Sleep Apnea

Sleep apnea occurs during sleep when a cessation of airflow occurs for at least 10 seconds (usually 20-30 s but rarely >2 min). The apneas (absences of breath) are accompanied by snoring, sleep arousals, and hypoxia (oxygen deprivation).

The term sleep apnea describes 2 major sleep-related clinical problems: (1) obstructive sleep apnea (OSA) and (2) central sleep apnea (CSA). OSA is caused by upper airway (UA) obstruction at the level of the pharynx and is the most common form of sleep apnea. CSA is the result of impairment in respiratory control of breathing.

Sleep apnea syndrome encompasses a spectrum of sleep- related breathing disorders ranging from simple snoring to severe sleep apnea with associated neurocognitive deficits, residual daytime sleepiness, pauses in breathing, and cardiovascular consequences such as hypertension and stroke. UA resistance syndrome is a condition within this spectrum that is intermediate in severity to these two extremes. Patients with UA resistance syndrome have clinical features closely related to OSA, but frank apneas are absent.

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The available evidence indicates that pharyngeal collapse is responsible for the recurrent UA obstruction during sleep in OSA. The mechanisms responsible for recurrent UA closure still are not completely understood. Compared to healthy subjects, patients with OSA appear to have a smaller pharyngeal airway during wakefulness. The loss of muscle tone during sleep could also precipitate UA obstruction in predisposed individuals. Inspiratory UA narrowing has been noted to be worse during sleep compared to wakefulness.

Decreases in transmural airway pressure and mucosal adhesive forces have been considered an essential factor in the causation of UA narrowing/obstruction in OSA. Other factors implicated in the pathophysiology of OSA include the following: patients with SDB may have blunted/abnormal UA neuromuscular reflexes that predispose to UA collapse; surface mucosal forces may play an important role in preventing UA opening; changes in vasomotor tone in the UA have been shown to affect UA resistance; alcohol and benzodiazepines have been shown to selectively depress UA muscle activity and may contribute to UA collapsibility.



Although previous studies estimated the prevalence of sleep apnea to be 2% for middle-aged women and 4% for middle- aged men, recent studies show much higher prevalence, at 4% for women and 9% for men. The National Commission on Sleep Disorders Research has estimated that sleep apnea affects 7-18 million people in the United States. Prevalence increases with age. Approximately 92% of affected women and 80% of affected men remain undiagnosed.


Clinically, little doubt exists that sleep apnea can affect quality of life in many ways. Sleep apnea is now known to be a public health hazard because of accidents due to sleepiness. Moreover, patients often have hypoxemia with each apnea, and end-organ systems can be affected by profound and repetitive hypoxia. This includes hypertension, cerebrovascular disease, heart disease, cardiac arrhythmias, and pulmonary artery hypertension. Other problems include excessive daytime sleepiness, performance and neurocognitive deficits, and motor vehicle accidents (patients with OSA have a 7-times higher rate of motor vehicle accidents compared with healthy controls).


Clinical history and physical examination are of paramount importance in the evaluation of a patient with suspected sleep apnea. Clinical screening is necessary to determine if a patient's symptoms are due to a condition other than OSA also known to produce increased daytime somnolence.

The typical history of a patient with OSA is that of a middle- aged man who is obese and snores loudly, is excessively sleepy, and is reported to stop breathing at night. Snoring is nearly ubiquitous in patients with OSA. When taking a patient's history, excluding other causes of frequent sleep arousals (eg, periodic limb movement disorder, depression, medical disorders, environmental interferences) is important.

The cardinal symptoms of sleep apnea include the 3 Ss, as follows: Snoring (loud, habitual), Spousal apnea report/witnessed apneas, Sleepiness (daytime).

Other symptoms include the following: Nonrestorative sleep, a choking sensation or gasping during the night, morning headaches, probably due to hypercapnia during sleep, insomnia, restless sleep, sore throat or dry mouth in the morning, cognitive deficits including memory and intellectual impairment, personality and mood changes, including depression and anxiety, sexual dysfunction, including impotence and decreased libido. Many patients also demonstrate gastroesophageal reflux due to the high negative intrathoracic pressure during apneas.



Obesity often is present, but not all patients are obese. Approximately 18-40% of affected patients are not more than 20% heavier than their ideal body weight.

The airway appears crowded and small. UA abnormalities include severe nasal obstruction, low-hanging soft palate, large (hypertrophied) uvula, enlarged tonsils/adenoids, and macroglossia. Large neck circumference (collar size >17.5 in) has been associated with SDB.

The diagnostic criteria for OSA according to the International Classification of Sleep Disorders: Diagnostic and Coding Manual produced by the ASDA states that monitoring demonstrates the following: More than 5 obstructive apneas greater than 10 seconds in duration per hour of sleep and 1 or more of the following: (1) frequent arousals from sleep associated with the apneas, (2) bradytachycardia, (3) arterial oxygen desaturation in association with apneic episodes.


Imaging Studies:

The modalities available for identifying the site of obstruction include lateral cephalometry, endoscopy, fluoroscopy, CT scan, and MRI. The accuracy of these methods in identifying the site(s) of obstruction is not clear. Routine radiographic imaging of the UA in the initial evaluation of sleep apnea is of uncertain benefit currently and should not be performed unless a specific indication is present.

UA imaging studies (cephalometrics, MRI, CT scan) should be performed in patients being evaluated for UA and craniofacial surgery. Cephalometrics may be useful in some patients being evaluated for oral appliance therapy. Other tests include in-laboratory overnight PSG (polysonography). Complete PSG is a multichannel recording of sleep and breathing and usually involves in-laboratory measurement of sleep architecture and EEG arousals, eye movements, chin movements, airflow, respiratory effort, oximetry, ECG, body position, snoring, and leg movements.

The multiple sleep latency test traditionally has been used to quantify sleepiness in patients with symptoms of daytime hypersomnolence. It must be performed on the day following a standard PSG. The patient is instructed to attempt sleeping for 20 minutes on each of 4 separate naps, each nap being 2 hours apart. The average latency to stage 1 sleep is determined for the 4 naps, and a mean sleep latency of less than 5 minutes is considered abnormal (ie, indicative of pathological sleepiness). A mean sleep latency of more than 10 minutes is normal.


Medical Care:

Little evidence supports the treatment of asymptomatic patients with sleep apnea. Patients with mixed apneas should be treated as if they have OSA because OSA is most life- threatening and central sleep apnea abates commonly with OSA treatment. Only health care professionals with adequate training in the evaluation and management of OSA should prescribe therapy for patients with sleep apnea. CPAP (continuous positive airway pressure) should not be prescribed without PSG confirmation of the correct CPAP pressure level because no standardized pressure value exists based on age or body mass index.

The primary treatment for OSA is positive pressure therapy, and nasal CPAP is the most commonly prescribed type of therapy. Other forms of positive airway pressure include bilevel positive airway pressure and variable CPAP. Nightly use of at least 4 hours of CPAP is required to produce consistent ameliorative effects. Data show that compliance at 1 month predicts compliance at 3 months. Whether patients like CPAP depends on their perception of improvement, not on the severity of their disease as judged by the clinician.

Other nonsurgical therapy includes general/behavioral measures such as weight loss and avoidance of alcohol, sedatives, and supine position. Pharmacologic therapy is not part of treatment. No clinically useful drug therapy is currently available.


Surgical Care:

A specific space-occupying lesion causing UA obstruction is found in only 3 of 200 adult patients with OSA. Although surgical correction of such an abnormality (ie, tonsillectomy) could potentially cure OSA, the majority of adult patients do not have such correctible lesions.

The level of obstruction in patients with OSA is classified into 3 types. Type I is obstruction in the retropalatal region only. Type II is obstruction in both the retropalatal and retrolingual regions. Type III is obstruction in the retrolingual region only.

Different surgical procedures have been proposed for patients with different levels of obstruction. Uvulopalatopharyngoplasty (UPPP) may correct type I obstruction. Genioglossus advancement with hyoid myotomy (GAHM) may correct type III obstruction. Maxillomandibular advancement osteotomy (MMO) may correct obstruction at all levels. Based on the recognition that several sites of obstruction could be responsible, a systematic approach for selecting surgery has been developed. This is the Riley- Powell-Stanford surgical protocol designed in 1988. The protocol has 2 phases. Phase I consists of the UPPP and GAHM procedures, and phase II consists of the more complicated MMO procedure. Patients who are not adequately treated with phase I surgery are offered phase II surgery.

A few words about UPPP: UPPP is the most common surgical procedure performed for adults with OSA and was introduced to the United States by Fujita and colleagues in 1981. It involves removal of the tonsils (if present), uvula, distal margin of the soft palate, and redundant pharyngeal tissue and reshaping of the soft tissues in the lateral pharyngeal walls. The surgical success rate is approximately 50% when surgical success is defined as a 50% reduction in severity of the condition. The outcome of UPPP is difficult to predict. Although the procedure usually is well tolerated and uneventful, complications can include the following: Pain upon swallowing and pain with speech, usually for 1-2 weeks postoperatively, hemorrhage (2-4%), swallowing difficulties, particularly regurgitation of food, long-term pharyngeal discomfort, disturbance in taste, numbness of tongue, and nasopharyngeal stenosis.

A few comments about other surgery options: Laser-assisted uvulopalatoplasty although successful in reducing snoring in 90% of patients, the success rate in patients with apnea is much lower; Radiofrequency volumetric tissue reduction of the soft palate (somnoplasty) is a new technique pioneered by Powell and associates that used radiofrequency energy to ablate the soft palate. This procedure has US Food and Drug Administration (FDA) approval for the treatment of snoring and OSA. Unfortunately, long-term follow-up (12-18 mo) revealed that almost half of patients undergoing radiofrequency volumetric reduction of the soft palate develop recurrence of snoring.


Medical/Legal Pitfalls:

The American Thoracic Society (ATS) has issued detailed guidelines on sleep apnea, sleepiness, and driving risks. Laws regarding impaired drivers, including those with OSA, vary from state to state. In some states, the physician is obligated to report patients under specific conditions (ie, mandatory reporting statute) while other states permit reporting but do not require it (ie, permissive reporting statute). Irrespective of whether statutory reporting is required, physicians may be liable for damages if a patient with OSA injures himself or someone else while driving.

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