COVID-19 pathology: experience of 2000 autopsies

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  • Authors: Zayratyants O.V.1,2,3, Samsonova M.V.4, Cherniaev A.L.3,4, Mishnev O.D.5, Mikhaleva L.M.3,6, Krupnov N.M.7, Kalinin D.V.8
  • Affiliations:
    1. «A.I. Evdokimov Moscow State University of Medicine and Dentistry» Ministry of Health of Russian Federation
    2. The State Budgetary Healthcare Institution of Moscow Area Moscows regional research clinical institute n.a. M.F. Vladimirskiy
    3. Research Institute of Human Morphology
    4. Federal State Budgetary Institution «Pulmonology Scientific Research Institute under Federal Medical and Biological Agency of Russsian Federation»
    5. ФГАОУ ВО «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова» Минздрава России
    6. City Clinical Hospital No. 31
    7. State Budgetary Institution «D.I. Mastbaum Forensic Medical Bureau»
    8. Federal State Budget Scientific Research Center «A.V. Vishnevsky Institute of Surgery» of the Ministry of Health of Russian Federation
  • Issue: Vol 6, No 4 (2020)
  • Pages: 10-23
  • Section: ORIGINAL STUDY ARTICLES
  • URL: https://journals.rcsi.science/2411-8729/article/view/122396
  • DOI: https://doi.org/10.19048/fm340
  • ID: 122396

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Abstract

Background: Pathological anatomy, patogenesis and the morphogenesis of manifestations and complications of COVID-19 remain insufficiently studied. The fullest information on structural bases of organs and tissues alterations by new coronavirus disease can be obtained as a result of autopsies.

Aims: The aim of the study was to study the morphological changes of lungs and other organs of the autopsies of COVID-19 deceased persons. Results of 2000 autopsies of people who died of a severe form of COVID-19 in Moscow, consisting of 1212 men and 788 women, from March 20 to May 22, 2020 (a ratio 1.54:1) aged from 20 to 99 years (on average 68.5±15.63 years) were presented. This experience was previously generalized in the Atlas COVID-19 pathology. Autopsies were made in the converted interstationary pathoanatomical offices at strict observance of rules of biosafety according to standard and legal documents of WHO, Russian Ministry of Health and Rospotrebnadzor.

Results: Morphological changes of lungs with varying severity and extent were detected in all examined cases; however, damage to other organs was also common, which in some cases prevailed over pulmonary changes and was the cause of death. The main morphological changes in lungs were diffuse alveolar damage and microangiopathy, alveolar hemorrhage syndrome, thrombosis, and thromboembolism.

Conclusion: The involvement of the lungs, other organs, and vascular system in the pathological process is a result of multiple factors. It is advisable to implement clinical and morphological «masks» of COVID-19.

About the authors

Oleg V. Zayratyants

«A.I. Evdokimov Moscow State University of Medicine and Dentistry» Ministry of Health of Russian Federation; The State Budgetary Healthcare Institution of Moscow Area Moscows regional research clinical institute n.a. M.F. Vladimirskiy; Research Institute of Human Morphology

Author for correspondence.
Email: ovzair@mail.ru
ORCID iD: 0000-0003-3606-3823

Dr. Sci. Med., professor

Russian Federation, 20/1 Delegatskaya street, 127473, Moscow; Moscow; Moscow

Maria V. Samsonova

Federal State Budgetary Institution «Pulmonology Scientific Research Institute under Federal Medical and Biological Agency of Russsian Federation»

Email: samary@mail.ru
ORCID iD: 0000-0001-8170-1260
SPIN-code: 9525-9085

Dr. Sci. Med.

Russian Federation, Moscow

Andrey L. Cherniaev

Research Institute of Human Morphology; Federal State Budgetary Institution «Pulmonology Scientific Research Institute under Federal Medical and Biological Agency of Russsian Federation»

Email: cheral12@gmail.com
ORCID iD: 0000-0003-0973-9250

Dr. Sci. Med., Professor

Russian Federation, Moscow; Moscow

Oleko D. Mishnev

ФГАОУ ВО «Российский национальный исследовательский медицинский университет имени Н.И. Пирогова» Минздрава России

Email: mishnevod@gmail.com
ORCID iD: 0000-0002-6466-9147

Dr. Sci. Med., Professor

Russian Federation, Москва

Liudmila M. Mikhaleva

Research Institute of Human Morphology; City Clinical Hospital No. 31

Email: mikhalevalm@yandex.ru
ORCID iD: 0000-0003-2052-914X
SPIN-code: 2086-7513

Dr. Sci. Med., Professor

Russian Federation, Moscow; Moscow

Nikolai M. Krupnov

State Budgetary Institution «D.I. Mastbaum Forensic Medical Bureau»

Email: Krupatan@yandex.ru
ORCID iD: 0000-0002-5162-1662
SPIN-code: 4814-3226

Cand. Sci. (Med.)

Russian Federation, Ryazan

Dmitry V. Kalinin

Federal State Budget Scientific Research Center «A.V. Vishnevsky Institute of Surgery» of the Ministry of Health of Russian Federation

Email: dmitry.v.kalinin@gmail.com
ORCID iD: 0000-0001-6247-9481

Cand. Sci. (Med.)

Russian Federation, Moscow

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Supplementary files

Supplementary Files
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1. JATS XML
2. Fig. 1. Incidence of fatal complications (immediate causes of death, %) in patients died of COVID-19 (n=2000) [18] Note. ARDS (acute respiratory distress syndrome) — 90% Pulmonary embolism — 6%, Brain edema with herniation — 0,5%, Sepsis — 1,5%, Acute myocardial infarction — 1,3%, Ischemic cerebral infarction — 0,3%, Gangrene of the intestine — 0,1%, Others — 0,3%.

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3. Fig. 2. Incidence (n and %) of thrombotic and thromboembolic complications in patients died of COVID-19 (n=2000) Note. Thrombosis of the coronary arteries of the heart, brain arteries and other organs, regardless of the presence and severity of atherosclerosis; pulmonary embolism and pulmonary thrombosis are presented together, due to a possible error of the diff erential morphological diagnosis during autopsy [18]. ДВС — disseminated intravascular coagulation.

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4. Fig. 3. Comorbid diseases (n) in patients died of COVID-19 (n=2000) Note. Diabetes mellitus (DM)was presented by 5 cases of DM type 1 and 433 cases of DM type 2 [18]. ХИБС — chronic form of ischaemic heart disease, ХОБЛ — chronic obstructive pulmonary disease, ДПК — duodenum, СКВ — systemic lupus erythematosus, ВИЧ — infection assosiated with HIV.

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5. Fig. 4. Diff use alveolar damage, exudative phase: a — lung tissue is diff usely compressed, with a bright red surface «lacquer» type, with hemorrhages; б, в — the cut surface of the lung shows a dark cherry or red-brown color, with areas of atelectasis, extensive confl uent hemorrhage and hemorrhagic infarctions; multiple parietal and obturating thrombi in the pulmonary veins and arteries of diff erent caliber (arrows); г — thromboembolus in the pulmonary artery (arrow)

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6. Fig. 5. Diff use alveolar damage, exudative stage: а, б — intra-alveolar edema with accumulation of red blood cells, mononuclear leucocytes and neutrophils, fi brin; Intra-alveolar hemorrhage (alveolar hemorrhage syndrome), hyaline membranes, vascular congestion with red blood cell aggregation (sludge) and thrombi (arrows); в — mononuclear leucocytes with some neutrophils interalveolar septs, perivascular tissue, vascular walls infi ltrate with endotelial alteration; г — cytopathic virus-induced eff ect: desquamated large deformed type II alveolocytes and their symplasts with intracytoplasmic inclusions in the lumina of alveoli; д — hyaline membranes lining the contour of the alveoli and respiratory bronhiols (red); е — fi brin thrombus (arrow) in vascular lumen with signs of endoteliitis Note. H&E (а–г, е); Lendrum-MSB stain (д); a, б, е — ×60, д —×120, в — ×250, г — ×1000.

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7. Fig. 6. Diff use alveolar damage, proliferative stage: lung tissue is diff usely compressed, airless, gray and light red-brown with grey reticular markings and subpleural hemorrhagic infarctions (arrows)

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8. Fig. 7. Diff use alveolar damage, proliferative stage: а — squamous metaplasia of the alveolar epithelium; а, б — granulation tissue, fi brinin and erythrocytes in the alveolar lumina Note. H&E; а —×60, б — ×250.

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9. Fig. 8. Diff use alveolar damage, proliferative stage: the phenomen of cytophagy in syndrome of macrophages activation (secondary hemophagocytic lymphohistiocytosis) Note. H&E; ×400.

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10. Fig. 9. Mucous membrane of the nose (superior nasal meatus). Edema, vascular congestion of the microvasculature, diffuse lymphoid infiltration, dystrophic and proliferative changes in the epithelium with intraepithelial lymphocytic infiltration, and edema of the basement membrane. Note. H&E; ×250.

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11. Fig. 10. Pia mater (а, б) and brain (в, г): а, б — thrombovasculitis of pia mater; в, г — thrombovasculitis of brain tissue Note. H&E; a, б — ×250, в — ×60, г — ×120.

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12. Fig. 11. Myocardium: а — diffuse lymphoid infiltration and stromal edema, destructive and productive vasculitis, dystrophic changes and necrosis of certain cardiomyocytes; б — focal, mainly perivascular, lymphocyte and macrophage infiltration, dystrophic changes and necrosis of certain cardiomyocytes, edema of stroma Note. H&E; ×400.

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13. Fig. 12. Kidney: a — necrosis of convoluted tubular epithelial cells; б — collaptoid glomerulopathy with the effusion in the lumen of glomerular capsules; в — virus alteration of convoluted tubular epithelial cells; г — microangiopathy with thrombi in glomerular capillars Note. H&E; a — ×250, б — ×60, в — ×120, г — ×400.

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14. Fig. 13. Liver: a — severe hepatic steatosis and focal hemorrhages; б — extensive hepatic necrosis

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15. Fig. 14. Small intestine, post-mortem autolysis: severe vascular congestion with red blood cell aggregation and confluent hemorrhages, especially in single preserved villi, almost destroyed, mucosal and submucosal edema of the intestinal wal Note. H&E; ×120.

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16. Fig. 15. Adenohypophysis. Vascular congestion, hemorrhage, and necrosis and degeneration of adenocytes Note. H&E; ×250.

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Copyright (c) 2021 Zayratyants O.V., Samsonova M.V., Cherniaev A.L., Mishnev O.D., Mikhaleva L.M., Krupnov N.M., Kalinin D.V.

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