Autopsies: In Addition to the Lungs, COVID-19 Damages Other Organs

COVID-19 not only triggers severe pneumonia but can also cause thromboses in the lungs.

Professor Sigurd Lax
Professor Sigurd Lax

The COVID-19 disease triggered by the coronavirus SARS-CoV-2 not only triggers severe pneumonia but can also cause thromboses of the lungs and subsequently damage other vital organs such as the kidneys, liver, and pancreas. The findings are from an initial, larger series of autopsies in Austria carried out as part of a study at the Pathology Department at the Graz II Regional Hospital, location West, in cooperation with the Medical University of Graz, the Johannes Kepler University of Linz, and the Medical University of Vienna. The study was recently published in the renowned journal Annals of Internal Medicine with a featured editorial.

According to Sigurd Lax (professor of pathology at the Johannes Kepler University Linz and Director of the Institute of Pathology at the Graz II State Hospital, an academic teaching hospital at the Medical University of Graz), COVID-19 damages more than just the lungs. Prof. Lax conducted autopsies on persons deceased from COVID-19, evaluating the results of the first 11 cases together with his Graz team including colleagues from the departments of Internal Medicine and Anaesthesiology at the LKH Graz II, the Diagnostic and Research Institute for Hygiene, Microbiology and Environmental Medicine at MedUni Graz, the Institute for Hospital Hygiene and Microbiology at KAGes, and Michael Trauner from the Department of Internal Medicine III at the MedUni Vienna and believes that "Our examinations shows that although damage to the lungs is the disease’s starting point, the consequences are often thromboses in the pulmonary circulation itself and other organs are also damaged."

Blood Vessels in the Lungs
Thromboses (when blood clots block blood vessels) can – as seen in heart attack and stroke patients - directly block vessels, leading to tissue death (infarction).

Although COVID-19 causes inflammation directly in the pulmonary alveoli, the co-reaction in the small arteries often appears to trigger blood clotting which can result in slower pulmonary blood flow, especially in patients who already suffer from cardiovascular diseases. This can subsequently cause additional thromboses in the lungs, leading to rapid lung and circulation failure as an immediate cause of death in connection to COVID-19.

COVID-19 affects a number of other organs such as the kidneys, liver, pancreas, adrenal gland, and lymphatic system. Michael Trauner added: "We can see that COVID-19 is a severe infectious disease that affects the entire organism." Doctors still are unsure if survivors of severe bouts with the disease will suffer long-term damage to the affected organs.

Other reports of COVID-19 patients who suffered leg vein thrombosis with pulmonary embolism and strokes confirm that the increased tendency to thrombosis with COVID-19 has far-reaching effects.

Benefit of Blood-Thinning Drugs still Unclear
The role blood-thinning medication plays to prevent and treat these thromboses is not yet clear as clinically treated patients can be given blood thinners preventatively anyway. However intensive care physicians at LKH Graz II emphasize these could not prevent the COVID-19-typical thromboses in the series. The study’s findings support the demand of coagulation specialists for a generous and timely indication of thrombosis prophylaxis - even for non-hospitalized patients. Further studies are needed to explore when - and to what extent - therapeutic blood thinning is appropriate, depending on laboratory findings and imaging. In order to develop new, effective treatments, follow-up studies will be necessary to explain the systemic and local mechanisms in pulmonary circulation that lead to an increased risk of thrombosis.

Service: Annals of Internal Medicine
Pulmonary Arterial Thrombosis in COVID-19 with Fatal Outcome: Results From a Prospective, Single-Center, Clinicopathologic Case Series

Sigurd F. Lax, Kristijan Skok, Peter Zechner, Harald H. Kessler, Norbert Kaufmann, Camillo Koelblinger, Klaus Vander, Ute Bargfrieder, Michael Trauner., opens an external URL in a new window

Editorial:, opens an external URL in a new window