COVID Autopsy Findings – What Doctors Are Learning From Autopsy Findings of COVID Patients

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COVID Autopsy Findings – What Doctors Are Learning From Autopsy Findings of COVID Patients

COVID Autopsy Findings – What Doctors Are Learning From Autopsy Findings of COVID Patients

Once the COVID is deeply embedded in the body, it begins to cause more severe disease. This is where the direct attack on other organs with ACE2 receptors can occur, including heart muscle, kidneys, blood vessels, liver, and the brain. Early findings, including those from multiple covid autopsies and biopsy reports, show that viral particles can only be found in the nasal passages and throat and 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 covid patients had meningitis.
So the covid is sometimes going to all these different organs by attaching to the ACE2 receptors there, but that’s not even the whole story.

⏩ Timestamps, click to skip ahead – COVID Autopsy Findings
00:00 – Common Symptoms of COVID
01:40 – What we know about COVID
02:25 – Early findings of Multiple Autopsy and Biopsy Reports of COVID
03:02 – Microscope Picture of the COVID and Kidney Cells
03:20 – COVID Autopsy Findings

Doctor Mike Hansen’s Programs ⏩

Because in some COVID 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 COVID gets into the alveolar cells, meaning the tiny little air sacs within the lungs, it makes many 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 covid invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. Early covid autopsy results are also showing widely scattered clots in multiple organs. In one study from the Netherlands, 1/3rd hospitalized with COVID got clots despite 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 – Yes!
2) Indirectly attacking organs by way of collateral damage from the cytokine storm – Yes!
3) Indirectly cause damage to organs through blood clots – Yes!
4) Indirectly cause damage due to low oxygen levels, improper ventilator settings, drug treatments themselves, and/or all of these things combined – Yes!

Endothelial cells are more vulnerable to dying in people with preexisting endothelial dysfunction, 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. For example, blood clots travel to the toes and cause blockages in blood flow, meaning ischemia or infarction can cause gangrene. 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 covid patients with APS have catastrophic APS, where these patients can have strokes, seizures, heart attacks, kidney failure, ARDS, skin changes like the ones I mentioned. In addition, viral infectious diseases, particularly those of the respiratory tract, have been reported as CAPS 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 cholesterol levels, smoking, diabetes, age, chemotherapy, and infection degree. All of these contribute toward developing arterial thrombosis.

Many patients with severe COVID have labs resembling DIC, such as increased PT/INR, increased PTT, and decreased platelet levels. But the reason these COVID patients who developed clots in the study I mentioned earlier, the reason they don’t have DIC is actually 2 reasons, one, they didn’t have extensive bleeding. Two, they did not have low fibrinogen levels. And if it’s truly DIC, you would have both of those things.

Doctor Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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