General anesthesia may impair pulmonary gas exchange (1,2), resulting in decreased blood oxygenation (2). Pulmonary atelectasis is a major cause of these detrimental effects (3,4). These pulmonary atelectasis occur in 85%–90% of healthy adults within minutes after the induction of general anesthesia, and up to 15% of the entire lung may be atelectatic, particularly in the basal regions (5), resulting in a true pulmonary shunt of approximately 5%–10% of cardiac output (6).
During general anesthesia (7), as well as during the immediate postoperative period (8), morbidly obese patients (MO) are more likely to have significant impairments of pulmonary gas exchange and respiratory mechanics (9). Because awake MO patients already have severe alterations of their respiratory mechanics (10) (decreased chest wall and lung compliance, decreased functional residual capacity [FRC]), we hypothesized that these patients were particularly prone to intra- and postoperative atelectasis. The aim of our study was, therefore, to compare intra- and postoperative pulmonary atelectasis between MO and nonobese patients until postoperative Day 1.
After local ethics committee approval and written, informed consent, 30 ASA physical status I–III patients aged 20 to 60 yr and scheduled for a laparoscopic procedure were enrolled into the study. The estimation of the sample size was based on previous studies. This size was calculated to detect a difference of 50% in atelectasis between the groups, with P = 0.05 and a power of 80%. Exclusion criteria were previous cardiac or pulmonary disease, except sleep apnea syndrome; carotid stenosis; and a history of vascular neurologic disorders. One group consisted of 20 MO patients (with a body mass index (BMI) of >35 kg/m2); 10 nonobese patients (BMI <30 kg/m2) were enrolled into the second group. The scheduled laparoscopic procedure was gastric bypass or gastric bending for the MO group and cholecystectomy for the nonobese subjects.
No premedication was given. General anesthesia was induced after 5 min of breathing 100% oxygen with 2 mg/kg of propofol and 0.75 μg/kg of remifentanil during the first 45 s, followed by an infusion of 0.1–0.5 μg · kg−1 · min−1. Maintenance of anesthesia was obtained with desflurane and remifentanil. The dosage of these drugs was adjusted to achieve a clinically adequate depth of anesthesia. During induction, the lungs were ventilated manually via a face mask with 100% oxygen. To facilitate orotracheal intubation, patients received 0.2 mg/kg of cisatracurium; additional doses of 1–4 mg were given when needed. The patients were mechanically ventilated with 50% oxygen in nitrogen with a tidal volume of 10 mL/kg in the nonobese patients and 10 mL/kg of ideal body weight for the MO group. The respiratory rate was adjusted to maintain an end-tidal carbon dioxide concentration of 35–45 mm Hg with an inspiratory/expiratory ratio of 1:2. A positive end-expiratory pressure of 6 cm H2O was applied in both groups. At the end of surgery, any residual effect of the muscle relaxant was reversed by 2.5 mg of neostigmine and 0.25 mg of glycopyrronium. Postoperative analgesia was provided by 2 g of propacetamol, 30 mg of ketorolac, and 0.1 mg/kg of morphine given 30 min before the end of the surgical procedure. Ten minutes before extubation, all patients were given 100% oxygen. After extubation, all patients were spontaneously breathing with a face mask (providing a fraction of inspired oxygen [Fio2] of 0.5) for 2 h or more when required. Postoperative analgesics consisted of propacetamol 2 g four times per day and ketorolac 30 mg three times per day. Metamizole 500 mg three times per day was added if needed in both groups.
During the surgical procedure, the peritoneum was insufflated with CO2 by a WOLF gas insufflator (Treier Endoscopie, Berommunster, Switzerland) up to an intraperitoneal peak pressure of 15 mm Hg. Patients were excluded from the study if the procedure was converted to laparotomy.
Measurements consisted of computed tomography (CT) performed at three different periods: before the induction of general anesthesia, immediately after awakening and tracheal extubation, and 24 h later. Before each CT, a front scout view was obtained, and three sections of 5 mm at 120 kV and 150 mA were acquired at end-expiratory position at the level of the interventricular septum with a lung algorithm (GE Light Speed; General Electric, Milwaukee, WI). The CT data were transferred on a GE Advantage Windows station.
Each right and left lung surface was manually extracted, and a window setting of −1000 to +100 Hounsfield units (HU) was selected to assess the total lung surface. A threshold of −1000 to 500 HU was applied to quantify the amount of normally ventilated lung, a second threshold of −500 to −100 was chosen to establish the surface of poorly ventilated lung, and third threshold of −100 to +100 HU was set to measure the surface of atelectatic lung area. The right and left lung surfaces of pulmonary atelectasis were summed and reported to the total lung surface. The amount of atelectatic tissue was expressed as a percentage of the total lung area (excluding the heart and the great vessels).
Data were compared by using analysis of variance, the unpaired Student’s t-test, and Dunnett’s test. P < 0.05 was considered significant. Values are expressed as mean ± sd. The statistical package used was JMP (Version 3.1.5; SAS Institute, Cary, NC).
There were differences between the two groups in the following demographic data: BMI, ASA status, and anesthesia duration (Table 1). The male/female ratio and the age of the patients showed no significant difference between the two groups.
Already before anesthesia induction, there was significantly more atelectasis in MO than in nonobese patients (2.1% ± 1.2% versus 1.0% ± 0.4%, respectively;P < 0.01) (Fig. 1). After tracheal extubation, the amount of pulmonary atelectasis had significantly increased in both groups but remained greater in the MO patients (MO patients, 7.6% ± 4.1% versus 2.8% ± 2.2%;P < 0.05) (Figs. 1 and 2). Twenty-four hours later, pulmonary atelectasis had returned to baseline in nonobese patients (1.9% ± 0.9%) but remained increased in MO patients (9.7% ± 6.4%;P < 0.01) (Figs. 1 and 2). Within MO patients, no correlation was found between BMI and the amount of atelectasis (R2 = 0.0042 after extubation;R2 = 0.0001 24 h later) (data not shown). Furthermore, when the two groups were pooled, there was no correlation between the BMI and the amount of pulmonary atelectasis at the three different times (before induction, after extubation, and 24 h later). Moreover, there was no correlation between anesthesia duration and the amount of pulmonary atelectasis after the extubation and 24 h later (R2 = 0.0211 and R2 = 0.154, respectively).
The major finding of this study is that MO patients develop more atelectasis during general anesthesia than nonobese patients. Moreover, 24 hours after the end of the surgical procedure, atelectasis persists in MO patients, whereas complete resorption occurs in nonobese patients.
Only one previous study has evaluated the correlation between obesity and atelectasis formation (11). It found a weak correlation between Broca’s index [weightkg/(heightcm − 100)] and the atelectatic surface (R2 = 0.12;P < 0.05). In our study, there was also a weak correlation between the amount of atelectasis and BMI when both groups were pooled, but not when the two groups were studied separately. Because of the design of our study, the BMI was not a continuous variable, and therefore we had to study this correlation in each group.
In general, compared with nonobese patients, functional residual capacity (FRC) is markedly decreased in MO patients, the alveolar-arterial oxygenation gradient is increased, and intraabdominal pressure is higher (7,8,12). This has been shown during general anesthesia and during surgical procedures (12), as well as after surgery in sedated/paralyzed MO patients (7,8). The authors postulated that the hypoxemia and the marked alterations of the mechanical properties of the respiratory system seen in the MO patients were largely explained by a reduction in lung volume because of excessive unopposed intraabdominal pressure (7). This was confirmed by another study showing an improvement of respiratory function in MO patients, but not in nonobese patients, when 10 cm H2O of positive end-expiratory pressure was applied (13). In our study, the surgical procedure was performed by laparoscopy with an intraperitoneal pressure of 15 mm Hg in both groups. Therefore, the intraabdominal pressure was probably not different between the two groups during the surgical procedure, and it was increased in the MO group only during general anesthesia before and after the surgical procedure. Moreover, it has been shown that the reverse Trendelenburg position, which was the position of both groups for all surgical procedures, improves oxygenation and lung mechanics in MO patients (14). We therefore consider the increased intraabdominal pressure as not only the explanation for the larger amount of atelectasis seen in the MO group, but also the reason why the decreased lung volume already shown in these patients (12) also participated in atelectasis formation.
The difference seen between the two groups at 24 hours in our study may have several explanations. First, it has been shown that FRC in MO patients was diminished and even worsened when they were in the supine position (15). This may explain why, in our study, before general anesthesia, MO patients already had more atelectasis than lean patients. Therefore, during the first postoperative night, this phenomenon will recur with persisting or even increased atelectasis surface. Second, despite the same type of surgical procedure, MO patients generally remain longer and are more immobilized in their beds than nonobese patients. Indeed, it is easier for the lean patients to mobilize themselves and for the nursing staff to stimulate them. Early mobilization certainly contributed to the rapid disappearance of atelectasis in the nonobese group. Third, the surgical procedure was twice as long in the MO group than in the nonobese group. However, no correlation was found between the duration of surgery and the percentage of atelectasis, which is confirmed by two studies showing no progressive decrease of the lung volume in normal-weight and obese subjects with the duration of general anesthesia (16,17). Therefore, the duration of the surgical procedure is not a main factor explaining atelectasis formation. Fourth, analgesia was the same in both groups. Because no postoperative opiates were given, postoperative respiratory depression might not have resulted from the analgesic regimen. Although the same surgical procedure was performed in both groups, one might argue that laparoscopic gastric bypass, or banding versus laparoscopic cholecystectomy, would produce a different intensity of postoperative pain. This difference between the two groups would then explain the difference in the amount of atelectasis seen 24 hours after tracheal extubation. Nevertheless, previous studies investigating different postoperative analgesic techniques, to improve respiratory efficiency, failed to show any or showed only a minor benefit of improving postoperative pain (18,19).
Consequently, the above-mentioned causes seem to explain only partially the difference seen at 24 hours. Therefore, the most likely explanation for this difference is obesity by itself.
The method of atelectasis measurement by CT scan is established (5,6). To avoid excessive radiation exposure, only the level of the interventricular septum was chosen. The interventricular septum level may not be representative of the whole lung, but it appeared to be a compromise between the most affected bases of the lungs and the less affected apex.
Fio2 was similar in both groups during general anesthesia and the immediate postoperative period. The MO patients needed a supplement of oxygen by face mask for a longer period of time (Fio2 0.5). This longer exposure to 50% oxygen may have contributed to the longer persistence of atelectasis in the MO group. Low Fio2 has no influence on atelectasis formation (20), and, therefore, the longer exposure to 50% oxygen had no effect on the amount of atelectasis seen in our study.
The increased amount of atelectasis found in MO patients explains, at least partially, postoperative pulmonary complications. Therefore, it seems important to further investigate any techniques for avoiding atelectasis formation in this high-risk group.
We conclude that pulmonary atelectasis appearing during general anesthesia will resolve in nonobese patients within hours. However, MO patients will already show atelectasis on the morning of surgery before any medication has been given. They will develop much more atelectasis, which will persist and even tend to increase, 24 hours after tracheal extubation.
1. Hedenstierna G, Tokics L, Strandberg A, et al. Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis. Acta Anaesthesiol Scand 1986; 30: 183–91.
2. Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia: an observer study. Br J Anaesth 1991; 66: 437–44.
3. Bendixen HH, Hedley-Whyte J, Laver MB. Impaired oxygenation in surgical patients during general anesthesia with controlled ventilation. N Engl J Med 1963; 269: 991–6.
4. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985; 62: 422–8.
5. Lundquist H, Hedenstierna G, Strandberg A, et al. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995; 36: 626–32.
6. Rothen HU, Sporre B, Englberg G, et al. Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth 1993; 71: 788–95.
7. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 1997; 82: 811–8.
8. Pelosi P, Croci M, Ravagnan I, et al. Total respiratory system, lung, and chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest 1996; 109: 144–51.
9. Tweed WA, Phua WT, Chong KY, et al. Tidal volume, lung hyperinflation and arterial oxygenation during general anaesthesia. Anaesth Intensive Care 1993; 21: 806–10.
10. Zerah F, Harf A, Perlemuter L, et al. Effects of obesity on respiratory resistance. Chest 1993; 103: 1470–6.
11. Strandberg A, Tokics L, Brismar B, et al. Constitutional factors promoting development of atelectasis during anaesthesia. Acta Anaesthesiol Scand 1987; 31: 21–4.
12. Pelosi P, Croci M, Ravagnan I, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998; 87: 654–60.
13. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology 1999; 91: 1221–31.
14. Perilli V, Sollazzi L, Bozza P, et al. The effects of the reverse trendelenburg position on respiratory mechanics and blood gases in morbidly obese patients during bariatric surgery. Anesth Analg 2000; 91: 1520–5.
15. Biring MS, Lewis MI, Liu JT, Mohsenifar Z. Pulmonary physiologic changes of morbid obesity. Am J Med Sci 1999; 318: 293–7.
16. Damia G, Mascheroni D, Croci M, Tarenzi L. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anaesth 1988; 60: 574–8.
17. Hewlett AM, Hulands GH, Nunn JF, Milledge JS. Functional residual capacity during anaesthesia. III. Artificial ventilation. Br J Anaesth 1974; 46: 495–503.
18. Englberg G. Single-dose intercostal nerve blocks with etidocaine for pain relief after upper abdominal surgery: preliminary communication. Acta Anaesthesiol Scand 1975; 60: S43–9.
19. Finer B. Studies of the variability in expiratory efforts before and after cholecystectomy. Acta Anaesthesiol Scand Suppl 1970; 38: 1–68.
20. Rothen HU, Sporre B, Englberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.
Submit Your Papers Online
You can now have your paper processed and reviewed faster by sending it to us through our new, web-based Rapid Review System. Submitting your manuscript online will mean that the time and expense of sending papers through the mail can be eliminated. Moreover, because our reviewers will also be working online, the entire review process will be significantly faster. You can submit manuscripts electronically via http://www.rapidreview.com. There are links to this site from the Anesthesia & Analgesia website (http://www.anesthesia-analgesia.org), and the IARS website (http://www.iars.org). To find out more about Rapid Review, go to http://www.rapidreview.com and click on “About Rapid Review.”© 2002 International Anesthesia Research Society