The purpose of study was to study the pathomorphological changes of COVID-19-associated pneumonia in its severe course on the basis of autopsies with substantiation of pathogenetic links of clinical and morphological manifestations. Materials and methods. The study of changes of COVID-19-associated pneumonia in its severe course was performed on the basis of autopsies of 16 deceased individuals using macroscopic and microscopic methods. All patients had chronic diseases during their lifetime, which contributed to the severe course of COVID-19. Results and discussion. The severe course of COVID-19 is manifested by conventional morphological signs of acute respiratory distress syndrome and vascular wall lesions with the development of hypercoagulable syndrome. Autopsy revealed characteristic macroscopic changes in the lungs that distinguish this disease from other infectious diseases of the respiratory system. Microscopically, changes were observed in the lung tissue, which corresponded to the proliferative phase of diffuse alveolar damage, which is a morphological sign of clinical manifestations of acute respiratory distress syndrome. Deposits of homogeneous eosinophilic masses were found in the lumens of the alveoli, which unevenly covered the walls of the respiratory parts. Hyperplasia and metaplasia of type II alveolocytes was characteristic morphological feature of COVID-19-associated pneumonia. Sporadic altered hyperchromic pneumocytes were detected, often with the formation of symplasts associated with the cytopathic effect of SARS-CoV-2. The development of acute respiratory distress syndrome in COVID-19-associated pneumonia is based on the mechanism involved in the release of SARS-CoV2 from affected type II pneumocytes, leading to their destruction. As a result, specific inflammatory mediators are released, which stimulate macrophages that synthesize biologically active substances, increasing the permeability of capillaries and leading to the accumulation of exudate in the alveoli. Destruction of type II pneumocytes also reduces surfactant production, causing alveolar collapse, impaired gas exchange, and refractory hypoxemia. Pulmonary vascular endotheliitis with widespread thrombosis is also the prominent sign of acute respiratory distress syndrome in severe COVID-19-associated pneumonia. Conclusion. Pathomorphological studies indicate that the direct effect of SARS-CoV-2 on the epithelium of the respiratory tract and alveoli leads not only to its damage, but also trigger a cascade of reactions that cause the development of acute respiratory distress syndrome
Keywords: respiratory distress syndrome, type II pneumocytes, hyperplasia, hypercoagulation
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