Wisconsin Medical Journal

Authors are with the Medical College of Wisconsin. Doctor Meyer is a resident in Otolaryngology and Communication Sciences; Dr. Woodson is Associate Professor Otolaryngology and Communication Sciences. INTRODUCTION Primary snoring and obstructive sleep apnea (OSA) lie at separate extremes of a continuum of sleep-related breathing disorders. In the 30-year-old population, 20% of men and 5% of women will snore. These numbers rise to 60% and 40% respectively by age 60. It is estimated that 4% of adult males and 2% of adult females have OSA, which makes the disease as common as asthma.1 Although snoring without any features of obstruction may not have detectable health consequences2 per se (aside from sleep interruption of bed partners), individuals suffering from OSA have substantially increased risks for high blood pressure (2x normal),3 heart attack (23x normal),4 stroke (1.5 x normal),5 headaches, sexual impotence, impaired intellectual function, and depression.6 These individuals also pose further risk to themselves and society as their excessive sleepiness may cause them to fall asleep in the work environment, with a 15 times increased incidence in motor vehicle accidents as compared to normal drivers.7 The fundamental abnormality of both snoring and OSA is a structurally small and unusually collapsible upper airway.8 These abnormalities may be skeletal or soft tissue, and interact with body mass index, ventilatory control mechanisms, or other undefined variables to determine apnea severity. The goal of surgery is to enlarge and reconstruct the upper airway to prevent collapse and obstruction. Multiple techniques are evolving to achieve this goal and to reduce both disease and surgical morbidity. There are at least 8 different sites at which obstruction can occur: nasal (deviated septum, enlarged turbinates, enlarged adenoids, nasal polyps), soft palate and uvula (retropalatal), tonsils (palatine and lingual), tongue base (retrolingual), mandible (retrognathism), lateral pharyngeal walls (pharyngeal muscle hypertrophy or laxity, mucosal redundancy), hyoid and epiglottis. In addition to anatomic obstruction from the above areas, decreased dilating forces of the pharyngeal musculature during sleep and negative inspiratory pressure generated by the diaphragm can contribute to the development of obstruction. Treatment and surgical procedures must keep all these factors in mind, and often therapy must be targeted to multiple anatomic sites to result in appreciable relief. There are multiple treatments for OSA (see Table 1). For individuals with severe OSA (Respiratory Disturbance Index [RDI] >40), continuous positive airway pressure (CPAP), maxillo-mandibular advancement (MMA), and tracheotomy are the only modalities shown to provide significant cure. The convenience and efficacy of CPAP make it the first line treatment for OSA.9,10 Many of the other surgical modalities used for OSA should be viewed as adjunct to CPAP or as a measure to improve tolerance to CPAP. When consistently used, CPAP can provide significant improvement in sleepiness, impaired intellectual function, and normalize increased cardiovascular risk. Unfortunately, compliance is the greatest hurdle. Up to 30% of patients will refuse CPAP at initial trial, and even when agreeing to use the device, only 50% of users will be compliant.11,12