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Sleep apnea

For patient information about sleep apnea click here

For patient information about central sleep apnea click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Clinical practice guidelines by the United States Preventive Services Task Force[1] and the American Academy of Sleep Medicine[2][3] address screening and diagnosis.

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Sleep apnea was first described in literature in the 19th century. It was often misdiagnosed as either narcolepsy or skepticism. In 1981, Collin Sullivan invented the continuous positive airway pressure (CPAP) for the treatment of sleep apnea. Prior to its recognition as a unique disorder, sleep apnea was viewed as either a type of insomnia or an age-related phenomenon.

Discovery

  • In 1890, Silas Weir Mitchell, a neurologist and American toxicologist, described sleep apnea as respiratory failure in sleep because of the “failure of the chest and diaphragmatic movements” [1]
  • During the second half of the 19th century, the clinical features of sleep apnea were thoroughly described:[1]

Development of Treatment Strategies

  • In 1981, Colin Sullivan and associates in Sydney improved the management of obstructive sleep apnea with continuous positive airway pressure (CPAP) [2]
  • By the late 1980s, CPAP was transformed from the bulky and noisy first models and became widely used, which lead to specialized clinics for diagnosis and treatment

Impact on Cultural History

  • April 18th is Sleep Apnea Awareness Day in recognition of Colin Sullivan (Australian physician, professor, and inventor)
  • Before sleep apnea was recognized as a separate sleep disorder, it was viewed as either a type of insomnia or an age-related phenomenon[3]

References

  1. 1.0 1.1 1.2 Lavie, [ill]etz (1984). “[ill]othing New Under the Moon”. Archives of Internal Medicine. 144 (10): 2025. doi:10.1001/archinte.1984.04400010145023. ISSN 0003-9926.
  2. Sullivan, ColinE.; Berthon-Jones, Michael; Issa, FaiqG.; Eves, Lorraine (1981). “REVERSAL OF OBSTRUCTIVE SLEEP APNOEA BY CONTINUOUS POSITIVE AIRWAY PRESSURE APPLIED THROUGH THE NARES”. The Lancet. 317 (8225): 862–865. doi:10.1016/S0140-6736(81)92140-1. ISSN 0140-6736.
  3. Shaw R, McKenzie S, Taylor T, Olafiranye O, Boutin-Foster C, Ogedegbe G; et al. (2012). “Beliefs and attitudes toward obstructive sleep apnea evaluation and treatment among blacks”. J Natl Med Assoc. 104 (11–12): 510–9. PMC 3740354. PMID 23560353.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

There are three types of sleep apnea: obstructive, central, and mixed. The majority of patients have obstructive sleep apnea (OSA). Individuals of untreated sleep apnea stop breathing repeatedly during the night usually for a minute or longer, during their sleep. Most of the time, these individuals are unaware of these episodes because the episodes don’t trigger an awakening. Obstructive sleep apnea results from the narrowing or total blockage of the airway. In central sleep apnea, there is failure of the central nervous system to send appropriate signals to the muscles of respiration. These signals control the individual’s breathing. It is also possible for an individual to have a combination of these two types, referred to as mixed apnea.

Classification

Sleep apnea can be classified into three categories:

Obstructive Sleep Apnea (OSA)

  • The majority of the three forms
  • It results from either the narrowing or total blockage of the respiratory airway which occurs when the soft tissue at the back of the throat collapses during sleep
  • OSA may be classified into three classes based on the severity of the disease[1]:
  • The severity of the disease is assessed by the Apnea Hypopnea index (AHI), which combines apneas and hypopneas
  • Apneas are defined as breathing pauses lasting 10 seconds
  • Hypopneas are defined as events lasting 10 seconds in which there is continued breathing but ventilation is reduced by at least 50% from the previous baseline during sleep
  • None/Minimal OSA: AHI < 5
  • Mild OSA: AHI = 5-14: Patients may either be asymptomatic or may complain of sleepiness when they are sedentary. The daytime sleepiness often does not impair the patients’ quality of life.
  • Moderate OSA: AHI = 15-29: Patients are usually symptomatic.
  • Severe OSA: AHI ≥ 30: Patients’ symptoms are severe enough to interfere with daily activities. They may fall asleep during activities that require attention (e.g. driving)

Central Sleep Apnea

  • The brain is unable to send appropriate signals to the muscles that control breathing due to the instability of the respiratory center
  • It is referred to as idiopathic central sleep apnea when an underlying etiology cannot be identified
  • Cheyne-Stokes breathing is a subtype of breathing in central sleep apnea, which is defined as periodic breathing with recurrent episodes of apnea that alternate with episodes of rapid breathing
  • In Cheyne-Stokes breathing, apnea episodes occur during sleep and during wakefulness

Mixed Apnea/Complex Sleep Apnea

References

  1. Loscalzo, Joseph; Longo, Dan L.; Fauci, Anthony S.; Dennis L. Kasper; Hauser, Stephen L (2011). Harrison’s Principles of Internal Medicine, 18th Edition. McGraw-Hill Professional. ISBN 0-07-174889-X.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

The pathogenesis of obstructive sleep apnea includes upper airway anatomy defects, the inability of the upper airway dilator muscles to respond to respiratory challenge during sleep, inadequate arousal threshold, loop gain, and potential for state-related changes in lung volume. The pathogenesis of central sleep apnea involves chemoreceptors that modulate ventilation.

Pathogenesis

Obstructive Sleep Apnea

The pathogenesis of obstructive sleep apnea results from a combination of the following components[1]:

  • Upper airway anatomy
  • The ability of the upper airway dilator muscles to respond to respiratory challenge during sleep
  • Arousal threshold
  • Loop gain
  • Potential for state-related changes in lung volume

Upper Airway Anatomy

  • The airway is composed of numerous muscles and soft tissues
  • It lacks rigid support
  • The collapsible portion is from the hard palate to the larynx
  • The upper airway can momentarily close during speech, swallowing, and during sleep

Upper Airway Dilator Muscles

  • Upper airway dilator muscles, particularly the genioglossus, keeps the airway patent via protective reflexes

Arousal Threshold

  • Low respiratory drive, that causes pleural pressure, induces arousal from sleep (examples are hypoxia and hypercapnia)

Loop Gain

  • Loop gain is stability of the ventilatory control system
  • There is a cyclical breathing pattern that develops between obstructive breathing events during sleep and wakefulness, which makes the ventilatory control system unstable

Changes in Lung Volume

  • Although the exact mechanism is not understood, there is an interaction between pharyngeal patency and lung volume

Central Sleep Apnea

  • Ventilation is modulated with chemoreceptor inputs (medullary neurons that respond to C02)
  • The ventilatory output is given in change in PaO2 or PaCO2
  • If the individual is extremely sensitive to the chemoreceptor inputs, that individual is at a risk for unstable breathing patterns
  • Therefore, individuals with high chemo-responsiveness will hyperventilate, lowering PaCO2 below the ideal level, leading to hypoventilation and potential apnea[2]

Genetics

  • The following may have some genetic basis[1]:
  • Obesity
  • Craniofacial structure
  • Size of upper airway
  • Ventilatory control abnormalities

References

  1. 1.0 1.1 Eckert DJ, Malhotra A (2008). “Pathophysiology of adult obstructive sleep apnea”. Proc Am Thorac Soc. 5 (2): 144–53. doi:10.1513/pats.200707-114MG. PMC 2628457. PMID 18250206.
  2. Eckert DJ, Jordan AS, Merchia P, Malhotra A (2007). “Central sleep apnea: Pathophysiology and treatment”. Chest. 131 (2): 595–607. doi:10.1378/chest.06.2287. PMC 2287191. PMID 17296668.

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Sleep apnea may be commonly caused by a large neck/abodminal circumference (e.g. obese individuals), administration of medications, diseases that narrow the respiratory airways (e.g. enlarged adenoids, enlarged tonsils), diseases that affect the central nervous system (e.g. cerebrovascular accident, spinal cord injury), or infectious diseases (e.g. polio).

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ Systems

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect Elosulfase alfa, galsulfase, laronidase
Ear Nose Throat Enlarged adenoids, enlarged tonsils, malformations of the nose, malformations of the throat
Endocrine Diabetic neuropathy, hypothyroidism
Environmental No underlying causes
Gastroenterologic Gastroesophageal reflux
Genetic Charcot-Marie-Tooth disease, Hallermann-Streiff syndrome, Joubert syndrome, Marfan syndrome, muscular dystrophy, myotonic dystrophy, Potocki-Lupski syndrome, WAGR syndrome
Hematologic No underlying causes
Iatrogenic Postoperative complication
Infectious Disease Common cold, meningoencephalitis, post-polio syndrome, sinusitis, tonsilitis
Musculoskeletal/Orthopedic Muscular dystrophy, myotonic dystrophy
Neurologic Amyotrophic lateral sclerosis, Arnold-Chiari malformation, cerebrovascular accident, Charcot-Marie-Tooth disease, diabetic neuropathy, idiopathic intracranial hypertension, Joubert syndrome, multiple system atrophy, post-polio syndrome, spinal cord injury
Nutritional/Metabolic Hurler syndrome, metabolic syndrome, obesity, Pompe disease
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Ophthalmologic No underlying causes
Overdose/Toxicity Alcohol intoxication, opioid overdose
Psychiatric No underlying causes
Pulmonary Obesity hypoventilation syndrome
Renal/Electrolyte Chronic kidney disease
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma Spinal cord injury
Urologic No underlying causes
Miscellaneous No underlying causes

Causes in Alphabetical Order

References

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Differentiating Sleep Apnea From Other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Sleep apnea must be differentiated from other diseases that cause loud snoring, fatigue, choking, coughing, and daytime sleepiness. To differentiate obstructive sleep apnea (OSA) and central sleep apnea, a polysomnogram should be performed. OSA will demonstrate evidence of thoracoabdominal effort, whereas central sleep apnea will not.

Differential Diagnosis

The table below summarizes the findings that differentiate sleep apnea from other conditions that cause loud snoring, fatigue, choking, coughing, and/or somnolence.

Disease/Condition Differentiating Clinical Features Differentiating Tests
Cheyne-Stokes breathing (CSB) Recurrent episodes of apnea with absence of respiratory effort; CSB is associated with cerebrovascular disease, CHF, and/or renal failure[1] In CSB, a crescendo-decrescendo change in breathing amplitude interpersed by episodes of central sleep apnea or hypoapnea would be seen
Narcolepsy Level of sleepiness in narcolepsy may be higher in Epworth Sleepiness Scale[2]; may have cataplexy hypnagogic hallucincations, and sleep paralysis A polysomnography should be performed to rule out OSA; a multiple sleep latency test (MLST) can assess for naroclepsy
Insufficient sleep Difficult to differentiate clinically from sleep apnea A polysomnography should be performed to rule out OSA; a sleep diary should used
Inadequate sleep hygiene Irregular sleep schedule with frequent napping; frequent use of alcohol, nicotine, and caffeine; poor bedroom environment A polysomnography should be performed to rule out OSA; diagnosis is usually clinical
Periodic limb movement disorder Urge to move legs due to discomfort during periods of inactivity (including sleep); patients have excessive sleepiness A polysomnography should demonstrate limb movements and rule out OSA
Nocturnal gastroesphageal reflux Nocturnal restlessness, choking episodes during sleep, frequent awakening, and labored breathing A polysomnography should be performed to rule out OSA
Nocturnal asthma Nocturnal choking, gasping, coughing, or dyspnea A polysomnography should be performed to rule out OSA; pulmonary function tests (PFTs) should be performed
Primary snoring More common than OSA A polysomnography should be performed to rule out OSA
Nocturnal panic attacks Nocturnal choking, gasping, coughing, or dyspnea A polysomnography should be performed to rule out OSA; a psychiatric history should be performed
Congestive heart failure Nocturnal choking, gasping, coughing, or dyspnea A polysomnography should be performed to rule out OSA; EKG, chest x-ray, blood tests, stress testing, and cardiac catheterization should be performed
Sleep-related laryngospasm Nocturnal choking, gasping, coughing, or dyspnea A polysomnography should be performed to rule out OSA
Chronic fatigue syndrome Daytime fatigue is usually the only complaint A polysomnography should be performed to rule out OSA
Depression Fatigue and feelings of hopelessness A polysomnography should be performed to rule out OSA; a psychiatric history should be performed
Pseudocentral sleep apnea Patients with diaphragmatic paralysis depend on accessory muscles during breathing and may have apnea during REM sleep (sleep apnea is mostly observed during non-REM sleep); history of neuromuscular disease A polysomnography should be performed to rule out OSA; various neuromuscular disease tests should be performed

References

  1. Lieber C, Mohsenin V (1992). “Cheyne-Stokes respiration in congestive heart failure”. Yale J Biol Med. 65 (1): 39–50. PMC 2589377. PMID 1509783.
  2. Vernet C, Arnulf I (2009). “Narcolepsy with long sleep time: a specific entity?”. Sleep. 32 (9): 1229–35. PMC 2737581. PMID 19750928.

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

The true prevalence of sleep apnea is difficult to estimate because mild cases may remain undiagnosed, and the majority of patients only present following the development of clinical manifestations. Sleep apnea is a chronic disorder, and clinical manifestations often develop as the disease progresses. Accordingly, elderly patients are more commonly diagnosed with sleep apnea than younger adults. Male gender and African American race are associated with higher prevalence of sleep apnea compared with female gender and other ethnicities.

Prevalence

  • The true prevalence of sleep apnea is difficult to estimate because mild cases may remain undiagnosed, and the majority of patients only present following the development of clinical manifestations.
  • In the general population, sleep apnea prevalence is estimated to range from 3,000 to 7,000 per 100,000 individuals[1]

Age

  • Sleep apnea is a chronic disorder, and clinical manifestations often develop as the disease progresses. Accordingly, elderly patients are more commonly diagnosed with sleep apnea than younger adults.
  • Compared with younger adults, the prevalence of sleep apnea is 2 to 3 greater among individuals older than 60-65 years of age[2]

Gender

  • Sleep apnea is more common among males
  • The male:female ratio ranges between 2:1 to 3:1[3]
  • The prevalence of sleep apnea is approximately 3,000-7,000 per 100,000 for adult men and 2,000-5,000 per 100,000 for adult women[4]
  • The increased prevalence among males may be attributable to the larger neck circumference and a longer pharyngeal airway

Race

  • Compared with Caucasian and Asian race, African-American race is associated with a 2-3 fold increased risk of obstructive sleep apnea[5]
  • Sleep apnea due to craniofacial factors is more frequently observed among Chinese patients than among Caucasians.[6]
  • The predilection of central sleep apnea based on race is unknown.

References

  1. Punjabi NM (2008). “The epidemiology of adult obstructive sleep apnea”. Proc Am Thorac Soc. 5 (2): 136–43. doi:10.1513/pats.200709-155MG. PMC 2645248. PMID 18250205.
  2. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A (1998). “Effects of age on sleep apnea in men: I. Prevalence and severity”. Am J Respir Crit Care Med. 157 (1): 144–8. doi:10.1164/ajrccm.157.1.9706079. PMID 9445292.
  3. Redline S, Kump K, Tishler PV, Browner I, Ferrette V (1994). “Gender differences in sleep disordered breathing in a community-based sample”. Am J Respir Crit Care Med. 149 (3 Pt 1): 722–6. doi:10.1164/ajrccm.149.3.8118642. PMID 8118642.
  4. Punjabi, N. M. (2008). “The Epidemiology of Adult Obstructive Sleep Apnea”. Proceedings of the American Thoracic Society. 5 (2): 136–143. doi:10.1513/pats.200709-155MG. ISSN 1546-3222.
  5. Cakirer B, Hans MG, Graham G, Aylor J, Tishler PV, Redline S (2001). “The relationship between craniofacial morphology and obstructive sleep apnea in whites and in African-Americans”. Am J Respir Crit Care Med. 163 (4): 947–50. doi:10.1164/ajrccm.163.4.2005136. PMID 11282771.
  6. Patil SP, Schneider H, Schwartz AR, Smith PL (2007). “Adult obstructive sleep apnea: pathophysiology and diagnosis”. Chest. 132 (1): 325–37. doi:10.1378/chest.07-0040. PMC 2813513. PMID 17625094.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

The most common risk factor for the development of sleep apnea is large neck circumference. Other risk factors of sleep apnea include smoking, alcohol, sedatives, tranquilizers, males, a positive family history, certain ethnic backgrounds such as African Americans, and individuals over 60-65 years. Continuous positive airway pressure (CPAP) is a risk factor for complex sleep apnea (also known as mixed sleep apnea).

Risk Factors

The table below lists the risk factors for sleep apnea:

Risk Factor Description
Physical Characteristics Most common risk factor. Thick neck, obstructed nasal passages, large tongue, narrow airway, receding chin, overbite, certain shapes and increased rigidity of the palate and jaw
Smoking Smoking may increase the amount of inflammation and fluid retention in the upper airway
Alcohol This relaxes the muscles in the throat
Sedatives/tranquilizers This relaxes the muscles in the throat the throat
Male Gender Men are more likely to suffer sleep apnea than women and children are, though it is not uncommon in the last two population groups
Genetic Factors A positive family history may have a higher risk of developing sleep apnea
Ethnic Background African Americans, people of Mexican origin, and Pacific Islanders
Age Sleep apnea occurs significantly in adults over 60-65

Medical conditions that are risk factors for obstructive sleep apnea (OSA)

  • Obesity is the most common risk factor for OSA
  • Facial deformities
  • Chronic respiratory tract conditions such as:

Medical conditions that are risk factors for central sleep apnea (CSA)

  • Problems after cervical spine surgery

Prolonged continuous positive airway pressure (CPAP) is a risk factor for complex sleep apnea (also known as mixed sleep apnea) because patients with obstructive sleep apnea may develop central sleep apnea.

References

  1. Young, T.; Skatrud, J.; Peppard, PE. (2004). “Risk factors for obstructive sleep apnea in adults”. JAMA. 291 (16): 2013–6. doi:10.1001/jama.291.16.2013. PMID 15113821. Unknown parameter |month= ignored (help)
  2. 2.0 2.1 Young, Terry (2004). “Risk Factors for Obstructive Sleep Apnea in Adults”. JAMA. 291 (16): 2013. doi:10.1001/jama.291.16.2013. ISSN 0098-7484.

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Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Clinical practice guidelines by the United States Preventive Services Task Force[1] address screening and do not recommend screening.

However, commercial drivers, operators of heavy equipment, pilots, and other occupations at risk of diurnal sleepiness should be screened by history and physical exam using standardizes questionnaires.

Obstructive Sleep Apnea Screening

  • Commercial drivers, operators of heavy equipment, pilots, and other populations at risk from diurnal sleepiness should with be screened with a history and physical exam
  • If OSA is suspected, a sleep study should be performed
  • For patients with obstructive sleep apnea, screening questionnaires may be useful for preoperative and high risk patients

STOP BANG questionnaire

  • Asks about the presence of loud snoring, apneas, excessive daytime sleepiness, and hypertension
  • STOP BANG questionnaire combines the STOP questionnaire questions and adds BMI age, and neck circumference (increased sensitivity but decreased specificity compared to STOP questionnaire)
  • A score of three or higher has a sensitivity and specificity of 84 and 56 percent for the diagnosis of OSA using an AHI threshold of >5 events per hour, and a sensitivity and specificity of 93 and 43 percent for an AHI >15 [2]
  • To view the STOP BANG questionnaire, click here

Sleep apnea clinical score (SACS)

  • A four-item questionnaire that incorporates neck circumference, hypertension, habitual snoring, and nocturnal gasping or choking to generate a score ranging from 0 to 100
  • Scores greater than 15 result in a probability of OSA (defined as an AHI >10 events per hour) of 25 to 50 percent[3]

Berlin questionnaire

  • The Berlin questionnaire consists of 10 items relating to snoring, nonrestorative sleep, sleepiness while driving, apneas during sleep, hypertension and BMI
  • The results categorize patients as having a high or low risk for OSA
  • A high risk score is associated with a sensitivity and specificity of 80 and 46 percent when OSA is defined as an AHI ≥5 events per hour, and 91 and 37 percent when OSA is defined as an AHI ≥15 events per hour[4]
  • To view the Berlin questionnaire, click here

Central Sleep Apnea Screening

There are no current screening guidelines for central sleep apnea.

References

  1. US Preventive Services Task Force. Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW et al. (2017) Screening for Obstructive Sleep Apnea in Adults: US Preventive Services Task Force Recommendation Statement. JAMA 317 (4):407-414. DOI:10.1001/jama.2016.20325 PMID: 28118461
  2. Chung F, Yegneswaran B, Liao P, Chung SA, Vairavanathan S, Islam S; et al. (2008). “STOP questionnaire: a tool to screen patients for obstructive sleep apnea”. Anesthesiology. 108 (5): 812–21. doi:10.1097/ALN.0b013e31816d83e4. PMID 18431116.
  3. Flemons WW, Whitelaw WA, Brant R, Remmers JE (1994). “Likelihood ratios for a sleep apnea clinical prediction rule”. Am J Respir Crit Care Med. 150 (5 Pt 1): 1279–85. doi:10.1164/ajrccm.150.5.7952553. PMID 7952553.
  4. Myers KA, Mrkobrada M, Simel DL (2013). “Does this patient have obstructive sleep apnea?: The Rational Clinical Examination systematic review”. JAMA. 310 (7): 731–41. doi:10.1001/jama.2013.276185. PMID 23989984. Review in: Evid Based Med. 2014 Apr;19(2):e10

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saarah T. Alkhairy, M.D.

Overview

Sleep apnea can begin with loud snoring and eventually lead to serious complications. Common symptoms include somnolence, depression, and headaches. More serious complications include cardiovascular diseases, stroke, and hypertension. If sleep apnea is adequately treated, the prognosis is very good. If it is left untreated, patients can develop serious complications and have a poor prognosis.

Natural History

  • Sleep apnea is a progressive disease. Snoring is the earliest manifestation of sleep apnea.[1]
  • Snoring in sleep apnea is often mild at first, but it often progresses as the disease becomes more severe.

Complications

Untreated sleep apnea is associated with the development of the following complications:

Prognosis

  • If adequately treated, the prognosis of sleep apnea is generally very good
  • Sleep apnea during surgery and anesthesia is associated with poor prognosis
  • Opioid-induced central sleep apnea is associated with poor prognosis[2]

References

  1. 1.0 1.1 Grunstein, R.R. (1994). “Sleep apnoea – evolution and doubt”. European Respiratory Journal. 7 (10): 1741–1743. doi:10.1183/09031936.94.07101741. ISSN 0000-0000.
  2. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.

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Diagnosis

Diagnosis

Diagnostic Criteria | History and Symptoms | Physical Examination | Laboratory Findings | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

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  1. US Preventive Services Task Force. Bibbins-Domingo K, Grossman DC, Curry SJ, Davidson KW, Epling JW et al. (2017) Screening for Obstructive Sleep Apnea in Adults: US Preventive Services Task Force Recommendation Statement. JAMA 317 (4):407-414. DOI:10.1001/jama.2016.20325 PMID: 28118461
  2. Kapur VK, Auckley DH, Chowdhuri S, Kuhlmann DC, Mehra R, Ramar K; et al. (2017). “Clinical Practice Guideline for Diagnostic Testing for Adult Obstructive Sleep Apnea: An American Academy of Sleep Medicine Clinical Practice Guideline”. J Clin Sleep Med. 13 (3): 479–504. doi:10.5664/jcsm.6506. PMC 5337595. PMID 28162150.
  3. Mokhlesi B, Cifu AS (2017). “Diagnostic Testing for Obstructive Sleep Apnea in Adults”. JAMA. 318 (20): 2035–2036. doi:10.1001/jama.2017.16722. PMID 29183053.

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