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Definition, Etiology, PathogenesisTop
Obstructive sleep apnea (OSA) is a disease 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 with normal function of the respiratory muscles. Apnea, hypopnea, or both cause episodes of nocturnal hypoxemia and arousals from sleep that lead to sleep fragmentation (patients are unaware of most of these episodes). This in turn causes daytime symptoms and in combination with repeated hypoxemia and an increase in sympathetic tone leads to an elevation in blood pressure and its complications.
Severe sleep apnea may occur in the absence of nighttime and daytime symptoms. Conversely, symptoms may occur with an apparently normal sleep study, particularly if nasal pressure monitoring is not done to detect flattening of the nasal pressure waveform, indicating increased upper airway resistance syndrome (UARS).
Apnea is a reduction of ≥90% in the amplitude of respirations lasting ≥10 seconds. Hypopnea is defined as a decrease of ≥30% in the pressure in the nasal cavity lasting ≥10 seconds and associated with a decrease of ≥3% in SaO2 and/or associated with (micro)arousal. The apnea-hypopnea index (AHI) is an index indicating the number of apneas and hypopneas per hour of sleep. Respiratory event–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 pharyngeal obstruction during sleep include obesity (neck circumference >43 cm in men and >40 cm in women), long uvula, tonsillar and/or adenoidal hypertrophy, nasal septal deviation, turbinate enlargement, nasal polyps, alcohol consumption (particularly before bedtime), tobacco smoking, certain sedatives and hypnotics, hypothyroidism, and acromegaly.
Clinical Features and Natural HistoryTop
1. Daytime symptoms: Sleepiness, morning headache, memory and concentration impairment, decreased libido, emotional disorders.
2. Nocturnal symptoms: Snoring (loud, irregular) and apneas, excessive sweating, arousal with a choking sensation, nocturia, palpitations, mouth dryness upon awakening.
3. Other symptoms: Overweight or obesity are observed in 70% of patients. Hypertension is observed in 50% of patients.
4. Sequelae: Untreated severe OSA increases the risk of cardiovascular diseases (hypertension, ischemic heart disease, arrhythmia, conduction disturbances, heart failure, stroke), increases perioperative risk, and likely increases the risk of death. Sleepiness and fatigue of drivers or operators from OSA of any severity increases accident risk.
A definite diagnosis requires sleep study. Polysomnography (overnight monitoring of sleep [electroencephalography, electrooculogram, and electromyography]) together with the monitoring of airflow, respiratory effort (chest and abdomen respiratory movements), hemoglobin oxygen saturation in arterial blood (SaO2), electrocardiography, body position, and limb movements is the gold standard. In patients without cardiorespiratory disease, potential respiratory muscle weakness (due to a neuromuscular condition), suspicion of sleep-related hypoventilation, chronic opioid medication use, or history of stroke or severe insomnia, the diagnosis 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 recording). However, when the home sleep apnea test is either negative or inconclusive and a clinical suspicion of significant OSA remains, polysomnography should be considered.
American Academy of Sleep Medicine 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.
During episodes of breathing disturbances it is necessary to confirm the presence of respiratory effort.
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 assessment of daytime sleepiness may be done using the Epworth Sleepiness Scale (www.epworthsleepinessscale.com). This scale asks the patient about the probability of falling asleep (or dozing) not related to tiredness in a number of normal daytime activities including:
1) Sitting or reading.
2) Watching TV.
3) Sitting inactive (eg, during meetings, in a theater).
4) Being a passenger in a car for over an hour.
5) Lying down in the afternoon.
6) Talking to somebody.
7) Sitting after eating lunch.
8) Being in a car while stopped for a few minutes.
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 ≤10 indicate normal daytime sleepiness, 11 to 12, mild sleepiness, 13 to 15, moderate sleepiness, and 16 to 24, severe excessive daytime sleepiness.
Although the sleep study remains the gold standard in the diagnosis of OSA, an approach requiring such a test for screening for severe diseases has limitations due to major technology and resources requirements. Questionnaires, such as NoSAS score, STOP-Bang (www.stopbang.ca), or the Berlin questionnaire, are sometimes used to evaluate the need for sleep study; however, their sensitivity and specificity are limited. Some clinicians suggest that the STOP-Bang score may be used to identify patients at risk of severe OSA. Overnight oximetry screening with the following results may be used to identify those who are likely to have subsequent moderate or severe OSA on polysomnography and should undergo such a test:
1) An oxygen desaturation index >10 (that is, 10 per-hour episodes of a drop in SaO2 by ≥4% for ≥10 s in comparison to preceding 120 s), or
2) More than 10% of total time with SaO2 <90%, or
3) Lowest SaO2 <85%.
This approach, although not fully tested, may limit the number of costly and time-consuming polysomnography studies, as a negative overnight oximetry study makes severe sleep apnea very unlikely. However, polysomnography or the home sleep study is mandatory to diagnose OSA and – in most if not all jurisdictions – to meet criteria for the continuous positive airway pressure (CPAP) funding as well as for screening patients in critical safety occupations.
Other causes of daytime sleepiness: central sleep apnea, obesity-hypoventilation syndrome, narcolepsy, periodic limb movement disorder, restless leg syndrome, and insomnia.
1. Patient education — lifestyle changes: Weight reduction in obese patients, sewing one or more golf balls into the back of the patient’s pajamas (to prevent the patient from sleeping on the back; may not be effective), avoidance of alcohol consumption in the evening, avoidance of muscle relaxants, and cessation of tobacco smoking.
2. CPAP therapy (or its modifications: auto-CPAP, bilevel positive airway pressure [BiPAP]) is the method of choice for treating moderate or severe OSA, as well as mild OSA in patients with severe daytime symptoms. This treatment should be offered to reduce the severity of symptoms and prevent profound hypoxia in patients who experience it irrespective of symptoms, although the effects of treatment on mortality and major cardiovascular morbidity are not clear.Evidence 1Strong 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 heterogeneity among outcomes. 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. PubMed 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. PubMed PMID: 27571048. CPAP provides upper airway patency by the use of a continuous positive pressure of 4 to 20 cm H2O. In patients with daytime sleepiness persisting despite effective CPAP treatment, you may consider a trial of medication, including modafinil.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). Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness and the risk of bias. Kuan YC, Wu D, Huang KW, et al. Effects of Modafinil and Armodafinil in Patients With Obstructive Sleep Apnea: A Meta-analysis of Randomized Controlled Trials. Clin Ther. 2016 Apr;38(4):874-88. doi: 10.1016/j.clinthera.2016.02.004. Epub 2016 Feb 28. PubMed PMID: 26923035. Mason M, Welsh EJ, Smith I. Drug therapy for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2013 May 31;(5):CD003002. doi: 10.1002/14651858.CD003002.pub3. Review. PubMed PMID: 23728641.
3. Oral devices: Most often these involve mandibular repositioning splints. These devices are suggested in patients with OSA in whom CPAP treatment is not feasible.Evidence 3Weak 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 the risk of bias and indirectness. Lim J, Lasserson TJ, Fleetham J, Wright J. Oral appliances for obstructive sleep apnoea. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD004435. Review. PubMed PMID: 16437488.
4. Surgical treatment may be considered as an adjunct to CPAP treatment (septoplasty, tonsillectomy, adenoidectomy, bariatric surgery) or in patients who do not tolerate CPAP (mandibular advancement, osteotomy of the hyoid bone). However, the effects of those treatments are not clear.Evidence 4Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to the risk of bias, inconsistency, heterogeneity of interventions, indirectness of outcomes, and imprecision. Sundaram S, Bridgman SA, Lim J, Lasserson TJ. Surgery for obstructive sleep apnoea. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001004. Review. PubMed PMID: 16235277.
5. Other methods: Implantation of a unilateral hypoglossal nerve stimulation device.