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{{Infobox_Disease | Name = {{PAGENAME--> | Image = | Caption = | DiseasesDB = | ICD10 = {{ICD10|G|47|3|g|40--> | ICD9 = {{ICD9|780.5--> pre-diagnosis, {{ICD9|327.23--> confirmed diagnosis | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = ped | eMedicineTopic = 2114 | MeshID = D012891 | -->

Sleep apnea, sleep apnoea or sleep apnœa is a sleep disorder characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough so one or more breaths are missed, and occur repeatedly throughout sleep. The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), or a blood oxygen desaturation of 3-4 percent or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram.

Clinically significant levels of sleep apnea are defined as 5 or more events of any type per hour of sleep time (from the polysomnogram). There are two distinct forms of sleep apnea: Central and Obstructive. Breathing is interrupted by the lack of effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite effort. In mixed sleep apnea, there is a transition from central to obstructive features during the events themselves.

Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. 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., but efforts to breathe are not only present, they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.

Obstructive sleep apnea is the most common category of sleep-disordered breathing. The prevalence of OSA among the adult population in western Europe and North America has not been confidently established, but in the mid-1990s was estimated to be 3-4% of women and 6-7% of men.

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 (American Academy of Sleep Medicine Task Force, 1999). 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 may be adequate and easier to obtain than formal polysomnography. High probability patients were indentified by Epworth Sleepiness Scale (ESS) of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater.

Populations at risk 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 obstructive sleep apnea. Men, whose anatomy is typified by increased body mass in the torso and neck, are more typical sleep apnea sufferers, especially through middle age and older. Adult women suffer typically less frequently and to a lesser degree than men do, owing partially to physiology, but possibly to emerging links to levels of progesterone. Prevalence in post-menopausal women approaches that of men in the same age range.

Adults In adults, the most typical individual with obstructive sleep apnea syndrome is obese, with particular heaviness at the face and neck. The hallmark symptom of obstructive sleep apnea syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing obstructive sleep apnea 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.

Children Although this so called "hyper-somnolence" (excessive sleepiness) may also occur in children, it is not at all typical of younger children with sleep apnea. Toddlers and young children with severe obstructive sleep apnea instead ordinarily behave as if "over-tired" or "hyper". Adults and children with very severe obstructive sleep apnea 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 high enough so 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. Obstructive sleep apnea in children, unlike adults, is almost always caused by obstructive tonsils and adenoids and is usually cured with tonsillectomy and adenoidectomy.

This problem can also be caused by excessive weight. The symptoms are more like the symptoms adults feel; restlessness, exhaustion, and more.

Common signs and symptoms (The signs and symptoms that follow apply to both adults and children suffering with sleep apnea)

Additional signs of obstructive sleep apnea include restless sleep, and loud snoring (with periods of silence followed by gasps). Other symptoms are non-specific: morning headaches, trouble concentrating, irritability, forgetfulness, mood or behavior changes, decreased sex drive, increased heart rate, anxiety, depression (mood), increased frequency of urination, nocturia (getting up during the night to urinate), Gastroesophageal reflux disease and heavy sweating at night.

The most serious consequence of 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).

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 obstructive sleep apnea 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 in 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 (de Miguel-Díez, et al 2003), and some physicians advocate routine testing of this group (Shott, et al 2006).

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 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.

Pharyngeal flap surgery may cause obstructive sleep apnea Obstructive sleep apnea is a serious complication that seems to be most frequently associated with pharyngeal flap surgery, compared to other procedures for treatment of velopharyngeal inadequacy (VPI).Sloan, G.M. (2000). Posterior pharyngeal flap and sphincter pharyngoplasty: The state of the art. Cleft Palate-Craniofacial Journal, 37(2), 112-122. In OSA, recurrent interruptions of Respiration (physiology) 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 (physiology).Pugh, M.B. et al. (2000). Apnea. Stedman’s Medical Dictionary (27th ed.) Retrieved June 18, 2006 from STAT!Ref Online Medical Library database.Liao, Y., Noordhoff, M.S., Huang, C., Chen, P.K.T., Chen N., Yun, C. et al. (2004). Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency. Cleft Palate-Craniofacial Journal, 41(2), 152-156. There have been documented instances of severe airway obstruction, and reports of post-operative OSA continue to increase as healthcare professionals (i.e. physicians, speech language pathologists) become more educated about this possible dangerous condition.Peterson-Falzone, S.J., Hardin-Jones, M.A., & Karnell, M.P. (2001). Cleft Palate Speech (3rd ed.). St. Louis: Mosby. 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 at the nose, and asking the subject to say "P". This p sound, a plosive, is normally produced with the nasal airway closed 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 obstructive sleep apnea syndrome in susceptible individuals, particularly in the days following surgery, when swelling occurs (see below: Special Situation: Anesthesia and Surgery)

{| class="wikitable" align="right" style="margin: 1em 1em "! AHI||Rating|-| 30||Severe|}

Treatment There are a variety of treatments for obstructive sleep apnea, depending on an individual’s medical history, the severity of the disorder and, most importantly, the specific cause of the obstruction.

In acute infectious mononucleosis, for example, although the airway may be severely obstructed in the first 2 weeks of the illness, the presence of lymphoid tissue (suddenly enlarged tonsils and adenoids) blocking the throat is usually only temporary. A course of anti-inflammatory steroids such as prednisone (or another kind of glucocorticoid drug) is often given to reduce this lymphoid tissue. Although the effects of the steroids are short term, in most affected individuals, the tonsillar and adenoidal enlargement are also short term, and will be reduced on its own by the time a brief course of steroids is completed. In unusual cases where the enlarged lymphoid tissue persists after resolution of the acute stage of the Epstein-Barr infection, or in which medical treatment with anti-inflammatory steroids does not adequately relieve breathing, tonsillectomy and adenoidectomy may be urgently required.

Most children with obstructive sleep apnea have the problem on the basis of chronically enlarged tonsils and adenoids. In these children, tonsillectomy and adenoidectomy is curative. The operation may be far from trivial, however, in the worst cases, in which growth is reduced and abnormalities of the right heart may have developed. Even in these extreme cases, however, the surgery tends to cure not only the apnea and upper airway obstruction - but to allow subsequent normal 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).

The treatment for obstructive sleep apnea in the case of adults with poor oropharyngeal airways secondary to heavy upper body type is varied. Unfortunately, in this most common type of obstructive sleep apnea, unlike some of the cases discussed above, reliable cures are not the rule.

Some treatments involve lifestyle changes, such as avoiding alcohol and medications that relax the central nervous system (for example, sedatives and muscle relaxants), losing weight, and quitting smoking. Some people are helped by special pillows or devices that keep them from sleeping on their backs, or oral appliances to keep the airway open during sleep. If these conservative methods are inadequate, doctors often recommend continuous positive airway pressure (CPAP), in which a face mask is attached to a tube and a machine that blows pressurized air into the mask and through the airway to keep it open. There are also surgical procedures that can be used to remove and tighten tissue and widen the airway, but the success rate is not high. Some individuals may need a combination of therapies to successfully treat their sleep apnea.

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 splints or holds open the relaxed muscles, just as air in a balloon inflates it. There are several variants:

• (Continuous positive airway pressure), or continuous positive airway pressure, in which a controlled air compressor generates an airstream at a constant pressure. This pressure is prescribed by the patient's physician, based on an overnight test or titration. Newer CPAP models are available which slightly reduce pressure upon exhalation to increase patient comfort and compliance. CPAP is the most common treatment for obstructive sleep apnea.
• (VPAP), or variable positive airway pressure, also known as bilevel or BiPAP, uses an electronic circuit to monitor the patient's breathing, and provides two different pressures, a higher one during inhalation and a lower pressure during exhalation. This system is more expensive, and is sometimes used with patients who have other coexisting respiratory problems and/or who find breathing out against an increased pressure to be uncomfortable or disruptive to their sleep.
• (Automatic positive airway pressure), or automatic positive airway pressure, is the newest form of such treatment. An APAP machine incorporates pressure sensors and a computer which continuously monitors the patient's breathing performance. It adjusts pressure continuously, increasing it when the user is attempting to breathe but cannot, and decreasing it when the pressure is higher than necessary. Although FDA approved, these devices are still considered experimental by many, and are not covered by most insurance plans.

A second type of physical intervention, a Mandibular advancement splint (MAS), is sometimes prescribed for mild or moderate sleep apnea sufferers. The device is a mouthguard similar to those used in sports to protect the teeth. For apnea patients, 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 for some patients.The FDA accepts only 16 oral appliances for the treatment of sleep apnea. A listing is available at their website

Oral appliance therapy is less effective than CPAP, but is more 'user friendly'. Side-effects are common, but rarely is the patient aware of them.

Pharmaceuticals There are no effective drug-based treatment for obstructive sleep apnea.

Oral administration of the methylxanthine theophylline (chemically similar to caffeine) can reduce the number of episodes of apnea, but can also produce side effects such as palpitations and insomnia. Theophylline is generally ineffective in adults with OSA, but is sometimes used to treat central sleep apnea (see below), and infants and children with apnea.

When other treatments do not completely treat the OSA, drugs are sometimes prescribed to treat a patient's daytime sleepiness or somnolence. These range from stimulants such as amfetamine to modern anti-narcolepsy medicines. The anti-narcoleptic modafinil is seeing increased use in this role as of 2004.

In most cases, weight loss will reduce the number and severity of apnea episodes. In the morbidly obese, a major loss of weight (such as what occurs after bariatric surgery) can sometimes cure the condition.

Neurostimulation {{update--> Many researchers believe that OSA is at root a neurological condition, in which nerves that control the tongue and soft palate fail to sufficiently stimulate those muscles, leading to over-relaxation and airway blockage. A few experiments and trial studies have explored the use of pacemakers and similar devices, programmed to detect breathing effort and deliver gentle electrical stimulation to the muscles of the tongue.

This is not a common mode of treatment for OSA patients as of 2004, but it is an active field of research.

Surgical intervention A number of different surgeries are available to improve the size or tone of a patient's airway. For decades, tracheostomy was the only effective treatment for sleep apnea. It is used today only in rare, intractable cases that have withstood other attempts at treatment. Modern operations employ one or more of several options, tailored to each patient's needs. Long term success rates are low, resulting in most doctors favoring CPAP.

• Nasal surgery, including turbinectomy (removal or reduction of a nasal turbinate), or straightening of the nasal septum, in patients with nasal obstruction or congestion which reduces airway pressure and complicates OSA.
• Tonsilectomy and/or adenoidectomy in an attempt to increase the size of the airway.
• Removal or reduction of parts of the soft palate and some or all of the uvula, such as uvulopalatopharyngoplasty (UPPP) or laser-assisted uvulopalatoplasty (LAUP). Modern variants of this procedure sometimes use radiofrequency waves to heat and remove tissue.
• Reduction of the tongue base, either with laser excision or radiofrequency ablation.
• Genioglossus Advancement, in which a small portion of the lower jaw that attaches to the tongue is moved forward, to pull the tongue away from the back of the airway.
• Hyoid Suspension, in which the hyoid bone in the neck, another attachment point for tongue muscles, is pulled forward in front of the larynx.
• Maxillomandibular advancement (MMA). A more invasive surgery usually only tried in difficult cases where other surgeries have not relieved the patient's OSA, or where an abnormal facial structure is suspected as a root cause. In MMA, the patient's upper and lower jaw are detached from the skull, moved forward, and reattached with pins and/or plates.
  • Pillar procedure, three small inserts are injected into the soft palate to offer support, potentially reducing snoring in mild to moderate sleep apnea.
  
  
  Special situation: surgery and anesthesia in patients with sleep apnea syndrome Many drugs and agents used during surgery to relieve pain and depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing.
  
  Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.
  
  Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction - swelling may negate some of the effects in the immediate postoperative period.
  
  Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons.
  
  Alternative treatments Breathing exercises, such as those used in Yoga, the Buteyko method, or didgeridoo playing can be effective. There are muscles which act to tension and open the airway during each inspiration. Exercises can, in some cases, restore sufficient function to these muscles to prevent or reduce apnea.
  
  Central sleep apnea In pure central sleep apnea or Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors it do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing, and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.
  
  While sleeping, a normal individual is "at rest", as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe. In central sleep apnea, the basic neurological controls for breathing rate malfunctions and fails to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (Hypoxia (medical)) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live; and, if the level of blood oxygen goes low enough for long enough, the terrible consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is, and the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.
  
  In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs due to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brains' mandate for the body to breathe. Even in severe cases of central sleep apnea, the effects almost always result in pauses that make breathing irregular, rather than cause the total cessation of breathing.
  • Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gasses with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. How do the changing blood levels of oxygen and carbon dioxide result in a breath? In any healthy animal, including humans, oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx (so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and Diaphragm (anatomy). These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it. The body inhales.
  • Physiologic effects of central apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures- even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications. In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction).With longstanding recurrent episodes of apnea, over months and years, increases in carbon dioxide levels may change the pH of the blood enough to cause a metabolic acidosis.
  
  
  Laboratory findings {| class="wikitable" align="right" style="margin: 1em 1em "! AHI||Rating|-| 30||Severe|}
  
  Polysomnography of sleep apnea shows pauses in breathing that are followed by drops in blood oxygen and increases in blood carbon dioxide. In adults, a pause must last 10 seconds to be scored as an apnea. However in young children, who normally breathe at a much faster rate than adults, the pause may be many seconds shorter and still be considered apnea. The cessation of airflow in central sleep apnea has an association with no physical attempts to breathe. On polysomnograms, there is an absence of rib cage and abdominal movements while airflow ceases at the nose and lips. Obstructive sleep apnea show pauses in breathing for at least 10 seconds causing a decrease in blood oxygen and associates with physical attempts to breathe.
  
  Hypopneas in adults are defined as a 50% reduction in air flow for more than 10 s, followed by a 4% desaturation, and/or arousal. The Apnea- Hypopnea Index (AHI) is expressed as the number of apneas and hypopneas per hour of sleep.
  
  Clinical details Any individual, no matter how healthy, who is given enough of a central respiratory depressant drug will develop apnea on a central basis. Generally, drugs that are respiratory depression also have sedation effects, and so the individual taking a toxic dose of such a drug is likely to be asleep, or at least in an altered state of consciousness, when breathing becomes irregular. Alcohol is such a central respiratory depressant in large doses, so are opioid, barbiturates, benzodiazepines, and many other tranquilizers. Some individuals have abnormalities that predispose them to central sleep apnea. The treatment for the condition depends on its specific cause.
  
  Similarly, in any person who has some form of sleep apnea (including obstructive sleep apnea), breathing irregularities during sleep can be dangerously aggravated by taking one of these drugs. Quantities that are normally considered safe may cause the person with chronic sleep apnea to stop breathing altogether. Should these individuals have general anesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea is likely to occur with even low levels of the drugs in their system.
  
  Premature infants with immature brains and reflex systems are at high risk for central sleep apnea syndrome, even if these babies are otherwise healthy. Fortunately, those premature babies who have the syndrome will generally outgrow it as they mature, providing they receive careful enough monitoring and supportive care during infancy to survive. Because of the propensity toward apnea, medications that can cause respiratory drive depression are either not given to premature infants, or given under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia. Caffeine has been found to help reduce apnea in preterm infants and to aid in care after general anesthesia.Henderson-Smart DJ. Steer P. Prophylactic caffeine to prevent postoperative apnea following general anesthesia in preterm infants. of Cochrane Database Syst Rev. 2000;(2):CD000048; PMID: 10796287. refs Article. Review Cochrane Database of Systematic Reviews. (4):CD000048, 2001.
  
  Sudden infant death syndrome is sometimes theorized to be attributable to sleep apnea.
  
  Congenital Central Hypoventilation Syndrome: This rare, inborn condition involves a specific gene, PHOX2B. This homeobox gene guides maturation of the autonomic nervous system, and loss-of-function mutations lead to the failure of the brain to effectively control breathing during sleep in patients with the syndrome. There may be a pattern of recognizable facial features among individuals affected with this 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 {{cite web|url=http://www.thoracic.org/sections/publications/press-releases/conference/articles/2007/press-releases/sleep-apnea-increases-risk-of-heart-attack-or-death-by-30.html |title=Sleep Apnea Increases Risk of Heart Attack or Death by 30% |last=N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, CT |date=May 20, 2007 |work=American Thoracic Society -->.
  
  Notes References
  • Sher, A. (1990). Obstructive sleep apnea syndrome: a complex disorder of the upper airway. Otolaryngologic Clinics of North America, 24, 600.
  
  
  External links
  • American Sleep Apnea Association
  • Sleep Apnea: Symptoms, Causes, Diagnosis, and Treatment
  • Mayo Clinic Discovers New Type of Sleep Apnea, Mayo Clinic, September 1, 2006.
  • Your Guide To Healthy Sleep, National Heart, Lung, and Blood Institute
  • Non-profit Sleep Apnea Studies forum
  • Apnea Board - non-profit Sleep Apnea info site & forum
  • Sleep Apnea The Merck Manual
  
  
  {{Infobox_Disease | Name = {{PAGENAME--> | Image = | Caption = | DiseasesDB = | ICD10 = {{ICD10|G|47|3|g|40--> | ICD9 = {{ICD9|780.5--> pre-diagnosis, {{ICD9|327.23--> confirmed diagnosis | ICDO = | OMIM = | MedlinePlus = | eMedicineSubj = ped | eMedicineTopic = 2114 | MeshID = D012891 | -->
  
  Sleep apnea, sleep apnoea or sleep apnœa is a sleep disorder characterized by pauses in breathing during sleep. These episodes, called apneas (literally, "without breath"), each last long enough so one or more breaths are missed, and occur repeatedly throughout sleep. The standard definition of any apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal (3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2), or a blood oxygen desaturation of 3-4 percent or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram.
  
  Clinically significant levels of sleep apnea are defined as 5 or more events of any type per hour of sleep time (from the polysomnogram). There are two distinct forms of sleep apnea: Central and Obstructive. Breathing is interrupted by the lack of effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite effort. In mixed sleep apnea, there is a transition from central to obstructive features during the events themselves.
  
  Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years, even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. 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., but efforts to breathe are not only present, they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.
  
  Obstructive sleep apnea is the most common category of sleep-disordered breathing. The prevalence of OSA among the adult population in western Europe and North America has not been confidently established, but in the mid-1990s was estimated to be 3-4% of women and 6-7% of men.
  
  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 (American Academy of Sleep Medicine Task Force, 1999). 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 may be adequate and easier to obtain than formal polysomnography. High probability patients were indentified by Epworth Sleepiness Scale (ESS) of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater.
  
  Populations at risk 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 obstructive sleep apnea. Men, whose anatomy is typified by increased body mass in the torso and neck, are more typical sleep apnea sufferers, especially through middle age and older. Adult women suffer typically less frequently and to a lesser degree than men do, owing partially to physiology, but possibly to emerging links to levels of progesterone. Prevalence in post-menopausal women approaches that of men in the same age range.
  
  Adults In adults, the most typical individual with obstructive sleep apnea syndrome is obese, with particular heaviness at the face and neck. The hallmark symptom of obstructive sleep apnea syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing obstructive sleep apnea 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.
  
  Children Although this so called "hyper-somnolence" (excessive sleepiness) may also occur in children, it is not at all typical of younger children with sleep apnea. Toddlers and young children with severe obstructive sleep apnea instead ordinarily behave as if "over-tired" or "hyper". Adults and children with very severe obstructive sleep apnea 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 high enough so 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. Obstructive sleep apnea in children, unlike adults, is almost always caused by obstructive tonsils and adenoids and is usually cured with tonsillectomy and adenoidectomy.
  
  This problem can also be caused by excessive weight. The symptoms are more like the symptoms adults feel; restlessness, exhaustion, and more.
  
  Common signs and symptoms (The signs and symptoms that follow apply to both adults and children suffering with sleep apnea)
  
  Additional signs of obstructive sleep apnea include restless sleep, and loud snoring (with periods of silence followed by gasps). Other symptoms are non-specific: morning headaches, trouble concentrating, irritability, forgetfulness, mood or behavior changes, decreased sex drive, increased heart rate, anxiety, depression (mood), increased frequency of urination, nocturia (getting up during the night to urinate), Gastroesophageal reflux disease and heavy sweating at night.
  
  The most serious consequence of 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).
  
  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 obstructive sleep apnea 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 in 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 (de Miguel-Díez, et al 2003), and some physicians advocate routine testing of this group (Shott, et al 2006).
  
  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 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.
  
  Pharyngeal flap surgery may cause obstructive sleep apnea Obstructive sleep apnea is a serious complication that seems to be most frequently associated with pharyngeal flap surgery, compared to other procedures for treatment of velopharyngeal inadequacy (VPI).Sloan, G.M. (2000). Posterior pharyngeal flap and sphincter pharyngoplasty: The state of the art. Cleft Palate-Craniofacial Journal, 37(2), 112-122. In OSA, recurrent interruptions of Respiration (physiology) 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 (physiology).Pugh, M.B. et al. (2000). Apnea. Stedman’s Medical Dictionary (27th ed.) Retrieved June 18, 2006 from STAT!Ref Online Medical Library database.Liao, Y., Noordhoff, M.S., Huang, C., Chen, P.K.T., Chen N., Yun, C. et al. (2004). Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency. Cleft Palate-Craniofacial Journal, 41(2), 152-156. There have been documented instances of severe airway obstruction, and reports of post-operative OSA continue to increase as healthcare professionals (i.e. physicians, speech language pathologists) become more educated about this possible dangerous condition.Peterson-Falzone, S.J., Hardin-Jones, M.A., & Karnell, M.P. (2001). Cleft Palate Speech (3rd ed.). St. Louis: Mosby. 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 at the nose, and asking the subject to say "P". This p sound, a plosive, is normally produced with the nasal airway closed 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 obstructive sleep apnea syndrome in susceptible individuals, particularly in the days following surgery, when swelling occurs (see below: Special Situation: Anesthesia and Surgery)
  
  {| class="wikitable" align="right" style="margin: 1em 1em "! AHI||Rating|-| 30||Severe|}
  
  Treatment There are a variety of treatments for obstructive sleep apnea, depending on an individual’s medical history, the severity of the disorder and, most importantly, the specific cause of the obstruction.
  
  In acute infectious mononucleosis, for example, although the airway may be severely obstructed in the first 2 weeks of the illness, the presence of lymphoid tissue (suddenly enlarged tonsils and adenoids) blocking the throat is usually only temporary. A course of anti-inflammatory steroids such as prednisone (or another kind of glucocorticoid drug) is often given to reduce this lymphoid tissue. Although the effects of the steroids are short term, in most affected individuals, the tonsillar and adenoidal enlargement are also short term, and will be reduced on its own by the time a brief course of steroids is completed. In unusual cases where the enlarged lymphoid tissue persists after resolution of the acute stage of the Epstein-Barr infection, or in which medical treatment with anti-inflammatory steroids does not adequately relieve breathing, tonsillectomy and adenoidectomy may be urgently required.
  
  Most children with obstructive sleep apnea have the problem on the basis of chronically enlarged tonsils and adenoids. In these children, tonsillectomy and adenoidectomy is curative. The operation may be far from trivial, however, in the worst cases, in which growth is reduced and abnormalities of the right heart may have developed. Even in these extreme cases, however, the surgery tends to cure not only the apnea and upper airway obstruction - but to allow subsequent normal 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).
  
  The treatment for obstructive sleep apnea in the case of adults with poor oropharyngeal airways secondary to heavy upper body type is varied. Unfortunately, in this most common type of obstructive sleep apnea, unlike some of the cases discussed above, reliable cures are not the rule.
  
  Some treatments involve lifestyle changes, such as avoiding alcohol and medications that relax the central nervous system (for example, sedatives and muscle relaxants), losing weight, and quitting smoking. Some people are helped by special pillows or devices that keep them from sleeping on their backs, or oral appliances to keep the airway open during sleep. If these conservative methods are inadequate, doctors often recommend continuous positive airway pressure (CPAP), in which a face mask is attached to a tube and a machine that blows pressurized air into the mask and through the airway to keep it open. There are also surgical procedures that can be used to remove and tighten tissue and widen the airway, but the success rate is not high. Some individuals may need a combination of therapies to successfully treat their sleep apnea.
  
  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 splints or holds open the relaxed muscles, just as air in a balloon inflates it. There are several variants:
  • (Continuous positive airway pressure), or continuous positive airway pressure, in which a controlled air compressor generates an airstream at a constant pressure. This pressure is prescribed by the patient's physician, based on an overnight test or titration. Newer CPAP models are available which slightly reduce pressure upon exhalation to increase patient comfort and compliance. CPAP is the most common treatment for obstructive sleep apnea.
  • (VPAP), or variable positive airway pressure, also known as bilevel or BiPAP, uses an electronic circuit to monitor the patient's breathing, and provides two different pressures, a higher one during inhalation and a lower pressure during exhalation. This system is more expensive, and is sometimes used with patients who have other coexisting respiratory problems and/or who find breathing out against an increased pressure to be uncomfortable or disruptive to their sleep.
  • (Automatic positive airway pressure), or automatic positive airway pressure, is the newest form of such treatment. An APAP machine incorporates pressure sensors and a computer which continuously monitors the patient's breathing performance. It adjusts pressure continuously, increasing it when the user is attempting to breathe but cannot, and decreasing it when the pressure is higher than necessary. Although FDA approved, these devices are still considered experimental by many, and are not covered by most insurance plans.
  
  
  A second type of physical intervention, a Mandibular advancement splint (MAS), is sometimes prescribed for mild or moderate sleep apnea sufferers. The device is a mouthguard similar to those used in sports to protect the teeth. For apnea patients, 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 for some patients.The FDA accepts only 16 oral appliances for the treatment of sleep apnea. A listing is available at their website
  
  Oral appliance therapy is less effective than CPAP, but is more 'user friendly'. Side-effects are common, but rarely is the patient aware of them.
  
  Pharmaceuticals There are no effective drug-based treatment for obstructive sleep apnea.
  
  Oral administration of the methylxanthine theophylline (chemically similar to caffeine) can reduce the number of episodes of apnea, but can also produce side effects such as palpitations and insomnia. Theophylline is generally ineffective in adults with OSA, but is sometimes used to treat central sleep apnea (see below), and infants and children with apnea.
  
  When other treatments do not completely treat the OSA, drugs are sometimes prescribed to treat a patient's daytime sleepiness or somnolence. These range from stimulants such as amfetamine to modern anti-narcolepsy medicines. The anti-narcoleptic modafinil is seeing increased use in this role as of 2004.
  
  In most cases, weight loss will reduce the number and severity of apnea episodes. In the morbidly obese, a major loss of weight (such as what occurs after bariatric surgery) can sometimes cure the condition.
  
  Neurostimulation {{update--> Many researchers believe that OSA is at root a neurological condition, in which nerves that control the tongue and soft palate fail to sufficiently stimulate those muscles, leading to over-relaxation and airway blockage. A few experiments and trial studies have explored the use of pacemakers and similar devices, programmed to detect breathing effort and deliver gentle electrical stimulation to the muscles of the tongue.
  
  This is not a common mode of treatment for OSA patients as of 2004, but it is an active field of research.
  
  Surgical intervention A number of different surgeries are available to improve the size or tone of a patient's airway. For decades, tracheostomy was the only effective treatment for sleep apnea. It is used today only in rare, intractable cases that have withstood other attempts at treatment. Modern operations employ one or more of several options, tailored to each patient's needs. Long term success rates are low, resulting in most doctors favoring CPAP.
  • Nasal surgery, including turbinectomy (removal or reduction of a nasal turbinate), or straightening of the nasal septum, in patients with nasal obstruction or congestion which reduces airway pressure and complicates OSA.
  • Tonsilectomy and/or adenoidectomy in an attempt to increase the size of the airway.
  • Removal or reduction of parts of the soft palate and some or all of the uvula, such as uvulopalatopharyngoplasty (UPPP) or laser-assisted uvulopalatoplasty (LAUP). Modern variants of this procedure sometimes use radiofrequency waves to heat and remove tissue.
  • Reduction of the tongue base, either with laser excision or radiofrequency ablation.
  • Genioglossus Advancement, in which a small portion of the lower jaw that attaches to the tongue is moved forward, to pull the tongue away from the back of the airway.
  • Hyoid Suspension, in which the hyoid bone in the neck, another attachment point for tongue muscles, is pulled forward in front of the larynx.
  • Maxillomandibular advancement (MMA). A more invasive surgery usually only tried in difficult cases where other surgeries have not relieved the patient's OSA, or where an abnormal facial structure is suspected as a root cause. In MMA, the patient's upper and lower jaw are detached from the skull, moved forward, and reattached with pins and/or plates.
    • Pillar procedure, three small inserts are injected into the soft palate to offer support, potentially reducing snoring in mild to moderate sleep apnea.
    
    
    Special situation: surgery and anesthesia in patients with sleep apnea syndrome Many drugs and agents used during surgery to relieve pain and depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing.
    
    Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.
    
    Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction - swelling may negate some of the effects in the immediate postoperative period.
    
    Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons.
    
    Alternative treatments Breathing exercises, such as those used in Yoga, the Buteyko method, or didgeridoo playing can be effective. There are muscles which act to tension and open the airway during each inspiration. Exercises can, in some cases, restore sufficient function to these muscles to prevent or reduce apnea.
    
    Central sleep apnea In pure central sleep apnea or Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors it do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and hyperpnea, even during wakefulness. The sleeper stops breathing, and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.
    
    While sleeping, a normal individual is "at rest", as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe. In central sleep apnea, the basic neurological controls for breathing rate malfunctions and fails to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation will drop to a lower than normal level (Hypoxia (medical)) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live; and, if the level of blood oxygen goes low enough for long enough, the terrible consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is, and the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.
    
    In any person, hypoxia and hypercapnia have certain common effects on the body. The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs due to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brains' mandate for the body to breathe. Even in severe cases of central sleep apnea, the effects almost always result in pauses that make breathing irregular, rather than cause the total cessation of breathing.
    • Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gasses with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. How do the changing blood levels of oxygen and carbon dioxide result in a breath? In any healthy animal, including humans, oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx (so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and Diaphragm (anatomy). These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it. The body inhales.
    • Physiologic effects of central apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures- even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications. In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction).With longstanding recurrent episodes of apnea, over months and years, increases in carbon dioxide levels may change the pH of the blood enough to cause a metabolic acidosis.
    
    
    Laboratory findings {| class="wikitable" align="right" style="margin: 1em 1em "! AHI||Rating|-| 30||Severe|}
    
    Polysomnography of sleep apnea shows pauses in breathing that are followed by drops in blood oxygen and increases in blood carbon dioxide. In adults, a pause must last 10 seconds to be scored as an apnea. However in young children, who normally breathe at a much faster rate than adults, the pause may be many seconds shorter and still be considered apnea. The cessation of airflow in central sleep apnea has an association with no physical attempts to breathe. On polysomnograms, there is an absence of rib cage and abdominal movements while airflow ceases at the nose and lips. Obstructive sleep apnea show pauses in breathing for at least 10 seconds causing a decrease in blood oxygen and associates with physical attempts to breathe.
    
    Hypopneas in adults are defined as a 50% reduction in air flow for more than 10 s, followed by a 4% desaturation, and/or arousal. The Apnea- Hypopnea Index (AHI) is expressed as the number of apneas and hypopneas per hour of sleep.
    
    Clinical details Any individual, no matter how healthy, who is given enough of a central respiratory depressant drug will develop apnea on a central basis. Generally, drugs that are respiratory depression also have sedation effects, and so the individual taking a toxic dose of such a drug is likely to be asleep, or at least in an altered state of consciousness, when breathing becomes irregular. Alcohol is such a central respiratory depressant in large doses, so are opioid, barbiturates, benzodiazepines, and many other tranquilizers. Some individuals have abnormalities that predispose them to central sleep apnea. The treatment for the condition depends on its specific cause.
    
    Similarly, in any person who has some form of sleep apnea (including obstructive sleep apnea), breathing irregularities during sleep can be dangerously aggravated by taking one of these drugs. Quantities that are normally considered safe may cause the person with chronic sleep apnea to stop breathing altogether. Should these individuals have general anesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea is likely to occur with even low levels of the drugs in their system.
    
    Premature infants with immature brains and reflex systems are at high risk for central sleep apnea syndrome, even if these babies are otherwise healthy. Fortunately, those premature babies who have the syndrome will generally outgrow it as they mature, providing they receive careful enough monitoring and supportive care during infancy to survive. Because of the propensity toward apnea, medications that can cause respiratory drive depression are either not given to premature infants, or given under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia. Caffeine has been found to help reduce apnea in preterm infants and to aid in care after general anesthesia.Henderson-Smart DJ. Steer P. Prophylactic caffeine to prevent postoperative apnea following general anesthesia in preterm infants. of Cochrane Database Syst Rev. 2000;(2):CD000048; PMID: 10796287. refs Article. Review Cochrane Database of Systematic Reviews. (4):CD000048, 2001.
    
    Sudden infant death syndrome is sometimes theorized to be attributable to sleep apnea.
    
    Congenital Central Hypoventilation Syndrome: This rare, inborn condition involves a specific gene, PHOX2B. This homeobox gene guides maturation of the autonomic nervous system, and loss-of-function mutations lead to the failure of the brain to effectively control breathing during sleep in patients with the syndrome. There may be a pattern of recognizable facial features among individuals affected with this 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 {{cite web|url=http://www.thoracic.org/sections/publications/press-releases/conference/articles/2007/press-releases/sleep-apnea-increases-risk-of-heart-attack-or-death-by-30.html |title=Sleep Apnea Increases Risk of Heart Attack or Death by 30% |last=N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, CT |date=May 20, 2007 |work=American Thoracic Society -->.
    
    Notes References
    • Sher, A. (1990). Obstructive sleep apnea syndrome: a complex disorder of the upper airway. Otolaryngologic Clinics of North America, 24, 600.
    
    
    External links
    • American Sleep Apnea Association
    • Sleep Apnea: Symptoms, Causes, Diagnosis, and Treatment
    • Mayo Clinic Discovers New Type of Sleep Apnea, Mayo Clinic, September 1, 2006.
    • Your Guide To Healthy Sleep, National Heart, Lung, and Blood Institute
    • Non-profit Sleep Apnea Studies forum
    • Apnea Board - non-profit Sleep Apnea info site & forum
    • Sleep Apnea The Merck Manual