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Sleep Apnea Syndrome

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Last Update: September 4, 2023.

Continuing Education Activity

Sleep apnea syndrome (SAS) is defined by frequent episodes of apnea and hypopnea associated with symptoms such as excessive daytime and cardiovascular morbidity and mortality. Obstructive sleep apnea syndrome is a condition in which there is a dynamic collapse of upper airway tissues during sleep. This may result in recurrent respiratory-related events and both short-term symptomatic consequences and long-term physiologic consequences. This activity reviews the evaluation, workup, and management of adult patients with obstructive sleep apnea and highlights the role of the healthcare team in evaluating and treating these patients.


  • Summarize the etiology of obstructive sleep apnea.
  • Outline appropriate evaluation of obstructive sleep apnea.
  • Review the management options for obstructive sleep apnea.
  • Describe how the interprofessional healthcare team can implement strategies to improve patient outcomes in sleep apnea syndrome.
Access free multiple choice questions on this topic.


Sleep apnea syndrome (SAS) is defined by frequent episodes of apnea and hypopnea associated with symptoms such as excessive daytime and cardiovascular morbidity and mortality.[1] SAS encompasses a broad spectrum of sleep-disordered breathing from central to mixed, obstructive apnea, and hypopnea. In obstructive SAS (i.e., obstructive sleep apnea-OSA), there is upper airway collapse and obstruction during sleep, which results in snoring, obstructive apneas (cessations of breathing), hypopneas (abnormally slow or shallow breathing), or respiratory-related arousals.[2][3] The etiology, epidemiology, history and physical manifestation, diagnostic approach, and complications of SAS are reviewed here. More specifics of central and obstructive sleep apnea are also described separately in more detail.[4][5][6]


Factors that contribute to the development of upper airway collapse are those that affect upper airway patency. Because the upper airway is enclosed by the craniofacial skeleton, which serves as the scaffold of the upper airway, the craniofacial skeleton is one of the key determinants of upper airway patency or collapse.[7][8] Thus, in situations such as retrognathia or maxillomandibular deficiency, the soft tissues of the upper airway exist within a more compact space, resulting in decreased upper airway patency.

Conversely, the size and compressibility of the soft tissues within the craniofacial skeleton also determine upper airway patency. Upper airway patency decreases with increased soft tissue mass within a given confined space within the craniofacial skeleton. This may be influenced by factors such as the amount of submucosal or lingual adipose tissue, as well as cervical lymphovascular tone, as well as neuromuscular influences on upper airway muscular tone.[9][10][11][12][13] 

Increased age, obesity, male gender, and craniofacial abnormalities are considered to be the primary risk factors for developing OSA. Other risk factors include smoking and a family history of OSA.[14][15][16][17][18]


The overall prevalence of SAS ranges from 21-59% in the general population and patients with cardiac disease, respectively. [19][20] Obstructive sleep apnea is the most common sleep-related breathing disorder. It is most common in adult males but may also be present in women and children, though rates of OSA in post-menopausal women approach those of men.[1][17][2] 

In North America, the prevalence of OSA is between 15 and 30 percent in males and 10 to 15 percent in females.[14][21][14] The prevalence of OSA varies by race, and in the United States is more prevalent in African Americans than in other groups, independent of body weight.[22][23] 

The prevalence of OSA also appears to be increasing, which is thought to be related to a combination of increasing rates of obesity as well as increased diagnosis and detection. In a study by Peppard et al., it was estimated that the prevalence of OSA increased from 11 to 14 percent from 1990 to 2010 among adult American males.[21]


Though many factors contribute to obstructive sleep apnea, changes in respiratory dynamics during sleep are the principal essence of the disorder which are influenced by multiple factors. During sleep, there is decreased tonic activity of the laryngeal, supraglottic, oropharyngeal, nasopharyngeal, and lingual musculature, which results in dynamic collapse with respiration.[9][24] This decreased upper airway tonic activity results in a dynamic decrease in the caliber of the upper airway and therefore increased resistance to airflow. The effects of this dynamic collapse can range from mild collapse without significant changes to respiration and no effect on oxygenation or arousal to complete airway obstruction, decreased oxygenation, and frequent arousals throughout sleep. Over time, this can have significant effects on cardiopulmonary and neurologic function. 

Obstruction during sleep can occur at various sites within the upper airway. These include the nasal cavity, the nasopharynx, the oropharynx, the base of the tongue, and the laryngeal complex. A patient may have one primary site of obstruction; however, many patients have an obstruction at multiple levels. A thorough evaluation and examination are essential to properly identify the most likely sites of obstruction so that treatment may be tailored appropriately. 

An understanding of definitions of respiratory events is imperative in understanding this disorder. An apnea is defined as the cessation of airflow for 10 seconds or more. A hypopnea is defined as either a reduction in airflow for at least ten seconds of 30 percent or more with an associated oxygen desaturation of at least four percent OR a reduction in airflow for at least ten seconds of 50 percent or more with an associated oxygen desaturation of three percent or associated arousal. Respiratory effort-related arousal (RERA) is a sequence of breaths that do not meet the criteria for apnea or hypopnea with increasing effort or with flattening of the nasal pressure waveform that increases for at least ten seconds, which results in arousal.[25]

There is an array of common findings that are characteristic of patients presenting with obstructive sleep apnea. Daytime sleepiness is the most common complaint for patients seeking evaluation and treatment for OSA. Sleepiness is defined as difficulty remaining alert while awake. Patients or their partners will often complain of loud snoring, coughing, or choking during sleep. Though snoring is sensitive for OSA, it has a low specificity and is not useful in diagnosing OSA alone.[26] Patients with OSA often complain of morning headaches. Less common complaints include difficulty remaining asleep, chest pain or palpitations, neuropsychiatric changes, or nocturia.[27][28]

History and Physical

A complete history for a patient presenting with signs or symptoms of OSA must be obtained, including symptoms of daytime sleepiness, associated sleep symptoms, snoring, coughing, or choking during sleep, morning headaches, chest pain, dyspnea, or neuropsychiatric changes. Inquiring regarding sleep hygiene and screening for other sleep-related diagnoses is also important. One of the key points is to determine whether the patient is experiencing sleepiness associated with OSA from fatigue, which indicates alternative medical diagnoses. 

A comprehensive history and physical examination are crucial in the workup for suspected OSA, with special attention to all possible sites of the upper airway obstruction. The nasal cavity is carefully evaluated for conditions that decrease the patency of the nasal airway, including septal deviation, inferior turbinate hypertrophy, masses or lesions, nasal valve collapse, or adenoid hypertrophy. The oropharynx is also carefully examined with attention to factors that may decrease patency, including an enlarged or elongated soft palate or uvula, which is often seen in patients with chronic obstructive respiratory disorders. The physician also evaluates palatine tonsil hypertrophy and macroglossia and their effect on oropharyngeal airway patency. The Updated Friedmann Staging System for Obstructive Sleep Apnea is a widely used screening tool for evaluating oropharyngeal patency, including tongue position, palatine tonsil size, and body mass index into stage I-IV.[29] This is a validated scale that is helpful not only in screening patients but also may be useful in determining optimal treatment modalities and tracking outcomes. 

The hypopharyngeal and laryngeal evaluation includes assessing lateral pharyngeal wall anatomy and collapse, epiglottis size and shape, lingual tonsillar hypertrophy, and assessment for any obstructive lesions or masses. The evaluation of the hypopharynx and laryngeal airway remains controversial. Some advocate an awake assessment of these structures using mirror laryngoscopy or flexible fiberoptic laryngoscopy. Scoring systems such as the Modified Cormack-Lehane scoring systems have been developed, which are useful for efficiently and effectively communicating laryngeal anatomy findings to evaluate obstructive sleep apnea.[30] However, such evaluation is limited as it does not assess the dynamic changes of the airway during sleep. As a result, efforts have been made to evaluate the dynamic collapse of the upper airway. Maneuvers have been previously described to simulate airway collapse in an awake patient; however, these have been shown to have limited utility as simulating the dynamic collapse that occurs during sleep with awake maneuvers is problematic.[31] 

Drug-induced sleep endoscopy (DISE) has emerged as an alternative evaluation of the upper airway during which the patient is evaluated by flexible fiberoptic laryngoscopy while lying supine under sedation, thus providing a more physiologic representation of sleep-related dynamics of the upper airway. DISE is believed to be useful in improving treatment outcomes for patients with OSA; however, controversy exists regarding its use due to lack of standardization as well as the most appropriate use in the workup and treatment for obstructive sleep apnea.[32]

The physical examination also includes evaluating the craniofacial skeleton with an assessment of mandibular anatomy, such as retrognathia, narrow mandibular or maxillary arches, maxillomandibular insufficiency, or any bony lesions that may affect obstruction, such as large mandibular tori. Neck anatomy should also be examined. A neck circumference greater than 17 inches for men and 15.5 inches for women is associated with an increased risk of OSA. Evaluation of general body habitus includes evaluation for obesity and adipose distribution, achondroplasia, or chest wall deformities. The physical examination should also include evaluation for possible cardiovascular sequelae, including arterial hypertension and peripheral edema.


Current recommendations are to obtain diagnostic testing for the workup of OSA in patients with excessive daytime sleepiness on most days as well as two or more of the following symptoms: diagnosed hypertension, loud snoring, witnessed apneas or gasping/choking episodes during sleep. In the absence of these symptoms, some recommend pursuing diagnostic testing for excessive daytime sleepiness alone if there is a concern for obstructive sleep apnea given the overall clinical presentation or if an evaluation for OSA must be ruled out during the workup for another disorder.[33]

A widely used, validated tool that helps differentiate sleepiness from fatigue used in diagnosing OSA, which evaluates daytime sleepiness, is the Epworth Sleepiness Scale. This survey asks the patient to rate the likelihood of falling asleep from 0-3 (0 would never fall asleep to 3-a high chance of dozing off) in various situations. A total score of greater than 10 is suspicious for OSA.[34]

The gold standard for the diagnosis of obstructive sleep apnea is an in-laboratory polysomnogram. This is preferred for all patients, but in certain populations/situations, an at-home polysomnogram is an acceptable alternative to an in-laboratory study. Patients in whom an at-home sleep study may be an appropriate alternative include those with no suspicion of another sleep-related diagnosis, an adequate device is available for at-home testing, and a sleep expert is available to interpret the data. If the study is inconclusive or suspicion of OSA remains despite a negative at-home polysomnogram result, an in-laboratory polysomnogram should be completed.[33][35]

An understanding of key indexes of sleep-disordered breathing is required to understand the data of a polysomnogram and diagnose obstructive sleep apnea. The Apnea Index (AI) refers to the total number of apneas per hour of sleep. The Hypopnea Index (HI) is the total number of apneas per hour of sleep. The AI and HI are used to calculate the Apnea-Hypopnea Index (AHI), which is the total apneas or hypopneas per hour of sleep. This calculation serves as one of the important determinants in the diagnosis of OSA. The RERA Index refers to the total number of RERAs that occur per hour of sleep. The Respiratory Disturbance Index (RDI) is an index that is calculated as the total number of apneas, hypopneas, and RERAs per hour of sleep. The Central Apnea Intex is another useful index calculated by the total number of central apneas per hour of sleep. Similarly, the Mixed Apnea Index may be calculated to find the total number of mixed apneas per hour of sleep. 

The diagnosis of OSA is confirmed on polysomnogram if there are five or more predominantly obstructive respiratory events per hour (which refers to an AHI or RDI 5 or greater) in a patient who has one or more sleep-associated symptoms or conditions (which include sleepiness, fatigue, sleep that is unrestful, insomnia, apneas, gasping or choking, consistent snoring breathing interruptions witnessed by a bed partner, mood disorder, diagnosed hypertension, cognitive dysfunction, cerebrovascular accident, coronary artery disease, atrial fibrillation, congestive heart disease, or diabetes mellitus type II). Alternatively, the diagnosis of OSA is also confirmed if there are fifteen or more predominantly obstructive respiratory events per hour (referring to an AHI or RDI of 15 or greater), regardless of associated symptoms or conditions. OSA is generally classified as mild, moderate, or severe. Mild OSA refers to an AHI or RDI between 5 and 14 on a polysomnogram. Moderate OSA refers to an AHI or RDI between 15 and 30. Patients with an AHI or RDI greater than 30 on a polysomnogram are categorized as having severe OSA.[36] 

Treatment / Management

Education and Behavior

Once a patient is diagnosed with OSA, counseling regarding risk factors, natural history, and complications of untreated OSA should be discussed. All patients should also be alerted of the increased risk of motor vehicle collisions (MVC) in patients with OSA. The patients should also be instructed to consult with their primary physician regarding their OSA prior to undergoing anesthesia or starting sedating medications. 

Appropriate behavioral modifications should be identified and discussed with all patients as these are modifiable and low-risk. For obese patients, regular exercise and a healthy diet should be encouraged. Weight loss has been shown to improve AHI/RDI, decrease daytime sleepiness, improve metabolic parameters, and improve blood pressure control.[37][38] Counseling regarding proper sleep hygiene should also be provided, as many patients with OSA also suffer from the simultaneous effects of poor sleep hygiene. Counseling may also be provided regarding recommending a change in sleep position if applicable.[39][40][41][42][43] All patients with OSA should be advised that alcohol and sedating medications may worsen their OSA. 

Positive Airway Pressure Therapy

In positive pressure therapy, the positive transmural pharyngeal pressure so that the upper airway remains patent as the intraluminal pressure exceeds the surrounding pressure.[44] In most patients with OSA, this is delivered via continuous positive airway pressure (CPAP), though in some patients, bilevel positive airway pressure (BI-PAP) or auto-titrating positive airway pressure (APAP) may be appropriate.

Positive airway pressure is the initial treatment for nearly all patients with OSA and remains the mainstay of treatment. Numerous randomized control trials and meta-analyses have concluded that positive airway pressure reduces respiratory event frequency, daytime sleepiness, and frequency of MVCs improves blood pressure control, and improves the overall quality of life.[45][46][47][48][49][50][51][52] The American Academy of Sleep Medicine recommends offering positive pressure therapy to all patients diagnosed with OSA.[53] Adherence to positive pressure therapy is one of the most important factors to assess once therapy is initiated. Twenty to forty percent of patients do not use their devices, and others often do not wear their devices for a sufficient amount of time.[54][55]

Alternative and Adjunctive Therapies 

Oral Appliances are an option for patients with mild to moderate OSA who fail to tolerate positive pressure therapy. In the appropriate patients, these devices decrease respiratory-related arousals, sleepiness, snoring, and oxygen desaturation.[56][57][58][59] Potential adverse effects secondary to oral appliances include dental pain, occlusal changes, temporomandibular joint disease, dry mouth, bruxism, and gingival irritation.[58] Younger patients with lower body-mass indexes with mild to moderate OSA have the greatest benefit from oral appliances.[60]

Surgery Intervention is generally not considered first-line therapy for OSA and instead is considered when therapy from positive pressure therapy and/or oral appliance therapy is either ineffective or declines over time. In these patients, identification of the most likely contributing site or sites of obstruction is assessed in a comprehensive exam as above. In addition, some surgeons advocate performing Drug-Induced Sleep Endoscopy (DISE) to further evaluate the airway under anesthetic conditions - however, there is no current consensus on the role of DISE in assessing patients with OSA.

Depending on the sites of obstruction, numerous surgical alternatives exist, including tonsillectomy, uvulopalatopharyngoplasty (for which complications include oropharyngeal bleeding and velopharyngeal insufficiency as well as velopharyngeal stenosis), adenoidectomy, surgical correction for nasal obstruction including septoplasty and inferior turbinate reduction. Craniofacial surgery, including maxillomandibular advancement, may also be performed for maxillomandibular insufficiency with improvement in obstructive sleep apnea for moderate to severe disease but carry the risk of damage to nearby structures, including the inferior alveolar/mental nerve, provides sensation to the chin and lower lip, and marginal mandibular nerve provides motor innervation to the lateral oral aperture. This also requires inpatient hospital stay and recovery and is not a good option for older patients with multiple comorbidities.[61]

An alternative to standard anatomic correction surgery is hypoglossal nerve stimulation, which protrudes the tongue forward via an implantable neurostimulation device that senses respiration to deliver stimulation at the appropriate time. This is indicated in patients with moderate to severe obstructive sleep apnea who have failed positive pressure ventilation or do not obtain enough benefit from positive pressure ventilation with a BMI of less than 32. In selected patients, these devices have shown reductions in AHI and oxygen saturation indexes and decreased subjective sleepiness.[62][63][64][65] 

It should also be noted that tracheostomy is another surgical treatment for obstructive sleep apnea as this bypasses the upper airway; however, this is rarely chosen for treatment of OSA alone but remains an option for patients with severe refractory disease or those with a concomitant disease for which tracheostomy may be appropriate.[66]

Differential Diagnosis

The consideration of alternative diagnoses to OSA is imperative not only for the correct diagnosis of OSA but because patients with OSA may have concomitant alternative sleep-related diagnoses that also must be considered.[67] It is important to differentiate obstructive apnea from central apnea. It is also important to differentiate OSA from primary snoring or laryngospasm. Other causes of excessive daytime sleepiness must be carefully considered, including narcolepsy, periodic limb movement disorder, restless leg syndrome, circadian rhythm disorders, and sleep hygiene-related effects. If one of these diagnoses is suspected, an appropriate workup, such as a multiple sleep latency test, may be considered if there is a concern for narcolepsy.


The short-term prognosis for patients with OSA is generally good. Treatments for patients with mild obstructive sleep apnea have shown improvement in symptoms but do not show differences in long-term cardiovascular outcomes. However, untreated OSA can be life-threatening. Excessive daytime sleepiness results in patients with OSA having increased death rates from MVCs and other sleepiness-related incidents; patients with moderate to severe OSA have an increased risk of developing cardiopulmonary disease, cerebrovascular incidents, and neuropsychiatric dysfunction if untreated. However, treatments have not been shown to decrease mortality, cardiovascular events, and neurocognitive function in the long term.[68][69]


Patients with OSA are at risk of multiple adverse clinical outcomes. One of the most common adverse outcomes in patients with obstructive sleep apnea is an increased rate of motor vehicle collisions. Patients with OSA are involved in motor vehicle collisions at a rate of 2 to 3 times that of the general population. Thus it is important to counsel patients diagnosed with OSA regarding this risk. In patients who spend a significant amount of time in motor vehicles, such as those in commercial transportation, appropriate treatment for obstructive sleep apnea is particularly important to avoid adverse outcomes.[68] 

Obstructive sleep apnea may also result in neuropsychiatric dysfunction, including difficulties with attention, memory, cognitive deficit, and impaired executive function. Patients with obstructive sleep apnea are also more likely to experience mood disorders, psychosis, and sexual dysfunction than the general population.[70][71][72] 

Cardiopulmonary mortality is another important factor to consider for patients with OSA. Multiple large studies have demonstrated that patients with moderate to severe OSA are at increased risk for coronary artery disease, systemic hypertension, cardiac arrhythmias, congestive heart failure, pulmonary hypertension, right heart failure, and cerebrovascular accident.[73] Patients with OSA also have an increased incidence of metabolic derangements incidence of insulin resistance as well as an increased incidence of the complications of type II diabetes mellitus.[74] There is also a two to threefold increase in non-alcoholic fatty liver disease incidence in patients with OSA independent of obesity.[75][76][77][78] 

Deterrence and Patient Education

Because OSA is so prevalent and has numerous negative health-related outcomes, physicians must appropriately evaluate and screen patients for symptoms and signs of OSA. When diagnosed, patients should be educated regarding the pathophysiology, expected course, and treatment options, including lifestyle modifications, positive pressure therapy, and alternative/additional therapies as indicated. They should also be counseled regarding the need for long-term follow-up and monitoring for potential complications of OSA.

Pearls and Other Issues

OSA is a condition caused by obstruction of the upper airway during sleep that can lead to symptoms including daytime sleepiness, snoring, gasping for air while sleeping, and morning headaches that are associated with adverse outcomes, including increased rates of MVCs and sleepiness-related accidents as well as increased rates of cardiopulmonary complications, cerebrovascular events, and neurocognitive effects in the long term. 

In addition to a comprehensive history and physical exam, in-lab polysomnography is the gold standard for treating obstructive sleep apnea. 

For patients with OSA, positive pressure therapy is the mainstay of treatment. However, additional treatments are available for those who fail positive pressure therapy or have an inadequate response to positive pressure therapy alone.

Enhancing Healthcare Team Outcomes

Enhancing healthcare outcomes for OSA is multifaceted and involves all interprofessional healthcare team members. Knowledge regarding OSA in the general population is currently poor, and initiatives are underway to address this but must be furthered to improve.[79] Clinicians (MDs, DOs, NPOs, and PAs), nurses, sleep specialists, and other health professionals must consider the implications on healthcare outcomes that may come into effect when treating patients with OSA in any healthcare setting because the complications of OSA are many and may affect patient outcomes if not addressed appropriately.[52] [Level 1]

The clinician will direct the overall direction of case management, but nurses, pharmacists, and other ancillary staff can provide valuable patient counsel, make recommendations from their areas of expertise, and alter other team members if they not any changes in the patient's condition. All interprofessional team members must maintain accurate, updated records, so everyone involved in care has the most accurate and current data to make decisions. This interprofessional paradigm will help drive improved patient outcomes. [Level 5]

Review Questions


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Disclosure: Evan Cumpston declares no relevant financial relationships with ineligible companies.

Disclosure: Philip Chen declares no relevant financial relationships with ineligible companies.

Copyright © 2023, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK564431PMID: 33232089


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