The exact incidence of OSA in the adult population is unknown. It was previously thought to be between 5% and 10%, but a recent study showed that one in four U.S. adults appears to be at high risk for OSA. This fact underscores the increased chance of having a patient with undiagnosed OSA as a candidate for general anesthesia.

The most clearly recognized risk factor for OSA is a narrow upper airway. The most common etiologies involve congenital abnormalities of the airway (e.g., Pierre-Robin syndrome, midface hypoplasia), hypertrophy of the adenoids and tonsils (especially in children), macroglossia (e.g., Down syndrome), and increased uvula size. Other important risk factors are obesity (body mass index >30 kg/m²), nasal polyps, deviated nasal septum, and chronic rhinitis. Neck circumference of >17 in for men and >16 in for women also represents an additional risk for OSA. Obesity by itself can lead to OSA or can worsen a pre-existing OSA. In the adult population the male-to-female ratio is 2:1, but this ratio does not apply to children or postmenopausal females. In women over the age of 65 years, the risk for OSA increases threefold. Other predisposing factors for OSA include a family history of OSA, smoking, and use of alcohol, tranquilizers, or sedatives.

The patient with OSA has a smaller and more easily collapsible upper airway. The risk of complete collapse of the airway is accentuated at the end of expiration, when the tissue pressure overcomes intraluminal pressure. The critical collapsible area is usually seen in the velopharynx, as evidenced
by imaging studies (computerized tomography, magnetic resonance, or fluoroscopy). Recurrent apnea will lead to intermittent hypoxemia, hypercapnia, and sleep fragmentation, with secondary increase of the sympathetic tone. OSA represents an independent risk factor for cardiovascular morbidity and mortality. A plausible explanation seems to be the increased oxidative stress secondary to alternate hypoxia/reoxygenation. The oxidative stress causes systemic inflammatory response with activation of endothelial cells, leukocytes, and platelets that culminates in early signs of atherosclerosis. OSA is one of the leading causes of systemic hypertension, left ventricular hypertrophy, pulmonary hypertension with right ventricular failure and congestive heart failure, cardiac dysrhythmias, ischemic heart disease, and stroke.

Sleep fragmentation leads to chronic fatigue, excessive daytime somnolence that markedly increases the risk of motor vehicle accidents, memory problems, anxiety, and depression.

The diagnosis of OSA is based on patient history, clinical presentation, physical examination, and sleep study (polysomnography). The classical symptoms of OSA are snoring, excessive daytime sleepiness, and witnessed episodes of breathing cessation during sleep. Usually, the patient with OSA is a man, over age 60 years, obese, with a short and thick neck. The “gold standard” for diagnosing OSA remains the polysomnography or sleep study performed overnight in a sleep laboratory. An accurate measurement requires 12 physiologic signals (Table 75.1) with a computer-based automated sleep analysis.

The final result of the analysis is the apnea-hypopnea index (AHI), which is the total number of apnea and hypopnea events per hour of total sleep time. According to the AHI, the severity of OSA can be stratified as shown in Table 75.2.

The mainstay of treatment for OSA is continuous positive airway pressure (CPAP) applied during sleep via a tight nasal or facial mask. Indications for CPAP therapy are an AHI >10 accompanied by symptoms or an AHI >30 regardless of symptoms. This technique has been proven to be efficient in preventing the collapse of the airway and improving breathing during sleep. CPAP therapy improves concentration, alertness, neurocognitive function, and mood. The CPAP has favorable effects on cardiovascular outcome but necessitates a strict commitment from the patient. The addition of humidification, bi-level positive airway pressure (BiPAP), and auto-titration of positive airway pressure has been tried to improve compliance and patient comfort. Mandibular repositioning appliances represent a simple and noninvasive alternative method of treatment for mild OSA (AHI 5 to 15) and are used in
patients who are unable to tolerate CPAP. The mechanism of action is similar to the jaw-thrust technique. Surgery is reserved for severe OSA or lack of response to CPAP. The main objective of any surgical technique is to enlarge the upper airway. Adenoidectomy, tonsillectomy, nasal polypectomy, septoplasty, uvulopalatopharyngoplasty, maxillomandibular advancement and hyoid expansion are all procedures used to alleviate the symptoms of OSA
surgically. If these are unsuccessful and the obstruction is severe, the last option is tracheostomy. As adjuvant therapy, the following may be helpful: losing weight, position therapy, topical application of soft tissue lubricant, and the use of acetazolamide to increase respiratory drive to compensate for the metabolic acidosis caused by hypoxia.

The natural history of sleep apnea is not yet fully described, but the mortality is increased with the development of cardiovascular complications, especially in the middle-aged population. CPAP, surgery, and dieting can improve the outcome and lower the risk of death from cardiovascular complications.