What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients Once the SARS-CoV-2 virus is deeply embedded in the body, it begins to cause more severe disease. This is where direct attack on other organs that have ACE2 receptors can occur, including heart muscle, kidneys, blood vessels, liver, and the brain. Early findings, including those from multiple autopsy and biopsy reports, show that viral particles can be found not only in the nasal passages and throat, but also in tears, stool, kidneys, liver, pancreas, and heart.
One case report found evidence of viral particles in the CSF, meaning the fluid around the brain. That patient had meningitis. So the virus is sometimes going to all these different organs by means of attaching to the ACE2 receptors that are there, but that’s not even the whole story. Because in some cases, by the time the body’s immune system figures out the body is being invaded, its like unleashing the military to stomp out the virus, and in that process, there’s a ton of collateral damage. This, is what we refer to as the cytokine storm.
When the virus gets into the alveolar cells, meaning the tiny little air sacs within the lungs, it makes a ton of copies of itself, and goes onto invade more cells. The alveoli’s next door neighbor is guess who, yeah, the tiniest blood vessels in our body, capillaries. And the lining of those capillaries is called endothelium, which also have ACE2 receptors. And once the virus invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. And Early autopsy results are also showing widely scattered clots in multiple organs.
In one study from the Netherlands, 1/3rd of hospitalized with COVID-19 got clots despite already being on prophylactic doses of blood thinners. So not only are you getting the inflammation with the cytokine storm, but you’re also forming blood clots, that can travel to other parts of the body, and cause major blockages, effectively damaging those organs.
So wait a minute doc, you’re telling me that this can cause organ damage by 1) Directly attacking organs by their ACE2 receptor? Yup 2) Indirectly attacking organs by way of collateral damage from the cytokine storm? Yup 3) Indirectly cause damage to organs by means of blood clots? yup 4) Indirectly casue damage as a result of low oxygen levels, improper ventilator settings, drug treatments themselves, and/or all of these things combined? Yeah Endothelial cells are more vulnerable to dying in people with preexisting endothelial dysfunction, which is more often associated with being a male, being a smoker, having high blood pressure, diabetes, and obesity.
Blood clots can form and/or travel to other parts of the body. When blood clots travel to the toes, and cause blockages in blood flow there, meaning ischemia or infarction, that can cause gangrene there. And lots of times patients with gangrene require amputation, and “COVID toes” So is antiphospholipid antibody syndrome (APS), the cause of all these blood clots in patients with severe COVID? Maybe. Some patients with APS have what’s called catastrophic APS, where these patients can have strokes, seizures, heart attacks, kidney failure, ARDS, skin changes like the ones I mentioned.
Viral infectious diseases, particularly those of the respiratory tract, have been reported as being the triggers for CAPS. The pathogenesis is complex and may involve the activation of Toll-like receptor 4 (TLR-4), which triggers a cytokine storm, followed by alterations to the endothelium of lung capillaries, which serves as the trigger for inducing the clotting storm. Various factors increase the risk of developing arterial thrombosis. Classically, the cardiovascular-dependent risk factors implicated in clotting have been hypertension, meaning high blood pressure, high levels of cholesterol, smoking, diabetes, age, chemotherapy, and degree of infection.
All of these contribute toward developing arterial thrombosis. A lot of patients with severe COVID-19 have certain labs that resemble DIC, such as increased PT/INR, increased PTT, decreased levels of platelets. But the reason why these COVID patients who developed clots in the study I mentioned earlier, the reason why they don’t have DIC, is actually 2 reasons, one, they weren’t having extensive bleeding, and two, they did not have low fibrinogen levels. And if its truly DIC, you would have both of those things.
