Reduced survival in patients requiring chest tubes with COVID-19 acute respiratory distress syndrome.

Background: Numerous complications requiring tube thoracostomy have been reported among critically ill patients with COVID-19; however, there has been a lack of evidence regarding outcomes following chest tube placement. Methods: We developed a retrospective observational cohort of all patients admitted to an intensive care unit (ICU) with confirmed COVID-19 to describe the incidence of tube thoracostomy and factors associated with mortality following chest tube placement. Results: In total, 1705 patients with laboratory confirmed COVID-19 patients were admitted to our ICUs from March 7, 2020, to March 1, 2021, with 69 out of 1705 patients (4.0%) receiving 130 chest tubes. Of these, 89 out of 130 (68%) chest tubes were indicated for pneumothorax. Patients receiving tube thoracostomy were much less likely to be alive 90 days post-ICU admission (52% vs 69%; P < .01), and had longer ICU (30 vs 5 days; P < .01) and hospital (37 vs 10 days; P < .01) lengths of stay compared with those without tube thoracostomy. Patients who received tube thoracostomy and survived at least 90 days post-ICU admission had shorter times to first chest tube insertion (8.5 vs 17.0 days; P = .01) and a nonsignificantly higher static compliance (20.0 vs 17.5 mL/cm H2O; P = .052) at the time of chest tube placement than those who had expired. Logistic regression analysis demonstrated an association between time to first chest tube and decreased survival when adjusted for covariates. Conclusions: Requiring a chest tube in COVID-19 is a negative prognostic end point. Delayed development of chest tube requirement was associated with a decreased survival and could reflect a poor healing phenotype.

Pdgfrα functions in endothelial-derived cells to regulate neural crest cells and the development of the great arteries.

Originating as a single vessel emerging from the embryonic heart, the truncus arteriosus must septate and remodel into the aorta and pulmonary artery to support postnatal life. Defective remodeling or septation leads to abnormalities collectively known as conotruncal defects, which are associated with significant mortality and morbidity. Multiple populations of cells must interact to coordinate outflow tract remodeling, and the cardiac neural crest has emerged as particularly important during this process. Abnormalities in the cardiac neural crest have been implicated in the pathogenesis of multiple conotruncal defects, including persistent truncus arteriosus, double outlet right ventricle and tetralogy of Fallot. However, the role of the neural crest in the pathogenesis of another conotruncal abnormality, transposition of the great arteries, is less well understood. In this report, we demonstrate an unexpected role of Pdgfra in endothelial cells and their derivatives during outflow tract development. Loss of Pdgfra in endothelium and endothelial-derived cells results in double outlet right ventricle and transposition of the great arteries. Our data suggest that loss of Pdgfra in endothelial-derived mesenchyme in the outflow tract endocardial cushions leads to a secondary defect in neural crest migration during development.