Clinical and pathomorphological analysis of deaths from COVID-19 in 2020

Abstract

The aim of the work – to conduct clinical and pathomorphological analysis of deaths from COVID-19 in 2020. Materials and methods. We analyzed 41 case histories and results of pathological-anatomical examination of patients who were died of COVID-19 during 2020. Results. The lethal outcome of COVID-19 disease was recorded at day 22 (16; 27) of the disease. Among the dead, there is a high percentage of men (73.2 %), early old age and middle old age patients (75.6 %) with comorbid pathology (92.7 %). Early lung damage with COVID-19 in the deceased was determined by pronounced interstitial and interstitial-alveolar edema, the presence of erythrocyte stasis in the pulmonary microvessels, blood clots and hypoperfusion leukocyte stasis, as well as the presence of erythrocytes in the alveoli. Bilateral polysegmental subtotal viral pneumonia in 90.2 % of dead patients was characterized by significant edema and thickening of the alveolar walls with their moderate infiltration by lymphocytes, focal peribronchial and perivascular inflammatory polymorphonuclear infiltration, multiple and small exfoliated alveolar epithelium (87.8 %), as well as metaplasia of a few alveolocytes preserved on the luminal surface of the alveoli (82.9 %). Every tenth person who died of COVID-19 had signs of secondary bacterial microflora. In 85.4 % of patients who died on day 22–27 of the disease focal or sublobar pneumofibrosis was diagnosed. In those who died due to COVID-19, multiorgan failure was characterized by focal necrosis of the renal tubular epithelium (73.2 %), focal lymphocytic-leukocyte infiltration (12.2 %) and renal microvascular thrombosis (17.1 %), focal centro-lobular necrosis (90.2 %) and focal lymphocytic-leukocyte infiltration of lobes (7.3 %) of the liver. Thrombotic complications were confirmed in 22.0 % of deceased patients: ischemic cerebral infarction, transmural myocardial infarction, pulmonary embolism, deep vein thrombosis of the lower extremities under the pathology. These thrombotic complications were not diagnosed during life in all patients. The majority of deaths due to COVID-19 had morphological signs of chronic cardiovascular pathology. Ischemic heart disease and hypertension during the life of patients were not diagnosed in all cases. Conclusions. Early lung damage in COVID-19 in the deceased was determined by pronounced interstitial-alveolar edema, blood clots and leukocyte stasis in microvessels, less often – the presence of “hyaline membranes”. In 90.2 % of the dead patients bilateral polysegmental subtotal pneumonia with edema and lymphocytic infiltration of the pulmonary interstitium, inflammatory peribronchial and perivascular focal polymorphonuclear infiltrates, foci of atelectasis and dyscryphaseses was found. In 9.7 % of patients bilateral subtotal viral-bacterial fibrinous-purulent bronchopneumonia developed. In those who died on the 22nd–27th day of the disease focal pneumofibrosis was determined. Pathomorphologically, thrombotic complications, which were not diagnosed in all patients during their lifetime, were confirmed in 22.0 % of deceased patients. Most deaths from COVID-19 had morphological signs of chronic cardiovascular disease.