Sleep apnea

Sleep apnea is a sleep-related breathing disorder in which repetitive pauses in breathing, periods of shallow breathing, or collapse of the upper airway during sleep results in poor ventilation and sleep disruption.^[10][11] Each pause in breathing can last for a few seconds to a few minutes and occurs many times a night.^[1] A choking or snorting sound may occur as breathing resumes.^[1] Common symptoms include daytime sleepiness, snoring, and non restorative sleep despite adequate sleep time.^[12] Because the disorder disrupts normal sleep, those affected may experience sleepiness or feel tired during the day.^[1] It is often a chronic condition.^[13]

Sleep apnea may be categorized as

Some people with sleep apnea are unaware they have the condition.[1] In many cases it is first observed by a family member.^[1] An in-lab sleep study overnight is the preferred method for diagnosing sleep apnea.^[15] In the case of OSA, the outcome that determines disease severity and guides the treatment plan is the apnea-hypopnea index (AHI).^[15] This measurement is calculated from totaling all pauses in breathing and periods of shallow breathing lasting greater than 10 seconds and dividing the sum by total hours of recorded sleep.^[10][15] In contrast, for CSA the degree of respiratory effort, measured by esophageal pressure or displacement of the thoracic or abdominal cavity, is an important distinguishing factor between OSA and CSA.^[18]

A systemic disorder, sleep apnea is associated with a wide array of effects, including increased risk of

The typical screening process for sleep apnea involves asking patients about common symptoms such as snoring, witnessed pauses in breathing during sleep and excessive daytime sleepiness.^[19] There is a wide range in presenting symptoms in patients with sleep apnea, from being asymptomatic to falling asleep while driving.^[19] Due to this wide range in clinical presentation, some people are not aware that they have sleep apnea and are either misdiagnosed or ignore the symptoms altogether.^[29] A current area requiring further study involves identifying different subtypes of sleep apnea based on patients who tend to present with different clusters or groupings of particular symptoms.^[19]

OSA may increase risk for driving accidents and work-related accidents due to sleep fragmentation from repeated arousals during sleep.^[19] If OSA is not treated it results in excessive daytime sleepiness and oxidative stress from the repeated drops in oxygen saturation, people are at increased risk of other systemic health problems, such as diabetes, hypertension or cardiovascular disease.^[19] Subtle manifestations of sleep apnea may include treatment refractory hypertension and cardiac arrhythmias and over time as the disease progresses, more obvious symptoms may become apparent.^[12] Due to the disruption in daytime cognitive state, behavioral effects may be present. These can include moodiness, belligerence, as well as a decrease in attentiveness and energy.^[30] These effects may become intractable, leading to depression.^[31]

Risk factors

Obstructive sleep apnea can affect people regardless of sex, race, or age.^[32] However, risk factors include:^[33]

• male gender^[33][34]
• obesity^[33][34]
• age over 40^[33]
• large neck circumference^[33]
• enlarged tonsils or tongue^[33]
• narrow upper jaw^[15]
• small lower jaw^[34]
• tongue fat/tongue scalloping^[15]
• a family history of sleep apnea^[33]
• endocrine disorders^[33] such as hypothyroidism^[34]
• lifestyle habits such as smoking or drinking alcohol^[33]

Central sleep apnea is more often associated with any of the following risk factors:^[18]

• transition period from wakefulness to non-REM sleep^[18]
• male gender^[18]
• older age^[18]
• heart failure^[18]
• atrial fibrillation^[18]
• stroke^[18]
• spinal cord injury^[18]

Mechanism

Obstructive sleep apnea

The causes of obstructive sleep apnea are complex and individualized, but typical risk factors include narrow pharyngeal anatomy and craniofacial structure.

There are two main mechanism that drive the disease process of CSA, sleep-related hypoventilation and post-hyperventilation hypocapnia.[18] The most common cause of CSA is post-hyperventilation hypocapnia secondary to heart failure.^[18] This occurs because of brief failures of the ventilatory control system but normal alveolar ventilation.^[18] In contrast, sleep-related hypoventilation occurs when there is a malfunction of the brain's drive to breathe.^[18] The underlying cause of the loss of the wakefulness drive to breathe encompasses a broad set of diseases from strokes to severe kyphoscoliosis.^[18]

Complications

OSA is a serious medical condition with systemic effects; patients with untreated OSA have a greater mortality risk from cardiovascular disease than those undergoing appropriate treatment.^[37] Other complications include hypertension, congestive heart failure, atrial fibrillation, coronary artery disease, stroke, and type 2 diabetes.^[37] Daytime fatigue and sleepiness, a common symptom of sleep apnea, is also an important public health concern regarding transportation crashes caused by drowsiness.^[37] OSA may also be a risk factor of COVID-19. People with OSA have a higher risk of developing severe complications of COVID-19.^[38]

There are three types of sleep apnea. OSA accounts for 84%, CSA for 0.9%, and 15% of cases are mixed.[46]

Obstructive sleep apnea

In a systematic review of published evidence, the United States Preventive Services Task Force in 2017 concluded that there was uncertainty about the accuracy or clinical utility of all potential screening tools for OSA,^[47] and recommended that evidence is insufficient to assess the balance of benefits and harms of screening for OSA in asymptomatic adults.^[48]

The diagnosis of OSA syndrome is made when the patient shows recurrent episodes of partial or complete collapse of the upper airway during sleep resulting in apneas or hypopneas, respectively.^[49] Criteria defining an apnea or a hypopnea vary. The American Academy of Sleep Medicine (AASM) defines an apnea as a reduction in airflow of ≥ 90% lasting at least 10 seconds. A hypopnea is defined as a reduction in airflow of ≥ 30% lasting at least 10 seconds and associated with a ≥ 4% decrease in pulse oxygenation, or as a ≥ 30% reduction in airflow lasting at least 10 seconds and associated either with a ≥ 3% decrease in pulse oxygenation or with an arousal.^[50]

To define the severity of the condition, the Apnea-Hypopnea Index (AHI) or the Respiratory Disturbance Index (RDI) are used. While the AHI measures the mean number of apneas and hypopneas per hour of sleep, the RDI adds to this measure the respiratory effort-related arousals (RERAs).^[51] The OSA syndrome is thus diagnosed if the AHI is > 5 episodes per hour and results in daytime sleepiness and fatigue or when the RDI is ≥ 15 independently of the symptoms.^[52] According to the American Association of Sleep Medicine, daytime sleepiness is determined as mild, moderate and severe depending on its impact on social life. Daytime sleepiness can be assessed with the Epworth Sleepiness Scale (ESS), a self-reported questionnaire on the propensity to fall asleep or doze off during daytime.^[53] Screening tools for OSA itself comprise the STOP questionnaire, the Berlin questionnaire and the STOP-BANG questionnaire which has been reported as being a very powerful tool to detect OSA.^[54][55]

Criteria

According to the International Classification of Sleep Disorders, there are 4 types of criteria. The first one concerns sleep – excessive sleepiness, nonrestorative sleep, fatigue or insomnia symptoms. The second and third criteria are about respiration – waking with breath holding, gasping, or choking; snoring, breathing interruptions or both during sleep. The last criterion revolved around medical issues as hypertension, coronary artery disease, stroke, heart failure, atrial fibrillation, type 2 diabetes mellitus, mood disorder or cognitive impairment. Two levels of severity are distinguished, the first one is determined by a polysomnography or home sleep apnea test demonstrating 5 or more predominantly obstructive respiratory events per hour of sleep and the higher levels are determined by 15 or more events. If the events are present less than 5 times per hour, no obstructive sleep apnea is diagnosed.^[56]

A considerable night-to-night variability further complicates diagnosis of OSA. In unclear cases, multiple testing might be required to achieve an accurate diagnosis.^[57]

Polysomnography

Nighttime in-laboratory Level 1 polysomnography (PSG) is the gold standard test for diagnosis. Patients are monitored with EEG leads, pulse oximetry, temperature and pressure sensors to detect nasal and oral airflow, respiratory impedance plethysmography or similar resistance belts around the chest and abdomen to detect motion, an ECG lead, and EMG sensors to detect muscle contraction in the chin, chest, and legs. A hypopnea can be based on one of two criteria. It can either be a reduction in airflow of at least 30% for more than 10 seconds associated with at least 4% oxygen desaturation or a reduction in airflow of at least 30% for more than 10 seconds associated with at least 3% oxygen desaturation or an arousal from sleep on EEG.^[58]

An "event" can be either an apnea, characterized by complete cessation of airflow for at least 10 seconds, or a

Home oximetry

In patients who are at high likelihood of having OSA, a

The diagnosis of CSA syndrome is made when the presence of at least 5 central apnea events occur per hour.^[11] There are multiple mechanisms that drive the apnea events. In individuals with heart failure with Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep.^[62] This results in ventilatory instability, caused by chemoreceptors that are hyperresponsive to CO2 fluctuations in the blood, resulting in high respiratory drive that leads to apnea.^[11] Another common mechanism that causes CSA is the loss of the brain's wakefulness drive to breathe.^[11]

CSA is organized into 6 individual syndromes: Cheyne-Stokes respiration, Complex sleep apnea, Primary CSA, High altitude periodic breathing, CSA from medication, CSA from comorbidity.^[11] Like in OSA, nocturnal polysomnography is the mainstay of diagnosis for CSA.^[18] The degree of respiratory effort, measured by esophageal pressure or displacement of the thoracic or abdominal cavity, is an important distinguishing factor between OSA and CSA.^[18]

Mixed apnea

Some people with sleep apnea have a combination of both types; its prevalence ranges from 0.56% to 18%. The condition, also called treatment-emergent central apnea, is generally detected when obstructive sleep apnea is treated with CPAP and central sleep apnea emerges.^[18] The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most likely related to incorrect settings of the CPAP treatment and other medical conditions the person has.^[63]

Management

The treatment of obstructive sleep apnea is different than that of central sleep apnea. Treatment often starts with behavioral therapy and some people may be suggested to try a continuous positive airway pressure device. Many people are told to avoid alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night.^[64] The evidence supporting one treatment option compared to another for a particular person is not clear.^[65]

Changing sleep position

More than half of people with obstructive sleep apnea have some degree of positional obstructive sleep apnea, meaning that it gets worse when they sleep on their backs.^[66] Sleeping on their sides is an effective and cost-effective treatment for positional obstructive sleep apnea.^[66]

Continuous positive airway pressure

For moderate to severe sleep apnea, the most common treatment is the use of a continuous positive airway pressure (CPAP) or automatic positive airway pressure (APAP) device.^[64][67] These splint the person's airway open during sleep by means of pressurized air. The person typically wears a plastic facial mask, which is connected by a flexible tube to a small bedside CPAP machine.^[64]

Although CPAP therapy is effective in reducing apneas and less expensive than other treatments, some people find it uncomfortable. Some complain of feeling trapped, having chest discomfort, and skin or nose irritation. Other side effects may include dry mouth, dry nose, nosebleeds, sore lips and gums.^[68]

Whether or not it decreases the risk of death or heart disease is controversial with some reviews finding benefit and others not.^[22][69][65] This variation across studies might be driven by low rates of compliance—analyses of those who use CPAP for at least four hours a night suggests a decrease in cardiovascular events.^[70]

Weight loss

Excess body weight is thought to be an important cause of sleep apnea.^[71] People who are overweight have more tissues in the back of their throat which can restrict the airway, especially when sleeping.^[72] In weight loss studies of overweight individuals, those who lose weight show reduced apnea frequencies and improved apnoea–hypopnoea index (AHI).^[71][73] Weight loss effective enough to relieve obesity hypoventilation syndrome (OHS) must be 25–30% of body weight. For some obese people, it can be difficult to achieve and maintain this result without bariatric surgery.^[74]

Rapid palatal expansion

In children, orthodontic treatment to expand the volume of the nasal airway, such as nonsurgical rapid palatal expansion is common. The procedure has been found to significantly decrease the AHI and lead to long-term resolution of clinical symptoms.^[75][76]

Since the palatal suture is fused in adults, regular RPE using tooth-borne expanders cannot be performed. Mini-implant assisted rapid palatal expansion (MARPE) has been recently developed as a non-surgical option for the transverse expansion of the maxilla in adults. This method increases the volume of the nasal cavity and nasopharynx, leading to increased airflow and reduced respiratory arousals during sleep.^[77][78] Changes are permanent with minimal complications.

Surgery

Several surgical procedures (sleep surgery) are used to treat sleep apnea, although they are normally a third line of treatment for those who reject or are not helped by CPAP treatment or dental appliances.^[22] Surgical treatment for obstructive sleep apnea needs to be individualized to address all anatomical areas of obstruction.^[10]

Nasal obstruction

Often, correction of the nasal passages needs to be performed in addition to correction of the

Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) are available to address pharyngeal obstruction.^[10]

The "Pillar" device is a treatment for snoring and obstructive sleep apnea; it is thin, narrow strips of polyester. Three strips are inserted into the roof of the mouth (the soft palate) using a modified syringe and local anesthetic, in order to stiffen the soft palate. This procedure addresses one of the most common causes of snoring and sleep apnea — vibration or collapse of the soft palate. It was approved by the FDA for snoring in 2002 and for obstructive sleep apnea in 2004. A 2013 meta-analysis found that "the Pillar implant has a moderate effect on snoring and mild-to-moderate obstructive sleep apnea" and that more studies with high level of evidence were needed to arrive at a definite conclusion; it also found that the polyester strips work their way out of the soft palate in about 10% of the people in whom they are implanted.^[81]

Hypopharyngeal or base of tongue obstruction

Base-of-tongue advancement by means of advancing the genial tubercle of the mandible, tongue suspension, or hyoid suspension (aka hyoid myotomy and suspension or hyoid advancement) may help with the lower pharynx.^[10]

Other surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat, procedures done at either a doctor's office or a hospital. Small shots or other treatments, sometimes in a series, are used for shrinkage, while the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues.^[64]

Multi-level surgery

Maxillomandibular advancement (MMA) is considered the most effective surgery for people with sleep apnea, because it increases the posterior airway space (PAS).^[82] However, health professionals are often unsure as to who should be referred for surgery and when to do so: some factors in referral may include failed use of CPAP or device use; anatomy which favors rather than impedes surgery; or significant craniofacial abnormalities which hinder device use.^[83]

Potential complications

Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to relieve pain and to 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 or collapses in a patient's airways.^[84] Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.^[10]

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. Once the swelling resolves and the palate becomes tightened by postoperative scarring, however, the full benefit of the surgery may be noticed.^[10]

A person with sleep apnea undergoing any medical treatment must make sure their doctor and anesthetist are informed about the sleep apnea. Alternative and emergency procedures may be necessary to maintain the airway of sleep apnea patients.^[85]

Other

Neurostimulation

Diaphragm pacing, which involves the rhythmic application of electrical impulses to the diaphragm, has been used to treat central sleep apnea.^[86][87]

In April 2014, the U.S. Food and Drug Administration granted pre-market approval for use of an upper airway stimulation system in people who cannot use a continuous positive airway pressure device. The Inspire Upper Airway Stimulation system senses respiration and applies mild electrical stimulation during inspiration, which pushes the tongue slightly forward to open the airway.^[88]

Medications

There is currently insufficient evidence to recommend any medication for OSA.^[89] This may result in part because people with sleep apnea have tended to be treated as a single group in clinical trials. Identifying specific physiological factors underlying sleep apnea makes it possible to test drugs specific to those causal factors: airway narrowing, impaired muscle activity, low arousal threshold for waking, and unstable breathing control.^[90][91] Those who experience low waking thresholds may benefit from eszopiclone, a sedative typically used to treat insomnia.^[90][92] The antidepressant desipramine may stimulate upper airway muscles and lessen pharyngeal collapsibility in people who have limited muscle function in their airways.^[90][93]

There is limited evidence for medication, but 2012 AASM guidelines suggested that acetazolamide "may be considered" for the treatment of central sleep apnea; zolpidem and triazolam may also be considered for the treatment of central sleep apnea,^[94] but "only if the patient does not have underlying risk factors for respiratory depression".^[89][67] Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects.^[95][96][97]

Oral appliances

An oral appliance, often referred to as a mandibular advancement splint, is a custom-made mouthpiece that shifts the lower jaw forward and opens the bite slightly, opening up the airway. These devices can be fabricated by a general dentist. Oral appliance therapy (OAT) is usually successful in patients with mild to moderate obstructive sleep apnea.^[98][99] While CPAP is more effective for sleep apnea than oral appliances, oral appliances do improve sleepiness and quality of life and are often better tolerated than CPAP.^[99]

Nasal EPAP

Nasal EPAP is a bandage-like device placed over the nostrils that uses a person's own breathing to create positive airway pressure to prevent obstructed breathing.^[100]

Oral pressure therapy

Oral pressure therapy uses a device that creates a vacuum in the mouth, pulling the soft palate tissue forward. It has been found useful in about 25 to 37% of people.^[101][102]

Prognosis

Death could occur from untreated OSA due to lack of oxygen to the body.^[68]

There is increasing evidence that sleep apnea may lead to liver function impairment, particularly

]

Epidemiology

The examples and perspective in this section may not represent a worldwide view of the subject. You may improve this section, discuss the issue on the talk page, or create a new section, as appropriate. (August 2016) (Learn how and when to remove this template message)

The Wisconsin Sleep Cohort Study estimated in 1993 that roughly one in every 15 Americans was affected by at least moderate sleep apnea.[110]^[111] It also estimated that in middle-age as many as 9% of women and 24% of men were affected, undiagnosed and untreated.^{[71][110][111]}

The costs of untreated sleep apnea reach further than just health issues. It is estimated that in the U.S., the average untreated sleep apnea patient's annual health care costs $1,336 more than an individual without sleep apnea. This may cause $3.4 billion/year in additional medical costs. Whether medical cost savings occur with treatment of sleep apnea remains to be determined.^[112]

Frequency and population

Sleep disorders including sleep apnea have become an important health issue in the United States. Twenty-two million Americans have been estimated to have sleep apnea, with 80% of moderate and severe OSA cases undiagnosed.^[113]

OSA can occur at any age, but it happens more frequently in men who are over 40 and overweight.^[113]

History

A type of CSA was described in the German

References