So are blood clots at least part of the reason why some people with COVID-19 are dying?
I can tell you that the number of clotting problems my colleagues are seeing in the ICU across the country, all related to Covid-19, is unprecedented. But this isn’t just a bunch of doctors and nurses that I know who are reporting this. A recent Dutch study found that of the 184 patients in the ICU with Covid-19 pneumonia, 20% were having clotting issues.
There was also a similar study in Wuhan, China where 25% hospitalized COVID patients had clots. Why, and how is SARS-CoV-2, which invades the cells of the lungs, specifically they type II alveoli, how is it causing blood clots to form in the body? When someone has a severe case of COVID-19, its causing a ton of inflammation within the lungs. This inflammation is what is triggering the blood clots to develop.
We knew that this happens with ARDS even before COVID-19 came around. In ARDS, these patients usually develop microthrombi, meaning tiny clots, that form in the tiny blood vessels in the lungs. And these microthrombi can combine to form bigger thrombi, meaning bigger clots.
This happens at least partly because of the cytokine storm that develops as a result of the infection. Blood clots are also a concern with seriously ill people in general, regardless of what illness they have, because these patients aren’t moving much, if at all, and lack of movement further predisposes one to having clots.
And that’s why when patients are admitted to an intensive care unit, we usually given them blood thinners, unless there is a reason not to, for example if they have bleeding, we don’t want to give those patients blood thinners. But when we give these blood thinners, we give them in prophylactic doses, meaning the intention is to reduce their risk of developing a clot in the first place.
But these prophylactic doses are considered low dose. And the chances of someone having severe bleeding from these small doses is very small. But the blood clots with COVID-19, these are just a whole ‘nother beast.
There’s something more going on here. So how, and why is COVID-19 causing more blood clots than usual?
Long story short, the virus enters the alveolar cells in the lungs using the ACE2 receptor, and once it does that, it causes the cell to have less ACE2 receptor on its surface. This increases the amount of 3 things within the lungs: 1) inflammation 2) formation of clots and 3) constriction of blood vessels going to the lungs, meaning pulmonary vasoconstriction.
And guess what, each and every one of these things by itself can lead to low oxygen levels. So you can imagine what that means when you have all 3 of these things going on at the same time. The way that oxygen gets into our blood from the alveoli, it has to diffuse from the alveoli to our capillaries.
The cytokine storm causes destruction of the alveolus and the endothelium, and this is a trigger for clotting. We knew this happens in ARDS even before COVID. But guess what, the virus that causes covid can actually invade the cells here in the endothelium because these cells have ACE2 receptors as well. And that can cause even more inflammation and more clotting.
And these clots can combine with other clots, to form bigger clots, and can travel to other parts of the body. And in another published report in the NEJM, there were 3 patients in the ICU who had COVID-19 , and these 3 patients developed blood clots that were significant enough to cause major blockages in blood vessels. These 3 patients were positive for antiphospholipid antibodies. These antibodies are not in the blood for the vast majority of people.
These antiphospholipid antibodies are bad because they attack phospholipid proteins in our body, and if severe enough, they can cause major clots to form in our blood vessels. Anti-phospholipid antibody syndrome is a condition that depends on someone’s genetics. But these antibodies can also arise transiently in patients with critical illness and various infections. So do all patients with COVID-19 who have blood clots, do they all have this transient anti-phospholipid antibody syndrome? We don’t know yet.
The cytokine storm that is triggered in the lungs, that can affect other organs in the body, such as heart, kidneys, and brain. And as if that’s not bad enough, just about all of the other organs in the body have ACE2 receptors, such as the heart, kidneys, and brain.
