Postoperative hypoxemia in morbidly obese patients with and without obstructive sleep apnea undergoing laparoscopic...

The increased incidence of morbid obesity has resulted in an increase of bariatric surgical procedures. Obstructive sleep apnea (OSA) is a commonly encountered comorbidity in morbidly obese patients. Sedatives, analgesics, and anesthetics alter airway tone, and airway obstruction and death have been reported in patients with OSA after minimal doses of sedatives and anesthetics, yet there is a lack of consensus regarding the care of these patients. In this study, we sought to determine whether obese patients with polysomnography-confirmed diagnosis of OSA were at significantly greater risk for postoperative hypoxemic episodes in the first 24 h after laparoscopic bariatric surgery than morbidly obese patients without a diagnosis of OSA.

Adult subjects (Body Mass Index, 35-75 kg/m(2)) scheduled to undergo laparoscopic bariatric surgery were studied. A finger pulse oximetry probe was placed preoperatively and oxygen saturation (Spo(2)) was recorded continuously. All subjects underwent preoperative polysomnography testing within 4 wk of surgery. Anesthetic management was standardized, using propofol for induction and desflurane and remifentanil for maintenance of anesthesia. Patient-controlled analgesia programmed to deliver morphine, 1 mg. every 10 minutes, was used for pain management postoperatively. Hypoxemic episodes were scored as Spo(2) >4% below the polysomnography study baseline and lasting for more than 10 s.

Eight men and 32 women were enrolled and 1 subject had incomplete data. Thirty-one of the 40 subjects had polysomnography-confirmed OSA. Eight subjects used home continuous positive airway pressure devices nightly, and six of these used their device postoperatively. Preoperatively, subjects with OSA had lower nadir Spo(2) during the polysomnography study and a larger number had an apnea/hypopnea index >10 episodes per hour compared with the non-OSA group. In the first 24 h postoperatively, there was no difference in the median Spo(2) with and without oxygen therapy, between OSA and non-OSA groups. The number of episodes of oxygen desaturation >4% below the polysomnography study baseline value and the mean number of desaturation episodes per hour did not differ between the groups.

In morbidly obese subjects, in the first 24 h after laparoscopic bariatric surgery, OSA does not seem to increase the risk of postoperative hypoxemia. Our data confirm that morbidly obese subjects, with or without OSA, experience frequent oxygen desaturation episodes postoperatively, despite supplemental oxygen therapy suggesting that perioperative management strategies in morbidly obese patients undergoing laparoscopic bariatric surgery should include measures to prevent postoperative hypoxemia.