Obstructive night apnea

Obstructive sleep apnea (sleep apnea) involves episodes of partial and/or complete closure of the upper airway during sleep, resulting in cessation of breathing lasting more than 10 seconds. Symptoms of obstructive sleep apnea include fatigue, snoring, repeated awakenings, morning headache, and excessive daytime sleepiness. Diagnosis is based on sleep history, physical examination, and polysomnography.

Treatment of obstructive sleep apnea includes nasal continuous positive airway pressure, oral appliances, and, in resistant cases, surgery. The prognosis is good with treatment, but most cases go unrecognized and untreated, leading to hypertension, heart failure, injury, and death from motor vehicle crashes and other accidents due to excessive sleepiness.

In high-risk patients, sleep destabilizes the upper airway, causing partial or complete obstruction of the nasopharynx, oropharynx, or both. When breathing decreases but does not stop, the condition is called obstructive sleep hypopnea.

The prevalence of obstructive sleep apnea (OSA) in developed countries is 2-4%; the condition is often unrecognized and underdiagnosed even in symptomatic patients. OSA is up to 4 times more common in men, possibly because it is underdiagnosed in women, who may be more likely to refuse to report snoring symptoms, or because of gender bias against seeing a specialist.

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What causes obstructive sleep apnea?

Anatomical risk factors include obesity (body mass index > 30); an oropharynx “packed” with a short or retracted lower jaw and a large tongue, tonsils, lateral pharyngeal walls, or lateral parapharyngeal fat pads; a rounded head; and a shirt collar size greater than 18 inches. Other known risk factors include postmenopausal age and use of alcohol or sedatives. A family history of sleep apnea is present in 25% to 40% of cases, possibly resulting from the characteristic function of the respiratory center or pharyngeal structure; the likelihood of developing the disease progressively increases with the number of family members with the pathology. Obstructive sleep apnea is also frequently associated with chronic diseases such as hypertension, stroke, diabetes, gastroesophageal reflux disease, nocturnal angina, heart failure, and hypothyroidism.

Because obesity is a common risk factor for both obstructive sleep apnea and obesity-hypoventilation syndrome, the two conditions may coexist.

Airway obstruction causes paroxysms of inspiratory effort, decreased gas exchange, disruption of normal sleep architecture, and partial or complete arousals from sleep. Hypoxia and/or hypercapnia and sleep fragmentation interact to produce characteristic symptoms and signs.

Obstructive sleep apnea is an extreme form of airway resistance during sleep. Less severe forms do not result in O ₂ desaturation and include primary snoring, pharyngeal airflow resistance that causes noisy inspiration but no arousals, and upper airway resistance syndrome, which is more severe pharyngeal resistance that causes snoring and intermittent sleep disturbances. People with upper airway resistance syndrome tend to be younger and less obese than those with obstructive sleep apnea, and complain of daytime sleepiness more than people with primary snoring. However, the symptoms, diagnosis, and treatment of snoring and upper airway resistance syndrome are the same as those of obstructive sleep apnea.

Symptoms of Obstructive Sleep Apnea

Symptoms of obstructive sleep apnea include loud, intermittent snoring, which is reported by 80-85% of patients with obstructive sleep apnea. However, most people who snore do not have obstructive sleep apnea, and only a few require intensive evaluation. Other symptoms of obstructive sleep apnea include choking, gasping, or snorting during sleep, restless sleep, and inability to sleep uninterrupted. Most patients are not aware of their symptoms during sleep, but others who sleep in the same bed or room with them do. Daytime symptoms of obstructive sleep apnea include general weakness, increased sleepiness, and decreased alertness. The frequency of sleep complaints and the severity of daytime sleepiness roughly correlate with the number and duration of awakenings during the night. Arterial hypertension and diabetes mellitus are twice as common among people who snore, even after taking into account age and obesity. Obstructive sleep apnea may be associated with cardiac arrhythmias (e.g., bradycardia, asystole) and heart failure.

Diagnostic criteria for obstructive sleep apnea

• Excessive daytime sleepiness not explained by other factors, plus more than 2 of the following:
• Loud, heart-rending snore
• Night snorting, noisy sonorous sighs
• Frequent awakenings at night
• Sleep that does not bring a feeling of vigor
• Daytime fatigue
• Decreased alertness and sleep monitoring results documenting more than 5 hypopnea and apnea episodes per hour

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Diagnosis of obstructive sleep apnea

The diagnosis is suspected in patients with identifiable risk factors and/or symptoms. The patient and sleep partner should be interviewed. The differential diagnosis of excessive daytime sleepiness is broad and includes altered sleep quantity or quality due to poor sleep hygiene; narcolepsy; sedation or altered mental status due to medications; chronic medical conditions including cardiovascular, respiratory, or metabolic disorders and concomitant medications (eg, diuretics, insulin); depression; substance abuse; and other primary sleep disorders (eg, periodic limb movements, restless legs syndrome). A sleep history should be obtained in all elderly patients; in patients with symptoms of daytime fatigue, sleepiness, and lack of energy; in overweight or obese patients and in patients with chronic medical conditions such as hypertension (which can be caused by obstructive sleep apnea), heart failure (which can cause and be caused by obstructive sleep apnea), and stroke. Most patients who complain only of snoring, without other symptoms or cardiovascular risk, probably do not need extensive workup for obstructive sleep apnea.

Physical examination should include evaluation for nasal obstruction, tonsillar hypertrophy, signs of inadequately controlled hypertension, and neck measurements.

The diagnosis is confirmed by a polysomnographic study, which includes a simultaneous study of respiratory effort using plethysmography; airflow in the nasal and oral cavities using flow sensors; O ₂ saturation using oximetry; sleep architecture using EEG (to determine sleep stages), electromyography of the chin (to detect hypotonia), and electrooculograms to record rapid eye movements. In addition, the patient is observed using a video camera. ECG is necessary to determine the presence of arrhythmia episodes with apnea episodes. Other diagnostic approaches include examination of muscle activity of the limbs (to identify non-respiratory causes of arousal from sleep, such as restless legs syndrome and periodic limb movement disorder syndrome) and body position (asphyxia may occur only in the supine position).

Some studies use portable monitors that measure only heart rate, pulse oximetry, and nasal airflow to diagnose obstructive sleep apnea. Although some studies show a high correlation between these monitors and polysomnography, there remains controversy in recommendations for their routine use because coexisting sleep disorders (eg, restless legs syndrome) may go undetected.

A common summary measure used to describe breathing disorders during sleep is the apnea-hypopnea index (AHI), which is the total number of apnea and hypopnea episodes during sleep divided by the number of hours of sleep. AHI values can be calculated for different stages of sleep. The respiratory disturbance index (RDI) is a similar measure that reflects the number of episodes of decrease in blood O ₂ saturation to less than 3% per hour. Using EEG, the arousal index (AI), which is the number of arousals per hour of sleep, can be calculated. AI may correlate with AHI or RHI, but approximately 20% of apnea and desaturation episodes are not accompanied by arousals or have other causes of arousal. An AHI greater than 5 requires the diagnosis of obstructive sleep apnea; values greater than 15 and greater than 30 indicate moderate and severe sleep apnea, respectively. Snoring increases the likelihood of having an AHI greater than 5 by 7 times. IP and IDN correlate moderately with patient symptoms.

Additional tests may include upper airway examination, thyroid stimulating hormone, and other tests needed to identify chronic conditions associated with obstructive sleep apnea.

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Treatment of obstructive sleep apnea

Initial treatment for obstructive sleep apnea is aimed at addressing underlying risk factors. Modifiable risk factors include obesity, alcohol and sedative use, and poorly treated chronic medical conditions. Weight loss is an important component of treatment for obstructive sleep apnea, but is extremely difficult for most people, especially those who are tired or sleepy.

Surgical correction of obstruction at the level of the altered upper airway caused by enlarged tonsils and nasal polyps should be considered; correction of macroglossia and micrognathia may also be the treatment of choice.

The goal of treatment for obstructive sleep apnea is to reduce the number of episodes of sleep fragmentation and hypoxia; treatment for obstructive sleep apnea is tailored to each patient and the severity of the changes. Cure is defined as the disappearance of symptoms and a decrease in AHI below a threshold, usually 10/hour. Moderate and severe sleepiness are predictors of successful treatment.

CPAP

Nasal CPAP is the drug of choice for most patients with subjective sleepiness, but is of questionable value in patients who deny sleepiness. CPAP improves upper airway patency by creating positive pressure in a collapsed upper airway. Effective pressures typically range from 3 cm to 15 cm H2O. Disease severity does not correlate with required pressure. If clinical improvement does not occur, pressure can be titrated by performing repeated polysomnographic studies. Independent of the AHI, CPAP may also improve neurocognitive impairment and blood pressure. If CPAP is discontinued, symptoms recur within a few days, although short interruptions in therapy are usually well tolerated in acute medical situations. Duration of therapy is not defined.

Failure of nasal CPAP usually occurs when patient compliance is low. Side effects include sore throat, which may be relieved in some cases by using warm, humidified air, and discomfort due to a poorly fitting mask.

CPAP may be augmented with respiratory support (bilevel positive airway pressure) in patients with obesity-hypoventilation syndrome.

Oral appliances. Oral appliances are designed to advance the mandible or at least prevent the mandible from sliding backward during sleep. Some are also designed to retract the tongue. The use of these devices to treat both snoring and obstructive sleep apnea is gaining acceptance. Comparative studies of these devices with CPAP are limited, and definitive indications and cost-effectiveness have not been established.

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Surgical treatment of obstructive sleep apnea

Surgery is reserved for patients who are refractory to atraumatic treatment. Uvulopalatopharyngoplasty (UPPP) is the most common procedure. It involves submucous resection of tonsillar tissue to the arytenoepiglottic folds, including resection of the adenoids, to enlarge the upper airway. One study demonstrated equivalence with CPAP, using CPAP as a bridge to surgery, but the two have not been directly compared. Patients with morbid obesity or anatomical airway narrowing may not be aware of the success of UPP. In addition, recognition of sleep apnea after UPP is difficult because snoring is absent. These hidden obstructions may be as severe as the apneic episodes before surgery.

Additional surgical interventions include tongue resection and mandibulomaxillary advancement. The latter is often suggested as a 2nd stage treatment when UFPP fails. There are no studies of this 2-stage approach in a cohort of patients across multiple centers.

Tracheostomy is the most effective therapeutic intervention for obstructive sleep apnea, but it is a procedure of last resort. It bypasses the obstruction during sleep and is reserved for patients who suffer most severely from obstructive sleep apnea and/or sleep hypopnea (e.g., patients with cor pulmonale). It may take 1 year or more before the opening can be closed.

Laser uvuloplasty is recommended for the treatment of loud snoring along with radiofrequency tissue ablation. It provides a 70-80% reduction in snoring intensity within 2 to 6 months; however, the effectiveness decreases after 1 year. Sleep apnea syndrome should be excluded in such cases so as not to delay the use of more adequate treatment.

Additional Treatments for Obstructive Sleep Apnea

Complementary therapies are used but have not been shown to be as effective as first-line treatments.

_O2 administration may cause respiratory acidosis and morning headache in some patients, and it is impossible to predict who will respond favorably to such administration.

Many drugs have been used as respiratory center stimulants (eg, tricyclic antidepressants, theophylline), but their use cannot be recommended for routine use due to limited efficacy and/or low therapeutic index.

Nasal dilators and commercial throat sprays have not been proven effective in treating snoring.

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Patient education and support

An informed patient and family are more likely to accept treatment strategies, including tracheostomy in patients who are refractory to other treatments. Support groups are effective in providing information and maintaining timely and effective treatment.

What is the prognosis for obstructive sleep apnea?

The prognosis is favorable with appropriate treatment. However, untreated obstructive sleep apnea, which is not uncommon because it is often undiagnosed, can have long-term complications, including poorly controlled hypertension and heart failure. Side effects of hypersomnolence, such as loss of ability to work and sexual dysfunction, can significantly disrupt family well-being.

Perhaps most importantly, excessive daytime sleepiness is a major risk factor for serious injury and death from accidents, particularly motor vehicle crashes. Sleepy patients should be counseled about the risks of driving or performing tasks during which sleep episodes would be hazardous. In addition, perioperative cardiac arrest may be associated with obstructive sleep apnea, probably due to the effects of anesthesia after cessation of mechanical ventilation. Therefore, patients should inform the anesthesiologist of the diagnosis before undergoing surgery and should have continuous positive airway pressure (CPAP) maintained during hospitalization.