For a more detailed discussion, see Douglas NJ: Sleep Apnea, Chap. 265, p. 2186, in HPIM-18.
Sleep apnea is defined by the presence of at least five episodes per hour of apnea (no airflow for ≥10 seconds) and/or hypopnea (reduction in airflow by at least 50% from baseline for ≥10 seconds). Obstructive sleep apnea/hypopnea syndrome (OSAHS) is the most common medical cause of daytime somnolence. OSAHS is caused by upper airway closure during inspiration, punctuated by brief arousals that terminate apneic episodes. Risk factors for OSAHS include obesity and anatomic shortening of the mandible or maxilla. Hypothyroidism and acromegaly are systemic diseases associated with OSAHS.
Central sleep apnea (CSA) is characterized by respiratory pauses during sleep related to absence of respiratory effort. CSA is commonly found in heart failure and stroke pts; spontaneous CSA is rare.
Symptoms of OSAHS include daytime somnolence, impaired cognitive performance and driving skills, nocturnal choking, nocturia, and decreased libido. Loud snoring is typically reported by sleeping partners. Depression and hypertension are associated with OSAHS, and cardiovascular disease risk may be increased. Differential diagnosis of OSAHS includes insufficient amount of sleep, somnolence related to shift work, depression, drug effects (both stimulants and sedatives), narcolepsy, and idiopathic hypersomnolence.
Severity of somnolence can be assessed with the Epworth Sleepiness Score, although somnolent pts who don’t fall asleep at inappropriate times may be missed with this questionnaire. Obtaining the sleep history from the pt’s partner can be very helpful. Daytime somnolence may be seen in CSA as well as OSAHS.
Physical examination should include assessment of body mass index, jaw and upper airway structure, and blood pressure. Potentially related systemic illnesses, including acromegaly and hypothyroidism, should be considered.
Diagnostic testing often includes a polysomnogram in a sleep laboratory. However, limited sleep studies without neurophysiologic monitoring may be used for screening. Significant daytime somnolence with a negative limited screening study should be followed by a full polysomnogram. Many apneic events previously labeled as central apneas in polysomnographic studies may have been obstructive events despite lack of thoracoabdominal movement.
TREATMENT Sleep Apnea
Pts with significant daytime somnolence and >15 apneic and/or hypopneic events per hour clearly benefit from treatment; benefits are less compelling with milder degrees of OSAHS. Efforts to reduce weight in obese pts, to limit alcohol use, and to carefully withdraw sedative medications should be pursued.
The primary therapy for OSAHS is continuous positive airway pressure (CPAP). Selecting a comfortable mask delivery system and titrating the appropriate amount of CPAP are essential. Airway drying related to CPAP can be reduced by including a heated humidification component in the CPAP system. Alternative OSAHS therapies include mandibular repositioning splints (oral devices), which hold the jaw and tongue forward to widen the pharyngeal airway. Several types of surgical procedures have been used in OSAHS, including bariatric surgery in obese pts, tonsillectomy, jaw advancement surgery, and pharyngeal surgery. Tracheostomy is curative since it bypasses the upper airway obstruction site, but it is rarely used. No drugs have been proven to reduce apneic events; however, modafinil may reduce sleepiness.
Treatment of CSA involves managing any predisposing conditions, such as congestive heart failure. CPAP may be effective in some CSA pts.
For a more detailed discussion, see Douglas NJ: Sleep Apnea, Chap. 265, p. 2186, in HPIM-18.