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Obstructive sleep apnea (OSA) is a disorder that involves frequent episodes of breathing reduction (hypopnea) or cessation (apnea) owing to upper airways obstruction caused by excessive soft tissue compliance, redundant upper airway mucosa, and inadequate motor tone of the tongue and/or pharyngeal dilator muscles. Hypopnea is defined as a decrease in airflow by 50% or more, and apnea is defined as a complete cessation of breathing for at least 10 seconds.1 Hypopneas and apneas are usually terminated by a brief transient awakening or arousal, followed by resumed sleep. The repetitive cycle of sleep interruption can cause marked daytime sleepiness and cognitive impairment, as well as mood disturbances, social withdrawal, and decreased sexual desire.

An estimated 3 to 7% of men and 2 to 5% of women in the United States are affected by OSA; among patients with a body mass index (BMI) greater than 28 kg/m², the prevalence is estimated to be nearly 50%.^2,3 However, OSA is likely significantly underdiagnosed owing to its often indolent and chronic nature. Patients are not always aware of snoring or apneic episodes, and not all patients present with daytime sleepiness.^4–6

Regardless of the presence or severity of subjective symptoms, OSA is independently associated with a significant number of adverse health-related outcomes, including systemic and pulmonary hypertension, cardiac arrhythmias, coronary artery disease, heart failure, and cerebrovascular disease, as well as an increased risk of motor vehicle accidents and perioperative complications.^6–10 Successful treatment of OSA attenuates each of these conditions and risks, effectively reducing the risk of morbidity and mortality in addition to improving quality of life^8–13; hence, early recognition and management of OSA is essential.

Anatomy

Several anatomic classification systems may be used in the assessment of airway patency among patients with OSA. The Fujita system describes the location airway collapse as retropalatal (type I), retropalatal and retrolingual (type II), and retrolingual (type III).14 Type I collapse is most commonly encountered in primary snorers and patients with mild OSA and type II in the majority of patients with OSA. Mallampati and Friedman scores describe the completeness of oropharyngeal visualization and suggest the extent of tongue base obstruction. The Mallampati score is determined with the tongue protruded, and the Friedman score is determined with the tongue retained in the oral cavity.^15,16

Signs and Symptoms

Snoring and excessive daytime sleepiness are the most common presenting symptoms in patients with OSA. Other frequently reported symptoms include fatigue, poor concentration, short-term memory loss, irritability, morning headaches, decreased libido, restless and unrefreshing sleep, gasping or choking while sleeping, repeated awakenings, and excessive nocturia. Bed partners may also report witnessing apneas.

Patients suspected of having OSA should also be assessed for secondary conditions that may occur as a result of OSA, including hypertension, coronary artery disease, heart failure, and stroke. A detailed sleep history is also important to identify other sleep disorders, including poor sleep hygiene, insomnia, and movement disorders, that may occur simultaneously with OSA.

OSA is often suspected in symptomatic patients who are obese or those with a large neck circumference (> 42 cm in men and > 37 cm in women). Additional physical examination findings that are suggestive of OSA include retroor micrognathia, nasal deformities (turbinate hypertrophy, polyps, valve abnormalities, and septal deviations), a high-arched or narrow hard palate, an enlarged or elongated uvula, macroglossia, tonsillar hypertrophy, and a Mallampati score of 3 or 4.

Diagnostic Testing

OSA’s variable and nonspecific clinical features make it nearly impossible to diagnose or exclude without objective testing. Because our ability to clinically predict which patients will meet OSA diagnostic criteria is poor and the consequences of untreated OSA are significant, diagnostic testing is currently recommended for any patient who presents with snoring and excessive daytime sleepiness.¹⁷ In the absence of excessive daytime sleepiness, testing is recommended for snorers with other comorbidities or suggestive clinical symptoms, and those working in mission-critical professions (i.e., truck and bus drivers and pilots).¹⁷

Polysomnography (PSG) is used to establish the diagnosis of OSA and determine its severity. PSG involves monitoring sleep state (electroencephalography and electrooculography), airflow, oxygen saturation, heart rate (electrocardiography), muscle activity (electromyography), and arousals during sleep. PSG allows for the determination of the apnea-hypopnea index (AHI; calculated by the number of apneas and hypopneas per hour of sleep) and the respiratory distress index (RDI; calculated by the number of apneas, hypopneas, and respiratory effort-related arousals per hour of sleep), which are the most widely used objective assessments of sleep-disordered breathing. The RDI is used to classify OSA severity as mild (5 to 15), moderate (16 to 30), or severe (> 30).

PSG can be performed at home or in a sleep laboratory, which requires an overnight hospital stay. Laboratory PSG offers the most comprehensive evaluation in a monitored, controlled setting and is the current gold standard for OSA diagnosis. However, despite its acceptance as the gold standard, laboratory PSG is associated with a high diagnostic variability, likely owing to various interpretations of nonuniform rules that are used to score events. Furthermore, laboratory PSG is expensive and not always accessible. Patients in rural communities often lack access to centers that perform PSG; and even when access is available, wait times may be exceedingly long.

A simplified version of the laboratory assessment that is performed at home by using a portable monitoring device may be offered as an alternative in select patients. Advantages to home PSG monitoring include the ability to record information in a natural sleep environment; increased access and availability and therefore shorter waiting time; considerably lower cost; and a centralized center for data analysis, which allows for decreased diagnostic variability.18 However, home PSGs have a higher false-negative rate and likely underestimate disease severity, because home PSG RDI is defined differently (as the number of apneas, hypopneas, and RERAs per hour of recording instead of hours of sleep).¹⁸ Consequently, home PSGs are most effectively used to include the diagnosis of OSA in otherwise-healthy patients with a high pretest probability of moderate to severe OSA.¹⁷ Home PSGs are not appropriate for the diagnosis of OSA in patients with significant comorbid medical conditions (severe pulmonary disease, neuromuscular disease, or congestive heart failure) or in those suspected of having other comorbid sleep disorders (central sleep apnea, periodic limb movement disorder, narcolepsy, insomnia, and circadian rhythm disorder).¹⁷ A repeated laboratory PSG is warranted if clinical suspicion for OSA is high in a patient with a negative home PSG.

Treatment

Treatment of OSA varies according to disease severity and usually involves a combination of behavioral modifications, such as weight loss, alcohol avoidance, and alteration of sleeping position; positive airway pressure (continuous positive airway pressure [CPAP], bilevel positive airway pressure, or automatic positive airway pressure); oral appliances (OAs); and a variety of upper airway surgical procedures.

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