Various procedures target relief of airway obstruction in patients with OSA.

 OSA is a common yet underrecognized disorder that affects approximately 4% of middle-aged adults and 20% to 50% of elderly persons.1,2 Of the approximately 75,000 patients seen annually in sleep disorder centers, roughly 75% are diagnosed with OSA.3 Projections of the prevalence of OSA in the United States range from 7 to 18 million people.3

OSA is a potentially life-threatening condition characterized by repeated collapse of the upper airway during sleep, cessation of breathing, and clinical associations with a variety of disease states. The spectrum and severity of clinical presentations of OSA are extremely variable.

Despite the prevalence of sleep apnea, the pathogenetic mechanisms of this disorder remain not completely understood. The occurrence of upper airway obstruction during sleep and not wakefulness implicates the removal of the wakefulness stimulus to breathe as a key factor underlying upper airway obstruction during sleep. Most of the data on sleep effect are derived from studies during NREM sleep, given the difficulty in achieving REM during invasive studies in the laboratory environment.

Rationale for Surgical Intervention
Increased upper airway resistance and collapsibility in patients with OSA can be the result of an anatomic compromise. Pharyngeal resistance during wakefulness is increased in patients with OSA compared with normal individuals, and pharyngeal resistance correlates with the severity of OSA.4 The pharynx of adults with OSA collapses when experimentally exposed to subatmospheric pressure during wakefulness, whereas that of normal controls does not.5 The upper airway is anatomically smaller in patients with OSA than in normal individuals, particularly at the retropalatal and retroglossal levels. Pharyngeal cross-sectional area correlates inversely with OSA severity.6

OSA has been associated with anatomic compromise resulting from neoplasia (benign or malignant), metabolic abnormalities, and traumatic compromise. Inflammatory disorders may cause diffuse enlargement of structure such as the tongue and pharyngeal lymphoid tissues (as in tonsillitis), resulting in a compromise of the airway; however, in the majority of patients with OSA, no specific focus of upper airway pathology can be identified.

The association between obesity and OSA is well recognized. Weight gain in patients with OSA usually results in an increase in the severity of apnea. It has long been hypothesized, and later documented by magnetic resonance imaging (MRI), that the region surrounding the collapsible segment of the pharynx in patients with OSA has a greater fat load than does the same region in equally obese patients who do not have OSA. This finding—in conjunction with the finding of an increase in airway resistance and a decrease in airway stability documented when applying lard-filled bags to the neck to simulate cervical fat accumulation—suggests that the effect of obesity on OSA might be related to local parapharyngeal fat deposits.7 Histopathologic studies of uvulas excised during uvulopalatopharyngoplasty (UPPP) for OSA have demonstrated higher amounts of both fat and muscle mass compared with those seen during normal postmortem studies.8

Many people who snore or have OSA mouth-breathe during sleep.9-11 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. With the mouth 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, 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 narrowing further the oropharyngeal lumen.

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. Furthermore, the nasal mucosa, which is bypassed in mouth breathing, might have receptors that respond to airflow and serve as afferent stimuli for the neural regulatory mechanisms of respiration. Eliminating this afferent input to reflex arcs involving upper airway muscles could predispose to OSA.12,13

Nonsurgical Approaches to Management
Nonsurgical approaches to the management of OSA include behavioral modification, drug therapy, and use of mechanical devices. Behavioral modifications include avoidance of alcohol and sedative medications, alteration of sleep position, avoidance of sleep deprivation, and weight loss. Drug therapy for OSA is of limited clinical value, with the exception of thyroxine replacement in patients with hypothyroidism.14

Nasal CPAP is the initial treatment of choice for OSA in adults and can reduce mortality associated with OSA.15 CPAP allows progressive restoration of air flow, as the pressure applied exceeds the airway opening pressure. Appropriate CPAP can resolve OSA in many patients. CPAP works by pneumatically splinting the collapsible upper airway. Although effective, CPAP is uncomfortable or intolerable for some patients, and variable patient compliance remains a significant problem. Studies have found that up to 25% of patients discontinue CPAP therapy.16-18

The primary surgical options for the management of severe OSA are tracheostomy, UPPP, and laser-assisted uvulopalatoplasty (LAUP).

Tracheostomy was the initial surgical procedure performed for OSA and is effective in decreasing the morbidity and mortality of OSA. Because tracheostomy bypasses the collapsible upper airway, it is the definitive surgical treatment for OSA.19 This procedure, however, is associated with complications and significant emotional and physical morbidity. From the patient’s perspective, tracheostomy is aesthetically and socially undesirable. Nevertheless, tracheostomy remains an important surgical option in patients with severe OSA who cannot tolerate CPAP, and for whom other interventions are ineffective or unacceptable.

UPPP is currently the most commonly performed surgical procedure for the treatment of OSA.20 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 OSA.21 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 after UPPP may also contribute to suboptimal results.

Laser-Assisted Uvulopalatoplasty
LAUP has been developed for the treatment of snoring and OSA. It is performed under local anesthesia on an outpatient basis. LAUP is a multistaged 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 to traditional UPPP. LAUP is also less expensive and requires less time off from work. In a recent study evaluating the effectiveness and safety of LAUP in patients with OSA,22 during a 6-month to 5-year follow-up period (mean, 40 months), 91.5% of the patients with habitual snoring reported significant short-term improvement based on post-treatment questionnaires, whereas 79.7% reported long-term subjective improvement.

Additional Procedures
Additional surgical procedures used in selected patients with severe OSA, all of which are designed to enlarge the retropalatal airway, include uvulopalatopharyngoglossoplasty; linguoplasty; laser midline glossectomy; inferior sagittal mandibular osteotomy and genioglossal advancement with hyoid myotomy and suspension (GAHM); and maxillomandibular osteotomy (MMO).20 Laser midline glossectomy involves laser extirpation of a portion of the posterior midline tongue. Laser lingual tonsillectomy, reduction of the aryepiglottic folds, and partial epiglottectomy may be performed in selected patients. Linguoplasty involves additional extirpation of posterior and lateral tongue tissue. In GAHM, the glenoid tubercle of the mandible (the anterior attachment of the tongue) is advanced by a limited osteotomy of the mandible. MMO enlarges the retrolingual airway maximally and provides some enlargement of the retropalatal airway as well. The major drawback of MMO is that it is a complex procedure limited to only a few institutions, and is associated with significant postoperative morbidity.

The determination as to which surgical procedure to perform in the patient with OSA is more complex than merely a consideration of polysomnographic results. These results must be weighed along with the current symptoms, diagnostic results, physical examination, and current health status to determine the most appropriate and potentially successful procedure.

The consequences of OSA can be significant for those affected as well as bed partners and 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 a thorough understanding of the pathophysiology and anatomical contributions to the disease, accurate diagnosis (which includes identification of possible triggers), and institution of the appropriate therapeutic modalities, including surgery if it is warranted.

John D. Zoidis, MD, is a contributing writer for Sleep Review.

1. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A. Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med. 1998;157:144-148.
2. Peter JH, Fuchs E, Kohler U, et al. Studies in the prevalence of sleep apnea activity: evaluation of ambulatory screening results. Eur J Respir Dis. 1986;146:S451-S458.
3. Netzer NC, Hoegel JJ, Loube D, et al. Prevalence of symptoms and risk of sleep apnea in primary care. Chest. 2003;124:1406-1414.
4. Stauffer JL, Zwillich CW, Cadieux RJ, et al. Pharyngeal size and resistance in obstructive sleep apnea. Am Rev Respir Dis. 1987;136:623-627.
5. Abbott MB, Donnelly LF, Dardzinski BJ, Poe SA, Chini BA, Amin RS. Obstructive sleep apnea: MR imaging volume segmentation analysis. Radiology. 2004;232:889-895.
6. Sher AE. An overview of sleep disordered breathing for the otolaryngologist. Ear Nose Throat J. 1999;78:694-707.
7. Suratt PM, McTier RF, Wilhoit SC. Collapsibility of the nasopharyngeal airway in obstructive sleep apnea. Am Rev Respir Dis. 1985;132:967-971.
8. Walker RP, Grigg-Damberger MM, Gopalsami C, et al. Laser-assisted uvulopalatoplasty for snoring and obstructive sleep apnea: results in 170 patients. Laryngoscope. 1995;105:938-943.
9. Aloia MS, Arnedt JT, Davis JD, Riggs RL, Byrd D. Neuropsychological sequelae of obstructive sleep apnea-hypopnea syndrome: a critical review. J Int Neuropsychol Soc. 2004;10:772-785.
10. Shepard JW, Pevernagie DA, Stanson AW, et al. Effects of changes in central venous pressure on upper airway size in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 1996;153:250-254.
11. Guilleminault C, Stoohs R, Clerk M, et al. A cause of excessive daytime sleepiness: the upper airway resistance syndrome. Chest. 1993;104:781-787.
12. Badr MS, Skatrud JB, Dempsey JA, et al. Effect of mechanical loading on expiratory and inspiratory muscle activity during NREM sleep. J Appl Physiol. 1990;68:1195-1202.
13. Henke KG, Dempsey JA, Badr MS, et al. Effect of sleep-induced increase in upper airway resistance on respiratory muscle activity. J Appl Physiol. 1991;70:158-168.
14. Rajagopal KR, Abbrecht PH, Derderian SS, et al. Obstructive sleep apnea in hypothyroidism. Ann Intern Med. 1984;101:491-494.
15. He J, Kryger MH, Zorick FJ, et al. Mortality and apnea index in obstructive sleep apnea: experience in 385 male patients. Chest. 1988;94:9-14.
16. Reeves-Hoche MK, Meck R, Zwillich CW, et al. Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Dis. 1994;149:149-154.
17. Waldhorn RE, Herrick TW, Nguyen MC, et al. Long-term compliance with nasal CPAP therapy of obstructive sleep apnea. Chest. 1990;97:33-38.
18. Carswell JJ, Koenig SM. Obstructive sleep apnea: Part I. Pathophysiology, diagnosis, and medical management. J Long Term Eff Med Implants. 2004;14:167-176.
19. Thatcher GW, Maisel RH. The long-term evaluation of tracheostomy in the management of severe obstructive sleep apnea. Laryngoscope. 2003;113:201-204.
20. Benedetti JA, Hoard M, Gampper TJ. Obstructive sleep apnea: Part II. Surgical approaches to sleep apnea. J Long Term Eff Med Implants. 2004;14:177-184.
21. Friedman M, Ibrahim H, Lee G, Joseph NJ. Combined uvulo-palatopharyngoplasty and radiofrequency tongue base reduction for treatment of obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg. 2003;129:611-621.
22. Kyrmizakis DE, Chimona TS, Papadakis CE, et al. Laser-assisted uvulopalatoplasty for the treatment of snoring and mild obstructive sleep apnea syndrome. J Otolaryngol. 2003;32:174-179.