Fig. 67-6). For example, OSA patients should avoid ethanol and sedative hypnotics, since these agents increase apneas in most patients. Weight loss is recommended for obese patients and may reduce apneas and improve oxygen saturation, particularly if the obesity is moderate. However, dietary weight reduction is difficult to achieve and maintain. Surgical procedures such as gastric stapling may help morbidly obese patients. Some patients benefit from adjustment of sleeping body position; many patients have fewer apneas when sleeping on their side than when supine. Reversible causes of nasal obstruction such as chronic rhinitis should be treated. Thyroid replacement may improve sleep-disordered breathing in hypothyroid patients with sleep apnea. Most patients, however, require additional therapy beyond these steps.
see Fig. 67-6). Introduced by Sullivan and co-workers in 1981, nasal CPAP is produced by a high-flow blower that delivers a continuous stream of room air into a sealed nasal mask, which the patient wears during sleep. The positive pressure created in the circuit pneumatically splints the pharynx open. Nasal CPAP can abolish apneas and hypopneas, oxygen desaturation, and apnea-related sleep fragmentation in most patients. Patients should be studied in the sleep laboratory to determine the optimal CPAP level, which will vary with individual upper airway characteristics. CPAP pressures ranging from 5 to 15 cm H2O are most commonly required. After the initiation of effective nasal CPAP therapy, patients experience a marked rebound of deep non-REM sleep and REM sleep. Sleep patterns gradually normalize over the first few weeks of therapy in association with symptomatic improvement, particularly daytime sleepiness and function. Side effects are generally minor but may affect compliance. Some patients experience problems with nasal congestion and mask and mouth airleaks, which can reduce CPAP effectiveness. Several recent studies have now clearly demonstrated that compliance with nasal CPAP therapy is suboptimal in many patients. OSA patients require long-term follow-up, and those who experience problems that cannot be solved or whom are noncompliant may need additional therapy.
Surgical procedures designed to alter upper airway structure have proved helpful in treating OSA patients. Uvulopalatopharyngoplasty (UPPP) surgery is designed to enlarge the upper airway by removing the uvula, part of the soft palate, and redundant pharyngeal tissue. UPPP can cure snoring and OSA. However, success with UPPP surgery for sleep apnea is variable and cannot be routinely predicted preoperatively. The uvula and some palatal tissue can also be removed with laser-assisted uvuloplasty (LAUP), an outpatient procedure recently developed for the treatment of snoring. However, there are currently no published data to recommend LAUP for the treatment of sleep apnea.
Surgical correction of a deviated nasal septum, tonsillar and adenoid hypertrophy, and maxillary and mandibular hypoplasia has been shown to improve sleep-disordered breathing in selected OSA patients. Tracheostomy effectively treats OSA because the occluded pharynx is by-passed. Patients can plug the tracheostomy tube while awake and sleep with it open. However, tracheostomy is now reserved for morbidly ill patients or those who do not respond to less invasive options.
Various oral appliances have been developed to treat OSA, with some reported success. Most appliances are designed to stabilize the mandible and reduce occlusion of the pharynx by the tongue during sleep. This may be a useful alternative approach for some patients with mild to moderate OSA. However, not all patients improve, and polysomnography is recommended to assess the response to the appliance. The major side effect is oral discomfort. More experience with oral appliances is needed before they will be widely used.
A number of studies have examined the effects of supplemental oxygen on sleep and respiration in OSA patients. Although some patients have less sleep-disordered breathing and better oxygen saturation with supplemental oxygen, apneas may occasionally worsen. Supplemental oxygen should not be considered first-line therapy and should be tested during sleep before it is prescribed for the treatment of OSA.
Pharmacologic therapy for OSA has not met with great success. Protriptyline, a tricyclic antidepressant, has been widely used in some countries such as Canada. Protriptyline suppresses REM sleep and may stimulate upper airway muscle activity. It has been shown to reduce apneas, but it has substantial side effects. Ventilatory stimulants such as medroxyprogesterone are used by some clinicians to improve gas exchange in the subgroup of OSA patients with awake alveolar hypoventilation. However, such drugs do not predictably improve sleep apnea.
Revision date: June 18, 2011
Last revised: by Janet A. Staessen, MD, PhD