Obstructive sleep apnea

Obstructive sleep apnea frequently goes undiagnosed, even as it impairs cardiovascular and cognitive function. The effects on quality of life and the economic costs are high.

Obstructive sleep apnea (OSA) affects up to 5% of the population in Western countries, but as many as 80% of cases remain undiagnosed. Prevalence increases with age, peaking at approximately 60 years. Although 1 in 5 adults has mild OSA, only 1 in 15 has a moderate to severe case.

Obesity is a significant risk factor, partly because layers of fat adjacent to the pharynx narrow its lumen. A 10% increase in weight leads to a six-fold risk of developing OSA.Other risk factors for OSA include male sex and abnormalities of craniofacial morphology. Frequent alcohol use has also been considered a risk factor since it depresses the central respiratory drive and enhances muscle relaxation.

Patients with untreated OSA may present with conditions such as hypertension, coronary artery disease (including MI), diabetes, heart failure, stroke, and cognitive dysfunction. Although these conditions are commonly treated without a search for underlying pathology, OSA can be a major contributor. Previous research has focused on the cardiac effects of untreated OSA, such as hypertension, stroke, and arrhythmias.However, a mechanism that causes cardiac dysfunction may also cause cognitive dysfunction resembling dementia. Failure to diagnose and treat OSA effectively may result in improper management of this dementia.

At present, no optimal treatment options are available for OSA. Continuous positive airway pressure (CPAP) therapy is the first-line treatment, but patient adherence is only 46% to 70% because of discomfort caused by the mask.

OSA is defined as periods of apnea (cessation of breathing for longer than 10 seconds) or hypopnea (reduction but not complete cessation of airflow to less than 50% of normal) that occur throughout sleep. These are caused by partial or complete obstruction of the upper airway, usually the oropharynx, which inhibits inspiratory airflow.

Airway closure results from the relaxation during sleep of skeletal muscles—specifically, the pharyngeal dilator muscles and the genioglossus, which maintain the tongue in the anterior position when the person is supine. Too much muscle relaxation allows the tongue to slide posteriorly, partially or completely occluding the airway and causing the typical loud snoring and sudden choking and gasping for air. Other contributing anatomic anomalies include excessive soft palate tissue and enlarged tonsils, tongue base,uvula or narrow arch of teeth.

Cyclical oxygen desaturation occurs with each pause in breathing that stimulates arousal from sleep. In rapid eye movement (REM) sleep, muscle tone is most relaxed and apnea episodes are prolonged, with severe desaturations, often 60% to 70% lower than normal.Following each apneic or hypopneic event, a surge of sympathetic nervous activity occurs, stimulating transient tachycardia and increasing BP, and stimulating the production of cortisol and stressor hormones. Each interruption of the sleep pattern prevents patients from reaching the deep sleep stage. Deep sleep is vital for recovery and repair of body tissue. They wake feeling unrested and experience daytime sleepiness.

Patients with OSA perform poorly on driving-simulator tests and have a 2% to 7% greater risk of a motor vehicle accident (MVA) caused by driver sleepiness, fatigue, and inattentiveness.Up to 21% of patients who present to the emergency department following an MVA have undiagnosed OSA.The true number may be even higher than reported, given that a significant number of crashes are attributed to comorbid conditions such as stroke and MI when OSA may have been a contributing cause.

Untreated OSA has been strongly implicated in contributing to cardiovascular disease by increasing the risk of atherosclerosis, ischemia, and stroke. Repeated transient hypopnea/apnea and reoxygenation events resulting from untreated OSA affect cerebral oxygenation and blood flow velocity.This produces a condition similar to myocardial hypoxia.

It has been hypothesized that severe oxygen desaturation and decreased blood flow velocity to brain tissue may cause an infarct, similar to a cardiac infarct, resulting in death of brain tissue with permanent neuropsychological dysfunction. After several years of untreated OSA, the impact may become clinically evident as dementia. This destructive process is thought to represent vascular dementia rather than the degenerative dementia commonly seen in Alzheimer’s disease and Parkinson’s disease.Patients currently classified as having dementia may not be treated properly if underlying OSA is not considered or treated.

Diagnosis The signs and symptoms associated with OSA are shared with other medical conditions . Patients (or their partners) complain of loud snoring and excessive daytime sleepiness, the two hallmark features of OSA. Other symptoms include restless sleep, choking during sleep, and morning headaches. A large number of patients with OSA will remain asymptomatic but will eventually develop long-term side effects. It is important to rule out other causes of daytime sleepiness and to recognize common signs found in patients with OSA, including obesity, a thick neck, tonsillomegaly, acromegaly, and craniofacial anomalies.

The diagnosis of OSA is confirmed by an overnight sleep study using polysomnography (PSG), a noninvasive modality that detects the pattern of repetitive oxygen desaturation associated with heart rate variability that is specific for OSA. A complete PSG study requires a minimum of 2 to 4 hours of continuous sleep and monitors three variables: assessment of sleep stages, respiration, and limb movements. A diagnosis of mild, moderate, or severe OSA is based on one of three classification criteria: an apnea index (the apnea index is the number of episodes of apnea per hour of sleep—more than 5, more than 15, or more than 30); an apnea/hypopnea index (the number of episodes of apnea and hypopnea per hour); or a respiratory disturbance index (5-15, 16-30, or more than 30 disturbances).

Treatment There are three main treatment options for OSA. The treatment of choice is CPAP therapy and weight loss. The second-line therapy is surgery. A last resort in patients with severe, life-threatening OSA who do not respond to CPAP or surgery is a tracheotomy, which is 100% curative but rarely used. Alternative treatment options for patients with mild OSA include oral prosthetic devices (mandibular repositioning device, tongue retaining devices, and soft palate lifters), avoiding alcohol and other sedatives, and altering sleeping positions, such as elevating the head of the bed or lying on one’s side rather than supine.There are no pharmacologic treatments for OSA.

Although not curative, CPAP therapy is considered the best treatment option for moderate to severe OSA. The CPAP device provides airway pressure throughout respiration to prevent airway collapse. During use, the patient places a mask over the mouth, which is held in place by headgear with tubing connected to an electrical unit that provides a constant flow of air into the mask. Patient adherence to this treatment is disappointing, in part because of the side effects, which include sleep disruption, dry mouth/nose, sore throat, nosebleeds, claustrophobia, and facial skin abrasions from mask straps.

If a trial of CPAP therapy fails, the next step is to consider uvulopalatopharyngoplasty (UPPP). The most common surgical procedure for OSA, UPPP involves a tonsillectomy, reorientation of the anterior/posterior pillars, and excision of the uvula and posterior rim of the soft palate.UPPP is effective for patients with mild to moderate cases of OSA. It reduces symptoms in 90% of patients, decreases the number of apneic events in 60%, and achieves a cure in 50%.

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