Pulmonary stromal expansion and intra-alveolar coagulation are primary causes of COVID-19 death
László Székely, Béla Bozóky, Mátyás Béndek, Masih Ostad, Pablo Lavignasse, Lars Haag, Jieyu Wu, Jing Xu, Soham Gupta, Elisa Saccon, Anders Sönnerborg, Yihai Cao, Mikael Björnstedt, Attila Szakos
Abstract
welve complete autopsies, including two rapid autopsies of young patients where the cause of death was COVID-19 ARDS. The main virus induced pathology was in the lung parenchyma and not in the airways. Most coagulation events occurred in the intra-alveolar and not in the intra-vascular space and the few thrombi were mainly composed of aggregated thrombocytes. The dominant inflammatory response was the massive accumulation of CD163 + macrophages and the disappearance of T killer, NK and B-cells. The virus was replicating in the pneumocytes and macrophages but not in bronchial epithelium, endothelium, pericytes or stromal cells. The lung consolidations were produced by a massive regenerative response, stromal and epithelial proliferation and neovascularization. We suggest that thrombocyte aggregation inhibition, angiogenesis inhibition and general proliferation inhibition may have a roll in the treatment of advanced COVID-19 ARDS.