Introduction

Sleep apnea, first described in 1965, is a disorder characterized by brief interruptions of breathing during sleep. There are two types: central and obstructive. Central sleep apnea occurs when the brain fails to send the appropriate signals to initiate respiration. Obstructive sleep apnea (OSA), which is more common, is due to partial blockage of airflow in or out of the nose or mouth, although efforts to breathe continue. A research review, summarized here, describes its diagnosis and treatment. Untreated OSA is associated with increased mortality, so that the condition deserves attention and appropriate treatment.

Apnea that is not coupled with total cessation of airflow - a 50% reduction in flow, accompanied by significant oxygen de-saturation (typically, -4%) - is termed hypopnea. The degree of disturbed breathing in OSA is described by the apnea-plus-hypopnea index (AHI), which is calculated by adding the number of apneic and hypopneic episodes and dividing by the duration of sleep in hours. Thus a patient who has 35 apneas and 7 hypopneas over 6 hours has an AHI of (35 + 7)/6 = 7. Patients with symptoms suggesting sleep apnea and an AHI of 5 or more meet the minimum criteria for the OSA syndrome.

Pathology

The pathological features responsible for partial upper airway obstruction commonly involve pharyngeal narrowing due to obesity, edema or enlarged tonsils. Slackness in the pharyngeal wall can be aggravated by a receding chin, nasal obstruction or increased respiratory difficulty related to obesity. Roughly half the obstructions are at the level of the palate, and half at the hypopharynx.

Risk factors for OSA

The condition is seen twice as often in men as in women. It occurs in roughly 4% of men and 2% of women in the USA. Obesity is a strong risk factor, so that patients with a body mass index (BMI) >28 kg/m2 are at risk. A neck circumference >17 inches (43cm) in males or >16 inches (41cm) in females is also a positive predictor. OSA is more prevalent in middle age than in young persons, and the number of asymptomatic persons who meet the numerical criteria for OSA increases with age. Genetics may underlie the causation e.g. a high-arched hard palate, or a receding chin. Lifestyle factors, such as cigarette smoking, problematic alcohol intake and use of sedatives or relaxant drugs (e.g. benzodiazepines) exacerbate OSA. Upper airway inflammation produced by infection, irritants or allergens can also worsen the problem.

Symptoms and signs

Symptoms include chronic loud snoring, gasping or choking episodes during sleep, excessive daytime sleepiness (which may be associated with falling asleep when driving or at work), and personality changes or cognitive difficult due to tiredness. The signs commonly observed include obesity (with a BMI >28 kg/m2), neck thickening, and nasopharyngeal narrowing. There is often systemic hypertension, but pulmonary hypertension is less common. Arterial oxygen saturation and AHI estimates can help in diagnosing severity, as can the use of a standardized questionnaire on daytime somnolence, such as the Epworth sleepiness scale.¹

Apart from the presenting symptoms, the physician should inquire about automobile accidents that may be related to daytime fatigue, and make a careful examination that includes measurement of the neck circumference, BMI calculation, and inspection of the upper respiratory passages. Possible cor pulmonale - a loud 2nd pulmonary heart sound (P2), right ventricular heave, and dependant edema - should also be sought. Suspected OSA should be confirmed by overnight polysomnography (PSG), which includes electroencephalography, electro-oculography, chin electromyography, airflow measurement, arterial oxygen saturation, respiratory effort and electrocardiography.

The PSG results allow precise calculation of the AHI, and discrimination between central, mixed and obstructive sleep apneas. They also show the severity of oxygen de-saturation, as well as excluding other sleep disorders (e.g. parasomnias, nocturnal seizures, narcolepsy). Although ambulatory sleep studies (i.e. non-sleep lab studies) have become popular, they do not provide adequate information for a correct diagnosis.

Pulmonary hypertension

This serious potential complication of OSA is seen in about 17% of patients. It is caused by the wide fluctuations in intra-thoracic pressure, reduced blood oxygen saturation and increased carbon dioxide levels, which cause bradycardia, decreased stroke volume, and finally vasoconstriction of certain vascular beds, leading to pulmonary hypertension. The condition is unrelated to other causes of impaired pulmonary function (e.g. COPD), increased body mass or smoking.

Essential hypertension

Half of all patients with OSA are hypertensive, while 30% of patients with essential hypertension have sleep apnea. The proposed mechanism is apnea-induced repeated sympathomimetic discharge. During sleep, blood pressure fluctuates to a greater extent in patients with sleep apnea, regardless of weight, age or sex. Snoring alone, however, has no effect on blood pressure.

Treatment

Therapy consists of nasal continuous positive airway pressure (CPAP) therapy, surgery, use of oral or dental devices, and/or behavioral changes. If there is a specific underlying correctable anatomic abnormality, surgery is recommended. Otherwise, nasal CPAP is suitable for patients with moderate to severe OSA.

Nasal CPAP. Positive pressure in the upper airway helps keep it open while the patient is asleep. CPAP decreases the AHI, improves arterial oxygen saturation, improves daytime somnolence scores, lowers blood pressure and normalizes life expectancy.

Nasal CPAP is best instituted in the sleep laboratory, with the pressure titrated to that which relieves apnea. Many centers use a "split-night" approach where CPAP is titrated in the 2nd half of the study night, after sleep apnea is documented.

The success of nasal CPAP depends on the patient's willingness to wear the device. Compliance rates range from 65% to 80%. The average duration of nightly use is about five hours. Half the users report at least one side effect related to the mask -- air leaks near the eyes can be irritating, and morning dryness of the nose or mouth occurs often. Less frequently, sneezing, nasal congestion and nasal drip occur. These effects can be helped by a good-fitting mask, judicious use of nasal saline sprays, and nasal corticosteroids.

Surgery. Tracheostomy is obviously effective in virtually all patients with obstructive sleep apnea. Tonsillectomy, adenoidectomy and nasal polypectomy are minor corrective approaches. More radical procedures, such as uvulopalatopharyngoplasty, have relatively high success rates - 30% to 50%. Reconstruction of the lower jaw can also be undertaken.

Devices. Sometimes dental or oral devices can be used to reposition the jaw or tongue - they are usually only of benefit in mild cases. Compliance is often a problem.

Behavioral therapy. Weight loss can be extremely beneficial in improving the structure and function of the upper airway, and decreasing pharyngeal collapsibility. Even slight weight loss can lead to major improvements. Patients should stop smoking, sedative and alcohol consumption, and attempt to sleep on their side.

Comment

The Epworth sleepiness scale is useful for assessing severity and progress of daytime somnolence, but its results do not help in diagnosing OSA from other conditions.

Alertness on the part of the family physician as to the possibility of OSA can be extremely rewarding. Treatment is often most successful, producing quite dramatic improvements in the patient's quality of life.