Proper management of sleep apnea can reduce the significant consequences of this disorder, which can include frequent arousals, daytime sleepiness, even death.

 Screening studies1,2 in the United States, Europe, and Australia have shown that a substantial proportion of the adult population has mild-to-moderate sleep apnea. According to the American Lung Association,3 as many as 18 million US residents have sleep apnea. Despite its prevalence, the mechanisms underlying this disorder remain incompletely understood. The reduction in dilating muscle tone of the upper airway caused by sleep is associated with reduced upper-airway caliber and increased pharyngeal-wall compliance.4 The resulting combination of increased resistance and decreased inspiratory flow leads to increased work of breathing, hypoventilation, and frequent arousals from sleep, with excessive daytime sleepiness. This distinct clinical entity is upper-airway resistance syndrome.5

Airway Patency
Some studies6 have suggested that the pharyngeal airway is smaller in patients with sleep apnea, even when they are awake. The airway also has an anteroposterior configuration.6 Negative intraluminal pressure generated by thoracic muscle activity is thought to induce upper-airway obstruction in patients with sleep apnea.7 In addition, when inspiratory narrowing during sleep occurs, the ensuing increase in air velocity results in decreased intraluminal pressure.8 Subsequently, intraluminal pressure becomes more negative and, hence, more conducive to upper-airway collapse.

The compliance of the pharyngeal wall is an important determinant of the effect of transmural pressure.8 A stiff pharyngeal wall (as seen during wakefulness) remains patent even with significant transmural pressure. In contrast, a compliant upper airway (as seen in patients with sleep apnea) closes even at atmospheric pressure.

The intrinsic stiffness of the pharyngeal wall is attributed to both neuromuscular and other factors. Upper-airway dilating muscles are presumed to be critical to the preservation of upper-airway patency, but there is conflicting evidence regarding the effect of upper-airway muscles on pharyngeal compliance.

The upper airway is connected to the thoracic cage and the mediastinum by several structures. Increased lung volume during inspiration is associated with larger upper-airway caliber in people who are awake, probably because thoracic inspiratory activity exerts caudal traction on the upper airway.9 Caudal traction may transmit subatmospheric pressure through the trachea and ventrolateral cervical structures to the soft tissues surrounding the upper airway, increasing transmural pressure and dilating the pharyngeal airway. This mechanism has been exhibited by sleeping subjects as reduced upper-airway resistance and increased retropalatal airway size when end-expiratory lung volume was increased using passive inflation.10

Caudal traction may either dilate or stiffen the pharyngeal airway.9 Patients with sleep apnea may be more dependent on the effects of increased lung volume because dilation and/or stiffening may be more pronounced in a highly compliant upper airway.

Increased upper-airway resistance and collapsibility in patients with sleep apnea can be the result of an anatomical compromise. Pharyngeal resistance during wakefulness is increased in patients with sleep apnea, and pharyngeal resistance correlates with the severity of sleep apnea.11 The pharynges of adults with sleep apnea collapse when experimentally exposed to subatmospheric pressure during wakefulness, whereas those of healthy controls do not.12 The upper airway is smaller in patients with sleep apnea, particularly at the retropalatal and retroglossal levels. Pharyngeal cross-sectional area correlates inversely with the severity of sleep apnea.13

Sleep apnea has been associated with anatomical compromise resulting from neoplasia (benign or malignant), metabolic abnormalities, and trauma.13 Inflammatory disorders may cause diffuse enlargement of structures such as the tongue and pharyngeal lymphoid tissues (as in tonsillitis), but in the majority of patients with sleep apnea, no specific focus of upper-airway pathology can be identified.

The association between obesity and sleep apnea is well recognized. Weight gain in patients with sleep apnea usually results in an increase in the severity of apnea. The region surrounding the collapsible segment of the pharynx in patients with sleep apnea is believed to have a greater fat load than does the same region in equally obese patients who do not have sleep apnea. This, in conjunction with an increase in airway resistance and a decrease in airway stability documented14 when lard-filled bags were applied to the neck to simulate cervical fat accumulation, suggests that the effect of obesity on sleep apnea might be related to local parapharyngeal fat deposits. Histopathological studies of uvulae excised during uvulopalatopharyngoplasty (UPPP) for sleep apnea had higher amounts of both fat and muscle mass than those seen during normal postmortem studies.15

Many people who snore or have sleep apnea mouth breathe during sleep. Although this has not been systematically investigated, increased nasal or nasopharyngeal resistance might explain it. The open-mouth posture unfavorably alters the pharyngeal airway by creating a relatively unstable passage. When the mouth is open, the tongue and soft palate are exposed to atmospheric pressure. This releases the anterior part of the tongue (producing a dorsal motion of the belly of the genioglossus muscle) and decreases the dimensions of the oropharyngeal lumen. The entire transmural pressure of the pharynx is exerted across the soft palate, moving it dorsally and further narrowing the oropharyngeal lumen.

The open-mouth posture further compromises the pharyngeal airway by diminishing the length of the axis of action of the genioglossus and, therefore, its efficacy in pulling the tongue forward out of the airway. Further, the nasal mucosa might have receptors, bypassed during mouth breathing, that respond to airflow and serve as afferent stimuli for the neural regulation of respiration. Eliminating this afferent input could predispose an individual to sleep apnea.

Clinical investigations13 have confirmed that nasal obstruction exacerbates a tendency toward sleep apnea. The larynx, as the other high-resistance structure in the upper airway, can also contribute to sleep apnea when compromised by space-occupying lesions or abductor paralysis.

Sleep apnea is associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleeping hours. This was demonstrated recently in a postmortem review16 of polysomnograms and death certificates for 112 patients who had undergone polysomnography and had died suddenly from cardiac causes. For four equal parts of the day, the investigators compared the rates of sudden death from cardiac causes for patients with sleep apnea with the rates for people without sleep apnea, the rates for the general population, and the rates expected according to chance alone. From midnight to 6 am, sudden death from cardiac causes had occurred in 46% of people with sleep apnea, compared with 21% of people without sleep apnea (P=.01). The increased risk of sudden cardiac death during sleeping hours among patients with sleep apnea contrasts strikingly with the low incidence of sudden cardiac death during sleeping hours in people without sleep apnea.

Nonsurgical Management
Nonsurgical approaches to the management of sleep apnea include behavioral modification, drug therapy, and the use of mechanical devices. Behavioral modifications consist of avoiding alcohol and sedative medications, changing sleep positions, avoiding sleep deprivation, and losing weight. Drug therapy for sleep apnea is of limited clinical value, with the exception of thyroxine replacement for patients with hypothyroidism.17

Nasal continuous positive airway pressure (CPAP) is the initial treatment of choice for sleep apnea in adults and can reduce mortality associated with sleep apnea.18 Patient compliance remains a significant problem; studies19,20 have found that up to 25% of patients discontinue CPAP therapy.

Surgical Management
There are numerous surgical options for the management of severe sleep apnea. Tracheostomy was the first procedure performed for sleep apnea, and is still considered effective in decreasing the morbidity and mortality associated with the disorder. This procedure, however, is associated with complications and significant emotional and physical morbidity.21 From the patient’s perspective, tracheostomy may be aesthetically and socially undesirable. Nevertheless, tracheostomy remains an important surgical option in patients with severe sleep apnea who cannot tolerate CPAP, and for whom other interventions are ineffective or unacceptable.

UPPP is the most commonly performed surgical procedure for the treatment of sleep apnea.21 UPPP enlarges the retropalatal upper airway by excising a portion of the posterior soft palate and uvula, with trimming and reorientation of the tonsillar pillars. The tonsils, if present, are excised as well. Historically, UPPP has been considered effective in about 50% of patients with sleep apnea.21,22 These suboptimal results are due largely to unresolved obstruction of the upper airway in sites other than the retropalatal region. Preoperative screening studies are now used to identify patients in whom the retropalate is the primary site of obstruction and in whom UPPP is more likely to be effective. Significant weight gain, if it occurs after UPPP, may also contribute to suboptimal results.

Laser-assisted uvulopalatoplasty (LAUP) has been developed for the treatment of snoring and sleep apnea. It is performed under local anesthesia on an outpatient basis. LAUP is a multistage procedure that involves carbon dioxide–laser excision of the uvula and a small portion of the soft palate at each stage. The goal of staging is to excise the least amount of palatal tissue needed to reduce snoring effectively while reducing the risk of velopharyngeal insufficiency. LAUP has been reported to reduce morbidity, such as pain and bleeding, as compared with traditional UPPP.23 LAUP is also less expensive, and patients may require less time off work for recovery.

Additional surgical procedures used in selected patients with severe sleep apnea are all designed to enlarge the retropalatal airway and include uvulopalatopharyngoglossoplasty, linguoplasty, laser midline glossectomy, inferior sagittal mandibular osteotomy and genioglossal advancement with hyoid myotomy and suspension, and maxillomandibular osteotomy.

The consequences of sleep apnea can be significant for patients, their bed partners, and their family members. Although many patients try to self-manage their symptoms, most will eventually seek treatment if symptoms are unrelenting and/or progressive. Optimal management depends on accurate diagnosis, which includes identification of possible triggers and institution of CPAP and other appropriate therapeutic modalities.

John D. Zoidis, MD, is a contributing writer for RT.

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