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.
The current prevalence of obstructive sleep apnea (OSA) in the United States is not well established; however, based on cohort and survey data, the estimated prevalence of moderate to severe OSA (defined as an apnea-hypopnea index [AHI] ≥15) among adults ages 30 to 70 years is 13% for men and 6% for women; estimated prevalence of at least mild OSA (defined as AHI ≥5) plus symptoms of daytime sleepiness are 14% for men and 5% for women.1 Severe OSA is associated with increased all-cause mortality.2,3 In addition to mortality, other adverse health outcomes associated with untreated OSA include cardiovascular disease and cerebrovascular events, diabetes, cognitive impairment, decreased quality of life, and motor vehicle crashes.3-23
The U.S. Preventive Services Task Force (USPSTF) concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for OSA in the general adult population.
Go to the Table for more information on the USPSTF recommendation rationale and assessment. For more details on the methods the USPSTF uses to determine the net benefit, see the USPSTF Procedure Manual.24
Patient Population Under Consideration
This recommendation applies to asymptomatic adults (age 18 years or older). It also applies to adults with unrecognized symptoms of OSA. This includes persons who are not aware of their symptoms or do not report symptoms as being a concern to their clinician. This recommendation does not apply to persons presenting with symptoms (e.g., snoring, witnessed apnea, excessive daytime sleepiness, impaired cognition, mood changes, or gasping or choking while asleep) or concerns about OSA, persons who have been referred for evaluation or treatment of suspected OSA, or persons who have acute conditions that could trigger the onset of OSA (e.g., stroke). Care of these persons should be managed as clinically appropriate. This recommendation also does not apply to children, adolescents, or pregnant persons.
OSA is a sleep disorder characterized by episodes of narrowing and obstruction of the pharyngeal airway during sleep resulting in reductions or cessations in breathing.25 Total airway obstruction for more than 10 seconds is defined as apnea, whereas hypopnea is a partial airway obstruction with at least a 4% reduction in blood oxygen saturation.26 OSA is defined as more than five apneic, hypoxic, or sleep arousal events per hour despite efforts to breathe.26 The AHI is used to define the severity of OSA. In general, mild OSA is defined as five to 15 events per hour, moderate OSA as 16 to 30 events per hour, and severe OSA as more than 30 events per hour.27 Common clinical signs and symptoms of OSA include excessive daytime sleepiness, unrefreshing sleep despite length of sleep, loud or irregular snoring, and choking or gasping while asleep.28
Risk factors associated with OSA include male sex, older age (40 to 70 years), postmenopausal status, higher body mass index, and craniofacial and upper airway abnormalities (e.g., enlarged tonsils or long upper airway). Black, Native American, and Latino/Hispanic populations have a higher prevalence of OSA compared with White populations; some evidence suggests that these differences are partially explained by higher rates of obesity, asthma, and tobacco use among these groups.4,29
There are several screening questionnaires and clinical prediction tools that attempt to identify persons at higher risk of OSA. Many combine questions about clinical findings (e.g., body mass index and neck circumference) with questions about symptoms associated with OSA. Potential screening questionnaires and clinical prediction tools include the Epworth Sleepiness Scale (ESS),30 STOP Questionnaire (Snoring, Tiredness, Observed Apnea, High Blood Pressure),31 STOP-Bang Questionnaire (STOP Questionnaire plus Body Mass Index, Age, Neck Circumference, and Gender),32 Berlin Questionnaire,33 Wisconsin Sleep Questionnaire,34 and the Multivariable Apnea Prediction tool.35 However, none of these instruments have been adequately validated in general populations enrolled from primary care settings.4
Persons suspected of having OSA are traditionally diagnosed using polysomnography, which combines several measurements, including an electroencephalogram, electrooculogram, chin electromyelogram, airflow monitor, oxygen saturation, respiratory effort, and electrocardiogram or heart rate. Additional recommended measurements include body position and leg movements.36 The resultant AHI measured during polysomnography is representative of the frequency of events and used to describe the severity of disease/condition.
Positive airway pressure (PAP) devices, which use compressed air to maintain the airway, are the primary treatment for OSA.4 For patients with overweight and obesity, weight loss is also an option. Mandibular advancement devices (MADs) are an alternative therapy to PAP for patients with OSA who prefer them or for those with adverse effects associated with PAP.4 Surgical interventions for OSA are available, but they generally are not considered first-line treatments and are rarely used.4
Suggestions for Practice Regarding the I Statement
Potential Preventable Burden
The exact prevalence of OSA in unknown; however, the estimated prevalence of OSA in the U.S. population has increased in the past few decades. For example, the diagnosis of OSA in the National Ambulatory Medical Care Survey rose by 442% between 1999 and 2010.37 The rise in prevalence is primarily attributed to the increase in prevalence of obesity.1 OSA is associated with multiple adverse health outcomes such as cognitive impairment, motor vehicle and other accidents, lost work days, work disability, impaired work performance, and decreased quality of life.4 OSA has also been associated with cardiovascular disease (e.g., coronary heart disease, stroke, or hypertension), type 2 diabetes, and metabolic syndrome. While OSA is associated with increased all-cause mortality, the role OSA plays in increasing overall mortality independent from other risk factors (older age, higher body mass index, and other cardiovascular risk factors), as well as the progression rates of OSA from mild to severe disease, is less clear.4
Commonly reported harms of treatment with PAP include claustrophobia, oral or nasal dryness, eye or skin irritation, rash, epistaxis, and pain. Commonly reported harms of treatment with MADs include oral mucosal, dental, or jaw symptoms, such as mucosal or dental pain, discomfort or tenderness, mucosal erosions, and jaw or temporomandibular joint pain or discomfort.4
Most primary care clinicians do not routinely screen for OSA and most patients do not discuss sleep-related symptoms with their primary care clinicians. One study found that only 20% of patients with sleep-related symptoms spontaneously reported them to their primary care clinicians.4 For persons with suspected OSA, current practice is usually referral to a specialist for appropriate diagnostic testing and treatment.38
When final, this recommendation will replace the 2017 USPSTF recommendation on screening for obstructive sleep apnea. In 2017, the USPSTF found insufficient evidence to assess the balance of benefits and harms of screening for OSA in asymptomatic adults (I statement). The current draft recommendation statement is consistent with the I statement from 2017.
Scope of Review
The USPSTF commissioned a systematic review to evaluate the benefits and harms of screening for OSA in adults.4 The systematic review also evaluated the evidence on the benefits and harms of treatment of OSA on intermediate outcomes (e.g., change in AHI and blood pressure) and health outcomes (e.g., mortality, quality of life, cardiovascular and cerebrovascular events, and cognitive impairment).
Accuracy of Screening Tests and Risk Assessment
Seven studies assessed one or more clinical prediction tools or screening questionnaires compared with facility-based polysomnography: two studies on the Berlin Questionnaire, four studies on the STOP-BANG, and two studies on the Multivariable Apnea Prediction tool. Study sizes ranged from 43 to 1,033 and studies were generally conducted in participants with underlying conditions such as hypertension, type 2 diabetes, or Alzheimer’s disease or in persons with symptoms. Findings for the both the Berlin and the STOP-BANG questionnaires were inconsistent. The Berlin questionnaire had sensitivity ranging from 37% to 80% and specificity ranging from 0% to 84% for mild OSA. In the two studies evaluating the original STOP-BANG questionnaire, both found good sensitivity (87% to 95%) but low specificity (0% to 23%) for detecting OSA at different AHI cut points.4,39,40 Two studies assessed a modified version of the STOP-BANG questionnaire (different scoring criteria) in different populations; sensitivity ranged from 61% to 79% and specificity ranged from 53% to 76% for detecting OSA at different AHI cut points.4,41,42
In the two studies that assessed the Multivariable Apnea Prediction tool, sensitivity ranged between 90% and 92% and specificity ranged between 44% and 64% to predict severe OSA syndrome (defined in the study as AHI ≥30 and ESS score >10).4 However, these studies were conducted in populations that had a high prevalence of OSA (and thus more likely to be symptomatic) and a high risk of spectrum bias (i.e., the study population does not represent the general primary care population).
Benefits of Early Detection and Treatment
The USPSTF found no studies that directly evaluated the effect of screening for OSA on health outcomes. The USPSTF did identify and review studies on the effect of treatment on intermediate outcomes and health outcomes.
The USPSTF reviewed evidence from four systematic reviews of good-quality treatment trials evaluating the effect of PAP or MADs on intermediate outcomes, including AHI and blood pressure.4
Three systematic reviews focused on the benefit of PAP for reducing blood pressure outcomes. One review limited to minimally symptomatic, asymptomatic, or nonsleepy populations pooled data comparing PAP with controls and demonstrated a small reduction in daytime diastolic blood pressure (-0.92 mm Hg [95% CI, -1.39 to -0.46 mm Hg]; 5 trials; 1,541 participants; I2=0) and no significant difference between groups in daytime systolic blood pressure (-0.51 mm Hg [95% CI, -3.39 to 2.38 mm Hg]; I2=84%). A second review of PAP that included trials of any OSA severity and symptoms pooled analyses and showed that PAP was associated with a reduction in mean 24-hour blood pressure of -2.63 mm Hg (95% CI, -3.86 to -1.39 mm Hg; 8 trials; 994 participants; I2=0%).4 The third review of PAP was limited to populations with resistant hypertension (23 trials; 4,905 participants); pooled analysis showed a reduction in mean 24-hour systolic blood pressure (-5.06 mm Hg [95% CI, -7.98 to 2.13 mm Hg]; I2=84%) and mean 24-hour diastolic blood pressure (-4.21 mm Hg [95% CI, -6.50 to -1.93 mm Hg]; I2=81%). One review of MADs found benefits associated with MADs compared with inactive control for improving blood pressure; however, differences between groups were imprecise and not statistically significant.4
Two reviews reported on the difference between groups in change from baseline AHI with PAP. The pooled estimates in AHI reduction favoring PAP were generally consistent. The review that limited inclusion to studies of asymptomatic adults with OSA or those of minimally symptomatic, nonsleepy adults found a pooled mean difference of -15.57 events per hour (95% CI, -29.32 to -1.82 events per hour; 3 trials; 1,541 participants).4
Health Outcomes: PAP
Sixty-three randomized, controlled trials (RCTs) comparing PAP with sham treatment or another active control reported on at least one health outcome. Most trials enrolled participants from sleep clinics and no trial enrolled screen-detected populations from a primary care setting.4
Thirty-one RCTs reported on mortality; however, the vast majority of trials (28 RCTs) reported mortality rates at 12 weeks or less, and most of these trials (25 RCTs) reported no death in any study group. Three RCTs assessed mortality over a longer duration, and none found a statistically significant difference between groups. Similarly, the short duration of most trials and the small number of total events makes it difficult to assess the effect of PAP on cardiovascular and cerebrovascular events.4
Forty-eight trials reported on changes in excessive daytime sleepiness using the ESS. The meta-analysis found that PAP reduced mean ESS scores more than controls (pooled mean difference, -2.30 [95% CI, -2.72 to -1.88]; 48 trials; 7,099 participants). This pooled mean difference is within the range considered as minimally clinically important for the ESS (-2 to -3).4
Twenty-eight RCTs reported measures of general health-related quality of life and eighteen RCTs reported measures of sleep-related quality of life (using a variety of questionnaires). Overall, PAP was associated with small improvements in both general health-related and sleep-related quality of life. However, these improvements are not considered clinically meaningful (i.e.. below a minimally clinically important difference).4
Health Outcomes: MADs
Twelve trials assessed the effect of MADs on health outcomes. All studies recruited participants with known or suspected OSA from specialty clinics. Treatment duration ranged from 4 to 12 weeks in most trials.4
Ten trials were included in a meta-analysis reporting on change in ESS score among groups randomized to MADs or an inactive control. It found that MADs improved ESS scores more than controls (pooled mean difference, -1.67 [95% CI, -2.09 to -1.25]; 10 trials; 1,540 participants; I2=36%); however, this change falls below the range considered a minimally clinically important difference for the ESS.4 Several studies reported on various quality of life metrics. Overall, the findings were inconsistent or imprecise, making it difficult to draw conclusions on the quality of life benefits related to MADs. Four trials reported on mortality; however, the duration of reporting was short (1 to 12 weeks) and few events were reported.4
Harms of Screening and Treatment
The USPSTF found no studies that directly evaluated harms associated with screening for OSA. Nineteen trials reported on harms associated with treatment of OSA using PAP or MADs.4 In general, reporting on harms related to treatment were sparse, and no trial included screen-detected persons identified from a primary care setting.
Ten studies (n=2,064) reported on harms of treatment with PAP. Followup in these studies was generally from 8 to 12 weeks. Overall, 1% to 47% of trial participants reported any harms from treatment with PAP, including oral or nasal dryness, eye or skin irritation, rash, epistaxis, and pain. In general, harms related to PAP treatment were short-lived and could be alleviated by discontinuing treatment or by supplementing PAP with additional interventions.4
Ten trials (n=684) reported on harms of treatment with MADs. Followup in these trials was generally from 4 to 8 weeks. In general, findings were imprecise and inconsistent. In seven trials, 17% to 74% of participants reported oral mucosal, dental, or jaw symptoms compared with 0% to 17% of participants in comparator groups (sham treatment, no treatment, or conservative management). In four trials, 5% to 33% of participants reported oral dryness compared with 0% to 3% in control groups, and in three trials, 23% to 68% of participants reported excessive salivation compared with 0% to 3% in comparator groups.4
More studies are needed that address the following areas.
- Studies of OSA screening in asymptomatic populations representative of the U.S. primary care population that evaluate the benefits and harms of screening on health outcomes (e.g., mortality, cardiovascular disease events, motor vehicle accidents, and quality of life) in screened vs. unscreened persons.
- Accuracy studies of screening tools in a general U.S. adult primary care population, especially in persons with unrecognized or mild symptoms.
- Development of accurate risk assessment tools that can identify populations most likely to benefit from OSA screening.
- More data on the natural history of OSA; in particular, the rates of progression from mild to severe OSA, the length of duration before progression, and the magnitude of benefit if OSA is identified and treated earlier.
Most groups do not recommend routine screening in primary care settings among populations without signs or symptoms of OSA. U.S. Department of Veterans Affairs guidelines suggest using the STOP Questionnaire to stratify the risk of OSA among patients who report sleep complaints (weak recommendation) and also suggest assessing for sleep-disordered breathing in patients with a history of cardiovascular or cerebrovascular events, congestive heart failure, and chronic opioid use (weak recommendation).43 The American Academy of Sleep Medicine recommends using polysomnography or a home sleep apnea test to diagnose OSA in uncomplicated adults presenting with signs and symptoms that indicate an increased risk of OSA.44 If the home test result is negative or inconclusive, polysomnography conducted in a sleep laboratory facility is recommended.44 The American Academy of Sleep Medicine also has a health advisory recommending annual OSA screening for adult patients who belong to certain high-risk groups.45 In 2014, the American College of Physicians recommended conducting a sleep study for patients with unexplained daytime sleepiness (weak recommendation, low-quality evidence).46
10. Shaw JE, Punjabi NM, Wilding JP, et al. Sleep-disordered breathing and type 2 diabetes: a report from the International Diabetes Federation Taskforce on Epidemiology and Prevention. Diabetes Res Clin Pract. 2008;81(1):2-12.
11. Vgontzas AN, Bixler EO, Chrousos GP. Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. J Intern Med. 2003;254(1):32-44.
12. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165(9):1217-1239.
13. Quan SF, Wright R, Baldwin CM, et al. Obstructive sleep apnea-hypopnea and neurocognitive functioning in the Sleep Heart Health Study. Sleep Med. 2006;7(6):498-507.
14. Kerner NA, Roose SP. Obstructive sleep apnea is linked to depression and cognitive impairment: evidence and potential mechanisms. Am J Geriatr Psychiatry. 2016;24(6):496-508.
15. Bubu OM, Andrade AG, Umasabor-Bubu OQ, et al. Obstructive sleep apnea, cognition and Alzheimer's disease: a systematic review integrating three decades of multidisciplinary research. Sleep Med Rev. 2020;50:101250.
16. Moyer CA, Sonnad SS, Garetz SL, Helman JI, Chervin RD. Quality of life in obstructive sleep apnea: a systematic review of the literature. Sleep Med. 2001;2(6):477-491.
17. Horstmann S, Hess CW, Bassetti C, Gugger M, Mathis J. Sleepiness-related accidents in sleep apnea patients. Sleep. 2000;23(3):383-389.
18. Young T, Blustein J, Finn L, Palta M. Sleep-disordered breathing and motor vehicle accidents in a population-based sample of employed adults. Sleep. 1997;20(8):608-613.
19. Wu H, Yan-Go F. Self-reported automobile accidents involving patients with obstructive sleep apnea. Neurology. 1996;46(5):1254-1257.
20. Terán-Santos J, Jiménez-Gómez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. Cooperative Group Burgos-Santander. New Engl J Med. 1999;340(11):847-851.
21. George CF, Nickerson PW, Hanly PJ, Millar TW, Kryger MH. Sleep apnoea patients have more automobile accidents. Lancet. 1987;2(8556):447.
22. Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis. 1988;138(2):337-340.
23. George CF, Smiley A. Sleep apnea & automobile crashes. Sleep. 1999;22(6):790-795.
32. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y. High STOP-Bang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth. 2012;108(5):768-775.
33. Netzer NC, Stoohs RA, Netzer CM, Clark K, Strohl KP. Using the Berlin Questionnaire to identify patients at risk for the sleep apnea syndrome. Ann Intern Med. 1999;131(7):485-491.
34. 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):1230-1235.
35. Maislin G, Pack AI, Kribbs NB, et al. A survey screen for prediction of apnea. Sleep. 1995;18(3):158-166.
36. Iber C, Ancoli-Israel S, Chesson A, et al. The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology and Technical Specifications. Westchester, IL: American Academy of Sleep Medicine; 2007.
37. Ford ES, Wheaton AG, Cunningham TJ, Giles WH, Chapman DP, Croft JB. Trends in outpatient visits for insomnia, sleep apnea, and prescriptions for sleep medications among US adults: findings from the National Ambulatory Medical Care survey 1999-2010. Sleep. 2014;37(8):1283-1293.
38. Sánchez-Quiroga M, Corral J, Gómez-de-Terreros FJ, et al. Primary care physicians can comprehensively manage patients with sleep apnea. A noninferiority randomized controlled trial. Am J Respir Crit Care Med. 2018;198(5):648-656.
39. Selvanathan J, Waseem R, Peng P, Wong J, Ryan CM, Chung F. Simple screening model for identifying the risk of sleep apnea in patients on opioids for chronic pain. Reg Anesth Pain Med. 2021;46(10):886-891.
40. Edmonds PJ, Gunasekaran K, Edmonds LC. Neck grasp predicts obstructive sleep apnea in type 2 diabetes mellitus. Sleep Disord. 2019;2019:3184382.
41. Jorge C, Benítez I, Torres G, et al. The STOP-Bang and Berlin questionnaires to identify obstructive sleep apnoea in Alzheimer's disease patients. Sleep Med. 2019;57:15-20.
42. Shin C, Baik I. Evaluation of a modified STOP-BANG questionnaire for sleep apnea in adults from the Korean general population. Sleep Med Res. 2021;12(1):28-35.
43. U.S. Department of Veterans Affairs; U.S. Department of Defense. Clinical Practice Guideline for Management of Chronic Insomnia Disorder and Obstructive Sleep Apnea (Insomnia/OSA). https://www.healthquality.va.gov/guidelines/CD/insomnia/index.asp. Accessed February 24, 2022.
44. Kapur VK, Auckley DH, Chowdhuri S, et al. Clinical practice guideline for diagnostic testing for adult obstructive sleep apnea: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(3):479-504.
45. American Academy of Sleep Medicine. Obstructive Sleep Apnea Screening Health Advisory. https://aasm.org/advocacy/position-statements/sleep-apnea-screening-health-advisory/. Accessed February 28, 2022.
46. Qaseem A, Dallas P, Owens DK, et al. Diagnosis of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014;161(3):210-220.