Covid 19 and Blood Clots: Why?

Less than four months ago, my colleagues in New York City began seeing something unusual and unexpected in their patients that required hospitalization for Covid 19 illness.   It became apparent, that despite ordering standard low dose daily blood thinner medications for most of these patients to prevent blood clots forming in leg veins while they lie in bed, a number of them went on to develop blood clots in both major veins and small arteries of the body.

Furthermore, a new and initially unexplainable observation was observed in patients who sought urgent medical help.  It seemed that these patients could initially function and were not in as severe distress as the measurement of their blood oxygen levels would predict.  But, not uncommonly they would suddenly decompensate without much warning and either require emergent placement on a ventilator or actually have a cardiac arrest and die.  It is now strongly suspected that the lack of oxygen levels and this sudden change in status was/is due to the silent accumulation of blood clots in the small arteries that supply the lung with blood.

In addition, doctors in NYC began to see younger patients with acute strokes that were due to clots forming in the arteries of the brain.  These patients often turned out to be Covid 19 positive and did not fit the description of the typical stroke patient.

Accordingly, there has been a rapid investigation into trying to understand the mechanisms in Covid 19 patients of what appears to be a “hyper-coagulable state” …a predisposition to developing blood clots.

Current thinking is that the SARS Cov-2 virus is doing something that is particular to our blood coagulation system, either directly or indirectly.  We now know that in patients who get particularly ill from this virus, there is an overproduction in the liver of certain blood proteins that are needed for normal blood clotting functions.  In addition, the platelet, a small component of our blood that helps to clot the blood and stop bleeding when we are injured, appears to acquire a revved up function which further promotes clotting when not necessarily indicated or warranted.

What we do not know yet is whether the virus itself is directly responsible for these blood clotting changes or whether these changes are an indirect effect of the virus attacking the inner lining of our blood vessels (which we are pretty sure is happening) and then subsequently triggering a body wide inflammatory response that leads to these changes in our blood.

While a vaccine would potentially prohibit the virus from making a home in our bodies when we are exposed, “therapeutic drugs” are medicines that are designed to blunt either the reproduction of the virus in our body or at least diminish its effects in provoking total body inflammation and blood clotting once the virus gets established in our system.

Until we understand more precisely what the exact mechanisms are for this predisposition to blood clotting, doctors are ordering patients who are hospitalized with Covid 19 to get larger doses of blood thinners and quite often once discharged, these patients are told to continue the blood thinners either orally or by self-injection for another 2 weeks.  For patients with Covid 19 who are not hospitalized, there is no recommendation yet for giving blood thinner medication or even daily aspirin use since we are not sure the low risks of using these medications for 2-4 weeks outweighs the potential benefits.