Continuing Education Activity

Obstructive sleep apnea (OSA) is a sleep disorder characterized by repeated episodes of complete (apnea) or partial (hypopnea) collapse of the upper airway, causing oxygen desaturation or sleep arousal. This disruption leads to fragmented, nonrestorative sleep. Symptoms include loud, disruptive snoring, witnessed apneas, and excessive daytime sleepiness. This condition has significant implications for cardiovascular health, mental well-being, quality of life, and driving safety. Diagnosis involves polysomnography or home sleep apnea testing. Treatment options include continuous positive airway pressure therapy, oral appliances, and surgical interventions.

This activity reviews the etiology, epidemiology, pathophysiology, clinical manifestations, and management of OSA, as well as examines its causes, risk factors, and advancements in diagnostic techniques. This activity also highlights the importance of interdisciplinary collaboration in managing OSA and fosters effective communication and teamwork among healthcare professionals. In addition, this activity provides interprofessional healthcare providers with insights into the latest advancements in diagnostic techniques and evidence-based treatment modalities, ensuring comprehensive care delivery and improved patient outcomes in OSA management.

Objectives:

• Identify key symptoms and risk factors associated with obstructive sleep apnea to accurately recognize at-risk individuals.
• Implement evidence-based management strategies, including continuous positive airway pressure therapy, oral appliances, and surgery, to improve patient care.
• Select the most appropriate diagnostic techniques and treatment options based on the individual patient's clinical presentation and preferences.
• Collaborate with the interprofessional healthcare team to improve outcomes and provide comprehensive care for patients affected by obstructive sleep apnea.

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Introduction

Obstructive sleep apnea (OSA) is characterized by episodes of complete (apnea) or partial (hypopnea) collapse of the upper airway, leading to decreased oxygen desaturation or arousal from sleep.[1] This disruption results in fragmented and nonrestorative sleep. Other symptoms include loud and disruptive snoring, witnessed apneas during sleep, and excessive daytime sleepiness.[2][3][4] OSA significantly affects cardiovascular health, behavioral conditions, quality of life, and driving safety.[5] Other types of sleep-disordered breathing, including central sleep apnea, upper airway resistance, and obesity hypoventilation, will be discussed separately. Please see StatPearls' companion resources, "Central Sleep Apnea" and "Upper Airway Resistance Syndrome," for more information. 

Etiology

Pharyngeal narrowing and closure during sleep is a complex phenomenon influenced by multiple factors. Sleep-related reductions in ventilatory drive, neuromuscular factors, and anatomical risk factors all contribute significantly to upper airway obstruction during sleep.[1] 

Anatomical factors that promote pharyngeal narrowing include a large neck circumference, excess soft tissue, bony structures, or blood vessels.[6] Many of these structures can increase pressure around the upper airway, leading to pharyngeal collapsibility and insufficient space for airflow in part of the upper airway during sleep.[7]

In addition, the upper airway muscle tone is crucial; when muscle tone decreases, it leads to a repetitive total or partial airway collapse. OSA in adults is most commonly associated with obesity, male sex, and advancing age.[8] 

Anatomical Factors

• Micrognathia and retrognathia
• Facial elongation
• Mandibular hypoplasia
• Adenoid and tonsillar hypertrophy
• Inferior displacement of the hyoid

Nonanatomical Risk Factors

• Central fat distribution
• Obesity
• Advanced age
• Male gender
• Supine sleeping position
• Pregnancy [9]

Additional Factors

• Alcohol use
• Smoking
• Use of sedatives and hypnotics

Associated Medical Disorders

• Endocrine disorders (eg, diabetes mellitus, metabolic syndrome, acromegaly, and hypothyroidism) [10][11]
• Neurological disorders (eg, stroke, spinal cord injury, and myasthenia gravis) [12][13]
• Prader-Willi syndrome [14]
• Down Syndrome [15]
• Congestive heart failure [16]
• Atrial fibrillation [17]
• Obesity hypoventilation syndrome

These associations between OSA and various medical disorders are primarily based on observational studies rather than randomized clinical trials.

Epidemiology

OSA is a common condition with significant adverse consequences.[18] Using the definition of 5 or more events per hour, OSA affects almost 1 billion people globally,[19] with 425 million adults aged between 30 to 69 having moderate-to-severe OSA (15 or more events per hour).[20] 

In the United States, it has been reported that 25% to 30% of men and 9% to 17% of women meet the criteria for OSA.[21][22] Prevalence is higher in Hispanic, Black, and Asian populations. Prevalence also increases with age, and when individuals are 50 years or older, and as many women as men develop the disorder. The increasing prevalence of OSA is related to the rising rates of obesity, ranging between 14% and 55%.[21] Some risk factors, including obesity and upper airway soft tissue structure, are genetically inherited.[23]

Pathophysiology

Upper airway obstruction during sleep is often caused by negative collapsing pressure during inspiration; however, progressive expiratory narrowing in the retropalatal area also has a significant role.[24] The magnitude of upper airway narrowing during sleep is often related to body mass index (BMI), indicating that both anatomical and neuromuscular factors contribute to airway obstruction.[25] The pressure-flow relationship through collapsible tubes is key to understanding the mechanisms of OSA.[26] Additional information on risk factors is available in the Etiology section. 

History and Physical

Patients with suspected OSA usually present with excessive daytime sleepiness, loud snoring, gasping, choking, or witnessed episodes of breathing cessation during sleep. Excessive daytime sleepiness is one of the most common symptoms.[22]

Many patients may only report daytime fatigue, with or without other associated symptoms. Therefore, it is important to objectively assess the distinction between sleepiness and fatigue. The Epworth Sleepiness Scale (ESS) can be used to quantitatively evaluate the severity of sleepiness.[27] The ESS score ranges from 0 to 24; a score above 9 suggests excessive daytime sleepiness and warrants additional assessment. The Fatigue Severity Scale (FSS) can also be used to assess the severity of fatigue symptoms.[28] 

The ESS and FSS are helpful tools, as sleepiness and fatigue symptoms may occur concurrently. Other symptoms may include morning headaches, nocturnal reflux, insomnia, and nocturia.[29][30][31] Symptoms of sleep-onset and sleep-maintenance insomnia are more commonly reported by women.[32]

The STOP-BANG questionnaire is one of the most widely accepted screening tools for OSA.[33]

• Snoring: Do you snore loudly (louder than talking or loud enough to be heard through closed doors)?
• Tired: Do you often feel tired, fatigued, or sleepy during the daytime?
• Observed: Has anyone observed you stop breathing during your sleep?
• Blood pressure: Are you currently being treated for high blood pressure?
• BMI: Is your BMI greater than 35 kg/m²?
• Age: Are you of age 50 or older?
• Neck circumference: Is your neck circumference greater than 40 cm?
• Sex: Are you male?

The STOP-BANG questionnaire can be used to assess the probability of moderate-to-severe OSA. A high risk is indicated if "YES" is selected for 5 or more items, while a low risk is indicated if "YES" is answered for fewer than 3 items.

Obesity is the most common finding in individuals with OSA. Other physical signs include a large neck circumference (17 inches or 43 cm in males and 16 inches or 40.5 cm in females), a crowded oropharynx (a Mallampati score of 3 to 4), retrognathia, micrognathia, tonsillar hypertrophy, low-lying palate, overjet, and a large tongue. However, lateral narrowing is the only independent predictor of OSA after adjusting for body weight and neck size (see Image. Clinical Assessment of Sleep Apnea).[34]

Evaluation

Adult patients with unexplained daytime or sleep-related symptoms, such as excessive sleepiness, fatigue, or unrefreshing sleep, should be evaluated for sleep apnea. However, universal screening for OSA is not recommended in asymptomatic patients, except for those at risk due to occupational hazards, such as drivers or pilots.[35][36] In addition, due to the high prevalence of OSA and its disease burden, patients with specific comorbidities, including refractory atrial fibrillation, resistant hypertension, and a history of stroke, should also be screened for sleep apnea, regardless of symptoms.[37] 

Nighttime in-laboratory level 1 polysomnography (PSG) is considered the gold standard for diagnosing OSA. During the test, patients are monitored using electroencephalogram (EEG) leads, pulse oximetry, temperature and pressure sensors to detect nasal and oral airflow, respiratory impedance plethysmography belts around the chest and abdomen to monitor motion, an electrocardiogram (ECG) lead, and electromyogram sensors to detect muscle contractions in the chin, chest, and legs (see Image. Polysomnography, 120-Second Window Showing Obstructive Sleep Apnea).

Scoring respiratory events in adults relies on 4 primary channels:

• Oronasal thermal sensor 
• Nasal air pressure transducer 
• Inductance plethysmography (with esophageal manometry or a pressure catheter may be used as alternatives) 
• Pulse oximetry [38] 

A snoring monitor is a required channel but does not contribute to the scoring of respiratory events. 

According to the American Academy of Sleep Medicine (AASM), hypopnea is defined by either 1 of 2 criteria:

• A reduction in airflow of at least 30% for more than 10 seconds, accompanied by at least 4% oxygen desaturation (eg, Medicare criteria).
• A reduction in airflow of at least 30% for more than 10 seconds, associated with either at least 3% oxygen desaturation or an arousal from sleep on EEG (recommended AASM criteria).[39] 

Scoring apnea requires both of the following criteria to be met:

• A drop in the peak signal excursion by more than or equal to 90% of the pre-event baseline flow.
• A duration of the flow reduction of more than or equal to 10 seconds.

As mentioned below, apneas are usually further classified based on respiratory effort, which is determined by respiratory inductance plethysmography signals (see Image. Polysomnography Showing Central and Obstructive Sleep Apneas).

• Obstructive sleep apnea: If an increased effort is present throughout the entire apnea.
• Central sleep apnea: If no effort is detected throughout the entire apnea.

Mixed apnea is characterized by an absence of effort during the initial portion of the event, followed by the resumption of effort in the latter part of the apnea.

Home sleep tests or portable monitoring have gained popularity due to their accessibility and lower cost. However, portable monitoring should be conducted following specific rules and procedures as outlined by the AASM Unattended Portable Monitoring Task Force guidelines.[40] These guidelines include the following criteria:

• At a minimum, the portable monitoring device must record airflow, respiratory effort, and blood oxygenation.
• The airflow, effort, and oximetric biosensors traditionally used in in-laboratory PSG should also be utilized in portable monitoring.
• Portable monitoring testing must be conducted under the oversight of an AASM-accredited comprehensive sleep medicine program, with established written policies and procedures.
• An experienced sleep technologist or technician must apply the sensors or provide direct patient education on proper sensor application.
• The portable monitoring device must display raw data and allow a trained sleep technologist or technician to manually score or edit automated scoring.
• A board-certified sleep specialist, or an individual meeting the eligibility criteria for the sleep medicine certification examination, must review the raw data from portable monitoring using scoring criteria that align with current AASM standards.[39] Under these specified conditions, portable monitoring may be used for unattended studies in the patient's home.
• A follow-up visit should be scheduled to review test results for all patients undergoing portable monitoring.
• Patients with a high pretest probability of moderate-to-severe OSA who receive negative or technically inadequate portable monitoring results should undergo in-laboratory PSG.

Unattended portable monitoring and home sleep tests are suitable for adults with a high pretest probability of sleep apnea and no significant medical comorbidities, such as advanced congestive heart failure, chronic obstructive pulmonary disease, or neurological disorders. These are level 3 sleep tests, which include pulse oximetry, heart rate monitoring, temperature and pressure sensors to detect nasal and oral airflow, resistance belts around the chest and abdomen to detect motion, and a sensor to monitor body position.

Moderate and severe sleep apnea can be detected using these tests. However, due to the potential underestimation of the apnea-hypopnea index (AHI) relative to the total recording time (which may exceed the total sleep time measured in an in-laboratory study), mild sleep apnea may go undiagnosed. In such cases, a repeat in-laboratory study may be necessary. A proposed algorithm for the appropriate use of portable monitoring and in-laboratory PSG is outlined in the Image. Sleep Apnea Testing Modalities.

One of the main limitations of home sleep testing is that most studies use total recording time as the denominator for calculating the AHI, rather than total sleep time, due to the absence of EEG sensors to differentiate sleep from wakefulness. This approach can lead to an underestimation of the AHI by at least 20%.[41] 

The AASM recommends using the term respiratory event index (REI) to differentiate the indices of respiratory events generated by a home sleep study (without recorded sleep). The AHI and REI represent the average number of obstructive events per hour, during sleep or recording time, respectively. Although most portable monitoring devices include flow sensors, other technologies, such as peripheral arterial tonometry (PAT), use alternative methods without flow to identify sleep-disordered breathing events. The severity of OSA obtained using PAT devices is referred to as pAHI, which has been reported to provide indices similar to those derived from PSG-based AHI.[42]

The severity of OSA in adults is classified based on AHI, REI, or pAHI as follows:

• Mild: 5 to 15 events per hour
• Moderate: Greater than 15 to 30 events per hour
• Severe: Greater than 30 events per hour

The disease burden in mild OSA is controversial and is primarily based on associated clinical sequelae, such as excessive daytime sleepiness, sleep maintenance insomnia, and cognitive dysfunction.[43]

Recent studies have challenged the traditional definition and scoring criteria of OSA in adults due to its limitations in capturing the pathophysiological impact on individual patients.[19] Various metrics have been proposed to improve the precision in diagnosing OSA,[44] including hypoxic burden, nocturnal heart rate changes, total sleep time with SpO₂ less than 90% (TST90), duration of obstructive events, sleep arousal burden, and even genetic factors.[45][46][47][48][49][50][51] 

Treatment / Management

Managing OSA requires a multifaceted approach that should be tailored to each patient. While treatment for moderate-to-severe OSA has demonstrated improvements in clinical outcomes,[52] evidence regarding the impact of therapy on mild OSA remains limited or inconsistent, particularly in relation to neurocognition, mood, vehicle accidents, cardiovascular events, stroke, and arrhythmias.[43]

Lifestyle Changes and Treating Underlying Medical Conditions

The importance of weight loss should be emphasized in patients with OSA who are overweight or have obesity.[53][54] Although weight loss is recommended and can often decrease the severity of OSA, it is usually not curative. Patients should be educated about the impact of sleep duration on their health and encouraged to prioritize getting at least 7 to 8 hours of sleep each night.[55] 

Patients should be advised to avoid alcohol, benzodiazepines, opiates, and certain antidepressants, as these may exacerbate their condition. Concomitant nasal obstruction should be addressed with nasal steroids for allergic rhinitis or surgically for nasal valve collapse. For patients with lung or heart conditions, such as asthma or heart failure, optimizing the treatment of these disorders is crucial.

Positional Therapy

OSA that is more pronounced in the supine position can be treated with a positioning device to maintain side-sleeping, which can be an effective option.[56][57]

Positive Airway Pressure Therapy

Continuous positive airway pressure (CPAP) is the most effective treatment for adults with OSA.[58] Bilevel PAP is also better tolerated by patients who require higher pressure settings (>15 cm H₂O). However, despite the high efficacy of CPAP in eliminating respiratory events, its effectiveness is limited by decreased usage during sleep and poor adherence. Adherence to CPAP remains a significant challenge, as nearly half of patients do not consistently follow treatment after the first month.[59] 

The American Thoracic Society recently published a statement on CPAP adherence tracking systems, optimal monitoring strategies, and outcome measures in adults.[60] Standardizing CPAP adherence reports is crucial, not only by tracking the number of hours used (>4 hours per night on >70% of nights) but also by including the amount of mask leak and the residual apnea and hypopnea index. However, what constitutes the optimal adherence goal for OSA treatment remains uncertain. Recent studies have explored the utility of telemedicine adherence interventions, remote CPAP monitoring, and more interactive features with patients and their families, which have been shown to increase CPAP adherence rates.[61][62][63][64]

Several studies have reported conflicting findings when assessing the effect of CPAP therapy on cardiovascular outcomes in patients with OSA.[44] In a recent randomized controlled trial, CPAP use for a minimum of 1 year in patients with acute coronary syndrome and OSA, without excessive daytime sleepiness, did not lower the incidence of cardiovascular events. These events were defined as cardiac-related deaths or one or more of the following outcomes—acute myocardial infarction, nonfatal stroke, hospital admission for heart failure, and new hospitalizations for unstable angina or transient ischemic attack. However, adherence to CPAP therapy was low (2.78 hours per night), and the follow-up period was insufficient, both of which are significant limitations of the study.[65] 

In another observational cohort study with long-term follow-up, CPAP use was associated with a lower all-cause mortality rate among patients with severe OSA, particularly around years 6 to 7 of follow-up.[66]

In a more recent study, patients with coronary artery disease and OSA who did not experience excessive sleepiness but exhibited greater changes in heart rate showed more benefit from CPAP therapy.[67]

Oral Appliance

For patients who are unable or unwilling to use CPAP, or those who lack reliable access to electricity, custom-fitted and titrated oral appliances or mandibular advancement devices (MAD) can help alleviate airway obstruction by advancing the lower jaw. This approach is typically most effective for candidates with appropriate dentition and mild-to-moderate sleep apnea. In a randomized clinical trial involving 126 patients with moderate-to-severe OSA, the 24-hour mean arterial pressure was similar between CPAP and MAD after the first month of therapy. However, MAD was found to be superior to CPAP in improving quality of life measures.[68] More recently, another randomized clinical trial demonstrated similar long-term improvements for both CPAP and MAD in self-reported neurobehavioral outcomes over a 10-year follow-up.[69]

The AASM and the American Academy of Dental Sleep Medicine (AADSM) have developed guidelines for using MAD in patients with OSA.[70] The AASM/AADSM guidelines recommend the following: 

• Oral appliances can be considered as an alternative to no treatment for adult patients with snoring (without OSA) or those with OSA who do not tolerate CPAP therapy or prefer an alternative treatment.
• When a sleep physician prescribes oral appliance therapy for an adult patient with OSA, a qualified dentist should use a custom, titratable appliance.
• A follow-up with a qualified dentist is necessary to assess for dental-related adverse effects after initiating oral appliance therapy in adult patients with OSA.
• Follow-up sleep testing is required to confirm the efficacy of the treatment.

Surgical Treatments

Uvulopalatopharyngoplasty (UPPP) involves the surgical removal of the uvula and tissue from the soft palate to create more space in the oropharynx.[71] This procedure is sometimes performed alongside a tonsillectomy and adenoidectomy. However, the long-term efficacy of UPPP is limited, with fewer than 50% of patients experiencing a significant improvement in the AHI after the first year.[72]

Maxillomandibular advancement (MMA) involves detaching both the upper and lower jaws and surgically advancing them anteriorly to increase space in the oropharynx.[73] This procedure is most effective for patients with retrognathia and tends to be less successful in older patients or those with larger neck circumferences. More recently, drug-induced sleep endoscopy has been used for preoperative planning, helping to identify multiple levels of obstruction in these patients and determining their candidacy for surgical treatments such as MMA or hypoglossal nerve stimulation (HNS).[74] This technique enables surgeons to address nasal, soft palate, and hypopharyngeal obstructions in a single surgery.[75] 

A newer treatment option is the implantable HNS, typically implanted unilaterally, although bilateral implantation has been reported recently.[76] This instrument works by stimulating the genioglossus muscle (an upper airway dilator) during apneas, causing tongue protrusion and relieving airway obstruction.[77] HNS effectively reduces the AHI, with a median AHI score at 12 months decreasing by 68%, from 29.3 events per hour to 9.0 events per hour. HNS also improves sleepiness symptoms in patients with moderate-to-severe OSA who are unable to tolerate CPAP treatment.[78] 

Adverse events following HNS, both short- and long-term, are relatively uncommon. In a study, 134 adverse events were reported from 132 patients over 5 years.[79] The most common adverse events reported after HNS are tongue abrasion (11.0%), pain (6.2%), and device malfunction (3% to 6%).[77] 

The eligibility criteria for HNS adopted from the original randomized trial include the following characteristics:

• Adults aged 18 or older
• Moderate-to-severe OSA (AHI between 20 and 50 with <25% central or mixed apneas)
• Inability to tolerate CPAP
• No complete concentric collapse at the palate on drug-induced sleep endoscopy [78]

Exclusion criteria for HNS include:

• BMI greater than 32.0 kg/m²
• Neuromuscular disease
• Hypoglossal nerve palsy
• Severe restrictive or obstructive pulmonary disease
• Moderate-to-severe pulmonary arterial hypertension
• Severe valvular heart disease
• Heart failure, New York Heart Association class III or IV
• Recent myocardial infarction or severe cardiac arrhythmias (within the past 6 months)
• Persistent uncontrolled hypertension despite medication use
• Active psychiatric disease and coexisting nonrespiratory sleep disorders

In extreme cases, OSA may be treated with a tracheostomy to bypass the oropharyngeal obstruction. This treatment is typically best managed at academic or specialty sleep centers with experience in handling tracheostomy cases. Patients undergoing tracheostomy face numerous challenges, including home care, durable medical equipment needs, and family or partner education on proper tracheostomy management. Additionally, many patients with severe OSA requiring a tracheostomy often have comorbidities that further complicate treatment.

Differential Diagnosis

Differential diagnoses for OSA include:

• Asthma
• Central sleep apnea
• Chronic obstructive pulmonary disease
• Depression
• Gastroesophageal reflux
• Hypothyroidism
• Narcolepsy
• Periodic limb movement disorder

Prognosis

The short-term prognosis of OSA with treatment is generally favorable, but the long-term outlook remains uncertain. The primary challenge is poor adherence to CPAP therapy, with nearly 50% of patients discontinuing its use within the first month despite education.[80] Many individuals with OSA have comorbidities or are at an increased risk for adverse cardiac events and stroke. Consequently, individuals who do not adhere to CPAP are at a higher risk for cardiac and cerebral events, as well as increased annual healthcare-related costs.[81][82] 

Furthermore, OSA is also associated with pulmonary hypertension, hypercapnia, hypoxemia, and daytime sedation, and these individuals have a high risk of motor vehicle accidents. The overall life expectancy of individuals with OSA is lower than that of the general population. OSA is known to impact cardiac function, especially in individuals with obesity.[83][84] Recent studies have shown that CPAP treatment improves left and right ventricular mechanics in patients with OSA.[85]

Complications

Complications from OSA can include:

• Hypertension
• Myocardial infarction
• Atrial fibrillation
• Congestive heart failure
• Cerebrovascular accident
• Depression
• Sleeplessness-related accidents

Deterrence and Patient Education

Weight loss should be encouraged in patients with OSA. They should be advised to avoid alcohol, benzodiazepines, opiates, and certain antidepressants, as these substances can worsen their condition. Patients should also be educated on the importance of proper sleep hygiene, ensuring sufficient sleep each night, and the risks of driving while drowsy. Adherence to CPAP use should be strongly encouraged, along with proper cleaning and maintenance of the machine to ensure optimal function.

Pearls and Other Issues

An association exists between posttraumatic stress disorder (PTSD) and OSA, although a definitive causal relationship has not been established. Up to 47% of patients with PTSD have difficulty maintaining sleep and are known to have a low arousal threshold.[86][87] Patients with both PTSD and OSA experience more severe symptoms of both disorders compared to those with only one condition.[88]

Enhancing Healthcare Team Outcomes

Managing OSA is most effectively achieved through an interprofessional team that includes a sleep specialist, primary care provider, cardiologist, otolaryngologist, dietitian, pulmonologist, neurologist, and nursing staff. Several treatment options are available for OSA, with the primary treatment being CPAP.

Although clinicians oversee overall therapy, nurses and sleep evaluation personnel have a critical role. Nurses are often the first providers to detect therapeutic failure or noncompliance (eg, with CPAP machines) and should prompt clinicians to address the issue and ensure appropriate diagnostic algorithms are followed. An interprofessional care model will lead to the best possible outcomes for OSA patients, particularly given the challenges in managing the condition.

Unfortunately, compliance with CPAP remains low. While some patients may benefit from an oral or nasal device, compliance remains challenging. Surgery is considered a last resort and should only be pursued after a thorough evaluation. Surgery does not cure the disorder, is expensive, and may lead to severe complications. The prognosis for most patients with OSA is guarded. Until weight loss is achieved, most therapies exhibit limited efficacy.

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Disclosure: Jennifer Slowik declares no relevant financial relationships with ineligible companies.

Disclosure: Abdulghani Sankari declares no relevant financial relationships with ineligible companies.

Disclosure: Jacob Collen declares no relevant financial relationships with ineligible companies.