Treatment of severe obstructive sleep apnea is imperative because the associated mortality and morbidity are high. A hallmark study showed that 40 percent of people with an apnea-hypopnea index greater than 20 died over an eight-year period if untreated.¹

The type of treatment for OSA in part depends on the severity. People with mild apnea have a wider variety of options, including oral appliances, while patients with moderate-to-severe apnea should be treated with nasal continuous positive airway pressure - the standard of care.

A growing number of people, though, are also finding that bariatric surgery leads to improvements in OSA symptoms.

Basics of Bariatric Surgery
Surgery for morbid (clinically severe) obesity (body mass index > 40 kg/m²) should be considered a treatment of last resort after dieting, exercise, psychotherapy, and drug treatments have all failed.

The 1991 National Institutes of Health Consensus Conference on Gastrointestinal Surgery for Severe Obesity concluded that "patients whose BMIs exceed 40 kg/m² are potential candidates for surgery if they desire substantial weight loss because obesity severely impairs the quality of their lives."

In certain instances, less severely obese patients (those with a BMI between 35 and 40 kg/m²) also may be considered for surgery. Patients in this category include those with high-risk co-morbid conditions such as life-threatening cardiopulmonary problems (e.g., OSA) or severe diabetes mellitus.²

Surgeons have performed a number of operations in the treatment of clinically severe obesity. They're known collectively as bariatric surgery, a term coined from the Greek words for weight and treatment.

Approximately 140,000 weight-reduction procedures were performed in the U.S. in 2004 alone. The number of such procedures rose by 450 percent from 1998 to 2002. Eighty percent of the patients are women; most are middle-aged or younger.

The current gold standard for the surgical treatment of clinically severe obesity is the gastric bypass (GB). This operation was first performed for obesity more than 30 years ago and was developed after surgeons observed massive weight loss in patients undergoing gastric surgery for ulcers or cancer. Approximately 75 percent of all operations performed for severe obesity in the U.S. are now of this type.

A small pouch (around 30 cc or one fluid ounce in size) is created by stapling across the top of the stomach, causing massive restriction in food intake.

A section of the small intestine (two to five feet in length) is attached to it so that food can bypass the duodenum and the first portion of the small intestine, reducing calorie and fat absorption.

The anastomosis from the gastric pouch to the jejunum is kept small (around 12 mm) so that food and fluids can only pass very slowly into the intestine, again limiting the number of calories that can be absorbed from food at any one time.

Most patients can expect to lose 67 percent of their excess weight two years after GB surgery.³ Long-term weight regain at nine years after surgery is approximately only 10 percent to 15 percent of initial weight loss.

Resolution of OSA After Surgery
GB surgery not only induces significant weight loss in successful patients but also leads to marked improvements in associated co-morbidities. A recent survey demonstrated that OSA occurs in up to 60 percent of patients undergoing bariatric surgery.

Researchers examined the effect of weight loss following bariatric surgery on OSA.⁴ One hundred consecutive patients with symptoms of OSA were prospectively evaluated by polysomnography before GB. The investigators compared preoperative and postoperative scores of Epworth Sleepiness Scale (ESS), respiratory disturbance index (RDI), and other parameters of sleep quality.

Preoperative RDI was 40 ± 4 (normal 5 events/hour). Thirteen patients had no OSA, 29 had mild OSA, while the remaining 58 patients were treated preoperatively for moderate-to-severe OSA.

At a median of six months follow-up, BMI and ESS scores improved (38 1 kg/m² vs. 54 1 kg/m², 6 ± 1 vs. 12 ± 0.1, postoperatively vs. preoperatively).

Eleven patients completed postoperative polysomnography (three to 21 months) after losing weight (postoperative BMI 40 ± 2 kg/m² vs. preoperative BMI 62 ± 3 kg/m²). They had significant improvement in ESS (3 ± 1 vs. 14 ± 2); minimum oxygen saturation (SpO₂ 86 ± 2 percent vs. 77 ± 5 percent); sleep efficiency (85 ± 2 percent vs. 65 ± 5 percent); and RDI (56 ± 13 vs. 23 ± 7, P = 0.041).

Regression analysis demonstrated no correlation between preoperative BMI, ESS score, and the severity of OSA, and no correlation between percent excess body weight loss and postoperative RDI.

A similar study compared sleep quality before and after bariatric surgery in 13 patients.⁵ Pretreatment polysomnographic recordings of patients with OSA demonstrated considerable reduction of deep and REM sleep stages with a correspondent prolongation of wake within sleep or non-REM sleep stages 1 and 2.

After surgical weight reduction, repeated polysomnographic recordings revealed considerable improvement or even a complete recovery of breathing in sleep and a normalization of sleep structure.

Non-REM deep sleep stages (3 and 4) augmented from 5.51 ± 2.53 percent (mean + SEM) to 22.69 ± 3.56 percent and the REM stage increased from 9.91 ± 1.78 percent to 18.15 ± 2.13 percent.

Obesity hypoventilation syndrome (OHS, characterized by hypoxemia and hypercarbia while awake) often is associated with OSA. One group showed that 126 (12.5 percent) of 1,010 patients undergoing GB surgery demonstrated OSA and/or OHS.⁶

In the 12 patients in whom arterial blood gases were available more than five years after surgery, PaO₂ increased from 54 ± 10 mm Hg to 68 ± 20 mm Hg and PaCO₂ fell from 53 ± 9 mm Hg to 47 ± 11 mm Hg.

Postoperative pulmonary function tests showed significant improvement in expiratory reserve volumes after surgery, suggesting improvement in the alveolar collapse and shunting during expiration typically seen in obesity-induced restrictive lung disease.

The researchers also saw reductions in pulmonary artery pressures in OHS patients after surgery. These were typically elevated before surgery but normal three to nine months after the procedure.

OSA as a Risk Factor
Although morbidly obese patients with OSA can anticipate significant amelioration in their sleep condition after GB surgery, it's important to realize that their apnea puts them at a higher risk of postoperative complications when compared to patients with similar BMI but no OSA.

Researchers retrospectively reviewed the hospital records of 311 patients who underwent GB in a six-month period.⁷ They found that a preoperative history of OSA predicted a longer length of stay after GB surgery.

Other investigators found that severe respiratory insufficiency of obesity (OSA with or without OHS) predicted a 2.4 percent perioperative mortality rate vs. 0.2 percent mortality in those patients with no significant pulmonary dysfunction.⁶

CPAP in the Postop Patient
Physicians haven't universally accepted the use of CPAP for patients with OSA following upper gastrointestinal surgery because of concerns that pressurized air will inflate the stomach and proximal intestine, resulting in anastomotic disruption.

A 2002 study assessed the safety and efficacy of postoperative CPAP for patients undergoing a gastrojejunostomy as part of a GB procedure.⁸ Researchers prospectively evaluated 1,067 patients (837 women and 230 men) for the risk of developing anastomotic leaks and pulmonary complications after the GB procedure. Of the 1,067 patients, 420 had OSA and 159 were dependent on CPAP.

There were 15 major anastomotic leaks, two of which occurred in CPAP-treated patients. Despite the theoretical risk of anastomotic injury from pressurized air delivered by CPAP, no anastomotic leaks were attributed to the device.

A more recent study of 415 laparoscopic GB patients, 64 of whom had OSA, confirmed that routine use of CPAP after GB doesn't convey added risk of anastomotic disruption to patients with significant OSA.⁹

Encouraging CPAP
OSA is a serious medical condition, linked to systemic hypertension, pulmonary hypertension, and cor pulmonale. Up to 24 percent of middle-aged men may be afflicted with this condition.

The most significant risk factor for OSA is obesity. Alterations in the severity of the condition are closely related to changes in an individual's weight. Medical and surgical treatment of severe obesity improves associated OSA. The presence of OSA in patients undergoing bariatric surgery, however, significantly increases the incidence of morbidity and mortality in the postoperative period.

The presence of OSA in patients who are less than 100 pounds above their ideal body weight can sometimes help to obtain approval for bariatric surgery from insurance companies who would otherwise deny services to patients requesting such surgery.

Most insurance companies cover bariatric surgery (including many state Medicaid programs and Medicare), although requirements for approval vary considerably. Preoperative evaluations from a dietician and a mental health provider are almost universally required, and many carriers now mandate six-to-12-month medically supervised weight loss programs prior to authorization.

The use of CPAP to treat OSA in the early postoperative period after GB surgery should be encouraged because it can be safely administered and should reduce the incidence of pulmonary complications occurring after the procedure.

Elliot R. Goodman, MD, is an attending physician in the department of surgery, Beth Israel Medical Center, New York City.

For a list of references, please visit http://Respiratory-care-sleep-medicine.advanceweb.com/Editorial/Content/editorial.aspx?CC=71744.