Do COVID-19 Vent Protocols Need a Second Look?

https://www.medscape.com/viewarticle/928156

John Whyte, MD, MPH: Hello. I’m Dr John Whyte, chief medical officer at WebMD. Welcome to “Coronavirus in Context.” Today we’re going to talk about whether we’re managing coronavirus correctly; do we need to think about a change in our treatment regiments? My guest is Dr Cameron Kyle-Sidell. He’s a physician trained in emergency medicine and critical care, and he practices at Maimonides in Brooklyn, New York. Welcome, Dr Sidell.

Cameron Kyle-Sidell, MD: Thank you very much. Thank you for inviting me.

Whyte: You’ve been talking a lot about the number of patients, the percentage of patients dying on ventilators. When did you first notice this trend?

Kyle-Sidell: In preparation of opening what became a full COVID-positive intensive care unit, we scoured the data just to see what was out there—those who have experienced it before us, primarily the Chinese and the Italians; it was hard to find exactly, like the rate of what we call successful extubation—meaning, someone was put on a ventilator and taken off. And that data are still hard to find. I imagine there are a lot of people still on ventilators. But from the data we have available, it appears to be somewhere between 50% and 90%. Most published data puts it around 70%. So, that’s a very, very high percentage in general, when one thinks of a medical disease.

Whyte: You’ve been talking on social media; you say you’ve seen things that you’ve never seen before. What are some of those things that you’re seeing?

Kyle-Sidell: When I initially started treating patients, I was under the impression, as most people were, that I was going to be treating acute respiratory distress syndrome (ARDS), similar in substance to AIDS, which I saw as a fellow. And as I start to treat these patients, I witnessed things that are just unusual. And I’m sure doctors around the country are experiencing this. In the past, we haven’t seen patients who are talking in full sentences and not complaining of overt shortness of breath, with saturations in the high 70s. It’s just not something we typically see when we’re intubating some of these patients. That is to say, when we’re putting a breathing tube in, they tend to drop their saturations very quickly; we see saturations going down to 20 to 30. Typically, one would expect some kind of reflexive response from the heart rate, which is to say that usually we see tachycardia, and if patients go too low, then we see bradycardia. These are things that we just weren’t seeing. I’ve seen literally a saturation of zero on a monitor, which is not something we ever want and something we actively try to avoid. And yet we saw it, and many of my colleagues have similarly seen saturations of 10 and 20. We try to put breathing tubes in to avoid this very situation. Now, these patients tend to desaturate extremely quickly, so these situations have occurred. Still, what we’re seeing—that there was no change in the heart rate—is just unusual. It’s just something that we are not used to seeing.

The Case for Quinine vs Covid-19

KR Paul 24 mins

I ran across this today and I’m wondering what you all think?

I don’t know who the author is or if this is true, but for all of you medical experts, here’s some information on Covid-19 and Hydroxychloroquine.

“In the last 3–5 days, a mountain of anecdotal evidence has come out of NYC, Italy, Spain, etc. about COVID-19 and characteristics of patients who get seriously ill. It’s not only piling up but now leading to a general field-level consensus backed up by a few previously little-known studies that we’ve had it all wrong the whole time. Well, a few had some things eerily correct (cough Trump cough), especially with Hydroxychloroquine with Azithromicin, but we’ll get to that in a minute.

There is no ‘pneumonia’ nor ARDS. At least not the ARDS with established treatment protocols and procedures we’re familiar with. Ventilators are not only the wrong solution, but high pressure intubation can actually wind up causing more damage than without, not to mention complications from tracheal scarring and ulcers given the duration of intubation often required… They may still have a use in the immediate future for patients too far to bring back with this newfound knowledge, but moving forward a new treatment protocol needs to be established so we stop treating patients for the wrong disease.

The past 48 hours or so have seen a huge revelation: COVID-19 causes prolonged and progressive hypoxia (starving your body of oxygen) by binding to the heme groups in hemoglobin in your red blood cells. People are simply desaturating (losing o2 in their blood), and that’s what eventually leads to organ failures that kill them, not any form of ARDS or pneumonia. All the damage to the lungs you see in CT scans are from the release of oxidative iron from the hemes, this overwhelms the natural defenses against pulmonary oxidative stress and causes that nice, always-bilateral ground glass opacity in the lungs. Patients returning for re-hospitalization days or weeks after recovery suffering from apparent delayed post-hypoxic leukoencephalopathy strengthen the notion COVID-19 patients are suffering from hypoxia despite no signs of respiratory ‘tire out’ or fatigue.

Here’s the breakdown of the whole process, including some ELI5-level cliff notes. Much has been simplified just to keep it digestible and layman-friendly.

Your red blood cells carry oxygen from your lungs to all your organs and the rest of your body. Red blood cells can do this thanks to hemoglobin, which is a protein consisting of four “hemes”. Hemes have a special kind of iron ion, which is normally quite toxic in its free form, locked away in its center with a porphyrin acting as it’s ‘container’. In this way, the iron ion can be ‘caged’ and carried around safely by the hemoglobin, but used to bind to oxygen when it gets to your lungs.

When the red blood cell gets to the alveoli, or the little sacs in your lungs where all the gas exchange happens, that special little iron ion can flip between FE2+ and FE3+ states with electron exchange and bond to some oxygen, then it goes off on its little merry way to deliver o2 elsewhere.
Here’s where COVID-19 comes in. Its glycoproteins bond to the heme, and in doing so that special and toxic oxidative iron ion is “disassociated” (released). It’s basically let out of the cage and now freely roaming around on its own. This is bad for two reasons:

1) Without the iron ion, hemoglobin can no longer bind to oxygen. Once all the hemoglobin is impaired, the red blood cell is essentially turned into a Freightliner truck cab with no trailer and no ability to store its cargo.. it is useless and just running around with COVID-19 virus attached to its porphyrin. All these useless trucks running around not delivering oxygen is what starts to lead to desaturation, or watching the patient’s spo2 levels drop. It is INCORRECT to assume traditional ARDS and in doing so, you’re treating the WRONG DISEASE. Think of it a lot like carbon monoxide poisoning, in which CO is bound to the hemoglobin, making it unable to carry oxygen. In those cases, ventilators aren’t treating the root cause; the patient’s lungs aren’t ‘tiring out’, they’re pumping just fine. The red blood cells just can’t carry o2, end of story. Only in this case, unlike CO poisoning in which eventually the CO can break off, the affected hemoglobin is permanently stripped of its ability to carry o2 because it has lost its iron ion. The body compensates for this lack of o2 carrying capacity and deliveries by having your kidneys release hormones like erythropoietin, which tell your bone marrow factories to ramp up production on new red blood cells with freshly made and fully functioning hemoglobin. This is the reason you find elevated hemoglobin and decreased blood oxygen saturation as one of the 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.

2) That little iron ion, along with millions of its friends released from other hemes, are now floating through your blood freely. As I mentioned before, this type of iron ion is highly reactive and causes oxidative damage. It turns out that this happens to a limited extent naturally in our bodies and we have cleanup & defense mechanisms to keep the balance. The lungs, in particular, have 3 primary defenses to maintain “iron homeostasis”, 2 of which are in the alveoli, those little sacs in your lungs we talked about earlier. The first of the two are little macrophages that roam around and scavenge up any free radicals like this oxidative iron. The second is a lining on the walls (called the epithelial surface) which has a thin layer of fluid packed with high levels of antioxidant molecules.. things like abscorbic acid (AKA Vitamin C) among others. Well, this is usually good enough for naturally occurring rogue iron ions but with COVID-19 running rampant your body is now basically like a progressive state letting out all the prisoners out of the prisons… it’s just too much iron and it begins to overwhelm your lungs’ countermeasures, and thus begins the process of pulmonary oxidative stress. This leads to damage and inflammation, which leads to all that nasty stuff and damage you see in CT scans of COVID-19 patient lungs. Ever noticed how it’s always bilateral? (both lungs at the same time) Pneumonia rarely ever does that, but COVID-19 does… EVERY. SINGLE. TIME.
— — — — — — — — — — — — –
Once your body is now running out of control, with all your oxygen trucks running around without any freight, and tons of this toxic form of iron floating around in your bloodstream, other defenses kick in. While your lungs are busy with all this oxidative stress they can’t handle, and your organs are being starved of o2 without their constant stream of deliveries from red blood cell’s hemoglobin, and your liver is attempting to do its best to remove the iron and store it in its ‘iron vault’. Only its getting overwhelmed too. It’s starved for oxygen and fighting a losing battle from all your hemoglobin letting its iron free, and starts crying out “help, I’m taking damage!” by releasing an enzyme called alanine aminotransferase (ALT). BOOM, there is your second of 3 primary indicators of whether the shit is about to hit the fan for a particular patient or not.
Eventually, if the patient’s immune system doesn’t fight off the virus in time before their blood oxygen saturation drops too low, ventilator or no ventilator, organs start shutting down. No fuel, no work. The only way to even try to keep them going is max oxygen, even a hyperbaric chamber if one is available on 100% oxygen at multiple atmospheres of pressure, just to give what’s left of their functioning hemoglobin a chance to carry enough o2 to the organs and keep them alive. Yeah we don’t have nearly enough of those chambers, so some fresh red blood cells with normal hemoglobin in the form of a transfusion will have to do.

The core point being, treating patients with the iron ions stripped from their hemoglobin (rendering it abnormally nonfunctional) with ventilator intubation is futile, unless you’re just hoping the patient’s immune system will work its magic in time. The root of the illness needs to be addressed.

Best case scenario? Treatment regimen early, before symptoms progress too far. Hydroxychloroquine (more on that in a minute, I promise) with Azithromicin has shown fantastic, albeit critics keep mentioning ‘anecdotal’ to describe the mountain, promise and I’ll explain why it does so well next. But forget straight-up plasma with antibodies, that might work early but if the patient is too far gone they’ll need more. They’ll need all the blood: antibodies and red blood cells. No help in sending over a detachment of ammunition to a soldier already unconscious and bleeding out on the battlefield, you need to send that ammo along with some hemoglobin-stimulant-magic so that he can wake up and fire those shots at the enemy.

The story with Hydroxychloroquine
All that hilariously misguided and counterproductive criticism the media piled on chloroquine (purely for political reasons) as a viable treatment will now go down as the biggest Fake News blunder to rule them all. The media actively engaged their activism to fight ‘bad orange man’ at the cost of thousands of lives. Shame on them.

How does chloroquine work? Same way as it does for malaria. You see, malaria is this little parasite that enters the red blood cells and starts eating hemoglobin as its food source. The reason chloroquine works for malaria is the same reason it works for COVID-19 — while not fully understood, it is suspected to bind to DNA and interfere with the ability to work magic on hemoglobin. The same mechanism that stops malaria from getting its hands on hemoglobin and gobbling it up seems to do the same to COVID-19 (essentially little snippets of DNA in an envelope) from binding to it. On top of that, Hydroxychloroquine (an advanced descendant of regular old chloroquine) lowers the pH which can interfere with the replication of the virus. Again, while the full details are not known, the entire premise of this potentially ‘game changing’ treatment is to prevent hemoglobin from being interfered with, whether due to malaria or COVID-19.

No longer can the media and armchair pseudo-physicians sit in their little ivory towers, proclaiming “DUR so stoopid, malaria is bacteria, COVID-19 is virus, anti-bacteria drug no work on virus!”. They never got the memo that a drug doesn’t need to directly act on the pathogen to be effective. Sometimes it’s enough just to stop it from doing what it does to hemoglobin, regardless of the means it uses to do so.

Anyway, enough of the rant. What’s the end result here? First, the ventilator emergency needs to be re-examined. If you’re putting a patient on a ventilator because they’re going into a coma and need mechanical breathing to stay alive, okay we get it. Give ’em time for their immune systems to pull through. But if they’re conscious, alert, compliant — keep them on O2. Max it if you have to. If you HAVE to inevitably ventilate, do it at low pressure but max O2. Don’t tear up their lungs with max PEEP, you’re doing more harm to the patient because you’re treating the wrong disease.

Ideally, some form of treatment needs to happen to:

Inhibit viral growth and replication. Here plays CHQ+ZPAK+ZINC or other retroviral therapies being studies. Less virus, less hemoglobin losing its iron, less severity and damage.

Therapies used for anyone with abnormal hemoglobin or malfunctioning red blood cells. Blood transfusions. Whatever, I don’t know the full breadth and scope because I’m not a physician. But think along those lines, and treat the real disease. If you’re thinking about giving them plasma with antibodies, maybe if they’re already in bad shape think again and give them BLOOD with antibodies, or at least blood followed by plasma with antibodies.

Now that we know more about how this virus works and affects our bodies, a whole range of options should open up.

Don’t trust China. China is ASSHOE. (disclaimer: not talking about the people, just talking about the regime). They covered this up and have caused all kinds of death and carnage, both literal and economic. The ripples of this pandemic will be felt for decades.

Developments in the Treatment of Acute COVID-19

https://talkingpointsmemo.com/edblog/possible-developments-in-the-treatment-of-acute-covid-19

This appears potentially quite important. Since it has to do with technical clinical details and treatment protocols I’ll try to be both as precise and general as possible. Yesterday I noticed this grainy youtube video posted on March 31st by a New York City emergency and critical care physician, Cameron Kyle-Sidell. Kyle-Sidell said that he thought the treatment protocol and basic understanding of acute COVID-19-induced respiratory distress were both wrong. He said that what he is seeing in his ICU does not look like pneumonia but rather oxygen deprivation (hypoxia). Thus the treatment shouldn’t be focused on high pressure for someone whose lungs aren’t able to function but rather more effective ways of delivering additional oxygen. Critically, he argued that the high pressure ventilation might be damaging the lungs. He also said his impressions were based both on his ICU work over the previous two weeks and conversations with other clinicians around the country.

I looked up Kyle-Sidell and he’s a real doctor in emergency and critical care. That checked out. So far so good.

The responses to his videos on social media, both pro and con, suggested he was saying that the COVID-19 virus wasn’t the cause of the sickness or that ventilators weren’t necessary. I listened closely. That was clearly not what he was saying. He was saying that the disease model most doctors are working with – pneumonia/ARDS – is not what these patients are presenting with and the treatment protocol is not suited to their disease.

He was cautious and tentative in his conclusions, just what you’d expect from a serious clinician. His argument was that it is a different syndrome requiring different treatments. Ventilators are the best treatment we have now, he said, but they should be used differently (different use of pressure, settings, all well beyond my understanding). It seemed legit. But obviously I have zero understanding about anything to do with respiratory disease or its treatment.

For all those reasons I was intrigued but didn’t write anything about it, though I was eager to hear from other clinicians who might be able to evaluate what he was saying.

I’m writing about it now because of this article I saw in Medscape, a publication for clinicians and researchers (you need to sign up for access but it’s free). The article discusses Kyle-Sidell’s findings along with others thinking along similar lines. There was also this interview which Dr. John Whyte, chief medical officer at WebMD, did with Kyle-Sidell discussing his ICU observations. So serious, credentialed people are taking this seriously.

The Medscape article notes that the American Journal of Respiratory and Critical Care and Intensive Care Medicine are publishing, respectively, a letter and an editorial by Dr. Luciano Gattinoni of the University of Gottingen who makes a similar set of observations and recommendations to those in Kyle-Sidell’s videos. Gattinoni’s findings were based on his and his colleagues clinical experience in Germany as well as discussions with doctors in northern Italy.

From Medcape

In the editorial, Dr. Gattinoni and his colleagues explained further that ventilator settings should be based on physiological findings — with different respiratory treatment based on disease phenotype rather than using standard protocols.

“This, of course, is a conceptual model, but based on the observations we have this far, I don’t know of any model which is better,” he said in an interview.

Anecdotal evidence is increasingly demonstrating that this proposed physiological approach is associated with much lower mortality rates among COVID-19 patients, he said.

While not willing to name the hospitals at this time, he said that one center in Europe has had a 0% mortality rate among COVID-19 patients in the intensive care unit when using this approach, compared with a 60% mortality rate at a nearby hospital using a protocol-driven approach.

Here is Kyle-Sidell’s first video from March 31st. He’s subsequently published two more. You can see why my initial impulse would be caution.

https://www.youtube.com/watch?time_continue=1&v=k9GYTc53r2o&feature=emb_logo

Given the discussion that this is getting from peer-reviewed publications and the write-ups in Medcape, I feel comfortable that this is at least a legitimate question and discussion, whether or not it ends up producing better treatment protocols for the treatment of COVID-19. While Kyle-Sidell’s videos were the first I’d heard about this approach or theory emerging from the New York City crisis it seems like at least some physicians in Europe have come to similar conclusions.

Drought Map for April 2nd 2020

Empty Shelves Sunday 3-29-20 at Red Wing Walmart

In the area where you would find toilet paper, paper towels, bleach, Kleenex, Lysol and other cleaning supplies etc etc.  Milk limited to 1 jug, no peroxide, no rubbing alcohol… not even oximeters… This situation is typical, day after day. One can only assume it’s worse for retailers with less sophisticated supply lines.

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55,000 DEAD IN MINNESOTA -BEST CASE

UNDER THE BEST CONDITIONS, MINNESOTA WILL SEE 50,000-55,000 COVID-19 DEATHS.
The StarTrib Headline Deliberately Downplays The Facts In Their Story
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Forecast for Minnesota predicts COVID-19 surge but fewer deaths, in summer
By Jeremy Olson and Christopher Snowbeck Star Tribune staff
March 27, 2020 — 8:49pm
https://www.startribune.com/4th-minnesotan-dies-from-covid-19-as-cases-rise-to-398/569161662/

Minnesota’s new “stay-at-home” strategy could reduce predicted COVID-19 deaths in the state by up to a third, according to the researchers who conducted the modeling.

Minnesota researchers provided the first detailed look Friday at the predictive modeling that influenced Gov. Tim Walz’s “stay-at-home” strategy — which began Friday at 11:59 p.m. — to slow the spread of a novel coronavirus that has caused four deaths in the state.

The good news is that the strategy could reduce predicted COVID-19 deaths by up to a third, according to the modeling, and even more if it buys the necessary time for researchers to come up with vaccines or drugs. But the death toll could still be steep, and the modeling still predicts a point this spring or summer when an overwhelming 2 million Minnesotans are infected all at once.

“My instinct was, ‘that can’t be right. That is so incredibly high it can’t be possible,’ ” said Stefan Gildemeister, the state health economist who conducted the modeling along with researchers from the U’s School of Public Health. While “shocking,” he said the results are only estimates based on assumptions about a still-unfolding global pandemic.

Health officials on Friday also reported two of the state’s four deaths from COVID-19, the respiratory illness caused by the virus. Both involved people in their 80s who lived in long-term care facilities in Hennepin and Martin counties. Minnesota’s confirmed case count is now 398 — with 34 people hospitalized with the illness and 17 receiving intensive care.

Walz issued a two-week stay-at-home order, with plans to follow that with three weeks of lesser restrictions — which will still include dine-in restaurant, bar and school closures. After that, restrictions could be reduced except for the elderly and people with other health problems who are most at risk of severe COVID-19 infection or deaths.

Two of the models by the state and university researchers compared the impact of this strategy vs. doing nothing at all and found that it could reduce deaths by as much as a third.

Both estimates are stark. The do-nothing model predicted 74,000 deaths in Minnesota over the entire course of the pandemic, but the model for the current state strategy still predicted 50,000 to 55,000 deaths, Gildemeister said.

State officials urged extreme caution in interpreting these figures, which are based on a number of assumptions, such as the amount of face-to-face time by Minnesotans that could spread the virus. Researchers also used the global average for the infection rate of the coronavirus, but it might not spread as quickly in Minnesota as in states or cities with more population density.

“We get nervous when we focus on the number,” said Shalini Kulasingam, one of the U researchers. “It’s an estimate based on the data we currently have in hand.

“What we’re all hoping for is at some point that we can actually deploy a vaccine” that dramatically changes the predicted outcomes, she added.

The goal of the “stay-at-home” intervention is to delay the peak of COVID-19 cases by as much as five weeks, which will buy hospitals time to acquire more supplies and ventilators and give researchers more time to study potential drugs and vaccines.

“The scenarios that had been run so far really do not reflect the precise mix of strategies the governor has chosen, and certainly don’t reflect the impact of any of those strategies,” said Jan Malcolm, state health commissioner.
Ventilators are of particular need. While 80% of those who contract corona¬virus infections have only mild to moderate symptoms, as many as 5% suffer severe symptoms and breathing problems that require intensive care.

While the state now has 1,268 ventilators for adults, Walz said that might not be enough at the peak and that “we are working on procuring what we think is going to be needed.”

Under the do-nothing model, the state would run out of intensive care beds in six weeks and see a peak in COVID-19 cases in nine weeks. Now, state officials hope the peak won’t come for 14 weeks.

Other national models haven’t predicted such severe outcomes, even for Minnesota, including those by the University of Washington Center for Health Trends and Forecasts, for the next four months. But each analysis is unique and based on different sets of assumptions.

Key assumptions by the Minnesota researchers included that face-to-face contact — the most likely method of virus transmission — will be reduced by 80% for the next two weeks due to the number of people staying at home and away from large gatherings.
Walz said Minnesotans have already practiced social distancing and that the results have shown up in various ways, including a 49% decline in traffic accidents.

Total predicted infection estimates for the state also rely on the current thinking that people are inoculated after initial infections and can’t get sick again — at least not right away.

Researchers in China recently infected monkeys with the virus, and then challenged them again and found no second cases of illness, said Michael Osterholm, director of the U’s Center for Infectious Disease Research and Policy. “We now have evidence to some immunity that occurs after infection, which is very important in terms of stopping ongoing transmission.”

Minnesota’s modeling shows a sharp decline in cases after the outbreak peaks, because so many people will have recovered and will no longer be infection risks. Osterholm said that presents an opportunity to mobilize people who have recovered.
So far, the state Health Department reports 180 confirmed cases of people who have recovered and are no longer required to be isolated.

“These are the people who can walk in the mouth of the lion and not worry about it,” Osterholm said.

State researchers have conducted dozens of models, including looking at ways to “flatten” the peak of cases through the extension of stay-at-home conditions for months. The researchers did not reveal those models on Friday, noting they are unrealistic in a U.S. democracy compared to countries with authoritarian governments that could force those conditions.

Osterholm said data modeling results can vary dramatically but still don’t change the looming impact of COVID-19 or the need for people to take it seriously right now.

Osterholm on Rogan Radio