Research Update Journal of Medicine
Open access (ISSN:)

Volume 1Issue 1
Medicine|Mini-Review|Pathology|COVID-19
| October 19, 2020
| Views: 146

Pulmonary pathology among individuals affected with COVID-19

Richa Jaiswal, Pragya Jaiswal, Priyanka Varma

Cite as: Jaiswal R, Jaiswal P, Varma P. Pulmonary pathology among individuals affected with COVID-19. Research Update Journal of Medicine. 2020;1(1):002.

Highlights

Prior knowledge about this subject

  • SARS-CoV-2 mainly affected the lung by causing severe pneumonitis which leads to acute respiratory distress syndrome which is often associated with multiorgan failure but only a few published data on autopsy are available.
  • Severe cases were identified by the presence of diffuse alveolar damage, severe endothelial injury, disseminated intravascular coagulation, and proinflammatory cytokines.

Findings of this study

  • Autopsies showed a remarkable increase in Interleukin 1 beta and Interleukin 6 mRNA, neutrophilic capillaritis, capillary micro thrombosis, and typical changes of ARDS.
  • Severe cases were identified by the presence of diffuse alveolar damage, severe endothelial injury, disseminated intravascular coagulation, and proinflammatory cytokines.
  • Early autopsy findings like capillary micro thrombosis, superimposed bronchopneumonia, pulmonary thromboembolism, and a sign of multi-organ failure showed ARDS as a predominant cause of death.

Impact of this study in clinical practice

  • Autopsies help us to improve our knowledge about the pathogenesis of COVID-19 by evaluating virus distribution, tissue damage, and cause of death.

Abstract

Worldwide 1.13M confirmed deaths occurred due to pandemic of coronal virus and very few publications on post mortem findings are available, this article presented four severe cases of deadly COVID-19 virus with different range of lung pathology which gives a better understanding of disease course and duration of disease. These autopsy reports showed that the early stage of diseases can be identified by the presence of high; levels of interleukin-1-beta and interleukin-6 with neutrophilic exudative capillaritis with micro thrombosis. Diffuse alveolar damage and the presence of thrombosis in small to medium-sized pulmonary vessels can be characteristics of late-stage and sometimes additional laboratory characteristics of disseminated intravascular coagulation can also be found in late stage. Autopsy results also described that organizing pneumonia with an extensive intra-alveolar proliferation of fibroblast and a distinct amount of metaplasia of alveolar epithelium can be present in late stages. In a lot of patients, multiorgan failure with critical liver damage was found which was a result of thrombotic microangiopathy with or without proinflammatory cytokine storm.

Keywords: COVID-19; pulmonary pathology; micro thrombosis; pro-inflammatory cytokines; acute respiratory distress syndrome

Introduction

Because of a pandemic caused by novel coronavirus SARS-CoV-2 almost 41 million people got affected and 1.12M people died, worldwide by mid-October [1]. This disease mainly affected the lung by causing severe pneumonitis which leads to acute respiratory distress syndrome (ARDS) which is often associated with multiorgan failure [2,3]. There are only a few published data on autopsy are available [4,5]. Severe cases were identified by the presence of diffuse alveolar damage, severe endothelial injury, disseminated intravascular coagulation, and proinflammatory cytokines [4,7]. Early autopsy findings like capillary micro thrombosis, superimposed bronchopneumonia, pulmonary thromboembolism, and a sign of multi-organ failure showed ARDS as a predominant cause of death.

Materials & Methods

Results

Discussion

Autopsy plays an important role to know the pathogenesis of severe SARS-CoV-2 infection. This article presented 4 autopsy cases that demonstrated pulmonary changes with different stages of severity. Patient 1 autopsy showed initial changes in the lung but a remarkable increase in Interleukin 1 beta and Interleukin 6 mRNA, neutrophilic capillaritis, capillary micro thrombosis but very less parenchymal inflammation in comparison to patient 2,3 and 4 where autopsy findings showed typical changes of ARDS. These autopsy findings revealed that pulmonary microvasculature findings can be differentiating factors of COVID-19 which can lead to hypoxemia and acute cardiac insufficiency [8]. SARS-CoV-2 RNA was found in all four patients’ lung tissues but viral RNA did not find in other organs. SARS-CoV-2 enters into host cells through angiotensin-converting enzyme 2 (ACE2) which is a metallopeptidase and having mRNA expression in human tissues, it is mostly found in alveolar epithelial cells, intestinal epithelium, and on arterial and venous endothelial cells [9,10].

In the patient 2 and 3 autopsies finding exhibited a large amount of D-dimer and fibrin degradation products which indicate hypercoagulability which is also a very common finding in COVID-19 [11,12]. Patients with high cardiovascular risk factors are at higher risk of mortality because of coagulopathy which can lead to thrombotic events and these autopsies finding support this phenomenon [4,13]. The autopsy report showed centriacinar necrosis which was due to cytokine-induced liver injury this injury can cause hypoxic damage which can be presented as centriacinar necrosis [14]. Autopsy also revealed massive vascular inflammation in medium-sized vessels which is uncommon in viral pneumonia and can be a distinguishing feature of fatal COVID-19 [15,16].

Conclusion

Autopsies help us to improve our knowledge about the pathogenesis of COVID-19 by evaluating virus distribution, tissue damage, and cause of death. Autopsy results explained that in severe SARS-CoV-2 infection not only the severe pulmonary disease but disseminated coagulation and thrombus formation is which is triggered by multifactorial endothelial damage are also frequently found.

References

  1. COVID-19 CORONAVIRUS PANDEMIC. Worldometer; 2020 [cited 2020 August 20]; Available from: https://www.worldometers.info/coronavirus/#countries
  2. Guan WJ, Ni ZY, Hu Y, et al. Clinical Characteristics of Coronavirus Disease 2019 in China. N Engl J Med. 2020;382(18):1708-1720. doi:10.1056/NEJMoa2002032
  3. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study [published correction appears in Lancet. 2020 Mar 28;395(10229):1038] [published correction appears in Lancet. 2020 Mar 28;395(10229):1038]. Lancet. 2020;395(10229):1054-1062. doi:10.1016/S0140-6736(20)30566-3
  4. Barnes BJ, Adrover JM, Baxter-Stoltzfus A, et al. Targeting potential drivers of COVID-19: Neutrophil extracellular traps. J Exp Med. 2020;217(6):e20200652. doi:10.1084/jem.20200652
  5. Wichmann D, Sperhake JP, Lütgehetmann M, et al. Autopsy Findings and Venous Thromboembolism in Patients With COVID-19: A Prospective Cohort Study. Ann Intern Med. 2020;173(4):268-277. doi:10.7326/M20-2003
  6. Li H, Liu L, Zhang D, et al. SARS-CoV-2 and viral sepsis: observations and hypotheses. Lancet. 2020;395(10235):1517-1520. doi:10.1016/S0140-6736(20)30920-X
  7. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-128. doi:10.1056/NEJMoa2015432
  8. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020;181(2):271-280.e8. doi:10.1016/j.cell.2020.02.052
  9. Hamming I, Timens W, Bulthuis ML, Lely AT, Navis G, van Goor H. Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol. 2004;203(2):631-637. doi:10.1002/path.1570
  10. Connors JM, Levy JH. COVID-19 and its implications for thrombosis and anticoagulation. Blood. 2020;135(23):2033-2040. doi:10.1182/blood.2020006000
  11. Spiezia L, Boscolo A, Poletto F, et al. COVID-19-Related Severe Hypercoagulability in Patients Admitted to Intensive Care Unit for Acute Respiratory Failure. Thromb Haemost. 2020;120(6):998-1000. doi:10.1055/s-0040-1710018
  12. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-1418. doi:10.1016/S0140-6736(20)30937-5
  13. Méndez-Sánchez N, Valencia-Rodríguez A, Qi X, et al. What Has the COVID-19 Pandemic Taught Us so Far? Addressing the Problem from a Hepatologist’s Perspective. J Clin Transl Hepatol. 2020;8(2):0024. doi:10.14218/JCTH.2020.00024
  14. Ruan Q, Yang K, Wang W, Jiang L, Song J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China [published correction appears in Intensive Care Med. 2020 Apr 6;:]. Intensive Care Med. 2020;46(5):846-848. doi:10.1007/s00134-020-05991-x
  15. Ruan Q, Yang K, Wang W, Jiang L, Song J. Correction to: Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020;46(6):1294-1297. doi:10.1007/s00134-020-06028-z
  16. Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. JAMA Cardiol. 2020;5(7):802-810. doi:10.1001/jamacardio.2020.0950

Electronic Supplementary Material

Acknowledgements

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