Dr. Pierre Daniel Kory (born 1970)

https://en.wikipedia.org/wiki/Pierre_Kory#/media/File:PierreKory.jpg2024-06-09-wikipedia-org-pierre-kory-senate-img-2020.jpg"An image of Dr. Pierre Kory during his government testimony in front of the US Senate in December 2020"

Wikipedia 🌐 Pierre Kory 

Saved Wikipedia (June 9, 2024) for "Pierre Kory"

https://en.wikipedia.org/wiki/Pierre_Kory

2024-06-09-wikipedia-org-pierre-kory.pdf

Alma mater

St. George's University

Known for

COVID-19 misinformation

Medical career


Field

Critical care medicine, Pulmonology

Institutions

University of Wisconsin (former), Front Line COVID-19 Critical Care Alliance (current)

Pierre Kory is an American critical care physician who gained attention during the COVID-19 pandemic for advocating widespread off-label use of certain drugs as treatments for COVID-19, as president and co-founder of the Front Line COVID-19 Critical Care Alliance (FLCCC).[1][2] Kory testified twice to the U.S. Senate regarding COVID-19. During his testimony in December 2020, Kory erroneously claimed that the antiparasitic medication ivermectin was a "wonder drug" with "miraculous effectiveness" against COVID-19.[3][4][5]

In August 2023 the American Board of Internal Medicine informed Kory his certification was to be revoked for spreading medical misinformation.[6]

Education and career[edit]

Kory graduated from NYU's school of Public Service with a Master's In Public Administration.[7] He completed his medical education at St. George's University in Grenada, West Indies, graduating with a Doctor of Medicine (MD) degree and completed residency and fellowship training in critical care and pulmonary medicine.[8] He did clinical rotations at the Weill Cornell School of Medicine.[8] Kory first practiced in Madison, Wisconsin, at UW Health, which is the academic medical center at the University of Wisconsin. He served there as the medical director for the Trauma and Life Support Center, in the outpatient pulmonary medicine clinic, where he performed bronchoscopic and pleural procedures.[8] Kory was the critical care service chief at the UW Health University Hospital (part of the University of Wisconsin School of Medicine and Public Health) until May 2020.[9][10] He later joined Aurora St. Luke's Medical Center in Milwaukee, Wisconsin,[11] before becoming a locum tenens physician.[12]

Kory is an expert in critical care ultrasonography. In 2015, along with his two co-editors, Kory won the British Medical Association's 2015 President’s Choice award in medical textbooks for their work on Point of Care Ultrasound.[8]

In August 2023 Kory was informed by the American Board of Internal Medicine that his board certification was to be revoked for "spreading false or inaccurate medical information".[6][13]

COVID-19[edit]

Further information: Ivermectin during the COVID-19 pandemic

Early in the COVID-19 pandemic, Kory advocated for using increasing doses of corticosteroids and anticoagulants for hospitalized people with COVID-19, at a time when the general recommendation was merely for supportive care.[10] Kory sees subsequent evidence from the RECOVERY Trial, which showed benefit from lower doses of corticosteroids, as vindicating his approach; medical researcher Kevin J. Tracey has said it is still unknown whether Kory's approach was beneficial or harmful. Kory has used other drugs off-label in his treatment regimens, including famotidine and intravenous vitamin C.[10] Kory gave testimony as a guest of U.S. Senator Ron Johnson at a May 5, 2020, Senate hearing in which he called for use of steroids in COVID-19 patients.[9][11] He resigned from UW Health in May out of frustration of its reluctance to implement such measures.[10][12]

Kory is president and co-founder of the Front Line COVID-19 Critical Care Alliance (FLCCC), a small U.S. organization of physicians and former journalists formed in April 2020 that advocates for ineffective COVID-19 treatments, including ivermectin.[14][1][2][15] The FLCCC falsely states that ivermectin reduces viral load and accelerates recovery in patients, while the World Health Organization, U.S. Food and Drug Administration, and European Medicines Agency advise against the use of ivermectin outside of clinical trials.[16][17][18]

On December 8, 2020, Kory was a witness at a Senate hearing called by the US Senate Homeland Security Committee Chair Ron Johnson,[19] which was criticized as promoting fringe ideas about COVID-19.[20] Kory described ivermectin as "miraculous" and as a "wonder drug" to be used against COVID-19. Video footage of his statements went viral on social media, receiving over one million views within a few days.[3] Kory became a leading advocate of the use of ivermectin throughout the pandemic, promoting a conspiracy theory that its true effectiveness was being suppressed by the "Gods of Science" who wanted to monopolize scientific information.[21] Kory resigned from Aurora St Luke's afterwards, claiming that new restrictions on his contract threatened to limit his freedom to speak.[11][12]

In November 2021 the Journal of Intensive Care Medicine retracted a paper written by Kory, Paul E. Marik, and others. The retraction was triggered when it was found the paper misreported the mortality figures of people treated for COVID-19 with the FLCCC's "MATH+" protocol, falsely making it appear to be an effective treatment.[22][23]

In February 2022, the American Journal of Therapeutics issued an expression of concern against a 2021 systematic review of which Kory had been lead author. The notice said there were suspicions about the integrity of the underlying data on which the paper depended to show that ivermectin was a viable treatment for COVID-19.[24][25]

By July 2022, Kory had begun endorsing misinformation about COVID-19 vaccines, downplaying the COVID-19 vaccines' effectiveness and spreading conspiracy theories about their safety and unreported fatalities. Kory claimed on a conservative podcast that COVID-19 vaccines "are not safe or effective", despite acknowledging that "There's just tons of papers in journals showing that the vaccines are safe and effective."[26] As of August 2021, studies reported that the COVID-19 vaccines available in the United States are "highly protective against severe illness, hospitalization, and death due to COVID-19".[27] In comparison with fully vaccinated people, the CDC reported that unvaccinated people were 10 times more likely to be hospitalized and 11 times more likely to die.[28][29]

Kory in August 2022 falsely claimed that vaccines can disrupt pregnancy and fertility, based on his reading of Pfizer data submitted to the FDA, an interpretation which is not supported by peer-reviewed evidence. He represented the rates of miscarriage after COVID vaccination as alarming,[30] when the rates are in fact consistent with background miscarriage rates of 11-16 percent in the general population.[31] Multiple studies have shown that COVID infection, not vaccination against COVID-19, is risky for pregnant women. One study found that the risk of fetal or newborn mortality is higher in unvaccinated pregnant women who contract COVID, than it is for vaccinated women infected with COVID at the same stage of pregnancy.[32] Further, according to studies cited by the CDC, there is no evidence of decreased fertility due to COVID vaccination now or in the future, and changes in menstrual cycles are small and temporary.[33]

Kory repeatedly questions peer-reviewed science on COVID, the COVID-19 vaccine emergency use authorization process overseen by federal agencies, and the profit motives of pharmaceutical companies, while he also profits from marketing off-label and "alternative" COVID treatments that are lacking in quality evidence.[34] His rhetoric carries many of the markings of conspiracy theory, which make emotional arguments that presume malfeasance and coordinated efforts and deliberate obfuscation of information. Such theories become ingrained in in-groups as a form of secret knowledge, which reinforces the fervor with which the ideas are believed. Kory's detractors such as David Gorski[35][36] have noted his efforts to promote and profit from alternative COVID treatments are similar to medical quackery going back centuries.[26][37]

In June 2022, Kory tweeted that the American Board of Internal Medicine had warned him that his board certification was in danger of being revoked for misinformation.[34] Effectively unable to practice within mainstream medicine, Kory launched his own “advanced COVID-19 care center", charging US$1,250 to 1,650 for a series of three appointments.[34]

In November 2022, Kory and the FLCCC began marketing a cocktail of supplements and drugs (e.g. ivermectin and nitazoxanide) for other viruses, influenza and Respiratory syncytial virus (RSV). Like the FLCCC-advocated COVID treatments, the recommendations lacked credible supporting scientific evidence. The Washington Post estimated that this cocktail could cost over $500.[38]

In March 2024, Kory and Paul Marik published an op-ed in The Hill claiming that long COVID was caused by COVID-19 vaccination instead of COVID-19 infection. The op-ed was republished by the German disinformation outlet Disclose.tv. The fact-checking website Health Feedback found that the op-ed relied on anecdotes that did not provide evidence to support the claim.[39]

Books[edit]

References

External links

Evidence Timeline

2019(March)  - Co-Autor with "Paul H. Mayo" , whom Kory writes CV19 opinion piece with in July 2020

https://www.researchgate.net/publication/331734170_Effectiveness_of_a_Transesophageal_Echocardiography_Course 


Effectiveness of a Transesophageal Echocardiography Course

March 2019Journal of Intensive Care Medicine 35(11):088506661983666

March 201935(11):088506661983666

DOI:10.1177/0885066619836665

Authors:

Marcos Silva Restrepo

Michel A Boivin

Pierre Kory

Pralay K. Sarkar

Gisela I. Banauch

Stephen Halpern

Paul H. Mayo

2020 (April)

"History

The FLCCC was founded by eight physicians and two former journalists in April 2020, at the start of the COVID-19 pandemic in the U.S.[3] According to its co-president, Paul E. Marik, the group has a shared interest in vitamin C.[2]

"

https://en.wikipedia.org/wiki/Front_Line_COVID-19_Critical_Care_Alliance#cite_note-fringedocs-3 

2020 (May 06) - "Senate committee explores COVID-19 recommendations from local expert"

By Taurean Small Washington, D.C.

https://spectrumnews1.com/wi/madison/politics/2020/05/06/senate-committee-explores-covid-19-recommendations-from-local-expert 

2020-05-06-spectrumnews1-com-senate-committee-explores-covid-19-recommendations-from-local-expert.pdf

2020-05-06-spectrumnews1-com-senate-committee-explores-covid-19-recommendations-from-local-expert-img-1.jpg

WASHINGTON (SPECTRUM NEWS) — Sen. Ron Johnson, R-Wisconsin is hoping lessons learned so far could steer the conversation about what the federal government should do next about the coronavirus pandemic.

But he’s cautioning his fellow lawmakers and the White House against acting out of fear rather than facts.

“We should take that new data into account in terms of how we modify our policy,” said Sen. Johnson during a virtual hearing for the Senate Homeland Security and Governmental Affairs Committee. “We have to look at the totality of the harm being done and not only just the tragedy from the standpoint of lives lost and lives destroyed but also the economic destruction and the human toll that is taking as well.”

Johnson opened the hearing by comparing COVID-19’s impact to other diseases and causes of death like influenza and cancer.

“I think those numbers are important to keep in mind as we eventually find out what the actual infection fatality rate, which as the denominator grows and that infection fatality rate decreases, hopefully some of the fear will be reduced,” said Sen. Johnson. “I'm not saying the fear is irrational — it’s absolutely legitimate — but in order to really regain our economy [and] open back up, we need to look at it from a proper perspective.”

But ranking Democrat on the committee Sen. Gary Peters, Michigan maintained the US’s struggle with disseminating medical and PPE supplies and testing capabilities show we’re not ready to let down our guards just yet.

“I'm ready to start getting America back to work but we need a clear plan backed by science and data,” said Sen. Peters.

Dr. Pierre Kory, the Critical Care Service Chief at the University of Wisconsin School of Medicine and Public Health was among the witnesses called to testify before the committee.

Johnson said he was invited because he’s one of the frontline specialists calling for the removal of red tape on medical solutions. 

"We are dismayed by the lack of proposal for an effective treatment protocol,” said Dr. Kory.

According to Dr. Kory, the current national medical directive is solely focused on supportive care.

He and a group of critical care specialists recently released their own recommendation

They want the Trump administration to green light their plan for early intervention protocols they believe would reduce the need for ventilators and ultimately prevent deaths.

“The lack of steroids may be a critical absence in the treatment strategies of these patients,” said Dr. Kory. “[And] the other thing that we’ve seen all around the world in many institutions and medical journals and editorials is this constant cry for randomized control trials or prospective trials. We, in our group, we all know the critical need for data and trials but we think there’s an over-emphasis.”

Johnson said he has sent Kory’s protocol to the White House for the president’s consideration.

“I sent it to [Chief of Staff] Mark Meadows today with the text: ‘I pray somebody will pay attention to this,” said Sen. Johnson.

The House is pressing oversight as a major part of its next steps in addressing this pandemic.

Likewise, Sen. Kamala Harris, D-California directly called on Sen. Johnson during Wednesday’s hearing to ask current high ranking officials to testify before his committee immediately.

“Our committee has the responsibility for oversight of all of FEMA that we bring current administration officials in to discuss with us what their plan is for the administration of taxpayer dollars,” said Sen. Harris. “And at the [Senate] Health Committee, they’re having Dr. [Anthony] Fauci (director of the National Institute of Allergy and Infectious Diseases) come. They’re having the point person at the top level of the administration. We should do no less."

2020 (May 25) - Death of George FLoyd

2020 (May 29 (estimated)) - Dr Kory is asked to provide an assessment paper of George Floyd death

2020 (June 08) - Dr Kory's assessment paper of George FLoyd death is completed and submitted

2020 (July 02)

https://www.newspapers.com/image/670557442/?match=1&terms=%22pierre%20kory%22

2020-07-02-florida-today-pg-a12.jpg

2020-07-02-florida-today-pg-a12-clip-kory-mayo-opinion.jpg

Note  - On July 8, the article was repeated elsewhere - https://www.newspapers.com/image/847490463/?match=1&terms=%22pierre%20kory%22 

Evdn USA today - https://www.newspapers.com/image/671246782/?match=1&terms=%22pierre%20kory%22 

2020 (August 05) - NYTImes : "The Covid Drug Wars That Pitted Doctor vs. Doctor;  How much freedom should front-line clinicians have in treating Covid-19 patients with unproven drugs? The question opened up a civil war in some hospitals."

https://www.nytimes.com/2020/08/05/magazine/covid-drug-wars-doctors.html

2020-08-05-nytimes-magazine-covid-drug-wars-doctors.pdf

2020-08-05-nytimes-magazine-covid-drug-wars-doctors-img-1.jpg

Image caption : In the absence of conclusive research for Covid-19 treatments, many doctors are having to rely on their experience to make judgment calls about medications.Credit...Adam Ferguson for The New York Times

Mangala Narasimhan, an intensive-care-unit doctor, started feeling impatient soon after the start of a meeting she attended at Long Island Jewish Medical Center on May 13. She wanted to get back to the unit, but instead she was sitting in a conference room with about a dozen colleagues. By then, the surge of Covid-19 cases, the waves of suffering that had crashed down on her hospital for months, was beginning, miraculously, to recede. The throngs of out-of-town health care workers who had come to New York City to help were also diminishing, heading home to regions whose own times would come. Narasimhan and her team now had fewer hands to oversee new patients coming in and the long-suffering ones on ventilators who were still in need of meticulous care. Long Island Jewish, in Queens, had, at the time, treated more Covid-19 patients than any other hospital in the country; the doctors there were still weary, still battered, their energy and time in need of careful rationing.

Narasimhan, who was in charge of more than 20 I.C.U.s across the Northwell Health system, knew heading into the meeting that it might be tense. Adey Tsegaye, a pulmonary-critical-care doctor who was calling in remotely, shared some of Narasimhan’s concerns. The meeting’s agenda included time for remarks from Alex Spyropoulos, a lead researcher at the Feinstein Institutes for Medical Research — the research arm of Northwell — who was running a clinical trial. The research was trying to determine whether a standard dose of an anticoagulant or a higher dose yielded better outcomes for Covid-19 patients who were already on oxygen or a ventilator and were at high risk of organ failure and clotting.

A doctor on Narasimhan’s unit had recently been at odds with a member of Spyropoulos’s research team. Stella Hahn, a pulmonary-critical-care doctor, arrived at work the day before the meeting to find that a Covid-19 patient had gone into cardiac arrest. She knew that the patient was enrolled in the clinical trial and had been randomly assigned to receive either the standard dose of the anticoagulant or the higher one. As is always the case in the most rigorous trials, neither the patient nor Hahn was supposed to know to which group this woman belonged. Double-blind, randomized, controlled trials — R.C.T.s — are considered the gold standard in research because they do not allow findings to be muddied by any individual doctor’s biases or assumptions. But Hahn believed that the patient’s condition now called for the higher dose, which could potentially require the patient’s removal from the trial.

Image

Alex Spyropoulos, a lead researcher at the Feinstein Institutes for Medical Research.

Credit...   Adam Ferguson for The New York Times

Word made it back to a doctor working with Spyropoulos, and that doctor called Hahn to urge her to reconsider, or at least to get more tests before acting. They exchanged heated words, as the colleague implored her to stay the course. Hahn pushed back: She had to rely on her clinical judgment and believed that it was unethical to wait for more information. How could researchers dictate care to a doctor right there at the bedside, especially when a patient’s condition was so dire?

The point of contention would be discussed at the May 13 meeting. Dozens of doctors from the Northwell system videoconferenced in, including Spyropoulos, who was seated in his home in Westchester. Hahn’s colleagues, a tightknit unit who had seen one another through so much, sat together in the conference room, occasionally checking their phones or exchanging glances as the meeting went on. As Spyropoulos recalls, he talked to the group about the importance of high-quality, randomized trials in making scientific progress, and the risks of trying experimental treatments without them. “I stressed to the group that we should not abandon this principle, even in the very stressful environment of a pandemic that was overwhelming our hospitals at Northwell,” he said. Relying on gut instinct rather than evidence, he told them, was essentially “witchcraft.”

Inside the Public Hospitals Trying to Save New York

For Tsegaye, the word landed like a blow. “There was a chill in the air,” said Tsegaye, who registered it even by videoconference. “Followed by rapid backpedaling.” Spyropoulos quickly explained that he had so much respect for what those doctors had done — he had not been in those critical-care units, in the emergency room, which he knew were unlike any other he had ever experienced. “But it was like a retraction sent to the newspaper the next day,” Tsegaye said. “The headline says it all. The retraction the next day? It doesn’t have the same impact.”

In the days to come, whenever Tsegaye thought about what Spyropoulos said in that meeting, she felt appalled all over again. She knew that she had never extended herself on behalf of her patients the way she had since March. She kept flashing back to a day when she was told that a ventilated patient’s endotracheal tube had fallen out, a situation that can be fatal for the patient and is also dangerous for the physician: Replacing it requires the doctor to come into close contact with the patient’s breath. Tsegaye was putting on her N95 mask to enter the patient’s room when its elastic snapped in two. There was no time to go to the supply area to get a new mask. What was the right thing to do? With a sense of dread, she found her feet and moved toward the patient’s room. As she prepared to enter, one of her fellows, whose mask was intact, told her to leave — she could manage it on her own.

Looking back, Tsegaye felt that the agony of making those kinds of decisions all day long compounded the grief she felt while treating so many patients she could not help. “These are the decisions we have had to face,” Tsegaye said. “For someone like me, who had been in that situation, to have someone tell you that you have been practicing witchcraft is kind of giving no value to the sacrifice that I have made — that my colleagues have made.”

Image

Stella Hahn, a pulmonary-critical-care doctor at Long Island Jewish Medical Center.

Credit...   Adam Ferguson for The New York Times

Image

Mangala Narasimhan, a doctor who is in charge of intensive-care units throughout the Northwell Health system.

Credit...   Adam Ferguson for The New York Times

As doctors face new spikes of Covid-19 cases around the country, they are also confronting a harsh reality: The virus’s deadly secrets remain largely intact. The medical community now has some research-backed drug treatments — remdesivir, an antiviral drug found to shorten hospital stays, and dexamethasone, a cheap, readily available steroid that seems to cut deaths of patients on ventilators by a third. But six months after the first patient tested positive on the West Coast, there is still no treatment that reliably slows progression of the illness, much less a cure. In July, the number of patients dying in this country topped 1,000 five days in a row, according to the Covid Tracking Project.

In these early months, doctors have faced two unknowns in trying to fight the devastation. The first is the virus itself: deadly, contagious and entirely novel. The standard of care for most intractable illnesses develops over years, as doctors build a body of research that tests various theories, compares and contrasts dosages, measures one drug’s power against another. Here doctors were starting from scratch: Any treatment protocol beyond supportive care — oxygen, hydration, antibiotics and ventilation — was conjecture. The second, equally novel challenge has been the sheer scale of the outbreak. Few doctors in this country had encountered the overwhelming volume of patients, the sense of helplessness, the exhaustion and the desperation to save lives. Hospital administrators found themselves plunging headlong into making difficult decisions in the absence of strong, unifying federal guidance. Most did so without the benefit of perfectly parallel case studies or personal experience in hospitals so overrun by suffering.

When there is no precedent, when there is an information vacuum, decisions are inevitably subject to challenge. In an already heated environment, some of the worst of the tensions played out between research-oriented doctors and those who saw themselves primarily as clinicians. Many treating patients on the floor considered it axiomatic that, with so many dying so fast and so little to go on, they would rely on their experience to make judgment calls about treatment options. They would try using medications that had been approved for other illnesses but not yet for this one — what the medical community calls off-label uses — if they felt they had good reasons to do so. They would take into consideration any information that was available: the observations of doctors in Milan and China, conversations among doctors in WhatsApp group texts and in Covid-19 physician Facebook groups, tidbits of research that made medical sense but had not yet been peer-reviewed.

Image

Remdesivir, an antiviral drug found to shorten hospital stays.

Credit...   Adam Ferguson for The New York Times

Other clinicians, and especially doctors more heavily involved in research, were frustrated that many of their colleagues were not sufficiently invested in the importance of empirical research to figure out which treatments worked best and were safest. Kevin Tracey, president of the Feinstein Institutes, tried to emphasize to the doctors affiliated with the Northwell hospital system that if they were going to try drugs off-label, they should always be doing so in the context of a clinical research trial: The drug might help some patients but could hurt even more of them. If that was the case, it was better to know than to operate out of a mix of hope and conviction. He understood, he said, the impulse for doctors to try drugs off-label out of compassion — and the “raw emotion of humans trying to help each other survive and not knowing what to do.” But he did not approve of it. “Emotions cannot carry the day,” he said. “You need evidence-based medicine, and you need clinical trials. You don’t make an exception in the middle of a pandemic.”

Ethan Weiss, a cardiologist at the University of California, San Francisco, who specializes in metabolic research, spent two weeks treating patients at a hospital in New York and was also distressed by how quickly doctors were trying untested therapies outside clinical trials. “I mean, it felt like it wasn’t even World War I medicine,” he said. “It was almost like Civil War-level medicine.” He asked that the name of that New York hospital be withheld out of respect for his colleagues, whom he knows were not only risking their lives but were also overwhelmed by their clinical demands and had no research to rely on. He nonetheless was surprised to see many of them making decisions “based on the sort of opinion or written protocol of one or a couple of people that was based on kind of nothing that I could see, other than just, ‘This seems like a good idea.’”

Many clinicians on the ground felt the urgency of treating the hundreds of patients dying in front of them; researchers, with their literal and intellectual distance from the I.C.U., were pressing them to think about the thousands of patients who were sure to follow — to slow down long enough to build a body of evidence that they knew with more certainty could help. The tensions between these two ways of thinking about medicine have always existed. But during the early months of the pandemic, the disagreements — what one critical-care doctor called, on his well-read blog, the profession’s “intellectual food fight” — provided another layer of painful stress to some doctors already near their limits. “It became like Republicans and Democrats,” said Pierre Kory, a critical-care doctor who faced that tension himself at the University of Wisconsin Hospital and Clinics. “The two sides can’t talk to each other.”

Image

Dexamethasone is a cheap, readily available steroid that seems to cut deaths of patients on ventilators by a third.

Credit...   Adam Ferguson for The New York Times

As they prepare to evaluate a given medication or procedure, researchers are expected to approach their task with a certain neutral mind-set. The official term for that stance sounds both scientific and strangely poetic: “clinical equipoise.” It’s a point at which a doctor’s curiosity is greater than her conviction that any one result is the most likely one. Clinical equipoise is an elegant characterization of a humble admission: I have no idea which of these two choices is better.

Equipoise gave way to unbridled enthusiasm among some physicians at Lenox Hill Hospital on the Upper East Side of New York in April when the city was in the thick of the surge. Many doctors there believed they were seeing great results by providing tocilizumab, an anti-inflammatory drug that tamps down the autoimmune response and is used for rheumatoid arthritis. The doctors were prescribing the drug, sometimes in conjunction with a steroid, to Covid-19 patients, particularly those who were not yet on ventilators but whose blood tests suggested that they were about to take a turn for the worse. In using it, doctors hoped to stave off what’s known as a cytokine storm, a potentially deadly immune-system overreaction in which a torrent of cytokines — proteins that can trigger infection-fighting forces — is released. Tocilizumab, which blocks the pathway of a cytokine called IL-6, might prevent that deadly storm from gathering force. But any anti-inflammatory carries risk, because in fighting inflammation, it can also hamper the body’s ability to clear the primary infection or others that follow; tocilizumab is also thought to carry some elevated risk of anaphylactic shock and lower-intestinal perforation.

Image

Tocilizumab, which might help prevent a potentially deadly immune-system overreaction but carries the risk of hampering the body’s ability to clear infections.

Credit...   Adam Ferguson for The New York Times

Patients with extreme flu in the I.C.U. sometimes received tocilizumab; it is also used to treat cytokine storms that some cancer patients experience as a side effect of treatment. Doctors at Lenox Hill did not believe it was a leap to think that the drug could address cytokine storms in Covid-19 patients. They knew that doctors in Milan were leaning heavily on the drug; they were in conversation with doctors at Yale New Haven Health, considered a fortress of research-heavy medicine, which also incorporated tocilizumab into their protocol. In addition, some small studies showed support for the drug’s effectiveness, though none were randomized, controlled trials.

“I understand that it has never been trialed,” John Boockvar, a neurosurgeon at Lenox Hill who is affiliated with the Feinstein Institutes, told me in late April. (Boockvar is one of the doctors featured on the documentary series “Lenox Hill.”) “But there is clearly enough data to support its use.” The doctors at Lenox Hill had also briefly participated in a randomized, controlled trial for another drug with a similar mechanism, called sarilumab. But to Boockvar, enrolling a patient in that trial, which might result in a patient receiving a placebo, posed an ethical challenge when he could simply prescribe tocilizumab — doctors refer to it as toci — instead. In April, he learned that Massachusetts General Hospital was starting a randomized, controlled trial for tocilizumab. “If that was my loved one,” he said, imagining a family member who might receive a placebo in that trial, “I’d be upset. I’d think, Why am I doing this? If it’s an off-label use with an approved drug — give the damn drug to everybody.”

At Long Island Jewish, some doctors who were hearing about the drug from colleagues at Lenox Hill, a part of the Northwell Health consortium, started clamoring for liberal access to it. And yet sometimes, when doctors placed orders with the hospital pharmacist, their prescriptions were declined; those patients didn’t meet criteria Northwell had established for administering tocilizumab, which was in short supply. Physicians were frustrated that patients who they believed would benefit from the drug could not receive it. Northwell wanted to be conservative about the off-label use of drugs outside clinical trials. “There’s no proof that anything works!” Tsegaye thought at the time. “Everything is experimental!” As for enrolling patients in a trial, as overwhelmed as she was, she hardly felt she was in a position to take that on.

Tsegaye’s supervisor, Narasimhan, also knew researchers were concerned that in prescribing tocilizumab so readily, physicians were possibly hampering enrollment in the trial underway at her hospital for sarilumab — a patient who received tocilizumab could not also receive sarilumab. She and her team did not prioritize the trials, she said; they wanted to provide the drugs they thought were needed. “We’ve always been allowed to choose treatment, right or wrong, based on what we thought was best,” Narasimhan said in May. “And that was gone. It was hard.”

In addition to fighting resistance from their administrators, the doctors were sometimes also at odds with their colleagues, especially infectious-disease doctors, many of whom believed that anti-inflammatories like tocilizumab and steroids could do more harm than good. “You’re killing these patients,” one infectious-disease doctor told Hahn at Long Island Jewish.

Image

Adey Tsegaye, a pulmonary-critical-care doctor at Long Island Jewish Medical Center in Queens.

Credit...   Adam Ferguson for The New York Times

In the Mount Sinai Health System, tocilizumab was also in demand. Administrators felt the stress of making decisions in the absence of clear data. Judith Aberg, the chief of the division of infectious diseases for Mount Sinai, fielded demands from doctors working on wards who wanted to use tocilizumab, early and often. “I have to give her credit; she was single-handedly fighting off a lot of pressure from hematologists,” said Keren Osman, a Mount Sinai oncologist and hematologist who was on some of those calls. As experts in blood cancers and diseases, hematologists had experience working with tocilizumab to treat cytokine storms that were a side effect of some cancer treatments. “She was saying, ‘I’m not comfortable just giving patients willy-nilly anything we have — we don’t know.’”

Patients and their families, who heard through the news media about the drug, also started to demand it, even for Covid-19 patients whose inflammatory markers were normal. “People were calling for us to give it, just to give it, because there were no other therapies,” Aberg said. At first, a medical team that included Aberg agreed to put some patients who were on ventilators on the drug — in those patients, it was obvious that systemic inflammation was already evident; also, the closer the patient was to dying, the more the risk seemed justified. Eventually, the thinking at Aberg’s hospitals and at others evolved to favor use of the drug earlier, before systemic inflammation did so much damage that the patient was already clinging to life.

By May, doctors at Long Island Jewish and Mount Sinai had stopped pressing for tocilizumab — if it was effective, it was not such a miracle drug that they could see its effects clearly. Many had started to pin their hopes instead on convalescent plasma, another experimental treatment in which sick patients are given plasma from recovered patients with antibodies, though its effectiveness is still unknown. “We did rush,” Aberg says now. “I mean, we were pushed. We were grasping for anything that we could possibly do.”

In early July, the drug company studying sarilumab, the drug similar to tocilizumab, announced that it was halting its trial; researchers found, as Aberg put it, “nada.” A few weeks later, the pharmaceutical company Roche announced preliminary results of a tocilizumab trial that was run on Covid patients with pneumonia. The drug’s effects were no better than a placebo. By then, Narasimhan was also starting to see preliminary reports of other research that showed the drug could, in fact, be dangerous, increasing the risk of fatal secondary and fungal infections.

“My take-home is that I wish we had done more randomized, controlled trials so we could have some real answers, so that we could tell Florida and Texas, ‘This works, and this doesn’t work,’” Narasimhan, who is now in charge of intensive-care units throughout the Northwell Health system, told me in July. “We could have had so many more answers in a way that was meaningful. We had this fixation that all these drugs were curative. And they weren’t.”

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Hydroxychloroquine, the drug that President Trump claimed was a “game changer” in mid-March.

Credit...   Adam Ferguson for The New York Times

The story of hydroxychloroquine will most likely be recalled as a classic medical parable of the pandemic. It was a drug that seemed so promising that physicians were desperate to use it, and researchers were equally driven to see if it actually delivered the hoped-for results. In the end, the enthusiasm of the first camp most likely slowed the speed with which the second could study the drug — only to find that the enthusiasm was never really justified in the first place.

In mid-March, Steven Libutti, director of the Rutgers Cancer Institute of New Jersey, read about a small hydroxychloroquine trial in France that was generating attention, having found that the anti-malarial might be effective in the treatment of Covid-19. “It looked interesting, exciting, promising, but it looked very far from convincing,” Libutti said. Although his specialty is cancer, he wanted to bring his extensive research knowledge to bear on the pressing question of the drug’s effectiveness. He wrote a proposal for a randomized, controlled trial that would measure the effectiveness of hydroxychloroquine on a patient’s viral load. (He was comparing the effect of the drug alone with placebo, as well as with the drug when administered with another drug called azithromycin.)

The Food and Drug Administration and the ethical review board at the Rutgers Cancer Institute approved his trial in record time, as has been typical for many proposed drug trials during the pandemic. He enrolled the first patient on April 1, hoping he could easily reach 150, calling on doctors to recruit patients at six hospitals in New Jersey.

By then President Trump had claimed in mid-March that the drug was a “game changer.” Some doctors in New York were quietly taking it prophylactically. That month, the F.D.A. authorized hydroxychloroquine for emergency use, a special dispensation that facilitated doctors’ access to the drug even outside the context of a trial. Many New York hospitals’ standard treatment protocols encouraged doctors to consider hydroxychloroquine for patients, even though the evidence that it worked remained slim and reports were emerging that in some patients it was causing heart problems.

Thousands of patients were pouring through those six New Jersey hospitals, but Libutti waited, for weeks, with great frustration as only a handful of patients were enrolled in his trial each day. Typically, in clinical trials, after a patient is admitted to the hospital, a doctor or nurse, often affiliated with the research, talks to the patient about the possibility of enrolling in a clinical trial. But Libutti’s team was finding that by the time a nurse could begin the conversation with the patient, that person had already been administered hydroxychloroquine — which meant the researchers could not get a baseline reading of that patient’s viral load. Patient after patient was disqualified from the study. They had “been handed hydroxychloroquine along with their toothbrush and slippers when they got to the emergency room,” Libutti told me. “They were giving it out like dinner mints.” The researcher said he “was shocked by the number of folks whom I thought were incredibly well-read, knowledgeable physicians but were just panic-prescribing hydroxychloroquine. I’ve never seen anything like it. It just shows how lost in the storm folks were.” (Michael Steinberg, who helps oversee trials as well as clinical care at Robert Wood Johnson University Hospital, which was involved in Libutti’s trial, said that although physicians use their clinical judgment to make decisions about treatment, they strongly encourage doctors to use evidence-based criteria.)

Other doctors shared Libutti’s experience. Arthur Caplan, a bioethicist at New York University’s medical school, said he is aware of three medical centers where researchers trying to study hydroxychloroquine felt that the early ardor for the drug among doctors and patients made it difficult for them to recruit subjects — to determine, essentially, whether the embrace of the drug was at all justified. Caplan and a colleague argued, in an article published online in April in The Journal of Clinical Investigation, that “panicked rhetoric about right-to-try must be aggressively discouraged in order for scientists to learn what regimens or vaccines actually work.” Communicating directly with doctors at various hospitals who were making the drug part of the official protocol, he used more plain language: “This is nuts!”

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Michelle Ng Gong, the director of critical-care research for the Montefiore Health System in New York.

Credit...   Adam Ferguson for The New York Times

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Steven Libutti, the director of the Rutgers Cancer Institute of New Jersey.

Credit...   Adam Ferguson for The New York Times

The Montefiore Health System in New York was one of the many that included hydroxychloroquine as an option in its treatment protocol, starting in late March. Michelle Ng Gong, the director of critical-care research, did not actively fight to have the drug removed from the protocol. But when she was working in her capacity as a critical-care doctor, she does not recall ever prescribing the medication, and she sometimes took patients who had received it in the emergency room off it. “When so many people are dying, you want to do something,” she said. But very sick patients are more susceptible to adverse events. “The problem is that we know from critical-care literature, as well as trials in the past, that we can always do more harm.”

In the end, the biggest randomized, controlled trial on hydroxychloroquine came out of Britain in June, and preliminary results found that the drug was not an effective treatment for Covid-19. In contrast to American doctors whose access to the use of the drug, even outside trials, had been eased by a federal agency, British physicians were given the opposite message. On April 1, the highest medical officials in England, Wales, Northern Ireland and Scotland each sent a letter to every hospital in their respective countries, urging doctors not to prescribe medications off-label outside trials. Instead they encouraged doctors to enroll their patients in large, multicenter, randomized, controlled trials, like a study run by the University of Oxford called Recovery, which looked at the efficacy of hydroxychloroquine, tocilizumab, convalescent plasma, dexamethasone and two other treatments. At some hospitals in Britain, as many as about 60 percent of patients were enrolled in Recovery trials; even the Northwell system, which is committed to research, was able to enroll, at its most trial-driven hospital, North Shore University Hospital, around only 20 percent of its patients in clinical trials.

A flood of patients all with the same illness presents logistical challenges to trials, but also the perfect conditions for them; that the American medical system could not harness more of those patients into randomized, controlled trials, said Peter Horby, one of the two chief investigators for Oxford’s Recovery trials, represents a lost opportunity. Whether or not convalescent plasma actually helps patients, for example, has not yet been resolved by a randomized, controlled trial despite the tens of thousands of doses that American patients have received, numbers that dwarf those in Britain. Given those numbers, American researchers “could have nailed it by now,” said Horby, whose own trial on convalescent plasma is still underway.

Caplan, the N.Y.U. bioethicist, acknowledges that doctors in the United States did manage to enroll more patients in trials more quickly than ever. But even still, he believes that the commitment to long-shot efforts to rescue patients was stronger than the commitment to science, which slowed results and possibly cost more lives. “We did a lot,” he said. “But we could have gone faster and resolved questions sooner.”

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Convalescent plasma, another experimental treatment in which sick patients are given plasma from recovered patients with antibodies, though its effectiveness is still unknown.

Credit...

Adam Ferguson for The New York Times

If researchers see hydroxychloroquine’s failure as a cautionary tale about the perils of acting without evidence, Pierre Kory, the Wisconsin critical-care doctor, sees a different medical lesson emerging from the pandemic: that the emphasis on randomized, controlled trials can get in the way of doctors’ providing common-sense, lifesaving treatments.

In April, supportive care alone was considered the best option for patients with Covid-19, given that there was no evidence yet to back other treatments. Kory, who was then the chief of critical-care service at the University of Wisconsin Hospital and Clinics, believed instead that medications commonly used in critical care would most likely help critically ill Covid-19 patients, too. That month, at a well-attended meeting with fellows, residents and leadership, including Lynn Schnapp, the chair of the department of medicine at the University of Wisconsin medical school, Kory suggested an approach that went beyond supportive care. He had been consulting with senior hematologists at the hospital and had observed alarming blood clotting in Covid-19 patients. He and the hematologists proposed that the hospital consider administering an aggressive dose of anticoagulants to patients whose blood tests showed elevated risks for clotting. (Many medical-society guidelines that once called for only supportive care now recommend the use of anticoagulants in Covid-19 patients, but not in doses as aggressive as those that Kory and specialists at the hospital had proposed.)

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Heparin, an anticoagulant now recommended by many medical-society guidelines in the treatment of Covid-19.

Credit...   Adam Ferguson for The New York Times

The meeting among Kory and his colleagues took an adversarial turn. “No one else is doing this,” said Lynn Schnapp, as Kory recalls. (She denies saying that, although a former colleague of Kory’s who attended the meeting confirmed Kory’s account.) “There is no evidence,” a fellow I.C.U. doctor said more than once, her voice raised. Kory, who pointed out at the meeting that his suggestion was based on the opinion of the hospital’s own experts, says he fired back with equal intensity. “And this is Wisconsin,” he told me. “People don’t yell here.” Other colleagues who were supposed to jump off the call to attend another meeting later confided to Kory that they couldn’t bring themselves to leave, for fear of missing out on this unusual hospital drama.

At a subsequent, smaller meeting, Kory brought up with Nizar Jarjour, a division chief, the possibility of giving steroids, commonly used on critical-care patients, to Covid-19 patients in the I.C.U. “I don’t want to talk about it,” Jarjour said.

In a lengthy email Jarjour later sent me, he explained that open discussion was welcome during that period of time; he also sympathized with the sentiments of the I.C.U. colleague who was urging caution while facing a novel virus.

Corticosteroids have a complicated and controversial history in critical-care medicine. Numerous trials over the past 50 years have been conducted on their efficacy in patients with acute respiratory distress syndrome, or ARDS, a diagnosis for patients who have reached a stage of perilous respiratory failure. Because many of those patients at that stage of illness have confounding factors, findings are far from definitive. But based largely on some meta-analyses, including those looking at how patients with MERS and SARS fared, the World Health Organization advised, early in the pandemic in this country, against the use of steroids in Covid-19 patients experiencing ARDS, which is to say, most patients on ventilators.

Kory and several colleagues at hospitals around the country noted that the studies that the W.H.O. cited, for example, were largely not randomized and controlled; other relevant institutions like the Society of Critical Care Medicine, whose doctors treat the most ill patients, and the European Society of Intensive Care Medicine did recommend the use of steroids for ventilated Covid-19 patients with ARDS. Also, in Kory’s own clinical experience, corticosteroids could be lifesavers. He did not see them as a wild-card drug for this disease, like hydroxychloroquine; he used them for non-Covid-19 patients who were facing cytokine storms or ARDS. He was surprised by the heat with which colleagues challenged him when he made the recommendation, and he believed that his own leadership role in conference calls subsequently diminished. He and Jarjour, he said, had more disagreements in three days than they had in the previous five years.

On April 7, Kory’s colleague Ellie Golestanian sent an email to Kory and others, at 1:32 a.m., in response to another colleague’s call for the use of corticosteroids and anticoagulants: “In patients with severe Covid-19, we are fumbling in the dark, clutching at anything that might work. But as you are well aware, just because a therapy ‘should’ work, or we desperately ‘want’ it to work — it does not follow that it ‘will’ work.”

“When I hear stuff like corticosteroids described as experimental and unproven, I want to jump out a window,” Kory told me later that month. “They make it sound like we are experimenting on people. I want to be respectful of my colleagues, but I feel like they are getting it 100 percent wrong. I’ve never seen smarter people get a problem more wrong. Because they are running hypotheses in a lab and so many of them fail, they think when I approach a patient, I am testing out a hypothesis. It’s not like a hypothesis, but more like a problem, and I have to figure out how to fix it with a couple of decades of experience to back me up. It’s a stretch to call it a hypothesis. It’s just me doctoring.”

Kory was so frustrated about the hospital’s approach that in May he resigned, taking a job instead at Aurora St. Luke’s Medical Center in Milwaukee. “Our differences were so far apart, I felt I couldn’t be a part of it,” said Kory, who foresaw, in April, a “catastrophe” if doctors at any hospital could apply only supportive care. A colleague of his in New York, an I.C.U. doctor affiliated with a major medical center, confirmed that he, too, resigned from his hospital, in part because of tensions around his decision to try an F.D.A.-approved medication off-label and outside a trial. In May, Kory, following his disagreement in Wisconsin, spent several weeks in New York treating patients, often with steroids.

In June, Oxford posted a preliminary report for its Recovery trial of more than 6,000 patients who received either standard care or dexamethasone, a steroid similar to the ones that Kory and other I.C.U. doctors had been advocating. At least when administered to patients who were already on oxygen or ventilators, the drug saved lives.

Why We’re Losing the Battle With Covid-19

July 14, 2020

Kory sees, in the Oxford results, a story of triumph. He believes that he successfully treated patients with steroids and that the Recovery trial results prove it. And yet if patients did not respond, he would go further, increasing the dose, in a few instances, to a level 10 times as strong as that in the trial. Did the higher dosage increase the risk? The answer to that question, a research purist like Kevin Tracey would point out, is still unknown. Despite the enthusiasm for the Recovery trial, Tracey maintains that even one stellar randomized, controlled trial does not settle the question of the use of steroids for patients with Covid-19. “It needs to be replicated,” he said. Given the long, complicated history of steroid studies, he predicts that sometime down the road another statistically powerful randomized, controlled trial will yield contradictory findings. In Tracey’s reservations, Kory sees not rational evaluation but bias. “That’s a 6,000-person trial he’s discrediting,” Kory said. “That’s a person who will never be convinced.”

Kory is also part of a group of critical-care doctors who widely disseminated a protocol for treating Covid-19 that includes anticoagulants and steroids but also other treatments — including Pepcid and intravenous vitamin C — whose efficacy is hotly contested among doctors.

Should Kory and his colleagues have been administering steroids when they did? Were they right? Kory thinks so. But Eric Rubin, the editor of The New England Journal of Medicine, thinks it’s not so clear-cut. “You could also say he was lucky,” Rubin said.

At times, over the course of several conversations, Rubin defended the bond between doctors and patients, the need for physician autonomy, the necessity of making judgments in the absence of evidence, especially when mortality rates were so high; at other times he seemed frustrated that doctors were still relying on treatments for which there was no evidence, concerned that a lack of equipoise had possibly muddled the course of research. “I know I seem to be saying opposite things,” he admitted. “And I agree with myself.”

Rubin is an infectious-disease doctor at Brigham and Women’s Hospital in Boston, and like many doctors in that specialty, he had strong reservations about steroids. He advised colleagues against using them. “And I was wrong,” he said. He also acknowledges that he was less opposed to the use of tocilizumab, although that, too, was untested and could also increase the risk of infection. I asked him whether perhaps there was something about tocilizumab’s novelty, even its scarcity, its high price, that may have given it a sheen of credibility? In the absence of evidence, we are all susceptible to predictable irrational biases. “We know less about toci,” is how Rubin said he thought about it at the time: It left open the possibility that it could be helpful, although of course that means it also left open the possibility that it could do more harm than supportive care, more harm even than steroids. Unlike steroids, tocilizumab was not yet the devil he knew. Rubin could see, months later, his decision-making process with humility. “I can’t argue that I was super rational either,” he finally said.

‘In patients with severe Covid-19, we are fumbling in the dark, clutching at anything that might work.’

At the peak of the surge, Rubin was far from the only doctor whose usual commitment to evidence faltered. “There would be a physician that would have said, ‘No, no, no,’ and all of the sudden, it’s his mother,” Aberg, the Mount Sinai doctor, told me. “All of a sudden, let me tell you, they wanted everything. We had some of our own physicians admitted, and people were just crazed about what they wanted to do to those individuals.” Kevin Tracey, the Feinstein researcher, says that overwhelming uncertainty was driving people’s reactions: “We just lived through a plague. It was life and death. Fear. Ignorance. You were seeing raw human behavior in survival mode, a classic reaction to threat.”

In recent months, a relative calm has set in. Since that tense mid-May meeting between the researcher Spyropoulos and his colleagues on the ground at Long Island Jewish Medical Center, clinicians and researchers have forged more compromise through a series of conversations. Looking back at that time, one critical-care doctor mentioned that Spyropoulos, when he called in by videoconference that day, seemed tired and stressed; perhaps, the critical-care doctor thought, that accounted for why Spyropoulos had spoken so harshly to the group.

Spyropoulos, the director of the anticoagulation program at Northwell, had in fact been working 19-hour days to try to get the trial up and running at breakneck speed. He also mentioned to me in passing, during an interview, that both he and his wife had been sick with Covid-19, his wife more so than him. Perhaps, like many doctors, he was laboring under the additional stress of having not just a professional but a deeply personal struggle with the power of the disease. In response to a text I sent asking about the extent of his wife’s illness, Spyropoulos wrote back on July 11. “My wife was very sick and bedridden for 3 days (I was mildly symptomatic) but she responded well to hydroxychloroquine,” he wrote.

His casual certainty about the cause and effect of her recovery was surprising. His wife had been ill, taken hydroxychloroquine and recovered. Whether the second event caused the third was at best unknown but statistically unlikely, given the now-significant body of research showing that the drug does not help. As if even Spyropoulos recognized that his comment was less than rational, he went on to rehearse the argument he made to his colleagues at Long Island Jewish about the importance of relying on research. Anything else, he repeated, was witchcraft.

NOTES: 
  • A correction was made on Aug. 5, 2020: An earlier version of this article misstated Lynn Schnapp's title at the University of Wisconsin medical school. She is chair of the department of medicine, not chair of the medical school.
  • Susan Dominus has worked for The New York Times since 2007, first as a Metro columnist and then as a staff writer with The New York Times Magazine. In 2009, she was a member of a team that won a Pulitzer Prize, for breaking news, for its coverage of a scandal that resulted in the resignation of Gov. Eliot Spitzer. In 2018, she was  part of a team that won a Pulitzer Prize, for public service, for reporting on workplace sexual-harassment issues.

2020 (Dec 10)

https://www.newspapers.com/image/699103747/?match=1&terms=ivermectin

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2020-12-10-wisconsin-rapids-daily-tribune-pg-2a-clip-johnson-hearing

2020 (Dec 17) - Kory describes Ivermectin as a "wonder drug"

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2023 (Oct 22) - Substack for "pierrekorymedicalmusings" : "George Floyd Did Not Die Of a Fentanyl Overdose ; Although the American public is lied to about nearly everything at this point, the cause of Floyd's death is not one of them. I should know as I was the medical expert who testified in his civil case."

https://pierrekorymedicalmusings.com/p/george-floyd-did-not-die-of-a-fentanyl

2023-10-22-pierrekorymedicalmusings-substack-george-floyd-did-not-die-of-a-fentanyl.pdf

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PIERRE KORY, MD, MPA  /   OCT 22, 2023

Recently, Tucker Carlson, who I consider to be a highly skilled, professional, and widely respected journalist, reported that the public was lied to about the cause of George Floyd's death and that he actually died of an opiate overdose. He is apparently basing this reporting on the opinion of the Hennepin County Prosecutor Amy Sweasy who claims that Dr. Andrew Baker, the medical examiner who performed Floyd’s autopsy, withheld Floyd’s true cause of death for fear of public retaliation.

As the pulmonologist expert witness retained in the civil case, I was provided access to all of the medical evidence. I spent dozens of hours reviewing video footage, ambulance records, medical records, toxicology reports and autopsy findings. I want Mr. Carlson to understand why my interpretation of all of the available evidence (still) strongly leads to the opposite conclusion of what the medical examiner is apparently now saying. I want to state at the outset that the medical examiner’s opinion then, as well as now, did not influence my conclusion so his changing of his interpretation has little relevance.

I am curious as to whether Mr. Carlson will correct his reporting if indeed he agrees with my below interpretation as an independant medical expert.

Before I go any further, a disclaimer: I recognize that the George Floyd case is a highly divisive and emotionally charged one for countless Americans. Many are profoundly saddened and outraged over the circumstances of his death; others are convinced he died of a drug overdose or believe he deserves little sympathy given his criminal background. Plenty are angered by the often supportive media coverage of the subsequent and sometimes violent Black Lives Matter movement protests.

So let me be clear: I am not a lawyer, a prosecutor or a judge. I am not a political scientist, or a sociologist, or a psychologist. I was not asked to deliver a moral or character assessment of Mr. Floyd. I have never met a saint, although I have known a few people that I feel come close. I never met Mr. Floyd. I was simply asked for my expert opinion as a lung and ICU specialist as to the proximate cause of his death based on all the available evidence, of which there was an extensive amount. It was an important task and one I felt confident I was expertly suited to perform.

Know that I have for years done expert witness reviews of medical malpractice cases as I find the work both interesting and challenging. The lawyers I worked for had consistently rated my work highly thus I was consulted often. The firm representing Mr. Floyd’s family in their wrongful death lawsuit interviewed me within days of his death and I was quickly retained (as an aside, this was 5 months before I became an expert in the use of ivermectin in Covid and was subsequently punished professionally for my resulting advocacy of the medicine). Had Mr. Floyd’s death occurred after that point, I am sure I would never have been retained.

The official expert testimony I submitted (found at the end of this post) is a lengthy and comprehensively detailed document which I’m honored to say my mentor Paul Mayo called, "a master class in pulmonary physiology."

My report concluded that George Floyd didn’t die from (just) a knee on the neck nor were the drugs found in his system a major contributor. Just as with the response to the Covid pandemic, I think it is important to understand exactly what happened to Mr. Floyd so that it never happens again.

For those not interested in reading the lengthy report, I will instead focus on clarifying what I think are the two most critical misinterpretations of the available evidence that I have seen on social media and in certain press outlets.

That Mr. Floyd died of an opiate overdose due to severely elevated levels of fentanyl measured in his bloodstream as documented in his toxicology report.

In order to properly interpret the levels found, one must first recognize that chronic opiate users, which Mr. Floyd was, can and do often develop significant levels of physiologic tolerance to opiates. Thus the absolute level measured in a chronic user is not accurately predictive of the degree of intoxication or death. However, I agree that if Mr. Floyd’s level was found in an opiate-naive user, it would almost certainly predict unconsciousness and/or risk of death.

Much more important than the level of opiates found in his blood is that clinically, throughout the videotaped arrest, Mr. Floyd was conscious and able to walk and communicate clearly. Due to his known claustrophobia, he was even able to struggle with officers on two separate occasions as they tried to force him into the back of a police car. His awake and physically active state was observed up until he was placed into prone restraint for many minutes. Also, when he was first placed in prone restraint, he was clearly awake, in distress, and begging to have the pressure of the officers bodies be removed from his back and neck.

The physical and cognitive abilities exhibited by Mr. Floyd are completely inconsistent with someone severely intoxicated with an opiate. In opiate intoxication, patients are lethargic, minimally arousable, and/or exhibit slowed breathing.

As a pulmonologist expert in physical examination, I did not observe shallow or slowed breathing until he was put into prone restraint (i.e. face and chest down on a hard surface). Recall that properly trained police officers are taught to never restrain a suspect in this position, because it is well known to cause death due to the inability of a suspect to sufficiently breathe. So, although he was probably somewhat high given the fentanyl found in his system, it was not severe clinically nor did it appear life-threatening.

Third, opiate overdoses occur within seconds to minutes of IV administration and the first physiologic effect is loss of consciousness prior to breathing then slowing and the heart then stopping minutes later (in massive IV overdoses, the first two can occur simultaneously and quickly). Thus, the prolonged time between when he would have last had access to IV opiates and when he stopped breathing in prone restraint was far too prolonged to blame on an IV opiate overdose. But what about if he had swallowed a bunch of pills containing opiates as the officers were approaching just prior to the arrest?

Certainly, if it was a really large amount of pills or a very high dosage form, this could lead to an overdose, but again, the absorption of oral opiates is much much slower and, if that was occurring, would have led to a slowly progressive intoxication evidenced by gradually diminishing consciousness and clarity, loss of muscle tone/activity, and slowed breathing. Although not directly relevant nor did it figure into my conclusion, I was provided no evidence of him having overdosed in the past.

But let’s just say, for the sake of argument, that the opiates he allegedly took prior to arrest just started to enter his bloodstream during the same time period he was put into prone restraint. A couple of problems with making this argument. First, I found no report of any witness or police officer who described him swallowing pills. That supposedly happened in a prior arrest in 2019 but was not documented in the 2020 arrest. From a media report, he had “foam” around his mouth and “semi-chewed pills” were allegedly found in his car but again, even if it were true, from the above, he was not initially severely intoxicated.

Second, know that prone restraint causes carbon dioxide (CO2) to slowly rise in the suspect’s blood as a result of their inability to inhale and exhale sufficiently, a condition called “CO2 narcosis.” C02 narcosis, as the name suggests, presents identically to opiate intoxication with increasing lethargy evolving into unconsciousness, slowed breathing, and then cardiac arrest.

Thus, in order to say that he died of an opiate overdose, you have to believe that it is more likely that his (supposedly) slowly rising opiate absorption reached a critical level at the same time that he was many minutes into a breath-restricting and C02 narcosis-causing prone restraint position. This is so improbable as to be near impossible. In medical malpractice causation, the evidence standard for cause is that which is “more likely than not.” The problem with this argument is that patients whose respiratory drive is being suppressed by opiates… never complain of it (Mr. Floyd was crying “I can’t breathe” repeatedly - with each plea ignored). In contrast, opiate overdose victims first descend into a sleep-like, highly pleasurable state, and then progress into unconscious, their breathing slows, stops, and they arrest.

But there’s more to disprove opiate overdose than a compelling probability assessment.

So lets entertain this hypothesis even further. Let’s again entertain that the (allegedly) rising oral opiate absorption hit a critical level causing gradual unconsciousness perfectly timed in the middle of a prolonged, three officer-weight bearing prone restraint episode.

Here is where you need to know that in one of the videos, there is a bystander who claimed he had specific training which led him to shout at the officers, over and over, “get off his neck man, you ain’t supposed to do that, get off his neck, get off his neck, he can’t breathe” which, after Mr. Floyd lost consciousness, changed to “check his pulse, check his pulse, he ain’t breathing, check his pulse, he is dead man.”

They did not take their weight off of Mr. Floyd, either at the time or for many minutes after. This is important because opiate overdoses are easily treatable as long as you can support breathing. For instance, I have taken care of many many dozens of opiate overdoses in the ICU. As long as the unconscious overdose patient is found with a pulse or pulse can be restored with CPR, all they need is a breathing tube and mechanical ventilator support until the opiate wears off. I cannot tell you how many young overdose victims I admitted on a ventilator. The majority would wake up hours later when the opiates wore off and then were quickly discharged alive from the ICU.

Certainly an uncomfortable minority never woke up due to anoxic brain injury from being in cardiac arrest for too long prior to successful CPR. However, in Floyd’s case, that would not and should not have happened because 4 police officers trained in CPR were present at the scene and could have identified pulselessness quickly (they were being begged to do so by bystanders). So, they were right there when he lapsed into unconsciousness, and thus they could have rapidly taken their body weight off of him, identified pulselessness, and initiated CPR.

But that didn’t happen until many minutes later when an ambulance paramedic showed up on the scene and tapped Officer Chauvin’s shoulder to get him to release his knee from the neck of the lifeless Mr. Floyd (I should point out that even the paramedic did not immediately check the pulse of unconscious Mr. Floyd, which to me as an intensivist, violated medical standards).

Thus, and I don’t want to litigate this, but I believe that based on the above actions, the crime would still have been homicide/unintentional murder/3rd degree murder based on the use of an aggressive and life-threatening prone restraint along with their indifference to Mr. Floyd’s unconscious and limp body. Lastly, all of the toxicology data and medical record data were presented and argued in the criminal case, and a jury of his peers found Chauvin guilty of same.

The second misinterpreted piece of evidence is that that no damage or fracture to his trachea (windpipe) was found on autopsy thus he did not die of asphyxiation.

What you need to know is that the windpipe is only half made of cartilage/bone. The posterior half is actually made of soft tissue. Windpipes can thus be occluded easily, either with hands around the neck via strangling, or just pressure from a knee. The trachea does not have to fracture to be occluded. Heck, when I was doing bronchoscopy and my scope was in the trachea, if the patient responded with a vigorous cough, the trachea would occlude transiently due to thoracic pressure “ballooning” the posterior membranous wall to contact the anterior wall and occlude. But that occurs transiently and is of no significant consequence. So, fracture of the trachea is not required for prolonged occlusion to have occurred.

Further, it is my opinion that Mr. Floyd did not die of asphyxiation solely due to the pressure on Mr. Floyd’s neck from Officer Chauvin’s knee. Had this been the sole cause, total occlusion of the trachea via external forces would have rendered communication impossible. When Chauvin’s knee was initially placed on Mr. Floyd’s neck, he could phonate (i,.e. make sounds) given that he was recorded pleading with the officers to “get off” of him and then later, just before he became unconscious, he began calling out for his mother. This is impossible with an occluded trachea. It is also impossible in severe opiate intoxication.

Instead, my conclusion was that Mr. Floyd died by the combined forces of three officers bearing weight on his thoracic cage (upper back, lower back, and neck/throat) against a concrete surface, rendering him unable to take in sufficient oxygen or expel sufficient carbon dioxide with each breath. It is a rapidly and extremely distressing sensation to not be able to take in a sufficient volume of air with each breath. Just think back to the last overly vigorous bear hug you received and how quickly you became uncomfortable and sought release.

Ultimately, it was my determination that Mr. Floyd was slowly suffocated as a result of the combined weight of multiple officers on this thoracic cage and windpipe after being placed in the prone position. It was a severely distressing way to die.

P.S My official submitted report follows but I first want to say thanks to all my subscribers, especially the paid ones. Your financial support is greatly appreciated as it allows me to devote what is often large amount of time I spend researching and writing my posts, so again, thanks. - Pierre

GEORGE FLOYD EXPERT OPINION REPORT

June 9, 2020

Dear Ms. Roman (not the attorneys name):

You have asked me to review materials and offer expert opinions concerning the cause of death of Mr. George Floyd during his videotaped apprehension and arrest which occurred on May 25, 2020, in Minneapolis, MN.

I am a physician licensed by the States of Wisconsin and Illinois.  I am a graduate of St. George’s University School of Medicine and I completed an Internal Medicine Residency at Columbia University’s St. Luke’s-Roosevelt Internal Medicine Residency Program in New York City followed by a Pulmonary Disease and Critical Care Medicine Fellowship at The Albert Einstein School of Medicine’s Beth Israel Medical Center in Manhattan. I am Board Certified in Internal Medicine, Pulmonary Diseases, and Critical Care Medicine. I have evaluated and treated a large number of patients over the past 15 years who have presented with a myriad of respiratory ailments with a large proportion of those patients having suffered acute respiratory failure in the ICU or on the hospital wards at multiple medical centers that I have worked at. Further, I had a large pulmonary and bronchoscopy practice for almost a decade in New York City where I performed numerous interventional and diagnostic procedures in the airway and thoracic cavity. I have also served as the Program Director of a large fellowship training program at Beth Israel Medical Center in New York City for a period of 3 years prior to being recruited by the University of Wisconsin where I then served as the Chief of the Critical Care Service and the Medical Director of the Trauma and Life Support Center for the past 5 years. I am also known as one of the pioneers and world experts in critical care ultrasonography, a skill set which has led to me becoming the senior editor of the best-selling textbook “Point of Care Ultrasound” which is in its 2nd edition and has been translated into 6 languages.

My expert opinions are based upon my skill, education, training, and experience, and my knowledge of the medical and scientific literature.  I have also considered the following materials in forming my opinions in this matter:

I have found with a reasonable degree of medical certainty that George Floyd died from asphyxiation as the direct result of the use of excessive restraining force by at least 3 of the police officers who participated in restraining Mr. Floyd. The forces that caused his asphyxiation (defined as “the state or process of being deprived of oxygen, which can result in unconsciousness or death; suffocation) resulted from the simultaneous application of near full body weight pressure by two grown men of unknown weight, with one who applied pressure with both knees on his back and one with his knee on his neck/spine while he lay prone on the ground in handcuffs, with the third officer restraining the movement of his legs such that Mr. Floyd could not change this threatened position.

The foundation of this expert opinion will be detailed in the summary of the evidence along with a review of respiratory system structure and function that follows. I will state at the outset that, based on the evidence presented, I am unable to determine precisely the relative contribution of each of the injurious forces that I have identified as it is my opinion that Mr. Floyd’s asphyxiation resulted from multiple, simultaneous injurious forces which limited his ability to take in sufficient volumes of air which led to him being deprived of sufficient oxygen to sustain his life. The simultaneous forces, combined with a disadvantageous mechanical respiratory position to support breathing are as follows; 1) excessive weight pressure on neck/upper back by Officer Chauvin which limited the superior expansion of the thorax during compromised positioning while also partially or completely occluding the upper airway “windpipe”, 2) excessive body weight pressure on lower/mid back by Officer Keung whose knees were positioned on top of Mr. Floyd and which limited diaphragmatic displacement to an extent which prevented sufficient inhaled air flow and volume, and 3) the prone positioning of Mr. Floyd on the ground which subsequently compressed his chest, limiting thoracic cage expansion which would allow for sufficient inhaled air flow and volume, and 4) the immobilization of Mr. Floyd’s legs by Officer Lane, preventing him from adjusting his body position in any manner which could relieve him of the aforementioned injurious restricting forces on his ventilatory ability.

Evidence

FORCE 1: As seen on the above listed videos taken from the sidewalk side of the police vehicle, and based on identification taken from a review of newspaper reports, Officer Chauvin can be seen applying pressure using his knee positioned on the upper neck and back of Mr. Floyd for a continuous period of approximately 10 minutes and 32 seconds.

FORCE 2: Officer Keung can be seen, during a shorter video taken from the street side of the car, with his 2 knees elevated off the street and placed on what appears to be the mid-lower back of Mr. Floyd. Given the limited duration of this video, I am unable to determine the length of time that Officer Keung’s body weight pressure was placed on Mr. Floyd’s mid-lower back beyond the time duration of this video.

FORCE 3: Officer Lane is positioned closest to Mr. Floyd’s feet with Officer’s Lanes arms extended over what appear to be the position of Mr. Floyd’s legs, thus rendering them immobile. The immobility of his legs further restricted Mr. Floyd’s ability to shift body position so as to relieve the injurious restricting ventilatory forces above.

MALPOSITION: Throughout both videos taken from street and sidewalk side of the car, Mr. Floyd can be seen in; 1) prone position and, 2) with his hands pulled behind him in a handcuff position preventing him from relieving the pressure on his chest or modifying his position so as to augment his breathing capacity.

Overview of the Critical Structures and Functions of the Respiratory System

In order to understand how the above forces and malposition led to the asphyxiation of Mr. Floyd, several concepts must be understood in order to understand the minimum amount of breathing (i.e. “minimum minute ventilation”) required to sustain life and how the above forces and malposition rendered Mr. Floyd unable to achieve this “minimum minute ventilation” so as to prevent his cardiac arrest/death.

Oxygen gas, present in atmospheric air, is required by all the cells in the body in order to create and use the energy to maintain each individual cell’s structure and function. These life sustaining oxygen molecules are absorbed by the air sacs in the lungs and then are transferred to the red blood cells circulating through the lung capillaries to then be pumped by the heart through the blood vessels of the body so that the oxygen molecules they carry can be delivered to each organ/cell. However, if these cells and/or organs are deprived of sufficient oxygen/energy, they begin to lose function, structural integrity, and if deprived of sufficient oxygen over a prolonged period, the cells and/or organs will sustain irreversible damage and cell/organ death.

Oxygen delivery is dependent on 2 main physiologic functions; 1) cardiac output, i.e. sufficient circulating blood flow per minute such that oxygen carrying red blood cells can “deliver” oxygen to each cell, with cardiac output dependent on the “pump function” of the heart, i.e. the heart must be able to receive sufficient oxygen to contract and forcefully eject enough blood flow throughout the circulation and 2) minute ventilation, i.e. the sufficient intake (inhalation) of a sufficient volume of fresh oxygen gas to be absorbed by these red blood cells while also transferring the carbon dioxide gas content from the blood to the open lung units in order to be able to exhale this gas into the atmosphere (carbon dioxide being the waste product of energy metabolism of the body).

Minute ventilation is defined by the volume of air inhaled/exhaled with each breath (i.e. “tidal volume”) multiplied by the rate at which this volume is exchanged per minute (i.e. “respiratory rate”).

Minute ventilation (MV) varies with the amount of energy being consumed which is dependent on the amount of activity being performed. For instance, at rest, an adult male will breathe, on average, approximately 12 times per minute and take in about 500 milliliters of air with each breath, thus the MV of an adult human at rest is approximately 6 liters per minute to support the energy required of a body at rest.  During light, moderate, and extreme exercise in highly trained male athletes, MV can be increased to approximately 12, 60, and up to 180 liters per minute respectively. Note that MV can only increase via 2 factors; 1) the “tidal volume” of each breath is increased by expanding the volume of the thoracic cage via; contraction of the diaphragmatic muscle which pulls the diaphragm lower into the abdominal cavity, contraction of the intercostal muscles which spread the ribs further apart, and contraction of multiple accessory muscles in the neck, chest and spine which extend the height of the thorax, and/or, 2) increasing the respiratory rate up to 40-50 times per minute at peak exercise.

Conversely, the minimum minute ventilation required to sustain life is the MV at which both oxygen and carbon dioxide levels remain in the normal range.

Hypoventilation is the condition where the MV is decreased such that carbon dioxide levels rise above normal and oxygen levels fall below normal, with the former becoming abnormal prior to the latter. Mild hypoventilation which causes slight abnormal fluctuations in oxygen or carbon dioxide levels are generally well-tolerated, especially if this hypoventilation occurs gradually over time, for example in morbid obesity, the slow and persistent accumulation of adipose tissue surrounding the thoracic cage and abdomen causes progressively worsening hypoventilation over months to years and is generally well tolerated. However, if acute, severe, or prolonged enough, both oxygen and carbon dioxide levels will become rapidly and severely abnormal. If hypoventilation is severe enough, patients will first lose consciousness due to the high carbon dioxide levels (a condition called “CO2 narcosis” given that high Co2 levels produce unconsciousness), and if MV persists at this low level, oxygen levels will then start to decrease to such an extent that the cells in the heart begin to lose energy/function, causing the heart as a whole to cease function, leading to a state of cardiac arrest/death.   

It is my opinion that Mr. Floyd suffered cardiac arrest as a result of prolonged hypoventilation, i.e. he was unable to inhale enough oxygen and exhale enough carbon dioxide such that he lost consciousness and then suffered cardiac arrest.

Causes of Hypoventilation

In order to achieve sufficient minute ventilation (MV) to sustain life, three factors must be present, which I have traditionally taught as the “three A’s” of breathing; 1) an “airway”, i.e. a windpipe that is patent/open to allow air to flow down through the airways to the lung tissues, 2) “ability” – i.e. both an intact neurologic respiratory drive combined with sufficient strength of the respiratory muscles to contract, along with sufficient “space” for the thoracic cavity to expand in size, thus creating a “vacuum” for fresh air to flow in on a pressure gradient from the atmosphere into the lungs, and 3) “area” – sufficient surface area of viable lung tissue so that oxygen can be absorbed from the inhaled air into the bloodstream while carbon dioxide can pass from the bloodstream into the inhaled air volume to then be expelled into the atmosphere during exhalation.

If any limitations in the above factors are present, hypoventilation will result, generally from three causes; 1) a reduced tidal volume (reduced volume of an inhaled breath),  2) a reduced respiratory rate, or 3) insufficient viable lung surface area, a cause only seen in acute and chronic lung conditions such as pneumonia, pulmonary edema, asthma, emphysema, pulmonary embolism etc.

I found no evidence that Mr. Floyd’s respiratory drive (rate) was significantly suppressed, despite the fact he had opiates in his bloodstream, an agent known to suppress respiratory rate. His intact respiratory rate is evidenced by observing him in the minutes prior to and at the beginning of the restraint by the officers whereby he was able to walk, sit, stand, answer questions, and cry out for help. It is clear from these observations that the opiates in his bloodstream at the time were not of sufficient concentration to suppress his respiratory rate.

I find no evidence, based on the reported autopsy results, that Mr. Floyd, despite his history of smoking and of a recent Covid-19 infection, had a chronic or acute lung disease which would lead to loss of sufficient lung tissue surface area that would lead to the degree of hypoventilation that would cause a cardiac arrest.

Therefore, given no evidence of either 1) a suppressed respiratory rate or 2) an acute or chronic lung disease, it is my opinion that Mr. Floyd died from 3) hypoventilation secondary to an insufficient volume of air with each breath, preventing him from exhaling sufficient carbon dioxide and inhaling sufficient oxygen to sustain life. The evidence for this is as follows:

1)    His complaints of “I can’t breathe” very soon after being restrained in a prone position with the weight of two grown men on his mid and upper back/neck. In my opinion, the fact that he was able to form words at that point in his prolonged restraint, leads to the following conclusion;

a.     Mr. Floyd, at least initially, was drawing enough air to “phonate” or “make sounds/speech”, (sounds are made on exhalation and require a sufficient volume of inhaled air to create sufficient exhaled flow through the vocal cords). The only conclusion I can draw from the fact that he was heard to phonate early on in the videos of his prolonged restraint is that “complete occlusion” of his airway was not occurring at that time because, if it had occurred, by definition, no sounds could have been produced by Mr. Floyd.

b.    Although his ability at the time to speak indicates that at least some air flow in and out of his airways/lungs was occurring, it is my opinion that this amount of airflow and inhaled volume was insufficient to sustain life if not reversed in minutes. I base this assertion on the fact that Mr. Floyd immediately communicated “I can’t breathe” indicating that he was suffering from a sensation termed “dyspnea” defined as “the sensation of difficulty breathing” which arises whenever airflow or air volume entering the chest is decreased to the point where gas exchange is compromised, a state immediately sensed by the nervous system, and is a well-described and uniquely distressing sensation (see below). 

c.     Thus, it is my belief, at least initially, that the force of Officer Chauvin’s knee on Mr. Floyd’s neck did not lead to complete collapse of his upper airway/windpipe but rather caused at least some “narrowing” given his diminished, but not absent, ability to phonate. It is my opinion that the most injurious impact of the officers weight on the knee placed over Mr. Floyds cervical spine/upper back was that it led to restriction of the respiratory accessory muscles of the neck such that it prevented him from drawing in sufficient air to counteract the pressure on his thoracic cage from Officer Keung (explained in detail below under “Compensatory Mechanisms of the Respiratory System).

d.    Although complete compression of the airway, by definition, was not present while Mr. Floyd was able to speak, there were prolonged periods in the video where no speech was heard and thus I cannot rule out the possibility that with subtle changes in neck position or weight directed by Officer Chauvin’s knee over Mr. Floyd’s neck that complete compression and lack of airflow occurred for transient or prolonged periods. Further, it is my opinion that, despite the fact that the autopsy reported no fracture or injury to the cartilaginous structures of the trachea (“windpipe”), the absence of such an injury does not in any way exclude the possibility that the airway was completely compressed at some point. The reason for this possibility is that only half the circumference of the windpipe is made of cartilage, i.e. the anterior trachea. The posterior trachea is “membranous” and is composed of soft tissue/mucosa and can easily be displaced/compressed such that it can oppose the anterior trachea thus leading to complete occlusion of the windpipe, either transiently through benign forces such as a vigorous cough or from sustained life threatening forces such as external body weight pressure applied over a knee to the cervical vertebrae which would then cause the vertebrae to compress the windpipe just anterior to it. In conclusion, the windpipe can be completely occluded without causing permanent damage to the tracheal rings.

DYSPNEA (“I can’t breathe”)

“Dyspnea” is a medical term defined as “the sensation of difficulty breathing” and most commonly occurs when the amount of muscle work required to draw in a sufficient volume of air is increased due to some “load” which restricts either airflow through the windpipe, ability of the lung to inflate, ability of the lung tissue to absorb sufficient oxygen with each breath, or the ability of the chest wall to expand to draw in a sufficient volume of air into the lung/chest. Many acute and chronic lung conditions cause this sensation, such as asthma where the airways are constricted and thus it requires increased, exaggerated muscular effort to inhale and exhale each breath through “smaller” airways, or pulmonary edema whereby water fills many lung units causing the lungs to become heavier and partially collapse, thus inflating them with each breath requires an increased and exaggerated effort.

It must be recognized that humans are exquisitely sensitive to any force that impairs our ability to breathe, and this “extreme sensitivity” likely developed as an evolutionary adaptation to promote our survival given that its intent is to immediately alert us to and reflexively correct via compensatory respiratory mechanisms (see below) any force which threatens or impairs our ability to sustain breathing. This is reflected by the fact that our thoracic cage (chest) is one of the most highly innervated parts of the body. Millions of nerves course over the skin and alongside the ribs of the thoracic cage. There are two types of nerves; “afferent” and “efferent” nerves. The former send “sensory” information to the brain, such as touch/movement, pain, temperature, and vibration thus allowing humans to constantly be aware of the amount of chest expansion or “stretch” that is occurring with each breath.

Efferent nerves conduct information from the brain to the muscles to direct muscle effort/movement. The normal amount of effort applied to a breath and the resulting amount of chest expansion that is sensed is generally perfectly matched and thus normal breathing is typically unconscious/not sensed. In other words, the unconscious automatic impulses sent from the brain to our respiratory muscles/diaphragms lead to volumes of air inspired which are perceived as “satisfying” or “non-distressing”, i.e. they are not perceived as insufficient but as adequate/normal, and thus are generally imperceptible. However, as soon as any force is applied such that it limits the ability of our chest to expand or “stretch” sufficiently with a normal or even increased respiratory effort, this immediately results in the sensation of “dyspnea”, or “inability to achieve a “satisfying” or sufficient volume of air intake, which, when severe and/or acutely severe, is known to be one of the more distressing sensations one can experience and can immediately create a superimposed sense of “panic”. Some examples of this sensation are when an over-exuberant or prolonged “bear hug” may be applied by a friend or family member and one feels immediately that “they cannot breathe”, a situation which is generally quickly reversed/decompressed upon release of the “hug” such that this distressing sensation is typically short-lived. Another example would be when a group of children (or adults) are wrestling or playing in a pile and the child/adult on the bottom of the pile suddenly experiences the cumulative weight of their playmates on their chest or back such that their normal or even exaggerated respiratory effort leads to the highly distressing, noxious, fearful feeling of insufficient air flow/chest expansion such that they immediately cry out “get off, I can’t breathe”.

Knowing the forces, diseases, situations, and positions that can restrict breathing, it is my opinion, that as soon as Mr. Floyd was placed prone on the ground and the weight of the two officers knees were applied to upper back/neck and mid-lower back, he immediately suffered acute, severe “dyspnea”, i.e. a sensation of difficulty breathing due to the resulting “restriction” of his ability to expand his chest preventing him from inhaling a sufficient “tidal volume” or a “satisfying breath.” This led to his immediate exclamation of “I can’t breathe”. In essence, he immediately sensed that the volume of air entering his chest was insufficient to maintain normal oxygen and carbon dioxide concentrations in the blood. It is my opinion that the severe and prolonged “hypoventilation” caused by the weight of the officers on his chest and shoulders/neck led to his loss of consciousness due to progressively increasing blood carbon dioxide levels followed by a cardiac arrest secondary to his progressively decreasing blood oxygen levels due to his inability to take in a sufficient volume of air to be able to absorb sufficient oxygen or expel sufficient carbon dioxide. In treating acute and chronic respiratory failure throughout my career, it should be recognized that this symptom/condition is one of the most distressing/noxious/panic inducing symptoms a human can suffer.

Respiratory System Compensation to Inspiratory or Ventilatory Deficits

Another important concept to understand are the compensatory abilities of the respiratory system that counteract limitations or restrictions in ventilatory function. Examples are as follows:

1)    INCREASING RESPIRATORY RATE: When we have insufficient ability to take in a large enough breath due to thoracic wall restriction, we typically compensate by increasing the respiratory rate, in this way sufficient minute ventilation can still be achieved, as per formula above. However, this compensatory mechanism fails if the volume of air inhaled with each breath is smaller than the volume of air in the windpipe and bronchi, a.k.a. smaller than the “dead space volume” (i.e. the volume of air that enters the thoracic cavity but does not come into contact with the lung tissue and thus the oxygen in this volume of air cannot be absorbed into the blood). This volume of air is equivalent to the air volume in the mouth/nose/trachea/proximal bronchi and is about 150ml in an adult male – i.e. any volume of air lower than this amount does not participate in gas exchange and thus cannot be compensated for by increasing the respiratory rate). It is my opinion that the volume of air entering Mr. Floyd’s lung was smaller than his dead space volume thus, his increased respiratory rate was unable to compensate for such a severely reduced tidal volume, again a condition which is immediately experienced as severely distressing or panic-inducing.

2)    INCREASING TIDAL VOLUME VIA USE OF ACCESSORY MUSCLES:

a.    If there is restriction to airflow through the windpipe or restriction to the descent of the diaphragms or a person suffers from a condition which limits lung inflation, the “accessory muscles of respiration” are recruited as follows:

   i. Diaphragm – the first response to an inspiratory load or restriction is to increase the rate and depth of descent of the diaphragm above normal “excursion” such that air flow rate and thoracic air volume is increased. It is my opinion that, in Mr. Floyds case, the ability of his diaphragm to descend further than normal, or even to descend the normal distance/excursion was impaired by two factors; 1) prone positioning on the ground which placed his body weight over his abdomen which compressed the abdominal contents such that they are displaced upwards against the diaphragm and thus limited the  descent of the diaphragm and 2) this upward displacement of abdominal contents/intestines against the diaphragm was further increased due to the added external weight of Officer Keung over Mr. Floyd’s mid back and consequently his abdomen.

ii.     Intercostal muscles – typically, when we make an exaggerated respiratory effort, the space between the ribs expand and the chest wall cavity/volume increases. When we exert increased respiratory effort using the intercostal muscles which run between the individual ribs, such expansion can be increased further. In Mr. Floyd’s case, the pressure on his back/abdomen and neck/shoulders by the two officers rendered the intercostal muscle contraction insufficient to overcome such severe restriction of the chest wall.

iii.     Accessory muscles of the neck/back/chest – after diaphragmatic effort, use of the accessory muscles are the next most powerful compensatory mechanism that humans employ to augment tidal volume or overcome an inspiratory resistance/load. These muscles include the sternocleidomastoid, spinal, neck and chest muscles. When these muscles are recruited/engaged, they serve to expand the thoracic cavity not only by expansion outwards such as with the intercostal muscles between the ribs, but by raising the thoracic cavity superiorly or “upwards.” It is my opinion that the knee of Officer Chauvin on Mr. Floyd’s neck/spine, rather than cutting off airflow at the windpipe, more than likely caused asphyxia/hypoventilation by limiting the neck/spine accessory muscles to achieve sufficient chest expansion to counteract the limitation produced by his prone position combined with the force of Officer #2’s weight on his chest/abdome

I have also identified a separate set of actions which caused Mr. Floyd further harm by making it less likely that cardiopulmonary resuscitation (CPR) could be successful which limited his ability to survive. These separate injurious actions were committed by the emergency medical personnel who appeared on the scene in the videos and were as follows:

1)    One emergency medical technician/paramedic clearly checks Mr. Floyd’s pulse at 11:50 of the youtube video entitled “Full Video of 2 officers murder George Floyd”. Although a determination of the presence or absence of a pulse is not audible on the video, it is my opinion that Mr. Floyd was pulseless at that time. If true, as an expert in the performance and training of CPR, it is my opinion that, in the setting of detecting the absence of a pulse of a patient who does not meet exclusion criteria for CPR delivery, chest compressions should immediately be initiated by the first trained bystander or personnel present.

2)    Instead of initiating immediate CPR on Mr. Floyd by; 1) directing Officer Chauvin to release his restraining knee pressure, 2) rolling Mr. Floyd supine and 3) beginning chest compressions, the medical technician/paramedic instead leaves to go to the ambulance to prepare a stretcher and transfer board/sheet. The period of time until the stretcher can be seen is 39 seconds later at 12:29 of the video, with the 39 second period beginning being from the first detection of an absent pulse. Further, it is not until 12:44, a full 54 seconds from absent pulse detection that the medical technician/paramedic directs Officer Chauvin to remove his knee so they can begin the process of transferring Mr. Floyd to a stretcher and into the ambulance. The last time Mr. Floyd can be seen on the video was at 13:29, and at that time, there is no evidence that CPR had been initiated on Mr. Floyd who had then been pulseless a minimum of one minute and 39 seconds since the initial pulse check.

3)    This delay towards attempting to restore circulation via chest compressions or other interventions that make up ACLS (advanced cardiac life support) prolonged the “no flow” period after circulatory arrest which severely limited Mr. Floyd’s chances of achieving successful “recovery of spontaneous circulation” (ROSC). Such an unnecessarily prolonged period of “no flow” clearly added further cellular and organ damage to the prior period of lack of blood flow to Mr. Floyd’s vital organs, namely his heart and brain.

In summary, the prolonged, simultaneously applied restraining forces by Minneapolis Police Officers Chauvin, Keung, and Lane on critical parts of Mr. Floyd’s respiratory and musculoskeletal system while he was in a handcuffed, prone position on the ground led to severe hypoventilation which caused a life-threatening elevation in blood carbon dioxide levels rendering him unconscious, which was then followed by a progressive and severe decrease in blood oxygen levels which directly caused his cardiac arrest and death. Further, the failure of emergency medical personnel to initiate CPR on Mr. Floyd immediately upon discovering he was pulseless led to an additional significant decrease in Mr. Floyd’s chances of achieving ROSC from the CPR that was eventually initiated in the ambulance.

The opinions in this report are expressed to a reasonable degree of medical certainty.

I reserve my right to amend or supplement my opinions based on any additional information that may become available to me.

Yours sincerely,

Pierre Kory, MD, MPA

June 9, 2020

Associate Professor of Medicine

Chief of the Critical Care Service

Medical Director of the Trauma and Life Support Center

Division of Allergy, Pulmonary and Critical Care

University of Wisconsin School of Medicine and Public Health

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Pierre D Kory

6006 N Highlands Ave, Madison, WI 53705

54 years old (May 3, 1970)

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Kory D Pierre, Pierre Daniel Kory, Tierre Kory

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President and Chief Medical Officer at Front-Line Covid-19 Critical Care Alliance

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Madison, WI 53705

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1970 - "Dr. Leslie Kory"

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Dr. Leslie Adam Kory, MD

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Diagnostic Radiology

Montefiore Medical Center Moses Campus

111 E 210th St, Bronx, NY, 104675 other location


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Dr. Kory graduated from the Universite De Lausanne Faculte De Biologie Et De Medecine in 1958. He works in Bronx, NY and 2 other locations and specializes in Diagnostic Radiology. Dr. Kory is affiliated with North Central Bronx Hospital.


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1984 ... working as a developer in Mass? 

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1985 - sold the land...

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?Leslie Kory, MD

Attending Physician, Body Imaging
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Jacobi Medical Center/Albert Einstein College of Medicine

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Blog posts (and Substacks) regarding Dr Pierre Kory

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Pierre Kory’s New York Story

Observations and questions for a doctor who arrived after The Main Hospital Death Event

JESSICA HOCKETT

JAN 22, 2024

In recent weeks,   Martin Neil Jonathan Engler & I have engaged in debate withPierre Kory, MD, MPA regarding characteristics and manifestations of COVID-19.1Despite being a relatively prominent American figure in the COVID Era, Dr. Kory is not someone I recall being familiar or engaging with on Twitter before 2023. After my suspended account was restored, I became more aware of his story, as a part of my ongoing interest in the New York City spring 2020 mass casualty event. Kory is a New York native who was living and working in Wisconsin when the WHO declared a coronavirus pandemic. In late April 2020, he was among the many out-of-state healthcare workers who traveled to “the epicenter” to work in hospitals.Unfortunately, official data related to the New York City’s staggering city death toll appear false. Authorities have not yet disclosed proof the event occurred as presented. There is no complete list of names, no way to obtain death certificates of all the deceased, no federal inquiry into what happened or why, and very little interest from American anti-mandate/health freedom advocates in probing what transpired. The unbelievable hospital mortality is not well- or fully-explained by ventilator use, extant data on nursing home residents who died in the hospital, orRemdesivir. We also have bizarre death processing reported by the medical examiner, and a taxpayer-funded hospital system refusing to release basic data to the public. Like Pietro, an anonymous doctor we interviewed, I believe Pierre Kory’s experience in New York is an asset to exposing the truth about the New York event. In this post, I present observations and questions about things he has said or that have been documented about what he saw and did in the first half of 2020.My aim is not to discredit Pierre Kory, nor to challenge his claim that he is anything other than a caring professional who did his best by the medical residents and patients he attended. His advocacy for Ivermectin and against the COVID shot are well-known and appreciated by many, but are beyond the scope of this post and my study of the New York event.2A delimited timeline and sources of interest follows:
  • October 2019 - April 2020 — Working in University of Wisconsin Hospital and Clinics, Madison, WI (Critical Care Service Chief, Medical Director, Trauma and Life Support Center)3
  • March/April 2020 – Involved in the formation of Frontline COVID-19 Critical Care Consortium (FLCCC). 
  • April 6, 2020 — Quoted in press release about COVID-19 treatment protocols, quoting Kory.
  • April 27, 2020 – First day in Mount Sinai Beth Israel Hospital, NYC, COVID-19 Emergency Critical Care Attending
  • May 6, 2020 – Testified as one of six witnesses at COVID-19 Roundtable, US Senate Homeland Security Committee  
  • July 1, 2020 — Published op-ed in USA Today with Dr. Paul Mayo, “ICU Doctors: Many More 
  • August 8, 2020 — Interviewed by Sean Burke, coinciding with New York Times article “The COVID Drug Wars that Pitted Doctor vs. Doctor”, which spotlighted Kory and others.
I present my observations and questions in categories:A. Before the Federal Emergency B. During the Spring 2020 Federal Emergency: UW Hospitals C. During the Spring 2020 Federal Emergency: Leaving for New York CityD. During the Spring 2020 Federal Emergency: In New York CityE. Witness at U.S. Senate Homeland Security & Governmental Affairs Committee Roundtable F. Interview on The Sean Burke ShowG. Younger-Adult Deaths in New York CityH. A Non-Coronavirus Explanation?All of the figures I reference are at the end of the post. I invite Dr. Kory’s responses, corrections, and clarifications and would welcome the opportunity for a face-to-face conversation.
A. Before the Federal Emergency 
  1. In fall 2019 and the first four months of 2020, you were working for University of Wisconsin Hospital and Clinics. Presumably, this means you were seeing patients. Was the 2019 flu season you observed more severe or markedly different than prior flu seasons? Do you recall patients presenting with symptoms or conditions that, in retrospect, you believe could have been “missed” SARS-CoV-2 infection?
  2. Clusters of EVALI cases were reported in Wisconsin in 2019. Did you treat any patients of any age in 2019 with symptoms resembling contemporaneous or subsequent case descriptions of EVALI?
  3. What/whose guidance were you following for “preparing” the hospital for COVID-19 patients (as you mentioned doing in an August 2020 interview with Sean Burke)? Were any existing patients moved into these ICUs, either before or after being tested?
B. During the Spring 2020 Federal Emergency: UW Hospitals
  1. You told a U.S. Senate committee that, in Madison, you “frantically prepared for the expected surge of patients.” Why was a surge expected? 
  2. In August 2020, you told Sean Burke, “I was chief of the critical care service and medical director of the main ICU at University of Wisconsin. And we were preparing like crazy for it to hit Wisconsin. Remember, there was a huge delay before you started seeing any– so I was really busy at work, helping teams prepare. We were almost re-inventing the hospital and workflows and processes.” Was there a surge? 
  3. At what point in time did you begin seeing new patients coming into the UW hospital presenting with symptoms that were new or unusual? What were the demographics of these patients? Did you get a sense of who they were and where they came from? 
  4. When did COVID testing begin at UW? Were all existing patients tested? Do you recall which/whose tests were being used?
  5. Were all patients who were admitted to the ED and/or as inpatients to the hospital in March and April tested for COVID-19? 
  6. Your description of the early weeks in Madison says you led daily COVID briefings at UW, “attended in person and remotely by all residents, hospitalists, and intensivists in charge of taking care of COVID patients.” Did you attend to COVID patients as well?
  7. You told Sean Burke you left for New York “once it seemed that the curve flattened in Wisconsin.” Whence the patients during the surge? Were they transferred from nursing homes? Moved from within the hospital to COVID wards? When did the surge end? Did you have a sense of why it ended? (What ended it?)
  8. Federal data show that Dane County, Wisconsin, did not experience a significant increase in hospital deaths in spring 2020 – or a high number of COVID-19 deaths (figure 1). Do you recall how many deaths you observed that attributed COVID-19 as the underlying cause? 
  9. You’ve suggested that a push for “early intubation” at UW came from other doctors who were scared. Were they scared because of what they were seeing clinically? How many doctors comprised (what you called) “the early intubation crowd”? How long did this early intubation last before [your words, “my colleagues and trainees carefully listened and for maybe the first and last time in the pandemic, simply trusted my judgement” and ceased the approach they were using?
  10. An April 6, 2020 FLCCC press release says, “If you can administer ascorbic acid and corticosteroids intravenously starting in the Emergency Room and every 6 hours thereafter while in the hospital, the mortality rate of this disease and the need for mechanical ventilators will likely be greatly reduced,” says Dr. Pierre Kory, the Medical Director of the Trauma and Life Support Center and Chief of the Critical Care Service at the University of Wisconsin in Madison. He explains that it is the severe inflammation sparked by the Coronavirus, not the virus itself, that kills patients. Inflammation causes a new variety of Acute Respiratory Distress Syndrome (ARDS), which damages the lungs. Should this be taken to mean you were successfully using these treatments with patients at UW?
  11. You’ve said on multiple occasions that you were in touch almost every day with ICU Directors in New York. How did their reports compare to what you were seeing in Madison? Did you report to those doctors what you and your colleagues were and weren’t seeing? 
C. During the Spring 2020 Federal Emergency: Leaving for New York City
  1. Regarding what prompted you to go to New York, you’ve said in various forums that you felt compelled to go help former colleagues and have referred as well to email lists of professional organizations. For example, you said [via Substack comment], “The Chiefs of critical care in NYC were sending out, via society email lists, ‘Intensivists Needed in NYC Now,” and that you showed up in New York in response to that call. Do you have examples of those solicitations? (They would be helpful to see, for archival/historical purposes re: the non-military “travel cadres” that descended on the city.) Were there people or factors that influenced your decision to go to New York, or was it largely those email lists?
  2. You told Sean Burke you left UW for New York on a Humanitarian Leave. Did you have to formally request/apply for the leave? Was anyone not employed by UW involved with initiating or approving the leave? 
  3. Senator Ron Johnson (R-WI) was your senator at the time. Did you and the Senator or the Senator’s staff communicate in late 2019 or the first months of 2020, prior to you leaving for New York City? Had you ever met the Senator (either virtually or in person) before 2020?
D. During the Spring 2020 Federal Emergency: In New York City
  1. You’ve said your first day in the Beth Israel ICU was April 27, 2020. This was after the main death event, per federal data (figure 2). Does this data surprise you, or does it seem consistent with what you witnessed in the timeframe?
  2. What was your date of arrival in New York City? Did you go to other hospitals, either before you started at Beth Israel or during your time in the city, whether in the five boroughs or metro area?
  3. You’ve said that you took over your “old ICU,” which was 16 beds, all filled with patients on ventilators with COVID, many of whom had been on vents for weeks. Although intubation data are incomplete and insufficient, what you’re saying fits with the state’s file, which shows a sharp rise in patients intubated, followed by a long, slow decline. Did you get a sense of who these patients were and what they were admitted for?  Did those 16 patients die? Are they examples of patients who were “actively dying” - a term you’ve usedto describe deteriorating patients who become “irrecoverable”?
  4. You’ve written about the number and nature of conversations that you had with families in New York regarding end-of-life care and decision-making. Did your hospital allow family members to visit their loved ones in the ICU? Did the conversations you reference take place in person over the phone/via Internet?  Did you witness DNR orders being given for COVID patients - unilaterally, without third-party witnesses?
  5. You’ve described being in a COVID ICU you were “leading,” with patients whose chest x-rays and presentation all looked the same.4 You’ve also said there were multiple COVID ICUs – which is consistent with descriptions of how hospitals “rearranged” in preparation for the so-called COVID surge. According to your CV, you were the director of simulation training at Beth Israel from 2008-2015 and COVID-19 Emergency Critical Care Attending in May 2020 at Beth Israel (which implies that you were overseeing residents).Such details are relevant to the theory that NYC hospitals ran a live-exercise simulation in those “surge” and post surge weeks. Do you think it’s possible that you (and others) may have been called in to follow up on or help oversee/evaluate the later stages of a simulation — one with live patients?Have you considered the possibility that NYC hospitals “ran” a live-exercise of some kind, to simulate disease spread, unbeknownst to most staff, including yourself?
  6. Officials, media reports, and healthcare worker stories indicate there was military presence in at least some NYC hospitals. Did you encounter military personnel (e.g., National Guard, Naval Health Officers) at Beth Israel? If so, did you speak or interact with any, and do you know why they were there and what they were doing? 
  7. On what day did you depart New York? What was the official reason for your departure? (Your CV indicates you were there for five weeks; elsewhere you’ve said four weeks. The use of present tense in the opening sentence in your 7/1/2020 USA Today op-ed with Dr. Paul Mayo indicates you were still there.)
  8. There is some confusing language in a  New York Times August 8, 2020 article regarding when you left UW. In an interview with Sean Burke on the same day, you seemed to suggest your resignation was in May. Can you clarify?
E. Witness at May 6, 2020 U.S. Senate Homeland Security & Governmental Affairs Committee Roundtable - COVID-19: How New Information Should Drive Policy
  1. When did you receive a request to testify at the May 6, 2020 meeting? When did you accept the request? 
  2. Were you given guidelines or parameters for your testimony, either in writing or via other communication? 
  3. Especially given your relatively late and then-very-recent arrival in New York City – the site of an incredible hospital mass casualty event – it’s curious that the Senate committee did not call a witness who had been in hospitals since February or March, at least. Do you know if other New York City doctors or administrators were asked to testify at the May 6, 2020 roundtable? 
  4. Introducing you at the May 6, 2020 meeting, Sen. Johnson said, “I just spoke with him last week,” which would have been sometime between April 26 and May 2, 2020. Was that the first time you ever had direct contact with Senator Johnson?
  5. You told the committee, ”The mortality and morbidity rates of this disease are unprecedented. I’ve been doing critical care for a decade and a half. I do not see mortality rates associated with any severe illness that I see in this one.” This was a very bold statement, even at the time — one that gives an impression of a very deadly illness which does not seem to have been observed in most places in the U.S. and around the world, including Chicago, which reported a first case six weeks prior to New York. Have you considered whether what you were seeing or your perception thereof was influenced by factors that didn’t involve a spreading flu-like pathogen?
  6. You told the committee, “Either I’ve been inundated with patients who are chronically on the vent who are dying of end-stage fibrotic lung disease, or I’m seeing patients who are crashing into my ICU, but as opposed to a month ago, where they were coming in with these mild abnormalities on chest x-rays and maybe mild abnormalities in their oxygen intake. Now, we’re seeing floridly abnormal x-rays, with very advanced disease.” You were not in the Beth Israel ICU “a month ago” (April 6, 2020), correct? Was this comparison based on what other employees of the hospital told you they witnessed? Who were these patients? Did you get a sense of their past medical history?
  7. You told the committee, “I’m throwing the book at ‘em, and it’s not working. I have to emphasize that the timing of the initiation of this therapy is critical. The world needs to know this.” What specific therapies were you using that weren’t working?
  8. You told the committee, “What happened here in New York is that the initial surge caused so many terrible reports of patients being unattended to, running out of resources, not enough physicians and nurses.” Who was supplying these "terrible reports"? 
  9. You went on to say, “They’re not coming to the hospital early enough. Now when they’re coming — they’re so far advanced that the medicines don’t work as well. And so we need to get the word out that things are better on the ground. We’re definitely much more stable in the hospitals. We’re much more resourced. We’re re-grouped. We’re ready to take care of patients, but the patients have to come. If they wait at home with these symptoms, we’re not going to be able to save them.” Who were the patients that were coming to the hospital but not early enough? From where were they coming (e.g., private residences, nursing homes, public housing) and how old were they? 
  10. In written testimony to the committee, you endorsed the use of Remdesivir as a potential outpatient treatment for COVID, stating, This is the phase anti-viral therapies should be focused on, i.e. before patients reach the hospital where medicines like hydroxychloroquine or Remdesivir would have the greatest impact to keep the patient away from the hospital and ICU, p 5). Did you administer, oversee the administration of, or have knowledge about the drug being used at Beth Israel? 
  11. Are your spoken and written testimonies to the committee inclusive and representative of COVID patients you saw in both Madison and New York City? 
F. Interview on the The Sean Burke Show, August 8, 2020
  1. You indicated you were using the MATH+ protocol with patients in New York, with little success, which you attributed to your late arrival. (Excerpt below.) Is it possible that the patients you saw – presumably patients who had tested positive for SARS-CoV-2 – were chronically ill patients that were transferred from nursing homes and elsewhere in the hospital and were not suffering from a new disease per se? 
Burke : Were you using  MATH+ there [in New York]?Kory: I was. I was using some forms of it. I was getting pushback on some of the Vitamin D, just little [ticky stacks?], but mostly I was using pretty aggressive anticoagulation and methylpred., as well as ascorbic acid. So, yeah actually, I was using MATH, the plus a little bit less so. But certainly MATH was standard for me.Burke: And the results that you were seeing?Kory: Well, not the same as my colleagues and there’s some really important reasons for that. And you even mentioned in your introduction is that, you know, especially in critical illness, we talk about this concept of the Golden Hour, or the Golden Hours, which is, when you intervene, before someone goes into multi-organ failure or severe organ failure, you gotta get to them early. The medicines have to be delivered early. And when I got to the ICU on April 27th, many of the patients that I took over had been on ventilators for 1-2 weeks. Some of them had gotten a little bit of steroids not. So I’m going tell you, if you ask me about my results? Not very good. But that’s not to say that the medicine doesn’t work. It was too late. These patients were really, really sick, you know.
  1. Along the same lines, a bit later in the interview you said,  “When I was in New York, I saw nothing but - what I would say were patients chronically ill with COVID, I didn’t see acute.” Did you see acutely ill COVID patients in Madison – i.e., patients with sudden onset of respiratory illness? 
  2. You also said, “By the time I left New York we had no new cases. So, this is end of May. There was just no new COVIDs that I saw. And since then I’ve been doing research and writing and other stuff.” In retrospect, does it strike you as odd that COVID cases in NYC hospitals simply disappeared in a city of 8.5 million people? Were you aware of any changes to testing protocols or the tests themselves that may have played a role? 
G. Younger-Adult Deaths in New York CityYou’ve said multiple times you saw younger adults dying of COVID-19 in NYC hospitals. Examples follow: 
  • The severity, morbidity and mortality of COVID-19 must be re-emphasized to all, both young and old, as it spares neither (7/1/2020, USA Today)
  • I had too many young and healthy (relatively) on vents suddenly - why/how would a bacterial pneumonia suddenly do this unless it was a new superbug which would have been quickly identified (2/23/2023, Substack).
Federal data show steep, simultaneous rises in the number of younger-adult deaths in hospital inpatient (figure 3).As far as colleagues in PANDA and I have been able to tell, New York City is a global outlier in the speed and magnitude of younger-adult deaths attributed to COVID-19. Nearly all the increase in hospital inpatient deaths among ages 25-54 cites COVID-19 as the underlying cause of death (figure 4). 
  1. Do you think a formal inquiry of NYC hospitals is warranted, if only on the basis of the number of COVID deaths among younger adults?
  2. Have you considered the possibility that COVID patient designation, as determined by testing positive, may have led you and other doctors to think it was caused by disease when in truth it was not? For example, people were sick and dying from something else, but being positive on a newly-developed PCR test for a newly-detected pathogen led you to focus on COVID as the main problem?
H. Not a Coronavirus?
  1. Multiple times in 2020 and thereafter, you’ve said that the COVID-19 disease you observed in the first wave of U.S. mortality was very severe and was transmitted from person to person. For example:
  • At the Senate Committee meeting on May 6 , you painted a picture of a war-zone that is inconsistent with hospital data and with what other doctors in most other cities and countries reported seeing during this timeframe. You said, “We’re at war right now with this virus,” and that “The mortality and morbidity rates of this disease are unprecedented. I’ve been doing critical care for a decade and a half. I do not see mortality rates associated with any severe illness that I see in this one.” Those are very strong words for a flu-like illness. Looking back, how confident are you that you were not observing a scene that was staged or set-up for you? 
  • You and Dr. Mayo said you were “perplexed as to why responsible people would choose not to wear a mask given the potential harm, including death, that they could cause to their fellow citizens.”
  • In your recent response to Martin Neil, Jonathan Engler, and me you admitted the possibility of "something as preposterous as deliberate widespread release in certain targeted cities and areas." 
It seems you may believe there was a point-release of SARS-CoV-2 or another agent or factor at work in NYC. Have you shared your concerns with federal officials? Do you have or are you aware of any specific data to support this hypothesis? If there was such a release, do you think it changes the WHO’s March 11, 2020 pandemic declaration (or your view thereof)?Finally, do you think your early impressions of the severity and threat of the COVID-19 – and the transmission mechanism – were warranted? If this perception was driven largely by what you observed in New York, have you considered that what you saw has alternate explanations that don’t involve a spreading coronavirus?