In 1964, Nunn1 showed that during routine general anesthesia, gas exchange was altered by shunt and uneven ventilation perfusion ratios. In 1985, Brismar et al.2 showed that within 5 min of induction of general anesthesia, chest radiographs showed that crest-shaped changes of increased density appeared in the dependent regions of both lungs. In 1989, Hedenstierna et al.3 also found densities in anesthetized animals, with the same location and attenuation as in anesthetized humans. Microscopy showed that these densities were atelectatic lung regions.4
Postoperative lung atelectasis develops with both IV and inhaled anesthesia and whether the patient is breathing spontaneously or is paralyzed and ventilated mechanically.5 The adverse effects of atelectasis persist into the postoperative period and can affect patient recovery.6
Up to 15% of the entire lung may be atelectatic during anesthesia, particularly in the basal region, resulting in a true pulmonary shunt of approximately 5%–10% of cardiac output.7 Laparoscopic surgery is usually performed by intraabdominal insufflation of carbon dioxide; this insufflation leads to an increase in intraabdominal pressure. The increase in intraabdominal pressure could induce shift of the diaphragm cranially and compression of basal lung regions. Thus, the increase in intraabdominal pressure could accentuate the effects of atelectasis already predisposed to by general anesthesia, and therefore laparoscopic surgeries are associated with a frequent incidence of lung atelectasis.8
During general anesthesia, as well as during the immediate postoperative period, obese patients are more likely than nonobese patients to develop atelectasis that resolves more slowly.9 This is because of a marked impairment of the respiratory mechanics (decreased chest wall and lung compliance and decreased function residual capacity) promoting airway closure with reduction of the oxygenation index (Pao2/PAo2) to a greater extent than in healthy-weight subjects.10 Also, the weight of the torso and abdomen makes diaphragmatic excursions more difficult, especially when recumbent or supine, which is intensified in the setting of diaphragmatic paralysis associated with neuromuscular blockade.11 In obese patients, avoiding atelectasis formation may be particularly difficult but at the same time particularly important.12
Over the last several decades, different strategies were used to reexpand collapsed lungs during general anesthesia to “optimize” oxygenation. Atelectatic lung tissue was fully reexpanded only with a pressure of 40 cm H2O maintained for 15 s. This pressure is equivalent to inflation to vital capacity, and thus this maneuver has been called the vital capacity maneuver (VCM).13 More recently, it has been shown that this maneuver needs to be maintained for only 7–8 s in order to reexpand all previously collapsed lung tissue,14 but in laparoscopic surgery, the recruitment effect of a single VCM may be lost after pneumoperitoneum, which necessitates a further recruitment maneuver to keep the alveoli opened. Indeed, there have been previous studies on this topic. Our study is focused on preventing atelectasis in obese patients undergoing laparoscopic bariatric surgeries. The aim of this study was to evaluate the safety and efficacy of the VCM followed by different levels of positive end-expiratory pressure (PEEP) used to prevent postoperative lung atelectasis in obese patients undergoing laparoscopic bariatric surgery.
After approval by our local Ethics and Research Committee, 66 adult obese patients with a body mass index (BMI) between 30 and 50 kg/m2, aged between 20 and 50 yr, and scheduled to undergo laparoscopic bariatric surgery, were included in this prospective, double-blind, controlled study after obtaining written informed consent. Patients were fasted for at least 8 h before the induction of anesthesia. Patients were excluded if they had been hospitalized more than 24 h before surgery, had a history of heart or lung diseases, had any clinical sign of cardiopulmonary disease during preoperative physical examination (jugular vein distension, gallop rhythm, hepatomegaly, tibial edema, or rales on auscultation of the chest, or any abnormalities in the preoperative 12-lead electrocardiogram or chest radiograph). If any complications occurred that necessitated laparotomy, the patient was excluded from the study.
Patients were premedicated with metoclopramide 10 mg IV, ranitidine 50 mg IV infusion, and oral lorazepam 1 mg 1 h before induction of anesthesia. Induction of anesthesia was achieved by administration of oxygen by facemask (100% O2) for 3–5 min followed by 2–3 mg/kg propofol, 2 μg/kg fentanyl, and 0.6 mg/kg rocuronium to facilitate tracheal intubation. Anesthesia was maintained using 2% sevoflurane, 1–2 μg · kg−1 · h−1 fentanyl, and 0.2 mg/kg rocuronium boluses every 30 min. In all patients, the lungs were ventilated with volume-controlled ventilation with a mixture of 50% oxygen in air, and a tidal volume of 8–10 mL/kg based on lean body weight. Breathing rate was adjusted to maintain end-tidal carbon dioxide partial pressure between 32 and 36 mm Hg. Carbon dioxide was insufflated into the peritoneal cavity until the intraabdominal pressure reached 11–15 mm Hg, which was maintained throughout the procedure.
Crystalloid solution at a rate of 20 mL · kg−1 · h−1 was administered to all patients starting immediately before induction of anesthesia until patient positioning (modified lithotomy position–anti-Trendelenburg), followed by 5 mL · kg−1 · h−1 until the end of the surgery. The arms and upper thorax of all patients were covered with a warm air-stream blanket to minimize heat loss. Intraoperative hypotension (decrease in mean arterial blood pressure [MAP] >25% of baseline) was treated with a bolus of normal saline 0.9% 250 mL and/or incremental doses of IV vasoactive drugs (ephedrine 5 mg or phenylephrine 50 μg). At the conclusion of surgery, sevoflurane was discontinued, and Fio2 was increased to 100%. The muscle relaxant was reversed by neostigmine 50 μg/kg and 0.015 mg/kg atropine sulfate. Tracheal extubation was performed in a semisitting position after reaching satisfactory criteria for extubation. Our extubation criteria were as follows:
- Intact neurological status; fully awake and alert; head lift >5 s
- Hemodynamically stable
- Normothermia; core temperature >36°C
- Full reversal of neuromuscular blocking drugs
- Respiratory rate >10 and <30 breaths/min
- Baseline peripheral oxygenation Spo2 >95% on Fio2 of 0.4
- Vital capacity >10 mL/kg ideal body weight; tidal volume >5 mL/kg ideal body weight
- Acceptable pain control in the postanesthesia care unit (PACU); patients were kept at head-up tilt of 30°–45°
To prevent development of immediate postextubation hypoxia, uninterrupted administration of oxygen was continued until patients were transferred to the PACU.
During the PACU stay, all patients were in a semisitting position with supplemental oxygen by Venturi facemask (Oximask; Tyco-Healthcare, Kendall) (Fio2 35%). A nonrebreathing oxygen mask was applied when oxygen saturation decreased to <94%. Postoperative analgesia was started in the PACU by patient-controlled analgesia, 1-mg bolus of morphine on demand with a lockout time of 6 min without background infusion. The patients were discharged to the ward after fulfilling the recovery criteria.15
Patients were randomly allocated into 3 groups according to the recruitment maneuver used: the zero end-expiratory pressure (ZEEP) group (n = 22) received the VCM maintained for 7–8 s applied immediately after intubation plus ZEEP, the PEEP 5 group (n = 22) received the VCM maintained for 7–8 s applied immediately after intubation plus 5 cm H2O of PEEP, and the PEEP 10 group (n = 22) received the VCM maintained for 7–8 s applied immediately after intubation plus 10 cm H2O of PEEP. All other variables were maintained constant throughout the procedure.
The study protocol was designed to 1) discontinue PEEP or VCM and start inotropic drugs in case of persistent hypotension (decrease MAP >25% of baseline) after giving vasoactive drugs; and 2) discontinue PEEP or VCM and change the ventilatory mode to pressure-controlled ventilation. Patients with high airway pressure >45 cm H2O were excluded from the study (Table 1).
Heart rate, noninvasive MAP, and arterial oxygen saturation were measured at the following times:
- T0: before induction of anesthesia breathing room air
- T1: immediately after induction of anesthesia
- T2: immediately after VCM
- T3: immediately after establishing pneumoperitoneum
- T4: immediately after patient positioning (modified lithotomy position with anti-Trendelenburg)
- T5: 30 min after establishing positioning
- T6: 60 min after establishing positioning/end of procedure
- T7: immediately after PACU admission
- T8: before discharge from PACU
Arterial blood gas samples were taken preoperatively (T0) and postoperatively (T8) to measure partial pressure of oxygen (Pao2) and to calculate alveolar-arterial Pao2 gradient (A-a Pao2).
Alveolar Po2 was calculated from the alveolar gas equation16:
where PAo2 is partial pressure of alveolar O2, Pio2 is partial pressure of inspired O2, PB is barometric atmospheric pressure (760 mm Hg), and PH2O is partial pressure of water vapor (47 mm Hg at normal body temperature).
Length of PACU stay and the need for nonrebreathing O2 mask (100% Fio2) or reintubation were recorded.
Computed Tomographic Imaging
The chest computed tomographic (CT) imaging was performed on hospital admission and after discharge from the PACU. CT scans were interpreted by radiologists who were aware of the experimental protocol but unaware of patient group assignment. Atelectasis was evaluated using a Siemens Volume Zoom CT Scanner (Siemens Volume Zoom CT Scanner, Erlangen, Germany). A tomogram film of the chest was done with the patient in supine position and his or her hand up. Four slices of 5-mm thickness were obtained above the diaphragm. The CT images were specifically evaluated for atelectasis, which was classified into 4 types depending on thickness: lamellar atelectasis (<3 mm), plate atelectasis (3–10 mm), segmental atelectasis (>10 mm but less than a lobe), and lobar atelectasis (atelectasis involving the entire lower lobe).17
The sample size for this study was based on the assumption that a reduction of atelectasis of 35% or more would be of clinical importance. Using the SPSS program (version 14), analysis of variance (ANOVA) test for numerical parametric data and χ2 test for ordinal and categorical data were applied, and a P value of 0.05 or less was considered significant. One-way ANOVA was used to compare the age, BMI, and surgery time among the 3 study groups. Mixed between-within subjects ANOVA (a combination of between-groups ANOVA and repeated-measures ANOVA) was used to compare the repeated measures and between groups. Nonparametric data, e.g., atelectasis or high Fio2 requirement were analyzed using the χ2 test.
There were no statistically significant differences among the 3 groups with regard to age, sex, ASA physical status classification, duration of surgery, or BMI (Table 2).
Sixty-six patients were included in this double-blind, prospective, randomized study. During the study, 3 patients in the ZEEP group, 3 patients in the PEEP 5 group, and 2 patients in the PEEP 10 group were excluded (Table 1). There were no significant differences in MAP and heart rate among the 3 study groups (Table 3), and there was a significant decrease of postoperative A-a gradient in the PEEP 10 compared with the ZEEP and PEEP 5 groups (Table 4 and Fig. 1). Time spent in the PACU was significantly shorter in the PEEP 10 group compared with both the ZEEP and PEEP 5 groups. During PACU stay, only 1 patient in the PEEP 10 group needed oxygen from a nonrebreathing O2 mask (Fio2 100%) compared with 5 patients in the ZEEP group (1 of them transferred to the intensive care unit because of persistent hypoxemia) and 3 patients in the PEEP 5 group (Table 5). During the first 48 h postoperatively, no significant desaturation, chest infection, or bronchospasm was noted in the PEEP 10 group, compared with 4 and 3 patients in the ZEEP and PEEP 5 groups, respectively (Table 6). All of the preoperative CT scans were normal in all 3 study groups. Postoperatively, patients in the PEEP 10 group had significantly less segmental and lobar atelectasis (4 patients) compared with the ZEEP and PEEP 5 groups (14 and 9 patients, respectively) (Table 7). The postoperative atelectasis score was comparable without significant differences between the ZEEP and PEEP 5 groups. No barotraumas (pneumothorax, air in mediastinum, or subcutaneous emphysema) were detected in chest CT scans in any patient in the 3 study groups.
Even though this study indicated positive benefits from the VCM and PEEP, there are potential disadvantages as well. Increased intrathoracic pressure as a result of PEEP or VCM may reduce the pressure gradient along which blood returns to the heart. This reduces right ventricular preload, right ventricular output, and ultimately cardiac output. This may lead to a reduction in MAP and pooling of blood in the abdomen and peripheries, especially in patients who are hypovolemic and in those whose adaptive cardiac reserves are blunted by intrinsic disease or medication.18
In this study, application of PEEP and VCM was not accompanied by a significant reduction in MAP, even after pneumoperitoneum and positioning (modified lithotomy position and anti-Trendelenburg). This can be explained by sufficient preoperative preload with crystalloid solution (20 mL · kg−1 · h−1) for all patients. Similarly, Azab et al.8 found in their study that application of 5 cm H2O PEEP was not accompanied by any reduction in MAP in patients undergoing laparoscopic cholecystectomy. In our study, there was no significant change in intraoperative or postoperative oxygen saturation and A-a gradient in patients who received 5 cm H2O PEEP compared with the ZEEP group. Also, there was no significant difference in the atelectasis score between the 2 groups, i.e., application of 5 cm H2O PEEP did not improve oxygenation and did not decrease atelectasis formation. This is in contrast to Azab et al.8 who concluded that PEEP (5 cm H2O) prevents deoxygenation during pneumoperitoneum and leads to a lower atelectasis score on CT scan examination up to 2 h postoperatively. However, their study used nonobese patients, whereas our study was conducted on obese patients with a BMI >30 kg/m2 who had lower functional residual capacity in whom PEEP 5 cm H2O may not be enough to reopen collapsed alveoli after induction of anesthesia.
In this study, a VCM followed by 10 cm H2O of PEEP was accompanied by better intraoperative and postoperative oxygenation in addition to a lower atelectasis score in chest CT scan done approximately 2 h postoperatively in comparison with the VCM alone. Coussa et al.19 had similar results and concluded that application of PEEP (10 cm H2O) in morbidly obese patients was very effective for preventing atelectasis during induction of general anesthesia.
This is in contrast to Rothen et al.13 who found that the VCM alone could completely abolish atelectasis that developed after induction of general anesthesia. This can be explained by the difference in patient populations because they applied the VCM to nonobese patients undergoing nonlaparoscopic surgery compared with obese patients undergoing laparoscopic surgery in our study.
In animal experiments, the VCM had no deleterious pulmonary effects as measured by extra vascular lung water, pulmonary clearance of 99mTc-diethylene triamine pentaacetic acid (DTPA) (which is a marker of the functional integrity of the alveolocapillary barrier), and light microscopy in pigs that received repeated VCM hourly for 6 h.20 Similarly, in this study, no pneumothorax, air in the mediastinum, or subcutaneous emphysema was detected in chest CT scan done postoperatively in any patient in the 3 study groups.
Many previous studies have investigated postoperative hypoxemia in the PACU. Mathes et al.21 found that, on arrival to the PACU, 20% of patients may have an oxygen saturation <92% and in 10% the saturation may be <90%. Xue et al.22 reported that, in the PACU within 3 h of surgery, 7% of patients will have at least 1 episode of desaturation <90% and 3% will desaturate to <85%. This incidence is increased for thoracoabdominal procedures, in which more than half of the patients will have oxygen saturation <90% and 20% of patients will have severe hypoxemia (<85%). Russell and Graybeal23 reported that, despite the use of 40% oxygen given by facemask, 15% of patients in the PACU will have oxygen saturation <92% lasting >30 s. This event seems to prolong the PACU stay and cause more intensive care admissions. In all previous studies, all patients were anesthetized for different types of surgeries with volume-controlled ventilation without any recruitment maneuver.
Postoperative pulmonary complications occurred only in the ZEEP and PEEP 5 groups, which can be explained by the increased frequency of atelectasis in those groups. The same finding was reached by Michelle et al.6 who reported that development of atelectasis is associated with decreased lung compliance, impairment of oxygenation, increased pulmonary vascular resistance, and development of lung injury. The adverse effects of atelectasis persist into the postoperative period and can affect patient recovery. The absence of pulmonary complications in group PEEP 10 patients can be attributed to less atelectasis in those patients.
The severity and effect of atelectasis are expected to be increased in super morbidly obese patients with a BMI >50 kg/m2 compared with obese patients with a BMI between 30 and 50 kg/m2, but the standard CT table cannot support a patient weighing >170 kg, which is why we did not include patients with BMI >50 kg/m2. We needed to be able to evaluate postoperative atelectasis by CT scan.
Intraoperative alveolar recruitment with the VCM followed by PEEP of 10 cm H2O is more effective than ZEEP or PEEP of 5 cm H2O for prevention of postoperative lung atelectasis and is associated with better oxygenation, shorter PACU stay, and fewer pulmonary complications in the immediate postoperative period in obese patients undergoing laparoscopic bariatric surgery.
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