In Reply:
We sincerely thank Jan van Egmond et al.1 for their interest in our review articles2,3 and relevant comments. We entirely agree that atelectasis is a prominent clinical issue and that there is great need for intervention methods to mitigate it. We also concur that negative pressure ventilation can increase the end-expiratory lung volume as observed with delivery of continuous negative extrathoracic pressure in healthy adults4 and anesthetized, surfactant-depleted rabbits.5 Continuous negative abdominal pressure has also been reported to selectively recruit dorsal atelectatic lung and correspondingly increase the volume of ventilated lung in animal models under general anesthesia.6,7 Accordingly, negative pleural pressure could resolve peripheral airway closure and atelectasis if that closure is secondary to insufficient transpulmonary pressures.
Of note, our reviews are focused on perioperative pulmonary atelectasis. As detailed in the reviews, abdominal and thoracic surgery are particularly relevant in that context as they are related to mechanisms promoting atelectasis and are associated with significant incidence of atelectasis and postoperative pulmonary complications.2,3 Unfortunately, in such surgical conditions, the mentioned negative pressure ventilatory support system is not applicable intraoperatively and may be challenging postoperatively due to concerns about sterility and access to the surgical site and wound. Finally, it is unclear whether application of negative pressure ventilation during the postoperative period could interfere with wound healing. Future studies on interventions to mitigate perioperative atelectasis should consider the mechanisms producing the process and the clinical context for optimal design and implementation.
Research Support
Supported by National Heart, Lung, and Blood Institute, National Institutes of Health (Bethesda, Maryland) grant Nos. R01 HL121228 and UH3 HL140177 (to Dr. Vidal Melo).
Competing Interests
The authors declare no competing interests.
