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Obstructive Sleep Apnea

Author: Jennifer M. Slowik Author: Abdulghani Sankari Editor: Jacob F. Collen Updated: 3/21/2024 1:31:35 PM

Introduction

Obstructive sleep apnea (OSA) is characterized by episodes of a complete (apnea) or partial collapse (hypopnea) of the upper airway with an associated decrease in oxygen saturation or arousal from sleep.[1] This disturbance results in fragmented, nonrestorative sleep. Other symptoms include loud, disruptive snoring, witnessed apneas during sleep, and excessive daytime sleepiness.[2][3][4] OSA has significant implications for cardiovascular health, mental illness, quality of life, and driving safety.[5]

This article discusses the etiology of OSA, its epidemiology, clinical manifestation, and management. Other types of sleep disorders and breathing (central sleep apnea,[6] upper airway resistance,[7] and obesity hypoventilation) will be discussed separately.[8] See Figures. Central and Obstructive Apnea, Polygraph; Sleep Polygraph, 30 Second Window; Sleep Polygraph, 120 Second Window; Sleep Apnea Clinical Assessment 'and Sleep Testing Modalities, Sleep Apnea. 

Etiology

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Etiology

Pharyngeal narrowing and closing during sleep is a complex phenomenon, and multiple factors play a role in this pathogenesis. Sleep-related reduced ventilatory drive and neuromuscular factors combined with anatomic risk factors are likely to play a significant role in upper airway obstruction during sleep.[1] 

The anatomic factors that promote pharyngeal narrowing include large neck circumference, soft tissue, bone, or vessels.[9] Many of these structures can lead to increased pressure surrounding the upper airway, resulting in pharyngeal collapsibility and insufficient space to accommodate airflow to a portion of the upper airway during sleep.[10] 

In addition, the upper airway muscle tone plays a role; when this muscle decreases, a repetitive total or partial airway collapse results. The most common cause of OSA in adults is obesity, male sex, and advancing age.[11] The severity of OSA decreases with age when adjusting for body mass index.[12]  

Anatomic Factors

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

Nonanatomic Risk Factors

  • Central fat distribution
  • Obesity
  • Advanced age
  • Male gender
  • Supine sleeping position
  • Pregnancy [13]

Additional Factors

  • Alcohol use
  • Smoking
  • Use of sedatives and hypnotics

Associated Medical Disorders

  • Endocrine disorders (eg, diabetes mellitus, metabolic syndrome, acromegaly, and hypothyroidism)[14][15]
  • Neurological disorders (eg, stroke, spinal cord injury, and myasthenia gravis)[16][17]
  • Prader Willi syndrome [18]
  • Down Syndrome [19]
  • Congestive heart failure [20]
  • Atrial fibrillation [21]
  • Obesity hypoventilation syndrome [8]

These relationships between OSA and various medical disorders are based mainly on observational studies and not necessarily randomized clinical trials. 

Epidemiology

Obstructive sleep apnea is a common condition with significant adverse consequences.[22] Using the definition of 5 or more events per hour, OSA affects almost 1 billion people globally,[23] with 425 million adults between 30 to 69 having moderate to severe OSA (15 or more events per hour).[24] 

In the United States, it has been reported that 25% to 30% of men and 9% to 17% of women meet the criteria for obstructive sleep apnea.[25][26] 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%.[25] Some risk factors, including obesity and upper airway soft tissue structure, are genetically inherited.[27]

Pathophysiology

Upper airway obstruction during sleep is often due to negative collapsing pressure during inspiration; however, progressive expiratory narrowing in the retro palatal area plays an important role.[28] The magnitude of upper airway narrowing during sleep is often related to body mass index, indicating that anatomical and neuromuscular factors contribute to airway obstruction.[29] The concept of the pressure-flow relationship through collapsible tubes is helpful in understanding the mechanisms of OSA.[30] 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 breathing cessation while sleeping that is witnessed by a bed partner. Excessive daytime sleepiness is one of the most common symptoms. However, most patients are asymptomatic.[26] 

Many patients only report daytime fatigue with or without other associated symptoms. Therefore, the distinction between sleepiness and fatigue should be objectively assessed. The Epworth Sleepiness Scale (ESS) can be used to evaluate the severity of sleepiness quantitatively.[31] The ESS score ranges from 0 to 24; more than 9 points indicate the presence of excessive daytime sleepiness and require additional assessment. The fatigue severity scale (FSS) can also assess the severity of symptoms of fatigue.[32] 

ESS and FSS are usually helpful as sleepiness and fatigue symptoms could be present concomitantly. Other symptoms vary from morning headaches and self-reported insomnia to nocturia.[33][34][35] Symptoms of sleep-onset insomnia and sleep maintenance insomnia were reported most by women.[36]

The STOP-BANG questionnaire is one of OSA's most widely accepted screening tools.[37]

  • 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 having or being treated for high blood pressure?
  • BMI: BMI greater than 35 kg/m2
  • Age: age greater than 50 
  • Neck circumference: Neck circumference greater than 40 cm
  • Sex: man

Use STOP-BANG to decide if there is a high probability of moderate-severe disease. There is a high risk if ‘YES’ was selected for 3 or more items; there is a low risk if ‘YES’ was answered for less than 3 items.

Obesity is the most common finding in individuals with OSA. Other physical findings are large neck circumference (17 inches or 43 cm in males and 16 inches or 40.5 cm in women), crowded oropharynx (Mallampati 3 to 4), retrognathia, micrognathia, tonsilar hypertrophy, low-lying palate, overjet, and a large tongue. However, only lateral narrowing is an independent predictor of OSA after adjusting for body weight and neck size.[38]

Evaluation

Any adult patient 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 those at risk of occupational hazards such as driving or pilots.[39][40]

In addition, due to the high prevalence of OSA and disease burden, patients with specific comorbidities such as refractory atrial fibrillation, resistant hypertension, and a history of stroke can be screened for sleep apnea regardless of symptoms.[41] 

Nighttime in-laboratory level 1 polysomnography (PSG) is the gold standard test for diagnosing obstructive sleep apnea. During the test, patients are monitored with 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 detect motion, an electrocardiogram lead, and electromyogram sensors to detect muscle contraction in the chin, chest, and legs. See Figure. Central and Obstructive Apnea, Polygraph.

Scoring respiratory events in adults relies on 4 channels:

  1. Oronasal thermal sensor 
  2. Nasal air pressure transducer 
  3. Inductance plethysmography (esophageal manometry or pressure catheter may be used instead) 
  4. Pulse oximetry [42] 

*A snoring monitor is a required channel but is not used to score any respiratory events. 

According to the American Academy of Sleep Medicine (AASM), hypopnea can be defined based on 1 of 2 criteria: a reduction in airflow of at least 30% for more than 10 seconds associated with at least 4% oxygen desaturation (eg, Medicare criteria) or a reduction in airflow of at least 30% for more than 10 seconds associated with at least 3% oxygen desaturation or an arousal from sleep on EEG (recommended AASM criteria).[43] 

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

  • A. Drop in the peak signal excursion by ≥90% of pre-event baseline flow
  • B. Duration of the drop in flow is ≥10 seconds
    • Apneas are usually further classified based on effort (respiratory inductance plethysmography signals)
    • Obstructive apnea, if there is increased effort throughout the entire apnea
    • Central apnea, if there is no effort throughout the entire apnea

Mixed apnea occurs if there is no effort in the first part and there is an effort in the second part of the apnea. See Figure 1. Polygraph depicting an example of central and obstructive apnea. 

Home sleep tests or portable monitoring (PM) have gained popularity due to their relative accessibility and lower cost. PM, however, should be used with specific rules and procedures based on the AASM unattended PM task force guidelines.[44] These guidelines outlined the following criteria:

  • At a minimum, the PM must record airflow, respiratory effort, and blood oxygenation.
  • The airflow, effort, and oximetric biosensors conventionally used for in-laboratory PSG should be used in PM.
  • PM testing must be performed under the auspices of an AASM-accredited comprehensive sleep medicine program with written policies and procedures.
  • An experienced sleep technologist/technician must apply the sensors or directly educate patients on sensor application.
  • The PM device must allow for the display of raw data with the capability of manual scoring or editing of automated scoring by a qualified sleep technician/technologist.
  • A board-certified sleep specialist or someone who fulfills the eligibility criteria for the sleep medicine certification examination must review the raw data from PM using scoring criteria consistent with current published AASM standards.[43] Under the specified conditions, PM may be used for unattended studies in the patient's home.
  • A follow-up visit should be performed to review test results for all patients undergoing PM.
  • Negative or technically inadequate PM tests should prompt in-laboratory polysomnography in patients with a high pretest probability of moderate to severe OSA.

Unattended PM and home sleep tests are appropriate for adults with a high pretest probability for sleep apnea and no significant medical comorbidities (advanced congestive heart failure, chronic obstructive pulmonary disease, and neurologic disorders). These are level 3 sleep tests consisting of 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 detect body position.

Moderate and severe sleep apnea is detected on these tests, but due to the chance of underestimating the apnea-hypopnea index relative to the total recording time (which may be longer than the total sleep time measured in an in-lab study), mild sleep apnea may go undiagnosed, and a repeat in-lab study may be needed. A proposed algorithm for the appropriate use of portable monitoring and in-lab PSG is outlined in Figure. Sleep Testing Modalities, Sleep Apnea. 

One of the main limitations of home sleep testing is that most studies rely on total recording time as the denominator instead of total sleep time in calculating the apnea-hypopnea index (AHI), as there are no EEG sensors to differentiate sleep from being awake. Using total recording time can result in an underestimation of the AHI by at least 20%.[45] 

The AASM recommended using the term respiratory event index (REI) to differentiate indices of respiratory events generated by a home sleep study (without recorded sleep). The AHI and REI are the average numbers of obstructive events per hour (during sleep or recording time, respectively).

While most portable monitoring devices include flow sensors, other technologies use an alternative method without flow, such as peripheral arterial tonometry (PAT), to identify sleep-disordered breathing events. The OSA severity obtained using PAT devices is called pAHI and is reported to provide similar indices to PSG-derived AHI.[46]

The severity of OSA in adults is 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 based on associated clinical sequelae (such as excessive daytime sleepiness, sleep maintenance insomnia, and cognitive dysfunction).[47]

Recent studies challenged the traditional definition and scoring criteria of OSA in adults due to its limitations in capturing the pathophysiological impact in individual patients.[23] Different metrics have been proposed to increase precision in diagnosing individuals with OSA.[48] These metrics include hypoxic burden, nocturnal heart rate changes, total sleep time with SpO2 <90% (TST90), duration of obstructive events, sleep arousal burden, and even genetics.[49][50][51][52][53][54][55] 

Treatment / Management

Treating OSA is a multi-pronged approach and should be individualized for each patient. While treatment of moderate to severe OSA has been shown to improve clinical outcomes,[56] there is limited or inconsistent evidence about the impact of therapy for mild OSA on neurocognition, mood, vehicle accidents, cardiovascular events, stroke, and arrhythmias.[47](A1)

Lifestyle Changes and Treating Underlying Medical Conditions

The importance of weight loss should be emphasized in patients with OSA who are overweight and obese.[57][58] Although weight loss is recommended and can often decrease the severity of obstructive sleep apnea, it is not usually curative. Patients should be educated on the impact of sleep duration on their health and prioritize getting at least 7 to 8 hours of sleep per night.[59] (A1)

Patients should be counseled to avoid alcohol, benzodiazepines, opiates, and some antidepressants, which may worsen their condition. Address any concomitant nasal obstruction with nasal steroids for allergic rhinitis or surgically for nasal valve collapse. For patients with lung or heart disease (such as asthma or heart failure), optimizing the treatment of these disorders is very important.

Positional Therapy

OSA that is more prominent in the supine position can be treated with a positioning device to keep a patient on their side, which can be an option.[60][61]

Positive Airway Pressure Therapy

Continuous positive airway pressure (CPAP) is the most effective treatment for adults.[62] 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 dampened by the decreased use of treatment during sleep and inadequate adherence. Adherence to CPAP among patients with OSA remains a significant challenge, as nearly half of the patients do not adequately adhere to treatment after the first month.[63] 

The American Thoracic Society published a recent statement on CPAP adherence tracking systems and the optimal monitoring strategies and outcome measures in adults.[64] Standardizing the CPAP adherence report not only the number of hours used more than 4 hours per night (>70% of nights) but also the amount of mask leak and residual apnea and hypopnea index is important. However, what is the optimal goal in adherence to OSA treatment? Recent studies are looking at the utility of telemedicine adherence interventions, remote monitoring of CPAP, and more interactive features with individual patients and their families have been shown to increase CPAP adherence rates.[65][66][67][68](A1)

Several study results have reported conflicting findings when assessing the effect of CPAP therapy on cardiovascular outcomes in patients with OSA.[48] In a recent randomized control trial, CPAP use for a minimum of 1 year in patients with acute coronary syndrome (ACS) and OSA without excessive daytime sleepiness did not lower the incidence of cardiovascular events (defined as cardiac-related death or 1 or more of the following outcomes: acute myocardial infarction, non-fatal stroke, hospital admission for heart failure, and new hospitalizations for unstable angina or transient ischaemic attack). The adherence to CPAP therapy was low (2.78 h/night), and follow-up was not long enough, which are significant limitations of this study.[69] (A1)

In another observational cohort study with long-term follow-up, CPAP use was associated with lower all-cause mortality among patients with severe OSA around years 6 to 7 of follow-up.[70]

In a more recent study, patients with coronary artery disease and OSA without excessive sleepiness who exhibited greater changes in heart rate benefited more from CPAP therapy.[71](A1)

Oral Appliance

For patients unable or unwilling to use CPAP or those unable to access electricity reliably, custom-fitted and titrated oral appliances or mandibular advancement devices (MAD) can bring the lower jaw forward and relieve airway obstruction. This typically works best for candidates with appropriate dentition and mild to moderate sleep apnea. In a randomized clinical trial on 126 patients with moderate-severe OSA, the 24-hour mean arterial pressure was similar between CPAP and MAD after 1-month of therapy. MAD was superior to CPAP for improving quality of life measures.[72] More recently, another randomized clinical trial demonstrated similar long-term improvement for CPAP and MAD in self-reported neurobehavioral outcomes during a 10-year follow-up.[73](A1)

The American Academy of Sleep Medicine (AASM) and the American Academy of Dental Sleep Medicine (AADSM) developed guidelines for using MAD in patients with OSA.[74] The AASM/AADSM guidelines recommend the following: (A1)

  • Oral appliances can be considered rather than no treatment for adult patients with snoring (without OSA) or those with OSA who do not tolerate CPAP therapy or prefer alternate treatment.
  • When a sleep physician prescribes oral appliance therapy for an adult patient with obstructive sleep apnea.
  • A qualified dentist should use a custom, titratable appliance.
  • A follow-up with a qualified dentist after oral appliance therapy is initiated in adult patients with OSA to assess for dental-related side effects.
  • A follow-up with sleep testing to confirm treatment efficacy is necessary.

Surgical Treatments

Uvulopalatopharyngoplasty (UPPP) surgically removes the uvula and tissue from the soft palate to create more space in the oropharynx.[75] This is sometimes done in conjunction with a tonsillectomy and adenoidectomy. Nevertheless, the long-term efficacy of UPPP is very limited, with less than 50% of patients having a significant increase in the apnea-hypopnea index after the first year.[76] (A1)

Maxillomandibular advancement (MMA) requires both the upper and lower jaws to be detached and surgically advanced anteriorly to increase space in the oropharynx.[77] This is best for patients with retrognathia and is less successful in older patients or those with larger neck circumferences. More recently, drug-induced sleep endoscopy has been used for preoperative planning to identify multiple levels of obstruction in these patients and candidacy for surgical treatment such as MMA and hypoglossal nerve stimulator.[78] This allows surgeons to address any nasal, soft palate, and hypopharyngeal obstructions that may be present during a single surgery.[79]

A newer option is the implantable hypoglossal nerve stimulator (HNS), usually implanted unilaterally, although bilateral implantation has been recently reported.[80] This instrument works by stimulating the genioglossus (upper airway dilator muscle) during apneas, resulting in tongue protrusion and relief of the obstruction.[81] (A1)

HNS effectively reduces AHI (median AHI score at 12 months decreased by 68%, from 29.3 events per hour to 9.0 events per hour) and improves sleepiness symptoms in those with moderate to severe OSA who are not tolerating CPAP treatment.[82] (A1)

Adverse events reported short- and long-term following HNS are not very common. In one study, 134 adverse events were reported from 132 patient reports over 5 years.[83] The most common adverse events reported after HNS are tongue abrasion (11.0%), pain (6.2%), and device malfunction (3% to 6%).[81] (A1)

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

  • Adults older than 18 years 
  • Moderate to severe OSA (AHI between 20 to 50 with <25% central or mixed apneas)
  • Inability to tolerate CPAP
  • No complete concentric collapse at the palate on drug-induced sleep endoscopy [82]
    • (A1)

Exclusion criteria for HNS include the following:

  • Body mass index 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 can also be treated with a tracheostomy to bypass the oropharyngeal obstruction. This management option is also best addressed at academic or specialty sleep centers that are experienced in treating patients with tracheostomy. Such patients encounter numerous challenges with home care, durable medical equipment, and family/partner education on tracheostomy management. Additionally, many patients with severe OSA requiring tracheostomy have comorbidities.

Differential Diagnosis

Differential diagnoses for OSA include the following:

  • 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 good, but the long-term prognosis is guarded. The biggest problem is the lack of adherence to CPAP, as nearly 50% of patients stop using CPAP within the first month despite education.[84] Many patients have comorbidities or are at risk for adverse cardiac events and stroke. Hence, those who do not use CPAP are at increased risk of cardiac and cerebral adverse events in addition to higher annual healthcare-related expenses.[85][86] 

Further, 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 patients with OSA is lower than the general population. OSA is known to affect cardiac function, particularly in obese individuals.[87][88] CPAP treatment was recently found to improve left and right ventricular mechanics in patients with OSA.[89]

Complications

Complications from OSA can include the following:

  • Hypertension
  • Myocardial infarction
  • Cerebrovascular accident
  • Depression
  • Sleeplessness-related accidents

Deterrence and Patient Education

Weight loss should be encouraged in patients with OSA. They should be counseled to avoid alcohol, benzodiazepines, opiates, and some antidepressants, which may worsen their condition. Additionally, they should be made aware of the importance of proper sleep hygiene, getting sufficient sleep every night, and the risks of driving while sleepy. Adherence to CPAP use should be encouraged, and the importance of properly cleaning and maintaining the machine should be emphasized.

Enhancing Healthcare Team Outcomes

Managing OSA is best accomplished with an interprofessional team that includes a sleep specialist, primary provider, cardiologist, otolaryngologist, dietitian, pulmonologist, neurologist, and nursing staff. There are many options to treat OSA, the primary one being CPAP.

As clinicians direct overall therapy, nurses and sleep evaluation personnel are critical. Nurses can often detect therapeutic failure or non-compliance (eg, with CPAP machines) and should prompt the clinician to address the situation and ensure the proper diagnostic algorithms are followed. The interprofessional care model will yield the best possible outcomes for OSA patients, especially given the difficulties in managing the condition. 

Unfortunately, compliance with CPAP remains low. Some patients may benefit from an oral or nasal device, but compliance remains an issue. Surgery is the last step and should only be considered after a thorough patient evaluation. Surgery does not cure the disorder, is expensive, and can be associated with severe complications. The prognosis for most patients with OSA is guarded. Until the patient starts to lose weight, most therapies have poor efficacy.

Media


(Click Image to Enlarge)
<p>Central and Obstructive Apnea, Polygraph. The image depicts an example of central and obstructive apnea.</p>

Central and Obstructive Apnea, Polygraph. The image depicts an example of central and obstructive apnea.

Contributed by A Sankari, MD

(Click Image to Enlarge)
<p>Sleep Polygraph, 30-Second Window

Sleep Polygraph, 30-Second Window. A polygraph recording during sleep; the panel shows electroencephalogram, electrooculogram, electrocardiogram, in addition to chin electromyogram signals from the lower limbs and respiratory signals, chest and abdomen respiratory plethysmography, and oxygen saturation during a 30-second window.

Contributed by A Sankari, MD, PhD

(Click Image to Enlarge)
<p>Sleep Polygraph, 120-Second Window

Sleep Polygraph, 120-Second Window. The polygraph, recorded during sleep, shows electroencephalogram, electrooculogram, electrocardiogram, in addition to chin electromyogram during a 120-second window. Note the repetitive obstructive apnea with persistent effort during cessation of both flow channels (nasal pressure flow and thermester followed by desaturation [light blue arrows] and arousals [dark blue arrows]).

Contributed by A Sankari, MD, PhD

(Click Image to Enlarge)
<p>Sleep Apnea Clinical Assessment

Sleep Apnea Clinical Assessment. The image demonstrates the clinical assessment of patients with suspected sleep apnea.

Contributed by A Sankari, MD, PhD

(Click Image to Enlarge)
<p>Sleep Testing Modalities, Sleep Apnea

Sleep Testing Modalities, Sleep Apnea. The available types of sleep apnea testing from level I (in-lab PSG) to portable monitoring devices (level II, III and IV). Note that only level II and III are acceptable for obstructive sleep apnea testing by the American Academy of Sleep Medicine guidelines.

Contributed by A Sankari, MD, PhD

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Level 1 (high-level) evidence