Obstructive Sleep Apnea

Obstructive Sleep Apnea Physician Writers Jay S. Balachandran, MD Sanjay R. Patel, MD, MS Section Editors Deborah Cotton, MD, MPH Jaya K. Rao, MD, MH...
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Obstructive Sleep Apnea

Physician Writers Jay S. Balachandran, MD Sanjay R. Patel, MD, MS Section Editors Deborah Cotton, MD, MPH Jaya K. Rao, MD, MHS Darren Taichman, MD, PhD Sankey Williams, MD

Screening and Prevention

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Diagnosis

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Treatment

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Practice Improvement

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Tool Kit

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Patient Information

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CME Questions

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The content of In the Clinic is drawn from the clinical information and education resources of the American College of Physicians (ACP), including ACP Smart Medicine and MKSAP (Medical Knowledge and Self-Assessment Program). Annals of Internal Medicine editors develop In the Clinic from these primary sources in collaboration with the ACP’s Medical Education and Publishing divisions and with the assistance of science writers and physician writers. Editorial consultants from ACP Smart Medicine and MKSAP provide expert review of the content. Readers who are interested in these primary resources for more detail can consult http://smartmedicine.acponline.org, http://www.acponline.org/products_services/ mksap/15/?pr31, and other resources referenced in each issue of In the Clinic. CME Objective: To review current evidence for the screening and prevention, diagnosis, treatment, and practice improvement of obstructive sleep apnea. The information contained herein should never be used as a substitute for clinical judgment. © 2014 American College of Physicians

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bstructive sleep apnea (OSA) is defined by repeated episodes of upper airway closure during sleep that result in recurrent oxyhemoglobin desaturation and sleep fragmentation (see the Box: Sleep Study Terminology and Obstructive Sleep Apnea Definitions). In the general adult population, the OSA syndrome occurs in 4% of men and 2% of women (1). The prevalence of OSA is rising in conjunction with increasing rates of obesity (2), with 5-year incidence rates of 7%–11% in middle-aged adults (3, 4).

O

Untreated OSA has long-term health consequences. The associated sleep fragmentation can result in daytime sleepiness and lead to increased risk for motor vehicle and occupational accidents (5) and reduced quality of life. In addition, the oxyhemoglobin desaturations and physiologic stresses from repetitive upper airway obstruction can lead to increased blood pressure and cardiovascular disease (6). However, only about 1 in 50 patients with symptoms suggestive of the OSA syndrome are evaluated and treated for the disease (7). Here, we aim to increase clinician familiarity with OSA and describe the importance of diagnosis and treatment.

Screening and Prevention

Sleep Study Terminology and Obstructive Sleep Apnea Definitions Terminology • Apnea: Breathing cessation for ≥ 10 seconds • Hypopnea: Breathing flow reduction for ≥ 10 seconds accompanied by either a ≥3% or ≥4% oxyhemoglobin desaturation or by arousal from sleep • AHI: Frequency of of apneas and hypopneas per hour of sleep • Oxygen desaturation index: Frequency of ≥ 3% or ≥ 4% oxyhemoglobin desaturations per hour of sleep • Time below SpO2 90%: Sleep or study time spent with oxyhemoglobin saturation less than 90%

Who should be screened for OSA? As part of a routine health maintenance evaluation, the American Academy of Sleep Medicine (AASM) recommends asking all adults whether they are dissatisfied with their sleep or have daytime sleepiness. Those with positive responses should be screened for OSA using further clinical history or screening instruments (8). Patients with risk factors should also be screened (see the Box: Risk Factors for Obstructive Sleep Apnea). Since obesity is the major risk factor for OSA, all obese patients should be screened for OSA. Excess weight is responsible for 41% of all cases and 58% of moderate-to-severe cases (9), and

Definitions

Risk Factors for Obstructive Sleep Apnea

AHI = apnea–hypopnea index; OSA = obstructive sleep apnea.

Obesity, especially with body mass index > 35 kg/m2 Family history of obstructive sleep apnea Retrognathia Treatment-resistant hypertension Congestive heart failure Atrial fibrillation Stroke Type 2 diabetes

• Mild OSA: AHI ≥ 5 but < 15 events per hour • Moderate OSA: AHI ≥ 15 but < 30 events per hour • Severe OSA: AHI ≥ 30 events per hour • The OSA syndrome: AHI ≥ 5 events per hour with daytime sleepiness

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the risk for OSA increases as obesity increases. Weight gain over time is also associated with OSA incidence: A 10% increase in weight predicts a 6-fold increase in the likelihood of developing clinically significant OSA (10). The AASM also recommends screening patients with a family history of OSA, those who have retrognathia, and those with diseases known to have a high coprevalence of OSA, such as type 2 diabetes, treatment-resistant hypertension, heart failure, atrial fibrillation, and stroke. Patients with pulmonary hypertension warrant screening for OSA because therapy may reduce pulmonary artery pressure (11). Patients who have high-risk driving occupations, such as commercial truck drivers and public transit operators, should be screened for OSA due to the potential public health impact, and any patient with a history of either a recent motor vehicle crash or near-miss attributable to sleepiness should be screened (12). What are the screening tools? Multiple screening questionnaires have been developed to identify

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high-risk patients (13), but none is accurate enough to preclude formal sleep testing. The Berlin questionnaire and the STOP-BANG screening test are 2 widely used, well-validated instruments. The Berlin questionnaire (Appendix Figure 1, available at www .annals.org) was developed for a primary care population and consists of 10 questions focused on the severity of snoring, witnessed apnea, the significance of daytime sleepiness, and the presence of obesity and hypertension. When

the questionnaire was evaluated in a primary care setting, more than 1 of 3 respondents were found to be at high risk for OSA, and the survey had an 86% sensitivity for predicting the presence of OSA (14). The STOP-BANG screening test (see the Box) was developed to assess patients in the preoperative setting. It is an 8-item tool with 1 point for each item. A STOP-BANG score of ≥ 3 among perioperative patients had an 84% sensitivity for predicting any OSA, and a score of ≥ 5 was more

STOP-BANG* STOP S Do you snore loudly (louder than talking or loud enough to be heard through closed doors)? T Do you often feel tired, fatigued, or sleepy during the day? O Has anyone observed you stop breathing during sleep? P Do you have or are you being treated for high blood pressure?

BANG B Body mass index > 35 kg/m2? A Age > 50 years? N Neck circumference > 40 cm? G Gender male? *In a perioperative setting, answering “yes” to ≥ 3 questions indicates a high risk for obstructive sleep apnea.

Consider how you have felt over the past week or two. How likely are you to doze off or fall asleep in the following situations? 0 1 2 3

= = = =

None Slight Moderate High

Situation

Score

Sitting and reading Watching television Sitting inactive in a public place (e.g., theater or meeting) As a passenger in a car for an hour without a break Lying down in the afternoon when able Sitting and talking to someone Sitting quietly after lunch without alcohol In a car while stopped for a few minutes in traffic Add above for total score Figure 1. Epworth Sleepiness Scale. Although imperfect, this scale can be a useful guide to quantifying the subjective concept of "sleepiness". Scores > 10 are consistent with excessive daytime sleepiness and should prompt further clinical evaluation.

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1. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleepdisordered breathing among middle-aged adults. N Engl J Med. 1993;328:1230-5. [PMID: 8464434] 2. Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177:1006-14. [PMID: 23589584] 3. Tishler PV, Larkin EK, Schluchter MD, Redline S. Incidence of sleep-disordered breathing in an urban adult population: the relative importance of risk factors in the development of sleep-disordered breathing. JAMA. 2003;289:2230-7. [PMID: 12734134] 4. Newman AB, Foster G, Givelber R, Nieto FJ, Redline S, Young T. Progression and regression of sleepdisordered breathing with changes in weight: the Sleep Heart Health Study. Arch Intern Med. 2005;165:2408-13. [PMID: 16287771] 5. Terán-Santos J, Jiménez-Gómez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. Cooperative Group BurgosSantander. N Engl J Med. 1999;340:847-51. [PMID: 10080847]

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6. Gottlieb DJ, Yenokyan G, Newman AB, O’Connor GT, Punjabi NM, Quan SF, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation. 2010;122:352-60. [PMID: 20625114] 7. Kapur V, Strohl KP, Redline S, Iber C, O’Connor G, Nieto J. Underdiagnosis of sleep apnea syndrome in U.S. communities. Sleep Breath. 2002;6:49-54. [PMID: 12075479] 8. 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;5:263-76. [PMID: 19960649] 9. Young T, Peppard PE, Taheri S. Excess weight and sleep-disordered breathing. J Appl Physiol (1985). 2005;99:1592-9. [PMID: 16160020] 10. Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284:3015-21. [PMID: 11122588] 11. Arias MA, García-Río F, Alonso-Fernández A, Martínez I, Villamor J. Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study. Eur Heart J. 2006;27:1106-13. [PMID: 16497687] 12. Strohl KP, Brown DB, Collop N, George C, Grunstein R, Han F, et al; ATS Ad Hoc Committee on Sleep Apnea, Sleepiness, and Driving Risk in Noncommercial Drivers. An official American Thoracic Society Clinical Practice Guideline: sleep apnea, sleepiness, and driving risk in noncommercial drivers. An update of a 1994 Statement. Am J Respir Crit Care Med. 2013;187:125966. [PMID: 23725615]

predictive of clinically relevant, moderate-to-severe OSA (15). Can OSA be prevented? Observational data suggest that weight loss can reduce the severity of preexisting OSA: A 10% weight loss among patients followed for over 10 years predicted a 26% decrease in severity (10). Among

patients with mild OSA, nearly 9 of 10 who lost an estimated 15% of body weight through diet and lifestyle modification achieved remission (16). Among patients with moderate-to-severe OSA, weight loss regimens can also lead to significantly reduced disease severity, even if total remission is less likely (17, 18).

Screening and Prevention... All adults should be asked if they have sleep problems or daytime sleepiness, and a positive response should prompt OSA screening via further clinical history or a validated questionnaire. Patients with significant obesity, cardiovascular disease, or a history of drowsiness while driving should be screened because of the high prevalence of OSA among these patients.

CLINICAL BOTTOM LINE

Diagnosis

© 2014 American College of Physicians

What symptoms should prompt consideration of OSA? Symptoms of OSA are described in the Box. Snoring is the symptom with the highest sensitivity for OSA but is nonspecific (19). To distinguish simple snoring from that suggestive of OSA, patients should be asked for details about the snoring: Patients with OSA are more likely than simple snorers to report loud, nightly snoring that is bothersome to others (14). Excessive daytime sleepiness is also a nonspecific finding but is important to elicit in determining therapy options and following the response to therapy. The Epworth Sleepiness Scale (ESS) (Figure 1) is an 8-item scale that quantifies sleepiness in everyday activities. Although it inconsistently correlates with objective measurements of sleepiness and has poor correlation with OSA severity, it can help standardize the evaluation of a patient’s subjective perception (20). It can also be used to follow response to OSA therapy. From a

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practical standpoint, the ESS has been adopted by most insurances as a required part of the sleep history before payment for a sleep study is authorized. A history of drowsiness or falling asleep while driving should be explicitly explored. Patients should also be questioned on consumption of caffeine or other stimulants because it may indicate attempts to self-treat sleepiness. Although relatively insensitive, choking or gasping during sleep is highly specific for moderate-to-severe OSA, as is the presence of morning headaches (19). Obtaining a history from a bed partner or cohabitant can be particularly helpful because many of these symptoms may not be apparent to the patient. Manifestations of untreated OSA may also include decreased libido, decreased concentration, or memory loss. Of note, OSA frequently presents in an atypical fashion, with insomnia and fatigue as the predominant symptoms, particularly in women. Despite population-based studies

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that find a 2:1 male–female prevalence, utilization data indicate that the ratio for referrals is 9:1 male, suggesting that clinicians do not adequately consider OSA in women (21). In the absence of symptoms, what other diseases should prompt evaluation? No high-level evidence currently supports routine evaluation for OSA in asymptomatic populations. However, routine diagnostic testing in asymptomatic, morbidly obese patients scheduled for bariatric surgery may be reasonable given the prevalence in this population (24) and low-level evidence that perioperative treatment reduces postoperative complications (23, 24).

opiates are at risk for opiateinduced central sleep apnea.

Symptoms of Obstructive Sleep Apnea

Finally, it is important to note that symptoms of OSA, such as sleepiness and sleep disturbances, are nonspecific. Other common sleep disorders, including insomnia, chronic sleep deprivation, and circadian rhythm disorders (such as shift work sleep disorder), may be responsible for the symptoms. What physical examination findings are important? The physical examination should include respiratory, cardiovascular, and neurologic systems. The presence and degree of obesity should

Witnessed episodes of apnea Loud, frequent, bothersome snoring Choking/gasping during sleep Excessive daytime sleepiness Drowsy driving (recent sleepinessassociated motor vehicle accident or near-miss) Unrefreshing sleep Sleep fragmentation Insomnia Nocturia Morning headaches Decreased concentration Memory loss Decreased libido

Evaluation for OSA may also benefit patients with hypertension refractory to medical therapy. Prevalence of OSA is high among these patients and randomized trials have shown that treatment leads to modest blood pressure reduction even when superimposed on aggressive antihypertensive medication regimens (25). What other conditions should be considered along with OSA? OSA frequently coexists with the obesity hypoventilation syndrome (OHS), a condition defined by daytime hypercapnia among obese patients without other causes of hypoventilation. This syndrome is present in up to 10%–20% of morbidly obese patients with OSA, and OHS patients have higher rates of cardiovascular complications, such as cor pulmonale. Observed episodes of apnea and nocturnal gasping may indicate a central sleep apnea syndrome rather than OSA. Patients with congestive heart failure are at risk for Cheyne-Stokes respiration, and patients receiving long-acting

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Figure 2. Modified Mallampati classification. The mouth is evaluated with the patient in a sitting position with the tongue protruded. A higher classification is associated with a higher risk for OSA. Grade I = soft palate, uvula, tonsillare fauces, and pillars visible; grade II = soft palate, uvular, and tonsillare fauces visible; grade III = only soft palate and base of uvula visible; grade IV = only hard palate visible.

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© 2014 American College of Physicians

13. Abrishami A, Khajehdehi A, Chung F. A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth. 2010;57:42338. [PMID: 20143278] 14. 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;131:485-91. [PMID: 10507956] 15. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y. High STOPBang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth. 2012;108:768-75. [PMID: 22401881]

be noted. Particular attention should be paid to the following signs of upper airway narrowing: enlarged neck circumference (>16 inches in women, >17 inches in men), a modified Mallampati score of 3 or 4 (Figure 2), macroglossia, tonsillar hypertrophy, an enlarged or elongated uvula, a high/arched palate, signs of nasal obstruction (polyps, septal deviation, turbinate hypertrophy, significant congestion), and retrognathia. What type of sleep study should be ordered? A “full-night” sleep study done in the laboratory is the recommended method to diagnose OSA (Figure 3); it also has the advantage of assessing for other sleep disorders. A “splitnight” study, in which an initial diagnostic recording of at least 2 hours documenting OSA is immediately

followed by positive airway pressure titration, is a reasonable alternative. What is the role of in-home sleep studies? Home sleep testing (HST) is increasingly being utilized in uncomplicated cases due to convenience and cost issues. HST devices offer a balance by eliminating cumbersome, full electroencephalographic (EEG) monitoring in the home while providing sufficient multichannel respiratory monitoring. Validation studies of HST devices for OSA diagnosis have been based on devices that record at least 4 signals, including oximetry, airflow, and measures of respiratory effort (25). Monitors limited to overnight oximetry alone have not been found to reliably diagnose OSA. In patients with a high clinical probability of OSA without comorbid

Figure 3. Sample recording from overnight polysomnography demonstrating obstructive sleep apnea. This 2-minute window demonstrates repeated episodes of obstructive apnea (denoted by brackets), characterized by airflow cessation lasting at least 10 seconds despite respiratory effort. Here, apnea is associated with oxyhemoglobin desaturation and is terminated by arousal from sleep. C4-M1 = electroencephalogram; LOC = left electro-oculogram; ROC = right electro-oculogram; CHIN = chin electromyogram; LEGS = leg electromyogram; EKG = electrocardiogram; SNORE = vibratory snore; THERM = airflow monitoring by thermal air sensor; NPT = airflow monitoring by nasal pressure transducer; CHEST = respiratory inductance plethysmography bands placed around the thorax; ABDM = respiratory inductance plethysmography bands placed around the abdomen; SaO2 =arterial oxyhemoglobin saturation.

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cardiopulmonary disease, high-level evidence supports HST for diagnosis of OSA (26, 27). Among these patients, a negative home study should be followed by an in-laboratory sleep study to definitively exclude the diagnosis. Evidence to support HST in patients with a low-to-intermediate pretest probability is currently lacking. HST has several limitations. Patients with reduced cognitive ability or limited manual dexterity may not reliably be able to apply the sensors at home and may therefore require technician-attended in-lab sleep studies. The validity and utility of HST in patients with serious comorbid conditions, such as chronic lung disease, congestive heart failure, or stroke, have not been fully evaluated. Finally, HST may underestimate OSA severity, which reduces the sensitivity of the test and limits the ability to directly compare results with in-lab studies. What variables are reported on a sleep study report, and what do they mean? The key metric used to stratify OSA severity is the apnea–hypopnea index (AHI), defined as the number of episodes of apnea (cessation of airflow for at least 10 seconds) and hypopnea (airflow reduction for at least 10 seconds accompanied by either a 3% or 4% oxyhemoglobin desaturation or arousal from sleep) per hour of sleep. Of note, varying definitions of hypopnea (e.g., 3% vs. 4% desaturation) can lead to different AHI calculations and can limit comparisons of polysomnography reports from different sleep laboratories. The AHI based on a 4% desaturation criteria for hypopnea has been more closely associated with cardiovascular risk (28) and is the metric preferred by the Centers for Medicare & Medicaid Services. However, this definition is more restrictive and may preclude diagnosis in some patients with

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classic symptoms, but without significant oxyhemoglobin desaturations, who would benefit from therapy. Sleep studies also collect other data that can provide important information about a patient’s sleep. Typically reported variables include total sleep time (or total recording time for home sleep tests), measures of sleep quality (sleep efficiency, wake time after sleep onset, quantity of sleep stages, and degree of overall sleep fragmentation), other measures of sleep-disordered breathing (number of central vs. obstructive respiratory events, frequency of oxyhemoglobin desaturation events, time spent with an oxyhemoglobin saturation < 90%, nadir oxyhemoglobin saturation), assessment of any EEG epileptiform activity, nocturnal arrhythmia, limb movements, and video/audio recording of sleeprelated behaviors. Do patients need to be seen by a sleep specialist before a sleep study is ordered? No high-level data suggest that sleep consultation is required before evaluation of uncomplicated OSA. However, clinicians should be able to adequately councel patients on OSA-related health risks, diagnostic testing, and rationale for therapy. Evaluation by a sleep specialist before polysomnography is recommended when complex sleep-disordered breathing (e.g., patients with significant cardiorespiratory disease or suspected OHS), parasomnias (unusual behaviors, emotions, or perceptions during sleep), or narcolepsy is suspected. Whenever possible, diagnostic testing should be done via an accredited sleep center. Recent evidence has found that such testing is associated with shorter delays in care and better overall patient satisfaction (29).

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16. Tuomilehto HP, Seppä JM, Partinen MM, Peltonen M, Gylling H, Tuomilehto JO, et al; Kuopio Sleep Apnea Group. Lifestyle intervention with weight reduction: first-line treatment in mild obstructive sleep apnea. Am J Respir Crit Care Med. 2009;179:320-7. [PMID: 19011153] 17. Johansson K, Neovius M, Lagerros YT, Harlid R, Rössner S, Granath F, et al. Effect of a very low energy diet on moderate and severe obstructive sleep apnoea in obese men: a randomised controlled trial. BMJ. 2009;339:b4609. [PMID: 19959590] 18. Foster GD, Borradaile KE, Sanders MH, Millman R, Zammit G, Newman AB, et al; Sleep AHEAD Research Group of Look AHEAD Research Group. A randomized study on the effect of weight loss on obstructive sleep apnea among obese patients with type 2 diabetes: the Sleep AHEAD study. Arch Intern Med. 2009;169: 1619-26. [PMID: 19786682] 19. Myers KA, Mrkobrada M, Simel DL. Does this patient have obstructive sleep apnea?: The Rational Clinical Examination systematic review. JAMA. 2013;310:731-41. [PMID: 23989984] 20. Benbadis SR, Mascha E, Perry MC, Wolgamuth BR, Smolley LA, Dinner DS. Association between the Epworth sleepiness scale and the multiple sleep latency test in a clinical population. Ann Intern Med. 1999; 130:289-92. [PMID: 10068387] 21. Young T, Hutton R, Finn L, Badr S, Palta M. The gender bias in sleep apnea diagnosis. Are women missed because they have different symptoms? Arch Intern Med. 1996;156:244551. [PMID: 8944737] 22. Frey WC, Pilcher J. Obstructive sleeprelated breathing disorders in patients evaluated for bariatric surgery. Obes Surg. 2003;13:676-83. [PMID: 14627460]

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23. Proczko MA, Stepaniak PS, de Quelerij M, van der Lely FH, Smulders JF, Kaska L, et al. STOP-Bang and the effect on patient outcome and length of hospital stay when patients are not using continuous positive airway pressure. J Anesth. 2014. [PMID: 24871541] 24. Hallowell PT, Stellato TA, Petrozzi MC, Schuster M, Graf K, Robinson A, et al. Eliminating respiratory intensive care unit stay after gastric bypass surgery. Surgery. 2007; 142:608-12; discussion 612.e1. [PMID: 17950355] 25. Martínez-García MA, Capote F, CamposRodríguez F, Lloberes P, Díaz de Atauri MJ, Somoza M, et al; Spanish Sleep Network. Effect of CPAP on blood pressure in patients with obstructive sleep apnea and resistant hypertension: the HIPARCO randomized clinical trial. JAMA. 2013;310:2407-15. 26. Rosen CL, Auckley D, Benca R, FoldvarySchaefer N, Iber C, Kapur V, et al. A multisite randomized trial of portable sleep studies and positive airway pressure autotitration versus laboratorybased polysomnography for the diagnosis and treatment of obstructive sleep apnea: the HomePAP study. Sleep. 2012;35:757-67. [PMID: 22654195] 27. Kuna ST, Gurubhagavatula I, Maislin G, Hin S, Hartwig KC, McCloskey S, et al. Noninferiority of functional outcome in ambulatory management of obstructive sleep apnea. Am J Respir Crit Care Med. 2011;183: 123844. [PMID: 21471093] doi:10.1164/rccm .201011-1770OC 28. Punjabi NM, Newman AB, Young TB, Resnick HE, Sanders MH. Sleep-disordered breathing and cardiovascular disease: an outcome-based definition of hypopneas. Am J Respir Crit Care Med. 2008;177:1150-5. [PMID: 18276938]

Diagnosis... Patients who snore loudly, have significant daytime sleepiness, or have a history of drowsy driving should be evaluated for OSA, particularly if they have associated symptoms of nocturnal choking or gasping or witnessed episodes of apnea. Even in asymptomatic patients, evaluation may be indicated for those undergoing bariatric surgery or who have treatment-resistant hypertension. Although in-lab sleep studies are considered the gold standard, in-home sleep testing can be considered for patients with a high clinical suspicion for OSA and no significant comorbid conditions.

CLINICAL BOTTOM LINE

Treatment

© 2014 American College of Physicians

Which patients with OSA require treatment? The decision to start treatment for OSA should include a discussion with the patient about the potential for alleviation of symptoms and cardiovascular risk reduction. High-level evidence indicates that patients with daytime sleepiness, regardless of severity, should be offered therapy (30, 31). In particular, those who have recently had a motor vehicle accident or near-miss attributable to sleepiness should be aggressively treated, specifically with continuous positive airway pressure (CPAP) therapy for any degree of OSA, because CPAP is the only treatment shown to reduce crash rates (12). The severity of OSA is also a major factor in deciding on therapy initiation. Observational data indicate that treatment of severe OSA, even if asymptomatic, is associated with a reduction in fatal and nonfatal cardiovascular events (6, 32). Whether asymptomatic patients with mild or moderate OSA should be treated remains controversial. Among asymptomatic patients with mild OSA, there is little evidence that treatment reduces cardiovascular risk in the absence of significant oxyhemoglobin desaturation.

severity and symptoms (16–18). Therefore, weight loss through dietary modification and regular exercise should be recommended to all overweight or obese OSA patients. Bariatric surgery can also substantially reduce the severity of OSA in morbidly obese patients, although notably, gastric banding was not found to be superior to intensive medical weight loss for reducing OSA (33). Can OSA be effectively managed by alterations in sleep position? In some patients, the supine position further narrows the upper airway and can worsen OSA. Avoiding this position can be an effective primary or supplementary therapy in patients documented to have a lower AHI in the nonsupine position than in the supine position (34). Position-dependent OSA is found in up to one third of patients with mild or moderate OSA. Wearable positional avoidance devices and monitoring or alarms may facilitate adherence better than traditional therapies, such as a tennis ball strapped to the back.

What is the role of weight loss and exercise? Studies show that intensive weight loss interventions help reduce OSA

How should CPAP be initiated? CPAP provides pneumatic splinting of the upper airway and is indicated as primary therapy for moderate-to-severe OSA, symptomatic OSA, and for any OSA in high-risk drivers. CPAP settings are traditionally determined with an in-lab overnight titration sleep study. A prescription for CPAP

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should include specification for the pressure setting, mask type and size, heated humidifier, and associated device supplies (tubing, filters, mask straps). For patients with uncomplicated OSA, empirical prescription of autotitrating CPAP (APAP) is an alternative to the in-lab overnight titration of CPAP. APAP devices detect upper airway narrowing and automatically adjust pressure to remain therapeutic. Overall, APAP performs as well as CPAP in terms of patient adherence and reducing sleepiness. However, APAP is contraindicated in patients at risk for Cheyne-Stokes breathing (e.g., those with congestive heart failure or stroke), given its increased potential to induce central apnea. APAP has also not been wellstudied in patients with significant pulmonary disease. APAP is typically prescribed with a wide initial pressure range, such as 5–20 cm H2O. It is imperative for the clinician to interrogate the device within 1–2 weeks of empirical APAP therapy initiation. Using downloaded therapy data, the clinician can narrow the pressure range or set it at a fixed CPAP setting. Although long-term APAP may not lower blood pressure to the same extent as CPAP (35), it may allow pressures to self-adjust if changes in therapy requirements are expected, such as during pregnancy, after bariatric surgery, or with fluctuating use of postoperative sedatives. When therapy is initiated, patients should be educated about equipment function, care, and maintenance; the benefits of therapy; and potential problems, such as mask or pressure intolerance, excessive dryness or moisture, or pressure leak around the mask. Successful primary care models of OSA management have included trained nursing support to facilitate patient counseling

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and education. Alternatively, early collaboration with a board-certified sleep specialist may increase adherence (29). What amount of CPAP use constitutes sufficient adherence? There is no threshold at which optimal benefit from CPAP therapy is derived. Strategies to maximize adherence to CPAP therapy are shown in Figure 4. Studies show a linear relationship between hours of CPAP use and improvements in sleepiness, quality of life, and blood pressure (36, 37); therefore, patients should use CPAP whenever they sleep. However, CMS has defined “adequate” CPAP adherence as use of ≥ 4 hours per night on 70% of nights, and requires, along with an increasing number of third-party payers, documentation of this level of adherence during a consecutive 30-day period within the first 90 days of therapy to continue reimbursement.

Support groups, bed partner support, and cognitive behavioral therapy focused on CPAP have also been shown to increase adherence (36). Other interventions that can increase adherence include adding heated humidification (now mostly standard) and nasal

29. Parthasarathy S, Subramanian S, Quan SF. A multicenter prospective comparative effectiveness study of the effect of physician certification and center accreditation on patient -centered outcomes in obstructive sleep apnea. J Clin Sleep Med. 2014;10:243-9. [PMID: 24634620] 30. Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med. 2003;163:565-71. [PMID: 12622603] 31. Weaver TE, Mancini C, Maislin G, Cater J, Staley B, Landis JR, et al. Continuous positive airway pressure treatment of sleepy patients with milder obstructive sleep apnea: results of the CPAP Apnea Trial North American Program (CATNAP) randomized clinical trial. Am J Respir Crit Care Med. 2012;186:677-83. [PMID: 22837377] 32. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoeahypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365:1046-53. [PMID: 15781100] 33. Dixon JB, Schachter LM, O’Brien PE, Jones K, Grima M, Lambert G, et al. Surgical vs conventional therapy for weight loss treatment of obstructive sleep apnea: a randomized controlled trial. JAMA. 2012;308:1142-9. [PMID: 22990273] 34. Morgenthaler TI, Kapen S, Lee-Chiong T, Alessi C, Boehlecke B, Brown T, et al; Standards of Practice Committee. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep. 2006;29:1031-5. [PMID: 16944671]

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What factors can optimize patient adherence to CPAP? Adherence patterns are determined within the first week after CPAP initiation, and a patient’s early perceived benefit of therapy is a strong predictor of long-term use. Accordingly, optimal management of OSA patients should include early followup (e.g., 1–2 weeks of therapy initiation) to identify and address any problems. Patients should be instructed to bring their CPAP devices and masks to clinic to review proper use. Adherence data can be obtained from the device and is important to review, because patients tend to overestimate actual use (38).

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CPAP intolerant

Assess patient knowledge and motivation Cognitive-behavioral therapy

Group support or bed partner involvement

Goal-setting

Consider nasal pathology Addition of heated humidification

Possible surgical intervention for severe anatomic defects

Nasal decongestants or steroids

Assess mask leak or mask discomfort Consider mask desensitization techniques

Try alternate mask interfaces

Assess for inability to sleep with CPAP Consider short course of sedative hypnotic to help patient acclimatize to device

Address healthy sleep habits (“sleep hygiene”)

Assess for pressure intolerance Consider autotitrating positive airway pressure (APAP) or bi-level positive airway pressure (BPAP)

Addition of expiratory pressure relief

Failed CPAP therapy in spite of efforts to address barriers Consider oral appliance therapy

Consider upper airway surgery

Consider novel treatments

Figure 4. Strategies to maximize adherence to continuous positive airway pressure (CPAP) therapy.

35. Ip S, D’Ambrosio C, Patel K, Obadan N, Kitsios GD, Chung M, et al. Auto-titrating versus fixed continuous positive airway pressure for the treatment of obstructive sleep apnea: a systematic review with meta-analyses. Syst Rev. 2012;1:20. [PMID: 22587875]

steroid therapy for patients with significant congestion.

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alternatives for selected patients with significant intolerance to pressure because these PAP modes lead to an overall lower mean pressure delivery than similar CPAP settings. For OSA patients without significant comorbid cardiorespiratory

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disease who have difficulty tolerating CPAP from the outset or who develop insomnia, short-term use of a sedative hypnotic, such as zolpidem or eszopiclone, may help to consolidate sleep and enable adherence so that the medication is no longer needed once the patient has habituated to CPAP (39). How should CPAP masks be chosen? Masks should be chosen to maximize patient comfort, since no one mask type is superior to another. Involving patients in mask selection can facilitate acclimatization. Nasal masks or nasal pillows (which sit under the nose and fit in the nares) may be better tolerated in patients with claustrophobia. Nasal pillows may be more effective in patients with unusual nasal bridge anatomy, facial hair, or absent dentition leading to lack of infranasal support. Patients who sleep with their mouth open may benefit from an oronasal (“fullface”) mask, because airflow delivered through a nasal mask or pillows may escape through an open mouth without effectively splinting the posterior airway. Poor fit or mask intolerance often does not become apparent until the mask has been used for a few nights. Patients should be encouraged to report mask problems early because masks can typically be replaced without cost in the first 30 days. What is the role of mandibular advancement devices? Custom-made mandibular advancement devices (MAD) are oral appliances that hold the mandible in a forward position and treat OSA by decreasing airway collapsibility and enlarging the upper airway. These devices are less effective than CPAP at normalizing the AHI and are therefore not recommended as initial therapy for severe OSA (34). For patients with mild or moderate OSA, however, MADs may be a reasonable initial therapy (41). Despite reduced efficacy, they tend to be more acceptable to

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patients and, as a result, are associated with greater adherence. Among patients with mild-to-moderate OSA, MADs have similar “real-world” effectiveness to CPAP regarding improvements in sleepiness and quality of life. For patients with severe OSA who do not tolerate CPAP despite attempts to address therapy barriers, MADs can be considered a secondary therapy option. Use of MADs requires adequate dentition and may exacerbate temporomandibular joint disease. Patients who need these devices should be referred to a dentist with expertise in OSA management, preferably with sleep dentistry accreditation. In addition, if a MAD is being used as primary therapy, a follow-up sleep study to document adequacy in reducing OSA is recommended. What is the role of surgical intervention? Most surgeries to decrease upper airway collapsibility do not significantly reduce OSA severity or symptoms (42). The uvulopalato-pharyngoplasty is perhaps best known, but reduction in symptoms with this procedure is generally small, and fewer than one half of patients have significant reduction in OSA severity over the long term. Maxillomandibular advancement is an invasive procedure with prolonged postoperative recovery but has an OSA cure rate of >90%, particularly in nonobese patients with retrognathia. Tracheostomy also cures OSA and can be used in lifethreatening situations. For very select patients, these 2 surgeries, which offer the potential for a cure, may be preferable to a lifetime of CPAP therapy. However, their intensity and associated morbidity preclude routine application. Predicting which patients will respond to a particular procedure can be difficult. However, in cases of known, severe anatomical defects predisposing the upper airway to

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36. Sawyer AM, Gooneratne NS, Marcus CL, Ofer D, Richards KC, Weaver TE. A systematic review of CPAP adherence across age groups: clinical and empiric insights for developing CPAP adherence interventions. Sleep Med Rev. 2011;15:343-56. [PMID: 21652236] 37. Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, et al. The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a metaanalysis of placebocontrolled randomized trials. Arch Intern Med. 2007;167:75764. [PMID: 17452537] 38. Schwab RJ, Badr SM, Epstein LJ, Gay PC, Gozal D, Kohler M, et al; ATS Subcommittee on CPAP Adherence Tracking Systems. An official American Thoracic Society statement: continuous positive airway pressure adherence tracking systems. The optimal monitoring strategies and outcome measures in adults. Am J Respir Crit Care Med. 2013;188:61320. [PMID: 23992588] 39. Lettieri CJ, Shah AA, Holley AB, Kelly WF, Chang AS, Roop SA; CPAP Promotion and Prognosis-The Army Sleep Apnea Program Trial. Effects of a short course of eszopiclone on continuous positive airway pressure adherence: a randomized trial. Ann Intern Med. 2009; 151:696-702. [PMID: 19920270] 40. Chai CL, Pathinathan A, Smith B. Continuous positive airway pressure delivery interfaces for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006:CD005308. [PMID: 17054251] 41. Phillips CL, Grunstein RR, Darendeliler MA, Mihailidou AS, Srinivasan VK, Yee BJ, et al. Health outcomes of continuous positive airway pressure versus oral appliance treatment for obstructive sleep apnea: a randomized controlled trial. Am J Respir Crit Care Med. 2013;187:87987. [PMID: 23413266]

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42. Aurora RN, Casey KR, Kristo D, Auerbach S, Bista SR, Chowdhuri S, et al; American Academy of Sleep Medicine. Practice parameters for the surgical modifications of the upper airway for obstructive sleep apnea in adults. Sleep. 2010;33:140813. [PMID: 21061864] 43. Pack AI, Black JE, Schwartz JR, Matheson JK. Modafinil as adjunct therapy for daytime sleepiness in obstructive sleep apnea. Am J Respir Crit Care Med. 2001;164: 1675-81. [PMID: 11719309] 44. Kaw R, Pasupuleti V, Walker E, Ramaswamy A, FoldvarySchafer N. Postoperative complications in patients with obstructive sleep apnea. Chest. 2012;141:436-41. [PMID: 21868464] 45. American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2014;120:268-86. 46. Chai-Coetzer CL, Antic NA, Rowland LS, Reed RL, Esterman A, Catcheside PG, et al. Primary care vs specialist sleep center management of obstructive sleep apnea and daytime sleepiness and quality of life: a randomized trial. JAMA. 2013;309:997-1004. [PMID: 23483174] 47. Bhasin S, Cunningham GR, Hayes FJ, Matsumoto AM, Snyder PJ, Swerdloff RS, et al. Testosterone therapy in adult men with androgen deficiency syndromes: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2006;91:1995-2010. [PMID: 16720669] 48. Gottlieb DJ, Punjabi NM, Mehra R, Patel SR, Quan SF, Babineau DC, et al. CPAP versus oxygen in obstructive sleep apnea. N Engl J Med. 2014;370:2276-85. [PMID: 24918372]

© 2014 American College of Physicians

collapse (e.g., marked tonsillar hypertrophy, severe septal deviation, severe congestion), surgeries to address these defects may have a role in treating OSA. These procedures (e.g., tonsillectomy, nasal septoplasty) are more often used to increase CPAP tolerability or reduce snoring than to “cure” OSA. How should treatment be monitored? All CPAP devices store and can report data regarding use, and many provide information about therapy effectiveness and mask leak (38). These data can be assessed by device interrogation and correlated with the patient’s responses. Clinicians should periodically ensure that CPAP equipment (e.g., masks, hose, filters) is being updated regularly by the device supplier and that it is being properly cleaned. Therapy monitoring should focus on ensuring CPAP use during all sleep sessions, assessing for symptom resolution, monitoring for side effects of CPAP use, and assessing for comorbid conditions commonly associated with OSA (discussed above). Patients with OSA remission due to weight loss or surgery should be monitored for return of symptoms. Those with a history of drowsy driving or sleepiness-related motor vehicle or occupational accidents should be closely monitored for continued remission of sleepiness. Relapse should prompt the clinician to investigate for the following possibilities in stepwise fashion: problems with CPAP delivery (mask leak, device malfunction), change in pressure needs, and non-OSA sleep factors (insufficient sleep duration, other sleep disorders). If sleepiness persists after these factors are addressed, a trial of modafinil should be considered as adjunctive treatment (43), although caution must be used in patients with a history of psychosis or mania, unstable angina, or recent myocardial infarction.

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No evidence supports routine follow-up sleep studies in patients whose symptoms do not recur. How should OSA be treated when a patient is admitted to the hospital? Little evidence supports any particular management strategy of patients with OSA admitted to a medical service. Nevertheless, they should be encouraged to use their CPAP or MAD while hospitalized, just as they would at home. Sedative and opiate medications can worsen OSA and should be used cautiously in OSA inpatients. In the surgical patient, untreated OSA in the perioperative setting is associated with a higher rate of cardiopulmonary complications and intensive care unit transfers (44). Accordingly, the American Society of Anesthesiology recommends that if moderate sedation is used intraoperatively, ventilation should be monitored by continuous oximetry and continuous capnography if feasible, and CPAP administration during sedation should be considered (45). When should a sleep specialist be consulted? For uncomplicated OSA, studies suggest that when primary care clinicians are educated about disease management and have trained support staff, treatment outcomes are similar to those of sleep specialists (46). However, if these prerequisites cannot be met, referral may be appropriate. In complicated situations, such as a CPAP-intolerant patient or one with persistent symptoms despite adequate therapy adherence and efficacy, a sleep specialist consultation may aid in further clinical evaluation and management (29, 46). In addition, for patients with multiple sleep disorders or with complex sleepdisordered breathing (e.g., OSA with comorbid severe cardiopulmonary disease, OHS, or central apnea), sleep specialist consultation may facilitate

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the use of more advanced PAP devices where necessary. What should patients know about the effects of medications and supplemental oxygen? Any sedative or opiate medication can worsen OSA and should be used with caution. There is low-level evidence that exogenous testosterone administration can exacerbate or induce OSA, so patients treated with androgen therapy should be screened and followed for OSA symptoms (47). Although supplemental oxygen is effective in treating oxyhemoglobin desaturation associated with OSA, there is little evidence to suggest that it reduces symptoms, blood pressure, or cardiovascular risk (48). Therefore, supplemental oxygen should not be used as a primary or sole therapy for OSA. Can treatment prevent or modify outcomes in other diseases? Among OSA patients with hypertension, and particularly those with daytime sleepiness or treatmentresistant hypertension, high-level evidence indicates that both CPAP

and MAD therapy can lead to modest reduction in blood pressure and that the degree of adherence correlates with the blood pressure response (25, 37, 49). Low-level evidence suggests that CPAP therapy is associated with lower rates of incident hypertension (50, 51). The effect of OSA therapy on cardiovascular outcomes remains unclear. Observational studies have found that OSA patients treated with CPAP have reduced risk for fatal and nonfatal cardiovascular events compared with untreated patients (6, 32). However, these findings may be confounded by treatment bias: Patients who adhered to CPAP may have been more likely to adhere to other cardioprotective measures. Other diseases may be modified by OSA therapy, but only low-level evidence exists. For example, among OSA patients with preexisting congestive heart failure, CPAP therapy may modestly increase ejection fraction. Among OSA patients with atrial fibrillation having cardioversion, therapy may be associated with a reduced likelihood of atrial fibrillation recurrence.

Treatment... All OSA patients should be encouraged to pursue conservative measures, such as weight control and avoidance of alcohol and sedatives before bedtime. Symptomatic OSA patients, patients with severe OSA, and patients with OSA associated with drowsy driving should be treated. CPAP is considered primary therapy for OSA, and therapy initiation requires close follow-up. Many factors may facilitate patient acceptance and adherence to CPAP therapy, including education, participation in mask selection, early counseling, and psychosocial support. For patients intolerant to CPAP, alternate therapy options included positional therapy devices, custom-fitted oral appliances, or surgical therapies. Adequate adherence to therapy is important because it is associated with symptom resolution and may reduce cardiovascular risk.

CLINICAL BOTTOM LINE

What do professional organizations recommend with regard to the care of patients with OSA? Organizations, such as the American College of Physicians, the

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AASM, and the Canadian Thoracic Society have produced guidelines for the diagnosis and management of OSA that reflect the themes of this article (8, 52–54).

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49. Durán-Cantolla J, Aizpuru F, Montserrat JM, Ballester E, Terán-Santos J, Aguirregomoscorta JI, et al; Spanish Sleep and Breathing Group. Continuous positive airway pressure as treatment for systemic hypertension in people with obstructive sleep apnoea: randomised controlled trial. BMJ. 2010;341:c5991. [PMID: 21106625] 50. Marin JM, Agusti A, Villar I, Forner M, Nieto D, Carrizo SJ, et al. Association between treated and untreated obstructive sleep apnea and risk of hypertension. JAMA. 2012;307:2169-76. [PMID: 22618924] 51. Barbé F, DuránCantolla J, Sánchezde-la-Torre M, Martínez-Alonso M, Carmona C, Barceló A, et al; Spanish Sleep And Breathing Network. Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: a randomized controlled trial. JAMA. 2012;307:2161-8. [PMID: 22618923] doi:10.1001/jama.201 2.4366 52. Qaseem A, Holty JE, Owens DK, Dallas P, Starkey M, Shekelle P. Management of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2014; 161:210-220. doi: 10.7326/M12-3187 53. Fleetham J, Ayas N, Bradley D, Fitzpatrick M, Oliver TK, Morrison D, et al. Canadian Thoracic Society 2011 guideline update: diagnosis and treatment of sleep disordered breathing Can Respir J. 2011;18:25-47. 54. 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;161:210-20. [PMID: 25089864] doi:10.7326/M123187

© 2014 American College of Physicians

What is the role of patient education in management? Patient education about OSA and involvement in deciding on appropriate therapy is accepted by consensus as standard of care. However, studies have shown that education needs to be combined with patient-specific information about treatment expectations and goal development in a

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Quality-of-Care Guidelines

Tool Kit

Clinical Guidelines

Obstructive Sleep Apnea

cognitive behavioral therapy–style intervention. In addition, education delivered via small group settings or with a spouse’s involvement is likely to be effective (36). What measures do stakeholders use to evaluate the quality of care for patients with OSA? The AASM and National Committee for Quality Assurance developed a set of performance measures for individual clinicians to assess quality of care in OSA management (56). Clinicians should 1) determine the severity of disease among all OSA patients, 2) offer a trial of positive airway pressure therapy for patients with symptomatic OSA or moderate-to-severe OSA, 3) assess therapy adherence objectively, and 4) follow OSA symptoms over time.

www.ama-assn.org/ama1/pub/upload/mm/pcpi/obst-sleep-apnea.pdf From the American Medical Association. www.aasmnet.org/practiceparameters.aspx?cid=102 From the American Academy of Sleep Medicine. www.thoracic.org/statements/pages/sleep.php From the American Thoracic Society. www.guideline.gov/content.aspx?id=47136 From the National Guideline Clearinghouse.

Patient Information http://patients.thoracic.org/information-series/en/resources/obstructive -sleep-apnea.pdf http://patients.thoracic.org/wp-content/uploads/2014/03/osa.pdf http://patients.thoracic.org/wp-content/uploads/2014/03/Oral _Appliances_for_Sleep_Apnea.pdf http://patients.thoracic.org/wp-content/uploads/2014/03/sleep -studies.pdf From the American Thoracic Society. www.nhlbi.nih.gov/health/health-topics/topics/sleepapnea/ www.nhlbi.nih.gov/health/health-topics/topics/cpap/ www.nhlbi.nih.gov/health/health-topics/topics/slpst/ www.nhlbi.nih.gov/health/health-topics/videos/living-with-and -managing-sleep-apnea.html From the National Institute of Health’s Heart, Lung, and Blood Institute. www.nlm.nih.gov/medlineplus/sleepapnea.html From the National Institutes of Health’s MedLine Plus. http://effectivehealthcare.ahrq.gov/index.cfm/search-for-guides-reviews -and-reports/?pageaction=displayproduct&productID=684 From the Agency for Healthcare Research and Quality.

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55. Montserrat JM, Ferrer M, Hernandez L, Farré R, Vilagut G, Navajas D, et al. Effectiveness of CPAP treatment in daytime function in sleep apnea syndrome: a randomized controlled study with an optimized placebo. Am J Respir Crit Care Med. 2001;164:608-13. [PMID: 11520724] 56. Strollo P, Metersky M, Berry R, Becker P, Collop N, Davidson T, et al. American Academy of Sleep Medicine (AASM)/Physician Consortium for Performance Improvement (PCPI)/National Committee for Quality Assurance – Obstructive Sleep Apnea Physician Performance Measurement Set. Accessed at www.ama-assn .org/ama1/pub/ upload/mm/pcpi/ obst-sleep-apnea.pdf on 15 July 2014.

Guidelines from the American College of Physicians on OSA management recommend focusing treatment on patients with daytime sleepiness (52). However, we believe that any OSA patient with symptoms attributable to OSA should be offered treatment. Although not studied as extensively as sleepiness, high-quality data show that such OSA symptoms as snoring, nocturia, unrefreshing sleep, and impaired quality of life improve with CPAP therapy (55).

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WHAT YOU SHOULD KNOW ABOUT OBSTRUCTIVE SLEEP APNEA

In the Clinic Annals of Internal Medicine

What is obstructive sleep apnea? Obstructive sleep apnea (OSA) is a common problem that disrupts breathing during sleep. People with OSA temporarily stop or decrease their breathing while sleeping, causing decreases in oxygen levels. These pauses can awaken a person or prevent the deepest and most restful sleep, causing daytime sleepiness. OSA is also associated with serious health effects. Poor sleep can lead to an increase in accidents and a reduced quality of life and is also associated with high blood pressure, heart disease, and stroke.

What are the warning signs?

How is it diagnosed? In addition to discussing your symptoms, your doctor will ask about your medical history and any medicines you are taking. Reports from others that you snore loudly or gasp during sleep are also important. Your doctor may order a sleep study (called a polysomnogram), which involves sleeping at a special lab that measures your breathing, heart rate, and oxygen levels during sleep. If polysomnography is not available, a study performed at home may be an option.

How is it treated? Treatments vary according to the severity of OSA. Your doctor may recommend lifestyle changes, such as losing weight or quitting smoking. He may suggest changing the position of sleep, avoiding sleeping on your back, and forcing yourself to sleep on your side. Alcohol should be avoided before sleep. Many patients are effectively treated and feel better with continuous positive airway pressure (CPAP) treatment. CPAP involves wearing a mask connected to a machine that blows air into the airway to prevent the path of air being blocked. Other options for treating OSA may be available, based on your particular situation. Talk with your doctor about the best treatment plan.

For More Information http://effectivehealthcare.ahrq.gov/ehc/products/117/684/sleep_ap _consumer.pdf

Agency for Healthcare Research and Quality. www.nlm.nih.gov/medlineplus/ency/article/000811.htm

Medline Plus. www.sleepapnea.org/learn/sleep-apnea/obstructive-sleep-apnea.html

American Sleep Apnea Association. http://patients.thoracic.org/information-series/en/resources/obstructive -sleep-apnea.pdf

American Thoracic Society.

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Patient Information

• Loud snoring (although everyone who snores does not have OSA and some people with OSA do not snore) • Daytime sleepiness • Choking or gasping during sleep (usually observed by a sleep partner) • Awakening with shortness of breath • Frequent awakening • Morning headaches • High blood pressure • Poor memory, trouble with concentration, or mood swings due to sleepiness and fatigue

CME Questions

1. A 64-year-old man is evaluated for a 3-month history of loud snoring and “gasping” during sleep. He also frequently falls asleep in a chair while reading in the evening. His medical history is otherwise unremarkable. On physical examination, temperature is 37.4°C (99.3°F), blood pressure is 130/82 mm Hg, pulse rate is 80/min, and respiration rate is 14/min; BMI is 36. Neck circumference is 45.7 cm (18 in), and a low-lying soft palate is noted. Polysomnography discloses severe obstructive sleep apnea, with an apnea–hypopnea index of 44 per hour. Which of the following is the most appropriate next step in treatment?

A. Continuous positive airway pressure B. Nocturnal oxygen therapy C. Oral appliance D. Upper airway surgery 2. A 55-year-old woman is evaluated in follow-up after starting nasal continuous positive airway pressure (CPAP) 6 weeks ago for obstructive sleep apnea. She is unable to wear the mask for more than 3 or 4 hours per night because of nasal congestion. She continues to have residual sleepiness during the day. Her husband notes that she does not snore or have apnea when the mask is on. On physical examination, temperature is 37.4°C (99.3°F), blood pressure is 122/74 mm Hg, pulse rate is 76/min, and respiration rate is 14/min. BMI is 26. Nasal mucosa is boggy and erythematous with a clear mucoid discharge. Which of the following management steps is most likely to improve this patient’s adherence to CPAP therapy?

A. Add heated humidification to the CPAP circuit B. Initiate oral modafinil C. Initiate oxymetazoline nasal spray D. Refer for nasal septal surgery

3. A 34-year-old man is evaluated for daytime fatigue of 9 months’ duration. He has never fallen asleep at the wheel, but falls asleep at other times during the day. He does not think he snores, but his wife is unavailable to confirm this. He reports no leg symptoms. He has no significant medical history and takes no medications. He does not smoke. He drinks two or three beers on Friday and Saturday nights. He does not exercise regularly and has gained 9.1 kg (20 lb) since getting married 18 months ago. On physical examination, temperature is normal, blood pressure is 125/76 mm Hg, and pulse rate is 88/min. BMI is 33. Neck circumference is 43 cm (17 in). Pharynx is normal. The thyroid is difficult to palpate owing to the patient’s large neck size. The lungs are clear. Cardiovascular and neurologic examinations are normal. In addition to counseling regarding sleep hygiene and weight loss, which of the following is the most appropriate management for this patient?

A. Advise alcohol abstinence B. Initiate therapy with zolpidem C. Order iron studies D. Refer for polysomnography 4. A 55-year-old man is evaluated for a 4-month history of worsening lower extremity edema and stable chronic dyspnea on exertion. His medical history is significant for dyslipidemia, hypertension, and type 2 diabetes mellitus. He does not drink alcohol. He has a 20-pack-year smoking history but has not used tobacco for the past 20 years. His current medications are simvastatin, lisinopril, aspirin, and insulin. On physical examination, temperature is 37.6°C (99.7°F), blood pressure is 144/86 mm Hg, pulse rate is 94/min, and respiration rate is 18/min. BMI is 42. Neck circumference is 47 cm (18.5 in). Bilateral breath sounds are normal with

no wheezing. Pigmented skin changes of chronic venous stasis are seen, and there is tense edema of both legs. Laboratory studies reveal a hemoglobin level of 16.8 g/dL (168 g/L). Blood gas studies on ambient air find a pH of 7.36, arterial PO2 of 52 mm Hg (6.9 kPa), and arterial PCO2 of 53 mm Hg (7.0 kPa). Echocardiogram shows left ventricular hypertrophy and a normal ejection fraction of 65%. The right ventricle is dilated, and pulmonary artery systolic pressure is estimated at 78 mm Hg. There is moderate tricuspid regurgitation, but the valves are otherwise normal. Chest radiograph shows shallow inspiration but clear lung fields. Which of the following is the most likely diagnosis?

A. Cheyne-Stokes breathing B. Chronic obstructive pulmonary disease C. Interstitial lung disease D. The obesity hypoventilation syndrome Disclosures: Dr. Balachandran, ACP Contributing Author, has disclosed the following conflict of interest: Payment for manuscript preparation: American College of Physicians. Dr. Patel, ACP Contributing Author, has disclosed the following conflicts of interest: Payment for manuscript preparation: American College of Physicians; Consultancy: Apnicure, Apnex Medical; Travel/ accommodations expenses covered or reimbursed: American Academy of Sleep Medicine, American Academy of Thoracic Medicine. Disclosures can also be viewed at www.acponline.org/ authors/icmje/ConflictOfInterestForms .do?msNumM14-1735.

Questions are largely from the ACP’s Medical Knowledge Self-Assessment Program (MKSAP, accessed at http://mksap.acponline.org/). Go to www.annals.org/intheclinic.aspx to complete the quiz and earn up to 1.5 CME credits, or to purchase the complete MKSAP program.

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