12 COVID Autopsy Cases Reveal the TRUTH "HOW COVID PATIENTS DYING"
In all 12 COVID Autopsy cases, the cause of death was found within the lungs or the pulmonary vascular system. Those who did not die of large pulmonary emboli died of extensive inflammation, meaning pneumonia with ARDS. In these COVID Autopsy cases, the lungs were wet and heavy, like a saturated water sponge. The lung surfaces often had a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish-blue Hypercapillarized areas.
This indicates areas of intense inflammation, with endothelial dysfunction that can be seen at the microscopic level. When they looked at the lungs' slices under the microscope, they found diffuse alveolar damage in 8 COVID Autopsy cases. Specifically, they saw hyaline membrane formation, tiny clots in the capillaries, capillaries engorged with red blood cells, and other inflammatory findings. All these findings represent ARDS. They also found lymphocytes, a type of white blood cell, infiltrated these areas of infiltration. This fits the picture of viral pathogenesis.
⏩ Timestamps 00:00 - Start 02:38 - The starting point of the COVID Autopsy Analysis 04:10 - Why we get COVID false Negative Test 04:34 - Rest of the Part of COVID Autopsy Analysis 09:45 - Big Takeaway's from the Findings in this COVID Autopsy Study 12:30 - Minimize the chances of having the severe disease if you were to get COVID
They also looked at the pharynx of these COVID patients, meaning in their throat. The lining of the throat, or mucosa, was hyperemic, meaning very red and irritated. They saw lymphocytes invading at the microscopic level, which is consistent with a viral infection. In one COVID case, a COVID patient had lymphocytes invade his heart muscle, findings that are consistent with what we call viral myocarditis. More than half of the COVID patients had large blood clots in this study. One-third of the COVID patients had pulmonary embolism as the direct cause of death.
All the others died of intense inflammation in their lungs related to pneumonia with ARDS (Acute Respiratory Distress Syndrome). Recently, studies show that about 1/3rd of COVID patients with severe COVID have blood clots. In another study of 191 COVID patients, half of those who died had clots, compared with 7% of survivors. And levels of D-dimer that were greater than 1000 µg/L were associated with a fatal outcome. So it's pretty clear now that the COVID has caused many clots to form in moderate to severe COVID disease.
How is this happening? It's likely a combination of reasons that have to do with downregulation of the ACE2 receptor in the lung alveoli, with a subsequent shift towards having more angiotensin II in the lungs, and less angiotensin 1-7 and 1-9 in the lungs, and when this happens, this leads to more cytokine storm with more inflammation, more constriction of pulmonary arteries, and more clots that develop. That, in turn, leads to more endothelial dysfunction in the capillaries surrounding the alveoli. Also, there is evidence that the virus attaches to the ACE2 receptors of those endothelial cells that line those capillaries, which further propagates inflammation and clotting.
And in the cytokine storm that develops there, RANTES, a chemokine, binds to the CCR5 receptor of CD4 and CD8 lymphocytes, and that causes those lymphocytes to infiltrate those areas of inflammation and, in doing so, further contributes towards the inflammatory reaction. This is why we see low levels of CD4 and CD8 lymphocytes in severe COVID. Endothelial damage can also lead to the development of antiphospholipid antibodies, which are harmful because they trigger blood clot formation. That's why COVID patients with clots with antiphospholipid antibody syndrome need to be on blood thinners.
Doctor Mike Hansen, MD Internal Medicine | Pulmonary Disease | Critical Care Medicine Website: https://doctormikehansen.com/ Doctor Hansen's Courses: https://doctormikehansen.com/courses/
