Postmortem pathological changes in extrapulmonary organs in SARS-CoV-2 rt-PCR-positive cases: a single-center experience

Abstract

Background: Although the lung is seen as the main target organ affected by SARS-CoV-2, other organs are also damaged.

Aim: We aimed to determine the extrapulmonary findings of autopsies performed on cases with positive results with postmortem polymerase chain reaction test.

Methods: Pathological changes in extrapulmonary organs were examined with light microscopy.

Results: Heart, liver, spleen, kidney, pancreas, and central nervous system samples of these cases were evaluated. About 80% of the cases were men, and 20% were women. In the examination of heart, 28 of the cases had scar, 14 had acute myocardial infarction, 6 had acute and previous myocardial infarction findings, 2 had myocarditis, and 4 had interstitial mononuclear inflammatory cell infiltration. In the examination of the liver, portal inflammation was observed in 84 of the cases, steatosis in 54, centrilobular necrosis in 9, and capillary endotheliitis in the portal area in 7 of them. In the evaluation of the kidney, 37 cases had chronic pyelonephritis, 36 had tubular damage, 15 had tubulointerstitial necrosis, 16 had subcapsular microhemorrhage, 10 had capillary endothelitis, and 9 had a microvascular fibrin trombosis in their glomerular capillaries. In the central nervous system, 8 cases had infarction and liquefaction, 56 had perivascular petechial hemorrhage, 54 had acute hypoxic ischemic change, 3 had parenchymal microhemorrhage, and 52 had capillary endotheliitis.

Conclusion: Autopsies play an important role in systematically examining the damage caused by the virus in all organs in order to elucidate the pathogenesis of SARS-CoV-2 infection and contribute to the clinical management of infected patients.

Keywords: Autopsy; COVID-19; Endotheliitis; Pathology; Postmortem; SARS-CoV-2; Thrombosis.

Fig. 1

A Coronary artery atheroma plaque and fibrin thrombosis, × 40; B Lymphohistiocytic myocarditis, × 400; C Interstitial mononuclear cells, × 400; D Lymphocytic pericarditis, × 400; E Perivascular and interstitial fibrosis, × 100; F Amyloidosis, × 200; G Subendocardial hemorrhage, × 200; H Myocardial infarction with granulation tissue, × 40; I Scarr tissue in the papillary muscle, × 40, H&E

Fig. 2

A Portal inflammation, macrovesicular ve microvesicular steatosis, × 400; B Centrilobular necrosis, × 100; C Lobular inflammation, × 400; D Capillary endoteliitis, × 400; E Cirrhosis, × 40; F Centrilobular congestion, cholestasis; × 100; G Microvascular thrombosis, × 200, H&E

Fig. 3

A Acute tubular damage, × 200; B Glomerular capillary microvascular thrombosis, × 400; C Glomeruler and peritubular capillary congestion, × 400; D Fibrin trombosis in arcuate branch of the renal artery, × 200; E Chronic pyelonephritis, × 200; F Acute tubular damage, capillary endoteliitis, × 200; G Subcapsular microhemorrhage, autolytic changes, × 100, H&E

Fig. 4

A Pituitary necrosis, × 100; B Perivascular petechial hemorrhage, × 400; C Capillary endoteliitis, × 400; D Acute hypoxic ischemic changes in the brain, × 200; E Acute hypoxic ischemic changes in the cerebellum, × 200; F Subacute infarction, × 40; G Intraparenchymal and petechial hemorrhage, × 40; H Microhemorrhages in infarct area, subarachnoid, × 40, I Menengitis, × 100, H&E

Fig. 5

Lymphocytic depletion and PMN leukocyte discharge in red pulp of the spleen, × 200, H&E

Fig. 6

A Necrotic changes in the epithelium of the small intestine, membrane-like fibrinous exudate on the mucosa, × 200; B Perivascular lymphocytic mononuclear inflammatory cells, × 200; C Necrotic changes in the epithelium of the stomach, membrane-like fibrinous exudate on the mucosa, mucosal hemorrhage, × 200, H&E

Fig. 7

Acut prostatitis, × 200, H&E