COVID-19

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.
Same reason insulin and Eli is hundreds of dollars. I don’t know. I doubt she was lying.
Probably because there is not a bunch of it laying around and companies were probably not making a bunch of it and then Covid came and demand shot up.
I don’t know.
When was the last time you ordered some IV Vitamin C?
Not in a long time. Last time was on someone admitted to ICU with rip roaring sepsis. They died the same day.

IV thiamine is my vitamin of choice!!

Members don't see this ad.
 
  • Like
Reactions: 1 user
This is so helpful. So sad to know that my aunt is postiuvie on Corona virus however she doesnt feel any symptoms yet.
 
Members don't see this ad :)
  • Like
Reactions: 1 user
I had a male patient who came with bilateral infiltrates on chest x-ray and CT scan and mildly hypoxic at rest but desating with exertion. I thought it was COVID but nasal PCR -ve times 2. Labs looked like COVID i.e inc fibrinogen , D Dimer , CRP . Infiltrates were felt to be ILD / IPF. No high fevers during hospital stay. Sent home 2 weeks later. Comes back 1 week later with worsening hypoxia and high fever. Now COVID PCR positive.
A negative nasal PCR means nothing when the clinical picture says COVID.
 
  • Wow
  • Like
Reactions: 1 users
I had a male patient who came with bilateral infiltrates on chest x-ray and CT scan and mildly hypoxic at rest but desating with exertion. I thought it was COVID but nasal PCR -ve times 2. Labs looked like COVID i.e inc fibrinogen , D Dimer , CRP . Infiltrates were felt to be ILD / IPF. No high fevers during hospital stay. Sent home 2 weeks later. Comes back 1 week later with worsening hypoxia and high fever. Now COVID PCR positive.
A negative nasal PCR means nothing when the clinical picture says COVID.

Have had 2 negative naso/oropharnygeal x2's that were positive on subsequent bronch. If everything fits COVID except the test, it's still COVID
 
Last edited:
  • Like
Reactions: 1 user
I had a male patient who came with bilateral infiltrates on chest x-ray and CT scan and mildly hypoxic at rest but desating with exertion. I thought it was COVID but nasal PCR -ve times 2. Labs looked like COVID i.e inc fibrinogen , D Dimer , CRP . Infiltrates were felt to be ILD / IPF. No high fevers during hospital stay. Sent home 2 weeks later. Comes back 1 week later with worsening hypoxia and high fever. Now COVID PCR positive.
A negative nasal PCR means nothing when the clinical picture says COVID.

Quite true. There's a decent false negative rate among symptomatic patients (which makes testing the asymptotic that much more absurd).
 
What annoys me is this false narrative that COVID virus resides in the body for only 2 weeks and after that any positive PCR is from dead virus.
Wrong COVID is like herpes simplex / zoster. Its going to hide in the cells and reinfect when the time is right.
Symptomatic patients have this relapsing remitting course where they are really sick with hypoxia and multiorgan failure and then rally a bit. I hypothesize that when they are kind of stable and not febrile the body may not be secreting virus and PCRs may be negative. But then another cytokine release syndrome starts and if you check PCR it will be positive. The virus wasn’t gone it was just intracellular.
 
What annoys me is this false narrative that COVID virus resides in the body for only 2 weeks and after that any positive PCR is from dead virus.
Wrong COVID is like herpes simplex / zoster. Its going to hide in the cells and reinfect when the time is right.
Symptomatic patients have this relapsing remitting course where they are really sick with hypoxia and multiorgan failure and then rally a bit. I hypothesize that when they are kind of stable and not febrile the body may not be secreting virus and PCRs may be negative. But then another cytokine release syndrome starts and if you check PCR it will be positive. The virus wasn’t gone it was just intracellular.
Do you have any evidence whatsover to back this up?
 
  • Like
Reactions: 1 users
Do you have any evidence whatsover to back this up?


I will say that I've seen this pattern a few times where someone looks like they're getting better and then off the cliff they go. It sucks because normally during that week I'm telling the family, "He's getting better... we're pretty far down on the FiO2."
 
I will say that I've seen this pattern a few times where someone looks like they're getting better and then off the cliff they go. It sucks because normally during that week I'm telling the family, "He's getting better... we're pretty far down on the FiO2."
Not what I asked him. Nobody is debating that some patients will have a waxing and waning course—but that holds for any critical illness.
I was asking that, aside from the refrain of “iTs a NovEL ViRuS” is there any evidence of viral dormancy/reactivation.
 
  • Like
Reactions: 1 users
I will say that I've seen this pattern a few times where someone looks like they're getting better and then off the cliff they go. It sucks because normally during that week I'm telling the family, "He's getting better... we're pretty far down on the FiO2."
Don’t tell them that. I tell them “he’s still critically ill and has a very good possibility of not making it home.”
I keeps it real.
 
Members don't see this ad :)
Are people now doing bronchs in these patients?
Has the risk gone down?

I’ve done one for a persistent plug, partner did a bronch for my bedside trach, and one other one also for a trach. All done with PAPR and a Stryker hood. So 3, at an institution that has treated >700 cases so far. Avoiding as much as possible.
 
Do you have any evidence whatsover to back this up?
I am hypothesizing. But at the same time I have seen so many patients who seem to be getting better with lower O2 requirements and CRP decreasing and then have a cytokine crisis with high fevers , hypoxia , CRP through the roof , multiorgan failure. I have seen people who tested -ve and a week later were again positive.
If we tested these COVID pts every day I bet during times they were better / CRP down they would be not secreting the virus and again secreting when in a crisis.
 
Don’t tell them that. I tell them “he’s still critically ill and has a very good possibility of not making it home.”
I keeps it real.

Yea, but when you go from a high PEEP and FiO2 of 1.0 to a PEEP of <10 and an FiO2 of 0.6, the hope becomes real. That was also in March/April... now every positive SARS conversation is hedged with, "but I've seen this before where the person gets better, and then ends up falling off of the metaphorical cliff." My most recent case was someone who was on a vent for over 2 months, trached, pegged, and awake/communicating, breathing decently on 10/5 pressure support, but couldn't get the patient's Fi below 0.6. The cliff still came. The patient still died.

Thankfully, to an extent, most terminal SARS cases is just a steady decline to being unsalvageable.
 
  • Like
Reactions: 1 user
I am hypothesizing. But at the same time I have seen so many patients who seem to be getting better with lower O2 requirements and CRP decreasing and then have a cytokine crisis with high fevers , hypoxia , CRP through the roof , multiorgan failure. I have seen people who tested -ve and a week later were again positive.
If we tested these COVID pts every day I bet during times they were better / CRP down they would be not secreting the virus and again secreting when in a crisis.
So you have a hypothesis, that seems to lack any backing in immunology or virology? That's pretty different than decrying a 'false narrative', as you put it, that does have strong backing in both.

It certainly is possible, but in my opinion ultimately unlikely.
 
  • Like
Reactions: 1 user


Levels of cytokines are lower in COVID than other forms of sepsis. I always thought looking at IL 6 and all those other markers never made sense when we have no idea what they look like in other septic states.
 


Levels of cytokines are lower in COVID than other forms of sepsis. I always thought looking at IL 6 and all those other markers never made sense when we have no idea what they look like in other septic states.
We use Anakinra on the MIS-C patients like it’s water... only, data shows that the sickest patients have the highest levels of IL-1ra. So we give the sickest patients something that they already have too much of in comparison to the less sicker patients.

Yep... it just makes sense for reasons.
 
We use Anakinra on the MIS-C patients like it’s water... only, data shows that the sickest patients have the highest levels of IL-1ra. So we give the sickest patients something that they already have too much of in comparison to the less sicker patients.

Yep... it just makes sense for reasons.

I look at the patient; septic patients look septic. I know, it's a crazy idea. I'm a fan of the old SIRS criteria (if all of your vitals are outta whack, you're in trouble). Do something.
 
  • Like
Reactions: 1 user
I look at the patient; septic patients look septic. I know, it's a crazy idea. I'm a fan of the old SIRS criteria (if all of your vitals are outta whack, you're in trouble). Do something.
Some what tangential but I agree that the Sepsis-3 definition with qSOFA, wasn’t a really helpful re-definition at all.
 
Seriously think every teenager with strep needs a lactate, cultures and vosyn?

But I would in in favor of redefining it as ‘looks septic’.
I'm not sure SIRS worked that well either. They are both kinda equivocal.

 
I'm not sure SIRS worked that well either. They are both kinda equivocal.

I'm not sure either of those studies have face validity.

When was the last time you saw an accurate RR charted. Seems most places nowadays use the number off a monitor which is typically a random number generator.

Hell, it can be difficult to get an accurate HR charted sometimes.

Big difference between having SIRS and meeting SIRS criteria. The former is clinically relevant, the latter give admin a hard-on.

Also, identifying infection is not the goal of either score. Why even bother publishing garbage like that?
 
I'm not sure either of those studies have face validity.

When was the last time you saw an accurate RR charted. Seems most places nowadays use the number off a monitor which is typically a random number generator.

Hell, it can be difficult to get an accurate HR charted sometimes.

Big difference between having SIRS and meeting SIRS criteria. The former is clinically relevant, the latter give admin a hard-on.

Also, identifying infection is not the goal of either score. Why even bother publishing garbage like that?
Well, there are a lot of problem with sepsis definitions. I mean 1/3 of patients have culture negative sepsis. I get there are viruses that are hard to detect, but with rapid PCR measurements nowadays, it's hard to imagine that 1/3 of patients who die with sepsis don't have an identifiable infectious source, which is literally required to have sepsis. But people still bill for it and treat it and I'm not blaming than other than to say its very hard to effectively treat a disease if people can't adequately define it to determine who has it and who doesn't. It's better than it used to be though, so that's good.

I would agree that isolated vital signs aren't helpful. A couple of data points are good though.
 
Seriously think every teenager with strep needs a lactate, cultures and vosyn?

But I would in in favor of redefining it as ‘looks septic’.

I mean... not every sepsis/severe sepsis/shock needs Vosyn (or the cefepime/flagyl/vanc combo). Don't get me started on antibiotics for "aspiration pneumonia."

Besides, I'll take the extra case mix index/GLOC/hospital reimbursement for playing the game and coding lactate >4 out as "septic shock (per SEP1/CMS standard)." It'll make my company look good and give us leverage for new toys.
 
Gonna be hard to get people to stop using it but it looks like it might be in the same category as plaquenil. I'm all for not wasting money on **** with marginal to no utility.
Well, it’s a nice thought but even marginal to no utility is likely to make it have continued use in critical care. Unless it has an actually signal of harm, it’ll be the same adage as countless other drugs:

“No one dies without a dose of... [insert Remdesivir]”
 
Well, it’s a nice thought but even marginal to no utility is likely to make it have continued use in critical care. Unless it has an actually signal of harm, it’ll be the same adage as countless other drugs:

“No one dies without a dose of... [insert Remdesivir]”

Except when cost is a factor. Giving an extra course of zosyn or vitamin c is one thing but nobody uses nitric in adults because it is so goddamn expensive and remdesivir ain't cheap. I am absolutely not sold on it and if subsequent subgroup analysis shows no signal I'd say we reserve it only for special cases (eg under 40 or no comorbid illness or something else).
 
  • Like
Reactions: 1 user
Except when cost is a factor. Giving an extra course of zosyn or vitamin c is one thing but nobody uses nitric in adults because it is so goddamn expensive and remdesivir ain't cheap. I am absolutely not sold on it and if subsequent subgroup analysis shows no signal I'd say we reserve it only for special cases (eg under 40 or no comorbid illness or something else).
Oh, we use nitric all the time in pediatrics. I mean, it does help SaO2 for refractory hypoxemia and is safer than ECMO. Plus just having ones torso in the ICU is expensive as it is.

I can’t actually fault people for trying one last Hail Mary treatment when the alternative is death anyway. I agree with your sentiment but that’s just not the way things are in the US, for better or worse.
 
  • Like
Reactions: 1 user
Oh, we use nitric all the time in pediatrics. I mean, it does help SaO2 for refractory hypoxemia and is safer than ECMO. Plus just having ones torso in the ICU is expensive as it is.

I can’t actually fault people for trying one last Hail Mary treatment when the alternative is death anyway. I agree with your sentiment but that’s just not the way things are in the US, for better or worse.
It is in adult medicine. I'm not saving people with 80+ years of life expectancy and throwing the entire kitchen sink at every patient would be preposterous... It's the same reason the angiotensin agonist is only used in post-op patients or transplants not diabetic septic foot wounds in the super obese.
 
  • Haha
  • Like
Reactions: 1 users
It is in adult medicine. I'm not saving people with 80+ years of life expectancy and throwing the entire kitchen sink at every patient would be preposterous... It's the same reason the angiotensin agonist is only used in post-op patients or transplants not diabetic septic foot wounds in the super obese.
Giapreza is miracle I tells ya...
 
Top