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.
In all 12 cases, the cause of death was found within the lungs or the pulmonary vascular system. For the ones who did not die of 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 hypercapillarized 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 8 cases. Specifically, they saw hyaline membrane formation, and 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 white blood cell, infiltrated these areas of infiltration. This fits the picture of viral pathogenesis.
They also looked at the pharynx of these patients, meaning in their throat. The lining of the throat, or mucosa, was hyperemic, meaning very red and irritated, and at the microscopic level, they saw lymphocytes invading there, 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. More than half of the patients in this study had large blood clots. One-third 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 with ARDS (Acute Respiratory Distress Syndrome). Recently there’s been studies showing that about 1/3rd of patients with severe COVID have blood clots. Another study of 191 patients with coronavirus aka COVID-19, 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 SARS-CoV-2 virus is causing a lot of clots to form in moderate to severe COVID disease.
How is this happening? It’s likely a combination of reasons, that has 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 the formation of blood clots. That’s why patients who have clots with the diagnosis of antiphospholipid antibody syndrome need to be on blood thinners.
Also, 11 out of the 12 patients in this 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. So the big takeaways from the findings in this study are that most people who die of COVID, it’s primarily a lung problem. Either related to inflammation with ARDS and/or blood clots.
Antiphospholipid syndrome might be a commonality among patients with thrombosis in COVID-19 patients.
Lämna ett svar