Doctors often want to keep pneumonia patients "dry", that is, somewhat dehydrated. (That's maybe contributing to the kidney failure.) To what extent could this also be resulting in increased clotting?
I'm in large part guessing here based on clinical observation, but my feeling is that you can extend this logic to other syndromes that accompany COVID-19. For example, we often see worsening liver function in the setting of this illness (albeit delayed by a few days). This could be explained in a number of ways, one of which is by impaired perfusion within capillary beds in the liver. Further, there is a myocarditis-like picture we sometimes see as well that could be explained by direct viral infection or again by impaired perfusion of the cardiac muscle by small vessel clotting.
When the thrombotic disease progresses, you start to see a more macro version: think strokes and pulmonary emboli in patients who are otherwise low risk at baseline. Thus, there's some interpolation going on here.
Hope that makes some sense.
A dear friend is dying of pancreatic cancer. And one of the key reasons that she's still alive was getting thrombosis under control. Initially with IV heparin, and now with Lovenox.
Are those commonly used for COVID patients? Or do they use oral anticoagulants?
Based on our institutional protocol, hospitalized COVID-19 patients receive therapeutic dose Lovenox, Eliquis, or IV heparin.[1] Lovenox is the first line treatment, but is contraindicated in patients with, among others things, severely impaired renal function. If these patients are able to tolerate oral medications, they can be given Eliquis. If not, they’re typically put on IV heparin drips (and are subject to the uncomfortable and burdensome blood draws that come with them).
Typically, all of these patients are discharged on two weeks of Eliquis if there are no major contraindications. The thinking is that the risk of damage to the body by microthrombi doesn’t necessarily end just because the patient is stable enough to go home.
Of course, with all of these medications, preventing clotting has to be balanced with preventing bleeding. We’ve had to stay vigilant for things like GI bleeds and hemorrhagic strokes, as these things become more common when everyone in the hospital is being heavily anticoagulated.
[1] Therapeutic dosing in this case is higher than typical prophylactic dosing. In the case of Lovenox, it would be something like 40 mg twice a day for the therapeutic dose versus 40 mg once a day for the prophylactic dose, which is what would be used in non-COVID-19 patients to prevent thromboembolism.
It's wild to see how much the thinking has changed on how this disease works.
ACE2 is expressed extensively in renal tissue, so the virus is transported there in the blood, infects cells, hijacks the cellular apparatus to replicate, and then explodes to cell to continue its march of death. So I think your speculation is a bit misplaced