What Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) PatientsWhat Doctors Are Learning From Autopsy Findings of Coronavirus (COVID-19) Patients
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Once the SARS-CoV-2 virus is deeply embedded in the body, it begins to cause more severe disease. This is where the 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 are being invaded, it's 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 invading more cells. The alveoli’s next-door neighbor is guessed who, yeah, the tiniest blood vessels in our body, capillaries. And the lining of those capillaries is called the endothelium, which also has ACE2 receptors. And once the virus invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. 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 it 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 cause 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, 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.
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.
Anyway, you can probably glean from this video why it's so hard for doctors to figure out what is going on with this virus. Between the variable ways this disease can present in different patients, and the different ways that organs can suffer damage, yeah, this is really, really really, complicated.
Are BLOOD CLOTS the reason why COVID19 patients are dying?
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Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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