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Obstructive sleep apnea (OSA) is a major problem in the United States and is associated with serious health complications. Noninvasive treatment with continuous positive airway pressure (CPAP) therapy remains the gold standard therapy, and it is typically recommended that patients try CPAP before considering alternative treatment options. For patients who are intolerant to CPAP therapy, surgical alternatives may be appropriate.
History and physical exam can help differentiate between snoring and sleep apnea. A thorough history and physical, input from a bed partner, and the Epworth Sleepiness Scale can help determine which patients need further diagnostic workup, such as polysomnography.
Identification of the site of airway obstruction should be performed prior to any attempted OSA surgery. Drug-induced sleep endoscopy may help to define the site of obstruction. A wide variety of surgical techniques are used for the treatment of OSA. Surgery should be tailored for each patient based on anatomic variations, severity of sleep apnea, and patient preference.
Elevated risk factors for OSA:
Age greater than 65 years
Body mass index (BMI) greater than 30 kg/m 2
Postmenopausal female
African American or Asian race
Male sex
Neck circumference greater than 17 inches in men and 16 inches in women
Although obesity is a risk factor for sleep apnea, an underweight patient may also have severe OSA.
Patients with OSA most likely to respond best to surgical therapy are those with “kissing” or 4+ tonsils.
Tracheotomy remains the most definitive surgical treatment for OSA. It bypasses the upper airway entirely and is effective in almost all patients, including those with severe disease.
Patients with craniofacial anomalies may benefit from correction of their skeletal deformity prior to soft tissue surgery for the treatment of OSA.
Snoring is simply noisy breathing during sleep that occurs due to the vibration of lax tissue in the upper airway. SDB is characterized by snoring along with symptoms suggestive of OSA, including daytime somnolence and snoring. Sleep-disordered breathing exists along a continuum of severity. UARS represents the mildest form of SDB and is characterized by a normal apnea-hypopnea index (AHI) with an elevated respiratory disturbance index (RDI), indicative of respiratory events that fragment sleep quality but are not severe enough to cause oxygen desaturation. OSA, the most severe form of SDB, affects quality of life and is potentially life-threatening. In adults, OSA is defined by an AHI of greater than five events per hour during sleep, as revealed by polysomnography. OSA is caused by upper airway tissue collapse resulting in airway obstruction.
Snoring is very common across the population. Based on self-report questionnaires and questionnaires, 40% of middle-aged men and 28% of middle-aged women snore. This increased to as high as 84% and 73%, respectively, in the seventh decade of life. It is estimated that as many as 3% to 7% of men and 2% to 5% of women have OSA. It has been shown that the prevalence is even higher in obese, senior, postmenopausal, and minority populations. The risk of OSA is higher when a person has a close relative (parent, child, or sibling) with OSA.
Snoring is caused by variations in airflow across dynamic portions of the upper airway, which results in the vibration of soft tissues. Most commonly, it occurs in the areas of the uvula, soft palate, tonsillar pillars, and/or pharyngeal walls. Occasionally, it may also occur at the base of the tongue or the epiglottis. OSA occurs secondary to collapse at the anatomic levels mentioned above, with airway collapse that is significant enough to not only result in vibratory snoring but also affect airflow and disruption in oxygen saturation. Obesity often contributes to snoring and apnea due to increased weight of the neck tissues; increased fat in the parapharyngeal space, which narrows the pharynx; redundancy in the soft palate; and fullness in the tongue base.
OSA refers to a collection of conditions and syndromes that have periods of apnea , a temporary cessation of breathing (defined as intermittent cessation of airflow during sleep that lasts 10 seconds or longer), and/or hypopneas (defined as a partial reduction in airflow that results in oxygen desaturation) as key occurrences. It was initially described in the early 1800s. One of the first accounts was written by Charles Dickens in 1837 and titled The Posthumous Papers of the Pickwick Club . Subsequently, William Osler coined the term “pickwickian” in 1918 to describe the obese, hypersomnolent patient. The pathogenesis and pathophysiology of OSA have been extensively studied. During sleep, the upper airway is occluded, resulting in an episode of obstructive apnea. As a result, the patient experiences brief arousal from sleep. With the return of breathing, the patient typically returns to sleep quickly. This sequence is repeated many times.
Over the years, various sleep apnea syndromes have been described and classified into three main types: central, obstructive, and mixed . Central sleep apnea refers to apneas notable for cessation of airflow due to cessation of breathing effort . Obstructive sleep apnea (OSA) refers to apnea due primarily to the collapse of the upper airway during sleep. Mixed apnea refers to apnea with both central and obstructive characteristics. Of the three main types of apneas, OSA is the most common and has received the most scientific interest and study.
Snoring, restless sleep, witnessed episodes of choking or gasping for air while sleeping, excessive daytime somnolence, morning headaches, nocturia, changes in mood (depression, irritability, anxiety, aggression), poor concentration, memory loss, night sweats, and bruxism.
Obesity: Obesity is very common in patients with OSA. Although being overweight is not necessary for OSA, truncal obesity predisposes patients to sleep apnea. In patients with a small airway diameter at baseline, even modest weight gain can cause OSA.
Hypothyroidism: There appears to be a link between hypothyroidism and OSA beyond increased BMI alone. It is thought that mucoprotein and hyaluronic acid deposition in the upper airway may be related to increased airway compression. Treating underlying hypothyroidism often improves sleep apnea, independent of weight change or pulmonary function.
Acromegaly: Tongue enlargement and skeletal changes, including increased head size, can also impact the airway and predispose patients to OSA.
Gastroesophageal reflux disease (GERD): GERD is commonly present alongside OSA. Changing intrathoracic pressures and obesity predispose patients to reflux, and the inflammation caused by untreated GERD has been shown to worsen sleep apnea.
Polycystic ovarian syndrome: Hormone dysregulation in PCOS can lead to increased frequency of apneic episodes in women with an anatomic predisposition for pharyngeal collapse. Hormonal changes associated with postmenopausal women have also been shown to cause a higher incidence of OSA.
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