SARS CoV-2 coronavirus / Covid-19 (No tin foil hat silliness please)

That’s the most peculiar thing about it. Why a serious scientist would even try to draw conclusions about such a trivial amount of data.

Week 1. 3.5% random test bearing virus of 750ish people in Stockholm.

Week 1.5. 7.5% of all pregnant woman coming in for child bearing virus in Stockholm

Week 2.5. 11% of 100 Stockholm blood donors have had virus on antibody test. Test is approx. 80%.

Not surprised you guys are playing the pessimists again though.
 
Stockholm had a random sample study end of March, result was 2,5% on that time had it (not antibody). So 5-8% when including recovered. So 11% isn't impossible at all in Stockholm city (1m), impossible for Sweden and unlikely for Greater stockholm (2.3m). And it isn't contradictory to what I have said before. But in general the more biased and smaller the sample the more Regulus likes it.

It’s definitely possible that the worst hit town at the centre of an epidemic can have 10-20% of people infected. The German town with the most cases apparently had 14% prevalence. This tells us feck all about the country as a whole, though. And herd immunity will be about the whole country, not specific hot spots.

Unless you find a way to stop all travel within that country. Somehow hope that Stockholm can work on herd immunity in complete isolation from the rest of Sweden. Which would be a completely bonkers and unworkable plan.
 
That’s consistent with the serology testing from blood donors in European countries. 1.5%. This fecking thing kills 1 in 100 people it infects. The idea that we’d find 10-30% of the population of an entire country already infected was always a pipe dream. The death toll from that would be astronomical.

69 deaths with a range of 48,000 and 81,000 infections is not 1%

@Revan

What am I missing?
 
Stockholm had a random sample study end of March, result was 2,5% on that time had it (not antibody). So 5-8% when including recovered. So 11% isn't impossible at all in Stockholm city (1m), impossible for Sweden and unlikely for Greater stockholm (2.3m). And it isn't contradictory to what I have said before. But in general the more biased and smaller the sample the more Regulus likes it.

I like optimistic, positive results in any form in fairness.
I’ll like it better when it’s done en masse and shows a huge percentage of infected in this City.
This result following on from the 2 previous studies is cause for optimism, if you’re that way inclined like. Which many here absolutely are not.
 
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It’s definitely possible that the worst hit town at the centre of an epidemic can have 10-20% of people infected. The German town with the most cases apparently had 14% prevalence. This tells us feck all about the country as a whole, though. And herd immunity will be about the whole country, not specific hot spots.

Unless you find a way to stop all travel within that country. Somehow hope that Stockholm can work on herd immunity in complete isolation from the rest of Sweden. Which would be a completely bonkers and unworkable plan.
Indeed.
 
That’s consistent with the serology testing from blood donors in European countries. 1.5%. This fecking thing kills 1 in 100 people it infects. The idea that we’d find 10-30% of the population of an entire country already infected was always a pipe dream. The death toll from that would be astronomical.

What are you basing this on?
 
?

There's 69 deaths from ~60,000 infections. So where did you get the "this disease kills 1 in 100"?

Isn't this very good news? Or would you rather be right?
That Santa Clara study has loads of problems. Also in NYC already 0,15% of total population has already died and 100% aren't infected obviously. So far I think our best study is the one from Gangelt, Germany, that had a 0,37% death rate, but it isn't published/finished yet.
 
?

There's 69 deaths from ~60,000 infections. So where did you get the "this disease kills 1 in 100"?

Isn't this very good news? Or would you rather be right?
Ah, ok, got it. These numbers do not match anything else right there. It puts the mortality rate at the flu's level. It also means that there should be 1/3 of the Iceland population be infected, in order for them to reach 10 deaths (but Iceland studies, show only 0.6% of people being infected). It also means that in Bergamo region (who has the same population as Stockholm, every person had to have been infected 4 times, in order to reach their 4500 deaths.

So, there are four options here:

- Stockhol's study is nonsense.
- Stockholm is hiding thousands of deaths.
- Stockholm people are hardcore badasses, and the virus does feck all to them.
- Stockholm does not have 60k infections.

Again, I am using your 69 as the number of deaths in Stockholm. Is this true?
 
This new test (see above) makes you sound like another know it all, know feck all.
Just because massi, the insufferable nitpicking pedant from redcafe “told me”, means naff all to me mate, I listen to experts.

Maybe take a step back and realise you don’t have all of the answers, if any. As I suggested, pregnant woman go into a completely different section of a hospital, nowhere near to where Covid-19 patients are doctors/nurses would be and weren’t/aren’t much more at risk, if at all.

Just want to add something to your comment about pregnant women going to a completely different section of the hospital from covid patients. Firstly im a doctor working in obstetrics, our unit for pregnant women has a covid 19 area and a ' clean' area. They are effectively on the same ward although there is some separation through a few doors and it has different entrances. However the staff that work in both areas are the same. We do get suspected covid patients into our unit who have symptoms but the reason the come into hospital is a pregnancy problem.

Also the same doctors who work in obstetrics in the UK also work in gynaecology in which part of the role will be going to A&E, covid 19 assessment areas and wards for patients that have come with gynaecology problems but also happen to currently have or suspected to have corona virus. Also our gynaecology ward is 5 foot away across a corridor from one of our coronvirus wards where pregnant women up to 20 weeks would be admitted.

That's not even counting the fact that all the interactions that all staff have with each other from different areas throughout a shift in hospital canteens, corridors, lifts, break rooms etc have
 
Ah, ok, got it. These numbers do not match anything else right there. It puts the mortality rate at the flu's level. It also means that there should be 1/3 of the Iceland population be infected, in order for them to reach 10 deaths (but Iceland studies, show only 0.6% of people being infected). It also means that in Bergamo region (who has the same population as Stockholm, every person had to have been infected 4 times, in order to reach their 4500 deaths.

So, there are four options here:

- Stockhol's study is nonsense.
- Stockholm is hiding thousands of deaths.
- Stockholm people are hardcore badasses, and the virus does feck all to them.
- Stockholm does not have 60k infections.

Again, I am using your 69 as the number of deaths in Stockholm. Is this true?
Think he talks about the Santa Clara/Stanford study. Stockholm city has around 400-500 death, lazy to check.
 
I don't understand your post without providing more context.

Sure, I'm referring to this study:

https://www.medrxiv.org/content/10.1101/2020.04.14.20062463v1.full.pdf

It suggests the amount of infections in Santa Clara ranges between 48,000 and 81,000 people infected in Santa Clara County by early April, 50- 85-fold more than the number of confirmed cases. As of Friday, there were 69 confirmed deaths Friday (72 today)

You wrote https://www.redcafe.net/threads/wuh...illiness-or-memes-please.452816/post-25496486
feck was expecting a bit more than this.

But then it might mean that heavy-hit places like New York or Italy/Spain might have a bit more. I think Italy is guesstimating to have 10% of the population who have been infected.

to which @Pogue Mahone replied:

That’s consistent with the serology testing from blood donors in European countries. 1.5%. This fecking thing kills 1 in 100 people it infects. The idea that we’d find 10-30% of the population of an entire country already infected was always a pipe dream. The death toll from that would be astronomical.

You replied:

I think it is less than that, but yep, it could well be in that region.

My hope was more based on Stockholm/New York's testing of women giving birth when they found something like 12% or so of them being infected (naturally, more would have been infected and have healed by the time of the testing).

So, 72 deaths out 70,000 infected does not imply this fecking thing kills 1 in 100 people it infects, it implies ~1 in 1000 people.
 
?

There's 69 deaths from ~60,000 infections. So where did you get the "this disease kills 1 in 100"?

Isn't this very good news? Or would you rather be right?

You seem to be assuming one - badly designed - study is the only mortality data that matters. Really weird way to look at this. I presume you’ve no scientific background?

Re the Santa Clara study, they estimated prevalence by advertising on fecking Facebook for volunteers to get tested. Which will inevitably get the vast majority of responses from people that have recently recovered from a viral illness. Which is a huge source of bias that will grossly inflate their prevalence estimates.

The Icelandic study (linked above) is far better designed and is the only one I’ve seen that sets out to test a properly random cross-section of society. Needless to say their calculation of prevalence is a tiny fraction of the Santa Clara study.
 
You seem to be assuming one - badly designed - study is the only mortality data that matters. Really weird way to look at this. I presume you’ve no scientific background?

Re the Santa Clara study, they estimated prevalence by advertising on fecking Facebook for volunteers to get tested. Which will inevitably get the vast majority of responses from people that have recently recovered from a viral illness. Which is a huge source of bias that will grossly inflate their prevalence estimates.

The Icelandic study (linked above) is far better designed and is the only one I’ve seen that sets out to test a properly random cross-section of society. Needless to say their calculation of prevalence is a tiny fraction of the Santa Clara study.

Physics and Math background + MBA thanks for asking.

So you're saying the sampling of the data from Stanford Univ was biased and not representative. Fair enough.
 
Sure, I'm referring to this study:

https://www.medrxiv.org/content/10.1101/2020.04.14.20062463v1.full.pdf

It suggests the amount of infections in Santa Clara ranges between 48,000 and 81,000 people infected in Santa Clara County by early April, 50- 85-fold more than the number of confirmed cases. As of Friday, there were 69 confirmed deaths Friday (72 today)

You wrote https://www.redcafe.net/threads/wuh...illiness-or-memes-please.452816/post-25496486


to which @Pogue Mahone replied:



You replied:



So, 72 deaths out 70,000 infected does not imply this fecking thing kills 1 in 100 people it infects, it implies ~1 in 1000 people.
Ah, ok. It is about Santa Clara instead of Stockholm.

69 deaths for 48k (assuming the conservative lower bound) puts the death rate at 0.14%, which might be a bit too good to be true, or a bit population skewed (I don't have the data about the demographics, but most people I see here are relatively young, probably cause tech workers, in general are young and there are a shitload of tech workers in this area). At upper bound, it puts the death rate to be lower than that of the flu, which probably is total nonsense.

And as Pogue explained, the data looks a bit biased. Though, I would have thought that in such an experiment it would have made sense to use only people who have not been diagnosed before. Are we sure that they did not do that?
 
Physics and Math background + MBA thanks for asking.

So you're saying the sampling of the data from Stanford Univ was biased and not representative. Fair enough.
I agree with Pogue. We need a true random sample or a whole population study. How do you explain that NYC already has 0,15% of total population died?
 
I agree with Pogue. We need a true random sample or a whole population study. How do you explain that NYC already has 0,15% of total population died?
Yep.

If Santa Clara'sstudy mortality rate gets extrapolated to NYC, then it means that everyone in NYC is infected (to reach the number of deaths).
 
Physics and Math background + MBA thanks for asking.

So you're saying the sampling of the data from Stanford Univ was biased and not representative. Fair enough.

I’m saying it’s a lot more prone to bias than the Icelandic study. The only way any of us can try and work out what the feck is going on is by trying to digest as much of the overall evidence base as we can. We can ignore the REALLY badly designed studies but I wouldn’t put Santa Clara in that category. Interestingly, their range of confidence for ‘true’ prevalence would include what we’re seeing in other studies, 1.5 - 2.5%. It’s only when they make some sketchy assumptions about the test missing cases with false negatives that they bump the prevalence up to a level which brings the mortality down to flu-type levels.

My “1 in 100” comment was a bit throwaway. Nobody knows for certain the mortality. We’re all guessing. And we won’t know until loads more countries do the same rigorous testing that Iceland did. 1% mortality does seem about right though. Hopefully a little lower. I’ve been hoping to see good evidence of prevalence being much higher than everyone thought but, so far, the better the evidence the lower the prevalence.
 
Cool - just coming online after the weekend and started reading this thread from Friday. Was excited when I saw this study at first cut, but as soon as I read Ioannidis' name in there I became a little more skeptical...
 
Yeah, but in practical terms the sensitivity must be limited by the sampling process... Whilst the specificity is not, I presume.

I say that because we had a patient (assymptomatic) whom went from positive to negative very shortly, unless we caught him exactly at the time of "recovery/cure" one of those should be false. I was arguing with my colleagues that it was much more likely that the negative was the false result.

I've seen at least one patient going pos-pos-neg-pos-neg-neg (cured) and that 4th test was very hard on him psychologically.

Unless other bugs that may cause cross-reactivity aren't being extracted either, I agree. And I doubt that is the case.

I think you'll be interested in figure 2 of this. You'll see recovering patients bounce back and forth between positive and negative until they are ultimately consistently negative. Check out they detected this in stool samples!

https://www.nature.com/articles/s41586-020-2196-x
 
Yup, they have overtaken Lombardy as the worst hit large area. Although Lombardy probably undercounts its deaths quite a lot.
I think a lot has to do that the deaths were not uniformly spread in Lombardy. Bergamo's region was much more hit than the other areas (which has only 1 million people or so, but 5k deaths or so).

But in any case yes, New York City is so far the worst-hit region in the world.
 
I agree with Pogue. We need a true random sample or a whole population study. How do you explain that NYC already has 0,15% of total population died?
Wait, where are you getting the 0.15 % from? That sounds a touch high.

EDIT: I'm getting 0.09 %.
 
Really interesting article about the Pneumonia part of Covid-19 and the possibility to use pulse oximetry to diagnose cov-19 and also help people before they get too sick.

https://www.nytimes.com/2020/04/20/opinion/coronavirus-testing-pneumonia.html

Gah. Pay-walled. I actually ordered a pulse oximeter off Amazon a while back. It’s the best way to know if you need to go into hospital. I was paranoid about getting sick but not knowing if I was sick enough to need to be hospitalised. Knowing my own O2 sats would be a big help if it ever comes to that. They’re pretty cheap too.
 
I think a lot has to do that the deaths were not uniformly spread in Lombardy. Bergamo's region was much more hit than the other areas (which has only 1 million people or so, but 5k deaths or so).

But in any case yes, New York City is so far the worst-hit region in the world.
Indeed. Maybe at the months end we get more data from Bergamo again.
 
Gah. Pay-walled. I actually ordered a pulse oximeter off Amazon a while back. It’s the best way to know if you need to go into hospital. I was paranoid about getting sick but not knowing if I was sick enough to need to be hospitalised. Knowing my own O2 sats would be a big help if it ever comes to that. They’re pretty cheap too.

HTH

I have been practicing emergency medicine for 30 years. In 1994 I invented an imaging system for teaching intubation, the procedure of inserting breathing tubes. This led me to perform research into this procedure, and subsequently teach airway procedure courses to physicians worldwide for the last two decades.
So at the end of March, as a crush of Covid-19 patients began overwhelming hospitals in New York City, I volunteered to spend 10 days at Bellevue, helping at the hospital where I trained. Over those days, I realized that we are not detecting the deadly pneumonia the virus causes early enough and that we could be doing more to keep patients off ventilators — and alive.

On the long drive to New York from my home in New Hampshire, I called my friend Nick Caputo, an emergency physician in the Bronx, who was already in the thick of it. I wanted to know what I was facing, how to stay safe and about his insights into airway management with this disease. “Rich,” he said, “it’s like nothing I’ve ever seen before.”

He was right. Pneumonia caused by the coronavirus has had a stunning impact on the city’s hospital system. Normally an E.R. has a mix of patients with conditions ranging from the serious, such as heart attacks, strokes and traumatic injuries, to the nonlife-threatening, such as minor lacerations, intoxication, orthopedic injuries and migraine headaches.

During my recent time at Bellevue, though, almost all the E.R. patients had Covid pneumonia. Within the first hour of my first shift I inserted breathing tubes into two patients.

Even patients without respiratory complaints had Covid pneumonia. The patient stabbed in the shoulder, whom we X-rayed because we worried he had a collapsed lung, actually had Covid pneumonia. In patients on whom we did CT scans because they were injured in falls, we coincidentally found Covid pneumonia. Elderly patients who had passed out for unknown reasons and a number of diabetic patients were found to have it.

And here is what really surprised us: These patients did not report any sensation of breathing problems, even though their chest X-rays showed diffuse pneumonia and their oxygen was below normal. How could this be?


We are just beginning to recognize that Covid pneumonia initially causes a form of oxygen deprivation we call “silent hypoxia” — “silent” because of its insidious, hard-to-detect nature.

Pneumonia is an infection of the lungs in which the air sacs fill with fluid or pus. Normally, patients develop chest discomfort, pain with breathing and other breathing problems. But when Covid pneumonia first strikes, patients don’t feel short of breath, even as their oxygen levels fall. And by the time they do, they have alarmingly low oxygen levels and moderate-to-severe pneumonia (as seen on chest X-rays). Normal oxygen saturation for most persons at sea level is 94 percent to 100 percent; Covid pneumonia patients I saw had oxygen saturations as low as 50 percent.

To my amazement, most patients I saw said they had been sick for a week or so with fever, cough, upset stomach and fatigue, but they only became short of breath the day they came to the hospital. Their pneumonia had clearly been going on for days, but by the time they felt they had to go to the hospital, they were often already in critical condition.

In emergency departments we insert breathing tubes in critically ill patients for a variety of reasons. In my 30 years of practice, however, most patients requiring emergency intubation are in shock, have altered mental status or are grunting to breathe. Patients requiring intubation because of acute hypoxia are often unconscious or using every muscle they can to take a breath. They are in extreme duress. Covid pneumonia cases are very different.

A vast majority of Covid pneumonia patients I met had remarkably low oxygen saturations at triage — seemingly incompatible with life — but they were using their cellphones as we put them on monitors. Although breathing fast, they had relatively minimal apparent distress, despite dangerously low oxygen levels and terrible pneumonia on chest X-rays.

We are only just beginning to understand why this is so. The coronavirus attacks lung cells that make surfactant. This substance helps keep the air sacs in the lungs stay open between breaths and is critical to normal lung function. As the inflammation from Covid pneumonia starts, it causes the air sacs to collapse, and oxygen levels fall. Yet the lungs initially remain “compliant,” not yet stiff or heavy with fluid. This means patients can still expel carbon dioxide — and without a buildup of carbon dioxide, patients do not feel short of breath.

Patients compensate for the low oxygen in their blood by breathing faster and deeper — and this happens without their realizing it. This silent hypoxia, and the patient’s physiological response to it, causes even more inflammation and more air sacs to collapse, and the pneumonia worsens until their oxygen levels plummet. In effect, the patient is injuring their own lungs by breathing harder and harder. Twenty percent of Covid pneumonia patients then go on to a second and deadlier phase of lung injury. Fluid builds up and the lungs become stiff, carbon dioxide rises, and patients develop acute respiratory failure.

By the time patients have noticeable trouble breathing and present to the hospital with dangerously low oxygen levels, many will ultimately require a ventilator.

Silent hypoxia progressing rapidly to respiratory failure explains cases of Covid-19 patients dying suddenly after not feeling short of breath. (It appears that most Covid-19 patients experience relatively mild symptoms and get over the illness in a week or two without treatment.)

A major reason this pandemic is straining our health system is the alarming severity of lung injury patients have when they arrive in emergency rooms. Covid-19 overwhelmingly kills through the lungs. And because so many patients are not going to the hospital until their pneumonia is already well advanced, many wind up on ventilators, causing shortages of the machines. And once on ventilators, many die.

Avoiding the use of a ventilator is a huge win for both patient and the health care system. The resources needed for patients on ventilators are staggering. Vented patients require multiple sedatives so that they don’t buck the vent or accidentally remove their breathing tubes; they need intravenous and arterial lines, IV medicines and IV pumps. In addition to a tube in the trachea, they have tubes in their stomach and bladder. Teams of people are required to move each patient, turning them on their stomach and then their back, twice a day to improve lung function.

There is a way we could identify more patients who have Covid pneumonia sooner and treat them more effectively — and it would not require waiting for a coronavirus test at a hospital or doctor’s office. It requires detecting silent hypoxia early through a common medical device that can be purchased without a prescription at most pharmacies: a pulse oximeter.

Pulse oximetry is no more complicated than using a thermometer. These small devices turn on with one button and are placed on a fingertip. In a few seconds, two numbers are displayed: oxygen saturation and pulse rate. Pulse oximeters are extremely reliable in detecting oxygenation problems and elevated heart rates.
Pulse oximeters helped save the lives of two emergency physicians I know, alerting them early on to the need for treatment. When they noticed their oxygen levels declining, both went to the hospital and recovered (though one waited longer and required more treatment). Detection of hypoxia, early treatment and close monitoring apparently also worked for Boris Johnson, the British prime minister.

Widespread pulse oximetry screening for Covid pneumonia — whether people check themselves on home devices or go to clinics or doctors’ offices — could provide an early warning system for the kinds of breathing problems associated with Covid pneumonia.

People using the devices at home would want to consult with their doctors to reduce the number of people who come to the E.R. unnecessarily because they misinterpret their device. There also may be some patients who have unrecognized chronic lung problems and have borderline or slightly low oxygen saturations unrelated to Covid-19.

All patients who have tested positive for the coronavirus should have pulse oximetry monitoring for two weeks, the period during which Covid pneumonia typically develops. All persons with cough, fatigue and fevers should also have pulse oximeter monitoring even if they have not had virus testing, or even if their swab test was negative, because those tests are only about 70 percent accurate. A vast majority of Americans who have been exposed to the virus don’t know it.

There are other things we can do as well to avoid immediately resorting to intubation and a ventilator. Patient positioning maneuvers (having patients lie on their stomach and sides) opens up the lower and posterior lungs most affected in Covid pneumonia. Oxygenation and positioning helped patients breathe easier and seemed to prevent progression of the disease in many cases. In a preliminary study by Dr. Caputo, this strategy helped keep three out of four patients with advanced Covid pneumonia from needing a ventilator in the first 24 hours.

To date, Covid-19 has killed more than 40,600 people nationwide — more than 10,000 in New York State alone. Oximeters are not 100 percent accurate, and they are not a panacea. There will be deaths and bad outcomes that are not preventable. We don’t fully understand why certain patients get so sick, or why some go on to develop multi-organ failure. Many elderly people, already weak with chronic illness, and those with underlying lung disease do very poorly with Covid pneumonia, despite aggressive treatment.

But we can do better. Right now, many emergency rooms are either being crushed by this one disease or waiting for it to hit. We must direct resources to identifying and treating the initial phase of Covid pneumonia earlier by screening for silent hypoxia.

It’s time to get ahead of this virus instead of chasing it.

Richard Levitan, an emergency physician in Littleton, N.H., is president of Airway Cam Technologies, a company that teaches courses in intubation and airway management.
 
Gah. Pay-walled. I actually ordered a pulse oximeter off Amazon a while back. It’s the best way to know if you need to go into hospital. I was paranoid about getting sick but not knowing if I was sick enough to need to be hospitalised. Knowing my own O2 sats would be a big help if it ever comes to that. They’re pretty cheap too.
There is a vaccine for pneumonia, does it help somewhat here (obviously not totally against covid) or is this pneumonia somehow different
 

This isn't anything shocking. They are saying they don't know how much immunity previous infection gives. Not that there won't be any but normal scientific caution. Which is entirely appropriate.

Another statement WHO made has been misinterpreted. They said that tests suggested that only 2% of people worldwide had been infected according to testing, this was taken as saying that people didn't get immunity after infection which wasn't what it said.

I think WHO and other experts are trying to temper the expectation that this WILL result in a vaccine in 12-18 months time. Things are looking promising but many promising medicines fail during the testing process.