Sleep apnea

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Template:Sleep Apnea
ICD-10	G47.3
ICD-9	780.57
MeSH	D012891

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]; Associate Editor(s)-In-Chief: Kashish Goel, M.D.

Keywords: Sleep apnea, obstructive sleep apnea, obesity hypoventilation, cor pulmonale

Types

There are two different type of sleep apnea. This section will focus on obstructive sleep apnea.

Obstructive sleep apnea

Obstructive sleep apnea (OSA) is not only much more frequent than central sleep apnea, it is a common condition in many parts of the world. If studied carefully in a sleep lab by polysomnography, approximately 1 in 5 American adults has at least mild OSA. Since the muscle tone of the body ordinarily relaxes during sleep, and since, at the level of the throat, the human airway is composed of walls of soft tissue, which can collapse, it is easy to understand why breathing can be obstructed during sleep. Although many individuals experience episodes of obstructive sleep apnea at some point in life, a much smaller percentage of people are afflicted with chronic severe obstructive sleep apnea.

Normal sleep/wakefulness in adults has distinct stages numbered 1 to 4, REM sleep, and wake. The deeper stages (3 to 4) are required for the physically restorative effects of sleep and in pre-adolescents are the focus of release for human growth hormone. Stages 2 and REM, which combined are 70% of an average person's total sleep time, are more associated with mental recovery and maintenance. During REM sleep in particular, muscle tone of the throat and neck, as well as the vast majority of all skeletal muscles, is almost completely attenuated, allowing the tongue and soft palate/oropharynx to relax, and in the case of sleep apnea, to impede the flow of air to a degree ranging from light snoring to complete collapse. In the cases where airflow is reduced to a degree where blood oxygen levels fall, or the physical exertion to breathe is too great, neurological mechanisms trigger a sudden interruption of sleep, called a neurological arousal. These arousals may or may not result in complete awakening, but can have a significant negative effect on the restorative quality of sleep. In significant cases of obstructive sleep apnea, one consequence is sleep deprivation due to the repetitive disruption and recovery of sleep activity. This sleep interruption in stages 3 and 4 (also collectively called slow-wave sleep), can interfere with normal growth patterns, healing, and immune response, especially in children and young adults.

Many people experience elements of obstructive sleep apnea for only a short period of time. This can be the result of an upper respiratory infection that causes nasal congestion, along with swelling of the throat, or tonsillitis that temporarily produces very enlarged tonsils. The Epstein-Barr virus, for example, is known to be able to dramatically increase the size of lymphoid tissue during acute infection, and obstructive sleep apnea is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of obstructive sleep apnea syndrome may also occur in individuals who are under the influence of a drug (such as alcohol) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms.

Diagnosis

History and Symptoms | Physical Examination | Lab Studies | Electrocardiogram | Polysomnography | Home Oximetry | Other imaging findings

Treatment

Medical Treatment | Surgical Treatment | Other Treatments

Prognosis

Although it takes some trial and error, most patients find a combination of treatments which reduce apnea events and improve their overall health, energy, and well-being. Without treatment, the sleep deprivation and lack of oxygen caused by sleep apnea increases health risks such as cardiovascular disease, high blood pressure, stroke, diabetes, clinical depression, weight gain and obesity.

The most serious consequence of untreated obstructive sleep apnea is to the heart. In severe and prolonged cases, there are increases in pulmonary pressures that are transmitted to the right side of the heart. This can result in a severe form of congestive heart failure (cor pulmonale).

Elevated arterial pressure (commonly called high blood pressure) can be a consequence of obstructive sleep apnea syndrome. When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping. Stroke is associated with obstructive sleep apnea. Sleep apnea sufferers also have a 30% higher risk of heart attack or death than those unaffected.

Many studies indicate that it is the effect of the "fight or flight" response on the body that happens with each apneic event that increases these risks. The fight or flight response causes many hormonal changes in the body; those changes, coupled with the low oxygen saturation level of the blood, cause damage to the body over time.

See also

• Marfan syndrome

References

• Maninder Kalra (March 2007). "Genetic susceptibility to obstructive sleep apnea in the obese child". Sleep Medicine. 8 (2): 169–175. PMID 17275401. CS1 maint: Date and year (link)
• American Academy of Sleep Medicine Task Force (1999). "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research". Sleep. 22 (5): 667–89. PMID 10450601.
• Bell, R. B. (2001). "Skeletal advancement for the treatment of obstructive sleep apnea in children". Cleft Palate-Craniofacial Journal. 38 (2): 147–54.
• Caples S, Gami A, Somers V (2005). "Obstructive sleep apnea". Ann Intern Med. 142 (3): 187–97. PMID 15684207.CS1 maint: Multiple names: authors list (link)
• Cohen, M. M. J. (1992). "Upper and lower airway compromise in the Apert syndrome". American Journal of Medical Genetics. 44: 90–93.
• de Miguel-Díez J, Villa-Asensi J, Alvarez-Sala J (2003). "Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children" (PDF). Sleep. 26 (8): 1006–9. PMID 14746382.CS1 maint: Multiple names: authors list (link)
• Mathur R, Douglas N (1994). "Relation between sudden infant death syndrome and adult sleep apnoea/hypopnoea syndrome". Lancet. 344 (8925): 819–20. PMID 7916096.
• Mortimore I, Douglas N (1997). "Palatal muscle EMG response to negative pressure in awake sleep apneic and control subjects". Am J Respir Crit Care Med. 156 (3 Pt 1): 867–73. PMID 9310006.
• Perkins, J. A. (1997). "Airway management in children with craniofacial anomalies". Cleft Palate-Craniofacial Journal. 34 (2): 135–40.
• Sculerati N. (1998 December). "Airway management in children with major craniofacial anomalies". Laryngoscope. 108 (12): 1806–12.
• Shepard, J. W. (1990). "Localization of upper airway collapse during sleep in patients with obstructive sleep apnea". American Review of Respiratory Disorders. 141: 1350–55.
• Sher, A. (1990). Obstructive sleep apnea syndrome: a complex disorder of the upper airway. Otolaryngologic Clinics of North America, 24, 600.
• Shott S, Amin R, Chini B, Heubi C, Hotze S, Akers R (2006). "Obstructive sleep apnea: Should all children with Down syndrome be tested?". Arch Otolaryngol Head Neck Surg. 132 (4): 432–6. PMID 16618913.CS1 maint: Multiple names: authors list (link)
• Shouldice RB, O'Brien LM, O'Brien C, de Chazal P, Gozal D, Heneghan C (2004). "Detection of obstructive sleep apnea in pediatric subjects using surface lead electrocardiogram features". Sleep. 27 (4): 784–92. PMID 15283015.CS1 maint: Multiple names: authors list (link)
• Slovis B. & Brigham K. (2001). "Disordered Breathing". In ed Andreoli T. E. Cecil Essentials of Medicine. Philadelphia: W.B. Saunders. pp. pp210–211.CS1 maint: Extra text (link)
• Strollo P, Rogers R (1996). "Obstructive sleep apnea". N Engl J Med. 334 (2): 99–104. PMID 8531966.
• Sullivan C, Issa F, Berthon-Jones M, Eves L (1981). "Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares". Lancet. 1 (8225): 862–5. PMID 6112294.CS1 maint: Multiple names: authors list (link)

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