Obstructive sleep apnea

Obstructive sleep apnea
Synonyms Obstructive sleep apnoea
Obstructive sleep apnea. As soft tissue falls to the back of the throat, it impedes the passage of air (blue arrows) through the trachea.
Classification and external resources
Specialty Sleep medicine
ICD-10 G47.3
ICD-9-CM 327.23
OMIM 107650
DiseasesDB 9135
MedlinePlus 000811
eMedicine ped/2114
Patient UK Obstructive sleep apnea
MeSH D012891

Obstructive sleep apnea (OSA) is the most common type of sleep apnea and is caused by complete or partial obstructions of the upper airway. It is characterized by repetitive episodes of shallow or paused breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation. These episodes of decreased breathing, called "apneas" (literally, "without breath"), typically last 20 to 40 seconds.[1]

Individuals with OSA are rarely aware of difficulty breathing, even upon awakening. It is often recognized as a problem by others who observe the individual during episodes or is suspected because of its effects on the body. OSA is commonly accompanied with snoring. Some use the terms obstructive sleep apnea syndrome or obstructive sleep apnea–hypopnea syndrome to refer to OSA which is associated with symptoms during the daytime.[2] Symptoms may be present for years or even decades without identification, during which time the individual may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. Individuals who generally sleep alone are often unaware of the condition, without a regular bed-partner to notice and make them aware of their symptoms.

As the muscle tone of the body ordinarily relaxes during sleep, and the airway at the throat is composed of walls of soft tissue, which can collapse, it is not surprising that breathing can be obstructed during sleep. Although a minor degree of OSA is considered to be within the bounds of normal sleep, and many individuals experience episodes of OSA at some point in life, a small percentage of people have chronic, severe OSA.

Many people experience episodes of OSA for only a short period. 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 OSA is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of OSA 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.

Signs and symptoms

Common signs of OSA include unexplained daytime sleepiness, restless sleep, and loud snoring (with periods of silence followed by gasps). Less common symptoms are morning headaches; insomnia; trouble concentrating; mood changes such as irritability, anxiety and depression; forgetfulness; increased heart rate and/or blood pressure; decreased sex drive; unexplained weight gain; increased urination and/or nocturia; frequent heartburn or gastroesophageal reflux disease; and heavy night sweats.

Adults

The hallmark symptom of OSA syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing OSA will fall asleep for very brief periods in the course of usual daytime activities if given any opportunity to sit or rest. This behavior may be quite dramatic, sometimes occurring during conversations with others at social gatherings.

The hypoxia (absence of oxygen supply) related to OSA may cause changes in the neurons of the hippocampus and the right frontal cortex. Research using neuro-imaging revealed evidence of hippocampal atrophy in people suffering from OSA. They found that in more than 25% of the OSA cases, this problem results in irreversible problems in mentally manipulating non-verbal information and in executive functions and working memory, despite years of optimal continuous positive airway pressure (CPAP) treatment.[3]

Diagnosis of obstructive sleep apnea is significantly more common among people in relationships, who are alerted to their condition by being informed by their sleeping partner since individuals with obstructive sleep apnea are often unaware of the condition. There is a stigma associated with loud snoring, and it is not considered a feminine trait. Consequently, females are less likely to be told by their partners that they snore, or to admit it to themselves or doctors. Furthermore, CPAP is also perceived negatively by females, and less likely to be utilized to its full extent in this group.[4]

Children

Although this so-called "hypersomnolence" (excessive sleepiness) may also occur in children, it is not at all typical of young children with sleep apnea. Toddlers and young children with severe OSA instead ordinarily behave as if "over-tired" or "hyperactive." Adults and children with very severe OSA also differ in typical body habitus. Adults are generally heavy, with particularly short and heavy necks. Young children, on the other hand, are generally not only thin but may have "failure to thrive", where growth is reduced. Poor growth occurs for two reasons: the work of breathing is intense enough that calories are burned at high rates even at rest, and the nose and throat are so obstructed that eating is both tasteless and physically uncomfortable. OSA in children, unlike adults, is often caused by obstructive tonsils and adenoids and may sometimes be cured with tonsillectomy and adenoidectomy.

This problem can also be caused by excessive weight in children. In this case, the symptoms are more like the symptoms adults feel such as restlessness, exhaustion, etc.

Children with OSA may experience learning and memory deficits and OSA has also been linked to lowered childhood IQ scores.[5]

Causes

Most cases of OSA are believed to be caused by:

In adults, the most individual with OSA syndrome are obese, however, obesity is not always present. Adults with normal body mass indices (BMIs) often have decreased muscle tone causing airway collapse and sleep apnea. The cause of this is not well understood.

OSA and recurrent tonsillitis (RT) are different in their mechanism and outcome.[6]

Risk factors

Old age is often accompanied by muscular and neurological loss of muscle tone of the upper airway. Decreased muscle tone is also temporarily caused by chemical depressants; alcoholic drinks and sedative medications being the most common. The permanent premature muscular tonal loss in the upper airway may be precipitated by traumatic brain injury, neuromuscular disorders, or poor adherence to chemical and or speech therapy treatments.

Individuals with decreased muscle tone increased soft tissue around the airway, and structural features that give rise to a narrowed airway are at high risk for OSA. Men, in which the anatomy is typified by increased mass in the torso and neck, are at increased risk of developing sleep apnea, especially through middle age and later. Women suffer typically less frequently and to a lesser degree than do men, owing partially to physiology, but possibly also to differential levels of progesterone. Prevalence in post-menopausal women approaches that of men in the same age range. Women are at greater risk for developing OSA during pregnancy.[7]

OSA also appears to have a genetic component; those with a family history of it are more likely to develop it themselves. Lifestyle factors such as smoking may also increase the chances of developing OSA as the chemical irritants in smoke tend to inflame the soft tissue of the upper airway and promote fluid retention, both of which can result in narrowing of the upper airway. An individual may also experience or exacerbate OSA with the consumption of alcohol, sedatives, or any other medication that increases sleepiness as most of these drugs are also muscle relaxants.[8]

Craniofacial syndromes

There are patterns of unusual facial features that occur in recognizable syndromes. Some of these craniofacial syndromes are genetic, others are from unknown causes. In many craniofacial syndromes, the features that are unusual involve the nose, mouth, and jaw, or resting muscle tone, and put the individual at risk for OSA syndrome.

Down syndrome is one such syndrome. In this chromosomal abnormality, several features combine to make the presence of obstructive sleep apnea more likely. The specific features of Down syndrome that predispose to obstructive sleep apnea include relatively low muscle tone, narrow nasopharynx, and large tongue. Obesity and enlarged tonsils and adenoids, conditions that occur commonly in the western population, are much more likely to be obstructive in a person with these features than without them. Obstructive sleep apnea does occur even more frequently in people with Down syndrome than in the general population. A little over 50% of all people with Down syndrome suffer from obstructive sleep apnea,[9] and some physicians advocate routine testing of this group.[10]

In other craniofacial syndromes, the abnormal feature may actually improve the airway, but its correction may put the person at risk for obstructive sleep apnea after surgery when it is modified. Cleft palate syndromes are such an example. During the newborn period, all humans are obligate nasal breathers. The palate is both the roof of the mouth and the floor of the nose. Having an open palate may make feeding difficult, but generally, does not interfere with breathing, in fact, if the nose is very obstructed, then an open palate may relieve breathing. There are a number of clefting syndromes in which the open palate is not the only abnormal feature; additionally, there is a narrow nasal passage - which may not be obvious. In such individuals, closure of the cleft palate – whether by surgery or by a temporary oral appliance, can cause the onset of obstruction.

Skeletal advancement in an effort to physically increase the pharyngeal airspace is often an option for craniofacial patients with upper airway obstruction and small lower jaws (mandibles). These syndromes include Treacher Collins syndrome and Pierre Robin sequence. Mandibular advancement surgery is often just one of the modifications needed to improve the airway, others may include reduction of the tongue, tonsillectomy or modified uvulopalatoplasty.

Post-operative complication

OSA can also occur as a serious post-operative complication that seems to be most frequently associated with pharyngeal flap surgery as compared to other procedures for the treatment of velopharyngeal inadequacy (VPI).[11] In OSA, recurrent interruptions of respiration during sleep are associated with temporary airway obstruction. Following pharyngeal flap surgery, depending on size and position, the flap itself may have an "obturator" or obstructive effect within the pharynx during sleep, blocking ports of airflow and hindering effective respiration.[12][13] There have been documented instances of severe airway obstruction, and reports of post-operative OSA continues to increase as healthcare professionals (i.e. physicians, speech language pathologists) become more educated about this possible dangerous condition.[14] Subsequently, in clinical practice, concerns of OSA have matched or exceeded interest in speech outcomes following pharyngeal flap surgery.

The surgical treatment for velopalatal insufficiency may cause obstructive sleep apnea syndrome. When velopalatal insufficiency is present, air leaks into the nasopharynx even when the soft palate should close off the nose. A simple test for this condition can be made by placing a tiny mirror on the nose, and asking the subject to say "P". This p sound, a plosive, is normally produced with the nasal airway closes off - all air comes out of the pursed lips, none from the nose. If it is impossible to say the sound without fogging a nasal mirror, there is an air leak - reasonable evidence of poor palatal closure. Speech is often unclear due to inability to pronounce certain sounds. One of the surgical treatments for velopalatal insufficiency involves tailoring the tissue from the back of the throat and using it to purposefully cause partial obstruction of the opening of the nasopharynx. This may actually cause OSA syndrome in susceptible individuals, particularly in the days following surgery, when swelling occurs (see below: Special Situation: Anesthesia and Surgery).

Finally, patients with OSA are at an increased risk of many perioperative complications when the present for surgery, even if the planned procedure is not on the head and neck. Guidelines intended to reduce the risk of perioperative complications have been published.[15]

Pathophysiology

The normal sleep/wake cycle in adults is divided into REM (rapid eye movement) sleep, non-REM (NREM) sleep, and consciousness. NREM sleep is further divided into Stages 1, 2 and 3 NREM sleep. The deepest stage (stage 3 of NREM) is required for the physically restorative effects of sleep, and in pre-adolescents, this is the period of release of human growth hormone. NREM stage 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 rarely result in complete awakening but can have a significant negative effect on the restorative quality of sleep. In significant cases of OSA, one consequence is sleep deprivation due to the repetitive disruption and recovery of sleep activity. This sleep interruption in stage 3 (also called slow-wave sleep), and in REM sleep, can interfere with normal growth patterns, healing, and immune response, especially in children and young adults.

Diagnosis

Diagnosis of OSA is often based on a combination of patient history and tests (lab- or home-based). These tests range, in decreasing order of cost, complexity and tethering of the patient (number and type of channels of data recorded), from lab-attended full polysomnography ("sleep study") down to single-channel home recording. In the USA, these categories are associated with insurance classification from Type I down to Type IV.[16] Reimbursement rules vary among European countries.[17] The STOP-Bang questionnaire has been found to be useful for screening people.[18] Those who test positive on the screening are then recommended to be tested by either a sleep study or home monitor.[19]

Polysomnography

AHIRating
<5Normal
5-15Mild
15-30Moderate
>30Severe

Polysomnography in diagnosing OSA characterizes the pauses in breathing. As in central apnea, pauses are followed by a relative decrease in blood oxygen and an increase in the blood carbon dioxide. Whereas in central sleep apnea the body's motions of breathing stop, in OSA the chest not only continues to make the movements of inhalation, but the movements typically become even more pronounced. Monitors for airflow at the nose and mouth demonstrate that efforts to breathe are not only present but that they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.

An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep.[20] To grade the severity of sleep apnea, the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.

Home oximetry

In patients who are at high likelihood of having OSA, a randomized controlled trial found that home oximetry (a non-invasive method of monitoring blood oxygenation) may be adequate and easier to obtain than formal polysomnography.[21] High probability patients were identified by an Epworth Sleepiness Scale (ESS) score of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater.[22] Home oximetry, however, does not measure apneic events or respiratory event-related arousals and thus does not produce an AHI value.

Treatment

Numerous treatment options are used in obstructive sleep apnea.[23] Avoiding alcohol and smoking is recommended,[24] as is avoiding medications that relax the central nervous system (for example, sedatives and muscle relaxants). Weight loss is recommended in those who are overweight. Continuous positive airway pressure (CPAP) and mandibular advancement devices are often used and found to be equally effective.[25][26] Physical training, even without weight loss, improves sleep apnea.[27] There is insufficient evidence to support widespread use of medications or surgery.[25]

Physical intervention

The most widely used current therapeutic intervention is positive airway pressure whereby a breathing machine pumps a controlled stream of air through a mask worn over the nose, mouth, or both. The additional pressure holds open the relaxed muscles. There are several variants:

Oral appliances or splints are often preferred but may not be as effective as CPAP.[28] This device is a mouthguard similar to those used in sports to protect the teeth. It is designed to hold the lower jaw slightly down and forward relative to the natural, relaxed position. This position holds the tongue farther away from the back of the airway and may be enough to relieve apnea or improve breathing.

Many people benefit from sleeping at a 30-degree elevation of the upper body[33] or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Sleeping on a side as opposed to sleeping on the back is also recommended.[34][35][36]

Some studies have suggested that playing a wind instrument may reduce snoring and apnea incidents.[37] This may be especially true of double reed instruments.[38]

Surgery

Surgical treatments to modify airway anatomy, known as sleep surgery, are varied and must be tailored to the specific airway obstruction needs of a patient. Surgery is not considered a frontline treatment for obstructive sleep apnea, as prospective, randomized, comparative clinical evidence against current front line treatments is lacking.[25][39] For those obstructive sleep apnea sufferers unable or unwilling to comply with front line treatment, a properly selected surgical intervention will be the result of considering an individual's specific anatomy and physiology, personal preference and disease severity.[23] There is little randomized clinical trial evidence for all types of sleep surgery.[25]

There are a number of different operations that may be performed including:

In the morbidly obese, a major loss of weight (such as what occurs after bariatric surgery) can sometimes cure the condition.

OSA in children is sometimes due to chronically enlarged tonsils and adenoids. Tonsillectomy and adenoidectomy are curative. The operation may be far from trivial, especially in the worst apnea cases, in which growth is retarded and abnormalities of the right heart may have developed. Even in these extreme cases, the surgery tends to cure not only the apnea and upper airway obstruction but allows normal subsequent growth and development. Once the high end-expiratory pressures are relieved, the cardiovascular complications reverse themselves. The postoperative period in these children requires special precautions (see "Surgery and obstructive sleep apnea syndrome" below).

Neurostimulation

For patients who cannot use a continuous positive airway pressure device, the U.S. Food and Drug Administration in 2014 granted pre-market approval for an upper airway stimulation system that senses respiration and delivers mild electrical stimulation to the hypoglossal nerve in order to increase muscle tone at the back of the tongue so it will not collapse over the airway. The device includes a handheld patient controller to allow it to be switched on before sleep and is powered by an implantable pulse generator, similar to one used for cardiac rhythm management. Approval for this active implantable neuromodulation device was preceded by a clinical trial whose results were published in the New England Journal of Medicine.[41][42]

Radiofrequency ablation

Radiofrequency ablation (RFA), which is conceptually analogous in some ways to surgery, uses low frequency (300 kHz to 1 MHz)[43] radio wave energy to target tissue, causing coagulative necrosis. RFA achieves its effects at 40 °C to 70 °C[44] unlike other electrosurgical devices which require 400 °C to 600 °C for efficacy.[45]

Subsequent evaluations of safety and efficacy have led to the recognition of RFA by the American Academy of Otolaryngology[39] as a somnoplasty treatment option in selected situations for mild to moderate OSA, but the evidence was judged insufficient for routine adoption by the American College of Physicians.[25]

RFA has some potential advantages in carefully selected medical settings, such as intolerance to the CPAP device. For example, when adherence is defined as greater than four hours of nightly use, 46% to 83% of patients with obstructive sleep apnea are non-adherent with CPAP[46] for a variety of reasons, including discomfort while sleeping.

RFA is usually performed in an outpatient setting, using either local anesthetics or conscious sedation anesthesia, the procedure itself typically lasting under 3 minutes. The targeted tissue, such as tongue or palate, is usually approached through the mouth without the need for incisions, although occasionally the target is approached through the neck using assisted imaging.[47] If the tongue is being targeted, this can be done from either dorsal or ventral side. Complications include ulceration, infection, nerve weakness or numbness and swelling. These complications occur in less than 1% of procedures.[43]

Medications

Evidence is insufficient to support the use of medications to treat obstructive sleep apnea.[25][48] This includes the use of fluoxetine, paroxetine, acetazolamide and tryptophan among others.[25][49]

Prognosis

Many studies indicate the effect of a "fight or flight" response on the body that happens with each apneic event is what increases health risks and consequences in OSA. 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.[50][51][52]

Without treatment, the sleep deprivation and lack of oxygen caused by sleep apnea increases health risks such as cardiovascular disease, aortic disease (e.g. aortic aneurysm),[53] high blood pressure,[54][55] stroke,[56] diabetes, clinical depression,[57] weight gain and obesity.[58]

The most serious consequence of untreated OSA is to the heart. Persons with sleep apnea have a 30% higher risk of heart attack or death than those unaffected.[59] In severe and prolonged cases, increased in pulmonary pressures are transmitted to the right side of the heart. This can result in a severe form of congestive heart failure known as cor pulmonale. Dyastolic function of the heart also becomes affected.[60] One prospective study showed patients with OSA, compared with healthy controls, initially had statistically significant increases in vascular endothelial growth factor (P=.003) and significantly lower levels of nitrite-nitrate (P=.008), which might be pathogenic factors in the cardiovascular complications of OSA.[61] These factors reversed to normal levels after 12 weeks of treatment by CPAP, but further long-term trials are needed to assess the impact of this therapy.[62]

Elevated arterial pressure (i.e., hypertension) can be a consequence of OSA syndrome.[63] When hypertension is caused by OSA, it is distinctive in that, unlike most cases (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping (non-dipper) or even increase (inverted dipper).[64]

Epidemiology

Two to four percent of adults are believed to have obstructive sleep apnea.[24] It is most commonly diagnosed in middle aged males.[24]

If studied carefully in a sleep lab by polysomnography (formal "sleep study"), it is believed that approximately 1 in 5 American adults would have at least mild OSA.[65]

Research

Neurostimulation is currently being studied as a method of treatment;[66] an implanted hypoglossal nerve stimulation system received European CE Mark (Conformité Européenne) approval in March 2012.[67] Also being studied are exercises of the muscles around the mouth and throat through activities such as playing the didgeridoo.[68][69]

See also

References

  1. ↑ "Obstructive Sleep Apnea Syndrome (780.53-0)". The International Classification of Sleep Disorders (PDF). Westchester, Illinois: American Academy of Sleep Medicine. 2001. pp. 52–8. Retrieved 2010-09-11.
  2. ↑ Barnes L (editor) (2009). Surgical pathology of the head and neck (3rd ed.). New York: Informa healthcare. ISBN 9781420091632.:226
  3. ↑ Gale SD, Hopkins RO (2004). "Effects of hypoxia on the brain: neuroimaging and neuropsychological findings following carbon monoxide poisoning and obstructive sleep apnea". J Int Neuropsychol Soc. 10 (1): 60–71. doi:10.1017/S1355617704101082. PMID 14751008.
  4. ↑ Henry, D; Rosenthal, L (Feb 2013). ""Listening for his breath:" the significance of gender and partner reporting on the diagnosis, management, and treatment of obstructive sleep apnea.". Social science & medicine (1982). 79: 48–56. doi:10.1016/j.socscimed.2012.05.021. PMID 22770968.
  5. ↑ Halbower AC, Degaonkar M, Barker PB, et al. (August 2006). "Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury". PLoS Med. 3 (8): e301. doi:10.1371/journal.pmed.0030301. PMC 1551912Freely accessible. PMID 16933960.
  6. ↑ Ezzedini R, Darabi M, Ghasemi B, Darabi M, Fayezi S, Moghaddam YJ, et al. (2013). "Tissue fatty acid composition in obstructive sleep apnea and recurrent tonsillitis.". Int J Pediatr Otorhinolaryngol. 77 (6): 1008–12. doi:10.1016/j.ijporl.2013.03.033. PMID 23643333.
  7. ↑ Edwards, Natalie; Sullivan, Colin E. (2008). "Sleep-Disordered Breathing in Pregnancy". Sleep Medicine Clinics. 3: 81–95. doi:10.1016/j.jsmc.2007.10.010.
  8. ↑ Sleep Apnea: Risk Factors, Mayo Clinic, June 29, 2010, Retrieved November 4, 2010.
  9. ↑ de Miguel-Díez J, Villa-Asensi JR, Alvarez-Sala JL (December 2003). "Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children". Sleep. 26 (8): 1006–9. PMID 14746382.
  10. ↑ Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R (April 2006). "Obstructive sleep apnea: Should all children with Down syndrome be tested?". Arch. Otolaryngol. Head Neck Surg. 132 (4): 432–6. doi:10.1001/archotol.132.4.432. PMID 16618913.
  11. ↑ Sloan GM (March 2000). "Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art". Cleft Palate Craniofac. J. 37 (2): 112–22. doi:10.1597/1545-1569(2000)037<0112:PPFASP>2.3.CO;2. PMID 10749049.
  12. ↑ Pugh, M.B. et al. (2000). Apnea. Stedman's Medical Dictionary (27th ed.) Retrieved June 18, 2006 from STAT!Ref Online Medical Library database.
  13. ↑ Liao YF, Noordhoff MS, Huang CS, et al. (March 2004). "Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency". Cleft Palate Craniofac. J. 41 (2): 152–6. doi:10.1597/02-162. PMID 14989690.
  14. ↑ McWilliams, Betty Jane; Peterson-Falzone, Sally J.; Hardin-Jones, Mary A.; Karnell, Michael P. (2001). Cleft palate speech (3rd ed.). St. Louis: Mosby. ISBN 0-8151-3153-4.
  15. ↑ Gross, JB; Bachenberg, KL; Benumof, JL; Caplan, RA; Connis, RT; Coté, CJ; Nickinovich, DG; Prachand, V; Ward, DS; Weaver, EM; Ydens, L; Yu, S; American Society of Anesthesiologists Task Force on Perioperative, Management (May 2006). "Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea.". Anesthesiology. 104 (5): 1081–93; quiz 1117–8. doi:10.1097/00000542-200605000-00026. PMID 16645462. Cite uses deprecated parameter |coauthors= (help)
  16. ↑ FAQ on www.sleepeducation.com
  17. ↑ Fietze I, Penzel T, Alonderis A, et al. (February 2011). "Management of obstructive sleep apnea in Europe". Sleep Med. 12 (2): 190–7. doi:10.1016/j.sleep.2010.10.003. PMID 21167776.
  18. ↑ Nagappa, M; Liao, P; Wong, J; Auckley, D; Ramachandran, SK; Memtsoudis, S; Mokhlesi, B; Chung, F (2015). "Validation of the STOP-Bang Questionnaire as a Screening Tool for Obstructive Sleep Apnea among Different Populations: A Systematic Review and Meta-Analysis.". PloS one. 10 (12): e0143697. PMID 26658438.
  19. ↑ Le Grande, MR; Neubeck, L; Murphy, BM; McIvor, D; Lynch, D; McLean, H; Jackson, AC (September 2016). "Screening for obstructive sleep apnoea in cardiac rehabilitation: A position statement from the Australian Centre for Heart Health and the Australian Cardiovascular Health and Rehabilitation Association.". European journal of preventive cardiology. 23 (14): 1466–75. PMID 27271098.
  20. ↑ "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force". Sleep. 22 (5): 667–89. August 1999. PMID 10450601.
  21. ↑ Mulgrew AT, Fox N, Ayas NT, Ryan CF (February 2007). "Diagnosis and initial management of obstructive sleep apnea without polysomnography: a randomized validation study". Annals of Internal Medicine. 146 (3): 157–66. doi:10.7326/0003-4819-146-3-200702060-00004. PMID 17283346.
  22. ↑ Flemons WW, Whitelaw WA, Brant R, Remmers JE (November 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.
  23. 1 2 Friedman: Sleep Apnea and Snoring, 1st ed. 2008
  24. 1 2 3 Azagra-Calero, E; Espinar-Escalona, E; Barrera-Mora, JM; Llamas-Carreras, JM; Solano-Reina, E (Nov 1, 2012). "Obstructive sleep apnea syndrome (OSAS). Review of the literature.". Medicina oral, patologia oral y cirugia bucal. 17 (6): e925–9. doi:10.4317/medoral.17706. PMID 22549673.
  25. 1 2 3 4 5 6 7 Qaseem, A; Holty, JE; Owens, DK; Dallas, P; Starkey, M; Shekelle, P; for the Clinical Guidelines Committee of the American College of, Physicians (Sep 24, 2013). "Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians.". Annals of Internal Medicine. doi:10.7326/0003-4819-159-7-201310010-00704. PMID 24061345.
  26. ↑ Bratton, DJ; Gaisl, T; Wons, AM; Kohler, M (1 December 2015). "CPAP vs Mandibular Advancement Devices and Blood Pressure in Patients With Obstructive Sleep Apnea: A Systematic Review and Meta-analysis.". JAMA. 314 (21): 2280–93. doi:10.1001/jama.2015.16303. PMID 26624827.
  27. ↑ Iftikhar, IH; Kline, CE; Youngstedt, SD (Sep 29, 2013). "Effects of Exercise Training on Sleep Apnea: A Meta-analysis.". Lung. 192: 175–184. doi:10.1007/s00408-013-9511-3. PMID 24077936.
  28. 1 2 Giles, TL; Lasserson, TJ; Smith, BH; White, J; Wright, J; Cates, CJ (Jul 19, 2006). "Continuous positive airways pressure for obstructive sleep apnoea in adults.". The Cochrane database of systematic reviews (3): CD001106. doi:10.1002/14651858.CD001106.pub3. PMID 16855960.
  29. ↑ Riaz, M; Certal, V; Nigam, G; Abdullatif, J; Zaghi, S; Kushida, CA; Camacho, M (2015). "Nasal Expiratory Positive Airway Pressure Devices (Provent) for OSA: A Systematic Review and Meta-Analysis.". Sleep disorders. 2015: 734798. PMID 26798519.
  30. ↑ Whitelaw WA, Brant RF, Flemons WW (January 2005). "Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea". Am. J. Respir. Crit. Care Med. 171 (2): 188–93. doi:10.1164/rccm.200310-1360OC. PMID 15486338. Review in: Caples SM (2005). "The accuracy of physicians in predicting successful treatment response in suspected obstructive sleep apnea did not differ between home monitoring and polysomnography". ACP J. Club. 143 (1): 21. PMID 15989309.
  31. ↑ Littner M, Hirshkowitz M, Davila D, et al. (March 2002). "Practice parameters for the use of auto-titrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. An American Academy of Sleep Medicine report". Sleep. 25 (2): 143–7. PMID 11902424.
  32. ↑ McNicholas, Walter T.; Bonsignore, Maria R.; Lévy, Patrick; Ryan, Silke (2016-05-27). "Mild obstructive sleep apnoea: clinical relevance and approaches to management". The Lancet. Respiratory Medicine. doi:10.1016/S2213-2600(16)30146-1. ISSN 2213-2619. PMID 27245915.
  33. ↑ Neill AM, Angus SM, Sajkov D, McEvoy RD (January 1997). "Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea". Am. J. Respir. Crit. Care Med. 155 (1): 199–204. doi:10.1164/ajrccm.155.1.9001312. PMID 9001312.
  34. ↑ Nakano H, Ikeda T, Hayashi M, Ohshima E, Onizuka A (March 2003). "Effects of body position on snoring in apneic and nonapneic snorers". Sleep. 26 (2): 169–72. PMID 12683476.
  35. ↑ Loord H, Hultcrantz E (August 2007). "Positioner--a method for preventing sleep apnea". Acta Otolaryngol. 127 (8): 861–8. doi:10.1080/00016480601089390. PMID 17762999.
  36. ↑ Szollosi I, Roebuck T, Thompson B, Naughton MT (August 2006). "Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration". Sleep. 29 (8): 1045–51. PMID 16944673.
  37. ↑ Learning To Play A Wind Instrument Could Lower Your Risk For Obstructive Sleep Apnea
  38. ↑ Risk of Obstructive Sleep Apnea Lower in Double Reed Wind Musicians
  39. 1 2 "Submucosal Ablation of the Tongue Base for OSAS". American Academy of Otolaryngology- Head and Neck Surgery. Retrieved 29 October 2013.
  40. ↑ Sleep apnea
  41. ↑ http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMA/pma.cfm?id=18437. FDA "Premarket Approval (PMA) Inspire II Upper Airway Stimulation System" U.S. Food and Drug Administration. April 30, 2014.
  42. ↑ Strollo PJ Jr, Soose RJ, Maurer JT, de Vries N, Cornelius J, Froymovich O, Hanson RD, Padhya TA, Steward DL, Gillespie MB, Woodson BT, Van de Heyning PH, Goetting MG, Vanderveken OM, Feldman N, Knaack L, Strohl KP; STAR Trial Group (January 9, 2014). "Upper-airway stimulation for obstructive sleep apnea". New England Journal of Medicine. 370 (2): 139–49. doi:10.1056/nejmoa1308659. PMID 24401051.
  43. 1 2 Farrar, J; Ryan, Olliver, Gillespie (October 2008). "Radiofrequency ablation for the treatment of obstructive sleep apnea: a meta-analysis.". The Laryngoscope. 118 (10): 1878–83. doi:10.1097/MLG.0b013e31817d9cc1. PMID 18806478. Cite uses deprecated parameter |coauthors= (help)
  44. ↑ Eick, Olaf J (1 July 2002). "Temperature Controlled Radiofrequency Ablation". Indian Pacing Electrophysiol. 3. 2 (3): 66–73. PMC 1564057Freely accessible. PMID 17006561.
  45. ↑ Bashetty, Kusum; Gururaj Nadig Sandhya Kapoor (19 November 2009). "Electrosurgery in aesthetic and restorative dentistry: A literature review and case reports". Journal of Conservative Dentistry. 12 (4): 139–144. doi:10.4103/0972-0707.58332. PMC 2879725Freely accessible. PMID 20543922.
  46. ↑ Weaver, Terri; Grunstein (2008). "Adherence to Continuous Positive Airway Pressure Therapy: The Challenge to Effective Treatment". Proceedings of the American Thoracic Society. 5 (2): 173–8. doi:10.1513/pats.200708-119MG.
  47. ↑ Steward, DL; Weaver, Woodson (2005). "Multilevel temperature-controlled radiofrequency for obstructive sleep apnea: extended follow-up". Otolaryngol Head Neck Surg. 132 (4): 630–5. doi:10.1016/j.otohns.2004.11.013. PMID 15806059.
  48. ↑ Mason, M; Welsh, EJ; Smith, I (May 31, 2013). "Drug therapy for obstructive sleep apnoea in adults.". The Cochrane database of systematic reviews. 5: CD003002. doi:10.1002/14651858.CD003002.pub3. PMID 23728641.
  49. ↑ Veasey SC (2003). "Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential". Am J Respir Med. 2 (1): 21–9. doi:10.1007/BF03256636. PMID 14720019.
  50. ↑ Weaver, Jacqueline (June 15, 2007). "Sleep apnea is linked to heart disease and diabetes". Yale Bulletin and Calendar. 35 (30).
  51. ↑ Dyugovskaya L, Lavie P, Lavie L (April 2002). "Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients". Am. J. Respir. Crit. Care Med. 165 (7): 934–9. doi:10.1164/ajrccm.165.7.2104126. PMID 11934717. Lay summary – ScienceDaily (Apr 4, 2002).
  52. ↑ Botros NA, Shah N, Mohsenin V, Roux F, Yaggi HK (May 21, 2007). Obstructive Sleep Apnea as a Risk Factor for Type II Diabetes (PDF). American Thoracic Society 2007 International Conference. Lay summary – ScienceDaily (May 21, 2007).
  53. ↑ Gaisl, Thomas; Bratton, Daniel J.; Kohler, Malcolm (2015-08-01). "The impact of obstructive sleep apnoea on the aorta". The European Respiratory Journal. 46 (2): 532–544. doi:10.1183/09031936.00029315. ISSN 1399-3003. PMID 26113685.
  54. ↑ Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. (May 11, 2000). "Prospective Study of the Association Between Sleep-Disordered Breathing and Hypertension" (PDF). The New England Journal of Medicine. Massachusetts Medical Society. 342 (19): 1378–1384. doi:10.1056/nejm200005113421901. Retrieved 2013-05-29. Conclusions: We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population.
  55. ↑ Peretz Lavie, Paula Herer, Victor Hoffstein (19 February 2000). "Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study" (PDF). BMJ. BMJ Publishing Group. 320: 479–82. doi:10.1136/bmj.320.7233.479. Retrieved 2013-05-29. Conclusion: Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors.
  56. ↑ Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V (November 2005). "Obstructive sleep apnea as a risk factor for stroke and death". N. Engl. J. Med. 353 (19): 2034–41. doi:10.1056/NEJMoa043104. PMID 16282178.
  57. ↑ Schröder CM, O'Hara R (June 2005). "Depression and Obstructive Sleep Apnea (OSA)". Ann Gen Psychiatry. 4: 13. doi:10.1186/1744-859X-4-13. PMC 1181621Freely accessible. PMID 15982424.
  58. ↑ "Women with sleeping problems at higher risk for Type 2 diabetes". American Sleep Association. Retrieved 30 January 2016.
  59. ↑ N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, Connecticut (May 20, 2007). "Sleep Apnea Increases Risk of Heart Attack or Death by 30%". American Thoracic Society. Archived from the original on May 24, 2009.
  60. ↑ Sun Y (Apr 2014). "Cardiac structural and functional changes in old elderly patients with obstructive sleep apnoea-hypopnoea syndrome.". J Int Med Res. 42 (2): 395–404. doi:10.1177/0300060513502890. PMID 24445697.
  61. ↑ Ciftci TU, Kokturk O, Demirtas S, Gulbahar O, Bukan N (2011). "Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome". Ann Saudi Med. 31 (1): 14–8. doi:10.4103/0256-4947.75772. PMC 3101718Freely accessible. PMID 21245593.
  62. ↑ Bahammam A (2011). "Obstructive sleep apnea: from simple upper airway obstruction to systemic inflammation". Ann Saudi Med. 31 (1): 1–2. doi:10.4103/0256-4947.75770. PMC 3101717Freely accessible. PMID 21245591.
  63. ↑ Silverberg DS, Iaina A, Oksenberg A (January 2002). "Treating obstructive sleep apnea improves essential hypertension and quality of life". Am Fam Physician. 65 (2): 229–36. PMID 11820487.
  64. ↑ Grigg-Damberger M (February 2006). "Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack". J Clin Neurophysiol. 23 (1): 21–38. doi:10.1097/01.wnp.0000201077.44102.80. PMID 16514349.
  65. ↑ Shamsuzzaman AS, Gersh BJ, Somers VK (October 2003). "Obstructive sleep apnea: implications for cardiac and vascular disease". JAMA. 290 (14): 1906–14. doi:10.1001/jama.290.14.1906. PMID 14532320.
  66. ↑ Kezirian, EJ; Boudewyns, A; Eisele, DW; Schwartz, AR; Smith, PL; Van de Heyning, PH; De Backer, WA (October 2010). "Electrical stimulation of the hypoglossal nerve in the treatment of obstructive sleep apnea". Sleep medicine reviews. 14 (5): 299–305. doi:10.1016/j.smrv.2009.10.009. PMID 20116305. Cite uses deprecated parameter |coauthors= (help)
  67. ↑ Editors (15 March 2012). "ImThera aura6000 System for Sleep Apnea Gets a Go in Europe". Medgadget. Retrieved 15 January 2014.
  68. ↑ Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O (February 2006). "Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial". BMJ. 332 (7536): 266–70. doi:10.1136/bmj.38705.470590.55. PMC 1360393Freely accessible. PMID 16377643.
  69. ↑ Guimarães KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G (May 2009). "Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome". Am. J. Respir. Crit. Care Med. 179 (10): 962–6. doi:10.1164/rccm.200806-981OC. PMID 19234106.

Further reading

This article is issued from Wikipedia - version of the 12/2/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.