Coussa, Marta MD; Proietti, Stefania MD; Schnyder, Pierre MD; Frascarolo, Philippe PhD; Suter, Michel MD, PhD; Spahn, Donat R. MD; Magnusson, Lennart MD, PhD
General anesthesia, even in healthy patients, increases intrapulmonary shunt, which may impair pulmonary gas exchange (1,2). Atelectasis formation during general anesthesia is the main cause of the increase in intrapulmonary shunt (3–5). Pulmonary atelectasis occurs in 85%–90% of healthy adults (6) within minutes after the induction of general anesthesia (7). The amount of atelectasis is larger in obese patients (8) or when a high fraction of inspired oxygen (Fio2) is used (9,10). Using a lower Fio2 while breathing oxygen diminishes this atelectasis formation during the induction of general anesthesia (10). This technique, however, is not recommended because it reduces the duration of nonhypoxic apnea (11). However, we have shown that application of positive airway pressure in nonobese patients during the induction of anesthesia prevents atelectasis formation despite breathing 100% oxygen (12).
During general anesthesia (13), as well as during the immediate postoperative period (14), morbidly obese patients are more likely to have significant impairment of pulmonary gas exchange and respiratory mechanics. Indeed, we have shown that morbidly obese patients will develop a larger amounts of atelectasis during general anesthesia than nonobese patients and that this atelectasis will resolve more slowly (8). Furthermore, morbidly obese patients will have oxygen desaturation more rapidly than nonobese patients (15) during apnea. Moreover, this population of patients is at an increased risk of difficult intubation (5%–15% of the patients) (16). Therefore, for morbidly obese patients, it would be particularly useful to prevent atelectasis formation during the induction of anesthesia despite the use of 100% oxygen.
The aim of this study was therefore to evaluate whether the application of positive airway pressure during anesthesia induction may prevent atelectasis formation despite the use of large concentrations of oxygen.
After approval by the local Ethic Committee and written informed consent, 23 adult morbidly obese patients, ASA II or III, aged 20 to 65 yr, and scheduled for bariatric surgery were enrolled in this prospective, randomized, single-blinded study. Two patients refused to participate in our study, two patients had a weight more than 160 kg, which is not tolerated by the computed tomography (CT) table, and one patient did not tolerate the face mask. They were excluded from the study.
Patients included in the study had a body mass index >35 kg/m2 and were scheduled for elective surgery. Patients were excluded if they were hospitalized more than 24 h before the operation or if they had a history or clinical signs of heart or lung disease. The estimation of the sample size was based on a previous study (8). This size was calculated to detect a difference of 50% in atelectasis between the groups, with P = 0.05 and a power of 80%.
Patients received no premedication. Anesthesia was induced with fentanyl 2 μg/kg and propofol 2 mg/kg followed by a continuous infusion at 4–6 mg · kg-1 · h-1. Patients received cisatracurium 0.2 mg/kg to facilitate endotracheal intubation.
In the positive end-expiratory pressure (PEEP) group, continuous positive airway pressure (CPAP) at 10 cm H2O was applied during the administration of oxygen for 5 min; then anesthesia was induced, and the patient was mechanically ventilated with a PEEP of 10 cm H2O (Vt = 10 mL/kg at 10 breaths/min) via a face mask for another 5 min (Fig. 1). PEEP was monitored by a pressure monitoring system measured directly at the face mask. The same induction and ventilation was applied for the control group but without CPAP or PEEP.
Atelectasis was evaluated by CT (6,17). The first CT scan was obtained while the patient was awake. A second CT scan was performed immediately after tracheal intubation. Patients were placed supine on the CT table with the arms above the head. A frontal scout view of the chest was obtained at end expiration. For analysis of atelectasis, three slice scans were performed at an end expiration of 1 cm above the right diaphragm with a section of 5 mm at 120 kV and 150 mA with a lung algorithm (GE LightSpeed, General Electric Company).
The CT data were transferred on a GE Advantage Window Station. The right and left lung surfaces were manually extracted, and a window setting of -1000 to +100 Hounsfield Unit (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 HU was chosen to establish the surface of poorly ventilated lung, and a third threshold of -100 to +100 HU was set to measure the surface of atelectatic lung area. The right and left lung surfaces of atelectasis were summed and reported to the total lung surface. Only one investigator (SP) performed these measurements and was blinded to the randomization.
Two arterial blood samples were obtained through radial artery puncture: one before the induction of anesthesia (on room air) and one directly after the second CT scan (approximately 3 min after intubation).
Values are expressed as mean ± sd. For values normally distributed, comparisons between and within groups were performed using unpaired and paired Student’s t-tests, respectively. For values not normally distributed, comparison between groups was performed with the Mann-Whitney test. Bonferroni correction for multiple comparisons was applied. Fisher’s exact test was used to compare discrete variables. P < 0.05 was considered significant.
The two groups were similar regarding demographic characteristics (Table 1). No patients had a difficult intubation, only one attempt was required, and the duration of intubation did not exceed 1 min in any patient.
Before the anesthesia induction, CT scans showed nearly no atelectasis in both groups (0.8% ± 1.2% in the control group versus 0.1% ± 0.2% in the PEEP group) (Figs. 2–4). Directly after intubation, the mean area of atelectasis increased significantly in both groups, but this increase was much more pronounced in the control group (10.4% ± 4.8% in the control group versus 1.7% ± 1.3% in the PEEP group; P < 0.001;Figs. 2–4).
Blood gas analysis showed no differences before the anesthetic induction (Table 2). Directly after the induction and intubation, there was a significantly higher Pao2 in the PEEP group (Table 2).
The main finding of this study is that despite the use of 100% oxygen, application of PEEP throughout the induction period nearly completely prevents atelectasis formation in morbidly obese patients.
The Fio2 used during the administration of oxygen will greatly influence atelectasis formation. If no oxygen administration (9) or an Fio2 of 0.3 is used, no atelectasis will occur (10). However, this technique is not recommended because decreasing Fio2 will also reduce the duration of nonhypoxic apnea. Even an Fio2 of 0.8 will prevent atelectasis formation compared with 100% oxygen but at the cost of a decrease in nonhypoxic apnea duration (11). However, preventing atelectasis formation in morbidly obese patients with the application of PEEP despite the use of 100% oxygen is more likely to maintain this duration of nonhypoxic apnea; it might even increase this duration by an increase in functional residual capacity and thus in the intrapulmonary oxygen store, as shown by a study in nonobese patients (18).
Atelectasis has been evaluated by CT scans. This method has been previously described (6). Atelectasis that appears after the induction of general anesthesia is located in dependent, basal parts of the lung (19). To avoid excessive radiation exposure, only the level of the interventricular septum was chosen. The interventricular septum level is the compromise between the most affected bases of the lung and the less affected apexes (20).
One limitation of the study is that the weight of the patients was limited to 160 kg. Indeed, the CT-scan table is not guaranteed for weights heavier than 160 kg. Two male patients were excluded from the study for this reason.
A potential risk of mechanical ventilation with PEEP is exposing a sedated, paralyzed patient to stomach insufflations and by consequence increasing the risk of regurgitation and broncho-aspiration. There is a risk with insufflation pressures more than 20 mm Hg, which is also obtained with manual ventilation (21,22). Alarm limits of the ventilator can be set to 20 mm Hg, and it is also possible to ventilate patients in the pressure-controlled mode, which will prevent the use of higher pressure via the face mask. Therefore, the proposed technique may even decrease these risks compared with manual ventilation via a face mask.
It is often believed that the combination of increased intraabdominal pressure, high volume, and low pH values of gastric contents, delayed gastric emptying, and an increased incidence of hiatus hernia and gastroesophageal reflux place the obese patient at a higher risk of broncho-aspiration (23). Studies, however, have challenged this contention. Zacchi et al. (24) showed that obese patients without symptoms of gastroesophageal reflux have a resistance gradient between the stomach and the gastroesophageal junction similar to that in nonobese subjects in both the lying and sitting positions. Although obese individuals have a 75% larger gastric volume than normal individuals, it has been shown that gastric emptying is actually faster in the obese. However, as a result of the larger gastric volume, the residual volume is still larger in obese individuals (25). Despite such conflicting evidence, it is sensible to take precautions against acid aspiration. This includes the use of H2 receptor antagonists, antacids, and prokinetics. Indeed, it has been shown that when administrating a single-dose of oral famotidine or a double-dose of oral ranitidine before surgery, mean gastric volume, aspirated through a gastric tube, was only of 13 mL and the mean gastric pH value was 6.5. With this premedication, no patient was considered “at risk” of developing aspiration pneumonitis (pH value <2.5 and gastric volume more than 25 mL) (26). Therefore, in our institution, H2 receptor antagonists, antacids, and prokinetics are given to all morbidly obese patients as premedication, but no rapid sequence induction is performed if the patient has no gastroesophageal reflux. The safety of this technique was confirmed by a study showing that no pulmonary aspiration occurred in 23 morbidly obese patients subjected to 349 general anesthetics for electroconvulsive therapy. In these patients, anesthesia was induced with methohexital and succinylcholine; ventilation was assisted using positive pressure with a face mask until the patient was able to resume adequate spontaneous respirations (27).
Moreover, obesity is significantly related to difficult intubation (28–30). In these cases, it is important to have as much time as possible to apply a difficult intubation algorithm. It is frequently believed that rapid sequence induction with succinylcholine will permit recovery of spontaneous ventilation in the case of impossibility to ventilate and intubate. In healthy young volunteers, after a single dose of succinylcholine, it takes five minutes to have a beginning of spontaneous ventilation, and 11% of these volunteers will desaturate to less than 90% within five minutes (31). In another study of 12 healthy volunteers, mean time to recovery of spontaneous ventilation was 5.2 minutes with four volunteers decreasing their Spo2 to <80% and requiring some form of assisted ventilation (32). Morbidly obese patients will desaturate faster (Spo2 <90% within two minutes), and recovery of spontaneous ventilation is more difficult (33). Therefore, it is not reasonable to hope that morbidly obese patients will recover spontaneous ventilation after a single dose of succinylcholine before lethal hypoxemia occurs. It is certainly more important to use an anesthesia induction technique, which gives the longest possible duration of nonhypoxic apnea, and the best intubating condition.
Application of CPAP for five minutes in conscious patients followed by five minutes of mechanical ventilation with PEEP in sedated patients is safe, simple, and well accepted by most patients. Only two patients refused to participate in our study because one suffered from claustrophobia and one did not tolerate the face mask, even without CPAP. Therefore, the limit of this technique is the tolerance of the patients. Nevertheless, in several studies, CPAP during the administration of oxygen was always tolerated without any problem (12,15,18). Even if CPAP cannot be applied in an individual patient, PEEP can still be used and will likely also be helpful in reducing atelectasis caused by anesthesia induction. Indeed, it has been shown that atelectasis occurs during the induction of general anesthesia and that prevention is probably most important directly after the induction (12). Nevertheless, we believe that application of CPAP is probably also helpful because some morbidly obese patients do develop atelectasis when they are supine.
1. Marshall BE, Wyche MQ Jr. Hypoxemia during and after anesthesia. Anesthesiology 1972;37:178–209.
2. Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia: an observer study. Br J Anaesth 1991;66:437–44.
3. 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.
4. Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003;91:61–72.
5. Tokics L, Hedenstierna G, Strandberg A, et al. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology 1987;66:157–67.
6. 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.
7. Strandberg A, Tokics L, Brismar B, et al. Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiol Scand 1986;30:154–8.
8. Eichenberger A, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg 2002;95:1788–92.
9. Reber A, Englberg G, Wegenius G, Hedenstierna G. Lung aeration: the effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia 1996;51: 733–7.
10. Rothen HU, Sporre B, Englberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995;345:1387–91.
11. Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003;98:28–33.
12. Rusca M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg. In press.
13. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 1997;82:811–8.
14. 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.
15. Berthoud MC, Peacock JE, Reilly CS. Effectiveness of preoxygenation in morbidly obese patients. Br J Anaesth 1991;67: 464–6.
16. Hood DD, Dewan DM. Anesthetic and obstetric outcome in morbidly obese parturients. Anesthesiology 1993;79:1210–8.
17. 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.
18. Herriger A, Frascarolo P, Spahn DR, Magnusson L. Effectiveness of positive end expiratory pressure during pre-oxygenation on duration of apnoea before arterial desaturation. Eur J Anaesthesiol 2003;20:A–268.
19. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985;62:422–8.
20. Neumann P, Rothen HU, Berglund JE, et al. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 1999;43:295–301.
21. Ho-Tai LM, Devitt JH, Noel AG, O’Donnell MP. Gas leak and gastric insufflation during controlled ventilation: face mask versus laryngeal mask airway. Can J Anaesth 1998;45:206–11.
22. Vyas H, Milner AD, Hopkin IE. Face mask resuscitation: does it lead to gastric distension? Arch Dis Child 1983;58:373–5.
23. Vaughan RW, Bauer S, Wise L. Volume and pH of gastric juice in obese patients. Anesthesiology 1975;43:686–9.
24. Zacchi P, Mearin F, Humbert P, et al. Effect of obesity on gastroesophageal resistance to flow in man. Dig Dis Sci 1991; 36:1473–80.
25. Wisen O, Hellstrom PM. Gastrointestinal motility in obesity. J Intern Med 1995;237:411–8.
26. Vila P, Valles J, Canet J, et al. Acid aspiration prophylaxis in morbidly obese patients: famotidine vs. ranitidine. Anaesthesia 1991;46:967–9.
27. Kadar AG, Ing CH, White PF, et al. Anesthesia for electroconvulsive therapy in obese patients. Anesth Analg 2002;94:360–1.
28. Rocke DA, Murray WB, Rout CC, Gouws E. Relative risk analysis of factors associated with difficult intubation in obstetric anesthesia. Anesthesiology 1992;77:67–73.
29. Rose DK, Cohen MM, Wigglesworth DF, DeBoer DP. Critical respiratory events in the postanesthesia care unit: patient, surgical, and anesthetic factors. Anesthesiology 1994;81:410–8.
30. Wilson ME, Spiegelhalter D, Robertson JA, Lesser P. Predicting difficult intubation. Br J Anaesth 1988;61:211–6.
31. Hayes AH, Breslin DS, Mirakhur RK, et al. Frequency of haemoglobin desaturation with the use of succinylcholine during rapid sequence induction of anaesthesia. Acta Anaesthesiol Scand 2001;45:746–9.
32. Heier T, Feiner JR, Lin J, et al. Hemoglobin desaturation after succinylcholine-induced apnea: a study of the recovery of spontaneous ventilation in healthy volunteers. Anesthesiology 2001; 94:754–9.
33. Farmery AD, Roe PG. A model to describe the rate of oxyhaemoglobin desaturation during apnoea. Br J Anaesth 1996;76: 284–91.