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You are here: HomePublic Comments and NominationsOpportunity for Public CommentDraft Recommendation Statement : Draft Recommendation Statement

Draft Recommendation Statement

Obstructive Sleep Apnea in Adults: Screening

This opportunity for public comment expired on July 11, 2016 at 8:00 PM EST

Note: This is a Draft Recommendation Statement. This draft is distributed solely for the purpose of receiving public input. It has not been disseminated otherwise by the USPSTF. The final Recommendation Statement will be developed after careful consideration of the feedback received and will include both the Research Plan and Evidence Review as a basis.

Recommendations made by the USPSTF are independent of the U.S. government. They should not be construed as an official position of the Agency for Healthcare Research and Quality or the U.S. Department of Health and Human Services.

Send Us Your Comments

In an effort to maintain a high level of transparency in our methods, we open our draft Recommendation Statements to a public comment period before we publish the final version.

Comment period is not open at this time.

Draft: Recommendation Summary

PopulationRecommendationGrade
(What's This?)
Asymptomatic adults

The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for obstructive sleep apnea (OSA) in asymptomatic adults.

I

Go to the Clinical Considerations section for suggestions for practice regarding the I statement.

Draft: Rationale

Importance

Based on older data, the estimated prevalence of OSA in the United States is 10% for mild OSA and 3.8% to 6.5% for moderate to severe OSA.1-3 Current prevalence may be higher due to rising rates of obesity.4, 5 The proportion of persons with OSA who are asymptomatic or have unrecognized symptoms is unknown. Obstructive sleep apnea is associated with increased all-cause mortality; however, the role OSA plays in increasing overall mortality, independent from other risk factors (age, body mass index [BMI], and other cardiovascular risk factors), is less clear.

Detection

Evidence on the use of screening questionnaires in asymptomatic adults to accurately identify which individuals will benefit from further testing for OSA is inadequate. The USPSTF identified this as a critical gap in the evidence.

Benefits of Early Detection and Intervention or Treatment

The USPSTF found inadequate direct evidence on the benefit of screening for OSA in asymptomatic populations. The USPSTF found no studies that evaluated the effect of screening for OSA on health outcomes. The USPSTF found at least adequate evidence that treatment with continuous positive airway pressure (CPAP) and mandibular advancement devices (MAD) can improve intermediate outcomes (e.g., the apnea–hypopnea index [AHI], Epworth Sleepiness Scale [ESS], and blood pressure) in populations referred for treatment. However, the applicability of this evidence to screen-detected populations is limited. The adequacy of the evidence varies based on the type of intervention and the reported intermediate outcomes. The USPSTF found inadequate evidence on the link between change in the intermediate outcome (AHI) and reduction in the health outcome (mortality). The USPSTF found evidence that treatment with CPAP can improve general and sleep-related quality of life in populations referred for treatment, but the applicability of this evidence to screen-detected populations is unknown. The USPSTF found inadequate evidence on whether treatment with CPAP or MAD improves other health outcomes (mortality, cognitive impairment, motor vehicle accidents, and cardiovascular or cerebrovascular events). The USPSTF also found inadequate evidence on the effect of treatment with various surgical procedures in improving intermediate or health outcomes.

Harms of Early Detection and Intervention or Treatment

The USPSTF found inadequate evidence on the direct harms of screening for OSA. The USPSTF found adequate evidence that the harms of treatment of OSA with CPAP and MAD are small. Reported harms include oral or nasal dryness; eye or skin irritation; rash; epistaxis; pain; excess salivation; and oral mucosal, dental, and jaw symptoms. The USPSTF found inadequate evidence on the harms of surgical treatment of OSA.

USPSTF Assessment

The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for OSA in asymptomatic adults. Evidence on screening tools to accurately detect persons who should receive further testing and treatment of subsequently diagnosed OSA to improve health outcomes in asymptomatic populations is lacking, and the balance of benefits and harms cannot be determined.

Draft: Clinical Considerations

Patient Population Under Consideration

This recommendation applies to asymptomatic adults (age 18 years and older) and adults with unrecognized symptoms of OSA. It does not apply to persons presenting with symptoms of or concerns about OSA, those who are being referred for evaluation or treatment of suspected OSA, or those who have acute conditions which could trigger the onset of OSA (e.g., stroke). It also does not apply to children, adolescents, or pregnant women.

Suggestions for Practice Regarding the I Statement

Potential Preventable Burden

Based on data from the 1990s, the estimated prevalence of OSA in the United States is 10% for mild OSA and 3.8% to 6.5% for moderate to severe OSA.1-3 Current prevalence may be higher due to rising rates of obesity.4, 5 Extrapolation from long-term followup data (from 1988–1994 to 2007–2010) from the Wisconsin Sleep Cohort Study results in an estimated prevalence of 16% for mild OSA and 10% for moderate to severe OSA.4 The prevalence of severe OSA in asymptomatic persons is unknown. In the Wisconsin Sleep Cohort Study, approximately 6% of adults with mild OSA progressed to moderate to severe OSA over 4 years.6

Risk factors associated with OSA include male sex, increasing age (from ages 40 to 70 years), postmenopausal status in women, higher BMI, and craniofacial and upper airway abnormalities. The evidence on other factors, such as smoking, alcohol and sedative use, and nasal congestion, is sparse or mixed.1

In theory, screening for OSA could improve mortality by identifying OSA early and providing treatment before it can adversely influence mortality. However, despite the observed association between severe AHI and increased mortality, no studies have demonstrated an improvement in mortality with treatment of OSA.

Although studies generally show that treatment of OSA with CPAP and MAD improves intermediate outcomes, such as AHI and ESS scores, there is a lack of studies demonstrating that change in AHI or ESS score improves health outcomes or mortality. In trials reviewed by the USPSTF, treatment with CPAP effectively reduced AHI to normal (<5) or near-normal (<10) levels. Treatment with MAD showed more modest improvements in AHI. Treatment with either CPAP or MAD improved ESS scores by approximately 2 points, and trials evaluating treatment with CPAP also found reductions in blood pressure. However, the clinical significance of these small reductions is unclear. Of note, trials that evaluated treatment with CPAP or MAD were primarily conducted in referral populations or patients of sleep clinics, not screen-detected patients from primary care settings.

Potential Harms

Direct evidence on the harms of screening for OSA is lacking. Commonly reported harms of treatment with CPAP include oral or nasal dryness, eye or skin irritation, rash, epistaxis, and pain.1 An estimated 14% to 32% of patients discontinue treatment with CPAP over 4 years.7 Commonly reported harms of treatment with MAD include oral mucosal, dental, or jaw symptoms. Less common harms include oral dryness and excess salivation. Limited study data suggest that 7% of patients discontinue treatment with MAD because of harms.1

Current Practice

Most primary care clinicians do not routinely screen for OSA.1 According to a practice-based research network study of 44 practices, only 20% of patients with sleep-related symptoms who regularly visit a primary care clinician spontaneously reported their symptoms to their primary care clinician.8 Some potential barriers to screening cited by providers include being unsure about how to identify and diagnose OSA, uncertainty regarding which type of sleep monitors are best for diagnosing OSA, and how to follow patients who have been diagnosed with OSA.1

Screening Tests

Potential screening questionnaires include the ESS, STOP Questionnaire, STOPBang Questionnaire, Berlin Questionnaire, and the Wisconsin Sleep Questionnaire. However, these tools have not been validated in a primary care setting.

Draft: Other Considerations

Research Needs and Gaps

The identification of valid and reliable clinical prediction tools that could accurately determine which asymptomatic persons (or persons with unrecognized symptoms) would benefit from further evaluation and testing for OSA is needed. In addition, studies that evaluate the effect of OSA treatments or interventions on health outcomes (e.g., all-cause and cardiovascular mortality, cardiovascular disease and cerebrovascular events, motor vehicle accidents, and cognitive impairment) that are adequately powered and have an appropriate length of followup are needed. Studies are also needed that evaluate whether improvement in AHI (for mild, moderate, and severe OSA) leads to improvement in health outcomes. These represent critical gaps in the current evidence base. The USPSTF has identified the need for further research on the effect of screening for OSA in asymptomatic persons from the general population on health outcomes, as well as the role of sleepiness in determining health outcomes. More data on the natural history of mild sleep apnea are also needed, in particular the rates of progression of mild to severe OSA, the length of duration before progression, and the magnitude of benefit if OSA is identified and treated earlier.

Draft: Discussion

Burden of Disease

Obstructive sleep apnea is the repeated collapse and obstruction of the upper airway during sleep, which results in reduced airflow (hypopnea) or complete airflow cessation (apnea), oxygen desaturation, and arousals from sleep.7 The severity of OSA can be categorized as mild, moderate, or severe based on the number of apnea and hypopnea events per hour (known as the AHI).1 An AHI of 5 to less than 15 is considered mild, 15 to less than 30 is considered moderate, and 30 or greater is considered severe. Obstructive sleep apnea syndrome (OSAS) is defined as having an AHI of 5 or greater with evidence of daytime sleepiness.

Reported estimates of OSA prevalence vary due to differing definitions of OSA, sampling bias, and year of study publication.9 A 2013 systematic review reported an estimated prevalence of 2% to 14% based on four community-based studies,10 while two U.S.-based studies conducted in the 1990s reported an estimated prevalence of 10% for mild OSA and 3.8% to 6.5% for moderate or severe OSA.1-3 Obstructive sleep apnea is more common in men than in women (odds ratio, 3.1 [95% CI, 2.5 to 3.8])10 and increases with age through the sixth and seventh decade and then plateaus.11-13 The prevalence difference between men and women narrows after menopause.2, 3, 12, 14 In both men and women, observational studies have found that the prevalence of OSA progressively increases as BMI increases. Using data from the Wisconsin Sleep Cohort Study, one study found that a 10% increase in weight was associated with a six-fold increase in risk of incident OSA over 4 years of followup.6

Patients with untreated, severe OSA have an increased risk of all-cause mortality. Based on prospective cohort studies, severe OSA has been found to be associated with a two-fold increased risk of all-cause mortality (hazard ratio, 2.07 [95% CI, 1.48 to 2.91]) and cardiovascular mortality (hazard ratio range, 2.87 to 5.9 [95% CI, 1.1–7.5 to 2.6–13.3).1 However, it is unclear whether OSA contributes to this increase in mortality independently, beyond the contributions of age, BMI, and other confounders.1 Other adverse outcomes have also been reported with OSA, such as increased risk of motor vehicle and other accidents; cognitive impairment; lost work days, work disability, and impaired work performance; and decreased quality of life.1

Scope of Review

The USPSTF commissioned a systematic review to evaluate the evidence on the accuracy, benefits, and potential harms of screening for OSA in asymptomatic adults seen in primary care, including those with unrecognized symptoms. The systematic review also evaluated the evidence on the benefits and harms of treatment of OSA on intermediate outcomes (e.g., change in AHI, sleepiness, and blood pressure) and health outcomes (e.g., mortality, quality of life, cardiovascular and cerebrovascular events, and cognitive impairment). The review focused on studies in adults age 18 years and older and excluded children, adolescents, and pregnant women.

Accuracy of Screening Tests

Several screening questionnaires and clinical prediction tools have been developed to identify persons who are at higher risk of sleep apnea. The USPSTF found evidence on two tools that have been evaluated in primary care or general populations (vs. referral populations): the Berlin Questionnaire and the Multivariable Apnea Prediction [MVAP] tool.1 The Berlin Questionnaire was evaluated in a single cross-sectional study that sampled Norwegian residents from the National Population Register; 16,302 participants completed the questionnaire and 518 went on to have polysomnography.15 Based on analyses that adjusted for oversampling of high-risk participants, the Berlin Questionnaire had a sensitivity of 37.2% (95% CI, 36.0% to 38.4%) and a specificity of 84% (95% CI, 83.2% to 84.7%) when using an AHI cutpoint of 5 or greater. Using an AHI cutpoint of 15 or greater, the Berlin Questionnaire had a sensitivity of 43% (95% CI, 41.2% to 44.8%) and a specificity of 79.7% (95% CI, 79.0% to 80.5%).1, 15 Overall, the study found poor accuracy. In addition, this is a single study that has not been externally validated, and it was found to have moderate risk of bias due to missing data, attrition bias, and spectrum bias. Two studies evaluated the MVAP in primary care settings. Although both studies were published by the same research group from Philadelphia, one study was conducted in Medicare patients who had daytime sleepiness (n=452),16 while the other was conducted in patients with hypertension visiting internal medicine practices (a Department of Veterans Affairs medical center system and a university-based hypertension clinic) (n=250).17 Among the Medicare patients with daytime sleepiness, the MVAP had a sensitivity of 90.0% and a specificity of 64.4% to predict severe OSAS (defined in the study as an AHI of >30 and ESS score of >10).16 Among patients with hypertension, the MVAP had a sensitivity of 91.5% and a specificity of 43.9% to predict severe OSAS.17 When unattended, in-home portable monitor testing was added, the sensitivity and specificity of the MVAP to predict severe OSAS increased to 90.9% and 75.7%, respectively,16 in the study of Medicare patients, while sensitivity decreased to 88.2% and specificity increased to 71.6% in the study of patients with hypertension.17 The two studies that evaluated the MVAP were both conducted in populations that had a high prevalence of OSAS (and thus were more likely to be symptomatic) and had a high risk of spectrum bias.

The USPSTF also evaluated the evidence on the accuracy of diagnostic tests for OSA. In particular, it evaluated the evidence on the various types of portable monitors to diagnose OSA compared to polysomnography. Evidence was obtained from two systematic reviews and 19 additional studies.1 Most studies evaluated type III and type IV portable monitors. The USPSTF reviewed evidence from three studies (n=160) on type II portable monitors, 21 studies (n=1,645) on type III portable monitors, and 84 studies (n=8,773) on type IV portable monitors.1 None of the studies were conducted in screen-detected populations, and most were conducted in referral populations being evaluated for suspected OSA. Studies were conducted in a variety of settings (home or laboratory) and used a variety of AHI cutpoints, which were not always well reported.1 The overall quality of evidence on type II and type IV portable monitors was found to be fair, while the overall quality of evidence on type III portable monitors was found to be good. A broad range of sensitivity and specificity was reported across multiple AHI cutpoints. Generally, studies on type II and type III portable monitors reported moderate to high sensitivity and specificity, while the reported sensitivity and specificity of type IV portable monitors was highly variable and inconsistent (see Table 5 of the full evidence report1). Overall, consistent with findings from other systematic reviews, it is believed that type III and type IV portable monitors are generally accurate in diagnosing OSA, but have a wide and variable bias in estimating actual AHI7, 18 in patients being evaluated for suspected OSA. It is unclear how these portable monitors would perform in asymptomatic, screen-detected persons.

Effectiveness of Early Detection and Treatment

The USPSTF found no studies that directly evaluated the effect of screening for OSA on final health outcomes, such as mortality, quality of life, and cardiovascular and cerebrovascular events. The USPSTF did identify and review studies on the effect of treatment on intermediate outcomes (e.g., AHI, ESS score, and blood pressure) and final health outcomes.

The USPSTF reviewed evidence from 76 good- or fair-quality treatment trials that described the effect of various interventions on intermediate outcomes, including AHI, ESS score, and blood pressure.1 The most evidence was available on CPAP and found that compared to sham intervention, CPAP reduced AHI (weighted mean difference [WMD], -33.8 [95% CI, -42.0 to -25.6]; k=13; n=543), ESS score (WMD, -2.0 [95% CI, -2.6 to -1.4]; k=22; n=2,721), and blood pressure (diurnal systolic blood pressure decreased by a WMD of -2.4 [95% CI, -3.9 to -0.9] and diurnal diastolic blood pressure decreased by a WMD of -1.3 [95% CI, -2.2 to -0.4]; k=15; n=1,190).1 Less evidence was available on the effect of treatment with MAD on intermediate outcomes. Meta-analyses found that compared to sham intervention, MAD reduced AHI (WMD, -12.6 [95% CI, -15.5 to -9.7]; k=6; n=307) and ESS score (WMD, -1.5 [95% CI, -2.8 to -0.2]; k=5; n=267); no statistically significant decrease in blood pressure was found. Five studies evaluated treatment with upper airway surgery; each evaluated a different surgical technique. Findings on AHI were inconsistent, and no statistically significant improvements in ESS score or blood pressure were found. Although studies generally showed that treatment with CPAP reduced AHI to near-normal levels, they found more modest reductions with MAD, and the clinical significance of the small reductions in ESS score and blood pressure is uncertain. Further, given that most of the trials were conducted in referred patients or patients of sleep clinics, the applicability of this evidence to a screen-detected population is limited.

The USPSTF reviewed evidence from 50 fair- or good-quality trials that evaluated the effect of various treatments or interventions on health outcomes.1 The most evidence was available on CPAP; however, the USPSTF found the evidence on most outcomes to be inadequate due to short length of followup and underpowered studies (i.e., too few events observed). Thirty-one trials (n=2,673) reported on the effect of treatment with CPAP on mortality; most (29/31) trials followed participants for only 12 weeks or less, and most (27/31) trials reported no deaths in either study group.1 Twelve trials reported on cognitive function; however, they used heterogeneous outcome measures, which made comparison difficult, and results were generally inconsistent. Five trials (n=1,529) reported on incidence of myocardial infarction. Most trials (4/5) followed participants for less than 1 year and when combined, only reported one death in the control group. Few trials reported on motor vehicle accidents, cerebrovascular events, or heart failure.1 Limited evidence was available on general and sleep-related quality of life. Small but statistically significant improvements in quality of life scores were seen, but the clinical significance of these improvements is unclear. Importantly, given the characteristics of included study participants (participants were from sleep clinics or referral populations, and were largely symptomatic, with sleepiness and more severe OSA), the applicability of this evidence to an asymptomatic, screen-detected population is questionable. Few studies reported on the effect of treatment with MAD (k=6; n=510) or upper airway surgery (k=4; n=187) on any health outcomes.

Despite the consistent observational findings of an association between severe OSA and increased mortality, the USPSTF identified no studies that reported on change in AHI and associated change in mortality. Thus, it is unclear whether treatments that improve AHI would also improve mortality.

Potential Harms of Screening and Treatment

The USPSTF identified no studies that directly evaluated the harms of screening for OSA. A subset of studies that evaluated the effectiveness of various OSA treatments also reported on harms of treatment. Nine studies (n=1,759) reported on harms of treatment with CPAP. Followup in these studies was generally from 8 to 12 weeks, and most participants were men, with a mean age range of 42 to 61 years and with overweight or obesity (mean BMI, 27 to 39 kg/m2). Overall, 2% to 47% of trial participants reported any adverse effects from treatment with CPAP, including oral or nasal dryness, eye or skin irritation, rash, epistaxis, and pain.1 Eight trials (n=443) reported on harms of treatment with MAD. Followup in these studies was generally from 4 to 6 weeks. In seven trials, 17% to 74% of participants reported oral mucosal, dental, or jaw symptoms compared to 0% to 17% of participants in comparator groups. In four studies, 5% to 33% of participants reported oral dryness compared to 0% to 3% in control groups, and in three studies, 23% to 68% of participants reported excessive salivation compared to 0% to 3% in comparator groups.1 Four trials (n=205) reported harms of treatment with upper airway surgery; 1% to 81% of participants reported any harms, which included pain, postoperative bleeding, difficulty speaking and swallowing, change in vocal quality, hematomas, ulcerations, infections, and temporary nasal regurgitation.1

Estimate of Magnitude of Net Benefit

Overall, the USPSTF found insufficient evidence on screening for OSA in asymptomatic adults or adults with unrecognized symptoms. No studies directly evaluated the benefits or harms of screening for OSA. Few studies evaluated the accuracy of specific screening tools to identify individuals at high risk for OSA who could benefit from further testing. Although numerous studies evaluated the effectiveness of treatment with CPAP or MAD to improve intermediate outcomes (e.g., AHI, ESS score, or blood pressure) in patients already receiving care or referred for care at a sleep clinic, the clinical significance of these changes and the applicability of this evidence to asymptomatic, screen-detected populations are unclear. Further, evidence is insufficient to determine whether treatment of screen-detected, asymptomatic or unrecognized OSA improves final health outcomes (e.g., mortality or cardiovascular events) or whether improving intermediate outcomes (e.g., AHI or ESS score) would improve these final health outcomes. Studies that evaluated the effect of treatment with CPAP or MAD on mortality were either underpowered or of too short duration to detect a difference between treated and untreated groups, and no studies reported on whether change in AHI or ESS score affects mortality. Fewer studies reported on the harms of treatment. Overall, the USPSTF was unable to determine the magnitude of the benefits or harms of screening for OSA and whether there is a net benefit or harm to screening in asymptomatic adults or adults with unrecognized symptoms.

How Does Evidence Fit With Biological Understanding?

According to observational studies, severe, untreated OSA has been found to be associated with an increased risk of all-cause and cardiovascular mortality.1 Other adverse outcomes that have been reported include increased risk of motor vehicle and other accidents; cognitive impairment; lost work days, work disability, and impaired work performance; and decreased quality of life.1 However, it is unclear what role OSA plays in causing these adverse outcomes, independent from other associated factors such as obesity, increased age, hypertension, and general lifestyle. One hypothesis is that OSA leads to chronic disturbances in gas exchange, sympathetic nervous system arousal, and fragmented sleep.1, 7

Draft: Recommendations of Others

The American College of Physicians recommends conducting a sleep study for patients with unexplained daytime sleepiness (grade: weak recommendation, low-quality evidence). It also recommends polysomnography for diagnostic testing in patients with suspected OSA. For patients without serious comorbid conditions, portable sleep monitors are recommended when polysomnography is not available (grade: weak recommendation, moderate-quality evidence).19 The American Academy of Sleep Medicine recommends that routine health maintenance evaluations include questions about OSA and evaluation for risk factors (obesity, retrognathia, and hypertension). Positive findings should trigger a comprehensive sleep evaluation.20 According to the National Institute for Health and Care Excellence, moderate to severe obstructive sleep apnea/hypopnea syndrome can be diagnosed from patient history and a sleep study using oximetry or other monitoring devices conducted in the patient’s home. In some cases, further studies that monitor additional physiological variables in a sleep laboratory or at home may be required, especially when alternative diagnoses are being considered.21

Send Us Your Comments

In an effort to maintain a high level of transparency in our methods, we open our draft Recommendation Statements to a public comment period before we publish the final version.

Comment period is not open at this time.

References:

1. Jonas DE, Amick HR, Feltner C, Weber RP, Arvanitis M, Stine A, et al. Screening for Obstructive Sleep Apnea in Adults: An Evidence Review for the U.S. Preventive Services Task Force. Evidence Synthesis No 146. AHRQ Publication No. 14-05216-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2016.
2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-5.
3. Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Leiby BE, Vela-Bueno A, Kales A. Association of hypertension and sleep disordered breathing. Arch Intern Med. 2000;160(15):2289-95.
4. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177(9):1006-14.
5. Young T, Palta M, Dempsey J, Peppard PE, Nieto FJ, Hla KM. Burden of sleep apnea: rationale, design and major findings of the Wisconsin Sleep Cohort study. WMJ. 2009;108(5):246-9.
6. Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284(23):3015-21.
7. Balk EM, Moorthy D, Obadan NO, Patel K, Ip S, Chung M, et al. Diagnosis and Treatment of Obstructive Sleep Apnea in Adults. Comparative Effectiveness Review No. 32.Report No. 11-EHC052. Rockville, MD: Agency for Healthcare Research and Quality; 2011.
8. Mold JW, Quattlebaum C, Schinnere E, Boeckman L, Orr W, Hollabaugh K. Identification by primary care clinicians of patients with obstructive sleep apnea: a practice-based research network (PBRN) study. J Am Board Fam Med. 2011;24(2):138-45.
9. Caples SM, Gami AS, Somers VK. Obstructive sleep apnea. Ann Intern Med. 2005;142(3):187-97.
10. Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea? The Rational Clinical Examination systematic review. JAMA. 2013;310(7):731-41.
11. Young T, Shahar E, Nieto FJ, Redline S, Newman AB, Gottlieb DJ, et al; Sleep Heart Health Study Research Group. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med. 2002;162(8):893-900.
12. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A. Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med. 1998;157(1):144-8.
13. Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Rein J, Vela-Bueno A, Kales A. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med. 2001;163(3 Pt 1):608-13.
14. Young T, Skatrud J, Peppard PE. Risk factors of obstructive sleep apnea in adults. JAMA. 2004;291(16):2013-6.
15. Hrubos-Strøm H, Randby A, Namtvedt SK, Kristiansen HA, Einvik G, Benth J, et al. A Norwegian population-based study on the risk and prevalence of obstructive sleep apnea. The Akershus Sleep Apnea Project (ASAP). J Sleep Res. 2011;20(1 Pt 2):162-70.
16. Morales CR, Hurley S, Wick LC, Staley B, Pack FM, Gooneratne NS, et al. In-home, self-assembled sleep studies are useful in diagnosing sleep apnea in the elderly. Sleep. 2012;35(11):1491-501.
17. Gurubhagavatula I, Fields BG, Morales CR, Hurley S, Pien GW, Wick LC, et al. Screening for severe obstructive sleep apnea syndrome in hypertensive outpatients. J Clin Hypertens (Greenwich). 2013;15(4):279-88.
18. Qaseem A, Holty JE, Owens DK, Dallas P, Starkey M, Shekelle P; Clinical Guidelines Committee of the American College of Physicians. Management of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2013;159(7):471-83.
19. Qaseem A, Dallas P, Owens DK, Starkey M, Holty JE, Shekelle P; Clinical Guidelines Committee of the American College of Physicians. Diagnosis of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014;161(3):210-20.
20. Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263-76.
21. National Institute for Health and Care Excellence. NICE Technology Appraisal Guidance 139: Continuous Positive Airway Pressure for the Treatment of Obstructive Sleep Apnoea/Hypopnoea Syndrome. London: National Institute for Health and Care Excellence; 2008.

Current as of: June 2016

Internet Citation: Draft Recommendation Statement: Obstructive Sleep Apnea in Adults: Screening. U.S. Preventive Services Task Force. June 2016.
https://www.uspreventiveservicestaskforce.org/Page/Document/draft-recommendation-statement166/obstructive-sleep-apnea-in-adults-screening

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