Hemostasis Complications in the Pathogeny of COVID-19
Safety Assessment
Florence Poitout

Hemostasis Complications in the Pathogeny of COVID-19

The latest worrisome phenomenon in SARS-CoV-2 infection--changes in the blood clotting properties of patients

When the COVID-19 pandemic began less than six months ago, many doctors and researchers considered SARS-CoV-2, the novel virus causing COVID-19 disease and of the same family as the severe acute respiratory syndrome (SARS) pandemic virus, a highly offensive respiratory virus. However, in recent months we are learning that virus also affect other organs, including the kidneys, heart, intestines and brain. 

Now, physicians are seeing another worrisome phenomenon—changes in the blood of patients with COVID-19, more specifically in the blood’s clotting properties (coagulation). Development of a clotting disorder is now one of the key features associated with poor outcomes of COVID-19. Autopsies have shown that people’s lungs fill with hundreds of microclots, a condition referred to as microvascular lung vessels obstructive thrombo-inflammatory syndrome (MicroCLOTS).(ref.1)

Several publications and societies have been highlighting the importance of screening for coagulation anomalies for the detection of COVID-19 -related complications.

What does this all mean? We know that the SARS-CoV-2 virus enters target cells through the angiotensin-converting enzyme 2 (ACE2) receptor. This receptor is expressed on the surface of lung epithelial cells and enterocytes of the small intestine. ACE2 receptors are also found on arterial and venous endothelial cells and arterial smooth muscle cells of multiple organs. Viral replication causes cellular damage, release of cytokines, activation of macrophages and induction of complement cascade.

It is hypothesized that this series of events leads to severe collateral tissue injury, massive vascular endothelial and alveolar epithelial damage, as well as blood clots that obstruct veins (microvascular thrombosis) in the lung and other organs. These lesions correlate clinically with progressive changes in blood oxygen levels and circulation. Microvascular thrombosis can also extend to the microvascular bed of kidneys, brain and other vital organs.  

In COVID-19 patients requiring hospitalization, the most common laboratory findings supporting the diagnosis of an anomaly of blood coagulation are increases in circulating concentrations of D-dimers (elevated fibrin fragments), prolonged prothrombin time, decreases in platelet counts and decreased fibrinogen concentration. (ref.2)

Interestingly, this type of hemostatic complication is not unfamiliar in animal models. For example, disseminated coagulopathy has been encountered in association with acute inflammatory syndromes in preclinical studies.

Future steps toward understanding COVID-19’s pathophysiological mechanisms and identifying treatments may benefit from our knowledge of inflammatory animal models and expertise in coagulation disorders.

Stay tuned!

  1. Ciceri, F et al. “Microvascular COVID-19 lung vessels obstructive thromboinflammatory syndrome (MicroCLOTS): an atypical acute respiratory distress syndrome working hypothesis.” Critical Care and Resuscitation: Journal of the Australasian Academy of Critical Care Medicine, April 15, 2020.
  2. Thachil, J. “The Versatile Heparin in COVID-19.” Journal of Thrombosis & Haemostosis, April 2020.

Anne Provencher, DVM, Dipl.ACVP, Executive Director of Clinical Pathology at Charles River's site in Sherbrooke, Canada contributed to this post.