We very much thank Zaouter et al. for their interest in our research, “Pressure Support versus Spontaneous Ventilation during Anesthetic Emergence—Effect on Postoperative Atelectasis: A Randomized Controlled Trial.”
The main questions of Zaouter et al. were why we defined atelectasis only when there were signs of atelectasis in three or more lung sections and why we used a modified scoring system to evaluate atelectasis severity. For the first question, as the authors noted, there is no established definition of atelectasis diagnosed by ultrasonography. We thought that at least 25% (3 of 12 sections) of lung areas should show signs of atelectasis to be a clinically significant atelectasis because almost all patients showed an atelectasis sign in at least one lung section. We admit that 25% of lung sections is arbitrary, but this threshold was determined before conducting the study.
For their second question, we thought that an atelectasis scoring system focused on anesthesia-induced atelectasis was needed because many protocols were developed for intensive care unit patients in previous studies. However, our protocol is still based on the protocols that are widely used. Anesthesia-induced atelectasis did not show definite B lines, which were used in the previous scoring system (B lines: hyperechoic vertical lines starting from the pleural line with the length of 8 cm or longer). Rather, anesthesia-induced atelectasis showed subpleural consolidations with short vertical lines starting from the margin of consolidation (pseudo B lines). Accordingly, loss of A line with multiple subpleural consolidations has been reported as a more common and helpful finding to diagnose anesthesia-induced atelectasis. In consideration of the development process of anesthesia-induced atelectasis, the grade 3 atelectasis, which is “loss of lung sliding and appearance of lung pulse,” was added to our grading system. We found that the collapse of small bronchioles and alveoli leads to “loss of lung sliding and appearance of lung pulse” as subpleural consolidation progresses to a larger parenchymal consolidation. This was also reported in previous studies. Although we modified the scoring system for a more accurate diagnosis of anesthesia-induced atelectasis, it was not validated. We described this in the limitations to our study.
For the third question (sample size), we found that the power of our study did not meet the expectations and needed a larger number of patients. However, we understand that the probability of type II error (false negative) would have decreased as the sample size (power) increased, but the type I error (false positive) usually remains the same. Therefore, we think our positive results would have been confirmed with more power if the sample size had increased.
We agree with Zaouter et al. that oxygen-free days or cumulative postoperative oxygen administration may be more important than the incidence of hypoxia as a secondary outcome. However, most patients received oxygen administration only on the night of surgery, and there was no difference in postoperative complications such as pneumonia and hospital stay between the two groups. So, we cautiously speculate that the time-weighted need for oxygen support would not have been different between the two groups.