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Pathophysiology and Management of Obstructive Sleep Apnea in Bariatric Patients

| January 1, 2016

This column is written by medical students and is dedicated to reviewing the science behind obesity and bariatric surgery.

Column Editor: Daniel B. Jones, MD, MS, FASMBS
Professor of Surgery, Harvard Medical School, Vice Chair, Beth Israel Deaconess Medical Center, Boston, Massachusetts

This month: Pathophysiology and Management of Obstructive Sleep Apnea  in Bariatric Patients

by Sally Tan
Medical Student, Harvard Medical School, Boston, Massachusetts

ABSTRACT
The author discusses the following four clinical questions most commonly asked by bariatric surgeons caring for patients with obstructive sleep apnea: 1) How is obstructive sleep apnea diagnosed? 2) What is the pathophysiology of obstructive sleep apnea in patients with obesity? 3) What are the treatment options for obstructive sleep apnea in this patient population? 4) Which bariatric surgical procedure is best for treating obstructive sleep apnea?

Bariatric Times. 2016;13(1):16–17.


Introduction
Obstructive sleep apnea (OSA) is a common comorbidity of obesity, estimated to afflict up to 71 percent of bariatric surgery patients.[1] OSA impairs quality of life for these patients, and emerging evidence suggests it may even perpetuate the endocrine imbalances that drive weight gain. Bariatric surgery is the most effective option for long-term weight loss, and patients often experience dramatic improvement in OSA symptoms following surgery. This article reviews the latest literature about OSA pathophysiology, diagnosis, and treatment as a practical guide for bariatric surgeons caring for patients with OSA.

Pathophysiology and Diagnosis of OSA
Sleep apnea is a disease involving intermittent collapse of the upper airways resulting in frequent episodes of apnea and hypopnea during sleep. Patients with obesity are particularly prone to developing sleep apnea because fat tissue deposition in the parapharyngeal region narrows airway luminal diameter and increases collapsing transmural pressure.[2] A dose-response relationship exists between sleep apnea and obesity, as the odds ratio of developing OSA increases by 1.14 with each unit increase in BMI.[3]

Intermittent obstruction of airways in OSA causes patients to report restless sleep and daytime somnolence, which can be quantified by the Epworth Sleepiness Scale.[4] Physiologically, apneic and hypopneic episodes lead to intermittent hypoxemia and hypercapnia, which stimulates pulmonary vasoconstriction and over the long-term causes pulmonary hypertension.[5]

Polysomnography, the definitive diagnosis for OSA, measures the number of apneic and hypopneic episodes during sleep. The Apnea Hypopnea Index (AHI) is defined as the total number of apneic and apneic plus hypopneic episodes divided by the total sleep duration in hours. Mild OSA is characterized by an AHI of 5 to 15 events/hour, moderate OSA 15 to 30 events/hour, and severe OSA more than 30 events per hour.[6]

OSA in the Bariatric Patient
Just as obesity increases risk for OSA, the reverse can also be true. Daytime somnolence associated with sleep apnea causes patients to generally exercise less, and this inactivity can perpetuate weight gain.[5]

New evidence suggests that OSA may also interfere with endocrine regulation. Leptin is a hormone that suppresses appetite, and obesity is associated with elevated leptin levels and resistance to leptin. Similarly, individuals with OSA also have 50-percent elevated leptin levels without the feeling of satiety.[7,8]

Endocrine dysfunction in OSA has additionally been independently linked to increased prevalence of type 2 diabetes mellitus and insulin resistance. Mechanistically, the intermittent hypoxia associated with sleep apnea is thought to cause insulin resistance by sympathetic activation and fragmentation of sleep cycles.[9] Moreover, metabolically dysfunctional adipose tissue in individuals with obesity contain macrophages that secrete pro-inflammatory cytokines IL-6 and TNF-α, while lean individuals’ macrophages secrete anti-inflammatory factors, such as IL-10 and adiponectin. Intermittent hypoxia in OSA is a potent pro-inflammatory stimulus, and has a synergistic effect on adipose tissue inflammation.[10]

Management of OSA
Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP) are first-line treatments for symptomatic OSA. By appropriately titrating positive airway pressure and selecting a well-fitted mouth appliance, these treatments decrease airway collapse during sleep.[11] Emerging evidence suggests that CPAP also improves OSA-associated comorbidities such as hypertension. Several studies have shown that CPAP decreases systemic blood pressure, though the effect size is small.[12–13]

For patients with refractory OSA symptoms on CPAP/BiPAP or with identifiable anatomic obstruction, surgical management of OSA is an option. Surgery aims to rectify often multiple levels of obstruction in the nasal, retropalatal, retroglossal, and hypopharyngeal regions. Uvulopalatopharyngoplasty (UPPP) is the most common surgical treatment for OSA in adults, and involves removal of the uvula, a portion of the soft palate and tonsils, and closure of the tonsillar pillars to increase the diameter of the pharyngeal airway and reduce obstruction. Nasal surgery, such as septoplasty or resection of inferior turbinates, improves CPAP compliance and produces subjective improvement in OSA symptoms. Tonsillectomy improves AHI scores and CPAP compliance, and is recommended as primary surgical treatment for select patients with tonsillar hypertrophy.[14]

Bariatric Surgery as OSA Treatment
Patients with obesity are often poor candidates for the aforementioned surgeries given their multiple comorbidities. In this population, bariatric surgery is widely recognized as an effective treatment for OSA, with most symptoms resolving within the first few months following surgery.[15] A recent review by Sarkhosh et al[16] compared OSA outcomes after various types of bariatric surgery and found significant OSA symptom improvement regardless of the type of surgery (Table 1). This study found preliminary evidence to suggest that malabsorptive procedures like biliopancreatic diversion (BPD) are more efficacious than purely restrictive ones like laparoscopic gastric banding (LAGB) at treating OSA.[16] Theoretically, both sleep apnea and obesity are linked to systemic inflammation, and malabsorptive procedures result in a protective anti-inflammatory state following surgery.[17] However, additional mechanistic studies to understand the post-surgical physiologic changes underlying OSA resolution are still needed.

Conclusion
OSA is a common comorbidity in bariatric patients, driven by shared pathophysiologic causes. CPAP/BiPAP are effective first-line treatments for OSA, though patients with refractory symptoms may benefit from surgical management. Patients with obesity are often poor candidates for these procedures, making bariatric surgery a definitive treatment for OSA in this patient population.

Acknowledgment
Ms. Tan would like to thank Stephanie B. Jones, MD, for her assistance with reviewing this article.

References
1.     Peromaa-Haavisto P, Tuomilehto H, Kössi J, et al. Prevalence of obstructive sleep apneoa among patients admitted for bariatric surgery: A prospective multicentre trial. Obes Surg. 2015 Nov 11. [Epub ahead of print]
2.    Maciel Santos MES, Rocha NS, Laureano Filho JR, et al. Obstructive sleep apnea-hypopnea syndrome—The role of bariatric and maxillofacial surgeries. Obes Surg. 2009;19:796–801.
3.    Pannain S, Mokhlesi B. Bariatric surgery and its impact on sleep architecture, sleep-disordered breathing, and metabolism. Best Pract Res Clin Endocrinol Metab. 2010;24(5):745–761.
4.    Fleisher KE, Krieger AC. Current trends in the treatment of obstructive sleep apnea. J Oral Maxillofac Surg. 2007;65(10):2056–2068.
5.    Fritscher LG, Mottin CC, Canani S, et al. Obesity and obstructive sleep apnea-hypopnea syndrome: The impact of bariatric surgery. Obes Surg. 2007;17:95–99.
6.    Caples SM, Gami AS, Somers IK. Obstructive sleep apnea. Ann Int Med. 2005;142:187–197.
7.    Marik P. Leptin, obesity, and obstructive sleep apnea. Chest. 2009;118:569–571.
8.    Wolk R, Ahamsuzzaman A, Somers VK. Obesity, sleep apnea, and hypertension. Hypertension. 2003;42:1067–1074.
9.    Kent B, McNicholas WT, Ryan S. Insulin resistance, glucose intolerance and diabetes mellitus in obstructive sleep apnoea. J Thorac Dis. 2015;7(8):1343–1357.
10.    Ouchi N, Parker JL, Lugus JJ, et al. Adipokines in inflammation and metabolic disease. Nat Rev Immunol. 2011;11:85–97.
11.    Ballard RD. Management of patients with obstructive sleep apnea. J Fam Pract. 2008;57(8 Suppl):S24–30.
12.    Martinez-Garcia MA, Capote F, Campos-Rodriguez F, et al. Effect of CPAP on blood pressure in patients with obstructive sleep apnea and resistant hypertension: the HIPARCO randomized clinical trial. JAMA. 2013;310(22):2407–2415.
13.    Fava C, Dorigoni S, Dalle Vedove F, et al. Effect of CPAP on blood pressure in patients with OSA/hypopnea: a systemic review and meta-analysis. Chest. 2014;145(4):762–771.
14.    Smith DF, Cohen AP, Ishman SL. Surgical management of OSA in adults. Chest. 2015;147(6):1681–1690.
15.    Ravesloot MJL, Hilgevoord AAJ, van Wagensveld BA, et al. Assessment of the effect of bariatric surgery on obstructive sleep apnea at two postoperative intervals. Obes Surg. 2014;24:22–31.
16.    Sarkhosh K, Switzer NJ, El-Hadi, M et al. The impact of bariatric surgery on obstructive sleep apnea: A systematic review. Obes Surg. 2013;23:414–423.
17.    Pallayova M, Steele KE, Magnuson TH et al. Sleep apnea determines soluble TNF-alpha receptor 2 response to massive weight loss. Obes Surg. 2011;21(9):1413–1423.

FUNDING: No funding was provided.

FINANCIAL DISCLOSURES: The author reports no conflicts of interest relevant to the content of this article.

 

Category: Past Articles, The Medical Student Notebook

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