Lessons learnt from COVID‐19 coagulopathy

Figures

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  FIGURE 1. Differentiating localised versus systemic coagulation activation in COVID‐19. In localised coagulation activation (left of the figure), viral invasion activates the host immune and coagulation systems. There is also interplay between the host systems termed immunothrombosis. Two situations with the viral infection can cause systemic coagulation activation – first, if there is a high viral load, it causes heightened immune response and thus extensive coagulation activation which spreads into the circulation to cause thrombi in the different circulatory beds. Similar dissemination of the coagulation can happen with moderate viral load but if the host immune response is aggressive

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  FIGURE 2. Platelet activation in COVID19. The severe acute respiratory syndrome coronavirus 2 has been shown to activate platelets in different studies. Platelet activation may be beneficial to an extent to limit the viral invasion but in other circumstances may be harmful by causing thrombi through platelet aggregation. What is crucial in these situations is to understand the key mechanisms involved so that appropriate platelet‐focused therapies can be instituted. Timing of such treatments is paramount to reap maximum benefits

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  FIGURE 3. Disseminated intravascular coagulation in 2021. In the presence of an underlying condition which can cause DIC, a combination of worsening laboratory parameters can be considered to be DIC but currently is considered as coagulopathy. This stage (middle section in the figure) is the best time for intervention and may be considered as non‐overt DIC. However, DIC is often entertained when the lab results are extremely deranged when the interventions may be futile