Obstructive Sleep Apnea (OSA)

Less severe forms may not produce oxygen desaturation, but they interrupt sleep.

Upper airway resistance syndrome is crescendo snoring terminated by snorts and respiratory effort-related arousals (RERAs). Breathing reductions do not meet strict criteria for obstructive apneas and hypopneas. Patients with upper airway resistance syndrome are typically younger and have less obesity than those with OSA. Patients are more often female, report fatigue, and complain of insomnia. Snoring and upper airway airflow resistance cause noisy inspiration but without arousals from sleep lasting > 2 seconds. Symptoms, diagnostic evaluation, and treatment of snoring and upper airway resistance syndrome are similar to those of OSA.

Obesity-hypoventilation syndrome is a related disorder in those with obesity, usually severe OSA, and hypoventilation without any other cause. Treatment of OSA in OHS with positive airway pressure (PAP) therapy can improve hypoventilation (3).

Obstructive sleep apnea has significant neurocognitive, cardiovascular, and metabolic consequences.

OSA is the leading medical cause of excessive daytime sleepiness. A more correct term is wake-time excessive sleepiness, because people who work during the night may be excessively sleepy during night hours. The excessive sleepiness actively increases the risk of automobile crashes, difficulties at work, and sexual dysfunction. There is often some degree of cognitive impairment and also increased risk of injury (eg, when operating heavy machinery or engaging in other activities during which unintentional sleep episodes would be hazardous).

Relationships with bed partners, roommates, and/or housemates may also be adversely affected because such people may have difficulty sleeping because of the patient's noisy, restless sleep.

Hypertension is strongly associated with OSA (4). Patients with untreated OSA who are normotensive are more likely to develop hypertension within 5 years of diagnosis. Repetitive nocturnal hypoxia and sleep disruption are associated with increased risk of medical disorders, including heart failure, coronary artery disease, atrial fibrillation (including recurrence after catheter ablation) and other arrhythmias, metabolic dysfunction–associated steatotic liver disease (MASLD), and stroke (5). The risk of stroke and all-cause mortality is increased even when controlling for other risk factors (eg, hypertension, diabetes) (6, 7). However, the contribution of OSA to these common disorders is often underappreciated (8).

Perioperative complications can occur with unrecognized OSA, because moderate or general anesthesia is a risk for airway obstruction. Patients with diagnosed OSA should inform an anesthesiologist of the diagnosis before undergoing any surgery and should receive continuous positive airway pressure (CPAP) when they receive preoperative medications and during recovery.

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Sleep studies include

• Traditional polysomnography conducted in a sleep laboratory

• Portable diagnostic tools that can be used by patients at home in their own bed

Polysomnography records and helps classify stages of sleep and the occurrence and duration of apneic and hypopneic periods. It is ideal for confirming the diagnosis of OSA and quantifying the severity of OSA (8). However, it requires an overnight stay in a sleep laboratory and is thus complicated and expensive. Polysomnography typically includes

• Continuous measurement of sleep architecture by EEG (electroencephalography)

• Chin electromyography to detect hypotonia

• Electro-oculography to assess the occurrence of rapid eye movements

• Airflow sensors at the nose and mouth to detect apneas and hypopneas

• Chest and/or abdominal sensors to detect respiratory effort

• Oxygen saturation by pulse oximetry

• ECG monitoring to detect arrhythmias associated with apneic episodes

The patient is also observed by video.

Other variables evaluated include limb muscle activity (to assess nonrespiratory causes of sleep arousal, such as restless legs syndrome and periodic limb movement disorder) and body position, because apnea may occur predominantly in the supine position.

Alternatively, patients may undergo a "split night" sleep study in which, after a diagnosis of OSA is made with polysomnography, CPAP is then administered and the pressure level is titrated to effect, allowing determination of appropriate therapy during the same overnight monitoring period. A whole night CPAP titration can also be performed, if needed, to assess the effectiveness of CPAP treatment after diagnosis.

Home sleep testing using portable diagnostic tools uses a limited subset of polysomnographic measures, typically just heart rate, pulse oximetry, respiratory effort, position, and nasal airflow to detect apnea and estimate its severity. The role of home sleep testing is expanding (9) because of the convenience, decreased cost, and ability to provide a reasonably accurate estimate of respiratory disturbances during sleep.

However, portable tools have some limitations. They do not actually detect the presence of sleep and instead depend on patients to self-report sleeping, which can be inaccurate; if patients were not sleeping during part of the study and they did not report this, sleep-disordered breathing will be underestimated. Thus, a negative home sleep test result in a patient with symptoms should be followed by polysomnography. Also, coexisting sleep disorders (eg, restless legs syndrome, seizures, REM behavior disorder, confusional arousals) are not detected. Follow-up polysomnography may still be needed to characterize these disorders as well as to accurately provide AHI and RDI values in the different stages of sleep and with changes in position, especially when surgery or therapy other than positive airway pressure is being considered.

Portable tools are often used in combination with questionnaires (eg, STOP-BANG, Berlin Questionnaire). If questionnaire results indicate a higher pre-test probability of disease, the sensitivity and specificity of the portable tools is higher.

The AHI is the total number of episodes of apnea and hypopnea occurring during sleep divided by the hours of sleep time. It is a commonly used measure of respiratory disturbance during sleep and is used to classify the severity of OSA. OSA is graded as:

• Mild: AHI ≥ 5 and < 15 per hour

• Moderate: AHI ≥ 15 and ≤ 30 per hour

• Severe: AHI > 30 per hour

The respiratory disturbance index (RDI) is a related measure that includes the number of arousals related to respiratory effort (called respiratory effort-related arousals or RERAs) plus the number of apnea and hypopnea episodes per hour of sleep.

The arousal index, which is the number of arousals per hour of sleep, can be computed if EEG monitoring is used. The arousal index is loosely correlated with AHI and RDI; about 20% of apneas and desaturation episodes are not accompanied by arousals, or other causes of arousals are present.

However, the AHI, arousal index, and RDI are only moderately associated with a patient’s symptoms. Some patients with a high or extremely high AHI (eg, > 60 per hour) have few or no symptoms. Additional metrics and combinations of metrics may prove useful in diagnosis (10). It is a composite of clinical and polysomnographic data (not just AHI) that is linked to outcome and to cardiovascular risk and mortality. For example, sleepiness regardless of AHI is linked to excess cardiovascular disease.

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Initial treatment aims to control risk factors such as obesity, hypertension, alcohol use, and sedative use. Exercise decreases the AHI and increases alertness, independent of any effect on body mass index (BMI).

Daytime sleepiness can be reduced by good sleep hygiene measures, including sleeping longer and discontinuing sedative medications, particularly antihistamines or antidepressants. Avoiding supine sleep can be useful and feasible for some patients who have primarily supine-related OSA.

Modest weight loss (≥ 15%) may result in clinically meaningful improvement (8, 9) but should not be considered curative for OSA. However, weight loss is extremely difficult for most people, especially those who are fatigued or sleepy. Weight loss as a result of bariatric surgery, however performed, can reduce the AHI and reduce symptoms (10, 11). Increasingly, medications such as GLP-1 receptor antagonists are used for weight loss and have decreased OSA severity (12).

CPAP is the treatment of choice for most patients with OSA and subjective daytime sleepiness, including those in whom it causes cognitive impairment (13, 14). Treatment of OSA with continuous positive airway pressure (CPAP) has been consistently shown to reduce sleepiness and snoring and improve bed partner sleep (15). There are reports of racial and socioeconomic bias in making this treatment available (16).

There are many different CPAP interfaces (masks) available, including those that insert into the nose (nasal pillows) and those that cover the nose (nasal mask), nose and mouth (full face mask), or the whole face. All have cushions to provide an air seal, which is essential for maintaining a pressure gradient. Cushions may be inflatable or made of silicone, foam, or gel. Proper fit and comfort vary widely among patients but must be optimized for both efficacy and adherence.

CPAP improves upper airway patency by applying positive pressure to the collapsible upper airway segment. Effective pressures typically range from 3 to 15 cm H2O. Pressure requirements are not correlated with disease severity. Many CPAP devices monitor CPAP efficacy and titrate pressures automatically (called adjustable or automatic positive airway pressure [APAP]), according to internal algorithms. If necessary, polysomnographic monitoring can be used to guide manual titration of pressure.

The level of CPAP necessary for airway patency is determined either by CPAP titration in the sleep laboratory or increasingly through the use of automatic positive airway pressure (APAP). With APAP, a range of pressures is prescribed (eg, 5 to 15 cm H2O), and the device uses internal algorithms to adjust the pressure up and down throughout the night as needed. CPAP improves upper airway patency by applying positive pressure to the collapsible upper airway segment. Pressure requirements are not correlated with disease severity. Effective pressures typically range from 3 to 15 cm H2O. If necessary, polysomnographic monitoring can be used to guide manual titration of pressure.

Although a reduction in AHI is one of the treatment goals, CPAP reduces tiredness and improves quality of life regardless of improvement in the AHI. CPAP also may reduce blood pressure, although the impact is usually modest. If CPAP is withdrawn, symptoms recur over several days, although short interruptions of therapy for acute medical conditions are usually well tolerated. Duration of therapy is indefinite.

If clinical improvement is not apparent, CPAP adherence should be reviewed, and patients should be reassessed for comorbid disorders. If patients have septal deviation or nasal polyps, nasal surgery may make CPAP treatment more successful but rarely cures OSA by itself.

Adverse effects of nasal CPAP include discomfort resulting from a poorly fitting mask, and dryness and nasal irritation, which can be alleviated in some cases with the use of warm humidified air. However, newer mask designs have improved comfort and ease of use.

Adherence is difficult for many people and is lower in patients who do not experience sleepiness. Overall, about 50% of patients adhere to use of CPAP long term. Adherence can be improved by efforts to foster a positive attitude toward device use combined with early attention to any problems, particularly mask fit, and close follow-up by a committed caretaker, with reinforcement by the primary care physician. There is also a need to recognize and address the decreased long-term CPAP adherence among patients who do not have obesity and have low respiratory arousal threshold (ie, awaken easily) and thus a propensity for increased arousals and irregular breathing. With many machines, adherence, pressure levels, leak, and residual respiratory events are tracked daily by the PAP devices and available to patients and clinicians.

Even when adherence is adequate, results may become unsatisfactory if patient factors change (eg, weight gain occurs, nasal obstruction develops).

CPAP can be augmented with inspiratory assistance (bilevel positive airway pressure) to increase tidal volume in patients with comorbid obesity-hypoventilation syndrome and sometimes, for comfort.

Oral appliances are designed to advance the mandible or, at the very least, prevent retrusion and tongue prolapse during sleep (17,18, 19). Some appliances are designed to pull the tongue forward. These appliances are considered mainstream treatments of both snoring and mild to moderate OSA. Comparisons of appliances to CPAP show equivalent effectiveness in mild to moderate OSA, but cost-effectiveness studies are focused on fixed initial costs of fabrication rather than on replacement and follow-up costs.

Surgical procedures to correct anatomic factors, such as enlarged tonsils and nasal polyps that contribute to upper airway obstruction, should be considered (19, 20). Surgery is a first-line treatment if specific anatomic encroachment is identified. However, in the absence of encroachment, evidence to support surgery as a first-line treatment is lacking. Surgery for macroglossia or micrognathia is also an option.

Uvulopalatopharyngoplasty (UPPP) involves resection of pharyngeal tissue. UPPP has been largely replaced by less aggressive approaches that attempt to stabilize the lateral walls of the pharynx and/or enlarge the velopharyngeal area without risk of altering speech or swallowing. CPAP and UPPP have not been directly compared in rigorous studies but UPPP may be efficacious in well selected individuals. Results are less predictable in patients who have severe obesity or anatomic narrowing of the airway (21). The procedure may reduce intrusive snoring, although apneic episodes may remain as severe (although silent) as before surgical intervention.

Other surgical procedures include midline glossectomy, hyoid advancement, and mandibulomaxillary advancement (22). Mandibulomaxillary advancement is sometimes offered as a second-stage procedure if soft-tissue approaches are not curative. The optimal multistage approach is not known.

Tracheostomy is the most effective therapeutic maneuver for OSA but is done as a last resort. It bypasses the site of obstruction and is indicated for patients most severely affected (eg, those with cor pulmonale) who cannot tolerate CPAP.

Upper airway stimulation using an implanted device to stimulate a branch of the hypoglossal nerve (23, 24) can activate muscles that protrude the tongue and other muscles that help open the airway. This therapy is successful in selected patients with moderate to severe disease. It is used mainly in those who are unable to tolerate CPAP therapy and in whom oral appliances are ineffective. The procedure may also be tried in those in whom mandibulomaxillary advancement is contemplated. Improvements in AHI to < 10 per hour occur in about 65% of these selected patients (25).

Various adjunctive treatments are sometimes used but have no proven benefit for OSA.

Supplemental oxygen improves blood oxygenation and may reduce AHI and arousal index among patients who did not respond to upper airway surgery (26). However, a beneficial clinical effect occurs mainly in those with high gain (tendency to have repeated apnea or hypopnea after an initial episode), and effects are hard to predict. Also, oxygen may provoke respiratory acidosis and morning headache. For these reasons, supplemental oxygen is not recommended for the treatment of OSA.

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31), but cannot be recommended because of factors including limited experience, a low therapeutic index, lack of replication of results, and lack of adequate trials. Better methods to recognize sleep apnea subtypes may allow better selection of patients for pharmacotherapy.

Exercises for upper airway muscles (myofunctional therapy) have been proposed on the theory that improved muscle strength and tone might help improve airway patency during sleep (32). There are a number of exercises that seem to reduce AHI and symptoms, making this approach interesting, particularly because it is noninvasive and with no adverse effects. However, this approach is not a mainstream recommendation because of the wide variety of techniques proposed, uncertainty about their mechanisms of action and efficacy, and practical difficulties with adherence. A least one device based on daytime electrical stimulation of the upper airway dilator muscles is available for treatment of snoring and mild OSA (33).

Nasal dilatory devices and throat sprays sold over-the-counter for snoring have not been studied sufficiently to prove value in OSA.

Laser-assisted uvuloplasty, uvular splints, and radiofrequency tissue ablation have been used to treat snoring in patients without OSA. Although they may transiently decrease snoring loudness, efficacy in treating OSA is neither predictable nor durable.

An informed patient and family are better able to cope with an OSA treatment strategy, including tracheostomy. Patient support groups provide helpful information and effectively support timely treatment and follow-up. The role of patient support groups and digital support tools for management is being investigated (34).

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