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32 m a s s a g e & b o d y w o r k j u l y / a u g u s t 2 0 2 0 education PATHOLOGY PERSPECTIVES COVID-19-Related Coagulopathy Blood Clotting—Through Thick and Thin By Ruth Werner Picture this: A person infected with SARS-CoV-2 is making blood clots. Gazillions of them. All over their body. Some are tiny, blocking the capillary supply to the skin and organs. Others are big enough to cause heart attacks, strokes, and pulmonary embolism. At the same time, the person has signs of bleeding in other parts of their body. Bruises form with little or no trigger. Their gums bleed with regular toothbrushing. Petechiae may develop in the skin: small, reddish, or purplish spots that are the result of microvascular bleeding under the skin. Somehow, their blood is simultaneously too thick and too thin. What in the world is going on here? And what should massage therapists know about this situation? To set up a conversation about blood-clotting problems related to COVID-19, we will do a cursory review of our wonderful capacity for hemostasis: maintaining our blood clotting functions within boundaries for health and safety. HEMOSTASIS: BALANCED BLOOD CLOTS Under normal circumstances, our blood fl ows through our thousands of miles of blood vessels, delivering oxygen and nutrients, removing carbon dioxide and wastes. The O2–CO2 exchanges happen at the alveoli in the lungs and at the capillary level in the tissues. It is meant to be a closed system, meaning that red blood cells are kept within the circulatory vessels. If they manage to escape, then something is wrong. Among our blood components, we have cell fragments called platelets or thrombocytes. These tiny, smooth corpuscles move through our circulatory system, scanning for possible breaches and rough spots. If something in the system is disrupted, then the platelets activate: they become spiky, they secrete a lot of chemicals that act on other platelets and clotting factors in the blood, a fi brin net is woven, and a plug—that is, a clot—is formed. The factors that prompt this process are identifi ed as the Virchow triad, named for a 19th-century German pathologist who made some early observations about blood clotting (Image 1). Blood clotting is not a bad thing; this mechanism serves an important life- preserving function, and we would be in a lot of trouble if it didn't work. But it must be balanced by clot-melting mechanisms, or we get into a different kind of trouble. Most of our clot-melting chemicals are produced by the liver; when they do their work, the fi brin nets are dismantled, clots are degraded, and blood fl ow is restored. The Virchow triad comprises any combination of impaired blood fl ow, endothelial injury, and hypercoagulability—a situation where pro-clotting chemicals are abundant. When any combination of these factors is present, blood clots will follow. 1 HYPERCOAGUL ABILIT Y THROMBOSIS ENDOTHELIAL INJURY STASIS OF BLOOD FLOW

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