Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem

Perturbation of respiratory mechanics produced by general anesthesia and surgery is more pronounced in morbidly obese (MO) patients. Because general anesthesia induces pulmonary atelectasis in nonobese patients, we hypothesized that atelectasis formation would be particularly significant in MO patients. We investigated the importance and resorption of atelectasis after general anesthesia in MO and nonobese patients. Twenty MO patients were anesthetized for laparoscopic gastroplasty and 10 nonobese patients for laparoscopic cholecystectomy. We assessed pulmonary atelectasis by computed tomography at three different periods: before the induction of general anesthesia, immediately after tracheal extubation, and 24 h later. Already before the induction of anesthesia, MO patients had more atelectasis, expressed in the percentage of the total lung area, than nonobese patients (2.1% versus 1.0%, respectively; P < 0.01). After tracheal extubation, atelectasis had increased in both groups but remained significantly more so in the MO group (7.6% for MO patients versus 2.8% for the nonobese; P < 0.05). Twenty-four hours later, the amount of atelectasis remained unchanged in the MO patients, but we observed a complete resorption in nonobese patients (9.7% versus 1.9%, respectively; P < 0.01). General anesthesia in MO patients generated much more atelectasis than in nonobese patients. Moreover, atelectasis remained unchanged for at least 24 h in MO patients, whereas atelectasis disappeared in the nonobese. IMPLICATIONS: We compared the resolution over time of pulmonary atelectasis after a laparoscopic procedure by performing computed tomography scans in two different groups of patients: 1 group had 10 nonobese patients, and in the other group there were 20 morbidly obese patients

Positive end-expiratory pressure during induction of general anesthesia increases duration of nonhypoxic apnea in morbidly obese patients.

Positive end-expiratory pressure (PEEP) applied during induction of anesthesia prevents atelectasis formation and increases the duration of nonhypoxic apnea in nonobese patients. PEEP also prevents atelectasis formation in morbidly obese patients. Because morbidly obese patients have difficult airway management more often and because arterial desaturation develops rapidly, we studied the clinical benefit of PEEP applied during anesthesia induction. Thirty morbidly obese patients were randomly allocated to one of two groups. In the PEEP group, patients breathed 100% O(2) through a continuous positive airway pressure device (10 cm H(2)O) for 5 min. After induction of anesthesia, they were mechanically ventilated with PEEP (10 cm H(2)O) for another 5 min until tracheal intubation. In the control group, the sequence was the same but without any continuous positive airway pressure or PEEP. We measured apnea duration until Spo(2) reached 90% and we performed arterial blood gases analyses just before apnea and at 92% Spo(2). Nonhypoxic apnea duration was longer in the PEEP group compared with the control group (188 +/- 46 versus 127 +/- 43 s; P = 0.002). Pao(2) was higher before apnea in the PEEP group (P = 0.038). Application of positive airway pressure during induction of general anesthesia in morbidly obese patients increases nonhypoxic apnea duration by 50%

Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients

Atelectasis caused by general anesthesia is increased in morbidly obese patients. We have shown that application of positive end-expiratory pressure (PEEP) during the induction of anesthesia prevents atelectasis formation in nonobese patients. We therefore studied the efficacy of PEEP in morbidly obese patients to prevent atelectasis. Twenty-three adult morbidly obese patients (body mass index >35 kg/m(2)) were randomly assigned to one of two groups. In the PEEP group, patients breathed 100% oxygen (5 min) with a continuous positive airway pressure of 10 cm H(2)O and, after the induction, mechanical ventilation via a face mask with a PEEP of 10 cm H(2)O. In the control group, the same induction was applied but without continuous positive airway pressure or PEEP. Atelectasis, determined by computed tomography, and blood gas analysis were measured twice: before the induction and directly after intubation. After endotracheal intubation, patients of the control group showed an increase in the amount of atelectasis, which was much larger than in the PEEP group (10.4% +/- 4.8% in control group versus 1.7% +/- 1.3% in PEEP group; P < 0.001). After intubation with a fraction of inspired oxygen of 1.0, PaO(2) was significantly higher in the PEEP group compared with the control group (457 +/- 130 mm Hg versus 315 +/- 100 mm Hg, respectively; P = 0.035) We conclude that in morbidly obese patients, atelectasis formation is largely prevented by PEEP applied during the anesthetic induction and is associated with a better oxygenation. IMPLICATIONS: Application of positive end-expiratory pressure during induction of general anesthesia in morbidly obese patients prevents atelectasis formation and improves oxygenation. Therefore, this technique should be considered for anesthesia induction in morbidly obese patients