Correctly diagnosing and treating SDB could result in millions in health care savings
The prevalence of obstructive sleep apnea (OSA) in the United States has been compared to the health care crisis presented by cigarette smoking.1 Mild OSA occurs in as many as one of five US adults, but ranges in severity from simple, asymptomatic snoring to profound, potentially lethal apneas.2 Physicians have identified a number of factors that may be associated with an increased risk of OSA, including:
• a family history of OSA or snoring;
• a small upper airway (large tongue, large uvula, recessed chin, or excess tissue in the throat or soft palate);
• gastroesophageal reflux;
• morning headaches; and
• cardiovascular disease.
Despite the high prevalence and seriousness of the condition, nearly 80% of people with OSA remain undiagnosed and untreated.2 This is due, in large part, to continued lack of awareness of the condition, its impact, and the relationship between high-quality sleep and health.3 Low awareness of OSA is especially alarming because of the abundant evidence linking the disease to several leading health concerns, including hypertension, heart failure, coronary artery disease, stroke, diabetes, and obesity. Untreated OSA has a significant negative impact on these conditions, leading to higher treatment costs, a higher risk of complications, and poor treatment outcomes. For example, there is a very high incidence of atrial fibrillation and stroke in patients with OSA.4,5 Studies3,6-8 have also shown that patients with untreated OSA are more likely to be involved in vehicle accidents. Beyond that, OSA leads to higher mortality risks in patients with cardiovascular disease and greater risks of complications in patients undergoing heart surgery.9,10 Untreated OSA has been identified as playing a significant role in decreased work productivity, resulting in an estimated US loss of $5 billion annually.3
OSA is highly prevalent among patients with cardiovascular disease. The respiratory disturbances associated with OSA can lead to decreased oxygen saturation and, occasionally, high blood levels of carbon dioxide. During each apnea episode, sympathetic nervous system activity increases, leading to arrhythmias and increased blood pressure. Sleep apnea was listed as an identifiable cause of hypertension by the US National Institutes of Health and is associated with congestive heart failure, coronary artery disease, and atrial fibrillation.11-14
OSA is also highly prevalent among stroke victims, and more than half of stroke patients also have OSA. The presence of OSA has been shown to increase the risk of stroke or death from any cause significantly, independently from other risk factors (including hypertension).15 It is known that the risk of stroke increases progressively with the increased severity of OSA, possibly due to acute hemodynamic changes occurring during episodes of apnea, decreased cerebral blood flow, paradoxical embolization, hypercoagulability, hypoxia-related cerebral ischemia, or atherosclerosis.15 Approximately 63% of patients with stroke or transient ischemic attack also experience OSA, and such patients are five times more likely to experience sleep disordered breathing (SDB) than the general population.16,17 Stroke patients with OSA also have worse functional outcomes and higher mortality rates a year after the stroke, compared with the general population.18
Over 80% of people with drug-resistant hypertension have OSA19; left untreated, OSA produces prolonged cardiovascular stress, leading to increased nocturnal and diurnal blood pressure levels (compared with levels of treated OSA patients).20 This pattern of consistently high (nondipping) blood pressure is of particular concern because nondipping hypertensive patients are at significantly increased risk for stroke.21
SDB is common in patients with moderate and severe heart failure, and it contributes to disease progression and worsening outcomes in congestive heart failure (CHF), including increased mortality.22 Over 50% of CHF patients have some form of SDB.22 Recent data23 suggest that these patients suffer equally from OSA and central sleep apnea (CSA). Heart failure patients with CSA also typically exhibit Cheyne-Stokes respiration (CSR), which is associated with severe left ventricular dysfunction,24 increased mortality,25 and high risk for cardiac transplantation.26 Recent evidence27 shows that treating CSR-CSA improves cardiac function.
Approximately 30% of patients with coronary artery disease have SDB, but the Sleep Heart Health Study12,28 suggested that the strongest influences of SDB and OSA are on stroke, CHF, and hypertension. Ischemic events are known to occur more frequently in the early morning hours, when patients are most vulnerable to SDB events related to the rapid–eye-movement stage of sleep.
OSA affects approximately 50% of all atrial fibrillation patients.13 In patients with OSA, intermittent hypoxemia, hypercapnia, chemoreceptor excitation, markedly increased sympathetic drive, and severe pressor surges, all of which occur nightly for years if untreated, may initiate or predispose a patient to atrial fibrillation. Nocturnal increases in sympathetic activation persist during wakefulness in patients with OSA, and increased sympathetic drive is associated with atrial fibrillation.13
OSA has been found to affect as many as 77% of bariatric-surgery candidates.20 The combination of OSA and bariatric surgery increases the risk of respiratory complications in obese patients.28,30,31 OSA is highly prevalent in morbidly obese patients and is associated with increased risk for cardiac arrhythmias.32 Significant weight gain may also increase a person’s chances of developing moderate to severe OSA.33,34
OSA is common among diabetes patients, affecting approximately 70%.35 Similarly, there is a high prevalence of diabetes and impaired glucose tolerance among patients with OSA. In one study, 50% of male sleep-apnea patients had abnormal glucose tolerance, and 30% of them had diabetes.36 OSA has also been demonstrated37 to be independently associated with an increased prevalence of metabolic syndrome.
Obesity is a common contributing factor to both sleep apnea and diabetes. Despite the importance of obesity in both disorders, however, OSA is an additional contributing factor that is independently associated with glucose intolerance and insulin resistance.33 Thus, it is difficult to control diabetes without addressing coexisting OSA.
Accumulated research7,8,38 has indicated that sleep-apnea patients have four to six times more risk of motor vehicle accidents than the general population. It is estimated4 that there are 310,000 OSA-related collisions per year in the United States, resulting in 1,400 fatalities and $15.9 billion in collision costs. Some experts39,40 have suggested that drivers with untreated OSA are as dangerous as drivers under the influence of alcohol.
OSA plays a significant role in fatigue-related productivity loss and has a tremendous impact on business. It has been estimated3,6 that fatigue caused by OSA leads to $5 billion worth of lost US productivity per year and leads to higher insurance, production, and consumer costs. Workers with OSA are also known to have more work-related accidents.3
Use of health care services costs as much as $2,000 more for patients with untreated OSA in the 2 years following initial diagnosis, compared with patients who receive treatment; untreated OSA patients also use approximately twice the resources of the general population, and spend twice as much time in the hospital in the year following diagnosis.41-43
Bariatric patients with OSA have three times the risk of postoperative complications of those without OSA.44 Complications associated with OSA increase hospital costs more than 80% for bariatric surgery.31 Patients with OSA undergoing hip or knee replacement surgery have twice the risk of postoperative complications, compared with control groups.45 Untreated OSA is also associated with increased hospitalization in patients with coronary artery disease.14 Hospitalizations are costly and can be reduced by providing treatment for patients with OSA.36,46,47
Although medicine is just beginning to discover and understand the links between SDB and anesthesia, a growing number of incidents nationwide have led many health care organizations to adopt OSA screening measures as standard practice. Risk of respiratory complications for untreated OSA patients receiving anesthesia is higher than that for patients without OSA, and there have been numerous lawsuits related to these circumstances.46,47 Screening for OSA may serve to prevent these complications and reduce associated hospital and legal costs. The American Society of Anesthesiologists48 recently completed a position paper specifically addressing the perioperative assessment and treatment of patients with OSA undergoing procedures requiring anesthesia.
Benefits of Treatment
There are numerous advantages of treating OSA patients with nasal continuous positive airway pressure (CPAP), particularly for patients with comorbidities. Effective CPAP treatment has been proven to decrease blood pressure significantly in OSA patients during sleep and wakefulness.20 CPAP is also known to lead to improved heart function (left ventricular ejection fraction) and a reduction in enlarged heart dimensions (left ventricular end-systolic dimension).20
CPAP treatment in patients with coronary artery disease is associated with a decrease in the occurrence of new cardiovascular events (death, hospitalization, or revascularization) and an increase in the time that elapses before such events.12 Patients with atrial fibrillation who receive effective CPAP treatment have a lower risk of recurrence than those with untreated OSA.5,13
For diabetes patients, CPAP treatment is known to improve glycemic control.49 OSA patients using CPAP experience improved insulin sensitivity and leptin levels.50
For increased risks of accidents, mortality, and loss of life, as well as for higher health care costs, CPAP treatment is an effective preventive measure. CPAP significantly reduces an OSA patient’s risk of motor vehicle accidents.3,6,38–40 Treating bariatric patients with CPAP results in a lower risk of postoperative complications and in reduced hospital stays.31 Heart-surgery patients who receive treatment for OSA have shorter hospital stays than patients with untreated OSA.9 Patients with sleep apnea who are treated with CPAP have reduced mortality rates, compared with those who do not receive treatment.10,11
Because OSA is highly prevalent in patients with other high-cost health conditions, it follows that treating OSA in those patient groups can reduce the associated costs (see Table).
For the conditions shown in the table, untreated OSA is known to lead to worsening outcomes, increased hospital stays, and higher medical costs. Conversely, treating patients for OSA reduces the risk of developing the disease and/or improves treatment outcomes. Treating OSA patients reduces per-person medical costs 50%.42
Identification and Treatment
Numerous tools are available to assist clinicians in screening for OSA. Clinically validated screening questionnaires include the Epworth Sleepiness Scale and the Berlin Questionnaire. These questionnaires may be used in conjunction with diagnostic screening tools such as portable sleep screeners and pulse oximeters. All are inexpensive, accurate ways to identify patients at high risk for OSA who should be referred for a full polysomnography (PSG) study. These tools are easy to use and provide fast, reliable results with the added benefit of streamlining the diagnosis process (by enabling those patients at highest risk to take priority on waiting lists for PSG). Sleep-laboratory access has expanded, and recent data51 suggest that waiting times have been substantially reduced.
CPAP therapy was first developed in 1980. In the past decade, there have been numerous advances that improved the convenience, comfort, and efficacy of CPAP devices. Portable monitoring advances have allowed highly sensitive, specific diagnosis to be done in the home or at a patient’s hospital bedside. In addition, most manufacturers are now producing very small, quiet, highly effective CPAP devices that allow significantly better patient acceptance and compliance than previously possible. CPAP devices have also become more sophisticated, including flow-limitation algorithms and measures of compliance and treatment efficacy. Of equal importance, nasal interfaces are now much smaller and more comfortable, and they leak less. In short, the technology of CPAP has advanced hugely over the past decade. Despite these advances in technology, costs remain reasonable.
In light of the hugely positive impact on health care outcomes and costs that treating OSA with CPAP would have, it would be grossly neglectful not to conduct a major national effort to address the health and public-safety problems that undiagnosed/untreated OSA presents. Diag-nosing and treating OSA must be a national priority.
Currently, the standard diagnostic process is inefficient and time-consuming. Patients often approach their primary care physicians with a variety of symptoms, and it may take several visits and/or referral to a pulmonologist or otolaryngologist to uncover the root cause. Too often, time is wasted treating superficial signs of sleep apnea with medications or other ineffective methods.
Specialists and generalists alike have an opportunity to improve this process by adopting a proactive approach to identifying and screening for sleep apnea. There are numerous past examples of early intervention as successful model for chronic-disease management. For instance, regular screening for diabetes and asthma has saved lives and provided significant cost savings. These models provide a valuable reference for interacting with patients and should inform the management of sleep patients. By taking advantage of various screening tools, clinicians can identify patients at risk for sleep apnea early and send them for sleep studies (and on to treatment) more efficiently.
1. Phillipson EA. Sleep apnea—a major public health problem. N Engl J Med 1993;328(17):1271-3.
2. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165(9):1217-39.
3. Hossain JL, Shapiro CM. The prevalence, cost implications, and management of sleep disorders: an overview. Sleep Breath. 2002;6(2):85-102.
4. Arzt M, Young T, Finn L, Skatrud JB, Bradley TD. Association of sleep-disordered breathing and the occurrence of stroke. Am J Respir Crit Care Med. 2005;172(11):1447-51.
5. Kanagala R, Murali NS, Friedman PA, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107(20):2589-94.
6. Sassani A, Findley LJ, Kryger M, Goldlust E, George C, Davidson TM. Reducing motor-vehicle collisions, costs, and fatalities by treating obstructive sleep apnea syndrome. Sleep. 2003;27(3):453-8.
7. Teran-Santos J, Jimenez-Gomez A, Cordero-Guevara J. The association between sleep apnea and the risk of traffic accidents. N Engl J Med. 1999;340(11):847-51.
8. Horstmann S, Hess CW, Bassetti C, Gugger M, Mathis J. Sleepiness-related accidents in sleep apnea patients. Sleep. 2000;23(3): 383-9.
9. Kindgen-Milles D, Muller E, Buhl R, et al. Nasal-continuous positive airway pressure reduces pulmonary morbidity and length of hospital stay following thoracoabdominal aortic surgery. Chest. 2005;128(2);821–8.
10. Campos-Rodriguez F, Pena-Grinan N, Reyes-Nunez N, et al. Mortality in obstructive sleep apnea–hypopnea patients treated with positive airway pressure. Chest. 2005;128(2);624–33.
11. Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005;365(9464):1046-53.
12. Shahar E, Whitney CW, Redline S. Sleep-disordered breathing and cardiovascular disease: cross sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med. 2001;163(1):19-25.
13. Gami AS, Pressman G, Caples SM, et al. Association of atrial fibrillation and obstructive sleep apnea. Circulation. 2004;110(4):364–7.
14. Milleron O, Pilliere R, Foucher A, et al. Benefits of obstructive sleep apnoea treatment in coronary artery disease: a long-term follow-up study. Eur Heart J. 2004;25(9):728–34.
15. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N Engl J Med. 2005;353(19):2034-41.
16. Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol. 2004;160(6):521-30.
17. Bassetti C, Aldrich MS. Sleep apnea in acute cerebrovascular diseases: final report on 128 patients. Sleep. 1999;22(2): 217-23.
18. Parra O, Arboix A, Montserrat JM, Quinto L, Bechich S, Garcia-Erols L. Sleep related breathing disorders: impact on mortality of cerebrovascular disease. Eur Respir J. 2004;24(2):267-72.
19. Logan AG, Perlikowski SM, Mente A, et al. J Hypertens. 2001;19(12);2271–7.
20. Becker HF, Jerrentrup A, Ploch T, et al. Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation. 2003;107(1):68-73.
21. Phillips RA, Sheinart KF, Godbold JH, Mahboob R, Tuhrim S. The association of blunted nocturnal blood pressure dip and stroke in a multiethnic population. Am J Hypertens. 2000;13(12):1250-5.
22. Wolk R, Kara T, Somers VK. Sleep-disordered breathing and cardiovascular disease. Circulation. 2003;108(1):9–12.
23. Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD. Risk factors for central and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir Crit Care Med. 1999;160(4):1101-6.
24. Kohnlein T, Welte T, Tan LB, Elliott MW. Assisted ventilation for heart failure patients with Cheyne-Stokes respiration. Eur Respir J. 2002;20(4):934-41.
25. Hanly PJ, Zuberi-Khokhar S. Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med. 1996;153(1):272-6.
26. Lanfranchi PA, Braghiroli A, Bosimini E, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation. 1999;99(11):1435-40.
27. Philippe C, Stoica-Herman M, Drouot X, et al. Compliance with and effectiveness of adaptive servoventilation versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in heart failure over a six month period. Heart. 2006;92(3): 337-42.
28. Schaefer H, Koehler U, Ewig S, Hasper E, Tasci S, Luderitz B. Obstructive sleep apnea as a risk marker in coronary artery disease. Cardiology. 1999;92(2):79–84.
29. O’Keeffe T, Patterson E. Evidence supporting routine polysomnography before bariatric surgery. Obes Surg. 2004;14(1): 23–6.
30. Valencia-Flores, Orea A, Castano VA, et al. Prevalence of sleep apnea and electrocardiographic disturbances in morbidly obese patients. Obes Res. 2000;8(3):262–9.
31. Cooney RN, Haluck RS, Ku J, et al. Analysis of cost outliers after gastric bypass surgery: what can we learn? Obes Surg. 2003;13(1):29–36.
32. Guardiano SA, Scott JA, Ware JC, Schechner SA. The long-term results of gastric bypass on indexes of sleep apnea. Chest. 2003;124(4):1615–9.
33. 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.
34. Charuzi I, Lavie P, Peiser J, Peled R. Bariatric surgery in morbidly obese sleep-apnea patients: short- and long-term follow-up. Am J Clin Nutr. 1992;55(2 suppl): S594S–6.
35. Einhorn et al. (TK) Prevalence and associations of sleep apnea in a population of adults with Type 2 diabetes mellitus. Abstract Number 2415-PO.Presented at the 2005 APSS Meeting; June 20-22, 2005; Denver.
36. Meslier N, Gagnadoux F, Giraud P, et al. Impaired glucose-insulin metabolism in males with obstructive sleep apnoea syndrome. Eur Respir J. 2003;22(1):156-60.
37. Coughlin SR, Mawdsley L, Mugarza JA, Calverley PM, Wilding JP. Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J. 2004;25(9):735-41.
38. Krieger J. Long-term compliance of nasal continuous positive airway pressure in sleep apnea patients and non-apneic snorers. Sleep. 1992;15(6 suppl):S42-6.
39. Hack MA, Choi SJ, Vijayapalan P, Davies RJ, Stradling JR. Comparison of the effects of sleep deprivation, alcohol and obstructive sleep apnoea (OSA) on simulated steering performance. Respir Med. 2001;95(7):594-601.
40. George CF, Boudreau AC, Smiley A. Simulated driving performance in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 1996;154(1):175-81.
41. Kapur V, Blough DK, Sandblom RE, et al. Medical cost of undiagnosed sleep apnea. Sleep. 1999; 22(6):749-55.
42. Kryger MH, Roos L, Delaive K, Walld R, Horrocks J. Utilization of health care services in patients with severe obstructive sleep apnea. Sleep. 1996;19(9 suppl):S111-6.
43. Peker Y, Hedner J, Johansson A, Bende M. Reduced hospitalization with cardiovascular and pulmonary disease in obstructive sleep apnea patients on nasal CPAP treatment. Sleep. 1997;20(8):645-53.
44.Perugini RA, Mason R, Czerniach DR, et al. Predictors of complication and suboptimal weight loss after laparoscopic roux-en-y gastric bypass: a series of 188 patients. Arch Surg. 2003;138(5): 541–5; discussion 545–6.
45. Gupta RM, Parvizi J, Hanssen AD, Gay PC. Postoperative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a case-control study. Mayo Clin Proc. 2001;76(9):897-905.
46. den Herder C, Schmeck J, Appelboom DK, de Vries N. Risks of general anaesthesia in people with obstructive sleep apnoea. BMJ. 2004;329(7472);955–9.
47. Hillman D, Platt PR, Eastwood PR. The upper airway during anesthesia. Br J Anaesth. 2003;91(1):31–9.
48. The American Society of Anesthesiologists Task Force on Perioperative Management of Patients with Obstructive Sleep Apnea. Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea.Park Ridge, Ill: American Societyof Anesthesiologists; 2005.
49. Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T. Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med. 2005;165(4):447-52.
50. Harsch I, Schahin S, Radespiel-Troger M, et al. Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome. Am J Respir Crit Care Med. 2004;169(2):156-62. Epub.
51. Collop N. Blue Light Special on CPAP, Aisle 11. Chest. 2006;129(1):6-7.
52. American Heart Association. Heart disease and stroke statistics–2005 update. Dallas: American Heart Association.
Ron F. Richard is senior vice president, strategic marketing for the Americas, ResMed Corp, Poway, Calif; Peter C. Gay, MD, is associate professor of medicine, Mayo College of Medicine, Rochester, Minn; Peter C. Farrell, PhD, is chairman and CEO, ResMed Corp