Postmortem examination of COVID-19 patients reveals diffuse alveolar damage with severe capillary congestion and variegated findings in lungs and other organs suggesting vascular dysfunction

Thomas Menter, Jasmin D Haslbauer, Ronny Nienhold, Spasenija Savic, Helmut Hopfer, Nikolaus Deigendesch, Stephan Frank, Daniel Turek, Niels Willi, Hans Pargger, Stefano Bassetti, Joerg D Leuppi, Gieri Cathomas, Markus Tolnay, Kirsten D Mertz, Alexandar Tzankov, Thomas Menter, Jasmin D Haslbauer, Ronny Nienhold, Spasenija Savic, Helmut Hopfer, Nikolaus Deigendesch, Stephan Frank, Daniel Turek, Niels Willi, Hans Pargger, Stefano Bassetti, Joerg D Leuppi, Gieri Cathomas, Markus Tolnay, Kirsten D Mertz, Alexandar Tzankov

Abstract

Aims: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has rapidly evolved into a sweeping pandemic. Its major manifestation is in the respiratory tract, and the general extent of organ involvement and the microscopic changes in the lungs remain insufficiently characterised. Autopsies are essential to elucidate COVID-19-associated organ alterations.

Methods and results: This article reports the autopsy findings of 21 COVID-19 patients hospitalised at the University Hospital Basel and at the Cantonal Hospital Baselland, Switzerland. An in-corpore technique was performed to ensure optimal staff safety. The primary cause of death was respiratory failure with exudative diffuse alveolar damage and massive capillary congestion, often accompanied by microthrombi despite anticoagulation. Ten cases showed superimposed bronchopneumonia. Further findings included pulmonary embolism (n = 4), alveolar haemorrhage (n = 3), and vasculitis (n = 1). Pathologies in other organ systems were predominantly attributable to shock; three patients showed signs of generalised and five of pulmonary thrombotic microangiopathy. Six patients were diagnosed with senile cardiac amyloidosis upon autopsy. Most patients suffered from one or more comorbidities (hypertension, obesity, cardiovascular diseases, and diabetes mellitus). Additionally, there was an overall predominance of males and individuals with blood group A (81% and 65%, respectively). All relevant histological slides are linked as open-source scans in supplementary files.

Conclusions: This study provides an overview of postmortem findings in COVID-19 cases, implying that hypertensive, elderly, obese, male individuals with severe cardiovascular comorbidities as well as those with blood group A may have a lower threshold of tolerance for COVID-19. This provides a pathophysiological explanation for higher mortality rates among these patients.

Keywords: COVID-19; SARS-CoV-2; autopsy; cardiovascular; kidney; lung; senile amyloidosis.

Conflict of interest statement

All authors declare that they have no conflicting interests.

© 2020 The Authors. Histopathology published by John Wiley & Sons Ltd.

Figures

Figure 1
Figure 1
Gross lung findings. A, Typical appearance of coronavirus disease 2019 (COVID‐19) lungs; note the perceptibly thickened alveolar septae and congestive interstitial aspects and a thrombembolus in the lower lobe. Insert: detailed view highlighting interstitial congestion. B, Extensive bronchopneumonic infiltrates in a COVID‐19 patient suffering from superimposed suppurative pneumonia.
Figure 2
Figure 2
Microscopic lung findings. A, Exudative diffuse alveolar damage (DAD) showing discrete hyaline membranes and prominent capillary congestion [haematoxylin and eosin (H&E)]. Insert: immunohistochemistry (IHC) for fibrin(ogen) showing the extent of hyaline membranes. B, Syncytial cells of pneumocyte II origin (H&E). Insert: IHC for thyroid transcription factor 1. C, Extensive capillary congestion without DAD (H&E). D, Microthrombi in alveolar capillaries (IHC for fibrin).
Figure 3
Figure 3
Findings in other organs. A, Kidney showing acute tubular damage without evidence of increased inflammatory infiltrates [periodic acid–Schiff (PAS) stain]. B, Kidney showing disseminated intravascular coagulation (PAS). C, Florid splenitis showing increases in neutrophil numbers in the perifollicular and marginal zones of the spleen (PAS). D, Lymph node showing an increase in the number of plasmablasts in the interfollicular zone as well as congestion (haematoxylin and eosin). Insert: immunohistochemistry for multiple myeloma 1.
Figure 4
Figure 4
Electron microscopy findings. A,B, Podocyte cytoplasm with its foot processes on top of a glomerular basement membrane containing mitochondria (upper left corner) and multiple vesicles, two of which contain several small possible virus‐like particles with sizes between 70 nm and 110 nm (arrow). At higher magnification, the vesicles contain double membranes and the virus‐like particles show a ring of electron‐dense granules and a ragged outer contour (electron microscopy). C, An activated glomerular endothelial cell, and a vesicle close to the luminal border with virus‐like particles (arrow and insert), adjacent to an erythrocyte (electron‐dense structure at the top left) (electron microscopy). D, Cytoplasm of a proximal tubular epithelial cell on top of a basement membrane and adjacent collagen fibres (left side). The cytoplasm contains mitochondria, rough endoplasmic reticulum, and multiple vesicles, one of which contains virus‐like particles (arrow and insert, electron microscopy).

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