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Updated: Nov 8, 2025

In Vitro Microfluidic Disease Model to Study Whole Blood-Endothelial Interactions and Blood Clot Dynamics in Real-Time
Published on: May 24, 2020
COVID-19 and thrombotic microangiopathies
Nishant R Tiwari1, Sanat Phatak2, Vivek R Sharma3
1Department of Internal Medicine, Byramjee Jeejeebhoy Government Medical College, Pune, India.
Insights
Severe COVID-19 may involve thrombotic microangiopathy (TMA), a condition characterized by microvascular blood clots. Identifying and treating TMA could improve outcomes for critically ill COVID-19 patients with organ dysfunction.
Area of Science:
- Critical Care Medicine
- Hematology
- Immunology
Background:
- Severe COVID-19 frequently causes multiorgan dysfunction, particularly affecting the lungs.
- An exaggerated immune response, including complement activation and cytokine storm, contributes to organ injury.
- COVID-19 patients exhibit hypercoagulability, high thrombosis rates, and anticoagulation failure.
Purpose of the Study:
- To investigate the potential role of thrombotic microangiopathy (TMA) in severe COVID-19.
- To explore TMA-like presentations within the published literature on COVID-19.
- To discuss the presentation, pathophysiology, and potential treatment strategies for TMA in COVID-19.
Main Methods:
- Systematic review of published literature on COVID-19.
- Identification of case reports and series describing TMA-like presentations in COVID-19 patients.
- Analysis of clinical data regarding presentation and pathophysiology.
Main Results:
- Extensive microvascular thromboses are frequently observed in severe COVID-19.
- Thrombotic microangiopathy (TMA) is a potential contributing factor to multi-organ complications.
- Findings suggest TMA may be implicated in the hypercoagulable state of COVID-19.
Conclusions:
- Thrombotic microangiopathy (TMA) may play a significant role in severe COVID-19 pathogenesis.
- Early identification and treatment of TMA could improve patient outcomes.
- Further research is warranted to elucidate the TMA-COVID-19 relationship and optimize management.
Abstract:
Severe COVID-19 can manifest as multiorgan dysfunction with pulmonary involvement being the most common and prominent. As more reports emerge in the literature, it appears that an exaggerated immune response in the form of unfettered complement activation and a cytokine storm may be a key driver of the widespread organ injury seen in this disease. In addition, these patients are also known to be hypercoagulable with a high rate of thrombosis and a higher-than-expected failure rate of anticoagulation. While macrovascular thrombosis is common in these individuals, the frequent finding of extensive microvascular thromboses in several series and case reports, raises the possibility of thrombotic microangiopathy (TMA) as being a contributing factor in the thrombotic and multi-organ complications of the disease. If this is correct, rapidly identifying a TMA and treating the underlying pathophysiology may allow for better outcomes in these critically ill patients. To further explore this, we reviewed the published literature on COVID-19, looking for reports describing TMA-like presentations. We summarize our findings here along with a discussion about presentation, pathophysiology, and a suggested treatment algorithm.
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