This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Ahmad, S. Articles by Prystowsky, J. Search for Related Content PubMed PubMed Citation Articles by Ahmad, S. Articles by Prystowsky, J. Related Collections Postanesthetic Care Unit Complications Patient Safety

---

PATIENT SAFETY

Postoperative Hypoxemia in Morbidly Obese Patients With and Without Obstructive Sleep Apnea Undergoing Laparoscopic Bariatric Surgery

From the Departments of Anesthesiology and Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.

Address correspondence and reprint requests to Shireen Ahmad, MD, Department of Anesthesiology, Northwestern University Feinberg School of Medicine, 251 E. Huron St., F5–704 Chicago, IL 0 60611. Address e-mail to sah704{at}northwestern.edu.

Abstract

INTRODUCTION: 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.

METHODS: Adult subjects (Body Mass Index, 35–75 kg/m²) scheduled to undergo laparoscopic bariatric surgery were studied. A finger pulse oximetry probe was placed preoperatively and oxygen saturation (Spo₂) 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 Spo₂ >4% below the polysomnography study baseline and lasting for more than 10 s.

RESULTS: 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 Spo₂ 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 Spo₂ 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.

CONCLUSIONS: 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.

The prevalence of obesity in the United States has markedly increased in the last several years and currently 31% of the adult population has a Body Mass Index (BMI) 30 kg/m². Four out of five obese persons have at least one debilitating illness related to obesity that results in an increased risk of death.1 Weight loss is generally difficult to achieve with exercise, medications, and diet in morbidly obese individuals and seems to be even more so in those with obstructive sleep apnea (OSA).2 Bariatric surgical procedures on the other hand, not only result in a sustained weight loss, but also lead to an improvement in co-morbidities such as diabetes, hypertension, hyperlipidemia, and OSA.3

Obesity is associated with a 12–30 fold increased risk of OSA relative to the normal population.4 OSA is found in 40% of obese females and 50% of obese males.5 Disastrous respiratory outcomes have been reported during the perioperative management of patients with OSA and are a major concern for anesthesia care providers.6 A review of recent malpractice claims for postoperative cardiopulmonary arrest in hospitalized patients with OSA revealed that reliance on traditional nursing assessment of respiratory rate in these patients is ineffective.7 Unexpected and unexplained postoperative deaths within 7 days of surgery occur most often at night and cardiopulmonary events related to sleep have been proposed as the most likely cause.8 However, postoperative episodic nocturnal hypoxemia with oxygen saturation (Spo₂) <85% has also been documented in healthy patients after elective abdominal surgery.9–12

Sedatives, analgesics, and anesthetics have been shown to alter airway tone in normal subjects,13 and airway obstruction and death have been reported in patients with OSA after minimal doses of sedatives and anesthetics.14,15 Routine oxygen administration may be ineffective as a prophylactic measure in these patients because diminished hypoxic drive may increase the incidence of airway obstruction.16,17 While there is an increased awareness among anesthesiologists regarding the vulnerability of these patients, few routinely screen preoperatively for OSA.18 Furthermore, despite reports of significant perioperative respiratory complications, there is a lack of consensus regarding the care of patients with OSA.

The purpose of this study was to determine whether morbidly obese patients with preoperative polysomnography (PSG)-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 undergoing these procedures who did not have a diagnosis of OSA. The hypothesis of this study was that OSA is an independent risk factor for postoperative hypoxemic episodes in morbidly obese subjects.

METHODS

After approval by the Institutional Review Board of Northwestern University, informed, written consent was obtained from 41 adult subjects who were scheduled to undergo laparoscopic bariatric surgery. Subjects were older than 18 years and their BMI ranged from 35 to 75 kg/m². Subjects were excluded if they were scheduled to be admitted to the intensive care unit postoperatively for nonrespiratory complications or if the American Society of Anesthesiology physical status was more than three.

Subjects underwent preoperative PSG testing (Nihon Kohden Polysmith version 5®) within 4 wk of surgery. The PSG test was attended by a technologist and included recording of four channels of electroencephalography, two channels of electrooculography, three channels of electromyography, one channel each of electrocardiogram, air flow, thoracic and abdominal respiratory motion, snoring and finger pulse oximetry. A diagnosis of OSA was made by the neurologist interpreting the sleep study. Subjects were evaluated by an anesthesiologist (S.A.) several days before surgery. A Berlin questionnaire was completed by the subject at the preoperative evaluation. At least 1 h before induction of anesthesia, an oximetry finger probe (LNOP®, Masimo, Irvine, CA) was placed on the index finger opposite to the side of the noninvasive blood pressure cuff. The probe was attached to a study-dedicated oximeter (Radical Version 4, Masimo, Irvine, CA) set-up to record Spo₂ continuously throughout surgery, the time period in the postanesthesia care unit (PACU) and for the 24 h after PACU discharge.

Perioperative management was standardized in accordance with an institutional clinical pathway. Subjects received sodium citrate, 30 mL orally, metoclopramide, 20 mg, and ranitidine, 50 mg, IV preoperatively. Anesthetic management was also standardized. Anesthesia was induced with propofol, 2 mg/kg based on the dosing body weight (ideal body weight (IBW) + [0.4 x (actual body weight – IBW)]),19,20 followed by succinylcholine 0.5 mg/kg, administered to facilitate tracheal intubation. Anesthesia was maintained with desflurane, titrated to achieve a Bispectral Index^TM (XP version 3.0, Aspect Medical Inc. Norwood, MA) between 50 and 60. Neuromuscular blockade was maintained with rocuronium, an initial dose of 0.5 mg/kg, with supplemental doses administered to maintain a T1 to T4 ratio of 2/4 (TOF Watch, Bluestar Enterprises, Inc., Chanhassen, MN). Remifentanil was administered at an initial rate of 0.2 µg · kg^–1 · min^–1 (IBW) and adjusted to maintain the blood pressure and heart rate within 20% of the preoperative value. Remifentanil was discontinued at the time of the removal of the laparoscope from the abdomen and morphine sulfate, 50 µg/kg IV (IBW), was administered. Residual neuromuscular block was reversed with neostigmine, 0.05 mg/kg IV (IBW), and glycopyrrolate, 0.005 mg/kg IV (IBW). Normothermia was maintained intraoperatively using warmed IV fluids (Hotline®, Level1 Technologies, Inc., Rockland, MA) and a forced warm air system (Bair Hugger®, Arizant Healthcare Inc., Eden Prairie, MN).

Subjects received IV morphine sulfate in divided doses as needed to achieve a verbal rating score (VRS) for pain <4 of 10 in the PACU. Patient-controlled analgesia, programmed to deliver 1 mg of morphine sulfate every 10 minute, was instituted before discharge from the PACU. Nausea and vomiting were treated with IV ondansetron. In accordance with the clinical pathway, subjects with a diagnosis of OSA were transferred to the intensive care unit, whereas subjects without OSA were transferred to the general clinical research center. All subjects received 3 L/min of supplemental oxygen by nasal cannula after tracheal extubation. Continuous positive airway pressure (CPAP) was applied at preoperative settings in the PACU in those subjects who had their appliances.

Spo₂ was recorded continuously for 24 h after discharge from the PACU with all subjects receiving 3 L/min of supplemental oxygen via nasal cannula. Twenty-four hours after discharge from the PACU the study coordinator evaluated all subjects, obtained a VRS for pain, and recorded the total dose of morphine sulfate consumed. Spo₂ was also recorded for 15 minutes after the discontinuation of oxygen therapy for 10 minutes. The incidence of cardiopulmonary complications during hospitalization was recorded.

After the monitoring period, the data were downloaded to a computer for analysis. Desaturation episodes (Spo₂ >4% below preoperative baseline values for >10 s in duration) were scored automatically by the analysis software. (Profox, Version PO Masimo 1/03, Escondido CA 92025). The pulse oximetry used in this study features read through motion technology that has been shown to be accurate during motion conditions. The oximeter also records a low quality signal alert. The software used to analyze the pulse oximetry signals eliminated from the analysis any periods of data containing low signal quality.

Data evaluated included the oxygen desaturation index (ODI), which is defined as the number of desaturation episodes per hour of recording. The ODI correlates with PSG-determined apnea/hypopnea index and has been used as a surrogate marker for postoperative apneic episodes. An ODI of 10 or more has been reported to have a sensitivity of (71%–85%) and specificity of (90%–93%) for the diagnosis of sleep apnea.21,22 Also determined from the oximetry data were the total number of desaturation episodes, the median Spo₂ during the collection period while the subject was receiving supplemental oxygen, and duration of the collection time that the Spo₂ was <90%.22

A priori sample size analysis using a two-sided Z test with pooled variance determined that an overall sample size of 36 subjects (OSA = 27, non-OSA = 9) would detect a difference of 0.5 in the proportion of subjects with an ODI more than 5 saturation episodes per hour during the first 24 h postoperatively assuming that the incidence is 0.6 in the OSA group and 0.1 in. the non-OSA group with a power of 80% at = 0.05. Pilot data from our institution suggested that 75% of eligible subjects undergoing bariatric surgery would have PSG-diagnosed OSA. To account for unanticipated subject dropout, 41 subjects were enrolled in the study.

Clinical characteristics, perioperative data, and postoperative oximetry outcomes were compared between OSA and non-OSA subjects using the Mann-Whitney U-test and the ² test. Estimates of exact P values were determined for the Mann-Whitney and the ² test using Monte Carlo method with 10,000 samples and confidence limits of 99%. Correlations between BMI, neck circumference, and total body mass with postoperative oximetry outcomes using Pearson correlation coefficients. The criterion for rejection of the null hypothesis was P < 0.05.

RESULTS

Forty-one subjects were enrolled, 8 males and 33 females. One subject was eliminated from the data analysis because the pulse oximeter was inadvertently discontinued prematurely during the data collection period. The median age of the subjects was 43 ± 10 Yr and the mean BMI was 50 ± 9 kg/m².

Thirty-one of the 40 subjects had PSG-confirmed OSA. Eight subjects with OSA were using a CPAP device nightly up to the time of surgery, and six of these eight used their device in the hospital postoperatively. Clinical characteristics of the subjects with OSA and those without OSA were comparable with respect to age, sex, comorbid conditions, ASA physical status, and neck circumference (Table 1). Baseline Spo₂ measured during the preoperative PSG studies were similar between groups; however the OSA-diagnosed subjects had lower nadir saturations. The incidence of apneic and/or hypopneic episodes >10 per hour (apnea/hypopnea index) was more frequent in OSA subjects compared with the non-OSA group. The percentage of subjects with positive Berlin questionnaires indicative of sleep-disordered breathing was larger in the OSA group than in the non-OSA group (Table 1).

Of the 29 subjects who underwent laparoscopic gastric bypass surgery, 23 had OSA and 6 did not; of the 11 subjects who underwent laparoscopic gastric banding surgery 8 subjects had OSA and 3 did not. Perioperative data stratified for type of surgery are shown in Table 2. The proportion of subjects undergoing laparoscopic gastric bypass or laparoscopic gastric banding and the duration of the surgeries were similar for both OSA and non-OSA groups. There was no difference in the duration of surgery, intraoperative remifentanil requirements, intraoperative morphine, and duration of hospitalization, between the OSA and non-OSA groups. In gastric bypass subjects, VRS for pain and 24 h morphine consumption were similar in OSA and non-OSA subjects. In contrast, VRS for pain and 24 h morphine consumption was greater in gastric banding subjects without OSA.

Postoperative oximetry data stratified for type of surgery are shown in Table 3. There was no significant difference in the median Spo₂ with or without oxygen therapy for both OSA and non-OSA groups. The ODI, the number of subjects with >5 desaturation per hour, the percent time that the Spo₂ was <90%, and the total number of desaturation episodes per hour did not differ between groups (Table 3). No preoperative patient characteristics (BMI, weight, and neck circumference) demonstrated a significant positive correlation with the ODI, the percent time below 90% Spo₂, total number of hypoxemic episodes, or the median Spo₂.

Eight of the subjects with OSA had used CPAP devices during sleep at home before surgery, and six of the eight used their home CPAP units in the first 24 h postoperatively. There were more hypoxemic episodes in the group that used their home CPAP units (median 149, 95% CI 118–166), compared with those who did not (median 42, 95% CI 23–98) (P = 0.02); this group had a larger percentage of the data collection period where the Spo₂ was below 90% (median 0.85, 95% CI 0.57–1.5), compared to the group not using CPAP (median 0.1, 95% CI 0.0–0.4, P = 0.001). The ODI, however, was not different in this subset of subjects.

One subject in the non-OSA group experienced respiratory compromise because of presumed aspiration pneumonitis necessitating reintubation on the second postoperative day. No other patients experienced cardiopulmonary complications during their hospital admission.

DISCUSSION

The important finding of this study was that there were no significant differences in the hourly frequency (ODI) or the total number of desaturation episodes during the first 24 h after laparoscopic bariatric surgery between obese subjects with OSA and obese subjects without OSA. Median Spo₂ with and without supplemental oxygen therapy and the duration that the Spo₂ was below 90% also did not differ between groups. Taken together, these findings suggest that OSA per se does not seem to be an independent risk of the occurrence of episodic hypoxemia in this subset of patients.

The increasing incidence of obesity in the United States has resulted in an increase in the number of patients presenting for bariatric surgeries. Obese patients have a more frequent incidence of comorbidities, including hypertension, diabetes, and OSA,1 which occurs 12 to 30 times more often in obese patients than in nonobese patients.4 Patients with OSA experience episodic upper airway obstruction and oxygen desaturation during sleep and the combination of residual anesthetics, postoperative analgesia, and pre-existing OSA is thought to increase morbidity and mortality from respiratory complications. The standardized anesthetic and postoperative analgesic management used in this study was designed to limit the amount of residual anesthesia and minimize excessive sedation.

Supplemental oxygen was administered during the first 24 h postoperatively, since it has been reported to reduce the frequency and severity of hypoxemic episodes and improve oxyhemoglobin saturation.12,23 The improvement in the nadir S_aO₂ may occur with some worsening in respiratory acidosis, a slight prolongation in mean apnea duration but an overall reduction of the duration of time spent in apnea.24 Oxygen therapy is ineffective in reducing the incidence of airway obstruction, and may diminish the stimulus to breathe.17 The use of supplemental oxygen, however, may have increased the median Spo₂ and reduced or masked the occurrence of desaturation episodes and may be a significant limitation of the findings of this study.

Impairment of pulmonary function is also affected by the type and location of surgery, with laparoscopic procedures resulting in less impairment than major abdominal surgery.25 A major limitation of the findings of this study is the lack of a uniform surgical procedure, which could affect the effect difference observed between groups and make the study under-powered to detect this difference. Nonetheless, the decrease in respiratory variables is greater in obese patients undergoing laparoscopic surgery than in nonobese subjects.26 Chest radiographs in morbidly obese patients performed on the first postoperative day after gastroplasty demonstrated that 19% had microatelectasis, 56% had focal atelectasis, and 6% had segmental atelectasis after laparoscopic surgery. Computed tomography revealed that morbidly obese patients develop more atelectasis during anesthesia than nonobese patients and more importantly, 24 h after surgery, the atelectasis persisted in the morbidly obese patients, whereas it was completely resolved in the nonobese patients.26

Postoperative episodic oxygen desaturation episodes occur exclusively during sleep.8 Another major limitation of the findings of this study is that we did not distinguish between sleep and wake periods in the 24 h postoperative period. Neural drive to the pharyngeal muscles is decreased during sleep resulting in atonia with airway obstruction and episodic hypoxemia.27 In addition, major abdominal surgery in normal patients is associated with postoperative sleep disordered breathing resembling OSA.10,28 Nocturnal breathing has been evaluated after a variety of ambulatory surgeries not involving the airway,29 and it has been found that the breathing abnormalities are no different than those noted in earlier studies after major inpatient surgeries.10,30,31 The patients who developed significant abnormalities were older and obese.

The episodes of airway obstruction in normal postoperative patients resemble those seen in patients with OSA. Since CPAP is successful in treating OSA,32 initiation of CPAP postoperatively has been advocated in obese patients to prevent acute airway obstruction.33 Despite the theoretical risk of damage to the bowel anastomoses from the pressurized air administered during CPAP use, none have been noted that could be attributed to the therapy and use is not contraindicated after bariatric surgery procedures.34 An interesting finding of this study was that subjects who used their preoperative home CPAP devices during the first 24 h postoperatively experienced a larger number of hypoxemic episodes and a larger percentage of time that the Spo₂ was below 90% compared with those that did not use CPAP. It has been reported that during normal sleep, effective CPAP pressure can vary from night to night and during the same night depending on body position, level of fatigue, sleep stage, upper airway edema, and ingestion of alcohol or sedatives.35 The effective CPAP is most likely altered after anesthesia and opioid analgesics and the preoperative setting may have been no longer adequate. Alternatively, subjects who used the CPAP devices may have been a more severe subset of the OSA group.

In conclusion, OSA does not seem to be an independent risk for postoperative hypoxemia in the first 24 h after laparoscopic bariatric surgery. Despite supplemental administration of oxygen, morbidly obese subjects with or without OSA experienced frequent desaturation episodes. These data suggest that perioperative management strategies for patients undergoing laparoscopic bariatric surgery should include measures to detect and prevent postoperative hypoxemia but that there may not need to be additional modifications for subjects with OSA.

ACKNOWLEDGMENTS

The authors thank Michael J. Arvam, PhD for his assistance in the conduct of this study and preparation of the manuscript.

Footnotes

Accepted for publication March 10, 2008.

Supported by National Center for Research Resources, National Institutes of Health Grant MO1 RR-00048 and Masimo Inc., Irvine, California.

This research was presented at the Annual Meeting of the American Society of Anesthesiologists, Chicago, 2006.

Reprints will not be available from the author.

REFERENCES

1. Mun EC, Blackburn GL, Mathews JB. Current status of medical and surgical therapy for obesity. Gastroenterology 2001;120:669–81[Web of Science][Medline]
2. Phillips BG, Hisel TM, Kato M, Pesek CA, Dyken ME, Narkiewicz K. Recent weight gain in patients with newly diagnosed obstructive sleep apnea. J. Hypertens 1999;17:1297–300[Web of Science][Medline]
3. Buchwald H, Avidor Y, Braunwald E, Jensen MD, Pories W, Fahrbach K, Schoelles K. Bariatric sur: a systematic review and meta-analysis. JAMA 2004;292:1724–8[Abstract/Free Full Text]
4. Peiser J, Lavie P, Ovnat A, Charuzi I. Sleep apnea syndrome in the morbidly obese as an indication for weight reduction surgery. Ann Surg 1984;199:112–5[Web of Science][Medline]
5. Kyzer S, Charuzi I. Obstructive sleep apnea in the obese. World J Surg 1998;22:998–1001[Web of Science][Medline]
6. Benumof JL. Creation of observational unit may decrease sleep apnea risk. Anesth Patient Safety Foundation Newslet 2002;17:39
7. Lofsky A. Sleep apnea and narcotic postoperative pain medication: a morbidity and mortality risk. Anesth Patient Safety Foundation Newslet 2002;17:24–5
8. Rosenberg-Ademsen S, Kehlet H, Dodds C, Rosenberg J. Postoperative sleep disturbances: mechanisms and clinical implications. Br J Anaesth 1996;76:552–9[Free Full Text]
9. Reeder MK, Goldman MD, Loh L, Muir AD, Casey KR, Lehane JR. Late postoperative nocturnal dips in oxygen saturation in patients undergoing major abdominal vascular surgery: predictive value of preoperative overnight pulse oximetry. Anaesthesia 1992;47:110–5[Web of Science][Medline]
10. Catley DM, Thornton C, Jordan C, Leehane JR, Royston D, Jones JG. Pronounced, episodic oxygen desaturation in the postoperative period: its association with ventilatory pattern and analgesic regimen. Anesthesiology 1985;63:20–8[Web of Science][Medline]
11. Knill RL, Moote CA, Skinner MI, Rose EA. Anesthesia with abdominal surgery leads to intense REM sleep during the first postoperative week. Anesthesiology 1990;73:52–61[Web of Science][Medline]
12. Rosenberg J, Wildschiodtz G, Pedersen MH, von Jessen F, Kehlet H. Late postoperative nocturnal episodic hypoxemia and associated sleep pattern. Br J Anaesth 1994;72:145–50[Abstract/Free Full Text]
13. Alexander CM, Gross JB. Sedative doses of midazolam depress hypoxic ventilatory responses in humans. Anesth Analg 1988; 67:377–82[Abstract/Free Full Text]
14. Dhonneur G, Combs X, Lerous B, Duvaldestin P. Postoperative obstructive apnea. Anesth Analg 1999;89:762–7[Abstract/Free Full Text]
15. Chung F, Crago RR. Sleep apnoea syndrome and anaesthesia. Can Anaesth Soc J 1982;29:439–45[Web of Science][Medline]
16. Catley DM. Postoperative analgesia and respiratory control. Int Anesthesiol Clin 1984;22:95–111[Web of Science][Medline]
17. Rosenberg J, Pedersen MH, Gebuhr P, Kehlet H. Effect of oxygen therapy on late postoperative episodic and constant hypoxemia. Br J Anaesth 1992;68:18–22[Abstract/Free Full Text]
18. Ogan OU, Plevak DJ. Anesthesia safety always an issue with obstructive sleep apnea. Anesth Patient Safety Foundation Newslet 1997;12:14–5
19. Green B, Duffull SB. What is the best size descriptor to use for pharmacokinetic studies in the obese? Br J Clin Pharmcaol 2004;58:119–33
20. De Baerdermaeker LE, Mortier EP, Struys MM. Pharmacokinetics in obese patients. Cont Educat in Anesth Crit Care Pain 2004;4:152–5
21. Rosenberg J, Kehlet H. Postoperative episodic oxygen desaturation in the sleep apnoea syndrome. Acta Anaesth Scand 1991;35:368–9[Web of Science][Medline]
22. Chiner E, Signes-Costa J, Arriero JM, Marco J, Fuentes I, Sergado A. Nocturnal oximetry for the diagnosis of the sleep apnoea hypopnoea syndrome: a method to reduce the number of polysomnographies? Thorax 1999;54:968–71[Abstract/Free Full Text]
23. Loredo JS, Ancoli-Israel S, Kim EJ, Lim WJ, Dimsdale JE. Effect of continuous positive airway pressure versus supplemental oxygen on sleep quality in obstructive sleep apnea: a placebo-CPAP-controlled study. Sleep 2006;26:564–71
24. Fletcher EC, Munafo DA. Role of nocturnal oxygen therapy in obstructive sleep apnea. When should it be used? Chest 1990;96:1497–1504
25. Nguyen NT, Lee SL, Goldman C, Fleming N, McFall AAR, Wilfe BM. Comparison of pulmonary function and postoperative pain after laparoscopic versus open gastric bypass: a randomized trial. J Am Coll Surg 2001;192:469–77[Web of Science][Medline]
26. Eichenberger AS, Proitti S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg 2002;95: 1788–92[Abstract/Free Full Text]
27. Cherniak NS. Respiratory dysrhythmias during sleep. N Engl J Med 1981;305:325–30[Web of Science][Medline]
28. Wheatley RG, Shepard D, Jackson IJB, Madej TH, Hunter D. Hypoxemia and pain relief after upper abdominal surgery: comparison of I.M. and patient controlled analgesia. Br J Anaesth 1992;69:558–61[Abstract/Free Full Text]
29. Bowdie TA. Nocturnal arterial oxygen desaturation and episodic airway obstruction after ambulatory surgery. Anesth Analg 2004;99:70–6[Abstract/Free Full Text]
30. Prinz P, Vitiello M, Raskind M, Thorpy M. Geriatrics: sleep disorders and aging. N Engl J Med 1990;323:520–6[Web of Science][Medline]
31. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230–35[Abstract/Free Full Text]
32. Strollo PJ Jr, Rogers RM. Obstructive sleep apnea. N Engl J Med 1996;334:99–104[Free Full Text]
33. Rennotte MT, Baele P, Aubert G, Rodenstein DO. Nasal continuous positive airway pressure in the perioperative management of patients with obstructive sleep apnea submitted to surgery. Chest 1995;107:367–74[Web of Science][Medline]
34. Huerta S, DeShields S, Shpiner R, Li Z, Liu C, Sarwicki M, Arteaga J, Livingston EH. Safety and efficacy of postoperative continuous positive airway pressure to prevent pulmonary complications after Roux-en-Y gastric bypass. J Gastrointest Surg 2002;6:354–8[Web of Science][Medline]
35. Noseda A, Kempenaers C, Kerkhofs M, Braun S, Linkowski P, Jann E. Constant vs auto-continuous positive airway pressure in patients with sleep apnea hypopnea syndrome and a high variability in pressure requirement. Chest 2004;126:31–7[Web of Science][Medline]

This article has been cited by other articles:

				Y. Al-Tamimi, L. De Baerdemaeker, and S. Jacobs Target controlled infusion of opioids for bariatric surgery and morphine loading dose Br. J. Anaesth., March 1, 2009; 102(3): 432 - 433. [Full Text] [PDF]

				H. Kinoshita, N. Hatakeyama, T. Minonishi, and Y. Hatano Severity of Obstructive Sleep Apnea Syndrome May Affect Postoperative Hypoxemia in Morbidly Obese Patients Anesth. Analg., March 1, 2009; 108(3): 1044 - 1044. [Full Text] [PDF]

				S. Ahmad and R. J. McCarthy Postoperative Monitoring of Obese Patients with Obstructive Sleep Apnea Anesth. Analg., March 1, 2009; 108(3): 1045 - 1045. [Full Text] [PDF]

				S. Ahmad and R. J. McCarthy Severity of Obstructive Sleep Apnea Syndrome May Affect Postoperative Hypoxemia in Morbidly Obese Patients Anesth. Analg., March 1, 2009; 108(3): 1044 - 1044. [Full Text] [PDF]

				F. J. Overdyk and Q. Ahmed Postoperative Monitoring of Obese Patients with Obstructive Sleep Apnea Anesth. Analg., March 1, 2009; 108(3): 1044 - 1045. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Ahmad, S. Articles by Prystowsky, J. Search for Related Content PubMed PubMed Citation Articles by Ahmad, S. Articles by Prystowsky, J. Related Collections Postanesthetic Care Unit Complications Patient Safety