Pathological Findings of Postmortem Biopsies From Lung, Heart, and Liver of 7 Deceased COVID-19 Patients

Abstract

Background. A novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been affecting almost all nations around the world. Most infected patients who have been admitted to intensive care units show SARS signs. In this study, we aimed to achieve a better understanding of pathological alterations that take place during the novel coronavirus infection in most presumed affected organs. Methods. We performed postmortem core needle biopsies from lung, heart, and liver on 7 deceased patients who had died of coronavirus disease 2019. Prepared tissue sections were observed by 2 expert pathologists. Results. Diffuse alveolar damage was the main pathologic finding in the lung tissue samples. Patients with hospitalization durations of more than 10 days showed evidence of organization. Multinucleated cells in alveolar spaces and alveolar walls, atypical enlarged cells, accumulation of macrophages in alveolar spaces, and congestion of vascular channels were the other histopathologic alteration of the lung. None of our heart biopsy samples met the criteria for myocarditis. Liver biopsies showed congestion, micro- and macro-vesicular changes, and minimal to mild portal inflammation, in the majority of cases. Conclusions. Similar to the previous coronavirus infection in 2003, the main pathologic finding in the lung was diffuse alveolar damage with a pattern of organization in prolonged cases. The SARS-CoV-2 infection does not cause myocarditis, and the ischemia of myocardium is the most probable justification of the observed pathologic changes in the heart. Liver tissue sections mostly showed nonspecific findings; however, ischemia of the liver can be identified in some cases.

Keywords: COVID-19; lung; pathology; postmortem examination; severe acute respiratory syndrome coronavirus 2.

Figure 1.

Pathologic findings of lung tissue of case 1. (A) Hyaline membrane formation; (B) intra-alveolar atypical enlarged cells; (C) multinucleated cells; (D) deposition of fibrinoid material in vessel walls.

Figure 2.

Pathologic findings of lung tissue of case 7. (A) Hyaline membrane formation; (B, C) necrosis and acute inflammatory reaction; (D) squamous metaplasia of bronchiole.

Figure 3.

Pathologic findings of lung tissue of case 3. (A, B) Proliferation of fibroblasts (organizing diffuse alveolar damage); (C) acute pneumonia; (D) enlarged atypical cell.

Figure 4.

Lung tissue samples immunohistochemistry study results. (A) CD3 stained major proportion of lymphocytes; (B) CD20 stained few lymphocytes; (C) CD68, a histiocytic marker, stained major population of intra-alveolar cells; (D) CD68 stained some multinucleated cells; (E) some multinucleated cells did not stain with LCA; (F) large atypical cells (arrow) did not stain with LCA; (G, H) large atypical cells stained with CKAE1/AE3 and TTF1.

Figure 5.

Pathologic findings of heart tissue biopsy of case 5.(A) Interstitial inflammatory infiltrate with ischemic necrosis; (B) immunohistochemical (IHC) staining for LCA; (C) IHC staining for CD68; (D) IHC staining for CD3.

Figure 6.

Pathologic findings of liver tissue samples. (A) Focal confluent necrosis (case 7); (B) moderate microvesicular changes (case 5); (C) mild portal tract mixed inflammation with focal interface hepatitis (case 1); (D) mild steatosis (predominantly macrovesicular) involves about 30% of lobular area admixed with mild microvesicular change (case 2).