Obstructive Sleep Apnea (OSA)

How to Cite This Chapter: Chari VM, Simms T, Powles ACP, Pływaczewski R, Niżankowska-Jędrzejczyk A, Mejza F. Obstructive Sleep Apnea (OSA). McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.3.16. Accessed April 16, 2024.
Last Updated: September 5, 2022
Last Reviewed: September 5, 2022
Chapter Information

Definition, Etiology, PathogenesisTop

Obstructive sleep apnea (OSA) is a disorder caused by recurrent episodes of upper airway collapse (causing apnea) or upper airway narrowing (causing hypopnea [a marked decrease in airflow]) at the level of the pharynx. Repetitive upper airway collapse can lead to swings in intrathoracic pressure, increased sympathetic nervous system activity, hypoxemia, hypercapnia, and sleep fragmentation, with associated neurocognitive and cardiovascular complications.

Apnea is defined as a ≥90% reduction of airflow lasting ≥10 seconds. Respiratory effort is present in obstructive apneas and absent in central apneas. Hypopnea is defined as a ≥30% reduction of airflow in the nasal pressure signal lasting ≥10 seconds, with an associated ≥3% decrease in oxygen saturation or electroencephalography (EEG)-defined arousal from sleep. The apnea-hypopnea index (AHI) indicates the number of apneas and hypopneas per hour of sleep. A respiratory effort–related arousal (RERA) is a disturbance of breathing lasting ≥10 seconds that does not meet the criteria for apnea or hypopnea and leads to arousal from sleep. The respiratory disturbance index (RDI) is the number of apneas, hypopneas, and RERAs per hour of sleep.

Factors contributing to upper airway obstruction during sleep include obesity, increased neck circumference (>43 cm in men and >40 cm in women), long uvula, tonsillar and/or adenoid hypertrophy, nasal obstruction, retrognathia, macroglossia, alcohol consumption (particularly before bedtime), use of sedative-hypnotic drugs, and tobacco smoking.

Clinical Features and Natural HistoryTop

1. Daytime symptoms: Excessive daytime sleepiness, morning headache, memory and concentration impairment, sexual dysfunction, depressed mood.

2. Nocturnal symptoms: Snoring, witnessed apneas, choking/gasping, excessive sweating, nocturia, palpitations, frequent awakenings.

3. Comorbidities and sequelae: OSA is an independent risk factor for hypertension and arrhythmias including atrial fibrillation. Severe OSA is associated with the development of coronary artery disease and increased risk of fatal and nonfatal cardiovascular events, independent of other risk factors including obesity. Untreated moderate to severe OSA increases perioperative risks including respiratory failure, myocardial infarction, heart failure, arrhythmias, stroke, and cardiac death. The presence of daytime sleepiness, regardless of OSA severity, increases the risk of motor vehicle collisions.

DiagnosisTop

A definitive diagnosis requires a sleep study. In-laboratory, technologist-attended polysomnography (PSG) is the gold standard and consists of overnight monitoring of sleep and sleep stages (using EEG, electrooculography, and electromyography), airflow, chest and abdominal respiratory effort, oxygen saturation (SpO2), electrocardiography, body position, and limb movements. In uncomplicated cases in adult patients (without cardiorespiratory disease, cerebrovascular disease, potential respiratory muscle weakness [due to a neuromuscular condition], suspicion of sleep-related hypoventilation, or chronic opioid medication use), the diagnosis of OSA can be made with home sleep apnea testing (involving at least recording of airflow, respiratory movement, and oximetry, or peripheral arterial tonometry with oximetry and actigraphy). However, when the home sleep apnea test is negative, inconclusive, or technically inadequate and a clinical suspicion of significant OSA remains, PSG is recommended.

American Academy of Sleep Medicine (AASM) diagnostic criteria:

1) At least 15 obstructed breathing events (apneas, hypopneas, RERAs) per hour of sleep (RDI ≥15; regardless of the presence or absence of symptoms).

2) RDI ≥5 in a patient with ≥1 of the following symptoms:

a) Unintentional sleeping episodes, excessive daytime sleepiness, unrefreshing sleep, fatigue, or insomnia.

b) Awaking with a feeling of apnea, dyspnea, or choking.

c) The patient’s partner reports habitual snoring or episodes of apnea during the patient’s sleep.

In addition to the above criteria (a-c), the European Sleep Research Society (based on the International Classification of Sleep Disorders) lists comorbidities that, if present, satisfy the diagnostic criteria for OSA with an RDI ≥5, for example, hypertension, coronary artery disease, stroke, congestive heart failure, atrial fibrillation, type 2 diabetes, mood disorder or cognitive dysfunction.

During episodes of breathing disturbances it is necessary to confirm the presence of respiratory effort and that the events are obstructive and not central in nature.

Classification of the severity of OSA based on the RDI:

1) RDI 5 to <15: Mild OSA.

2) RDI ≥15 to <30: Moderate OSA.

3) RDI ≥30: Severe OSA.

The severity of OSA is mainly classified by RDI or AHI, but other factors such as SpO2 nadir, average oxygen saturation, percentage of time with SpO2 <90%, and oxygen desaturation index (ODI) (see below) also reflect the severity of OSA.

Daytime Sleepiness Assessment

The assessment of daytime sleepiness may be done using the Epworth Sleepiness Scale (www.epworthsleepinessscale.com). This self-report questionnaire asks the patient about the probability of dozing off or falling asleep (in contrast to feeling tired) in a number of normal daytime activities including:

1) Sitting and reading.

2) Watching TV.

3) Sitting inactive in a public place (eg, during meetings, in a theater).

4) Being a passenger in a car for over an hour without a break.

5) Lying down to rest in the afternoon.

6) Sitting and talking to someone.

7) Sitting quietly after eating lunch (without alcohol).

8) Being in a car while stopped for a few minutes in traffic.

The probability of falling asleep or dozing in each of those situations is scored from 0 (never), through slight (1), moderate (2), to high (3). Scores of 11 to 24 represent increasing levels of excessive daytime sleepiness: 11 to 12, mild; 13 to 15, moderate; and 16 to 24, severe.

Screening for Severe OSA

Diagnostic PSG remains the gold standard in the diagnosis of OSA. The AASM recommends that clinical tools, questionnaires, or prediction algorithms not be used in the diagnosis of OSA in the absence of PSG or home testing. However, screening patients who are at high risk of having OSA is recommended by the AASM, even in the absence of significant sleep-related symptoms. Such populations include those with obesity, cardiac disease such as congestive heart failure, atrial fibrillation, treatment for resistant hypertension, stroke, and type 2 diabetes.

The STOP-Bang questionnaire (www.stopbang.ca) is a screening tool for OSA consisting of 8 questions, which helps determine whether a patient is at low (0-2), moderate (3-4), or high risk (5+) of having OSA. Although initially developed for the perioperative setting, it is used in clinic patients presenting with signs and symptoms suggestive of OSA and has been validated in multiple languages. The sensitivity of a STOP-Bang score of ≥3 in detecting mild OSA is 88% and increases to 93% to 100% for moderate-to-severe OSA. Another widely used screening tool is the Berlin questionnaire, which includes 11 questions across 3 categories (www.1800cpap.com). The sensitivity of the questionnaire in the detection of mild OSA is 76% and increases to 84% for severe disease.

There is no guideline-based recommendation for the use of overnight oximetry as a screening measure to identify those with suspected OSA. The ability to discern between obstructive and central events is questionable, not only due to the absence of respiratory effort monitoring but due to lack of distinguishing characteristics on the desaturation/resaturation pattern and waveform. The oxygen desaturation index (ODI) on oximetry is the per hour index of episodes of a ≥4% drop in SpO2 from the average SpO2 in the preceding 120 seconds and lasting >10 seconds. An ODI of >10 has been found to demonstrate an 85% to 93% sensitivity to detect moderate and severe sleep-disordered breathing (AHI ≥15) as determined by PSG. The ODI severity correlates well with the AHI severity for obstructive events but not central events.Evidence 1Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness. Series F, Kimoff RJ, Morrison D, et al. Prospective evaluation of nocturnal oximetry for detection of sleep-related breathing disturbances in patients with chronic heart failure. Chest. 2005 May;127(5):1507-14. PMID: 15888821. Chung F, Liao P, Elsaid H, et al. Oxygen Desaturation Index from Nocturnal Oximetry: A Sensitive and Specific Tool to Detect Sleep-Disordered Breathing in Surgical Patients. Anesth Analg. 2012 May;114(5):993-1000. PMID: 22366847. However, it is important to recognize that in-lab PSG or a home sleep study is required to confirm a diagnosis of OSA and further—mandatory in most if not all jurisdictions—criteria for continuous positive airway pressure (CPAP) funding should be met, and patients in safety critical occupations should undergo screening. At our institution we have incorporated overnight oximetry screening criteria of ODI >10 and >10% of the night spent with SpO2 <90% or nadir SpO2 <85% to identify high-risk bariatric surgery candidates needing PSG.

Differential Diagnosis

Other causes of excessive daytime sleepiness include insufficient sleep syndrome/sleep deprivation, other forms of sleep disordered breathing (eg, obesity hypoventilation syndrome, central sleep apnea), central disorders of hypersomnolence (eg, narcolepsy types 1 and 2, idiopathic hypersomnia, Kleine-Levin syndrome), sleep disturbances secondary to sleep movement disorders (eg, restless leg syndrome), and sedating medications.

TreatmentTop

Although upper airway narrowing is the most important factor, several others nonanatomical factors such as impaired upper airway muscle function during sleep, unstable respiratory control, and low respiratory arousal threshold may also play a contributory role in the occurrence of OSA. While the majority of established therapies for OSA address the anatomical contributors, personalized and optimal management may need to consider the nonanatomical contributors as well.

1. Lifestyle changes: Weight reduction may improve the AHI in patients with obesity; positional therapy (eg, anti-snore belt or shirt) can be an effective secondary or supplementary therapy in patients who have a low AHI in the nonsupine position; avoidance of alcohol consumption in the evening; avoidance of sedatives; and tobacco smoking cessation.

2. CPAP therapy (or its modifications: auto-CPAP, bilevel positive airway pressure [BiPAP]) CPAP maintains upper airway patency by the use of a continuous positive pressure of 4 to 20 cm H2O. This is the method of choice for treating moderate or severe OSA, as well as mild OSA in patients with severe daytime symptoms. CPAP therapy has established benefits on sleep-related quality of life, self-reported sleepiness, risk of motor vehicle collisions, and hypertension (particularly nocturnal blood pressure). The impact of CPAP on primary and secondary prevention of vascular events remains unclear, given the study population characteristics (notably “nonsleepy” patients) and suboptimal CPAP adherence in some landmark trials, such as the SAVE trial.Evidence 2Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to heterogeneity among outcomes and indirectness of intervention (limited compliance). Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice Parameters for the Medical Therapy of Obstructive Sleep Apnea. SLEEP 2006 Aug;29(8):1031-35. PMID: 16944671. Giles TL, Lasserson TJ, Smith BJ, White J, Wright J, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD001106. Review. Update in: Cochrane Database Syst Rev. 2006;(3):CD001106. PMID: 16437429. McEvoy RD, Antic NA, Heeley E, et al; SAVE Investigators and Coordinators. CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea. N Engl J Med. 2016 Sep 8;375(10):919-31. doi: 10.1056/NEJMoa1606599. Epub 2016 Aug 28. PMID: 27571048. Barbe F, Duran-Cantolla J, Sanchez-de-la-Torre M, et al. Effect of continuous positive airway pressure on the incidence of hypertension and cardiovascular events in nonsleepy patients with obstructive sleep apnea: a randomized controlled trial. JAMA. 2012 May 23;307(20):2161-8. PMID: 22618923.

3. Oral appliance therapy: This method uses devices that reposition the patient’s tongue and/or jaw to splint open the upper airway. It is recommended that custom, titratable devices be used over noncustom devices. Prescription and oversight of such oral appliances is recommended, rather than no treatment, in adult patients who are either intolerant to positive airway pressure (PAP) therapy or prefer an alternative.Evidence 3Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to risk of bias and indirectness. Ramar K, Dort LC, Katz SG, et al. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy: an update for 2015. J Clin Sleep Med 2015 July 15;11(7):773-827. PMID: 26094920. Given the lower effectiveness of AHI reduction compared with PAP therapy, oral appliances can be used in those with mild to moderate OSA.Evidence 4Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to risk of bias and indirectness. Ramar K, Dort LC, Katz SG, et al. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy: an update for 2015. J Clin Sleep Med 2015 July 15;11(7):773-827. PMID: 26094920.

4. Surgical treatment is generally considered a salvage treatment for those in whom CPAP or other conservative strategies failed. Options include tonsillectomy/adenoidectomy, maxillo-mandibular advancement, multilevel upper airway surgery (eg, modified uvulopalatopharyngoplasty with radiofrequency tongue reduction), or tracheostomy. The AASM recommends discussing sleep surgery referrals with patients with OSA and a body mass index (BMI) <40 kg/m2 who are intolerant to or not accepting PAP therapy.Evidence 5Moderate Quality of Evidence (moderate confidence that we know true effects of the intervention). Quality of Evidence lowered due to risk of bias and imprecision in observational RCTs but increased due to the effect size. Kent D, Stanley J, Aurora RN, et al. Referral of adults with obstructive sleep apnea for surgical consultation: an American Academy of Sleep Medicine clinical practice guideline. 2021 Dec 1;17(12):2499-2505. PMID: 34351848. Sundaram S, Bridgman SA, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001004. Review. PMID: 16235277. Bariatric surgery referral can be considered in those with OSA and class II or greater obesity (BMI ≥35 kg/m2) who are intolerant to or not accepting PAP therapy. The relative effects of surgical procedures on the AHI, excessive daytime sleepiness, and other outcomes vary and are difficult to predict at an individual level. There is a nonlinear relationship between post–bariatric surgery weight loss and AHI reduction, and a repeat sleep study should be pursued.

5. Experimental methods: Hypoglossal nerve stimulation, if available, may be an effective treatment in those with moderate-to-severe OSA. Optimal patient selection and surgical technique are unclear.Evidence 6Weak recommendation (benefits likely outweigh downsides, but the balance is close or uncertain; an alternative course of action may be better for some patients). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to risk of bias. Woodson BT, Soose RJ, Gillespie MB, et al. Three-Year Outcomes of Cranial Nerve Stimulation for Obstructive Sleep Apnea: The STAR Trial. Otolaryngol Head Neck Surg. 2016 Jan;154(1):181-8. PMID: 26577774. Strollo PJ, Roose RJ, Maurer JT, et al. Upper-Airway Stimulation for Obstructive Sleep Apnea. NEJM. 2014; 370:139-149. PMID: 24401051.

6. Oral medications: Use of wake-promoting medications to decrease residual sleepiness should be restricted to sleep medicine specialists after verifying the adequacy of PAP therapy and excluding other etiologies of persistent excessive daytime sleepiness.

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