Obstructive sleep Apnea
Obstructive sleep apnea is the most common sleep-related breathing disorder. It causes you to repeatedly stop and start breathing while you sleep.
There are several types of sleep apnea, but the most common is obstructive sleep apnea. This type of apnea occurs when your throat muscles intermittently relax and block your airway during sleep. A noticeable sign of obstructive sleep apnea is snoring.
Upper airway obstruction during sleep occurs when loss of normal pharyngeal muscle tone allows the pharynx to collapse passively during inspiration. Patients with anatomically narrowed upper airways (eg, micrognathia, macroglossia, obesity, tonsillar hypertrophy) are predisposed to the development of obstructive sleep apnea. Ingestion of alcohol or sedatives before sleeping or nasal obstruction of any type, including the common cold, may precipitate or worsen the condition.
Hypothyroidism and cigarette smoking are additional risk factors for obstructive sleep apnea. Before making the diagnosis of obstructive sleep apnea, a drug history should be obtained and a seizure disorder, narcolepsy, and depression should be excluded.
Symptoms and Signs
Most patients with obstructive or mixed sleep apnea are obese, middle-aged men. Arterial hypertension is common. Patients may complain of excessive daytime somnolence, morning sluggishness and headaches, daytime fatigue, cognitive impairment, recent weight gain, and impotence. Bed partners usually report loud cyclical snoring, breath cessation, witnessed apneas, restlessness, and thrashing movements of the extremities during sleep.
Personality changes, poor judgment, work-related problems, depression, and intellectual deterioration (memory impairment, inability to concentrate) may also be observed. The US Preventive Services Task Force does not recommend screening asymptomatic adults for sleep apnea.
Physical examination may be normal or may reveal systemic and pulmonary hypertension with cor pulmonale. The patient may appear sleepy or even fall asleep during the evaluation. The oropharynx is frequently found to be narrowed by excessive soft tissue folds, large tonsils, pendulous uvula, or prominent tongue. Nasal obstruction by a deviated nasal septum, poor nasal airflow, and a nasal twang to the speech may be observed. A “bull neck” appearance is common.
Erythrocytosis is common. Thyroid function tests (serum, TSH, FT4 ) should be obtained to exclude hypothyroidism.
Observation of the sleeping patient may reveal loud snoring interrupted by episodes of increasingly strong ventilatory effort that fail to produce airflow. A loud snort often accompanies the first breath following an apneic episode. Definitive diagnostic evaluation for suspected sleep apnea includes otorhinolaryngologic examination and overnight polysomnography (the monitoring of multiple physiologic factors during sleep).
Screening may be performed using home nocturnal pulse oximetry, which when normal has a high negative predictive value in ruling out significant sleep apnea. A complete polysomnography examination includes electroencephalography, electro-oculography, electromyography, ECG, pulse oximetry, and measurement of respiratory effort and airflow.
Polysomnography reveals apneic episodes lasting as long as 60 seconds. Oxygen saturation falls, often to very low levels. Bradydysrhythmias, such as sinus bradycardia, sinus arrest, or atrioventricular block, may occur. Tachydysrhythmias, including paroxysmal supraventricular tachycardia, atrial fibrillation, and ventricular tachycardia, may be seen once airflow is reestablished.
Weight loss and strict avoidance of alcohol and hypnotic medications are the first steps in management. Weight loss may be curative, but most patients are unable to lose the 10–20% of body weight required. Nasal continuous positive airway pressure (nasal CPAP) at night is curative in many patients. Polysomnography is frequently necessary to determine the level of CPAP (usually 5–15 cm H2 O) necessary to abolish obstructive apneas. Unfortunately, only about 75% of patients continue to use nasal CPAP after 1 year.
Pharmacologic therapy for obstructive sleep apnea is disappointing. Supplemental oxygen may lessen the severity of nocturnal desaturation but may also lengthen apneas; it should not be routinely prescribed without polysomnography to assess the effects of oxygen therapy. Mechanical devices inserted into the mouth at bedtime to hold the jaw forward and prevent pharyngeal occlusion have modest effectiveness in relieving apnea; however, patient compliance is not optimal.
Uvulopalatopharyngoplasty (UPPP), a procedure consisting of resection of pharyngeal soft tissue and amputation of approximately 15 mm of the free edge of the soft palate and uvula, is helpful in approximately 50% of selected patients. It is more effective in eliminating snoring than apneic episodes. UPPP may be performed on an outpatient basis with a laser.
Nasal septoplasty is performed if gross anatomic nasal septal deformity is present. Tracheostomy relieves upper airway obstruction and its physiologic consequences and represents the definitive treatment for obstructive sleep apnea.
However, it has numerous adverse effects, including granuloma formation, difficulty with speech, and stoma and airway infection. Furthermore, the long-term care of the tracheostomy, especially in obese patients, can be difficult. Tracheostomy and other maxillofacial surgery approaches are reserved for patients with life-threatening arrhythmias or severe disability who have not responded to conservative therapy.
A randomized trial of adaptive servo-ventilation in sleep apnea patients with predominant central apnea and impaired left ventricular ejection fraction (less than 45%) reported increased cardiovascular and all-cause mortality in the treatment group.