Microclot Update

Hot off the press!!! "TEG®, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy" by Dr. Pretorius at Stellenbosch University was published this week in the Journal of Clinical Medicine.

Abstract (edited by rosecottagedoc)

An important component of severe COVID-19 disease is virus-induced endothelilitis. This is inflammation of the cells of the smallest blood vessels.

This leads to:

  • Disruption of normal endothelial function, initiating a state of failing normal clotting physiology.

  • Massively increased levels of von Willebrand Factor, a clotting factor in the blood which initiates more clotting.

  • Overwhelming platelet activation, as well as activation of the enzymatic (intrinsic) clotting pathway.

  • There is an impaired fibrinolysis (the breaking down of clots), caused by increased levels of alpha-(2) antiplasmin.

The end result is hypercoagulation (proven by (TEG®)* and reduced fibrinolysis, inevitably leading to a difficult-to-overcome hypercoagulated physiological state.

TEG® results. * Note - TEG® stands for ThromboElastoGraphy® is a real time analyser of whole blood. It can express function and pinpoint dysfunction in the haemostatic process. It can quickly provide patient results to allow for faster treatments and decision-making*

A hypercoagulable state means the overriding tendency of the blood to clot with not enough balancing clot breakdown. In Covid-19 this leads to the formation of Microclots.

Stages 1-4 of mild to severe Microclots formation

Platelets in circulation also plays a significant role in clot formation, but they themselves may also drive hypercoagulation when they are overactivated due to the interactions of their receptors with the endothelium, immune cells or circulating inflammatory molecules.

4 stages of platelet clumping

From the literature it is clear that the role of platelets in severely ill COVID-19 patients has been markedly underestimated or even ignored. We here highlight the value of early management of severe COVID-19 coagulopathy as guided by TEG®, microclot and platelet mapping.

We also argue that the failure of clinical trials, where the efficacy of prophylactic versus therapeutic clexane (low molecular weight heparin (LMWH)) were not always successful, which may be because the significant role of platelet activation was not taken into account during the planning of the trial. We conclude that, because of the overwhelming alteration of clotting, the outcome of any trial evaluating an any single anticoagulant, including thrombolytic, would be negative.

"Here we suggest the use of the degree of platelet dysfunction and presence of microclots in circulation, together with TEG®, might be used as a guideline for disease severity".

A multi-pronged approach, guided by TEG® and platelet mapping, would be required to maintain normal clotting physiology in severe COVID-19 disease.

Dr Pretorius and her team, in this paper, are only writing about intervention at a very early stage in patients with severe Covid-19 identified through TEG® to have a hyper coagulable state.

We know from Dr Asad Khan, a British doctor with Long Covid, that people with Long Covid are undergoing the same treatment "apheresis" at various centres around the world to remove the Microclots and to stop the hyper coagulable state to improve fatigue, cognitive dysfunction, breathlessness and dysautonomia. Currently members of Doctors with Long Covid are trying to source TEG® in the UK.


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