madman
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Diagnosis and Management of Obstructive Sleep Apnea A Review (2020)
Daniel J. Gottlieb, MD, MPH; Naresh M. Punjabi, MD, PhD
IMPORTANCE Obstructive sleep apnea (OSA) affects 17% of women and 34% of men in the US and has a similar prevalence in other countries. This review provides an update on the diagnosis and treatment of OSA.
OBSERVATIONS The most common presenting symptom of OSA is excessive sleepiness, although this symptom is reported by as few as 15% to 50% of people with OSA in the general population. OSA is associated with a 2- to 3-fold increased risk of cardiovascular and metabolic disease. In many patients, OSA can be diagnosed with home sleep apnea testing, which has a sensitivity of approximately 80%. Effective treatments include weight loss and exercise, positive airway pressure, oral appliances that hold the jaw forward during sleep, and surgical modification of the pharyngeal soft tissues or facial skeleton to enlarge the upper airway. Hypoglossal nerve stimulation is effective in select patients with a body mass index of less than 32. There are currently no effective pharmacological therapies. Treatment with positive airway pressure lowers blood pressure, especially in patients with resistant hypertension; however, randomized clinical trials of OSA treatment have not demonstrated significant benefits on rates of cardiovascular or cerebrovascular events.
CONCLUSIONS AND RELEVANCE OSA is common and its prevalence is increasing with the increased prevalence of obesity. Daytime sleepiness is among the most common symptoms, but many patients with OSA are asymptomatic. Patients with OSA who are asymptomatic, or whose symptoms are minimally bothersome and pose no apparent risk to driving safety, can be treated with behavioral measures, such as weight loss and exercise. Interventions such as positive airway pressure are recommended for those with excessive sleepiness and resistant hypertension. Managing asymptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by high-quality evidence.
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of a partial or complete collapse of the upper airway during sleep, resulting in reduced (hypopnea) or absent (apnea) airflow lasting for at least 10 seconds and associated with either cortical arousal or a fall in blood oxygen saturation. OSA is present in approximately 25% of adults in the US and is a major cause of excessive sleepiness, contributing to reduced quality of life, impaired work performance, and increased motor vehicle crash risk.1,2 OSA is associated with an increased incidence of hypertension, type 2 diabetes mellitus, atrial fibrillation, heart failure, coronary heart disease, stroke, and death.3-6OSA can be diagnosed with either home- or laboratory-based sleep testing, and effective treatments are available. This review provides an update on the epidemiology, pathophysiology, diagnosis, and management of OSA.
Pathophysiology
OSA is characterized by the repetitive partial or complete collapse of the upper airway during sleep, resulting in episodic reduction (hypopnea) or cessation (apnea) of airflow despite the respiratory effort. Contraction of upper airway dilator muscles is necessary to maintain airway patency during inspiration. The most important upper airway dilator muscle is the genioglossus muscle, which contracts with each inspiration to prevent the posterior collapse of the tongue, assisted by the levator and tensor palatini muscles (advancing and elevating the soft palate) and the geniohyoid and stylopharyngeus muscles (opposing medial collapse of the lateral pharyngeal walls).3 Most people with OSA have a narrow upper airway, typically caused by fat deposition in the parapharyngeal fat pads and pharyngeal muscles15,16 or abnormalities in craniofacial structure (Figure 1). These abnormalities include both clinically evident anatomic abnormalities, such as micrognathia and retrognathia, or subtle radiographic findings, such as inferior positioning of the hyoid bone and shorter mandibular and maxillary length, which result in a small maxillomandibular volume.2,17 The relative contribution of soft tissue and bony abnormalities to OSA differs among individuals and between populations; for example, for the same severity of OSA, Caucasian individuals tend to be more overweight, while Chinese individuals have more craniofacial bony restrictions.18 In the presence of a small pharyngeal airway, upper airway collapse is prevented when an individual is awakened by the activity of pharyngeal dilator muscles. A decrease in both basal and compensatory dilator muscle tone during sleep permits airway collapse.3,19
Obstructive apneas and hypopneas result in large changes in intrathoracic pressure, intermittent hypoxemia, and arousal from sleep (Figure 2). Although these arousals generally do not wake the patient, this sleep fragmentation is the primary cause of excessive sleepiness in individuals with OSA. Intermittent hypoxemia, particularly with concomitant hypercapnia, activates the sympathetic nervous system and is the major contributor to both acute and chronic elevation of blood pressure (Figure 3).3,4 Increased catecholamine levels decrease insulin sensitivity and, in animal models, promote pancreatic beta-cell apoptosis, suggesting a possible mechanism underlying the association of OSA with type 2 diabetes mellitus,20 which persists after adjustment for demographic factors and BMI.21 Repetitive episodes of hypoxemia increase reactive oxygen species, which may further contribute to vascular disease, metabolic abnormalities, and inflammation.3
Clinical Presentation
The most common symptom of OSA is unrefreshing sleep, with excessive sleepiness reported by up to 90% of patients with OSA referred to sleep clinics22,23 (Table 1). Patients may also report fatigue, tiredness, or lack of energy.24 In some studies, these symptoms are more common than sleepiness.24 Excessive sleepiness is reported by 15% to 50% of people with OSA identified through general population screening.7,12,13,25 While some patients experience awakenings accompanied by gasping or choking, awakenings without accompanying symptoms are more typical. A systematic review concluded that on history and physical examination, nocturnal gasping or choking is the most reliable indicator of OSA, while snoring is not specific.26 A population study reported nocturia at least 2 times per night in 37.4% of individuals with an AHI of at least 20 per hour compared with 25.6% of those with an AHI of less than 20 per hour (adjusted odds ratio, 1.64 [95% CI, 1.03-2.55]).27 Chronic morning headache (occurring at least half of the day) is twice as common in individuals with OSA as in the general population.28 These headaches, characterized by a bilateral pressure sensation, resolve within hours of awakening and are of unknown etiology. Nocturnal gastroesophageal reflux is approximately twice as common in patients with OSA in the general population.29 Difficulty falling asleep is unlikely to be caused by OSA.30 Typical signs of OSA include habitual snoring, present in 50% to 60% of those with OSA, and witnessed apneas during sleep, present in 10% to 15% of those with OSA. The latter is twice as common as in those without OSA.11,14,31 Recent studies estimate the prevalence of OSA at 73% to 82% in individuals with resistant hypertension,32,33 76% to 85% in individuals with atrial fibrillation,34,35 65% to 85% in individuals with type 2 diabetes,36 71% in individuals with stroke,37 and 71% to 77% in patients undergoing bariatric surgery.38,39
*Assessment and Diagnosis
*Treatment
*Asymptomatic OSA
*Prognosis
Limitations
This review has some limitations. First, it was restricted to English-language publications and was developed primarily from published systematic reviews, meta-analyses, and clinical practice guidelines. Second, the literature search may have missed some relevant publications. Third, not all aspects of OSA were discussed. Fourth, high-quality data are lacking for some covered topics.
Conclusions
OSA is common and the prevalence is increasing. Daytime sleepiness is among the most common symptoms, but many patients with OSA are asymptomatic. Patients with OSA who are asymptomatic, or whose symptoms are minimally bothersome and pose no apparent risk to driving safety, can be treated with behavioral measures, such as weight loss and exercise. Interventions such as PAP are recommended for those with excessive sleepiness and resistant hypertension. Treating individuals with asymptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by high-quality evidence.
Daniel J. Gottlieb, MD, MPH; Naresh M. Punjabi, MD, PhD
IMPORTANCE Obstructive sleep apnea (OSA) affects 17% of women and 34% of men in the US and has a similar prevalence in other countries. This review provides an update on the diagnosis and treatment of OSA.
OBSERVATIONS The most common presenting symptom of OSA is excessive sleepiness, although this symptom is reported by as few as 15% to 50% of people with OSA in the general population. OSA is associated with a 2- to 3-fold increased risk of cardiovascular and metabolic disease. In many patients, OSA can be diagnosed with home sleep apnea testing, which has a sensitivity of approximately 80%. Effective treatments include weight loss and exercise, positive airway pressure, oral appliances that hold the jaw forward during sleep, and surgical modification of the pharyngeal soft tissues or facial skeleton to enlarge the upper airway. Hypoglossal nerve stimulation is effective in select patients with a body mass index of less than 32. There are currently no effective pharmacological therapies. Treatment with positive airway pressure lowers blood pressure, especially in patients with resistant hypertension; however, randomized clinical trials of OSA treatment have not demonstrated significant benefits on rates of cardiovascular or cerebrovascular events.
CONCLUSIONS AND RELEVANCE OSA is common and its prevalence is increasing with the increased prevalence of obesity. Daytime sleepiness is among the most common symptoms, but many patients with OSA are asymptomatic. Patients with OSA who are asymptomatic, or whose symptoms are minimally bothersome and pose no apparent risk to driving safety, can be treated with behavioral measures, such as weight loss and exercise. Interventions such as positive airway pressure are recommended for those with excessive sleepiness and resistant hypertension. Managing asymptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by high-quality evidence.
Obstructive sleep apnea (OSA) is characterized by recurrent episodes of a partial or complete collapse of the upper airway during sleep, resulting in reduced (hypopnea) or absent (apnea) airflow lasting for at least 10 seconds and associated with either cortical arousal or a fall in blood oxygen saturation. OSA is present in approximately 25% of adults in the US and is a major cause of excessive sleepiness, contributing to reduced quality of life, impaired work performance, and increased motor vehicle crash risk.1,2 OSA is associated with an increased incidence of hypertension, type 2 diabetes mellitus, atrial fibrillation, heart failure, coronary heart disease, stroke, and death.3-6OSA can be diagnosed with either home- or laboratory-based sleep testing, and effective treatments are available. This review provides an update on the epidemiology, pathophysiology, diagnosis, and management of OSA.
Pathophysiology
OSA is characterized by the repetitive partial or complete collapse of the upper airway during sleep, resulting in episodic reduction (hypopnea) or cessation (apnea) of airflow despite the respiratory effort. Contraction of upper airway dilator muscles is necessary to maintain airway patency during inspiration. The most important upper airway dilator muscle is the genioglossus muscle, which contracts with each inspiration to prevent the posterior collapse of the tongue, assisted by the levator and tensor palatini muscles (advancing and elevating the soft palate) and the geniohyoid and stylopharyngeus muscles (opposing medial collapse of the lateral pharyngeal walls).3 Most people with OSA have a narrow upper airway, typically caused by fat deposition in the parapharyngeal fat pads and pharyngeal muscles15,16 or abnormalities in craniofacial structure (Figure 1). These abnormalities include both clinically evident anatomic abnormalities, such as micrognathia and retrognathia, or subtle radiographic findings, such as inferior positioning of the hyoid bone and shorter mandibular and maxillary length, which result in a small maxillomandibular volume.2,17 The relative contribution of soft tissue and bony abnormalities to OSA differs among individuals and between populations; for example, for the same severity of OSA, Caucasian individuals tend to be more overweight, while Chinese individuals have more craniofacial bony restrictions.18 In the presence of a small pharyngeal airway, upper airway collapse is prevented when an individual is awakened by the activity of pharyngeal dilator muscles. A decrease in both basal and compensatory dilator muscle tone during sleep permits airway collapse.3,19
Obstructive apneas and hypopneas result in large changes in intrathoracic pressure, intermittent hypoxemia, and arousal from sleep (Figure 2). Although these arousals generally do not wake the patient, this sleep fragmentation is the primary cause of excessive sleepiness in individuals with OSA. Intermittent hypoxemia, particularly with concomitant hypercapnia, activates the sympathetic nervous system and is the major contributor to both acute and chronic elevation of blood pressure (Figure 3).3,4 Increased catecholamine levels decrease insulin sensitivity and, in animal models, promote pancreatic beta-cell apoptosis, suggesting a possible mechanism underlying the association of OSA with type 2 diabetes mellitus,20 which persists after adjustment for demographic factors and BMI.21 Repetitive episodes of hypoxemia increase reactive oxygen species, which may further contribute to vascular disease, metabolic abnormalities, and inflammation.3
Clinical Presentation
The most common symptom of OSA is unrefreshing sleep, with excessive sleepiness reported by up to 90% of patients with OSA referred to sleep clinics22,23 (Table 1). Patients may also report fatigue, tiredness, or lack of energy.24 In some studies, these symptoms are more common than sleepiness.24 Excessive sleepiness is reported by 15% to 50% of people with OSA identified through general population screening.7,12,13,25 While some patients experience awakenings accompanied by gasping or choking, awakenings without accompanying symptoms are more typical. A systematic review concluded that on history and physical examination, nocturnal gasping or choking is the most reliable indicator of OSA, while snoring is not specific.26 A population study reported nocturia at least 2 times per night in 37.4% of individuals with an AHI of at least 20 per hour compared with 25.6% of those with an AHI of less than 20 per hour (adjusted odds ratio, 1.64 [95% CI, 1.03-2.55]).27 Chronic morning headache (occurring at least half of the day) is twice as common in individuals with OSA as in the general population.28 These headaches, characterized by a bilateral pressure sensation, resolve within hours of awakening and are of unknown etiology. Nocturnal gastroesophageal reflux is approximately twice as common in patients with OSA in the general population.29 Difficulty falling asleep is unlikely to be caused by OSA.30 Typical signs of OSA include habitual snoring, present in 50% to 60% of those with OSA, and witnessed apneas during sleep, present in 10% to 15% of those with OSA. The latter is twice as common as in those without OSA.11,14,31 Recent studies estimate the prevalence of OSA at 73% to 82% in individuals with resistant hypertension,32,33 76% to 85% in individuals with atrial fibrillation,34,35 65% to 85% in individuals with type 2 diabetes,36 71% in individuals with stroke,37 and 71% to 77% in patients undergoing bariatric surgery.38,39
*Assessment and Diagnosis
*Treatment
*Asymptomatic OSA
*Prognosis
Limitations
This review has some limitations. First, it was restricted to English-language publications and was developed primarily from published systematic reviews, meta-analyses, and clinical practice guidelines. Second, the literature search may have missed some relevant publications. Third, not all aspects of OSA were discussed. Fourth, high-quality data are lacking for some covered topics.
Conclusions
OSA is common and the prevalence is increasing. Daytime sleepiness is among the most common symptoms, but many patients with OSA are asymptomatic. Patients with OSA who are asymptomatic, or whose symptoms are minimally bothersome and pose no apparent risk to driving safety, can be treated with behavioral measures, such as weight loss and exercise. Interventions such as PAP are recommended for those with excessive sleepiness and resistant hypertension. Treating individuals with asymptomatic OSA to reduce cardiovascular and cerebrovascular events is not currently supported by high-quality evidence.
