COVID-19

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Not really news, just confirmation: the Italians are already splitting their vents.


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To change the subject, a bit of "relaxation material":

 
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This is amazing!

Could be big. Worry about the confounding of coinfection without a cardiac muscle biopsy...
I figured that if we ever reached a steady state in this disease spread, IVIG would end up being a potentially useful tool, but without enough COVID exposure was unsure of the utility at this point.
 
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One of my patients died in week 3. Was getting better but suddenly developed refractory hypoxia. He was on vent throughout and also on hydroxychloroquine. Another was also getting better on 1 L but suddenly day 8 we have gone from 1 to 15 L. I don’t understand this infection at all. Why does it rebound ?
 
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Anybody seen a picture of these Tesla vents? curious to see how they produced so many in such a short period of time
 
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One of my patients died in week 3. Was getting better but suddenly developed refractory hypoxia. He was on vent throughout and also on hydroxychloroquine. Another was also getting better on 1 L but suddenly day 8 we have gone from 1 to 15 L. I don’t understand this infection at all. Why does it rebound ?
This virus causes multiorgan pathology, because we have no immunity to it (and it causes a hell of a cytokine storm). Anything can go wrong, even late in the disease. It's the kind of adversary you need to beat more than once.


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One of my patients died in week 3. Was getting better but suddenly developed refractory hypoxia. He was on vent throughout and also on hydroxychloroquine. Another was also getting better on 1 L but suddenly day 8 we have gone from 1 to 15 L. I don’t understand this infection at all. Why does it rebound ?
Maybe it was flash pulmonary edema from acute CHF?
 
Do you guys have any idea why there is such a huge discrepancy in outcomes for infected patients? On the one hand, this disease is 10 to 50 times more lethal than the flu, and it's fairly common for people under 50 to end up intubated in the ICU, something that is almost unheard of with the regular flu. But then on the other hand, they say a huge fraction of patients have very mild symptoms or may be completely asymptomatic and never even know they had it!

This is truly bizarre, because if you get the flu, you get smashed and definitely feel it, so why would this much more virulent disease have a median presentation that is milder than the median influenza presentation?
 
Do you guys have any idea why there is such a huge discrepancy in outcomes for infected patients? On the one hand, this disease is 10 to 50 times more lethal than the flu, and it's fairly common for people under 50 to end up intubated in the ICU, something that is almost unheard of with the regular flu. But then on the other hand, they say a huge fraction of patients have very mild symptoms or may be completely asymptomatic and never even know they had it!

This is truly bizarre, because if you get the flu, you get smashed and definitely feel it, so why would this much more virulent disease have a median presentation that is milder than the median influenza presentation?
There were at least two strains in China, with different levels of severity of disease. In the meanwhile, they have tracked even more than two, AFAIK.

Viruses mutate, Actually, one of the ways we could get out of this mess would be a lucky mutation which would make the infections milder.

Not everybody has the same level of symptoms with the flu either. For example, I can't remember the last time I had myalgias in my life.
 
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There were at least two strains in China, with different levels of severity of disease. In the meanwhile, they have tracked even more than two, AFAIK.

Viruses mutate, Actually, one of the ways we could get out of this mess would be a lucky mutation which would make the infections milder.

Not everybody has the same level of symptoms with the flu either. For example, I can't remember the last time I had myalgias in my life.

My guess is that some people simply have more random circulating natural immunity and or some cross over from other corona viruses they have been exposed to with similar enough phenotypes that have antibodies with mild activity against the current virus.
 
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My guess is that some people simply have more random circulating natural immunity and or some cross over from other corona viruses they have been exposed to with similar enough phenotypes that have antibodies with mild activity against the current virus.
That, too. Also the immune response differs from individual to individual, and, since the cytokine storm seems to be more dangerous than the virus itself, that's why we are seeing multiple people dead in the same family, I guess. I think genetics matter, like in malaria.
 
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There were at least two strains in China, with different levels of severity of disease. In the meanwhile, they have tracked even more than two, AFAIK.

Viruses mutate, Actually, one of the ways we could get out of this mess would be a lucky mutation which would make the infections milder.

Not everybody has the same level of symptoms with the flu either. For example, I can't remember the last time I had myalgias in my life.

It's arguable that different strains actually impact disease severity.

See: Response to “On the origin and continuing evolution of SARS-CoV-2”

There were multiple methodological errors in the paper that claimed that and one of their figures basically doesn't even make sense.

I think overall we're getting a flood of open access papers that have undergone very quick or minimal reviewing as this thing progresses. Likely literally papers that seem that they must have had a turnaround time of a couple weeks based on the data they're presenting. Also getting some very iffy papers out of China to take with a grain of salt. It's hard to derive anything significant from a lot of the papers coming out except descriptive information or if the paper is demonstrating very solid methods and outcomes.
 
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Darn, the Spanish flu must have had no idea of this theory.

har har

Should I rephrase that into something easier for you to understand? Just because a virus has a mutations doesn’t mean the mutations necessarily impact virulence. You literally said that in the post I quoted. The point of the paper I referenced was that there isn’t great evidence to show that these strains actually have different levels of virulence at this time.
 
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There were at least two strains in China, with different levels of severity of disease. In the meanwhile, they have tracked even more than two, AFAIK.
Viruses mutate, Actually, one of the ways we could get out of this mess would be a lucky mutation which would make the infections milder.
Could the virus mutate into a more lethal strain over time ? Is the Italy and Spanish strain more lethal than the South Korean strain ?
 
Could the virus mutate into a more lethal strain over time ? Is the Italy and Spanish strain more lethal than the South Korean strain ?
That's the debate, whether it has mutated or not, and whether that now affects clinical course.

It definitely can (it's a virus, they mutate, and many times that changes their virulence), but, after the exchange right above your post, I don't think there is evidence that its mutations have changed anything,
 
UK portal about Covid- 19
 
@FFP thanks for sharing all this info.
I can't remember if I read it in something that you've shared, but have you seen anything about proning patients early in the course of disease and not waiting until on ventilator? I thought I read something about that, and wanted to share it with someone.
 
From the article:

"When Drosten's university medical center developed what became the test recommended by the World Health Organization, they rolled these tests out to their colleagues throughout Germany in January.
"And they of course rolled this out to labs they know in the periphery and to hospital labs in the area where they are situated," Drosten said. "This created a situation where, let's say, by the beginning or middle of February, testing was already in place, broadly."
Drosten said that has meant quicker, earlier and more widespread testing for COVID-19 in Germany than in other countries."

And that's it. Test, isolate the positives until they're well, everyone else stays healthy. Individual labs aren't overrun, timely results, the system is able to handle the load.
 
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This really doesn't tell me much other than they are testing early. So what are they doing with those patients who test positive afterwards? Quarantining them, hospitalizing them? I mean we can only guess, but there are no actual answers in the article.
 
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From the article:

"When Drosten's university medical center developed what became the test recommended by the World Health Organization, they rolled these tests out to their colleagues throughout Germany in January.
"And they of course rolled this out to labs they know in the periphery and to hospital labs in the area where they are situated," Drosten said. "This created a situation where, let's say, by the beginning or middle of February, testing was already in place, broadly."
Drosten said that has meant quicker, earlier and more widespread testing for COVID-19 in Germany than in other countries."

And that's it. Test, isolate the positives until they're well, everyone else stays healthy. Individual labs aren't overrun, timely results, the system is able to handle the load.
How come the ones who test positive aren't getting that sick? Or am I missing something? So does that mean that if you catch the illness early enough in the course and isolate, the symptoms are much milder? Since there's no actual proven treatment, how are these 35K people fighting this illness and preventing it from getting severe?
 
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How come the ones who test positive aren't getting that sick? Or am I missing something? So does that mean that if you catch the illness early enough in the course and isolate, the symptoms are much milder? Since there's no actual proven treatment, how are these 35K people fighting this illness and preventing it from getting severe?
Fair question.
My comment was more about avoiding the run on resources.
 
@FFP thanks for sharing all this info.
I can't remember if I read it in something that you've shared, but have you seen anything about proning patients early in the course of disease and not waiting until on ventilator? I thought I read something about that, and wanted to share it with someone.
I would definitely try proning cooperative and non-altered patients on NIV, before intubating them. You remember correctly; some doctors have been doing this, but don't ask me where.
 
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I would definitely try proning cooperative and non-altered patients on NIV, before intubating them. You remember correctly; some doctors have been doing this, but don't ask me where.
I asked an awake person to prone themself. Their sats went up within the next hour. Unfortunately they did not like being prone so went back supine and continued texting on their phone. Due to precautions I’m not going back in the room to keep reminding them. They’re still on high flow but not intubated at least!
 
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I think this is our best chance for severe cases. I'm surprised we haven't been talking more about this.
 
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I think this is our best chance for severe cases. I'm surprised we haven't been talking more about this.

I too am surprised and disappointed that this old science hasn't been pursued more aggressively. That said, I think we will find that it works much better for prevention or early treatment than for already seriously ill cases.
 
I think this is our best chance for severe cases. I'm surprised we haven't been talking more about this.
This is five patients... I didn’t read the whole article but just the summary didn’t sounds right to me

“Pao2/Fio2 increased within 12 days (range, 172-276 before and 284-366 after). Viral loads also decreased and became negative within 12 days after the transfusion”... like two weeks isn’t the normal time frame for a lot of pts to recover oxygenation and stop shedding viruses?

why did you like this study?
 


Following identification of a case of coronavirus disease 2019 (COVID-19) in a health care worker, 76 of 82 residents of an SNF were tested for SARS-CoV-2; 23 (30.3%) had positive test results, approximately half of whom were asymptomatic or presymptomatic on the day of testing.
 
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