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Lung Doctor Analyzes George Floyd Autopsy Report (MEDICAL EXPLANATION)


Lung Doctor Analyzes George Floyd Autopsy Report (MEDICAL EXPLANATION)

Lung Doctor Analyzes George Floyd Autopsy Report (MEDICAL EXPLANATION)

Let’s be clear..we’ve all seen the video by now. It's obvious that these police officers killed George Floyd. The Hennepin County Medical Examiner, and the independent medical examiner hired by the family of George Floyd, Dr. Michael Baden, have concluded that his death was a homicide….but their opinion differs on the cause of death. But if both of them declared that his death was a homicide, does the cause of death really matter? (YES). I want justice for George Floyd, and that is why I’m making this video, because the medical explanation for his cause of death, is not a simple explanation. As a lung doctor, part of my job is to figure out why people can’t breathe. As an intensive care doctor, part of my job is to care for people who are on the brink of death. Like when someone can’t breathe. So when someone dies of asphyxia, as is the case of George Floyd, the determination of the cause of death is dependent on information elicited based on the investigation, which includes, the deceased personal medical history namely, autopsy, and crime scene investigation, which of course includes video evidence. Asphyxia is a Greek term that translates to “loss of pulse.”

Mechanical asphyxia involves some physical force or physical abnormality that interferes with the uptake and/or delivery of oxygen. With asphyxia, the brain doesn’t get enough oxygen, and when the pons and the medulla aren’t getting enough oxygen, they can no longer function. This means they can no longer tell the diaphragm to contract, and breathing then stops. While this happens, the heart is also not getting enough oxygen, and typically the heart pumps slower and slower until it stops. Prolonged continuous application of extreme pressure on the thorax, such as with the bodyweight of several officers, is capable of causing death. This is important, because this contributed to the death of George Floyd, in addition to the knee to the neck. The neck contains our airway, the trachea, and it also contains carotid and vertebral arteries and jugular veins. The arteries here deliver oxygenated blood to the brain, while the jugular veins allow the deoxygenated blood to flow back to the heart. So what happens when pressure is placed on the neck? Well, it depends, on a lot of different factors (amount and duration of pressure, etc). And looking at the George Floyd video, he was unconscious for more than 2 minutes with the knee still on his neck. There’s no doubt, that during this time, he took his last breath, and right around the same time, lost his pulse. By the time the EMS guy checks his pulse, I highly doubt he actually felt a pulse, because it was more than two minutes after George lost consciousness. It was obvious that when they moved George onto the stretcher, he was completely limp because he was dead. And it wasn’t until much later, did they start CPR, in the ambulance. Now let’s get to what the medical examiners had to say about this case.

Dr. Michael Baden, who did the independent autopsy says Floyd died of asphyxiation from sustained pressure when his back and neck were compressed, with the neck pressure cutting off blood flow to his brain.” I agree with that assessment. I would also add that partial compression of the trachea, causing airway compromise, was also possible. The weight on George’s back made the work of breathing much harder for his diaphragm, and the neck pressure at the very least meant less blood (and thus oxygen) was being delivered to his brain, and less carbon dioxide could be removed from his brain. After a while, the diaphragm becomes fatigued, and no longer has the strength to contract, which means the lungs can’t get oxygen into the blood, and can’t get carbon dioxide out of the blood. And all of this caused him to lose consciousness. And probably within seconds, he lost a pulse. And despite losing consciousness, and despite losing a pulse, they continued to apply pressure on the neck, and put their weight on his back. The Hennepin County medical examiner's office said that the cause of death is cardiopulmonary arrest complicating law enforcement subdual, restraint, and neck compression. This statement doesn’t really make sense to me. But the Hennepin County release also says heart disease was an issue; the independent examiner didn't find that. The county said that fentanyl and methamphetamine use were among significant conditions, but its report didn't say how much of either drug was in Floyd's system or how that may have contributed. But Dr. Michael Baden got it right.

- Doctor Mike Hansen

Coronavirus Autopsy Report Analysis by Dr. Mike | COVID-19 Autopsy

Coronavirus Autopsy Report Analysis by Dr. Mike | COVID-19 Autopsy
#coronavirus #covid19 #covid_19

⏩ Timestamps, click to skip ahead!
00:00 - Introduction
01:00 - Current Positive COVID Cases Details
02:05 - New Studies of COVID and Autopsy Report Analysis of a COVID Patient

Coronavirus | COVID-19 YouTube Video Playlist:

Coronavirus is the virus responsible for the COVID-19 outbreak. Wuhan, China has been the epicenter of this epidemic, but some experts, like Dr. Anthony Fauci, are now saying that we are on the verge of a pandemic.

Before I get to the Coronavirus autopsy report of a patient with COVID-19, its important to understand the context of the numbers of total people infected, total people with coronavirus pneumonia, number of people who developed ARDS, and the total number of deaths.

When looking at the numbers, we should realize that they are almost certainly being underreported in China, and there are multiple reasons for that, which I won't get into right now.

Although these are not concrete numbers, its what we have to go by at this point. The percentage of people.

Also, up to this point, there has not been any pathology reported on this disease because of limited access to autopsy and biopsy reports.

But finally, we now have a new case report study in Lancet Respir Med, published Feb 17, that has autopsy reports for a patient who died from COVID-19.

Pathological findings of COVID-19 associated with acute respiratory distress syndrome.

A patient is a 50-year-old man from China, who visited Wuhan Jan 8–12. On Jan 14, he developed a dry cough and some mild chills, so this is day 1 of the illness. However, he did not initially seek medical attention and kept working until Jan 21. He then went to a medical clinic on Jan 21, because by that time, he had developed worsening symptoms. He had fever, chills, fatigue, cough, and shortness of breath.
On Jan 22 (day 9 of illness), the Beijing Centers for Disease Control (CDC) confirmed by reverse real-time PCR assay that the patient had COVID-19.

He was immediately admitted to the isolation ward and received supplemental oxygen through a face mask.

He was given several different medications, which included the inhaled version of interferon alfa-2b, lopinavir plus ritonavir as antiviral therapy, and Moxifloxacin, to prevent secondary bacterial infection.

He was also given a steroid, methylprednisolone, to attenuate lung inflammation.

On day 12 of illness, after the initial presentation, his symptoms did not improve, other than his fever, which he received medication for.

His chest x-ray on day 12 showed progressive bilateral infiltrates. He repeatedly refused ventilator support in the intensive care unit repeatedly, apparently because he suffered from claustrophobia.

His oxygen saturation values decreased to 60%, and the patient had a cardiac arrest. At that point he was intubated with mechanical ventilation, he had chest compressions and epinephrine.

Unfortunately, they are unable to revive him.

An autopsy is done, and biopsy samples were taken from the lung, liver, and heart.

The heart tissue was essentially normal.

The liver biopsy of this patient showed moderate microvascular steatosis and
mild lobular and portal activity, indicating the injury could have been caused by either Coronavirus infection or as a result drug-induced liver injury.

Histological examination of lung tissue showed diffuse alveolar damage with cellular fibromyxoid exudates, along with the desquamation of pneumocytes and hyaline membrane formation.

These findings are consistent with acute respiratory distress syndrome ( ARDS ).

Interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, was seen in both lungs. There were multinucleated syncytial cells with atypical large alveoli characterized with prominent nucleoli, consistent with viral cytopathic-like changes.

These pathological features of COVID-19 greatly resemble those seen in SARS and Middle Eastern respiratory syndrome (MERS) coronavirus infection.

Acute Respiratory Distress Syndrome ( ARDS )
To watch the video please visit this link:

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine

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#coronavirus #covid19 #covid_19

188 Coronavirus Autopsies (COVID-19) – Possible Heart Inflammation (Myocarditis)?

Coronavirus Autopsy Report | 188 Coronavirus Autopsies (COVID-19) – Possible Heart Inflammation (Myocarditis)?

One-third of Big Ten athletes who contracted COVID-19 show signs of heart inflammation. Is SARS-CoV-2 really causing this?

Coronavirus | COVID-19 YouTube Video Playlist:

This video is a summary of all the coronavirus autopsy findings that have been done on coronavirus patients. This is based on 8 published studies and/or case reports. Here are the links to those studies:

SARS-CoV-2 exhibits selectivity for the lungs. Specifically, type II pneumocytes, meaning type II alveolar cells. Alveoli are the tiny microscopic air sacs of the lungs, which is the part of our lungs that is responsible for gas exchange. Air is brought down into the lungs, to the alveoli, and the oxygen diffuses from the alveoli into our tiny blood vessels there, called capillaries. At the same time, carbon dioxide, a waste product from our body, travels from the capillaries into our alveoli, and we then exhale out that carbon dioxide. Alveoli are made up of mainly type I alveolar cells. But to a lesser degree, they are also made up of type II alveolar cells, and these guys are sort of like the maintenance guys for the alveoli. They play a part in making surfactant, a sort of lubricant for the alveoli. But these cells also play a part in defending against foreign pathogens, like viruses and bacteria.

Well as it turns out these type II alveolar cells have the ACE2 receptors on them, and SARS-CoV-2 binds to this receptor, and that’s how it gains entry into these cells, and into our body. When the SARS-CoV-2 invades the type II alveolar cells, it precipitates a cascade of reactions that causes the body to react to it, with inflammation, and lots of damage to the alveoli, known as diffuse alveolar damage. Clinically, this is what we call ARDS, acute respiratory distress syndrome. This is what causes oxygen levels to go down, and what causes the so-called cytokine storm. When people die of COVID, this is what’s going. Also, there is a propensity for blood clots to develop, and some people with COVID died as a result of pulmonary emboli, meaning blood clots in their lungs. The capillaries in the lung surround the alveoli. Here, they serve to bring red blood cells in close proximity to the alveoli, to allow gas exchange to occur, as I mentioned earlier. The lining of these capillaries is called the endothelium, the cells that make up the endothelium here, also have ACE2 receptors. The virus, at least in those with severe disease, seems to be infiltrating the endothelium and causing inflammation and injury to the capillaries, not just the alveoli. This likely at least partially explains why this virus is causing blood clots to develop here.

So we are seeing a common theme here, and that is microthrombi that are being found in blood vessels of pretty much all the organs, including brain, kidneys, heart, liver, and of course lungs. This is likely all because of endothelial damage that occurs as a result of the virus binding to the ACE2 receptors that are located there.

After all, in some of these coronavirus autopsy studies, they used electron microscopy to find what appeared to be viral particles in the endothelial cells not only in the lungs, but also in the heart and kidneys.The endothelial damage serves to trigger the clotting process, something known as a coagulation cascade. But its also possible that the endothelial damage is mainly occurring in the lung capillaries, and that’s where the tiny clots first develop, and then they end up traveling to other parts of the body, eventually lodging in blood vessels of other organs. Or it could be both of these things. It's interesting to note that 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. So overall, organ damage that occurs in severe COVID- is likely a result of a multitude of factors.

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
Instagram Account:

#coronavirus #covid19 #covid_19

What Doctors Are Learning From Autopsy Findings of New CORONAVIRUS Patients

What Doctors Are Learning From Autopsy Findings of New CORONAVIRUS Patients

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

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 autopsies 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 coronavirus 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 COVID-19 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 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 coronavirus 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 - Yes!
2) Indirectly attacking organs by way of collateral damage from the cytokine storm - Yes!
3) Indirectly cause damage to organs by means of blood clots - Yes!
4) Indirectly cause damage as a result of 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, 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 Coronavirus 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 COVID-19 patients are dying?
Video Link -

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine

Coronavirus vs Flu vs Normal Lungs | Autopsy Comparison

Coronavirus vs Flu vs Normal Lungs | Autopsy Comparison

Both Coronavirus aka COVID-19 and the flu (influenza) can cause pneumonia, and ARDS, acute respiratory distress syndrome. Both of these can cause respiratory failure and death. We know that COVID is more likely to cause severe disease compared to influenza, and has a higher case fatality rate. We also know that COVID is much more likely to cause blood clots than influenza. In this recent study published in the NEJM, they actually compared lung autopsy findings from deceased patients of COVID and Influenza and compared those findings to people who died of other causes, who had normal lungs. This group with the normal lungs served as the control group. Pneumonia is a very broad medical term that refers to an inflammation within parts of a lung, or parts of both lungs. This entails the tiny air sacs of the lungs, called alveoli, to fill up with inflammatory fluid, which impairs the flow of oxygen from the air to the bloodstream.

The consequences of pneumonia, whether caused by Coronavirus or influenza, can result in dangerously low oxygen levels in the bloodstream and if not treated, can result in death. Sometimes if pneumonia is severe enough, it can cause ARDS, which refers to severe inflammation within both lungs, which causes extreme difficulty with getting oxygen into the blood. This is a well-known syndrome that can occur with either COVID or influenza pneumonia. SARS-CoV-2 inflicts a particular type of damage in human lungs that is somewhat different from the picture we see with influenza. To understand the differences, researchers looked at the lungs of seven patients who died of respiratory failure from Coronavirus and then compared them to the lungs of seven patients who died of pneumonia caused by influenza A.

They also compared them to the lungs of ten uninfected lungs which came from people whose organs had been donated for transplant but were not used, so these were normal lungs. The researchers were careful to match as well as they could, the gender and age of the patients so their comparisons among the groups of patients would be meaningful. All of the lungs came from patients who were older and whose average age in the Coronavirus group ranged from 68 years old for the females and 80 for the males. The average age in the influenza group ranged from 62 years for the females and 55 for the males. Perhaps the most interesting and important finding of this research revealed damage to the small blood vessels of the lungs, meaning lung capillaries. The lining of these capillaries is called the endothelium, and the cells that make up the endothelium have ACE2 receptors. The cells were in fact infected with SARS-CoV-2. The researchers in this study found severe microscopic injuries to the endothelium here, with actual disruptions of the cell membranes.

The also found widespread clotting in these lung capillaries surrounding the alveoli, which included actual blockage of the capillaries, and microangiopathy which involves thickening and weakening of the small blood vessel walls, which begin to leak blood and protein, further slowing the flow of blood. Although fibrin clots in the capillaries of the alveoli were present in the lungs from both the Coronavirus and influenza patients, micro-clots in the capillaries surrounding the alveoli were nine times as prevalent in the lungs of patients with COVID-19 as compared with the lung tissue of the influenza patients. What’s more, is that COVID-19 patients showed actual new blood vessel growth, primarily through a process known as intussusceptive angiogenesis. The word “angiogenesis” means the formation of new blood vessels. The term “intussusceptive” refers to something telescoping inside itself. In this context, it's referring to new blood vessels being formed by a pillar of tissue within another blood vessel, effectively splitting the vessel into two. The researchers believe this process contributes to more problems with clotting and inflammation of the lining of the blood vessels than is seen in the lungs of patients with influenza. Angiogenesis was seen much less frequently in the lungs of patients with influenza as well as the control group of normal lungs. The researchers also looked at the ACE2 receptor, which is what allows the SARS-CoV-2 virus to gain entry into cells. Compared to the lungs of the control group, there were more ACE2-positive cells in the lungs of both COVID-19 and influenza patients. The researches in the study speculate that the reason for more angiogenesis in the COVID group is because of the evidence of viral invasion of these endothelial cells. Also, endothelial cells in the specimens in the COVID group showed cellular swelling and disruption of the junctions in-between cells.

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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ABC News Live update: Officers charged with George Floyd’s death appear before judge

Calls for justice reverberated outside the courthouse following the hearing for four former Minneapolis police officers where no major decisions were announced on future proceedings.

George Floyd death: Floyd family attorney says only overdose was excessive force, racism

The attorney for George Floyd's family, Ben Crump, alongside other lawyers involved in the case against four police officers charged in Floyd's death, criticized the lawyers defending the officers for attempting to use a defence that the 46-year-old Black man was a danger to the community.

The officers' lawyers are reportedly using a defence in which they are highlighting Floyd's past crimes and history of drug use, seen as a blame the victim approach. They are also seizing on Floyd's reported medical issues and addiction, saying he likely died from fentanyl and not after officer Derek Chauvin kneeled on his neck for more than eight minutes.

Crump said in a press conference after a hearing, in which the officers' lawyers argued for their trials to be held separately, that the only overdose that killed Floyd was an overdose of excessive force and racism by the Minneapolis Police Department.

Asked about the arguments for separate trials, attorney Scott Masterson responded with three words: Guilty is guilty.

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George Floyd's death became a symbol for racial injustice. Racism also played a role in his life.

George Floyd’s death became a symbol of injustice and police brutality around the world. Those who knew him best in his Houston neighborhood say it was a stark reminder of the racism they’ve faced all their lives. Read more: Subscribe to The Washington Post on YouTube:

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Lawyers angry at claim drugs killed George Floyd

Prosecutors in the case of four former Minneapolis officers charged in George Floyd's death told a judge Friday the men should face trial together. Lawyers for Floyd's family were angered by claims his death was caused by a drug overdose. (Sept. 11)

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Protesters Call To Defund The Police After Death Of George Floyd | NBC Nightly News

As protests grow over police brutality against black Americans, many are demanding departments be defunded. At its core, that would mean rerouting a city’s policing budget into community programs.» Subscribe to NBC News:
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Protesters Call To Defund The Police After Death Of George Floyd | NBC Nightly News

How George Floyd's death unified community activists in Minneapolis

The death of George Floyd at the hands of Minneapolis police sparked protests nationwide against police brutality and racial injustice. CBS News' Brandi Kellam spoke with local leaders in Minneapolis to find out what has changed in their community outreach in the aftermath of Floyd's death.

Meet The Young Artist Behind Iconic Portrait Of George Floyd | TODAY

High school student Faith Blackstone has long been using art to educate others about Black history and activism. Following the death of George Floyd, she was inspired to create a portrait that went on to be displayed by his family at his funerals and viewed by people around the world.
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Meet The Young Artist Behind Iconic Portrait Of George Floyd | TODAY

At least 7 Minneapolis police officers quit after George Floyd's death

Several Minneapolis Police Department officers have decided to leave their jobs in the aftermath of George Floyd's death. They also cite a lack of support from the department.

Police ignored George Floyd's 'I can't breathe' plea: transcript

The former U.S. police officer charged in the death of George Floyd told him to stop shouting and save his breath as he knelt on his neck and Floyd gasped for air, according to a newly released transcript of police body camera footage.


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Minneapolis Native & UGA Player Jermaine Johnson Reacts to George Floyd's Death in His Hometown

Jermaine Johnson, who grew up in metropolitan Minneapolis, talks about his feelings after George Floyd was killed in his hometown.

George Floyd Is Reminding France of Its Own Systemic Racism

In June, while the U.S. took to the streets demanding justice for George Floyd, Parisians reignited their calls for justice for Adama Traoré. A Black man who died exactly 4 years ago while being detained by the French national guard.

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George Floyd’s Family Speaks Out After Hearing

Members of George Floyd’s family came to Minnesota to be at Friday's hearing, reports Jennifer Mayerle (1:41).
WCCO 4 News At 6 - September 11, 2020

Attorney for Thomas Lane asks for dismissal of charges in George Floyd's death

The attorney for former Minneapolis police officer Thomas Lane has filed a motion to dismiss charges in the death of George Floyd.

Attorney Earl Gray filed a motion to dismiss in Hennepin County District Court on Tuesday, citing lack of probable cause based on the entire record. Gray filed several exhibits as evidence, including body camera footage and a transcript of Lane's interview with investigators.

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One of the former officers arrested in George Floyd's death posts bail

Thomas Lane, one of the four former Minneapolis officers arrested in connection with the death of George Floyd, posted bail on Wednesday according to jail records.



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