Pulmonary Atelectasis

BackgroundPostoperative pulmonary complications (PPCs) are associated with poor outcomes following thoracotomy and lung resection. Video-assisted thoracoscopic surgery (VATS) for lobectomy is now frequently utilised as an alternative to thoracotomy, however patients remain at risk for development of PPC. There is little known of the short-term outcome associated with PPC following VATS lobectomy and if there are any potential risk factors that could be modified to prevent PPC development; our study aimed to investigate this.MethodsA prospective observational study of consecutive patients undergoing VATS lobectomy for lung cancer over a 4-year period in a regional centre was performed (2012-2016). Exclusion criteria included re-do VATS or surgery for pulmonary infection. All patients received physiotherapy as necessary from postoperative day 1 (POD1) and PPC was determined using the Melbourne Group Scale. Outcomes included hospital LOS, intensive therapy unit (ITU) admission and hospital mortality.ResultsOf the 285 patients included in the study, 137 were male (48.1%), the median (IQR) age was 69 (13) years and the mean (±SD) FEV1% predicted was 87% (±19). Patients that developed a PPC (n = 21; 7.4%) had a significantly longer hospital LOS (4 vs. 3 days), higher frequency of ITU admission (23.8% vs. 0.5%) and higher hospital mortality (14.3% vs. 0%) (p ConclusionsPatients undergoing VATS lobectomy remain at risk of developing a PPC, which is associated with an increase in physiotherapy requirements and a worse short-term morbidity and mortality. Current smoking is the only independent risk factor for PPC after VATS lobectomy, thus vigorous addressing of preoperative smoking cessation is urgently needed.

Acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure yet has few pharmacologic therapies, reflecting the mechanistic heterogeneity of lung injury. We hypothesized that damage to the alveolar epithelial glycocalyx, a layer of glycosaminoglycans interposed between the epithelium and surfactant, contributes to lung injury in patients with ARDS. Using mass spectrometry of airspace fluid noninvasively collected from mechanically ventilated patients, we found that airspace glycosaminoglycan shedding (an index of glycocalyx degradation) occurred predominantly in patients with direct lung injury and was associated with duration of mechanical ventilation. Male patients had increased shedding, which correlated with airspace concentrations of matrix metalloproteinases. Selective epithelial glycocalyx degradation in mice was sufficient to induce surfactant dysfunction, a key characteristic of ARDS, leading to microatelectasis and decreased lung compliance. Rapid colorimetric quantification of airspace glycosaminoglycans was feasible and could provide point-of-care prognostic information to clinicians and/or be used for predictive enrichment in clinical trials.

Partnership between anesthesia providers and proceduralists is essential to ensure patient safety and optimize outcomes. A renewed importance of this axiom has emerged in advanced bronchoscopy and interventional pulmonology. While anesthesia-induced atelectasis is common, it is not typically clinically significant. Advanced guided bronchoscopic biopsy is an exception in which anesthesia protocols substantially impact outcomes. Procedure success depends on careful ventilation to avoid excessive motion, reduce distortion causing computed tomography (CT)-to-body-divergence, stabilize dependent areas, and optimize breath-hold maneuvers to prevent atelectasis. Herein are anesthesia recommendations during guided bronchoscopy. An FiO2 of 0.6 to 0.8 is recommended for pre-oxygenation, maintained at the lowest tolerable level for the entire the procedure. Expeditious intubation (not rapid-sequence) with a larger endotracheal tube and non-depolarizing muscle relaxants are preferred. Positive end-expiratory pressure (PEEP) of up to 10-12 cm H2O and increased tidal volumes help to maintain optimal lung inflation, if tolerated by the patient as determined during recruitment. A breath-hold is required to reduce motion artifact during intraprocedural imaging (e.g., cone-beam CT, digital tomosynthesis), timed at the end of a normal tidal breath (peak inspiration) and held until pressures equilibrate and the imaging cycle is complete. Use of the adjustable pressure-limiting valve is critical to maintain the desired PEEP and reduce movement during breath-hold maneuvers. These measures will reduce atelectasis and CT-to-body divergence, minimize motion artifact, and provide clearer, more accurate images during guided bronchoscopy. Following these recommendations will facilitate a successful lung biopsy, potentially accelerating the time to treatment by avoiding additional biopsies. Application of these methods should be at the discretion of the anesthesiologist and the proceduralist; best medical judgement should be used in all cases to ensure the safety of the patient.

BackgroundAtelectasis is common during general anaesthesia and contributes to postoperative pulmonary complications. Despite preventive strategies targeting established underlying mechanisms, extensive atelectasis still often occurs, suggesting that additional factors may be involved. We tested the hypothesis that hypotension contributes to atelectasis formation during anaesthesia.MethodsWe conducted a randomised, evaluator-blinded crossover study in 12 anaesthetised, mechanically ventilated pigs under conditions simulating anaesthesia induction, in which preoxygenation was followed by either normotension or profound hypotension induced with nitroprusside. The primary outcome was total atelectasis volume, measured by computed tomography. Pulmonary blood flow distribution was assessed using [15O]-water positron emission tomography.ResultsAtelectasis volume was greater during induced hypotension (median MAP 46 mmHg [interquartile range: 43-49]), compared with normotension (median MAP 85 mmHg [81-93]) in 11 of 12 pigs (median difference 20 ml [95% CI 9-38]; PConclusionsIn this experimental model of anaesthesia induction, profound hypotension increased atelectasis compared with normotension. The findings are consistent with redistribution of pulmonary blood flow with low oxygen saturation towards dorsal lung regions that are prone to develop absorption atelectasis. Hypotension during induction of general anaesthesia might therefore be a hitherto unrecognised contributor to pulmonary atelectasis.Trial registrationwww.animalstudyregistry.org (https://doi.org/10.17590/asr.0000369).