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Obstructive sleep apnea: Overview of management in adults

Obstructive sleep apnea: Overview of management in adults
Author:
Atul Malhotra, MD
Section Editor:
Nancy Collop, MD
Deputy Editor:
Geraldine Finlay, MD
Literature review current through: Jan 2024.
This topic last updated: Nov 20, 2023.

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 including excessive daytime sleepiness, impaired daytime function, metabolic dysfunction, and an increased risk of cardiovascular disease and mortality.

An overview of the management of OSA is reviewed here. Other related OSA topics are discussed separately and include the following:

●(See "Clinical presentation and diagnosis of obstructive sleep apnea in adults".)

●(See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea".)

●(See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)

●(See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)

●(See "Downloading data from positive airway pressure devices in adults".)

●(See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea".)

●(See "Hypoglossal nerve stimulation for adult patients with obstructive sleep apnea".)

●(See "Oral appliances in the treatment of obstructive sleep apnea in adults".)

●(See "Surgical treatment of obstructive sleep apnea in adults".)

The recommendations discussed in this topic are for, the most part, consistent with guidelines issues by several national organizations, including the American Academy of Sleep Medicine, American Thoracic Society, American College of Physicians, International Geriatric Sleep Medicine Force, and others [1-9].

GENERAL ISSUES FOR ALL PATIENTS

Supportive care — General measures include the following:

●All patients with OSA should exercise as tolerated, receive routine vaccinations (figure 1), be counselled against cigarette and cannabis smoking (and vaping), and maintain a normal body mass index (BMI). (See "Standard immunizations for nonpregnant adults" and "Overview of smoking cessation management in adults".)

●Patients with OSA should be additionally treated for any comorbidities known to be associated with or worsen OSA. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Risk factors and associated conditions'.)

Treatment providers vary from primary care clinicians to sleep subspecialists. We prefer sleep care to be delivered by providers with training and expertise in sleep. A meta-analysis of five randomized trials and three observational studies found that treatment provided by sleep and nonsleep specialists resulted in similar symptom scores, quality of life, and adherence [10]. However, many of the nonsleep specialists also had extensive training or experience in sleep medicine, which may have biased the outcomes. Other studies have suggested similar results [11].

Patient education — Once the diagnosis of OSA is confirmed and its severity determined (see "Clinical presentation and diagnosis of obstructive sleep apnea in adults"), we educate the patient regarding the following:

●We inform the patient about risk factors that worsen OSA as well as the consequences of untreated OSA. Importantly, we warn patients about the increased risk of motor vehicle crashes associated with untreated OSA and the potential consequences of driving or operating other dangerous equipment while sleepy [3]. We also counsel patients to avoid activities that require vigilance and alertness and inform them about the cardiovascular risks associated with OSA. (See "Drowsy driving: Risks, evaluation, and management", section on 'Prevention and countermeasures' and "Obstructive sleep apnea and cardiovascular disease in adults" and "Sleep-related breathing disorders and stroke".)

●We also counsel patients about informing their medical providers that they have OSA, especially if they are to have surgery, become pregnant, or start opiate medications [12]. (See "Surgical risk and the preoperative evaluation and management of adults with obstructive sleep apnea" and "Postoperative management of adults with obstructive sleep apnea" and "Obstructive sleep apnea in pregnancy".)

●We also inform patients that positive airway pressure (PAP) therapy is a life-long therapy that does not cure OSA. Complete remission of OSA using risk factor modification is rare. (See 'Weight loss and exercise' below.)

●We inform females of childbearing age regarding the risk of worsening OSA control and possible fetal harm during pregnancy. (See "Obstructive sleep apnea in pregnancy".)

Behavior modification — For patients who have OSA and a modifiable risk factor, we advise behavior modification. These include weight loss (for those who are overweight), altered sleep position (for those with positional OSA), and avoidance of alcohol and sedatives.

Weight loss and exercise — In patients with OSA who are overweight or obese, we recommend weight loss and participation in an exercise regimen [1,2,13,14]. Available strategies for weight loss include behavioral modification, dietary therapy, exercise, drug therapy, and surgery. In particular, for adults with OSA and obesity (class II/III, BMI ≥35 kg/m2) who are intolerant of or decline PAP therapy, we consider early referral to a bariatric surgeon [15,16]. Further details regarding strategies for weight loss are provided separately. (See "Outcomes of bariatric surgery", section on 'Obstructive sleep apnea' and "Obesity in adults: Overview of management".)

For patients with OSA who lose weight, we rely on clinical judgement to inform a repeat sleep study. Some patients demonstrate a dose-response effect while others have a threshold effect with weight loss. We usually base our decision to perform a repeat sleep study on factors including improved symptoms, significant weight loss that is currently stable, or intolerance of PAP.

Weight loss, including that from bariatric surgery, has several benefits from an OSA standpoint, although complete remission of OSA is rare. Weight loss has been shown to 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 [17-29]. As examples:

●In one study of 72 patients with mild OSA and obesity (ie, mean AHI 10 events per hour of sleep and mean BMI 32 kg/m2), patients who underwent a low-calorie diet for three months plus nutrition and exercise counseling for one year had significantly greater weight loss (11 versus 2 kg), reduction in AHI (mean change from baseline -4 versus 0.3 events per hour), and improvement in quality of life compared with patients who underwent a single session of general nutrition and exercise advice [18]. There was no difference in the degree of improvement in daytime sleepiness, but the relevance of this is uncertain since the OSA was mild and the degree of daytime sleepiness was barely abnormal at baseline.

●A smaller study that included patients with more severe OSA and more daytime sleepiness at baseline suggested that weight loss also improves daytime sleepiness [30].

●Another retrospective study suggested a dose-response relationship between weight loss and OSA severity [28].

●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 [19].

●Patients with severe OSA have a lower likelihood of achieving clinically meaningful reductions in AHI and complete remission from weight loss [22,29].

For patients whose OSA improves or resolves after weight loss, we advise that they maintain their weight loss since weight gain has been associated with worsening or recurrence of OSA [31-34]. Counseling regarding ongoing diet modification and exercise, as well as referral to a nutritionist, may facilitate weight loss maintenance. Although weak data suggest that continuous PAP therapy itself may be associated with weight gain [35-38], longer-term follow-up of several randomized studies suggest that the initial improvement in AHI achieved through weight loss can persist for several years (as long as 10 years) despite up to 50 percent weight regain [14,22,39,40]. Such sustained improvement may be most relevant for patients with mild to moderate OSA at baseline rather than those with severe OSA. The impact of PAP on weight gain is discussed below. (See 'Efficacy' below.)

Exercise itself may modestly improve OSA even in the absence of significant weight loss. In a 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 [41].

The general benefits of weight loss and impact of bariatric surgery on health outcomes are described separately. (See "Obesity in adults: Overview of management", section on 'Importance of weight loss' and "Outcomes of bariatric surgery".)

Nonsupine sleep position — Some patients have OSA that develops or worsens during sleep in the supine position (typically observed during the diagnostic sleep study). These patients tend to have less severe OSA, be less obese, and be younger than patients who do not have positional OSA [42]. For such patients, we encourage sleeping in a nonsupine position (eg, lateral recumbent), which may correct or improve OSA, but is not generally relied upon as the sole therapy [43-47].

Several commercial devices are available that use vibratory feedback around the chest or neck to restrict supine sleep [48-51]. However, there is a lack of long-term efficacy and adherence data on these devices.

Alcohol, sedating, and select medications avoidance — We encourage avoidance of substances that can act as central nervous system depressants, disrupt sleep architecture, and potentially worsen OSA and daytime sleepiness. When medications are felt to be necessary despite the patient's OSA, we clinically monitor sleep quality and if feasible, carefully titrate the dose of the selected agent. (See "The effects of medications on sleep quality and sleep architecture".)

●We advise all patients with untreated OSA to avoid or reduce alcohol within two to four hours prior to sleep because it can depress the central nervous system, exacerbate OSA, worsen sleepiness, and promote weight gain [52,53]. 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 [54] The impact of alcohol avoidance on OSA control has not been formally studied.

●We also advise the avoidance of certain medications, provided reasonable alternatives exist. These include the following:

•Sedatives, in particular, benzodiazepines should be avoided in untreated patients with OSA due to their potential to worsen OSA control and symptoms of daytime sleepiness.

•Other medications that may exacerbate OSA and theoretically worsen daytime sleepiness include benzodiazepine receptor agonists, barbiturates, other antiepileptic medications (eg, gabapentin [55]), sedating antidepressants (eg, tricyclic antidepressants), antihistamines, and opiates. Select antidepressants may also worsen OSA control by causing weight gain (eg, mirtazapine) or worsen sleep quality by causing restless legs syndrome or periodic limb movements. (See "Management of restless legs syndrome and periodic limb movement disorder in adults", section on 'Avoidance of aggravating factors'.)

●We do not support cannabis use as a therapy for OSA. The American Academy of Sleep Medicine states that "medical cannabis and/or its synthetic extracts should not be used for the treatment of OSA due to unreliable delivery methods and insufficient evidence of effectiveness, tolerability, and safety" [56].

POSITIVE AIRWAY PRESSURE (PAP) THERAPY — Positive airway pressure (PAP) therapy is the mainstay of therapy for adults with OSA. PAP therapy prevents respiratory events due to upper airway collapse (eg, apneas, hypopneas) by maintaining a positive pharyngeal transmural pressure so that the intraluminal pressure exceeds the surrounding pressure and by increasing end-expiratory lung volume [57].

Indications — Different organizations advocate different thresholds for the initiation of PAP therapy in OSA. These are discussed below.

Our approach — Our approach is the following:

●Apnea-hypopnea index (AHI; number of apneas and hypopneas per hour of sleep) ≥15 – For patients with OSA and an AHI ≥15 events per hour of sleep, even in the absence of symptoms, we recommend PAP as initial therapy rather than no therapy or other therapies such as oral devices and hypoglossal nerve stimulation (HNS) (algorithm 1) [4]. This recommendation is based upon randomized trials in this population, which have demonstrated that PAP therapy reduces obstructive events during sleep, reduces daytime symptoms of sleepiness, lowers the risk of motor vehicle crashes, and improves systemic blood pressure (BP), erectile dysfunction, and quality of life. However, a mortality benefit has not been demonstrated. PAP therapy appears to be effective across a range of disease severities; however, patients with severe OSA (AHI ≥30 events per hour) are most likely to benefit. Limited clinical trial data comparing PAP therapy with oral devices suggest that PAP therapy is more effective in reducing AHI. There are no data comparing PAP therapy and HNS. (See 'Efficacy' below.)

●Other groups – We also suggest initiating therapy in several additional patients including the following:

•Patients with an AHI >5 and <15 events per hour of sleep who perform mission critical work (eg, airline pilots, air traffic controllers, locomotive engineers, bus and truck drivers), even in the absence of clinical or physiologic sequelae 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. While this is a common indication for PAP, there are no data to support it.

•Patients with an AHI ≤5 events per hour who have an increased number of respiratory effort-related arousals (RERAs) (eg, ≥10 per hour) and excessive daytime sleepiness. Noteworthy is that RERAs can only be reliably identified on polysomnography.

While patients in these categories were underrepresented in the available clinical trials, it is reasonable to expect that they would have similar benefits from PAP therapy.

For patients who decline PAP therapy, options are discussed below. (See 'Patients who fail, do not tolerate, or decline PAP therapy' below.)

The American Academy of Sleep Medicine — The American Academy of Sleep Medicine (AASM) recommends offering PAP therapy to all patients who have been diagnosed with OSA [1,58]. OSA is defined as either of the following [59,60]:

●An obstructive respiratory disturbance index (RDI) ≥15 events per hour of sleep

●An obstructive RDI >5 and <15 events per hour that is accompanied by any of the following: sleepiness, fatigue, insomnia, or other symptoms leading to impaired sleep-related quality of life; waking up with breath-holding, gasping, or choking; habitual snoring or breathing interruptions during sleep

The obstructive RDI is the number of obstructive apneas, obstructive hypopneas, and RERAs per hour of sleep; it is usually higher than the AHI. It behooves the clinician to be aware of the AASM definitions for apneas, hypopneas, and RERAs. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Respiratory disturbance index'.)

The Centers for Medicare and Medicaid Services — The Centers for Medicare and Medicaid Services (CMS) in the United States has its own guidelines for reimbursement of PAP therapy.

PAP therapy for OSA is reimbursed for the following [61]:

●When the AHI is ≥15 events per hour

●When the AHI is between 5 and 14 events per hour and associated with excessive daytime sleepiness

CMS will also reimburse for PAP therapy if the OSA was diagnosed on the basis of an abnormal RDI (similar to that listed for the AASM above (see 'The American Academy of Sleep Medicine' above)) or an RDI/AHI equivalent (eg, respiratory event index [REI]). The latter permits therapy to be instituted on the basis of home testing. However, it is important to realize that the REI is the number of apneas and hypopneas per hour of recording. This is different than the usual definition of the RDI or AHI because it does not count RERAs and it is calculated per hour of recording rather than per hour of sleep. A discussion on definitions, advantages, and disadvantages of AHI, REI, and RDI is provided separately. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults", section on 'Apnea-hypopnea index' and "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Criteria'.)

Efficacy — PAP has been compared with no therapy and with other therapies.

●PAP compared with no therapy – There is high-quality evidence from randomized trials and meta-analyses that in most adults, including older adults, PAP therapy reduces the frequency of respiratory events during sleep, decreases daytime sleepiness, lowers the risk of crashes, and improves systemic BP, erectile dysfunction, symptoms of gastroesophageal reflux, glycemic control (in patents with diabetes), and quality of life when compared with no therapy [62-75]. These benefits are evident across a range of disease severities, but those with severe OSA are most likely to benefit (eg, AHI ≥30 events per hour). The effect on cognition and depressive symptoms is unclear. However, the effect on cardiovascular events or mortality is less certain. As examples:

•In a 2019 meta-analysis from the AASM, compared with no therapy, CPAP had a significant impact on OSA severity (-23 events per hour, 95% CI -29 to -18 events/hour), Epworth Sleepiness Scale score (-2.4 points, 95% CI -2.8 to -1.9 points), nighttime systolic BP (-4.2 mmHg, 95% CI -6.0 to -2.5 mmHg), diastolic BP (-2.3 mmHg, 95% CI -3.7 to -0.9), and 24-hour mean BP (-2.6 mmHg, 95% CI -3.4 to -1.4 mmHg) [7]. Continuous PAP (CPAP) also positively impacted the rate of motor vehicle crashes (risk ratio 0.3, 95% CI 0.2-0.4) and quality of life. However, CPAP had no impact on cardiovascular events (eg, myocardial infarction, stroke), mortality, neurocognitive function, mood, fasting glucose or hemoglobin A1C, left ventricular ejection fraction, or risk of hospitalization.

•Although multiple observational studies have reported an association between CPAP use and decreased mortality [76-78], no randomized trial has demonstrated a mortality benefit from PAP therapy in patients with OSA. This may be because most randomized trials that have compared PAP 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 a measurable mortality benefit [79].

•The impact of PAP therapy (mostly fixed-level CPAP) in older adults and impact on cardiovascular events including heart failure, atrial fibrillation, and nocturnal arrhythmias are described separately. (See "Causes of impaired sleep including sleep apnea in older adults", section on 'Positive airway pressure' and "Obstructive sleep apnea and cardiovascular disease in adults" and "Sleep-disordered breathing in heart failure", section on 'Positive airway pressure therapy'.)

•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 [38]. Although comparison 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.

•Whether there is a difference in therapeutic effect when oronasal rather than nasal masks are used is unclear. However, one network meta-analysis of 29 studies (6378 patients) reported that nasal masks or pillows were associated with lower residual AHI, lower PAP pressure, and greater PAP adherence compared with oronasal masks [80].

•CPAP may improve glycemic control among patients with diabetes. In a meta-analysis of 11 trials totaling nearly 1000 patients, CPAP therapy reduced the hemoglobin A1c (HbA1c) (mean difference -0.24 percent, 95% CI -0.43 to -0.06%) compared with patients not receiving CPAP [75]. The degree of improvement was proportional to the hours of nightly use.

●PAP compared with other therapies – Limited studies have compared PAP with other OSA therapies.

•A network meta-analyses of 80 randomized trials reported that CPAP was the most effective therapy for reducing AHI when compared with other OSA therapies including mandibular advancement devices (MADs), exercise training, and weight loss [81]. Data on the efficacy of surgical therapy was not included in the analysis.

•Most clinical trials and several meta-analyses that compared MADs with PAP (usually CPAP) report that PAP is superior at improving the AHI and oxyhemoglobin saturation, but not the arousal index, or sleep architecture [63,82-92]. However, patients generally preferred and adhered better to the oral appliance. The procedure and efficacy of MADs are described separately (see "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Efficacy and outcomes').

CPAP has not been directly compared with other therapies such as HNS or other surgical therapies since surgical trials generally enroll patients who fail CPAP.

Mode selection, titration, initiation — In patients with OSA, in whom PAP is indicated, the two most common initial modes of PAP administration include auto-titrating PAP (APAP) and fixed-level CPAP. Other modes that are less commonly used include bilevel PAP (BPAP) and rarely adaptive servo-ventilation (ASV). While CPAP was more commonly used in the past, in the era of home sleep testing, APAP is now more commonly used and is the mode of preference during pregnancy.

●Types — The available modes of PAP therapy and mechanism of action are as follows:

•Fixed-level CPAP delivers PAP at a level that remains constant throughout the respiratory cycle. It is the simplest mode, most extensively studied, and associated with the most clinical experience. A pressure-relief setting (ie, lowers the PAP at the onset of exhalation) is sometimes used to improve comfort and tolerance of the device. Determining the optimal fixed-level of CPAP requires titration. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'In-laboratory fixed-level continuous positive airway pressure (CPAP)'.)

•APAP increases or decreases the level of PAP in response to a change in airflow, change in circuit pressure, or vibratory snore (ie, signs that generally indicate that upper airway resistance has changed). The degree of improvement of major outcomes conferred by APAP and CPAP is similar [93-97]. 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-level CPAP have not identified definitive benefits over CPAP. Patient selection for APAP and its titration are discussed separately. (See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea", section on 'Uncomplicated obstructive sleep apnea' and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Titration'.)

•BPAP delivers a preset inspiratory PAP (IPAP) and expiratory PAP (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 or APAP for the routine management of OSA [98]. BPAP should not be confused with BiPAP, the brand name of a single manufacturer and is just one of many devices that can deliver BPAP. Patient selection for BPAP and its titration are discussed separately. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Initial settings and titration'.)

•ASV provides a varying amount of inspiratory pressure superimposed on a low level of CPAP. It can be helpful in patients who have OSA and 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, caution should be exercised when using ASV in patients with concomitant 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 [99]. (See "Central sleep apnea: Treatment", section on 'Patients with ejection fraction ≤45 percent'.)

●Mode selection, settings titration, and initiation — Once the indication is met, we select a mode, typically APAP or a PAP titration for fixed-level CPAP (algorithm 2 and table 1). When adequate, good, or optimal PAP settings are identified, PAP therapy is initiated at home. Selection of a mode, titration of the PAP level, adequacy of PAP settings, and other aspects of initiating PAP therapy are described in detail separately. (See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)

Device selection — Device selection is determined by the mode selected and often chosen by the homecare provider (eg, APAP devices, CPAP device). We prefer FDA-approved (not cleared) devices. We also avoid ozone cleaning devices for PAP machines (which also invalidate the device's warranty). It is prudent that the clinician be aware of what device the patient has and encourage appropriate maintenance.

Most Philips CPAP and BPAP devices were recalled in June 2021 due to potential health risks related to polyester-based polyurethane (PE-PUR) foam that is used as a sound abatement tool in these units. Potential harms and reported complaints include headache, airway irritation, cough, chest pressure, and sinus infection. Carcinogenic risks may also exist, though attributable cases are not at this time reported in association with machine use. The American Academy of Sleep Medicine and the American Thoracic Society advise that patients discuss with their provider what steps to take, which may include switching to an alternate device, if available, or to an alternate mode of therapy. Patients can register online with Philips Respironics to have the foam, or their machine, replaced. The US Food and Drug Administration is investigating whether the replacement foam may also be problematic, but has not advised that patients stop using machines with replaced foam. A retrospective study of PAP devices that were claimed from 2012 to 2021 (median follow-up 7.5 years) reported no difference in the rate of cancer (including lung cancer) among those who had Philips or non-Philips manufacturer devices (adjusted hazard ratio 0.94, 95% CI 0.71-1.25) [100]. Study limitations include its retrospective nature, potential confounding variables, and median follow-up of only 7.5 years. Further data are necessary before making firm conclusions regarding the risk of cancer or other adverse effects from PE-PUR-containing devices.

FOLLOW-UP — Patients with OSA in whom positive airway pressure (PAP) therapy is initiated, require follow-up. Throughout follow-up, we remind the patient of the potential benefits of successfully treating OSA in the long-term, including clinical improvement (eg, less daytime sleepiness and reduced risk of vehicle crashes) and improved systemic blood pressure, erectile dysfunction, and quality of life. Data that support these outcomes are discussed above. (See 'Efficacy' above.)

Goals of PAP therapy — The goals of OSA therapy are to resolve signs and symptoms of OSA, improve sleep quality, and normalize the apnea-hypopnea index. This information is often obtained from the device itself and does not necessitate a repeat sleep study. Another goal is normalization of oxyhemoglobin saturation levels, which requires overnight oximetry that we perform, if available.

The goals of PAP titration are described separately. (See "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Titration goals'.)

Initial follow-up — Following PAP therapy initiation, we perform frequent evaluations during the first few weeks of therapy (eg, between 30 and 90 days). This support varies from center to center but generally involves any combination of frequent telephone calls and as-needed opportunities to meet face-to-face with a clinician. The purpose of frequent evaluations is to quickly identify and manage any side effects that develop since early intervention has been shown to improve long-term adherence to PAP therapy. Trouble-shooting common adverse effects that can occur during or following titration and initiation are described separately. (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Factors that influence initial success' and "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea", section on 'Evaluate and manage the suspected etiology'.)

Long-term follow-up — We approach OSA as a chronic disease that requires long-term, multidisciplinary management.

●For those who tolerate PAP therapy and reach their targeted goals, we schedule annual visits, 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, alteration in medications, and fluctuations in body weight. (See 'Goals of PAP therapy' above and 'Patients who achieve goals' below.)

●For those who do not tolerate or decline PAP therapy, we offer other therapeutic options so that patients may still gain some benefit from OSA treatment. (See 'Patients who fail, do not tolerate, or decline PAP therapy' below.)

Adherence and efficacy can also be monitored remotely with newer PAP devices that include modems. Communication with the devices can be bidirectional so that settings can be adjusted remotely. For those devices without modems, manual adjustment of settings or device accessories can be performed in the home by a home-care provider. (See "Downloading data from positive airway pressure devices in adults".)

OSA has been associated with medical conditions such as diabetes, systemic and pulmonary 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 [101], although in most patients the impact of OSA therapy on comorbidities is relatively minor and does not resolve any underlying condition. (See "Obstructive sleep apnea and cardiovascular disease in adults".)

PATIENTS WHO ACHIEVE GOALS — For patients who achieve the above-stated goals, positive airway pressure (PAP) should be continued and patients clinically monitored over their lifetime of PAP use. Details regarding long-term follow up is described above. (See 'Long-term follow-up' above.)

PATIENTS WHO DO NOT ACHIEVE GOALS — Possible causes of treatment failure include nonadherence, alternate etiology for symptoms, and/or inadequate therapy, the management of which is mostly discussed in the linked topics below. (See 'Nonadherence' below and 'Alternative etiology' below and 'Inadequate therapy' below.)

Once resolved, we reassess the patient during follow-up to evaluate whether they meet the goal of positive airway pressure (PAP) therapy. (See 'Follow-up' above.)

Nonadherence — Nonadherence or suboptimal adherence is common (eg, up to 50 percent) and should be assessed in all patients who have residual symptoms after PAP initiation (table 2 and algorithm 3). (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)

Alternative etiology — Although less common than nonadherence, we always keep in mind, alternative etiologies for sleepiness that may contribute to residual symptoms. Potential etiologies are listed on the table (table 3) and discussed separately. (See "Approach to the patient with excessive daytime sleepiness" and "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea", section on 'Exclude alternative etiologies'.)

Inadequate therapy — Inadequate therapy is often due to insufficient pressure or mode to meet the patient's need, which in turn, may be due to weight gain, inadequate initial titration, new medications, device malfunction, poorly fitting mask, air leaks, and/or treatment emergent central sleep apnea.

This evaluation involves clinical assessment focused on these potential etiologies and may also involve a repeat titration study. Once the etiology is identified, we address it and re-evaluate clinically during follow-up. Further details on the evaluation of adequate therapy and titration of PAP are provided separately. (See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea", section on 'Evaluate adequacy of therapy' and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Titration goals'.)

PATIENTS WHO FAIL, DO NOT TOLERATE, OR DECLINE PAP THERAPY — For patients who fail, do not tolerate, or decline positive airway pressure (PAP) therapy, options include an oral appliance or upper airway surgery (among which there are several types). This assessment is individualized and involves evaluating factors including the patient's suitability for an oral device or surgery, the patient's expected response to a specific therapy, the patient's preference, and available expertise. For most patients, we recommend not using pharmacologic therapies to treat OSA.

Surgically correctable pathology

Upper airway surgery — A minority of patients with OSA may have a surgically correctable airway obstruction (eg, tonsil enlargement) or anatomy (eg, retrognathia) contributing to OSA. In such cases, surgery may be effective in treating OSA (eg, tonsillectomy, maxillomandibular advancement, uvulopalatoplasty). In some cases, nasal surgery (eg, polypectomy) is sometimes performed as an adjunctive procedure to improve the efficacy of PAP therapy. These issues are discussed separately. (See "Surgical treatment of obstructive sleep apnea in adults".)

No surgically correctable pathology — For patients who fail, do not tolerate, or decline PAP therapy, but do not have surgically correctable airway obstruction or anatomy, other management options include hypoglossal nerve stimulation (HNS) or a mandibular oral device. Both treatments have advantages and disadvantages and the choice between them depends upon comorbidities, fitness for surgery, values and preferences of the individual, cost, and availability. Insurance restrictions can be a limitation in some cases.

Oral appliances — Oral appliances (eg, mandibular advancement devices, tongue retaining devices) are an alternative therapeutic strategy for patients with OSA. The table summarizes factors that influence patient selection for oral appliance therapy (table 4). Details regarding patient selection for and efficacy of oral appliance therapy compared with PAP therapy are provided separately. (See "Oral appliances in the treatment of obstructive sleep apnea in adults", section on 'Patient selection' and 'Efficacy' above.)

Hypoglossal nerve surgery — HNS is becoming increasingly used in patients with OSA. The tables summarizes factors that influence patient selection for an oral appliance therapy (table 4). Details regarding patient selection for oral appliance therapy are provided separately. (See "Surgical treatment of obstructive sleep apnea in adults", section on 'Patient selection' and "Hypoglossal nerve stimulation for adult patients with obstructive sleep apnea", section on 'Patient selection'.)

Refractory patients — There are limited options in patients who are refractory to therapy (eg, pharmacologic agents). Tracheostomy is no longer used.

Pharmacologic — We generally avoid pharmacologic agents and only use them as a last resort in patients who fail or decline PAP therapy who are also not suitable for oral appliance therapy or surgery.

A variety of pharmacologic agents have been investigated in randomized trials as primary therapeutic agents for the management of sleep-disordered breathing in OSA. This includes drugs that might act to stimulate respiratory drive directly (eg, theophylline) or indirectly (eg, acetazolamide, sulthiame), drugs that reduce upper airway collapsibility (eg, desipramine), antimuscarinics (eg, oxybutynin), or noradrenergic agents (eg, atomoxetine, reboxetine) [102-106]. However, no pharmacologic agent has proven to be sufficiently effective to warrant replacement of routine therapies [13,107]. No pharmacologic therapy has been approved by the FDA for OSA treatment.

Carbonic anhydrase inhibitors have been proposed as agents that potentially stimulate respiratory drive. Preliminary findings in 56 patients with moderate or severe OSA who were intolerant of PAP reported that the carbonic anhydrase inhibitor sulthiame reduced the AHI from 55.2 to 33.0 events/hour (400 mg group; placebo group 53.9 events/hour) and from 61.1 to 40.6 events/hour (200 mg; placebo 50.9 events/hour) [108]. Although there were no serious adverse events, intermittent paraesthesias were common and six patients withdrew due to side effects when on the higher dose of sulthiame. Further studies are required before sulthiame can be used routinely in patients with OSA.

We agree with the American Academy of Sleep Medicine who do not support the use of medical cannabis and/or synthetic extracts as pharmacologic therapy in patients with OSA [56]. Preliminary data in a phase II study of 73 adults with moderate or severe OSA reported that the cannabinoid dronabinol, administered one hour before bedtime reduced the AHI from 25.9 events per hour to 15.2 events per hour (2.5 mg dose) and 13.0 events per hour (10 mg dose), findings that were statistically significant when compared with placebo [109]. However, the mental wakefulness test scores did not improve significantly, suggesting that the clinical significance of the drop in AHI is uncertain. Adverse events were equal among the groups, were rare, and included diarrhea, vomiting, dizziness, and visual disturbances. Phase III trials should highlight whether this drug is effective as a therapy for moderate to severe OSA.

Several trials have examined the value of an atomoxetine-oxybutynin combination [104,110-112]. One randomized study of 20 patients reported that one dose of atomoxetine-oxybutynin administered prior to sleep lowered AHI by 63 percent (28.5 to 7.5 events/h) [104]. Further studies are needed before this combination can be used routinely.

PERSISTENT SLEEPINESS DESPITE GOOD OSA CONTROL — Patients with persistent sleepiness who have adequately treated OSA and in whom other causes of daytime sleepiness have been reasonably excluded may be candidates for wakefulness-promoting agents, such as modafinil, armodafinil, or solriamfetol. This evaluation is discussed in detail separately. (See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea".)

COVID-19 — Guidance for clinicians and patients regarding the administration of PAP therapy for OSA during the coronavirus disease 2019 (COVID-19) pandemic is provided by the American Academy of Sleep Medicine, Canadian Thoracic Society, and Australasian Sleep Association. (See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection" and 'Society guideline links' below.)

In brief:

●Sleep facility leaders suggest vaccination in accordance with the United States Centers for Disease Control and Prevention guidelines. Sleep apnea is not by itself a risk factor for severe disease or hospitalization, but obesity or other comorbidities may increase this risk. (See "COVID-19: Vaccines".)

●Increased vigilance regarding infection prevention when patients with OSA have COVID-19 is also preferred especially with the increased aerosolization of viral particles due to PAP therapy. Patients should not stop their PAP therapy during infection. (See "COVID-19: Infection prevention for persons with SARS-CoV-2 infection".)

INVESTIGATIONAL — The use of neuromuscular training and/or stimulation during the daytime has shown some promising results in early studies, but further data will be required before this approach can be widely recommended. Efforts to identify the subset of OSA patients that may benefit from this type of intervention are ongoing [113].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders in adults" and "Society guideline links: COVID-19 – Index of guideline topics".)

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: Sleep apnea in adults (The Basics)" and "Patient education: Daytime sleepiness (The Basics)")

●Beyond the Basics topic (see "Patient education: Sleep apnea in adults (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●General care for all patients – 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. General management involves the following (see 'General issues for all patients' above):

•Supportive care (eg, routine vaccinations, avoidance of smoking, treatment of comorbidities). (See 'Supportive care' above.)

•Patient education regarding the risk factors for and complications of untreated OSA, particularly the increased risk of motor vehicle crashes. (See 'Patient education' above.)

•Behavior modification for those with a modifiable risk factor. This includes losing weight (if overweight or obese), exercising, changing the sleep position (if OSA is positional), and avoiding alcohol and certain medications that can interfere with sleep or worsen daytime sleepiness. (See 'Behavior modification' above.)

●Positive airway pressure (PAP) – The indications for PAP therapy varies. Our approach is shown in the algorithm (algorithm 1).

•Apnea-hypopnea index (AHI) ≥15 events per hour – For patients with OSA and an AHI ≥15 events per hour of sleep, we recommend PAP as initial therapy rather than no therapy (Grade 1B) and we suggest PAP therapy rather than other therapies, such as oral devices and hypoglossal nerve stimulation (HNS) (Grade 2C). (See 'Positive airway pressure (PAP) therapy' above and 'Our approach' above.)

This recommendation is based upon randomized trials in this population that have demonstrated that PAP therapy reduces obstructive events during sleep, decreases daytime symptoms of sleepiness, lowers the risk of motor vehicle crashes, and improves systemic blood pressure, erectile dysfunction, and quality of life. However, a mortality benefit is less certain. PAP therapy appears to be effective across a range of disease severities; however, patients with severe OSA (AHI ≥30 events per hour) are most likely to benefit. Limited clinical trial data comparing PAP therapy with oral devices suggest that PAP therapy is more effective in reducing AHI. There are no data comparing PAP therapy with HNS. (See 'Efficacy' above.)

•Other indications – We also suggest PAP therapy for select patients with OSA who have an AHI <15 if there are circumstances that place them at increased risk (Grade 2C):

-Patients with an AHI >5 and <15 events per hour of sleep who perform mission critical work (eg, airline pilots, air traffic controllers, locomotive engineers, bus and truck drivers).

-Patients with an AHI ≤5 events per hour who have an increased number of respiratory effort-related arousals (eg, ≥10 per hour) and excessive daytime sleepiness.

While patients in these categories were underrepresented in clinical trials, it is reasonable to expect that they would have similar benefits from PAP therapy.

•Titration and initiation – Once the indication is met, PAP therapy is typically initiated at home. Details are found in the algorithm and table (algorithm 2 and table 1) and discussed separately. (See "Mode selection for titration of positive airway pressure in adults with obstructive sleep apnea" and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea".)

●Follow-up goals – We follow patients frequently during the first few weeks of PAP therapy to look for resolution of the signs and symptoms of OSA, improvement in sleep quality, and normalization of the AHI and oxyhemoglobin saturation levels. (See 'Follow-up' above and 'Goals of PAP therapy' above.)

•Treatment success – For patients who achieve the above-stated goals, PAP should be continued and patients clinically monitored over their lifetime of PAP use. (See 'Patients who achieve goals' above.)

•Treatment failure – Possible causes of treatment failure include any combination of the following, which are mostly discussed in the linked topics below:

-Nonadherence (table 2 and algorithm 3) – (See "Assessing and managing nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep apnea".)

-An alternate etiology for symptoms (table 3) – (See "Approach to the patient with excessive daytime sleepiness" and "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea", section on 'Exclude alternative etiologies'.)

-Inadequate therapy – (See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea", section on 'Evaluate adequacy of therapy' and "Titration of positive airway pressure therapy for adults with obstructive sleep apnea", section on 'Titration goals'.)

●Patients who fail, do not tolerate, or decline PAP – For patients who fail, do not tolerate, or decline PAP therapy, the assessment is individualized. Our general approach is as follows (see 'Patients who fail, do not tolerate, or decline PAP therapy' above):

•A minority of patients with OSA may have surgically correctable airway obstruction (eg, tonsil enlargement) or anatomy (eg, retrognathia) contributing to OSA. In such cases, surgery may be effective in treating OSA (eg, tonsillectomy, maxillomandibular advancement, uvulopalatoplasty). In some cases, nasal surgery (eg, polypectomy) is sometimes performed as an adjunctive procedure to improve the efficacy of PAP therapy. These issues are discussed separately. (See 'Surgically correctable pathology' above and "Surgical treatment of obstructive sleep apnea in adults".)

•For patients who fail, do not tolerate, or decline PAP therapy and do not have surgically correctable pathology, other management options include HNS or an oral appliance. Both treatments have advantages and disadvantages and the choice between them depends upon comorbidities, fitness for surgery, values and preferences of the individual, cost, and availability. Insurance restrictions can be a limitation in some cases. The tables summarize selection criteria for HNS (table 5) and oral appliances (table 4). These treatments are discussed in greater detail separately. (See 'No surgically correctable pathology' above and "Hypoglossal nerve stimulation for adult patients with obstructive sleep apnea" and "Oral appliances in the treatment of obstructive sleep apnea in adults".)

•For most patients, we recommend not using pharmacologic therapies to treat OSA (Grade 1B). A variety of medications have been investigated as potential therapeutic agents for OSA (including theophylline, acetazolamide, sulthiame, desipramine, oxybutynin, atomoxetine, reboxetine, sulthiame, dronabinol). However, none have been proven to be sufficiently effective to warrant routine use. These agents are reserved as a last resort option for individuals who fail, do not tolerate, or decline PAP therapy, an oral appliance, and surgery. (See 'Pharmacologic' above.)

●Persistent sleepiness – Patients with persistent sleepiness who have adequately treated OSA and in whom other causes of daytime sleepiness have been reasonably excluded may be candidates for wakefulness promoting agents such as modafinil, armodafinil, or solriamfetol. This evaluation is discussed in detail separately. (See "Evaluation and management of residual excessive sleepiness in adults with obstructive sleep apnea".)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Meir H Kryger, MD, FRCPC, who contributed to earlier versions of this topic review.

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  98. 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.
  99. 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.
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  103. Eskandari D, Zou D, Grote L, et al. Acetazolamide Reduces Blood Pressure and Sleep-Disordered Breathing in Patients With Hypertension and Obstructive Sleep Apnea: A Randomized Controlled Trial. J Clin Sleep Med 2018; 14:309.
  104. Taranto-Montemurro L, Messineo L, Sands SA, et al. The Combination of Atomoxetine and Oxybutynin Greatly Reduces Obstructive Sleep Apnea Severity. A Randomized, Placebo-controlled, Double-Blind Crossover Trial. Am J Respir Crit Care Med 2019; 199:1267.
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Topic 7695 Version 101.0

References

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2 : Management of obstructive sleep apnea in adults: A clinical practice guideline from the American College of Physicians.

3 : An official American Thoracic Society Clinical Practice Guideline: sleep apnea, sleepiness, and driving risk in noncommercial drivers. An update of a 1994 Statement.

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5 : 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.

6 : Management of Obstructive Sleep Apnea in Commercial Motor Vehicle Operators: Recommendations of the AASM Sleep and Transportation Safety Awareness Task Force.

7 : Treatment of Adult Obstructive Sleep Apnea With Positive Airway Pressure: An American Academy of Sleep Medicine Systematic Review, Meta-Analysis, and GRADE Assessment.

8 : Treatment of Adult Obstructive Sleep Apnea with Positive Airway Pressure: An American Academy of Sleep Medicine Clinical Practice Guideline.

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10 : Provider Types and Outcomes in Obstructive Sleep Apnea Case Finding and Treatment: A Systematic Review.

11 : Management of obstructive sleep apnoea in a primary care vs sleep unit setting: a randomised controlled trial.

12 : A matched cohort study of postoperative outcomes in obstructive sleep apnea: could preoperative diagnosis and treatment prevent complications?

13 : Non-CPAP therapies in obstructive sleep apnoea.

14 : Effects of Weight Loss on Obstructive Sleep Apnea Severity. Ten-Year Results of the Sleep AHEAD Study.

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16 : Referral of adults with obstructive sleep apnea for surgical consultation: an American Academy of Sleep Medicine systematic review, meta-analysis, and GRADE assessment.

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18 : Lifestyle intervention with weight reduction: first-line treatment in mild obstructive sleep apnea.

19 : Surgical vs conventional therapy for weight loss treatment of obstructive sleep apnea: a randomized controlled trial.

20 : Effectiveness of lifestyle interventions on obstructive sleep apnea (OSA): systematic review and meta-analysis.

21 : A randomized study on the effect of weight loss on obstructive sleep apnea among obese patients with type 2 diabetes: the Sleep AHEAD study.

22 : Long-term effect of weight loss on obstructive sleep apnea severity in obese patients with type 2 diabetes.

23 : Weight loss from lifestyle interventions and severity of sleep apnoea: a systematic review and meta-analysis.

24 : CPAP, weight loss, or both for obstructive sleep apnea.

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28 : Dose-response relationship between weight loss and improvements in obstructive sleep apnea severity after a diet/lifestyle interventions: secondary analyses of the "MIMOSA" randomized clinical trial.

29 : 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].

30 : Obstructive sleep apnea and body weight.

31 : Progression and regression of sleep-disordered breathing with changes in weight: the Sleep Heart Health Study.

32 : Longitudinal study of moderate weight change and sleep-disordered breathing.

33 : Recurrence of sleep apnea without concomitant weight increase 7.5 years after weight reduction surgery.

34 : Effects of a weight reduction program on sleep apnea: A two year follow-up

35 : Impact of treatment with continuous positive airway pressure (CPAP) on weight in obstructive sleep apnea.

36 : Does CPAP lead to change in BMI?

37 : Weight and metabolic effects of CPAP in obstructive sleep apnea patients with obesity.

38 : Effects of CPAP on body weight in patients with obstructive sleep apnoea: a meta-analysis of randomised trials.

39 : Longer term effects of very low energy diet on obstructive sleep apnoea in cohort derived from randomised controlled trial: prospective observational follow-up study.

40 : Sustained improvement in mild obstructive sleep apnea after a diet- and physical activity-based lifestyle intervention: postinterventional follow-up.

41 : Effects of exercise training on sleep apnea: a meta-analysis.

42 : Practice parameters for the medical therapy of obstructive sleep apnea.

43 : Positional treatment vs continuous positive airway pressure in patients with positional obstructive sleep apnea syndrome.

44 : A comparative study of treatments for positional sleep apnea.

45 : Usage of positional therapy in adults with obstructive sleep apnea.

46 : A randomized, controlled trial of positional therapy versus oral appliance therapy for position-dependent sleep apnea.

47 : Evaluation of a Trial Period With a Sleep Position Trainer in Patients With Positional Sleep Apnea.

48 : Long-term effectiveness and compliance of positional therapy with the sleep position trainer in the treatment of positional obstructive sleep apnea syndrome.

49 : The sleep position trainer: a new treatment for positional obstructive sleep apnoea.

50 : Assessment of a neck-based treatment and monitoring device for positional obstructive sleep apnea.

51 : Sleep position trainer versus tennis ball technique in positional obstructive sleep apnea syndrome.

52 : Alcohol and the risk of sleep apnoea: a systematic review and meta-analysis.

53 : Bedtime ethanol increases resistance of upper airways and produces sleep apneas in asymptomatic snorers.

54 : Alcohol, snoring and sleep apnea.

55 : Gabapentin acutely increases the apnea-hypopnea index in older men: data from a randomized, double-blind, placebo-controlled study.

56 : Medical Cannabis and the Treatment of Obstructive Sleep Apnea: An American Academy of Sleep Medicine Position Statement.

57 : Adult obstructive sleep apnoea.

58 : 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.

59 : Metrics of sleep apnea severity: beyond the apnea-hypopnea index.

60 : Metrics of sleep apnea severity: beyond the apnea-hypopnea index.

61 : Metrics of sleep apnea severity: beyond the apnea-hypopnea index.

62 : Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares.

63 : Continuous positive airways pressure for obstructive sleep apnoea in adults.

64 : Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis.

65 : A systematic review of continuous positive airway pressure for obstructive sleep apnoea-hypopnoea syndrome.

66 : Obstructive sleep apnoea in the elderly: role of continuous positive airway pressure treatment.

67 : A Randomized Controlled Trial of Continuous Positive Airway Pressure on Glucose Tolerance in Obese Patients with Obstructive Sleep Apnea.

68 : Effect of Continuous Positive Airway Pressure on Glycemic Control in Patients with Obstructive Sleep Apnea and Type 2 Diabetes. A Randomized Clinical Trial.

69 : CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea.

70 : Effects of CPAP and Mandibular Advancement Devices on Health-Related Quality of Life in OSA: A Systematic Review and Meta-analysis.

71 : CPAP therapy improves erectile function in patients with severe obstructive sleep apnea.

72 : Effect of Positive Airway Pressure Therapy on Drowsy Driving in a Large Clinic-Based Obstructive Sleep Apnea Cohort.

73 : The HIPARCO-2 study: long-term effect of continuous positive airway pressure on blood pressure in patients with resistant hypertension: a multicenter prospective study.

74 : Effect of CPAP Therapy on Symptoms of Nocturnal Gastroesophageal Reflux among Patients with Obstructive Sleep Apnea.

75 : Effects of continuous positive airway pressure therapy on glucose metabolism in patients with obstructive sleep apnoea and type 2 diabetes: a systematic review and meta-analysis.

76 : Cardiovascular mortality in women with obstructive sleep apnea with or without continuous positive airway pressure treatment: a cohort study.

77 : Mortality in obstructive sleep apnea-hypopnea patients treated with positive airway pressure.

78 : Mortality in severe sleep apnoea/hypopnoea syndrome patients: impact of treatment.

79 : 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.

80 : In search of a better CPAP interface: A network meta-analysis comparing nasal masks, nasal pillows and oronasal masks.

81 : Comparative efficacy of CPAP, MADs, exercise-training, and dietary weight loss for sleep apnea: a network meta-analysis.

82 : Oral appliances for snoring and obstructive sleep apnea: a review.

83 : Titrated mandibular advancement versus positive airway pressure for sleep apnoea.

84 : Health outcomes of continuous positive airway pressure versus mandibular advancement device for the treatment of severe obstructive sleep apnea: an individual participant data meta-analysis.

85 : Oral appliances for obstructive sleep apnoea.

86 : Efficacy and co-morbidity of oral appliances in the treatment of obstructive sleep apnea-hypopnea: a systematic review.

87 : Mandibular advancement splints and continuous positive airway pressure in patients with obstructive sleep apnoea: a randomized cross-over trial.

88 : Oral appliance therapy versus nasal continuous positive airway pressure in obstructive sleep apnea: a randomized, placebo-controlled trial.

89 : Health outcomes of continuous positive airway pressure versus oral appliance treatment for obstructive sleep apnea: a randomized controlled trial.

90 : 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.

91 : Effects of CPAP and mandibular advancement device treatment in obstructive sleep apnea patients: a systematic review and meta-analysis.

92 : Effectiveness of oral appliances versus continuous positive airway pressure in treatment of OSA patients: An updated meta-analysis.

93 : Equivalence of autoadjusted and constant continuous positive airway pressure in home treatment of sleep apnea.

94 : Automatic pressure titration with APAP is as effective as manual titration with CPAP in patients with obstructive sleep apnea.

95 : Auto-titrating versus standard continuous positive airway pressure for the treatment of obstructive sleep apnea: results of a meta-analysis.

96 : Efficacy of Bilevel-auto Treatment in Patients with Obstructive Sleep Apnea Not Responsive to or Intolerant of Continuous Positive Airway Pressure Ventilation.

97 : Fixed-pressure CPAP versus auto-adjusting CPAP: comparison of efficacy on blood pressure in obstructive sleep apnoea, a randomised clinical trial.

98 : Continuous versus bilevel positive airway pressure for obstructive sleep apnea.

99 : Adaptive Servo-Ventilation for Central Sleep Apnea in Systolic Heart Failure.

100 : An Association between Positive Airway Pressure Device Manufacturer and Incident Cancer? A Secondary Data Analysis.

101 : An Association between Positive Airway Pressure Device Manufacturer and Incident Cancer? A Secondary Data Analysis.

102 : Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation.

103 : Acetazolamide Reduces Blood Pressure and Sleep-Disordered Breathing in Patients With Hypertension and Obstructive Sleep Apnea: A Randomized Controlled Trial.

104 : The Combination of Atomoxetine and Oxybutynin Greatly Reduces Obstructive Sleep Apnea Severity. A Randomized, Placebo-controlled, Double-Blind Crossover Trial.

105 : The norepinephrine reuptake inhibitor reboxetine alone reduces obstructive sleep apnea severity: a double-blind, placebo-controlled, randomized crossover trial.

106 : One Month Dosing of Atomoxetine plus Oxybutynin in Obstructive Sleep Apnea: A Randomized, Placebo-controlled Trial.

107 : Drug therapy for obstructive sleep apnoea in adults.

108 : A Randomized Controlled Clinical Trial Exploring Safety and Tolerability of Sulthiame in Sleep Apnea.

109 : Pharmacotherapy of Apnea by Cannabimimetic Enhancement, the PACE Clinical Trial: Effects of Dronabinol in Obstructive Sleep Apnea.

110 : Combination of atomoxetine with the novel antimuscarinic aroxybutynin improves mild to moderate OSA.

111 : Efficacy of atomoxetine plus oxybutynin in the treatment of obstructive sleep apnea with moderate pharyngeal collapsibility.

112 : Atomoxetine and fesoterodine combination improves obstructive sleep apnoea severity in patients with milder upper airway collapsibility.

113 : Daytime Neuromuscular Electrical Therapy of Tongue Muscles in Improving Snoring in Individuals with Primary Snoring and Mild Obstructive Sleep Apnea.

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