Nasal polyposis is a risk factor for nonadherence to CPAP treatment in sleep apnea: the population-based DISCOVERY study
ABSTRACT
Study Objectives:
The aim was to evaluate nasal polyposis as a risk factor for nonadherence to continuous positive airway pressure (CPAP) treatment in patients with obstructive sleep apnea (OSA).
Methods:
This was a population-based, longitudinal analysis of patients starting CPAP treatment for OSA in the Swedish quality registry Swedevox between 2010 and 2018. Data were cross-linked with national registries. The impact of nasal polyposis on CPAP adherence was analyzed using uni- and multivariable logistic and linear regression models. Relevant confounders (age, sex, usage of nasal and oral steroids) were identified using a direct acyclic graph.
Results:
Of 20,521 patients with OSA on CPAP treatment (29.5% females), 331 (1.6%) had a diagnosis of nasal polyposis at baseline. At the 1-year follow-up, nasal polyposis was associated with an increased risk of CPAP usage < 4 hours/night (unadjusted odds ratio [OR] 1.21; 95% confidence interval [CI] 0.95–1.55); adjusted OR 1.38; 95% CI 1.08–1.77). In this group, unadjusted nocturnal mean CPAP usage was 15.4 minutes (95% CI −31.62 to 0.83) shorter and was an adjusted 24.1 minutes (95% CI −40.6 to −7.7) shorter compared with patients with OSA without nasal polyposis.
Conclusions:
Nasal polyposis is associated with reduced CPAP usage per night. These results highlight the importance of diagnosing nasal polyposis in patients with OSA before the start of CPAP treatment. Treatment of the condition may improve adherence, efficacy, and patient outcomes.
Citation:
Bengtsson C, Grote L, Ljunggren M, Ekström M, Palm A. Nasal polyposis is a risk factor for nonadherence to CPAP treatment in sleep apnea: the population-based DISCOVERY study. J Clin Sleep Med. 2023;19(3):573–579.
BRIEF SUMMARY
Current Knowledge/Study Rationale: Nasal obstruction has been associated with negative outcomes of continuous positive airway pressure (CPAP) treatment in patients with obstructive sleep apnea (OSA). CPAP adherence in patients with OSA and nasal polyposis, of which nasal obstruction is a main symptom, has not been previously investigated prospectively.
Study Impact: This first population-based, longitudinal, cohort study of nasal polyposis and CPAP adherence in patients with OSA adds new knowledge to the field of research regarding nasal obstruction and CPAP adherence. Our results underline the importance of investigating nasal symptoms and treating nasal polyposis in patients with OSA before the start of CPAP treatment, since it may improve CPAP adherence, efficacy, and patient outcomes.
INTRODUCTION
The main treatment worldwide for moderate to severe obstructive sleep apnea (OSA) is nasal continuous positive airway pressure (CPAP). Despite the efficacy of CPAP in reducing associated symptoms and diseases, adherence rates are poor.1 Nonadherence to CPAP treatment, defined as a nocturnal CPAP usage < 4 hours, varies between 29% and 83% in different populations.2 Many predictors for CPAP adherence have been explored and analysis in our population-based study identified sex, age, OSA severity, degree of daytime sleepiness, socioeconomic status, and use of a humidifier as strong predictors for CPAP adherence.3
Nasal obstruction has been identified as a main cause of CPAP nonadherence.4–8 However, the number of prospective studies investigating nasal obstruction and specific nasal diseases and their impact on CPAP adherence is limited. Only a few randomized controlled trials studied the positive effect of anti-obstructive nasal surgery on CPAP outcomes.9 Further investigations exploring this relationship are needed, as 35% of patients with OSA report nasal obstruction10 and have a significant sinonasal disease burden.4 Consequently, a large group of patients with OSA may be at risk of CPAP treatment failure due to sinonasal conditions, increasing the risk for adverse long-term health consequences.4,11
An important cause of nasal obstruction in patients with OSA is nasal polyposis, which affects approximately 2–4% of the general population.12,13 Nasal polyposis is a chronic inflammatory disease of the nasal mucosa, with nasal obstruction as a cardinal symptom of the disease. Since nasal polyposis is a treatable condition, further studies are needed. Therefore, the aim of the present study was to investigate if nasal polyposis is a predictor of nonadherence to CPAP treatment in patients with OSA. We also aimed to analyze the prevalence of nasal polyposis and its association with OSA disease characteristics. The “Course of DISease in patients reported to the Swedish CPAP Oxygen and VEntilator RegistrY” (DISCOVERY) study cohort, including data from the nationwide, population-based Swedish quality register Swedevox, was used to study our aims in more than 20,000 patients with OSA on CPAP treatment.14
METHODS
Study design and study population
This population-based longitudinal cohort study included patients aged ≥ 16 years starting CPAP for OSA treatment between July 1, 2010, and March 12, 2018, in the DISCOVERY database.14 In short, the DISCOVERY database cross-linked data on patients reported to the Swedish National Respiratory Failure Registry, Swedevox,15 with several national quality and governmental registries. Patients with follow-up data on adherence at the scheduled 1-year follow-up visit were included in the study (n = 20,521) (Figure 1, flowchart).
CPAP = continuous positive airway pressure.
Variables
At initiation of CPAP treatment at baseline, data on age, sex, body mass index, apnea-hypopnea index (AHI), oxygen desaturation index, Epworth Sleepiness Scale (ESS) score, and the usage of a humidifier were collected.
Data on medications at baseline were retrieved from the Swedish Prescribed Drug Registry with data of all dispensed outpatient drug prescriptions since July 2005 using Anatomical Therapeutic Chemical codes (nasal corticosteroids [NCS] R01AD, oral corticosteroids H02AB).16 Diagnoses at baseline of nasal polyposis and comorbidities were retrieved from the National Patient Registry with information about admissions to public hospitals since 1987 and outpatient hospital-based visits since 2001 using International Classification of Diseases, 10th Revision, codes (nasal polyposis [J33], asthma [J45], rheumatic disease [M05–08], cardiovascular disease [I00–99], and diabetes mellitus [E10–14]).17,18 Data on highest completed educational level (≥ 13 years, 10–12 years, ≤ 9 years) at baseline was retrieved from Statistics Sweden.19
At the 1-year follow-up, ESS and use of CPAP treatment were analyzed. Objective data on usage time were collected from the CPAP memory card and registered in Swedevox. The widely used limit of nonadherence of < 4 hours was used for comparability.
Ethical consideration
Patients are informed about the registration in the Swedevox database during their clinical visit at the respective sleep center. According to Swedish law, no written informed consent is required for registration in the national quality registries. The study protocol was approved by the Ethics Committee at the Medical Faculty at Lund University and the Swedish Ethical Review Authority, diary number 2018/51, 2019/01420 and 2021/04984, which waived individual consent due to the use of registry data.
Statistical analyses
Differences between groups were analyzed with chi-square test for categorical variables and unpaired t test for normally distributed continuous variables. The association between nasal polyposis and nocturnal CPAP usage as a continuous variable was analyzed using linear regression models with the estimates (β-coefficients) quantified in minutes to make the results interpretable to a clinical context. Nocturnal CPAP nonadherence was also dichotomized as < 4 hours/night and was analyzed using logistic regression. Confounders to adjust for in the regression models were based on subject matter knowledge and using a direct acyclic graph (DAG) (Figure 2) created by DAGitty (Johannes Textor, Tumour Immunology Lab and Institute for Computing and Information Sciences, Radboud University, Nijmegen, the Netherlands).20 Identified confounders adjusted for in the multivariable regression models were age, sex, and nasal and oral steroids. A 2-sided P value < .05 was considered to be statistically significant. Statistical analyses were conducted using the software packages Stata, version 16.0 (StataCorp LP, College Station, TX, USA).
Red dots indicate the minimal sufficient adjustment set for estimating the total effect of nasal polyposis on adherence to CPAP. Green arrows: causal path. Red arrows: biasing path. AHI = apnea-hypopnea index, BMI = body mass index, CPAP = continuous positive airway pressure, ESS = Epworth Sleepiness Scale.
RESULTS
Patient characteristics
The study population consisted of 20,521 patients (29.5% females) of whom 331 (1.6%) had been diagnosed with nasal polyposis. Patients with nasal polyposis were more often men, were slightly older, and had a lower body mass index compared with those without nasal polyposis (Table 1). Asthma was more prevalent among those with nasal polyposis, whereas other comorbidities did not differ between the groups, nor did educational level. Use of both nasal and oral steroids was more common in the group with nasal polyposis, as was nasal polyp surgery.
| Variable | No Nasal Polyposis (n = 20,190) | Nasal Polyposis (n = 331) |
|---|---|---|
| Age at therapy start, y | 57.7 ± 12.2 | 60.9 ± 11.1 |
| Sex, male | 14,226 (70.5) | 275 (83.1) |
| Body mass index, kg/m2 | 32.1 ± 6.2 | 30.3 ± 5.1 |
| Asthma | 765 (3.8) | 50 (15.1) |
| Rheumatic disease | 249 (1.2) | 4 (1.2) |
| Cardiovascular disease | 7,964 (39.4) | 128 (38.7) |
| Diabetes | 2,104 (10.4) | 33 (10.0) |
| Regular intake of nasal steroids | 2,649 (13.1) | 196 (59.2) |
| Regular intake of oral steroids | 1,391 (6.9) | 60 (18.1) |
| Nasal polyp surgery | 11 (0.1) | 25 (7.6) |
| Educational level | ||
| ≥13 years | 5,099 (26.2) | 69 (22.0) |
| 10–12 years | 10,058 (51.7) | 163 (51.9) |
| ≤9 years | 4,312 (22.1) | 82 (26.1) |
The severity of OSA, based on commonly used AHI cutoffs, did not differ between groups, but the mean AHI and oxygen desaturation index were significantly and slightly lower among those with nasal polyposis. At the 1-year follow-up there was no difference between the groups in delta ESS (the difference between the follow-up and baseline score), mean CPAP use, or in the proportion of patients adherent to CPAP ≥ 4 hours per night (Table 2).
| Variable | No Nasal Polyposis (n = 20,190) | Nasal Polyposis (n = 331) | P |
|---|---|---|---|
| Baseline | |||
| AHI, events/h | 37.0 ± 22.1 | 34.3 ± 20.3 | .03 |
| AHI categories (events/h) | .30 | ||
| <5 | 198 (1.0) | 4 (1.2) | |
| 5 to < 15 | 2,452 (12.3) | 39 (11.9) | |
| 15 to < 30 | 6,170 (31.0) | 117 (35.7) | |
| ≥30 | 11,084 (55.7) | 168 (51.2) | |
| ODI, events/h | 34.4 ± 22.2 | 31.6 ± 21.1 | .02 |
| Humidifier at initiation of | |||
| CPAP treatment | 9,851 (49.2) | 177 (53.8) | .10 |
| ESS, score | 10.4 ± 5.0 | 9.9 ± 4.6 | .09 |
| Follow-up data | |||
| Delta ESS, score | 4.5 ± 4.8 | 4.6 ± 4.7 | .74 |
| CPAP use (mean h/night) | 5.2 ± 2.5 | 4.9 ± 2.6 | .06 |
| Proportion of patients adherent ≥ 4 h/night | 15,273 (75.7) | 238 (71.90) | .12 |
Nasal polyposis and adherence
In the unadjusted logistic regression analysis, no association was found between nasal polyposis and nonadherence to CPAP (< 4 hours/night). However, after adjusting for confounders, nasal polyposis was associated with an increased risk of nonadherence to CPAP at follow-up (odds ratio [OR] 1.38; 95% confidence interval [CI] 1.08–1.77) (Table 3). CPAP usage measured continuously in minutes tended to be lower in the unadjusted linear regression analysis and was significantly reduced by 24.1 minutes (95% CI –40.6 to –7.7) in the fully adjusted model (Table 4). A sensitivity analysis was performed including both AHI at baseline and an asthma diagnosis at baseline, and our results remained significant with an increased risk of nonadherence to CPAP at follow-up (OR 1.32; 95% CI 1.03–1.70), and CPAP usage was significantly reduced by 21.0 minutes (95% CI –37.4 to –4.7).
| Variable | Unadjusted Odds Ratio | Adjusted Odds Ratio* |
|---|---|---|
| Nasal polyposis | 1.21 (0.95–1.55) | 1.38 (1.08–1.77) |
| Age (years) | ||
| 30 to < 45 | 0.95 (0.76–1.20) | 0.95 (0.76–1.20) |
| 45 to < 60 | 0.80 (0.64–0.99) | 0.78 (0.63–0.98) |
| >60 | 0.65 (0.52–0.80) | 0.62 (0.50–0.77) |
| Female sex | 0.92 (0.86–0.98) | 0.88 (0.82–0.94) |
| Nasal steroids | 0.87 (0.79–0.96) | 0.83 (0.75–0.91) |
| Oral steroids | 1.11 (0.98–1.25) | 1.16 (1.03–1.32) |
| Variable | Unadjusted | Adjusted* |
|---|---|---|
| Nasal polyposis | −15.40 (−31.62 to 0.83) | −24.11 (−40.56 to −7.66) |
| Age (years) | ||
| 30 to < 45 | −6.28 (−21.94 to 9.37) | −6.33 (−21.98 to 9.31) |
| 45 to < 60 | 9.67 (−5.25 to 24.59) | 10.16 (−4.76 to 25.09) |
| >60 | 27.65 (12.82 to 42.49) | 28.83 (13.98 to 43.69) |
| Female sex | −1.09 (−5.58 to 3.40) | 2.44 (−2.07 to 6.96) |
| Nasal steroids | 9.13 (3.22 to 15.05) | 11.97 (5.97 to 17.97) |
| Oral steroids | −0.96 (−8.93 to 7.02) | −4.99 (−12.99 to 3.02) |
DISCUSSION
The main finding of the present study was that the diagnosis of nasal polyposis at the start of CPAP treatment is associated with reduced CPAP usage and was identified as a significant predictor of nonadherence to CPAP after 1 year. This large, population-based, longitudinal study of nasal polyposis and CPAP outcomes provides strong evidence for the role of nasal obstruction in CPAP adherence. One potential explanation of our findings may include that smaller nasal dimensions and high nasal resistance, as measured by acoustic rhinometry, rhinomanometry, and peak nasal inspiratory flow, predict poor CPAP adherence according to earlier reports.4–7 This effect increases the risk for discontinuation of therapy soon after CPAP initiation.8 Nasal polyposis obstructs the nasal cavities and reduces nasal patency.21 Indeed, an experimental study of nasal polyposis and CPAP exposure for 2 hours found that CPAP worsened nasal patency, as measured by peak nasal inspiratory flow.22 A further finding that supports our results is that chronic rhinosinusitis, which often includes nasal polyposis, has been found to impair self-reported sleep quality in population-based studies, which, in turn, may contribute to difficulties in adhering to CPAP treatment.23,24
Nasal polyposis and asthma are known comorbidities,25 and asthma is associated with insomnia symptoms and nasal congestion.26 In the present study, comorbid asthma was more frequent in patients with nasal polyposis compared with patients without nasal polyposis. It is therefore likely that a diagnosis of asthma at baseline may have influenced CPAP adherence in the present study. Furthermore, the combination of insomnia and sleep apnea (COMISA) has been reported to negatively influence CPAP adherence.27 Unfortunately, our data do not allow for a COMISA classification in the study population. There was also a significant difference in AHI at baseline between those with and without nasal polyposis. It is known that disease severity of OSA defined by AHI affects CPAP adherence.15 When exploring the relationship between nasal polyposis, asthma, AHI, and CPAP adherence using our DAGitty model, asthma and AHI were not found to be confounding factors. However, a sensitivity analysis including both asthma and AHI at baseline did not change the significance of our results. The clinical relevance of the difference in AHI is also considered minor and should not have a decisive effect on our results.
The prevalence of nasal polyposis in the study was 1.6%, which is slightly lower compared with findings in the general population in previous studies of 2–4%.12,13 In Sweden, nasal polyposis is diagnosed and treated by both otorhinolaryngologists in private care and by specialists in public hospitals, but only in- and outpatient contacts at public hospitals are reported to the National Patient Registry. In addition, nasal endoscopy is not routinely performed on patients with OSA before the start of CPAP treatment in Sweden and nasal polyposis can be asymptomatic to a certain extent. Consequently, nasal polyposis in patients with OSA in our cohort may be undiagnosed at the start of CPAP treatment and the true effect of nasal polyposis on CPAP adherence may be underestimated in our study.
A strength of the present study is the longitudinal study design using a large, national, multicentric database including almost 80% of all CPAP cases in Sweden, which increases the generalizability of our findings. Further strengths include the high degree of external and internal validity of the registry data compared against medical records together with the link of our sleep apnea data to multiple nationwide registries with socioeconomic and drug prescription data.28
Some limitations need to be considered. Information on cigarette smoking was not available. Cigarette smoking is a potential confounder of the present study, since it has been associated with a negative impact on both objective and self-reported/subjective nasal function29,30 and may also affect sleep quality31 and CPAP adherence negatively.32 However, according to the Swedish Sleep Apnea Registry (SESAR), only 9–10% of CPAP users are smokers,33 and it is therefore most likely that smoking would have had only limited impact on our current findings.
The clinical relevance of our study is significant as we can clearly show that nasal polyposis, a treatable condition, has a significant impact on overall CPAP outcomes. For instance, we show that nasal polyposis reduces CPAP adherence by almost half an hour and increases the risk for CPAP failure by almost 40%. These numbers need to be considered as highly clinically relevant. For instance, in the recent meta-analysis of CPAP treatment performed by the American Academy of Sleep Medicine, educational intervention was advocated as standard of care for CPAP follow-up procedures due to its positive impact on CPAP adherence in the order of 33 minutes/day.34 Interestingly, the newly published national guidelines for the diagnosis of sleep apnea in Sweden recommend inspection of the upper airways including nose, pharynx, and oral cavity as a routine procedure in all patients referred for the evaluation of suspected sleep apnea.35 This recommendation is highly supported by our study findings.
CONCLUSIONS
This first population-based cohort study of nasal polyposis and CPAP adherence adds new knowledge to the field of research regarding nasal obstruction and CPAP adherence. We conclude that nasal polyposis is a risk factor for nonadherence to CPAP and it reduces the average time of CPAP usage per night. Clinically, our results underline the importance of investigating nasal symptoms in general, and nasal polyposis in particular, in patients with OSA before the start of CPAP treatment. Treatment of nasal polyposis may improve CPAP adherence, efficacy, and patient outcomes.
DISCLOSURE STATEMENT
All authors have seen and approved the manuscript. Work for this study was performed at the Department of Surgical Sciences, Otorhinolaryngology, Head and Neck Surgery, Uppsala University; Department of Medical Sciences, Respiratory, Allergy and Sleep Research, Uppsala University; and Centre for Research and Development, Region of Gävleborg/Uppsala University, Gävle Hospital. Caroline Bengtsson was supported by the Bror Hjerpstedt’s Foundation. Andreas Palm was supported by the Swedish Society for Sleep Research and Sleep Medicine, Uppsala-Örebro Regional Research Council (log number RFR-931234); Centre for Research and Development, Uppsala University/Region Gävleborg (log number CFUG-925881); Bror Hjerpstedt’s Foundation, Uppsala County Association against Heart and Lung Diseases; and the Fagerström Foundation. Ludger Grote was supported by the Swedish Heart and Lung Foundation (number 2018-567) and the agreement concerning research and education of doctors (ALFGBG-725601). Magnus Ekström was supported by unrestricted grants from the Swedish Society for Medical Research and the Swedish Research Council (log number 2019-02081). The sponsors had no roles in study design, data collection, data analysis, data interpretation, or writing of the report. Outside the submitted work, Ludger Grote reports nonfinancial research support from Itamar Medical and Resmed, research grant and clinical trial support from Desitin, and speaker bureau activities for Itamar Medical, Resmed, Philips, AstraZeneca, and Breas. In addition, Ludger Grote reports ownership in a licensed patent on sleep apnea therapy. The authors report no conflicts of interest.
ABBREVIATIONS
| AHI | apnea-hypopnea index |
| CI | confidence interval |
| CPAP | continuous positive airway pressure |
| ESS | Epworth Sleepiness Scale |
| OR | odds ratio |
| OSA | obstructive sleep apnea |
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