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Obstructive
sleep apnea consists of episodes of partial or complete closure
of the upper airway that occur during sleep and lead to breathing cessation
(defined as a period of apnea > 10 sec). Symptoms
include restlessness, snoring, recurrent awakening, morning headache,
and excessive daytime sleepiness. Diagnosis is based on sleep history,
and polysomnography. Treatment is with nasal continuous positive
airway pressure, oral appliances, and, in refractory cases, surgery.
Prognosis is good with treatment. Most cases remain undiagnosed
and untreated and are often associated with hypertension, heart
failure, and injury or death from motor vehicle crashes and other
accidents resulting from hypersomnolence.
In at-risk patients, sleep destabilizes patency of the upper airway, leading to partial or complete obstruction of the nasopharynx, oropharynx, or both. When breathing is diminished but not absent, the condition is called obstructive sleep hypopnea.
The prevalence of obstructive sleep apnea (OSA) is 2 to 9% in adults ; the condition is underrecognized and often undiagnosed even in symptomatic patients. OSA is up to 4 times more common in men, and 7 times more common in people who are obese (ie, body mass index [BMI] > 30).
Etiology
Anatomic risk factors include obesity, an oropharynx “crowded” by a short or retracted mandible, a prominent tongue base or tonsils, a rounded head shape and a short neck, a neck circumference > 43 cm, thick lateral pharyngeal walls, or lateral parapharyngeal fat pads. Other identified risk factors include postmenopausal status, aging, and alcohol or sedative use. A family history of sleep apnea is present in 25 to 40% of cases, perhaps reflective of intrinsic ventilatory drive or pharyngeal structure. The likelihood of other family members having sleep apnea increases as more family members have it.
Many people with OSA have disorders such as hypertension, stroke, diabetes, gastroesophageal reflux disease, nocturnal angina, heart failure, acromegaly, and hypothyroidism. OSA can also be associated with cardiac arrhythmias (eg, bradycardia, asystole).
Because obesity is a common risk factor for both OSA and the obesity-hypoventilation syndrome (see Obesity and the Metabolic Syndrome: Complications), the two conditions may coexist.
Airway obstruction causes paroxysms of inspiratory effort, reductions in gas exchange, disruption of normal sleep architecture, and partial or complete arousals from sleep. Factors that may interact to produce the characteristic symptoms and signs include hypoxia, hypercapnia, and sleep fragmentation.
OSA is an extreme form of sleep-related upper airway resistance. Less severe forms that do not produce O2 desaturation include snoring; pharyngeal airflow resistance causing noisy inspiration but without sleep arousals; and the upper airway resistance syndrome, characterized by crescendo snoring terminated by respiratory effort-related arousals (RERAs). People with the upper airway resistance syndrome are typically younger and less obese than those with OSA and they complain of daytime sleepiness more than do those with primary snoring. The symptoms, diagnostic evaluation, and treatment of snoring and upper airway resistance syndrome are otherwise the same as for OSA.
Symptoms and Signs
Although loud disruptive snoring is reported by 85% of OSA patients, most people who snore do not have OSA. Other symptoms of OSA may include choking, gasping, or snorting during sleep, restless and unrefreshing sleep, and difficulty staying asleep. Most patients are unaware of these symptoms (because they occur during sleep) but are informed of them by bed partners, roommates, or housemates.
When awake, patients may experience hypersomnolence, fatigue, and impaired concentration. The frequency of sleep complaints and the degree of daytime sleepiness correlate only roughly with number of nocturnal arousals.
Diagnosis
The diagnosis is suspected in patients with identifiable risk factors, symptoms, or both. Criteria for diagnosis consist of daytime symptoms, nighttime symptoms, and sleep monitoring that documents > 5 episodes of hypopnea and apnea per hour. Specifically, in regard to symptoms, there should be ≥ 1 of the following:
The patient and any bed partners, roommates, or housemates should be interviewed. The differential diagnosis of excessive daytime sleepiness is broad (see Sleep and Wakefulness Disorders: Insomnia and Excessive Daytime Sleepiness (EDS)) and includes
An extended sleep history should be taken in all patients who
Most patients who report only snoring, without other symptoms or cardiovascular risks, do not need an extensive evaluation for OSA.
The physical examination should include evaluation for nasal obstruction, tonsillar hypertrophy, and pharyngeal structure, measurement of neck circumference, and identification of clinical features of hypothyroidism and acromegaly.
The diagnosis is confirmed with polysomnography (see Sleep and Wakefulness Disorders: Testing), which includes continuous measurement of breathing effort by plethysmography, airflow at the nose and mouth using flow sensors, O2 saturation by oximetry, sleep architecture by EEG, chin electromyography (looking for hypotonia), and electro-oculograms to assess the occurrence of rapid eye movements. Polysomnography records and helps classify stages of sleep and the occurrence and duration of apneic and hypopneic periods. The patient is also observed by video, and ECG monitoring is used to determine whether arrhythmias occur in conjunction with the apneic episodes. Other variables evaluated include limb muscle activity (to assess nonrespiratory causes of sleep arousal, such as restless legs syndrome and periodic limb movements disorder) and body position (apnea may occur only in the supine position).
The common summary measure used to describe respiratory disturbances during sleep is the apnea-hypopnea index (AHI), which is the total number of episodes of apnea and hypopnea occurring during sleep divided by the hours of sleep time. AHI values can be computed for different sleep stages. The respiratory disturbance index (RDI) is a similar measure, describing the number of times per hour that blood O2 saturation falls > 3%. If EEG monitoring is used, an arousal index (AI) can be computed, which is the number of arousals per hour of sleep. The AI may be correlated with AHI or RDI, but about 20% of apneas and desaturation episodes are not accompanied by arousals, or other causes of arousals are present. An AHI > 5 is required for the diagnosis of OSA; values > 15 and > 30 indicate moderate and severe levels of sleep apnea, respectively. Snoring loudly enough to be heard in the next room confers a 10-fold increase in the likelihood of having AHI > 5. The AI and RDI correlate only moderately with a patient's symptoms.
Because the number of polysomnographic studies that can be done in a sleep laboratory cannot meet the demand, ambulatory diagnostic tools are being used more often. Portable monitors can measure heart rate, pulse oximetry, effort, position, and nasal airflow to provide estimates of respiratory disturbances during self-reported sleep, thereby diagnosing OSA. Ambulatory diagnostic tools are often used in combination with tools that calculate patients' risk (the sensitivity and specificity of the test depend on pre-test probability). When ambulatory diagnosis is used, coexisting sleep disorders (eg, restless legs syndrome) must be based on clinical suspicion.
Adjunctive testing may include upper airway imaging, measurement of thyroid-stimulating hormone, and other tests as appropriate to assess chronic medical conditions associated with OSA.
Prognosis
Prognosis is excellent if effective treatment is prescribed and used.
Untreated or unrecognized OSA leads to cognitive impairment as a result of sleeplessness, which, in turn, can lead to serious injury or death from accidents, especially motor vehicle crashes. Sleepy patients should be warned of the risk of driving, operating heavy machinery, or engaging in other activities during which sleep attacks would be hazardous.
Adverse effects of hypersomnolence, such as loss of employment and sexual dysfunction, can affect families considerably.
Long-term cardiovascular sequelae of untreated OSA include poorly controlled hypertension and heart failure.
In addition, perioperative complications, including cardiac arrest, have been attributed to OSA, probably because anesthesia can cause airway obstruction after a mechanical airway is removed. Patients should therefore inform their anesthesiologist of the diagnosis before undergoing surgery and should expect to receive continuous positive airway pressure (CPAP) when they receive preoperative drugs and during recovery.
Treatment
The aim of treatment is to reduce episodes of hypoxia and sleep fragmentation; treatment is tailored to the patient and to the degree of impairment. Cure is defined as a resolution of symptoms with AHI reduction below a threshold, usually 10/h.
Treatment is directed first at risk factors and then at OSA itself. Specific treatments for OSA include CPAP, oral appliances, and airway surgery.
Control of
risk factors:
Initial treatment aims at optimal control of modifiable risk factors, including obesity, alcohol and sedative use, hypothyroidism, acromegaly, and other chronic disorders. Although only modest weight loss may result in clinically meaningful improvement, weight loss is extremely difficult for most people, especially those who are fatigued or sleepy. Bariatric surgery reverses symptoms and improves AHI in 85% of morbidly obese (BMI > 40) patients.
CPAP:
Nasal CPAP is the treatment of choice for most patients with OSA and subjective daytime sleepiness; compliance is lower in patients who do not report sleepiness. CPAP improves upper airway patency by applying positive pressure to the collapsible upper airway. Effective pressures typically range from 3 to 15 cm H2O. Disease severity does not correlate with pressure requirements. If clinical improvement is not apparent, pressure can be titrated during monitoring with repeat polysomnography. Regardless of improvement in the AHI, CPAP will reduce cognitive impairment and BP. If CPAP is withdrawn, symptoms recur over several days, though short interruptions of therapy for acute medical conditions are usually well tolerated. Duration of therapy is indefinite.
Failures of nasal CPAP are common because of limited patient compliance. Adverse effects include dryness and nasal irritation, which can be alleviated in some cases with the use of warm humidified air, and discomfort resulting from a poorly fitting mask.
CPAP can be augmented with inspiratory assistance (bi-level positive airway pressure) for patients with the obesity-hypoventilation syndrome (see Obesity and the Metabolic Syndrome: Complications).
Oral
appliances:
Oral appliances are designed to advance the mandible or, at the very least, prevent retrusion with sleep. Some are also designed to pull the tongue forward. Use of these appliances to treat both snoring and OSA is gaining acceptance. Comparisons of appliances to CPAP show equivalence in mild to moderate OSA, but results of cost-effectiveness studies are not available.
Airway surgery:
Surgical correction of upper airway obstruction caused by enlarged tonsils and nasal polyps should be considered. Surgery for macroglossia or micrognathia is also an option. Surgery is a first-line treatment if anatomic encroachment is identified; otherwise, surgery is a second-tier approach.
Uvulopalatopharyngoplasty (UPPP) is the most commonly used procedure. It involves resection of submucosal tissue from the tonsillar pillars to the arytenoepiglottic folds, including resection of the adenoids, to enlarge the upper airway. Equivalence with CPAP was demonstrated in one study using CPAP as a bridge to surgery, but the interventions have not been directly compared. UPPP may not be successful in patients who are morbidly obese or who have anatomic narrowing of the airway. Moreover, recognition of sleep apnea after UPPP is obscured because of a lack of snoring. Such silent obstructions may be as severe as apneic episodes before surgical intervention.
Adjunctive surgical procedures include midline glossectomy, hyoid advancement, and mandibulomaxillary advancement. The latter is often offered as a 2nd-stage procedure if UPPP is not curative. Studies of multistage approaches across centers in unselected patients are not available.
Tracheostomy is the most effective therapeutic maneuver for OSA but is a procedure of last resort. It bypasses the site of obstruction and is indicated for those most severely affected (eg, those with cor pulmonale).
Laser-assisted uvuloplasty, uvular splints, and radiofrequency tissue ablation have been promoted as treatments for loud snoring in patients without OSA. Although they may transiently decrease snoring loudness, efficacy declines over months to years.
Adjunctive treatments:
Adjunctive treatments are commonly used but have no proven role as first-line treatment.
Modafinil can be used for residual sleepiness in OSA in patients who are effectively using CPAP.
Supplemental O2 improves blood oxygenation, but a beneficial clinical effect cannot be predicted. Also, O2 may provoke respiratory acidosis and morning headache in some patients.
A number of drugs have been used to stimulate ventilatory drive (eg, tricyclic antidepressants, theophylline ) but cannot be routinely advocated because of limited efficacy, a low therapeutic index, or both.
Nasal dilatory devices and throat sprays sold OTC for snoring have no proven benefits for OSA.
Patient education
and support:
An informed patient and family are better able to cope with a treatment strategy, including tracheostomy. Patient support groups provide helpful information and effectively support timely treatment and follow-up.
Last full review/revision November 2007 by Kingman P. Strohl, MD
Content last modified November 2007
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