Purple rashes, swollen legs, clogged catheters and sudden death — blood clots, large and small, are a frequent complication of COVID-19, and researchers are just beginning to untangle why. For weeks, reports have poured in of the disease’s effects throughout the body, many of which are caused by clots. “This is like a storm of blood clots,” says Behnood Bikdeli, a fourth-year cardiology fellow at Columbia University in New York City. Anyone with a severe illness is at risk of developing clots, but hospitalized patients with COVID-19 appear to be more susceptible.

Studies from the Netherlands and France suggest that clots appear in 20% to 30% of critically ill COVID-19 patients. Scientists have a few plausible hypotheses to explain the phenomenon, and they are just beginning to launch studies aimed at gaining mechanistic insights. But with the death toll rising, they are also scrambling to test clot-curbing medications.

Double whammy

Blood clots, jelly-like clumps of cells and proteins, are the body’s mechanism to stop bleeding. Some researchers view clotting as a key feature of COVID-19. But it’s not just their presence that has scientists puzzled: it’s how they show up. “There are so many things about the presentations that are a little bit unusual,” says James O’Donnell, director of the Irish Centre for Vascular Biology at the Royal College of Surgeons in Dublin.

Blood thinners don’t reliably prevent clotting in people with COVID-19, and young people are dying of strokes caused by the blockages in the brain. And many people in hospital have drastically elevated levels of a protein fragment called D-dimer, which is generated when a clot dissolves. High levels of D-dimer appear to be a powerful predictor of mortality in hospitalized patients infected with coronavirus.

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