2/8/22, 19:23 Management of obstructive sleep apnea in adults - UpToDate

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Management of obstructive sleep apnea in adults

Authors: Meir H Kryger, MD, FRCPC, Atul Malhotra, MD
Section Editor: Nancy Collop, MD
Deputy Editor: Geraldine Finlay, MD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2022. | This topic last updated: May 23, 2022.

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.

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
"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.

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), the International Geriatric

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Sleep Medicine Force, and others [1-9]. 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 [10]. 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.)

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 [11]; however, many of the nonsleep specialists also had extensive training or
experience in sleep which may have biased the outcomes. Other studies have suggested similar
results [12].

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 [1]. 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 [1]. 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 [3]. Patients

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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'.)

Patients should be counselled that they should always inform their medical providers that they
have sleep apnea, especially if they are to have surgery or start opiate medications [13].

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 opioids, may
worsen their 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” [14]. Thus, smoking cannabis
should not be encouraged at this point.

Weight loss and exercise — Weight loss and exercise should be recommended to all patients
with OSA who are overweight or obese [1,2,15,16]. 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 [17-26]. (See "Overweight and 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".)

Several trials have demonstrated an impact of weight loss on OSA control [18,27,28]. 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) [18]. 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
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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 [27]. 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]. We consider
referral to a bariatric surgeon in adults with OSA and obesity (class II/III, BMI ≥35 kg/m2) who
are intolerant of or decline positive airway pressure therapy (PAP) therapy [29,30]. Further
details are provided separately. (See "Outcomes of 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 [31-
34]. In addition, CPAP therapy itself may be associated with weight gain [35-37]. 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 [16,22,38,39]. 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 [22,40].

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 [41].

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 [42]. 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 [43-47].

Several commercial devices are available that use vibratory feedback around the chest or neck
to restrict supine sleep [48-51]. 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

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has been confirmed by polysomnography and adherence can be verified [1,42]. 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 [52]. 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 theoretically worsen daytime sleepiness
include benzodiazepine receptor agonists, barbiturates, other antiepileptic medications,
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
"Management of restless legs syndrome 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 [53].
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.

Most Philips CPAP and bilevel PAP devices are being recalled 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
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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 else an alternate mode of therapy. Patients can register online with Philips
Respironics to have the foam in their recalled PAP machines 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 [HR] 0.94, 95% CI 0.71–1.25) [54]. 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.

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 (BP), lowers the risk of crashes, improves erectile dysfunction, and improves quality of
life across a range of disease severities [26,55-66]. 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 [26]. 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 [56].

● In a 2019 meta-analysis of the American Academy of Sleep Medicine (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 (ESS) 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]. 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,
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myocardial infarction, stroke), mortality, neurocognitive function, mood, fasting glucose or

hemoglobin A1C, left ventricular ejection fraction, or risk of hospitalization.

More limited data also suggest that positive airway pressure therapy can improve
symptoms of gastroesophageal reflux [67], heart failure outcomes, and reduce the risk of
recurrent atrial fibrillation and nocturnal arrhythmias. (See "Obstructive sleep apnea and
cardiovascular disease in adults" 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 [10]. 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 [68]. The related MAD trials are
described separately. (See "Oral appliances in the treatment of obstructive sleep apnea in
adults", section on 'Efficacy and outcomes'.)

Although multiple observational studies have reported an association between CPAP use and
decreased mortality [69-71], no randomized trial has demonstrated a mortality benefit from
positive airway pressure therapy in patients with OSA [26]. 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
[72].

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 [73].
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.

Whether there is a difference in therapeutic effect when oronasal rather than nasal masks are
used is unclear. While observational studies suggested reduced adherence with oronasal

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masks, a small cross-over randomized trial reported no difference in AHI or adherence with
either mask [74].

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 [1,75]. 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 [76]. 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
[77]. 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) [4]. Our approach is to also initiate therapy in the following
groups of patients:
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● 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 auto-titrating positive airway pressure (APAP). We generally favor CPAP as
initial therapy because it is the most familiar and best studied. However, APAP is an alternative
to CPAP in suitable candidates.

The available modes of positive airway pressure therapy are summarized as follows [1]:

● 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 [78].
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.

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● 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 [79-83]. 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.

● 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 [84].
(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 "Titration of
positive airway pressure therapy for adults with obstructive sleep apnea".)

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 [85-91]. 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 educational, behavioral and troubleshooting 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 "Assessing and
managing nonadherence with continuous positive airway pressure (CPAP) for adults with
obstructive sleep apnea".)

Follow-up — Patients who elect to be treated with positive airway pressure should be evaluated
frequently, especially during the first few weeks of therapy [1]. 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
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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 "Assessing and managing
nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep
apnea".)

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 [1]. 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 "Assessing and managing
nonadherence with continuous positive airway pressure (CPAP) for adults with obstructive sleep
apnea".)

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 [1]. 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 [92]. (See "Obstructive sleep apnea and cardiovascular disease in adults".)

COVID-19 — Guidance for clinicians and patients regarding the administration of PAP therapy
for OSA during the COVID-19 pandemic is provided the American Academy of Sleep Medicine,

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the Canadian Thoracic Society, and the Australasian Sleep Association. (See "COVID-19:
Infection prevention for persons with SARS-CoV-2 infection" and 'Society guideline links' below.)

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 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 [56,93], 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 'Efficacy and outcomes'.)

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.

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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 'Efficacy and outcomes'.)

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 — We and other 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) [29,30].

Optimal screening or imaging procedures have not been established that accurately predict
which patients are most likely to benefit from surgery. In our experience, surgical treatment
appears to be most effective in patients who have OSA due to a severe, surgically correctable,
obstructing lesion of the upper airway, although PAP remains first-line therapy in many patients
with anatomic abnormalities of the upper airway. Examples of surgically correctable lesions that
may obstruct the upper airway include tonsillar hypertrophy, adenoid hypertrophy, or
craniofacial abnormalities [1,15,94].

Hypoglossal nerve stimulation via an implantable neurostimulator device ( picture 1) is a

treatment strategy that may have a role in selected patients with moderate to severe OSA, who
have failed continuous positive airway pressure with a body mass index <32 kg/m2, (BMI <35
kg/m2 is used in some centers) and no unfavorable collapse on drug-induced sleep endoscopy.
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 [95-105].

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), drugs that reduce upper airway collapsibility (eg, desipramine), antimuscarinics
(eg, oxybutynin), or noradrenergic agents (eg, atomoxetine) [106-108]. However, no

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pharmacologic agent has proven to be sufficiently effective to warrant replacement of such

therapies [15,109].

Initial findings in a phase II study of 73 adults with moderate or severe OSA reported that
compared with placebo, the cannabinoid, dronabinol, administered one hour before bedtime
reduced the apnea-hypopnea index (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) [110]. 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. A position statement of the American
Academy of Sleep Medicine does not support the use of medical cannabis and/or synthetic
extracts for the treatment of OSA until reliable data exist to support the efficacy and safety of
these products [14].

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)
[1,111,112]. 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 excessive sleepiness in adults with obstructive sleep
apnea".)

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

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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 severe OSA (AHI ≥30 events per hour), we recommend positive airway
pressure as initial therapy (Grade 1B). (See 'Positive airway pressure therapy' above.)
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● 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 excessive sleepiness in adults with obstructive sleep apnea".)

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GRAPHICS

Treatment of obstructive sleep apnea algorithm

AHI: apnea-hypopnea index; RDI: respiratory disturbance index.

* Determining RDI is not always feasible on home sleep apnea

testing (HSAT) but can be reliably identified on polysomnography
testing. However, in those with excessive daytime sleepiness and an
AHI ≤5 events per hour during HSAT, third party payers may
determine who gets further testing or therapy.

Graphic 70443 Version 10.0

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Upper airway stimulation device for obstructive sleep apnea

Graphic 93258 Version 3.0

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