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

Thanks- has reviews seem decent. I'm sure I read somewhere about a doctor worried he was going to catch coronavirus citing the oximeter as a crucial bit of kit.

This was the article that made me go shopping:
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.
 
Can someone please tell me if this article on oximeters is just another mask-fiasco or whether it carries some authority?

https://qz.com/1832464/pulse-oximeters-for-coronavirus-unnecessary-but-selling-strong/

Some pulmonologist is saying it's a waste of money. And my wife has been convinced.

They’re right that they’re pointless if you don’t have any symptoms. And shouldn’t be used to screen for infection. Definitely useful to have if you do get sick and feel super rough but are not sure if you should go to hospital or not.
 
Interesting to read that the state of Missouri has launched a legal action against China for loss of life and economic damages.

Good luck to them and hopefully they will be successful.

Then the fun will begin.

A waste of time and some noisy statement for headlines, it needs to be done at an international level. There's no civil jurisdiction of such claims in US courts.
 
Will doctors really take any notice of a DIY test though?

It depends. There can be false pulse oximeter readings sure, in cases of hypoperfusion (e.g Raynaud's disease), nail varnish or incorrect use but finger tip sats probe are fairly easy to use, if somebody called me with COVID symptoms with repeated Sats readings in the 80s yeah I'd be confident they should be phoning 111 or an ambulance if symptoms suggestive of respiratory distress

There are some instances for example where we accept low Sats readings, e.g. COPD patients or a recovering infant with bronchiolitis. But its an important clinical vital sign, and in the case of COVID (after respiratory rate) probably the most important factor in deciding whether somebody needs an admission or not. There are plenty of clinical symptoms though however people need to be mindful of, severe shortness of breath and fatigue are red flags.

Thanks! I have two kids (5 and 4). Won't the adult one give accurate readings for them too?

I'd recommend the paediatric ones still, there's one for kids aged around 2-12 years old, neonatal ones for younger than that. Accuracy for adult ones on kids is less, I think its to do with finger diameter and the sensors
 
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It depends. There can be false pulse oximeter readings sure, in cases of hypoperfusion (e.g Raynaud's disease) or incorrect use but finger tip sats probe are fairly easy to use, if somebody called me with COVID symptoms with repeated Sats readings in the 80s yeah I'd be confident they should be phoning 111 or an ambulance if symptoms suggestive of respiratory distress

There are some instances for example where we accept low Sats readings, e.g. COPD patients or a recovering infant with bronchiolitis. But its an important clinical vital sign, and in the case of COVID (after respiratory rate) probably the most important factor in deciding whether somebody needs an admission or not.



I'd recommend the paediatric ones still, there's one for kids aged around 2-12 years old, neonatal ones for younger than that. Accuracy for adult ones on kids is less, I think its to do with finger diameter and the sensors

I’m probably just being tight but I got a “one size fits all” version. Probably going to be a few % out when doing our kids but the main thing is spotting a drop from baseline, so it doesn’t need to be perfect. Plus our kids are basically invulnerable anyway. Jammy gits.
 
This was the article that made me go shopping:
That might have been what I read, not sure- guess we're on page 758.
I might still add it to the blood pressure monitor we have from previous health worries.
Do wonder what the hospital will say if you run in screaming that the reading was only 96%!
 
I’m probably just being tight but I got a “one size fits all” version. Probably going to be a few % out when doing our kids but the main thing is spotting a drop from baseline, so it doesn’t need to be perfect. Plus our kids are basically invulnerable anyway. Jammy gits.

That's true I've worked in practices with probes for both and never really had an issue.
I was in paeds minor injuries the other day, 3 cases between me and the A&E registrar in a 10 hour shift. Crazy.
 
Warning after infection rate rises in Germany as lockdown measures eased

Health officials in Germany have warned the public not to be complacent after a rise in the country’s coronavirus infection rate.

Germany has been widely seen as a world leader in how to handle the spread of COVID-19, and this week eased lockdown measures.

However, its government agency responsible for disease control has warned there is no end in sight to the coronavirus pandemic and that the number of cases could increase again.

On Tuesday, the Robert Koch Institute (RKI) said Germany’s reproduction rate, or RO, had risen from 0.7 on Friday to 0.9, meaning someone with coronavirus is infecting roughly one other person.

Why it is to early to talk of opening up.
 
That's true I've worked in practices with probes for both and never really had an issue.
I was in paeds minor injuries the other day, 3 cases between me and the A&E registrar in a 10 hour shift. Crazy.

Ha! Living the dream. I worked in an A&E in in a rural hospital in Aus and that often happened. Two of us on night shift, taking it in turns to have a kip. Friends back home couldn’t believe it.
 
Urgh it's 'unavailable'.
The specific one that I bought is also sold out.

However, looking at this:

https://www.amazon.co.uk/Oximeter-Saturation-Fingertip-Omnidirectional-Display(black/dp/B086Q142ZD/ref=lp_2826263031_1_15_s_it?s=drugstore&ie=UTF8&qid=1587504946&sr=1-15

... it seems to be built on the same hardware as mine. It was probably manufactured in the same factory, and all. But it obviously has a slightly different logo embossed on the outside.

Delivery seems a long way out, so you may want to look at an alternative. Assuming that they're all identical on the inside, I can recommend any of the oximeters that have the yellow/blue LED displays.
 
Warning after infection rate rises in Germany as lockdown measures eased



Why it is to early to talk of opening up.

I wonder if the US States who have talked of reopening bars etc will take note?











Don’t forget to tip your waiters, I’m here all week
 
The specific one that I bought is also sold out.

However, looking at this:

https://www.amazon.co.uk/Oximeter-Saturation-Fingertip-Omnidirectional-Display(black/dp/B086Q142ZD/ref=lp_2826263031_1_15_s_it?s=drugstore&ie=UTF8&qid=1587504946&sr=1-15

... it seems to be built on the same hardware as mine. It was probably manufactured in the same factory, and all. But it obviously has a slightly different logo embossed on the outside.

Delivery seems a long way out, so you may want to look at an alternative. Assuming that they're all identical on the inside, I can recommend any of the oximeters that have the yellow/blue LED displays.
Wonder how much these were selling for in December.
 
Warning after infection rate rises in Germany as lockdown measures eased



Why it is to early to talk of opening up.
What's the news here? Of course infection rate will rise when some restrictions are listed. It's literally the parameter they're looking at when trying to figure out how much of society they can open.
 
It seems that NY is hit by a particularly nasty strain of the virus and that death rates vary a lot depending on strains:
https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1

There has been an LA study suggesting a 0.12% death rate, similar to the Stockholm one from a few days ago.
Warning after infection rate rises in Germany as lockdown measures eased



Why it is to early to talk of opening up.

Why?

This will inevitably happen any time you open up.
 
Heard from a few different people that live down in Cork. Quite a few English tourists came over to holiday homes during the Easter holidays.
how the duck is this allowed to happen?
 
It seems that NY is hit by a particularly nasty strain of the virus and that death rates vary a lot depending on strains:
https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1

That study looks at viral isolates from patients in China. Where did you read about New York having a particularly bad strain?

On a side note, the study above is done in vitro. In a non-human cell line. So certainly doesn’t tell us anything about death rates.
 
It was always the plan in my opinion. I'm expected us to release measures around May 20-25th. Personally I think the plan was always a 2month lockdown but if he'd come and said that straight off the bat people would have lost their heads - 50% through mental breakdowns and depression and 50% through thinking 'sod THAT' and defying the rules from day one.

3 + 3 + 2 was always the most likely for me, anyway.
I was under the impression a 6 week lockdown was inevitable and speaking as someone who's well and truly on the train of thought that a lockdown for any serious length of time won't work i fully agreed with it.

However unless there's a concerning spike in the next two weeks some sort of rope has to be shown now, something like can visit non elderly relitves and freinds homes if nothing else.
 
It seems that NY is hit by a particularly nasty strain of the virus and that death rates vary a lot depending on strains:
https://www.medrxiv.org/content/10.1101/2020.04.14.20060160v1

There has been an LA study suggesting a 0.12% death rate, similar to the Stockholm one from a few days ago.

Why?

This will inevitably happen any time you open up.
Not sure this has much to do with what you said. The study was totally done in China, and had a sample of 11 infected people.
 
@Pogue Mahone @Revan

I am aware that it is regarding China. The point is that it suggests that there are different strains wtih significantly different outcomes.

Comparing numbers from NY and Italy and numbers elsewhere, combined with the above, a possible explanation is that those places are dominantly being struck by more lethal strains.
 
A waste of time and some noisy statement for headlines, it needs to be done at an international level. There's no civil jurisdiction of such claims in US courts.

Entirely agree with you. It's pointless as it's impossible to prove in a Court of law that they did something they shouldn't have done. Furthermore more there is no international law about this specifically what any country has to do.
 
@Pogue Mahone @Revan

I am aware that it is regarding China. The point is that it suggests that there are different strains wtih significantly different outcomes.

Comparing numbers from NY and Italy and numbers elsewhere, combined with the above, a possible explanation is that those places are dominantly being struck by more lethal strains.

This is what I have heard too. There are different strains discovered in different countries.
 


Technically you don't die of coronavirus unless you're diagnosed for it, and I guess unless there's a coroners investigation after death. I can see the latter not happening because 1) there's too many deaths 2) govt pressure not to investigate the cause - especially for those who are not dying in hospitals.
 
What's the news here? Of course infection rate will rise when some restrictions are listed. It's literally the parameter they're looking at when trying to figure out how much of society they can open.

The news is that Germany, seen by many as a positive example for other big countries, has taken a very small step on Monday. Measures which were critcized as too careful by some and which haven't even been fully implemented yet, especially for schools which are supposed to be rebooted deliberately one school year at a time (or not at all in some states). I also assume that testing data won't show the full impact of these changes within two days. And still R is basically already back at the sustainable limit. There is still some potential from masks which aren't mandatory in public yet, but if that doesn't compensate for the bump then we might even see a roll back of what little easment was attempted.
 
I don’t think anyone who’s been able to do their job from home should - or will be allowed to - return to their office again when current lockdown is eased. And that will likely be the status quo for the next year or two.
Working in the public sector in a job that can be done remotely, I’ll be very surprised if I am back in the office this year. My employer would both have to be incredibly irresponsible on a pastoral level and lose sight of the bigger picture to expect us to routinely commute in packed public transport and sit in a heavily populated office for virtually no benefit.
 
That paper isn't peer reviewed and also says "However, no mutation has been directly linked with functional changes in viral pathogenicity."

Not too many hard facts available at the moment, are there?

I was just throwing out an idea that might explain a few things. We will obviously find out for sure over the coming months.
 
This is what I have heard too. There are different strains discovered in different countries.

SARS-CoV-2 is a strain of the original SARS virus. To be a new strain genetic variation isn't enough. From what I have read I believe that you have to demonstrate a phenotypic (physical) change such as a antigen variation that alters the behaviour of a virus before it can be designated as a strain.

There are slight genetic variations in SARS-CoV-2 in different places with some researchers speculating that there may be 2 or even 3 main strains of SARS-CoV-2 but everything I've read so far suggests that these are not truly strains and that the genetic mutation rate of the virus is quite low which is encouraging for vaccine development.

Some papers do talk about strains of SARS-CoV-2 but reading the rest of the paper makes me wonder if a) I don't understand the term strain properly, b) the paper doesn't use the term strain correctly or c) strain isn't a firmly defined nomenclature?
https://www.sciencedirect.com/science/article/pii/S1567134820300915

The Daily Mail went with a headline claiming there were 30 strains which is just typically irresponsible Mail bullshit.
 
Not too many hard facts available at the moment, are there?

I was just throwing out an idea that might explain a few things. We will obviously find out for sure over the coming months.

There is evidence albeit often incomplete and in some cases conflicting (which will be explained in due course). And while there is some talk of strains from researchers (often in very small isolated studies) the big picture data so far suggests that there isn't enough variation to prevent the development of a vaccine and if we do so (not a given of course) then the immunity will last a reasonable time. Most of the talk of different strains seems to be bad reporting from idiots like the Daily Mail.
 
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Interesting paper that proposes variations in human genetics rather than virus genetics for regional variations in prevalence and mortality. No idea how good, bad or indifferent the publication is which makes it hard to judge the quality of the paper. This is a problem with much of what is being written at the moment as full peer review in top quality peer reviewed primary literature takes much longer and demands far more rigorous data collection and analysis than is possible in such a rapidly evolving situation.

https://www.degruyter.com/view/jour...-2020-0425/article-10.1515-cclm-2020-0425.xml
 
Interesting paper that proposes variations in human genetics rather than virus genetics for regional variations in prevalence and mortality. No idea how good, bad or indifferent the publication is which makes it hard to judge the quality of the paper. This is a problem with much of what is being written at the moment as full peer review in top quality peer reviewed primary literature takes much longer and demands far more rigorous data collection and analysis than is possible in such a rapidly evolving situation.

https://www.degruyter.com/view/jour...-2020-0425/article-10.1515-cclm-2020-0425.xml

Here is to hoping that this is indeed the case.
 
Here we go with the deadlier strains thing again. I give it two days before we’re round to “Herd Immunity” and then back to “it was leaked from
a Chinese lab”.....
 
SARS-CoV-2 is a strain of the original SARS virus. To be a new strain genetic variation isn't enough. From what I have read I believe that you have to demonstrate a phenotypic (physical) change such as a antigen variation that alters the behaviour of a virus before it can be designated as a strain.

There are slight genetic variations in SARS-CoV-2 in different places with some researchers speculating that there may be 2 or even 3 main strains of SARS-CoV-2 but everything I've read so far suggests that these are not truly strains and that the genetic mutation rate of the virus is quite low which is encouraging for vaccine development.

Some papers do talk about strains of SARS-CoV-2 but reading the rest of the paper makes me wonder if a) I don't understand the term strain properly, b) the paper doesn't use the term strain correctly or c) strain isn't a firmly defined nomenclature?
https://www.sciencedirect.com/science/article/pii/S1567134820300915

The Daily Mail went with a headline claiming there were 30 strains which is just typically irresponsible Mail bullshit.

I don’t think it is true that SARS 2 is a different strain of SARS. More like being different viruses which are similar to each other (probably comparable to two influenza A viruses like H1N1 and H3N2 but might be wrong).

Also, a virus having different strains does not necessarily means that a vaccine won’t be developed. For example there are many strains of H1N1, but the vaccine is definitely efficient against it (though you expect a strain to dominate for some period of time - typically vaccines are updated every year for some new strain). Only when some strain differs significantly (probably by recombining with some other virus or some strain of the same virus in a different animal which is what happened in 2009 for the swine pandemic) the vaccine might not be effective.

Maybe @berbatrick can shed some light here.
 
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I don’t think it is true that SARS 2 is a different strain of SARS. More like being different viruses which are similar to each other (probably comparable to two influenza A viruses like H1N1 and H3N2 but might be wrong).

Also, a virus having different strains does not necessarily means that a vaccine won’t be developed. For example there are many strains of H1N1, but the vaccine is definitely efficient against it (though you expect a strain to dominate for some period of time - typically vaccines are updated every year for some new strain). Only when some strain differs significantly (probably by recombining with some other virus or some strain of the same virus in a different animal which is what happened in 2009 for the swine pandemic) the vaccine might not be effective.

Maybe @berbatrick can shed some light here.

I'm not sure either. SARS-CoV-2 is often referred to as a strain but I also keep finding conflicting definitions of what constitutes a strain. Some involve genetic variation only and other require a phenotypic change that alters the behaviour of the virus. The former won't necessarily impact vaccine development but the later will (or could).