial therapies are not helpful.

DISCLOSURE STATEMENT

All authors have seen and approved the manuscript. The authors report no conflicts of interest.

ABBREVIATIONS

AHI

apnea-hypopnea index

CPAP

continuous positive airway pressure

CRS

chronic rhinosinusitis

OSA

obstructive sleep apnea

PAP

positive airway pressure