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Correspondence  |   January 2015
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Author Notes
  • Hospital Privado de Comunidad, Mar del Plata, Argentina (G.T.). gtusman@hotmail.com
  • (Accepted for publication September 18, 2014.)
    (Accepted for publication September 18, 2014.)×
Article Information
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Correspondence   |   January 2015
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Anesthesiology 01 2015, Vol.122, 214-215. doi:10.1097/ALN.0000000000000500
Anesthesiology 01 2015, Vol.122, 214-215. doi:10.1097/ALN.0000000000000500
Thank you very much for giving us the opportunity to reply the letter by Dr. Girard et al. about our recent paper in Anesthesiology.1  In their interesting letter, Dr. Girard et al. describe different theories about the genesis of B lines in the setting of atelectasis and commented that this very lung sonography (LUS) sign has already been described. Their argument is based on publications related to patients with pre-existing pulmonary diseases and on data derived from ex-vivo animal and laboratory models.2–5  As practicing anesthesiologists who simply apply LUS as a diagnostic tool, we focused our literature search primarily on clinical studies employing LUS and thereby may have missed important evidence coming from primary ultrasound research, however, we do not only agree with the criticism but are grateful to the authors for having raised our awareness for the complexity of LUS.
To our knowledge, the occurrence of anesthesia-induced atelectasis in children has never before been studied by LUS in detail. For this reason, we cannot infer with certainty that the LUS signs—including B lines—found in adults and in atelectasis of different origins are similar to or even identical with the ones we saw in anesthesia-induced atelectasis by compressive mechanism in our children. This lack of reliable information made us define anesthesia-induced atelectasis a posteriori and analyze the prevalence of LUS signs associated with such atelectasis (please see table 11 ). This is the reason why we presented our results—including those related to B lines—as novel contributions to the clinical understanding and diagnosis of atelectasis in children undergoing general anesthesia.
In the second part of their letter, Dr. Girard et al. highlight the role anesthesia-induced atelectasis may play in creating local inflammatory responses within the lungs and in causing postoperative pulmonary complications.6  Such lung inflammation appears any time cyclic ventilation is applied to a partially collapsed lung, the root cause being tidal recruitment (the opening and closing of an atelectatic area during the breathing cycle) and tidal overdistension (the excess volume or pressure that normally aerated areas receive during inspiration).6–9  This sequence of events calls for the use of protective ventilator settings also during anesthesia if such kind of lung injury was to be prevented.10–14  However, even in the light of recent studies, our knowledge on how to best implement protective ventilation strategies is scarce.15,16  These latest attempts to provide convincing scientific support for the hypothesis that particular ventilator settings (a combination of high vs. low tidal volume or high vs. low positive end-expiratory pressure, with and without recruitment maneuvers) would have proven effects on both, the mechanisms of lung injury during anesthesia and on postoperative pulmonary complications failed.
Furthermore, Dr. Girard et al. suggested that the link between atelectasis and postoperative pulmonary complications should be established by an imaging tool capable of detecting atelectasis. We totally agree with this statement. Although the presence of atelectasis might be suspected when respiratory mechanics and gas exchange are suboptimal, in vivo it can only be diagnosed with 100% certainty by imaging means. Therefore, the cited studies fail to demonstrate a causative relationship between particular ventilator settings and atelectasis, let alone postoperative pulmonary complications.
Therefore, before we could address such clinically relevant hypotheses, we first had to validate LUS by magnetic resonance imaging as a noninvasive reliable tool to detect atelectasis—at least in children. Now that LUS has demonstrated its high sensitivity and specificity for diagnosing atelectasis, we have a good chance to reveal tidal recruitment as the main mechanism of ventilator-associated lung injury in partially collapsed lungs. However, due to methodological reasons, LUS will fail as a diagnostic tool when the lungs become overdistended. To detect this other important injurious condition the monitoring of dead space by way of volumetric capnography is a valid option.17,18  Thus, today at least two noninvasive bedside methods are available to detect the main mechanisms of ventilator-induced lung injury. We believe it is about time to start using them in our daily practice for the benefit of our patients.
Competing Interests
The authors declare no competing interests.
Gerardo Tusman, M.D., Cecilia M. Acosta, M.D., Stephan H Bohm, M.D. Hospital Privado de Comunidad, Mar del Plata, Argentina (G.T.). gtusman@hotmail.com
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