12 Autopsy Cases Reveal TRUTH About How Patients Die From Coronavirus (COVID-19)

Posted on

Deprecated: implode(): Passing glue string after array is deprecated. Swap the parameters in /home/tipslibu/viruscorona.org/wp-content/themes/superfast/inc/template-tags.php on line 335

This is actually the connect to the primary study within this video:

https://world wide web.acpjournals.org/doi/10.7326/M20-2003

In most 12 cases, the reason for dying was discovered inside the lung area or even the lung vascular system. For those who didn’t die of huge lung emboli, they died from the extensive inflammation inside the lung area, meaning pneumonia with ARDS. In these instances, the lung area were wet and high, similar to a sponge that’s saturated with water. The surfaces from the lung frequently were built with a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish-blue hypercapillarized areas. This really is suggestive of regions of intense inflammation, with endothelial disorder that may be seen in the microscopic level. Once they take a look at slices from the lung area underneath the microscope, they found diffuse alveolar damage in 8 cases. Particularly, they saw hyaline membrane formation, and small clots within the capillaries, and capillaries which were engorged with red bloodstream cells, along with other inflammatory findings. Each one of these findings represent ARDS. Additionally they found lymphocytes, a kind of white-colored bloodstream cell, infiltrated these regions of infiltration. This fits the image of the viral pathogenesis.

Additionally they checked out the pharynx of those patients, meaning within their throat. The liner from the throat, or mucosa, was hyperemic, meaning very red and inflammed, and also at the microscopic level, they saw lymphocytes invading there, that is in line with a viral infection. In a single situation, someone had lymphocytes invade his heart muscle, findings which are in line with what we should call a viral myocarditis. Over fifty percent of the sufferers within this study had large thrombus. One-third of the sufferers had lung embolism because the direct reason for dying. All of the others died of intense inflammation within their lung area associated with pneumonia with ARDS (Acute Respiratory system Distress Syndrome). Lately there’s been studies showing that about 1/3rd of patients with severe COVID have thrombus. Another study of 191 patients with COVID-19, 1 / 2 of individuals who died had clots, in contrast to 7% of survivors. And amounts of D-dimer which were more than 1000 µg/L were connected having a fatal outcome. Therefore it is pretty obvious since the SARS-CoV-2 virus causes lots of clots to create in moderate to severe COVID disease.

How’s this happening? It’s likely a mix of reasons, that is due to downregulation from the ACE2 receptor within the lung alveoli, having a subsequent shift towards getting more angiotensin II within the lung area, and fewer angiotensin 1-7 and 1-9 within the lung area, and at these times, this can lead to more cytokine storm with increased inflammation, more constriction of lung arterial blood vessels, and much more clots that develop. That, consequently, results in more endothelial disorder within the capillaries that surround the alveoli. Also, there’s evidence the virus attaches towards the ACE2 receptors of individuals endothelial cells that line individuals capillaries, which further propagates inflammation and clotting. As well as in the cytokine storm that develops there, RANTES, a chemokine, binds towards the CCR5 receptor of CD4 and CD8 lymphocytes, which causes individuals lymphocytes to infiltrate individuals regions of inflammation, and by doing this, further contributes for the inflammatory reaction. For this reason there has been lower levels of CD4 and CD8 lymphocytes in severe COVID. Endothelial damage may also result in the growth and development of antiphospholipid antibodies, which antibodies can be harmful simply because they trigger the development of thrombus. That is why patients who’ve clots with detecting antiphospholipid antibody syndrome have to be on bloodstream thinners.

Also, 11 from the 12 patients within this study had underlying cardiovascular disease, and were obese. They are known risks not only for coronary disease, but additionally known risks for endothelial disorder, and therefore are known risks for COVID. Therefore the big takeaways in the findings within this study is the fact that many people who die of COVID, it’s mainly a lung problem. Either associated with inflammation with ARDS, and/or thrombus.

Antiphospholipid syndrome may well be a commonality among patients with thrombosis in COVID-19 patients.

Leave a Reply

Your email address will not be published. Required fields are marked *