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Pathological findings of COVID-19 associated with acute respiratory distress syndrome
Zhe Xu*, Lei Shi*, Yijin Wang*, Jiyuan Zhang, Lei Huang, Chao Zhang, Shuhong Liu, Peng Zhao, Hongxia Liu, Li Zhu, Yanhong Tai, Changqing Bai, Tingting Gao, Jinwen Song, Peng Xia, Jinghui Dong, Jingmin Zhao, Fu-Sheng Wang
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Our results imply that overactivation of T cells, manifested by increase of Th17 and high cytotoxicity of CD8 T cells, accounts for, in part, the severe immune injury in this patient. X-ray images showed rapid progression of pneumonia and some differences between the left and right lung.
In addition, the liver tissue showed moderate microvascular steatosis and mild lobular activity, but there was no conclusive evidence to support SARS-CoV-2 infection or drug-induced liver injury as the cause.
There were no obvious histological changes seen in heart tissue, suggesting that SARS-CoV-2 infection might not directly impair the heart.
Although corticosteroid treatment is not routinely recommended to be used for SARS-CoV-2 pneumonia, according to our pathological findings of pulmonary oedema and hyaline membrane formation, timely and appropriate use of corticosteroids together with ventilator support should be considered for the severe patients to prevent ARDS development.
Lymphopenia is a common feature in the patients with COVID-19 and might be a critical factor associated with disease severity and mortality.
Our clinical and pathological findings in this severe case of COVID-19 can not only help to identify a cause of death, but also provide new insights into the pathogenesis of SARS-CoV-2-related pneumonia, which might help physicians to formulate a timely therapeutic strategy for similar severe patients and reduce mortality
