Obstructive sleep apnea syndrome (OSAS) has significant acute and chronic impact on the cardiovascular and pulmonary systems (1). After general anesthesia, especially during the first hours after an operation, patients with OSAS are at risk of hypoxemia (2,3) that might evoke cardiac ischemia and ventricular arrhythmia (4,5). Perioperative management of patients with OSAS includes postoperative intensive care monitoring and nasal continuous positive airway pressure to reduce the amount of apnea and oxygen desaturation (6–8). The importance of postoperative intensive care monitoring of patients with OSAS after the first few postoperative hours has been questioned, as perioperative cardiac and respiratory complications of patients with OSAS were found to be infrequent after that time (9–12).
Nasal septum surgery is often performed, and the prevalence of OSAS among these patients is more frequent than in other patients (13). Patients with OSAS, who do not tolerate nasal continuous positive airway pressure because of obstructed nasal breathing, require nasal septum surgery to enable adequate nasal continuous positive airway pressure therapy. Postoperative nasal packing (PNP) is often needed after nasal septum surgery. PNP and artificial nasal obstruction increase apnea and oxygen desaturation in healthy patients (14–16) while making it impossible to use nasal continuous positive airway pressure.
As the impact of PNP in patients with OSAS is unknown, we prospectively evaluated the impact of anesthesia and/or PNP on sleep-disordered breathing and oxygen desaturation in healthy patients as well as in patients with OSAS. Our first hypothesis was that in patients with PNP, with and without OSAS, oxygen desaturation index (ODI) will increase by more than 5 n/h after general anesthesia. Second, we hypothesized that in patients without PNP and without OSAS, ODI would not increase or would only minimally increase after general anesthesia.
The study was approved by the Ethics Committee of the University of Basel, Switzerland. Informed written consent was obtained from each patient before inclusion. Sixty patients with overall ASA physical status I-II scheduled for either elective nasal surgery receiving PNP or for ear or minor neck surgery were consecutively included in this prospective study. Before surgical treatment, patients were routinely screened for OSAS by our Ear, Nose and Throat Department and, when appropriate, were further evaluated with polysomnography by our Pneumology Division for the presence or absence of OSAS, all within two months prior to surgery. Based on the preoperative diagnosis of OSAS, patients receiving PNP were placed in a group with established OSAS (Group 2) or in a group without OSAS (Group 1). Patients scheduled for elective ear or neck surgery who did not have OSAS, PNP, or nose surgery served as the control group. We excluded patients who had the following: bronchial asthma requiring medical therapy, cardiac disease with a New York Heart Association functional class >II or with a Canadian Cardiovascular Society functional class >I, malignancy, severe psychiatric disorders, or who were pregnant or younger than 18 yr.
All patients received 7.5 mg oral midazolam 60 min before surgery. General anesthesia was induced with propofol 2 mg/kg and fentanyl 2 μg/kg IV. Tracheal intubation was facilitated by atracurium 0.5 mg/kg IV. For maintenance, propofol 6–10 mg · kg−1 · h−1 and repeated doses of fentanyl were given as necessary based on clinical signs. Increments of atracurium 5 mg IV were given to maintain muscle relaxation, which was monitored by train-of-four nerve stimulation. Neostigmine 2.5 mg and glycopyrrolate 0.5 mg were given IV as needed to reverse neuromuscular blockade. Naloxone or flumazenil was given IV if considered to be necessary by the attending anesthesiologist. Criteria to extubate the trachea were defined as four equal twitches in the train-of-four and no tetanic fade (50 Hz over 5 s) during nerve stimulation, recovery of consciousness (eye opening to speech), protective airway reflexes, and return of spontaneous breathing.
Depending on the attending senior anesthesiologist and the availability of beds in the intensive care unit (ICU), OSAS patients were either monitored overnight in the ICU or were monitored in the postanesthesia care unit for 2 h before returning to the ward.
PNP consisted of an 80-mm plastic coated foam pack (Netcell 5000, Network, Ripon, UK). Each patient with PNP received a cotton bandage between the nose and mouth to reduce blood dripping from their nose.
Patients in the control group and Group 1 did not receive overnight oxygen after the operation. Group 1 received postoperative humidified air via a nebulizer to improve open-mouth breathing. Patients in Group 2 received postoperative oxygen (4 L/min) via standard adult facemasks without a reservoir system (Salter Labs, Arvin, CA). Because of the cotton bandage, the facemasks did not fit properly. We did not measure the inspiratory oxygen concentration.
Before the operation, the nasal septum was infiltrated with 10 mL lidocaine 1% containing epinephrine 1:200,000. Basic postoperative analgesia consisted of paracetamol 1000 mg orally every 6 h. If pain persisted, patients without renal impairment first received ketorolac 30 mg IV every 8 h and/or methadone 2 mg IV in the postoperative anesthesia care unit/ICU to achieve a pain score ≤30 mm on the 100-mm visual analog scale (where 0 mm represented “no pain” and 100 mm “worst possible” pain). On the ward, methadone was administered subcutaneously in a dose of 0.1 mg/kg body weight every 6 h, if necessary, to achieve a pain score ≤30 mm on the visual analog scale.
Before the operation, weight and height were measured to calculate the body mass index (kg/m2) in all patients. Maximal mouth opening and modified Mallampati score were assessed (17). Neck circumference was measured and the percentage of the predicted normal neck circumference was calculated (18). All patients completed a questionnaire assessing the daytime sleepiness using the German version of the Epworth sleepiness scale (19) and the frequency of snoring (nil = I do not know; 1 = never; 2 = just a few times; 3 = sometimes; 4 = quite often; 5 = usually, almost always).
A level III portable polygraphic device (Poly-MESAM; MAP, Martinsried, Germany) was used for measuring oronasal airflow, thoracoabdominal movements with piezoelectric belts, arterial oxygen saturation (finger pulse oximetry), and body position with a position sensor (20,21). During the preoperative and postoperative nights, the polygraphic device was set up at 9 pm and recordings were taken from 10 pm to 6 am of the following morning. During routine ward rounds, the night nurse noted the sleep state of patients at 0, 2, 4, and 6 am and the percentage of time a patient was observed sleeping was calculated from these data (25%, 50%, 75%, or 100%).
Apnea was defined as a cessation and hypopnea as a decrease of more than 50% of airflow or thoracoabdominal movements for more than 10 s. Desaturation was defined as a decrease of oxygen saturation <95% exceeding 4% from the preceding baseline. Polygraphic raw data were analyzed and verified independently by an observer and a senior chest physician, who were both blinded to the patient data other than the raw data. We used the software Poly-MESAM for windows (version 2.0, MAP) to automatically analyze and manually verify respiratory and desaturation events. Obvious patient movements and artifacts were removed before calculation of respiratory events and oxygen desaturations. Apnea-hypopnea index (AHI), apnea index (AI), ODI, mean baseline oxygen saturation (BLSAT), mean oxygen desaturation (ODSAT), lowest oxygen saturation (LSAT), number of oxygen desaturations <90% (ODI <90%), number of positional changes, and the time spent supine were calculated automatically.
For sample size calculation, we used nQuery Advisor for windows (Version 4; Statistical Solutions, Saugus, MA). For the control group, to detect a difference in ODI smaller or equal to 4 with a power of 80% using a paired Student’s t-test with a 0.05 one-sided significance level, a sample size of 12 patients was calculated, assuming a standard deviation of the differences of 5.2 (based on a separate pilot data). For Group 2, a sample size of 15 patients was calculated to detect a mean difference in ODI of 5 (from 15 to 20) with a power of 80% using a paired Student’s t-test with a two-sided significance level of 0.05, assuming a standard deviation of difference of 6.4 (based on separate pilot data). Data are presented as median (interquartile range). We used a Wilcoxon’s signed rank test to compare data within the groups. We used a Mann-Whitney U-test or a χ2 test to compare measurements among the groups where appropriate. P < 0.05 within the groups and P < 0.016 among the groups were considered significant. For statistical calculations, we used StatView for windows (Version 5.0.1; SAS Institute Inc., Cary, NC).
From 60 patients recruited, eight patients had to be excluded: in four, technical problems occurred (missing data recording), three patients declined to continue and in one, the surgical procedure was altered (septoplastic surgery with one-sided PNP). The demographics of the remaining 52 patients are described in Table 1.
Patients with PNP included in the study consisted of 25 without OSAS (Group 1) and 15 with OSAS (Group 2). In Group 2, the preoperative AHI values were 21 (18–37) measured by our Pneumology Division with a polysomongraph, all within 2 mo before surgery.
Patients in the control group (n = 12) underwent ear (n = 8) or minor neck (n = 4) surgery without receiving postoperative PNP. Elective intranasal surgery included septoplasty, turbinectomy, or paranasal sinus surgery, but not uvulopalatopharyngoplasty.
Results for AHI, AI, ODI, ODI <90%, BLSAT, ODSAT, and LSAT as well as percentage of observed time sleeping, time spent supine, and positional changes are given in Table 2. For preoperative versus postoperative values, AHI significantly increased in Group 1 (from 11 (5–9) to 37 [22–49]) and in Group 2 (from 14 [10–21] to 39 [26–50]) but not in the control group (6 [2–9] versus 5 [2–13]). ODI significantly increased in Group 1 (from 4 [2–8] to 13 [6–21]) but not in the control group (3 [1–7] versus 6 [3–9]) or in Group 2 (13 [8–27] versus 11 [4–37]).
In Group 2, 7 patients (47%) were sent to the ICU and 8 patients (53%) to the surgical ward for the first postoperative night. Preoperative AHI, AI, and ODSAT values were significantly different between the patients of the two subgroups. AHI was 22 (17–25) versus 11 (6–14), AI was 6 (3–6) versus 1 (0–2), and ODSAT was 88 (85–89) versus 90 (89–91) for the patients sent to the ICU compared with the patients sent to the surgical ward, respectively. After the operation, there were no significant differences between the two subgroups for any of the observed variables.
The duration of anesthesia was 150 (129–186) min and was not significantly different among the groups. The amount of postoperative methadone was not significantly different among the groups (Table 2).
The main results of our study show that in patients with propofol-based general anesthesia (control group), neither AHI nor ODI significantly increased after the operation. In patients with PNP without OSAS (Group 1), AHI and ODI significantly increased after the operation, whereas in patients with PNP and OSAS (Group 2), receiving overnight oxygen, AHI, but not ODI, significantly increased after the operation.
General anesthesia and postoperative analgesia can elicit postoperative sleep-disordered breathing and oxygen desaturation in healthy patients after abdominal surgery (22–24). In contrast to these studies, none of the measured variables in the patients of the control group changed significantly except for a small but significant increase in ODI <90%. As this increase in ODI <90% was minimal, its clinical implication is questionable. The finding that propofol-based general anesthesia for minor surgery has no significant impact on sleep-disordered breathing and oxygen desaturation shows that these patients do not need postoperative respiratory monitoring or overnight oxygen on a routine basis. There are no reports measuring the impact of propofol, fentanyl, and/or atracurium on postoperative sleep-disordered breathing and oxygen desaturation.
Artificial nasal obstruction (without anesthesia or surgical intervention) (15,16) and PNP (14) in healthy patients increases sleep-disordered breathing, which is consistent with our present study. None of these patients (14–16) received supplemental overnight oxygen, nor did our Group 1 patients.
In contrast to other studies (14–16), we found a significant increase in oxygen desaturation in patients with PNP. Artificial nasal obstruction and PNP increases oxygen desaturation, but until the present study, the increase was not found to be significant, presumably because of the small numbers of patients who were evaluated.
Oxygen facemasks are designed for standard nose anatomy. When PNP and a cotton bandage under the nose (to reduce blood dripping) are applied, facemasks often slide or cause patient discomfort and if placed incorrectly may even put the surgical result at risk. Because of these difficulties, until now, patients in our hospital with PNP did not routinely receive overnight oxygen. The exception was for patients diagnosed with OSAS, inasmuch as they are thought to be more prone to hypoxemia with its attendant adverse cardiovascular effects (1).
After endonasal surgery with PNP, in Group 1 (without overnight oxygen) oxygen desaturation (ODI, ODI <90%) significantly increased after the operation in contrast to Group 2 (with overnight oxygen). This finding suggests that all patients with PNP, regardless of whether or not they have OSAS, should receive overnight oxygen, although the facemask must be handled with special care so as not to jeopardize the surgical result.
In patients with OSAS, the impact of acute hypoxemia on the cardiovascular system is more than the impact of obstructive apnea (1). There is a clear relationship between the duration and the severity of hypoxemia and the occurrence of myocardial ischemia in the perioperative period (1,4,5). Perioperative cardiac morbidity is increased because of hypoxemia, whereas the short-term effect of obstructive respiratory events on perioperative morbidity and mortality remains unclear (1).
Many studies describe the increased perioperative cardiovascular and pulmonary risk in patients with OSAS (2–4,6,22). PNP alone significantly increases AHI in healthy patients (14), but until now it was unclear as to whether PNP further affects sleep-disordered breathing and oxygen desaturation in patients with OSAS receiving PNP. Although more recent studies have questioned the necessity of postoperative intensive care monitoring in patients with OSAS (9–12), the additional impact of PNP, which might jeopardize oxygenation in patients with OSAS, has not been studied.
Our study showed that patients with OSAS who received PNP and overnight oxygen had a significant increase in AHI after the operation. However ODI and ODI <90% did not significantly increase and BLSAT, ODSAT, and LSAT did not significantly decrease in Group 2 after the operation. After the operation, AHI and ODI were similarly affected in both groups receiving PNP; thus, there was no additional effect of OSAS on sleep-disordered breathing and oxygen desaturation in patients receiving PNP and overnight oxygen.
Using the preoperative AHI values (AHI 21) determined by our Pneumology Division using polysomnography, Group 2 had moderate OSAS as described by Piccirillo et al. (25) Our results demonstrated that patients with mild-to-moderate OSAS who received overnight oxygen were not further endangered by the potentially detrimental effects of hypoxemia, even after PNP, and therefore did not need routine postoperative intensive care monitoring. This is important because intensive care resources are limited and economic optimization is a constant theme within the health care sector. Because we did not evaluate patients with severe OSAS receiving PNP we cannot provide recommendations concerning the postoperative monitoring of these patients. Sick patients (ASA III) or patients with ischemic heart disease might need postoperative intensive care monitoring, as obstructive apnea in patients with ischemic heart disease is sufficient to cause myocardial ischemia (1).
The difference in preoperative AHI values between the 2 groups receiving PNP, although significant, was small (AHI 11 in Group 1 versus AHI 14 in Group 2). The large preoperative AHI values found in Group 1 might have reflected an increased prevalence of patients with undiagnosed OSAS (13) who were scheduled for septoplastic surgery.
We found significantly smaller preoperative AHI values in Group 2 than those obtained from our Pneumology Division. This is because for practical reasons we used a portable level III polygraphic device instead of the polysomnograpic device used by our Pneumology Division. There is a good correlation between the values obtained with polysomnographic and portable polygraphic devices (20,21). The portable polygraphic device calculates AHI and ODI as the number of events per total observed hours. In contrast, the polysomnograpic device calculates AHI and ODI on the basis of per hour of sleep and will therefore give more precise and larger values for AHI and ODI (20,21).
In conclusion, general anesthesia with propofol, fentanyl, and atracurium for minor surgery showed only a small impact on sleep-disordered breathing and oxygen desaturation, and overnight oxygen does not appear to be necessary for these patients.
In both groups receiving PNP, regardless of OSAS and overnight oxygen, AHI significantly increased after the operation. However, ODI significantly increased in the patients without OSAS and without overnight oxygen (Group 1) in contrast to the patients with OSAS receiving overnight oxygen (Group 2). Therefore, all patients regardless of OSAS should receive overnight oxygen.
In the patients with OSAS receiving PNP (Group 2), except for an increase in AHI, neither the number nor depth of oxygen desaturation increased significantly. After the operation, AHI was similar in both groups receiving PNP, whereas ODI only significantly increased in Group 1; thus moderate OSAS did not have an additional effect on sleep-disordered breathing and oxygen desaturation in patients receiving PNP and overnight oxygen. Because ODI did not significantly increase in patients with OSAS and PNP who received postoperative overnight oxygen, postoperative intensive care monitoring is not necessary on a routine basis for all patients with PNP and moderate OSAS.
The authors are indebted to the ward nurses of our Ear, Nose and Throat Department for their great help. The authors thank Joan Etlinger for editorial assistance. The Department of Anesthesia, University Hospital, Basel, Switzerland and the Swiss Society of Anesthesia and Reanimation supported this study.
1. Leung RS, Bradley TD. Sleep apnea and cardiovascular disease. Am J Respir Crit Care Med 2001;164:2147–65.
2. Esclamado RM, Glenn MG, McCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989;99:1125–9.
3. Gupta RM, Parvizi J, Hanssen AD, Gay PC. Postoperative complications in patients with obstructive sleep apnea syndrome undergoing hip or knee replacement: a case-control study. Mayo Clin Proc 2001;76:897–905.
4. Gill NP, Wright B, Reilly CS. Relationship between hypoxaemic and cardiac ischaemic events in the perioperative period. Br J Anaesth 1992;68:471–3.
5. Shepard JW Jr, Garrison MW, Grither DA, Dolan GF. Relationship of ventricular ectopy to oxyhemoglobin desaturation in patients with obstructive sleep apnea. Chest 1985;88:335–40.
6. Burgess LP, Derderian SS, Morin GV, et al. Postoperative risk following uvulopalatopharyngoplasty for obstructive sleep apnea. Otolaryngol Head Neck Surg 1992;106:81–6.
7. Meoli AL, Rosen CL, Kristo D, et al. Upper airway management of the adult patient with obstructive sleep apnea in the perioperative period–avoiding complications. Sleep 2003;26:1060–5.
8. 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.
9. Terris DJ, Fincher EF, Hanasono MM, et al. Conservation of resources: indications for intensive care monitoring after upper airway surgery on patients with obstructive sleep apnea. Laryngoscope 1998;108:784–8.
10. Mickelson SA, Hakim I. Is postoperative intensive care monitoring necessary after uvulopalatopharyngoplasty? Otolaryngol Head Neck Surg 1998;119:352–6.
11. Ulnick KM, Debo RF. Postoperative treatment of the patient with obstructive sleep apnea. Otolaryngol Head Neck Surg 2000;122:233–6.
12. Gessler EM, Bondy PC. Respiratory complications following tonsillectomy/UPPP: is step-down monitoring necessary? Ear Nose Throat J 2003;82:628–32.
13. Verse T, Maurer JT, Pirsig W. Effect of nasal surgery on sleep-related breathing disorders. Laryngoscope 2002;112:64–8.
14. Taasan V, Wynne JW, Cassisi N, Block AJ. The effect of nasal packing on sleep-disordered breathing and nocturnal oxygen desaturation. Laryngoscope 1981;91:1163–72.
15. Zwillich CW, Pickett C, Hanson FN, Weil JV. Disturbed sleep and prolonged apnea during nasal obstruction in normal men. Am Rev Respir Dis 1981;124:158–60.
16. Suratt PM, Turner BL, Wilhoit SC. Effect of intranasal obstruction on breathing during sleep. Chest 1986;90:324–9.
17. Friedman M, Tanyeri H, La Rosa M, et al. Clinical predictors of obstructive sleep apnea. Laryngoscope 1999;109:1901–7.
18. Davies RJ, Stradling JR. The relationship between neck circumference, radiographic pharyngeal anatomy, and the obstructive sleep apnoea syndrome. Eur Respir J 1990;3:509–14.
19. Bloch KE, Schoch OD, Zhang JN, Russi EW. German version of the Epworth Sleepiness Scale. Respiration 1999;66:440–7.
20. Verse T, Pirsig W, Junge-Hulsing B, Kroker B. Validation of the POLY-MESAM seven-channel ambulatory recording unit. Chest 2000;117:1613–8.
21. Ferber R, Millman R, Coppola M, et al. Portable recording in the assessment of obstructive sleep apnea. ASDA standards of practice. Sleep 1994;17:378–92.
22. Catley DM, Thornton C, Jordan C, et al. Pronounced, episodic oxygen desaturation in the postoperative period: its association with ventilatory pattern and analgesic regimen. Anesthesiology 1985;63:20–8.
23. Rosenberg J, Ullstad T, Rasmussen J, et al. Time course of postoperative hypoxaemia. Eur J Surg 1994;160:137–43.
24. Rosenberg J, Rasmussen GI, Wojdemann KR, et al. Ventilatory pattern and associated episodic hypoxaemia in the late postoperative period in the general surgical ward. Anaesthesia 1999;54:323–8.
25. Piccirillo JF, Duntley S, Schotland. Obstructive sleep apnea. JAMA 2000;284:1492–4.