Ventilator management and risk of air leak syndrome in patients with SARS-CoV-2 pneumonia: a single-center, retrospective, observational study

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia is reportedly associated with air leak syndrome (ALS), including mediastinal emphysema and pneumothorax, and has a high mortality rate. In this study, we compared values obtained every minute from ventilators to clarify the relationship between ventilator management and risk of developing ALS. This single-center, retrospective, observational study was conducted at a tertiary care hospital in Tokyo, Japan, over a 21-month period. Information on patient background, ventilator data, and outcomes was collected from adult patients with SARS-CoV-2 pneumonia on ventilator management. Patients who developed ALS within 30 days of ventilator management initiation (ALS group) were compared with those who did not (non-ALS group). Of the 105 patients, 14 (13%) developed ALS. The median positive-end expiratory pressure (PEEP) difference was 0.20 cmH O (95% confidence interval [CI], 0.20-0.20) and it was higher in the ALS group than in the non-ALS group (9.6 [7.8-20.2] vs. 9.3 [7.3-10.2], respectively). For peak pressure, the median difference was -0.30 cmH O (95% CI, -0.30 - -0.20) (20.4 [17.0-24.4] in the ALS group vs. 20.9 [16.7-24.6] in the non-ALS group). The mean pressure difference of 0.0 cmH O (95% CI, 0.0-0.0) (12.7 [10.9-14.6] vs. 13.0 [10.3-15.0], respectively) was also higher in the non-ALS group than in the ALS group. The difference in single ventilation volume per ideal body weight was 0.71 mL/kg (95% CI, 0.70-0.72) (8.17 [6.79-9.54] vs. 7.43 [6.03-8.81], respectively), and the difference in dynamic lung compliance was 8.27 mL/cmH O (95% CI, 12.76-21.95) (43.8 [28.2-68.8] vs. 35.7 [26.5-41.5], respectively); both were higher in the ALS group than in the non-ALS group. There was no association between higher ventilator pressures and the development of ALS. The ALS group had higher dynamic lung compliance and tidal volumes than the non-ALS group, which may indicate a pulmonary contribution to ALS. Ventilator management that limits tidal volume may prevent ALS development.