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INTRODUCTION — Obstructive sleep apnea (OSA) is a disorder that is characterized by obstructive apneas and hypopneas due to repetitive collapse of the upper airway during sleep. Untreated OSA has many potential consequences and adverse clinical associations, including excessive daytime sleepiness, impaired daytime function, metabolic dysfunction, and an increased risk of cardiovascular disease and mortality. (See "Overview of obstructive sleep apnea in adults", section on 'Complications and adverse outcomes'.)
The management of obstructive sleep apnea is reviewed here. The prevalence, risk factors, natural history, clinical manifestations, and diagnosis of OSA are discussed separately. (See "Overview of obstructive sleep apnea in adults" and "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)
GENERAL APPROACH — The goals of OSA therapy are to resolve signs and symptoms of OSA, improve sleep quality, and normalize the apnea-hypopnea index (AHI) and oxyhemoglobin saturation levels. OSA should be approached as a chronic disease that requires long-term, multidisciplinary management. The potential benefits of successfully treating OSA include clinical improvement (eg, less daytime sleepiness), reduced health care utilization and costs, and, possibly, decreased cardiovascular morbidity and mortality. (See "Overview of obstructive sleep apnea in adults", section on 'Complications and adverse outcomes'.)
Several national organizations have published clinical practice guidelines for the management of OSA in adults, including the American Academy of Sleep Medicine (AASM), the American Thoracic Society (ATS), the American College of Physicians (ACP), and the International Geriatric Sleep Medicine Force [1-6]. The recommendations discussed below are generally consistent with these guidelines.
Common to all guidelines is the recommendation that, in addition to reviewing the behavioral modifications reviewed in the next section, all patients diagnosed with OSA should be offered positive airway pressure as initial therapy. Issues relating to the precise definition of OSA, discrepancies between the consensus definition of OSA and the criteria used by the Centers for Medicare and Medicaid Services (CMS) to reimburse positive airway pressure therapy, and potential exceptions to this approach are discussed below. (See 'Indications for treatment' below.)
In patients with mild to moderate OSA who prefer not to use positive airway pressure or who fail to respond to it, oral appliances are an alternative therapy that have been shown to improve signs and symptoms of OSA and may be better tolerated in some patients than positive airway pressure . Upper airway surgery may supersede oral appliances as alternative therapy in patients with severe, surgically correctable, obstructing lesions of the upper airway. These alternatives to positive airway pressure therapy are discussed below. (See 'Alternative therapies' below.)
EDUCATION AND BEHAVIOR
Patient education — The management of a patient with OSA begins by firmly establishing the diagnosis and its severity. Disease severity guides management by identifying patients who are at greatest risk for adverse outcomes and by providing a baseline from which to measure the effectiveness of treatment . Diagnosis and disease severity are described separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)
Once the diagnosis of OSA is confirmed and its severity determined, the results of all testing should be reviewed with the patient. The patient should be educated about the risk factors, natural history, and consequences of OSA . Importantly, all patients should be warned about the increased risk of motor vehicle accidents associated with untreated OSA and the potential consequences of driving or operating other dangerous equipment while sleepy . Patients should also be counseled to avoid activities that require vigilance and alertness if sleepy. (See "Drowsy driving: Risks, evaluation, and management", section on 'Prevention and countermeasures'.)
Behavior modification — Behavior modification is indicated for all patients who have OSA and a modifiable risk factor. The types of behavior modification that should be instituted depend upon the characteristics of the patient. Overweight or obese patients should be encouraged to lose weight. Patients with positional OSA should change their sleep position accordingly. All patients should be advised that alcohol and certain common medications, such as benzodiazepines, may worsen their OSA.
Weight loss and exercise — Weight loss and exercise should be recommended to all patients with OSA who are overweight or obese [1,2,8]. While rarely leading to complete remission of OSA, weight loss, including that from bariatric surgery, has been shown to improve overall health and metabolic parameters, decrease the apnea-hypopnea index (AHI, the number of apneas and hypopneas per hour of sleep), reduce blood pressure, improve quality of life, and probably decrease daytime sleepiness [9-18]. (See "Obesity in adults: Health consequences".)
Initial treatment for weight loss should be aimed at decreasing food intake and, when possible increasing energy expenditure. Available strategies for weight loss include behavioral modification, dietary therapy, exercise, drug therapy, and surgery. These are discussed in detail separately. (See "Obesity in adults: Overview of management".)
The effects of weight loss on OSA were illustrated by a trial that enrolled 72 consecutive overweight patients (mean BMI 32 kg/m2) with mild OSA (mean AHI 10 events per hour of sleep) . The patients were randomly assigned to receive a single session of general nutrition and exercise advice, or a more intensive program that included a low calorie diet for three months plus nutrition and exercise counseling for one year. Patients in the latter group had significantly greater weight loss (11 versus 2 kg), reduction in the AHI (mean change from baseline, -4 versus 0.3 events per hour), and improvement in quality of life compared with the control group. There was no difference in the degree of improvement in daytime sleepiness, but the relevance of this is uncertain since the degree of daytime sleepiness was barely abnormal at baseline. Smaller studies that included patients with more severe OSA and more daytime sleepiness at baseline suggest that weight loss also improves daytime sleepiness .
The effect of weight loss achieved via bariatric surgery on OSA appears to be similar, with reductions in AHI proportional to weight loss but few complete remissions . (See "Medical outcomes following bariatric surgery", section on 'Obstructive sleep apnea'.)
Patients whose OSA improves or resolves after weight loss should strive to maintain their weight loss, since weight gain has been associated with worsening or recurrence of OSA [20-23]. In addition, CPAP therapy itself may be associated with weight gain [24-26]. Counseling regarding ongoing diet modification and exercise, as well as referral to a nutritionist, may be beneficial. Nevertheless, longer term follow up of several randomized studies suggests that the initial improvement in AHI achieved through weight loss can persist for several years despite up to 50 percent weight regain [14,27,28]. Such sustained improvement may be most relevant for patients with mild to moderate OSA at baseline rather than those with severe OSA, who have a lower likelihood of achieving clinically meaningful reductions in AHI and complete remission from weight loss at both early and late time points [14,29].
Exercise may modestly improve OSA even in the absence of significant weight loss. In a 2014 meta-analysis that included five small randomized trials, a supervised exercise program was associated with significantly improved AHI (mean change, -6 events/hour), sleep efficiency, subjective sleepiness, and cardiorespiratory fitness with minimal change in body weight .
Sleep position — During the diagnostic sleep study, some patients will be observed to have OSA that develops or worsens during sleep in the supine position. Such patients tend to have less severe OSA, to be less obese, and to be younger than non-positional patients . Sleeping in a non-supine position (eg, lateral recumbent) may correct or improve OSA in such patients and should be encouraged but not generally relied upon as the sole therapy [32-35].
Several commercial devices are available that use vibratory feedback around the chest or neck to restrict supine sleep [36-39]. However, sleeping in a non-supine position should not be used as the primary therapy unless normalization of the AHI when sleeping in a non-supine position has been confirmed by polysomnography and adherence can be verified [1,31]. In addition, there is a lack of long-term efficacy and adherence data on these devices.
Alcohol avoidance — All patients with untreated OSA should avoid alcohol, even during the daytime, because it can depress the central nervous system, exacerbate OSA, worsen sleepiness, and promote weight gain. Acute alcohol consumption often worsens the duration and frequency of obstructive respiratory events during sleep as well as the degree of oxyhemoglobin desaturation and snoring . In patients who snore but do not have OSA at baseline, alcohol consumption can prompt frank OSA.
Concomitant medications — Any clinician who prescribes medication for the patient should be informed that the patient has OSA, since certain medications with inhibitory effects on the central nervous system should be avoided if reasonable alternatives exist. In particular, benzodiazepines should be avoided in untreated patients.
Other medications that may exacerbate OSA and worsen daytime sleepiness include benzodiazepine receptor agonists, barbiturates, other antiepileptic drugs, sedating antidepressants, antihistamines, and opiates. Antidepressants that cause weight gain (eg, mirtazapine) might be particularly problematic in these patients. Some antidepressants may worsen sleep by causing restless legs syndrome or periodic limb movements. (See "Treatment of restless legs syndrome/Willis-Ekbom disease and periodic limb movement disorder in adults", section on 'Avoidance of aggravating factors'.)
When such medications are felt to be necessary despite the patient's OSA, their use should be monitored closely and the dose carefully titrated if possible. (See "The effects of medications on sleep quality and sleep architecture".)
POSITIVE AIRWAY PRESSURE THERAPY — Positive airway pressure therapy is the mainstay of therapy for adults with OSA. The mechanism of continuous positive airway pressure (CPAP) involves maintenance of a positive pharyngeal transmural pressure so that the intraluminal pressure exceeds the surrounding pressure . CPAP also stabilizes the upper airway through increased end-expiratory lung volume. As a result, respiratory events due to upper airway collapse (eg, apneas, hypopneas) are prevented.
Efficacy — There is high quality evidence from randomized trials and meta-analyses that in most adults, including the elderly, positive airway pressure therapy reduces the frequency of respiratory events during sleep, decreases daytime sleepiness, improves systemic blood pressure, lowers the risk of crashes, and improves quality of life across a range of disease severities [18,42-49]. However, no convincing effect on mortality has been demonstrated. As examples:
●In a meta-analysis of 35 randomized trials, CPAP compared with sham resulted in a significant reduction in the apnea-hypopnea index (AHI; mean difference -33.8 events/hour) as well as improved daytime sleepiness as assessed by the Epworth Sleepiness Scale (mean difference -2 points), systolic and diastolic blood pressure, and sleep-related quality of life . No appreciable effect on mortality was reported.
●In a meta-analysis of 22 randomized trials (1160 patients) that compared nocturnal CPAP with a control (sham CPAP, placebo tablets, or conservative management), nocturnal CPAP significantly improved both subjective and objective sleepiness, quality of life, cognitive function, and depression .
More limited data also suggest that positive airway pressure therapy can improve symptoms of gastroesophageal reflux , heart failure outcomes, and reduce the risk of recurrent atrial fibrillation and nocturnal arrhythmias. (See "Obstructive sleep apnea and cardiovascular disease" and "Sleep-disordered breathing in heart failure", section on 'Positive airway pressure therapy'.)
Direct comparisons of positive airway pressure to mandibular advancement devices (MAD) have used CPAP as the mode of positive airway pressure. Trials indicate that CPAP is more effective than MADs at reducing the frequency and severity of both respiratory events and oxyhemoglobin desaturation episodes during sleep, but symptomatic improvement is similar. Some studies have indicated that patients prefer oral appliances over CPAP therapy, at least with short-term follow-up . Similarly, a network meta-analyses of 80 randomized trials reported that CPAP was the most effective at reducing AHI, when compared to other OSA therapies including MADs, exercise training, and weight loss . The related MAD trials are described separately. (See "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Compared with positive airway pressure'.)
Although multiple observational studies have reported an association between CPAP use and decreased mortality [52-54], no randomized trial has demonstrated a mortality benefit from positive airway pressure therapy in patients with OSA . This may be because most randomized trials that have compared positive airway pressure with either no therapy or a sham therapy usually measured short-term outcomes, such as the frequency of respiratory events during sleep, daytime sleepiness, and quality of life, or because average CPAP usage achieved in most trials has not been sufficient to translate into measurable mortality benefit .
The effect of CPAP on body weight is unclear. One meta-analysis of 25 randomized controlled trials of mostly middle-aged men with moderate to severe OSA reported that three months of CPAP was associated with a small but significant increase in weight and body mass index . Although comparisons of CPAP patients with active lifestyle changes were excluded from the analysis, the effect was small and may not be clinically meaningful, especially in those in whom weight loss interventions are prescribed.
Indications for treatment — Different organizations advocate different thresholds for the initiation of positive airway pressure therapy in OSA, as the following examples demonstrate:
●The American Academy of Sleep Medicine (AASM) recommends offering positive airway pressure therapy to all patients who have been diagnosed with OSA [1,57]. OSA is defined as either an obstructive respiratory disturbance index (RDI) ≥15 events per hour with or without symptoms, or an obstructive RDI between 5 and 14 events per hour that is accompanied by any of the following: sleepiness, nonrestorative sleep, fatigue, or insomnia symptoms; waking up with breath holding, gasping, or choking; habitual snoring and/or breathing interruptions; hypertension, mood disorder, cognitive dysfunction, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, or type 2 diabetes . The obstructive RDI is the number of obstructive apneas, obstructive hypopneas, and respiratory effort related arousals (RERAs) per hour of sleep; it is usually higher than the AHI (the number of apneas and hypopneas per hour of sleep). (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Respiratory disturbance index'.)
●The Centers for Medicare and Medicaid Services (CMS) in the United States has its own guidelines for reimbursement of positive airway pressure therapy. Positive airway pressure therapy for OSA is reimbursed when the apnea-hypopnea index (AHI) is ≥15 events per hour, or between 5 and 14 events per hour and associated with excessive daytime sleepiness, impaired neurocognitive function, mood disorders, insomnia, cardiovascular disease (eg, hypertension, ischemic heart disease), or a history of stroke . The AHI is the number of apneas and hypopneas per hour of sleep. CMS will also reimburse for positive airway therapy if the OSA was diagnosed on the basis of an abnormal RDI. This permits therapy to be instituted on the basis of home testing. However, it is important to realize that the CMS defines the RDI as the number of apneas and hypopneas per hour of recording. This is different than the usual definition of the RDI because it does not count respiratory effort related arousals (RERAs) and it is calculated per hour of recording rather than per hour of sleep. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Apnea-hypopnea index'.)
While the AASM consensus guideline parameters are useful for the majority of patients, we and others suggest having a lower threshold for initiating therapy in several additional circumstances (algorithm 1) . Our approach is to also initiate therapy in the following groups of patients:
●Patients with an AHI >5 events per hour of sleep plus one or more clinical or physiologic sequelae attributable to OSA.
●Patients with an AHI ≥15 events per hour of sleep, even in the absence of symptoms.
●Patients who perform mission critical work (eg, airline pilots, air traffic controllers, locomotive engineers, bus and truck drivers) and have an AHI between 5 and 15 events per hour of sleep, even if there are no clinical or physiological symptoms attributable to OSA. Individuals with an AHI in this range who are truly asymptomatic may or may not be at risk for impaired driving. However, individuals tend to under-report symptoms when their occupation may be at risk, so judging whether a patient is symptomatic or not can be difficult. The decision to initiate therapy therefore requires some clinician judgement as well as recognition that the driver may be poorly motivated to report symptoms.
●Patients with an increased number of RERAs (eg, ≥10 per hour) and excessive daytime sleepiness, even if the AHI is ≤5 events per hour.
Modes of administration — The most common modes of positive airway pressure administration include continuous positive airway pressure (CPAP), bilevel positive airway pressure (BPAP), and autotitrating positive airway pressure (APAP). We generally favor CPAP as initial therapy because it is the most familiar and best studied.
The available modes of positive airway pressure therapy are summarized as follows :
●CPAP delivers positive airway pressure at a level that remains constant throughout the respiratory cycle. It is used most often because it is the simplest, the most extensively studied, and associated with the most clinical experience. A pressure relief setting (ie, lowers the positive airway pressure at the onset of exhalation) is sometimes used to improve comfort and tolerance of the device.
●BPAP delivers a preset inspiratory positive airway pressure (IPAP) and expiratory positive airway pressure (EPAP). The degree of pressure support and consequently tidal volume is related to the difference between the IPAP and EPAP. As an example, the tidal volume is greater using an IPAP of 15 cm H2O and an EPAP of 5 cm H2O (difference of 10 cm H2O), than an IPAP of 10 cm H2O and an EPAP of 5 cm H2O (difference of 5 cm H2O). There is no proven advantage to using BPAP instead of CPAP for the routine management of OSA . BPAP should not be confused with BiPAP, which is the brand name of a single manufacturer and is just one of many devices that can deliver BPAP.
●APAP increases or decreases the level of positive airway pressure in response to a change in airflow, a change in circuit pressure, or a vibratory snore (signs that generally indicate that upper airway resistance has changed). The degree of improvement of major outcomes conferred by APAP and CPAP is similar [61-65]. However, the performance of APAP can be highly variable, the body of evidence supporting its efficacy is more limited than that of fixed CPAP, and direct comparisons with fixed CPAP have not identified definitive benefits. (See "Initiation of positive airway pressure therapy for obstructive sleep apnea in adults", section on 'Auto-titrating CPAP'.)
●Adaptive servo-ventilation (ASV) provides a varying amount of inspiratory pressure superimposed on a low level of CPAP. It can be helpful in patients who have concomitant central apneas, which may occur as a consequence of CPAP (treatment-emergent central apneas), patients on long-acting opioids (narcotic-induced central sleep apnea), and patients who have had a stroke or kidney disease (central sleep apnea due to other conditions). However, based upon the SERVE-HF trial, caution should be exercised when using ASV in patients with heart failure and a Cheyne-Stokes breathing pattern, specifically those with a left ventricular ejection fraction of less than 45 percent, since a higher cardiovascular mortality in association with ASV use was reported in this population . (See "Central sleep apnea: Treatment", section on 'Patients with ejection fraction ≤45 percent'.)
Selection of a mode, titration of the positive airway pressure level, and other aspects of initiating positive airway pressure therapy are described in detail separately. (See "Initiation of positive airway pressure therapy for obstructive sleep apnea in adults".)
Adherence — Decreased adherence can lessen the potential benefits of CPAP therapy. It is estimated that 20 to 40 percent of patients do not use their positive airway pressure device and many others do not use it all night, every night [67-73]. In most studies, the average nightly usage of CPAP is only about four hours. Recognition of nonadherence is important because there are a variety of interventions that can help promote CPAP use, including troubleshooting device side effects and behavioral therapy. Adherence with positive airway pressure therapy is reviewed separately. (See "Adherence with continuous positive airway pressure (CPAP)".)
Follow-up — Patients who elect to be treated with positive airway pressure should be evaluated frequently, especially during the first few weeks of therapy . This may include frequent telephone calls and as-needed opportunities to meet face to face with a clinician. Adherence and efficacy can be monitored remotely with PAP devices that include modems. Communication with the devices can be bidirectional so that pressures can be adjusted remotely. The purpose of frequent evaluations is to quickly identify and manage any side effects that develop, since this may affect long-term adherence with the therapy. (See "Adherence with continuous positive airway pressure (CPAP)".)
Once any side effects of the positive airway pressure are successfully managed and the patient is adhering to the therapy, the patient should be asked whether the symptoms of OSA have resolved. In addition, objective data on compliance and effectiveness can be downloaded from the patient's device and reviewed, although studies on the accuracy of the information are mixed. An objective sleep evaluation is generally unnecessary if the symptoms of OSA have resolved, but repeat testing is indicated for patients who do not improve or who have recurrent or persistent symptoms such as daytime sleepiness . Objective testing may consist of polysomnography or type 3 home sleep apnea testing (HSAT) with concurrent CPAP use. (See "Home sleep apnea testing for obstructive sleep apnea in adults" and "Adherence with continuous positive airway pressure (CPAP)", section on 'Identification'.)
The purpose of such testing is to help the clinician determine the reason for the treatment failure. Possible causes of treatment failure include nonadherence or suboptimal adherence, weight gain, an inappropriate level of prescribed positive pressure, or an additional disorder causing sleepiness (eg, narcolepsy) that may require alterations in the therapeutic regimen. A review of medications should also be undertaken since many drugs may lead to sleepiness. Inadequate sleep time may also negate the expected effects from treatment of OSA.
Once the patient's positive airway pressure therapy has been optimized and symptoms resolved, a regimen of long-term follow-up should be established. Annual visits are reasonable, with more frequent visits in between if new issues arise . The purpose of long-term follow-up is to assess usage and monitor for recurrent OSA, new side effects, air leakage, and fluctuations in body weight.
OSA has been associated with other medical conditions, such as diabetes, hypertension, heart failure, and ischemic heart disease. Any comorbid condition that may be impacted by OSA should be monitored closely following the initiation of OSA-specific therapy. Therapy directed at such comorbidities may need to be modified once therapy for OSA is instituted. As an example, dosages of antihypertensive medications may need to be reduced after successful treatment of OSA . (See "Obstructive sleep apnea and cardiovascular disease".)
ALTERNATIVE THERAPIES — Oral appliances (eg, mandibular advancement devices, tongue retaining devices) are an alternative therapeutic strategy in OSA that may be offered to patients with mild to moderate OSA who decline or fail to adhere to positive airway pressure therapy and who have a preference for such treatment. (See 'Oral appliances' below.)
A variety of surgical approaches have also been explored in OSA; their role is primarily in patients with severe, obstructing lesions of the upper airway who have failed positive airway pressure therapy and an oral device. (See 'Upper airway surgery' below.)
Hypoglossal nerve stimulation is a novel strategy that is emerging as a potential treatment option in selected patients. (See "Surgical treatment of obstructive sleep apnea in adults", section on 'Global upper airway procedures'.)
Oral appliances — For patients with mild or moderate OSA who decline or fail to adhere to positive airway pressure therapy, an oral appliance is a reasonable alternative to positive airway pressure. This is based upon the recognition that while positive airway pressure is generally more effective than an oral appliance at normalizing respiratory events and oxyhemoglobin desaturation episodes during sleep [43,75], most patients prefer an oral appliance, adherence is an essential aspect of successful treatment, both modalities are effective compared to no treatment or a sham treatment, and both modalities have a similar effect on symptoms and quality of life. (See "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Compared with positive airway pressure'.)
Oral appliances have variable efficacy in patients with severe OSA and/or significant sleep-related hypoxemia; such patients are not good candidates for an oral appliance as first-line therapy and should be encouraged to use positive airway pressure therapy. (See "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Patient selection'.)
There are an increasing number of oral appliances that are designed to either protrude the mandible forward (ie, mandibular advancement/repositioning splints, devices, or appliances) or hold the tongue in a more anterior position (ie, tongue retaining devices). Either design holds the soft tissues of the oropharynx away from the posterior pharyngeal wall, thereby maintaining upper airway patency.
Oral appliances decrease the frequency of respiratory events, arousals, and episodes of oxyhemoglobin desaturation, compared to no treatment or a sham intervention. They may also improve daytime sleepiness, quality of life, and neurocognitive function. Their impact on mortality is unknown. These outcomes are discussed in detail separately. (See "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Outcome'.)
Patient assessment, device selection, device titration, follow-up, and adverse effects related to the use of oral appliances are discussed separately. (See "Oral appliances in the treatment of obstructive sleep apnea in adults".)
Upper airway surgery — There is no consensus regarding the role of surgery in patients with OSA of varying degrees of severity, nor have optimal screening or imaging procedures been established that accurately predict which patients are most likely to benefit from surgery. We generally consider surgical therapy when positive airway pressure or an oral appliance is declined or ineffective (after at least a three month trial of therapy). Surgical treatment appears to be most effective in patients who have OSA due to a severe, surgically correctable, obstructing lesion of the upper airway. Examples of surgically correctable lesions that may obstruct the upper airway include tonsillar hypertrophy, adenoid hypertrophy, or craniofacial abnormalities [1,8,76].
Hypoglossal nerve stimulation via an implantable neurostimulator device (picture 1) is a novel treatment strategy that may have a role in selected patients with moderate to severe OSA, although early results are mixed and further data are needed. Uncontrolled studies and a meta-analysis of such studies have shown significant reductions in AHI and oxygen saturation index as well as improvement in subjective measures of sleepiness after device implantation in selected patients [77-85].
Surgical treatments and hypoglossal nerve stimulation for patients with OSA are discussed separately. (See "Surgical treatment of obstructive sleep apnea in adults".)
Pharmacologic — A variety of pharmacologic agents have been investigated in randomized trials as primary therapeutic agents for the management of sleep-disordered breathing on OSA, with the goal of replacing the more burdensome therapies described above. This includes drugs that might act to stimulate respiratory drive directly (eg, theophylline) or indirectly (eg, acetazolamide) or drugs that reduce upper airway collapsibility (eg, desipramine) . However, no pharmacologic agent has proven to be sufficiently effective to warrant replacement of such therapies [8,87].
PERSISTENT SLEEPINESS — Pharmacologic therapy (with agents such as modafinil or armodafinil) may be beneficial as adjunctive therapy for excessive daytime sleepiness that persists despite documentation of adequate and successful conventional therapy (eg, positive airway pressure, oral appliances) [1,88,89]. Prior to the initiating pharmacologic therapy, adherence with conventional therapy should be confirmed and alternative causes of daytime sleepiness should be excluded. The use of pharmacologic therapy to treat persistent sleepiness is discussed in detail separately. (See "Evaluation and management of residual sleepiness in obstructive sleep apnea".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Daytime sleepiness (The Basics)")
●Beyond the Basics topics (see "Patient education: Sleep apnea in adults (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Obstructive sleep apnea (OSA) is a common disorder that is characterized by obstructive apneas and hypopneas due to repetitive collapse of the upper airway during sleep. (See 'Introduction' above.)
●OSA should be approached as a chronic disease that requires long-term, multidisciplinary care. Management begins with patient education. Importantly, patients should be warned about the increased risk of motor vehicle accidents associated with untreated OSA and the potential consequences of driving while sleepy. (See 'Patient education' above.)
●The desired outcomes of treatment include resolution of signs and symptoms of OSA and the normalization of sleep quality, the apnea-hypopnea index (AHI), and oxyhemoglobin saturation levels. A variety of effective behavioral and airway-specific therapies are available for the treatment of OSA, including weight loss, positive airway pressure therapy, oral appliances, and surgical procedures. (See 'General approach' above.)
●Behavior modification is indicated for most patients who have OSA. This includes losing weight (if overweight or obese), exercising, changing the sleep position (if OSA is positional), abstaining from alcohol, and avoiding certain medications. (See 'Behavior modification' above.)
●For patients with mild to moderate OSA, we suggest positive airway pressure as initial therapy rather than an oral appliance (Grade 2B). For patients who anticipate problems with positive airway pressure therapy adherence, an oral appliance is a reasonable alternative as first-line therapy. (See 'Oral appliances' above.)
●Surgical therapy is generally reserved for selected patients in whom positive airway pressure or an oral appliance was either declined, not an option, or ineffective. A notable exception is patients whose OSA is due to a surgically correctable obstructing lesion. For such patients, surgical resection of the obstructing lesion is first-line therapy. Hypoglossal nerve stimulation via an implantable neurostimulator device is a novel treatment strategy that may have a role in selected patients with moderate to severe OSA who decline or fail to adhere to positive airway pressure therapy, but further data are required. (See 'Upper airway surgery' above and "Surgical treatment of obstructive sleep apnea in adults".)
●Patients who continue to have excessive daytime sleepiness despite adequate OSA-specific therapy that is severe enough to warrant treatment may benefit from adjunctive pharmacologic therapy. This is discussed in detail separately. (See "Evaluation and management of residual sleepiness in obstructive sleep apnea".)
- Epstein LJ, Kristo D, Strollo PJ Jr, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009; 5:263.
- Qaseem A, Holty JE, Owens DK, et al. Management of obstructive sleep apnea in adults: A clinical practice guideline from the American College of Physicians. Ann Intern Med 2013; 159:471.
- Strohl KP, Brown DB, Collop N, et al. 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; 187:1259.
- Chowdhuri S, Quan SF, Almeida F, et al. An Official American Thoracic Society Research Statement: Impact of Mild Obstructive Sleep Apnea in Adults. Am J Respir Crit Care Med 2016; 193:e37.
- Netzer NC Chair, Ancoli-Israel S Co-Chair, Bliwise DL, et al. Principles of practice parameters for the treatment of sleep disordered breathing in the elderly and frail elderly: the consensus of the International Geriatric Sleep Medicine Task Force. Eur Respir J 2016; 48:992.
- Gurubhagavatula I, Sullivan S, Meoli A, et al. Management of Obstructive Sleep Apnea in Commercial Motor Vehicle Operators: Recommendations of the AASM Sleep and Transportation Safety Awareness Task Force. J Clin Sleep Med 2017; 13:745.
- Phillips CL, Grunstein RR, Darendeliler MA, 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; 187:879.
- Randerath WJ, Verbraecken J, Andreas S, et al. Non-CPAP therapies in obstructive sleep apnoea. Eur Respir J 2011; 37:1000.
- Smith PL, Gold AR, Meyers DA, et al. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985; 103:850.
- Tuomilehto HP, Seppä JM, Partinen MM, et al. Lifestyle intervention with weight reduction: first-line treatment in mild obstructive sleep apnea. Am J Respir Crit Care Med 2009; 179:320.
- Dixon JB, Schachter LM, O'Brien PE, et al. Surgical vs conventional therapy for weight loss treatment of obstructive sleep apnea: a randomized controlled trial. JAMA 2012; 308:1142.
- Araghi MH, Chen YF, Jagielski A, et al. Effectiveness of lifestyle interventions on obstructive sleep apnea (OSA): systematic review and meta-analysis. Sleep 2013; 36:1553.
- Foster GD, Borradaile KE, Sanders MH, et al. 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.
- Kuna ST, Reboussin DM, Borradaile KE, et al. Long-term effect of weight loss on obstructive sleep apnea severity in obese patients with type 2 diabetes. Sleep 2013; 36:641.
- Mitchell LJ, Davidson ZE, Bonham M, et al. Weight loss from lifestyle interventions and severity of sleep apnoea: a systematic review and meta-analysis. Sleep Med 2014; 15:1173.
- Chirinos JA, Gurubhagavatula I, Teff K, et al. CPAP, weight loss, or both for obstructive sleep apnea. N Engl J Med 2014; 370:2265.
- Ng SS, Chan RS, Woo J, et al. A Randomized Controlled Study to Examine the Effect of a Lifestyle Modification Program in OSA. Chest 2015; 148:1193.
- Jonas DE, Amick HR, Feltner C, et al. Screening for Obstructive Sleep Apnea in Adults: Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA 2017; 317:415.
- Browman CP, Sampson MG, Yolles SF, et al. Obstructive sleep apnea and body weight. Chest 1984; 85:435.
- Newman AB, Foster G, Givelber R, et al. Progression and regression of sleep-disordered breathing with changes in weight: the Sleep Heart Health Study. Arch Intern Med 2005; 165:2408.
- Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000; 284:3015.
- Pillar G, Peled R, Lavie P. Recurrence of sleep apnea without concomitant weight increase 7.5 years after weight reduction surgery. Chest 1994; 106:1702.
- Kajaste S, Telakivi T, Pihl S, Partinen M. Effects of a weight reduction program on sleep apnea: A two year follow-up. Sleep Res 1991; 20A:332.
- Quan SF, Budhiraja R, Clarke DP, et al. Impact of treatment with continuous positive airway pressure (CPAP) on weight in obstructive sleep apnea. J Clin Sleep Med 2013; 9:989.
- Redenius R, Murphy C, O'Neill E, et al. Does CPAP lead to change in BMI? J Clin Sleep Med 2008; 4:205.
- Garcia JM, Sharafkhaneh H, Hirshkowitz M, et al. Weight and metabolic effects of CPAP in obstructive sleep apnea patients with obesity. Respir Res 2011; 12:80.
- Johansson K, Hemmingsson E, Harlid R, et al. Longer term effects of very low energy diet on obstructive sleep apnoea in cohort derived from randomised controlled trial: prospective observational follow-up study. BMJ 2011; 342:d3017.
- Tuomilehto H, Gylling H, Peltonen M, et al. Sustained improvement in mild obstructive sleep apnea after a diet- and physical activity-based lifestyle intervention: postinterventional follow-up. Am J Clin Nutr 2010; 92:688.
- Tuomilehto H, Seppä J, Uusitupa M, et al. Weight reduction and increased physical activity to prevent the progression of obstructive sleep apnea: A 4-year observational postintervention follow-up of a randomized clinical trial. [corrected]. JAMA Intern Med 2013; 173:929.
- Iftikhar IH, Kline CE, Youngstedt SD. Effects of exercise training on sleep apnea: a meta-analysis. Lung 2014; 192:175.
- Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep 2006; 29:1031.
- Jokic R, Klimaszewski A, Crossley M, et al. Positional treatment vs continuous positive airway pressure in patients with positional obstructive sleep apnea syndrome. Chest 1999; 115:771.
- Cartwright R, Ristanovic R, Diaz F, et al. A comparative study of treatments for positional sleep apnea. Sleep 1991; 14:546.
- de Vries GE, Hoekema A, Doff MH, et al. Usage of positional therapy in adults with obstructive sleep apnea. J Clin Sleep Med 2015; 11:131.
- Benoist L, de Ruiter M, de Lange J, de Vries N. A randomized, controlled trial of positional therapy versus oral appliance therapy for position-dependent sleep apnea. Sleep Med 2017; 34:109.
- van Maanen JP, de Vries N. Long-term effectiveness and compliance of positional therapy with the sleep position trainer in the treatment of positional obstructive sleep apnea syndrome. Sleep 2014; 37:1209.
- van Maanen JP, Meester KA, Dun LN, et al. The sleep position trainer: a new treatment for positional obstructive sleep apnoea. Sleep Breath 2013; 17:771.
- Levendowski DJ, Seagraves S, Popovic D, Westbrook PR. Assessment of a neck-based treatment and monitoring device for positional obstructive sleep apnea. J Clin Sleep Med 2014; 10:863.
- Eijsvogel MM, Ubbink R, Dekker J, et al. Sleep position trainer versus tennis ball technique in positional obstructive sleep apnea syndrome. J Clin Sleep Med 2015; 11:139.
- Issa FG, Sullivan CE. Alcohol, snoring and sleep apnea. J Neurol Neurosurg Psychiatry 1982; 45:353.
- Jordan AS, McSharry DG, Malhotra A. Adult obstructive sleep apnoea. Lancet 2014; 383:736.
- Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981; 1:862.
- Giles TL, Lasserson TJ, Smith BJ, et al. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev 2006; :CD001106.
- Patel SR, White DP, Malhotra A, et al. 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.
- McDaid C, Durée KH, Griffin SC, et al. A systematic review of continuous positive airway pressure for obstructive sleep apnoea-hypopnoea syndrome. Sleep Med Rev 2009; 13:427.
- Martínez-García MÁ, Chiner E, Hernández L, et al. Obstructive sleep apnoea in the elderly: role of continuous positive airway pressure treatment. Eur Respir J 2015; 46:142.
- Salord N, Fortuna AM, Monasterio C, et al. A Randomized Controlled Trial of Continuous Positive Airway Pressure on Glucose Tolerance in Obese Patients with Obstructive Sleep Apnea. Sleep 2016; 39:35.
- Martínez-Cerón E, Barquiel B, Bezos AM, et al. Effect of Continuous Positive Airway Pressure on Glycemic Control in Patients with Obstructive Sleep Apnea and Type 2 Diabetes. A Randomized Clinical Trial. Am J Respir Crit Care Med 2016; 194:476.
- McEvoy RD, Antic NA, Heeley E, et al. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. N Engl J Med 2016; 375:919.
- Tamanna S, Campbell D, Warren R, Ullah MI. Effect of CPAP Therapy on Symptoms of Nocturnal Gastroesophageal Reflux among Patients with Obstructive Sleep Apnea. J Clin Sleep Med 2016; 12:1257.
- Iftikhar IH, Bittencourt L, Youngstedt SD, et al. Comparative efficacy of CPAP, MADs, exercise-training, and dietary weight loss for sleep apnea: a network meta-analysis. Sleep Med 2017; 30:7.
- Campos-Rodriguez F, Martinez-Garcia MA, de la Cruz-Moron I, et al. Cardiovascular mortality in women with obstructive sleep apnea with or without continuous positive airway pressure treatment: a cohort study. Ann Intern Med 2012; 156:115.
- Campos-Rodriguez F, Peña-Griñan N, Reyes-Nuñez N, et al. Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure. Chest 2005; 128:624.
- Marti S, Sampol G, Muñoz X, et al. Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment. Eur Respir J 2002; 20:1511.
- Barbé F, Durán-Cantolla J, Sánchez-de-la-Torre M, et al. 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.
- Drager LF, Brunoni AR, Jenner R, et al. Effects of CPAP on body weight in patients with obstructive sleep apnoea: a meta-analysis of randomised trials. Thorax 2015; 70:258.
- Berry RB, Budhiraja R, Gottlieb DJ, et al. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. Deliberations of the Sleep Apnea Definitions Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med 2012; 8:597.
- American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, Darien, IL 2014.
- www.cms.hhs.gov/Transmittals/Downloads/R35NCD.pdf (Accessed on July 14, 2009).
- Reeves-Hoché MK, Hudgel DW, Meck R, et al. Continuous versus bilevel positive airway pressure for obstructive sleep apnea. Am J Respir Crit Care Med 1995; 151:443.
- Nussbaumer Y, Bloch KE, Genser T, Thurnheer R. Equivalence of autoadjusted and constant continuous positive airway pressure in home treatment of sleep apnea. Chest 2006; 129:638.
- Fietze I, Glos M, Moebus I, et al. Automatic pressure titration with APAP is as effective as manual titration with CPAP in patients with obstructive sleep apnea. Respiration 2007; 74:279.
- Ayas NT, Patel SR, Malhotra A, et al. Auto-titrating versus standard continuous positive airway pressure for the treatment of obstructive sleep apnea: results of a meta-analysis. Sleep 2004; 27:249.
- Carlucci A, Ceriana P, Mancini M, et al. Efficacy of Bilevel-auto Treatment in Patients with Obstructive Sleep Apnea Not Responsive to or Intolerant of Continuous Positive Airway Pressure Ventilation. J Clin Sleep Med 2015; 11:981.
- Pépin JL, Tamisier R, Baguet JP, et al. Fixed-pressure CPAP versus auto-adjusting CPAP: comparison of efficacy on blood pressure in obstructive sleep apnoea, a randomised clinical trial. Thorax 2016; 71:726.
- Cowie MR, Woehrle H, Wegscheider K, et al. Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure. N Engl J Med 2015; 373:1095.
- Waldhorn RE, Herrick TW, Nguyen MC, et al. Long-term compliance with nasal continuous positive airway pressure therapy of obstructive sleep apnea. Chest 1990; 97:33.
- Rolfe I, Olson LG, Saunders NA. Long-term acceptance of continuous positive airway pressure in obstructive sleep apnea. Am Rev Respir Dis 1991; 144:1130.
- Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis 1992; 145:841.
- Krieger J, Kurtz D. Objective measurement of compliance with nasal CPAP treatment for obstructive sleep apnoea syndrome. Eur Respir J 1988; 1:436.
- Meurice JC, Dore P, Paquereau J, et al. Predictive factors of long-term compliance with nasal continuous positive airway pressure treatment in sleep apnea syndrome. Chest 1994; 105:429.
- Reeves-Hoche MK, Meck R, Zwillich CW. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med 1994; 149:149.
- Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993; 147:887.
- Somers V, Javaheri S. Heart failure and arrhythmias in obstructive sleep apnea. In: Principles and Practice of Sleep Medicine, 4th ed, Kryger MH, Roth T, Dement WC (Eds), Saunders, Philadelphia 2005.
- Bratton DJ, Gaisl T, Schlatzer C, Kohler M. Comparison of the effects of continuous positive airway pressure and mandibular advancement devices on sleepiness in patients with obstructive sleep apnoea: a network meta-analysis. Lancet Respir Med 2015; 3:869.
- Senchak AJ, McKinlay AJ, Acevedo J, et al. The effect of tonsillectomy alone in adult obstructive sleep apnea. Otolaryngol Head Neck Surg 2015; 152:969.
- Eastwood PR, Barnes M, Walsh JH, et al. Treating obstructive sleep apnea with hypoglossal nerve stimulation. Sleep 2011; 34:1479.
- Goding GS Jr, Tesfayesus W, Kezirian EJ. Hypoglossal nerve stimulation and airway changes under fluoroscopy. Otolaryngol Head Neck Surg 2012; 146:1017.
- Schwartz AR, Barnes M, Hillman D, et al. Acute upper airway responses to hypoglossal nerve stimulation during sleep in obstructive sleep apnea. Am J Respir Crit Care Med 2012; 185:420.
- Van de Heyning PH, Badr MS, Baskin JZ, et al. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope 2012; 122:1626.
- Mwenge GB, Rombaux P, Dury M, et al. Targeted hypoglossal neurostimulation for obstructive sleep apnoea: a 1-year pilot study. Eur Respir J 2013; 41:360.
- Strollo PJ Jr, Soose RJ, Maurer JT, et al. Upper-airway stimulation for obstructive sleep apnea. N Engl J Med 2014; 370:139.
- Certal VF, Zaghi S, Riaz M, et al. Hypoglossal nerve stimulation in the treatment of obstructive sleep apnea: A systematic review and meta-analysis. Laryngoscope 2015; 125:1254.
- Strollo PJ Jr, Gillespie MB, Soose RJ, et al. Upper Airway Stimulation for Obstructive Sleep Apnea: Durability of the Treatment Effect at 18 Months. Sleep 2015; 38:1593.
- Woodson BT, Soose RJ, Gillespie MB, et al. Three-Year Outcomes of Cranial Nerve Stimulation for Obstructive Sleep Apnea: The STAR Trial. Otolaryngol Head Neck Surg 2016; 154:181.
- Taranto-Montemurro L, Sands SA, Edwards BA, et al. Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation. Eur Respir J 2016; 48:1340.
- Mason M, Welsh EJ, Smith I. Drug therapy for obstructive sleep apnoea in adults. Cochrane Database Syst Rev 2013; :CD003002.
- Sukhal S, Khalid M, Tulaimat A. Effect of Wakefulness-Promoting Agents on Sleepiness in Patients with Sleep Apnea Treated with CPAP: A Meta-Analysis. J Clin Sleep Med 2015; 11:1179.
- Chapman JL, Vakulin A, Hedner J, et al. Modafinil/armodafinil in obstructive sleep apnoea: a systematic review and meta-analysis. Eur Respir J 2016; 47:1420.