12 COVID Autopsy Cases Reveal the TRUTH How COVID Patients Dying - Doctor Explains

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By Dr Mike Hansen

Original YouTube description:

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, much 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 look 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, click to skip ahead: 12 COVID Autopsy Cases Reveal!
00:00 - Introduction
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

This is the link to the main study in this video:
https://www.acpjournals.org/doi/10.73...

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. At the microscopic level, they saw lymphocytes invading there, 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 in this study had large blood clots. 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 that surround 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 are seeing low levels of CD4 and CD8 lymphocytes in severe COVID. Endothelial damage can also lead to the development of antiphospholipid antibodies, and these antibodies are bad because they trigger blood clot formation. That’s why COVID patients who have clots with antiphospholipid antibody syndrome need to be on blood thinners.

11 out of the 12 COVID patients in this study had underlying heart disease and were obese. These are known risk factors for cardiovascular disease and known risk factors for endothelial dysfunction and are known risk factors for COVID. So the big takeaways from the findings in this study are that most people who die of COVID are primarily lung problems. Either related to inflammation with ARDS and/or blood clots.

Antiphospholipid syndrome might be a commonality among patients with thrombosis in COVID patients.

Doctor Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
Website: https://doctormikehansen.com/
IG Account: http://instagram.com/doctor.hansen/
FB Page: https://www.facebook.com/DoctorMikeHa...

Before I say anything,
I just want to say

that if you are squeamish
you might not want to watch this video

because there will be some pictures 
of lungs that have a blood clot in them

and other organs of the body.
In my opinion it's nothing that bad

but I wanted to give you a warning,
regardless.

This video is a follow-up
to my last video which was called,

"What Doctors Are Learning From Autopsy
Findings of COVID Patients. "

Just after I published that video,
not even a day later, this study came out,

published in the
Annals of Internal Medicine

which I'll put a link in to the description below.

And what makes this study such a big deal
is that it's the first study that

looked at this many autopsies of
patients who died of COVID.

Not only do they do complete autopsies,
but they use CT scans

to scan the entire body for blood clots.

All 12 of the deceased had tested
positive for SARS Coronavirus-2

by means of RT-PCR.

Now, I want to say something.
Not everyone on this planet is

going to get COVID.
For those who do get the virus,

80% of them will either have mild
or no symptoms.

Roughly 15%-20% of them will 
have pneumonia.

Roughly 4% will develop ARDS, or Acute
Respiratory Distress Syndrome

and/or shock with
multi-organ failure.

And about 1% will die of
the infection.

When I'm in the ICU and 
someone dies it's obviously horrible.

Sometimes autopsies have to be done
irrespective of family consent

when it's a legal matter.

Rarely, depending on the
circumstances,

we ask familys' permission to 
do an autopsy.

Most families decline the option for
autopsy,

but during this pandemic, it's especially 
important for autopsies to be done

because they often provide
incredibly valuable information,

especially when we still know so little
about COVID.

Especially when it can present in so many 
different ways.

So in this study that was
done in Germany,

autopsies were mandated for patients 
who died of COVID.

And to the families of those victims
of COVID, my condolences.

And we're still trying to figure out
why some people do so poorly

when they get the virus,
while others do just fine

and then there's everyone in between.

So, the point of this video
is not to scare people.

The point is to learn about
the disease,

and to ultimately benefit from that
learning

with the hope of developing treatment
options

and ultimately reduce morbidity and mortality in other 
words to save lives and by making this video the

goal is to educate myself and others about what 
we're learning and getting the medical truth out

there to the public so in this study there were 
12 patients total nine men three women and the

median age was 73 all patients had some type of 
pre-existing medical condition most of them had

obesity and/or underlying heart disease such as 
coronary heart disease some had type 2 diabetes

hypertension peripheral artery disease asthma 
COPD initial lab tests revealed elevated levels

of d-dimer lactate dehydrogenase meaning LD H 
and C reactive protein or CRP all of these are

nonspecific markers of inflammation there is also 
mild thrombocytopenia in some patients meaning low

platelet counts this isn't an unusual finding in 
patients who are critically ill they also looked

at levels of viral RNA using rt-pcr studies all 
twelve patients had the SARS-CONORA-VIRUS 2

RNA in their lungs nine out of the twelve had it 
in their throat and six had in their bloodstream

in five patients they had viral RNA in other 
tissues like heart liver brain and kidney not

only did they have the virus there but the levels 
were higher in those tissues compared to the blood

here's a picture from a different autopsy that 
was not part of this study where the virus was

actually visualized in the kidney using electron 
microscopy so what is this telling us it tells us

that the virus is binding to those h2 receptors 
in those organs so in some people who die of COVID

they had the virus in other organs besides the 
lungs. But, and this is a big BUT, they did not die

as a result of that virus being in those different 
organs they died as a result of lung complications

also an important takeaway from this is that all 
twelve had in their lungs and nine out of the 12

had it in their throat so when you go to do a throat 
swab with someone who has COVID the virus might

not even be there and that's just another reason 
why you can get a false negative test okay so they

also did post-mortem CT scans of these patients 
which demonstrated mixed patterns of reticular

infiltrations in severe dense consolidations in 
both lungs this CT scan is a patient with covid

pneumonia in ARDS not from this study 
that we're talking about now but basically

demonstrating the exact same thing both lungs have 
extensive consolidations ground-glass opacities

which represent an extensive inflammation these 
are also known as pulmonary infiltrates and you

can see the difference compared to a normal 
CT scan of the chest which doesn't have any

pulmonary infiltrates in four cases out of the 12 
massive pulmonary embolism meaning massive blood

clots in the pulmonary arteries was the cause of 
death in another three cases out of the 12 they

had blood clots in their large veins of their legs 
meaning DVT without having pulmonary embolism so

in six of the nine men they had clots in the veins 
that surround the prostate gland in all 12 cases

the cause of death was found within the lungs or 
the pulmonary vascular system meaning within the

pulmonary arteries for the ones who didn't die of 
having a large pulmonary emboli they died of the

extensive inflammation within the lungs meaning 
pneumonia with ARDS in these cases the lungs were

wet and heavy much like a sponge that is saturated 
with water. The surfaces of the lung often had

a distinct patchy pattern with pale areas 
alternating with slightly protruding and firm

deep reddish blue hyper capitalized areas this 
is indicative of areas of intense inflammation

with endothelial dysfunction that can be seen at 
the microscopic level. When they look at slices

of the lungs under the microscope they found 
diffuse alveolar damage in eight cases out of 12

specifically they saw hyaline membrane formation 
tiny clots in the capillaries and capillaries

that were engorged with red blood cells and 
other inflammatory findings. All these findings

represent ARDS they also found lymphocytes 
a type of a white blood cell that infiltrated

these specific tissues this fits the picture of a 
viral pathogen ASIS. They also look at the pharynx

of these patients meaning the throat. The lining of 
the throat where the mucosa was hyperemic meaning

very red and irritated and at the microscopic 
level they saw lymphocytes invading there as well

again which is consistent with a viral infection 
in one case a patient had lymphocytes invade his

heart muscle findings that are consistent with 
what we call viral myocarditis. In other words the

heart muscle had evidence of viral infection more 
than half the patients in this study had large

blood clots. 1/3 of the patients had pulmonary 
embolism as the direct cause of death. All the

others died of intense inflammation in their lungs 
related to pneumonia and ARDS. Recently there's

been studies showing that about 1/3 of patients 
with severe COVID have blood clots. Another study

of 191 patients with Covid 19, half of those who 
died had clots compared with 7% of the survivors

and levels of d-dimer that were greater than 
1,000 were associated with a fatal outcome so

it's pretty clear now that sars-covid-2 virus 
is causing a lot of clots to form and moderate

to severe COVID disease. But how is this happening?
it's likely a combination of reasons they have

to do with down regulation of the h2 receptor in 
the lung alveoli with a subsequent shift towards

having more angiotensin 2 in the lungs and less 
angiotensin 1:7 and less in angiotensin 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 that 
surround the alveoli. Also there's evidence that

the virus attaches to the ACE 2 receptors of the 
endothelial cells that line those capillaries

which further propagates inflammation in clotting 
and in the cytokine storm that develops there

Randy's Okemo kine bind 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're seeing low levels of cd4 and cd8 lymphocytes

and severe COVID. Endothelial damage can also lead 
to the development of antiphospholipid antibodies

and these antibodies are bad because they trigger 
the formation of blood clots and that's why

patients who have clots with the diagnosis 
of antiphospholipid antibody syndrome they

need to be on blood thinners also 11 out of the 12 
patients in the study had underlying heart disease

and were obese these are known risk factors not 
just for cardiovascular disease but also known

risk factors for endothelial dysfunction, and are
known risk factors for COVID the endothelium is

more susceptible to damage based on cardiovascular 
risk factors such as men aged 45 or older, women

age 55 or older, smoking, high blood pressure, high 
cholesterol, diabetes, obesity, and lack of physical

activity. So the big takeaways from the findings 
in this study is that most people who die of Covid

it's primarily a lung problem either related to 
inflammation with ARDS and/or blood clots even

though blood thinners are not a cure for Covid per 
se they do have the potential to save lives. The

hard part is figuring out who is likely to develop 
clots and who should we give blood thinners to and

which blood thinners should we give and should 
we give high doses of blood thinners or just the

low-dose prophylactic doses? To further complicate 
matters it's often hard to diagnose blood clots in

hospitalized patients even before COVID came along 
usually it's easy to diagnose large blood clots in

the veins of the legs, meaning DVT by doing an 
ultrasound of the legs even though ultrasound

isn't a hundred percent accurate. The way we 
typically diagnose pulmonary emboli is by getting

a CT scan of the chest while at the same time 
giving IV contrast and this is called a CT angio

or CT A of the chest the downsides of doing this,
well there's several. One, you have to transport a

patient to the CT scanner and sometimes patients 
aren't stable enough to do that. Two, you risk

spreading the virus to others in the hospital by 
transporting that patient. And this will also require

more PPE use. Three, CT scans require larger doses of 
radiation. Four giving someone IV contrast has some

risks such as the risk of serious allergic 
reaction and the risk of causing some kidney

damage. On top of that the CTA of the chest can 
only visualize bigger clots so you might not see

the small clots that are there. Right now more and 
more hospitals are giving high-dose blood thinners

to COVID patients who have severe disease even 
if they haven't been diagnosed as having blood

clots. But what about patients without moderate or 
severe Covid, should they take a blood thinner or

maybe a low dose blood thinner, or should they take 
an antiplatelet medication like aspirin either 81

milligrams of aspirin or 162 milligram dose or 325 
milligrams dose, or should the general public take

a low dose aspirin like 81 milligrams in order to 
help prevent blood clots from forming if they do

get COVID or should it just be certain people in 
the population who are at higher risk of getting

severe COVID should they take aspirin? These are 
the questions we don't know the answers to at

this point. It's going to take a lot of studies 
to answer these questions because not only do

we need to know that there's a benefit in doing so, 
we have to know that these benefits will outweigh

the risks such as the risk of bleeding and then 
there's all the other drugs that are being looked

at right now and randomized control trials we 
should start seeing some of these results pretty

soon. What we do know is that in order to improve 
the capillary endothelium and also to minimize

your chances of having severe disease if you 
were to get COVID you want to do several things.

This includes exercise, eating healthy, getting 
good sleep, minimizing stress, not smoking, what

about vaping? generally not good either but not as 
bad as smoking. too much alcohol not good either

have your medical conditions under control 
whether that's diabetes, high blood pressure,

COPD, asthma, allergies, whatever the case may be. 
Now what about vitamin D? probably a good thing

but that's a whole another topic which I should 
make my next video on because there's a lot to

say about that and possibly other vitamins too 
if you're deficient in certain vitamins. Anyway

to catch that video subscribe to this channel and 
hit that bell notification so you know when I post

here on YouTube so many topics I want to cover in 
so little time but I will see you in the next one