COVID-19

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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.

No money from pharmaceutical companies.

On the plus side though, I think this is something that could be set up pretty easily locally comparitively. Get COVID follow up clinics going (and put some out of work surgeons back to work in them!) and get a high rate of plasma donation from those survivors to use on the next set of patients. Agree that ideally would be given early per below

I
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?

Because of this, I think early treatment would be key, get ahead of the virus and mitigate host response/cytokine storm.

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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?
I was glad that all of them got much better. Nobody died, even after a month, and these were sick puppies. That's very encouraging. This disease is mostly about buying enough time for the body to learn how to deal with the virus.

ARDS resolved in 4 patients at 12 days after transfusion, and 3 patients were weaned from mechanical ventilation within 2 weeks of treatment. Of the 5 patients, 3 have been discharged from the hospital (length of stay: 53, 51, and 55 days), and 2 are in stable condition at 37 days after transfusion.

Of course I would like more and better studies. One can argue that two patients seem to remain intubated after a month (suggesting complications). I am not saying we should use it now, unproven, except in the sickest patients, but I wouldn't be surprised if it works.
 
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I'm highly skeptical of any of these 'magic bullet' type papers.

Remember the reports from Thailand about combining oseltamivir (no biological rationale) w/ kaletra? Cocktail of flu, HIV drugs appears to help fight coronavirus: Thai doctors | Physician's Weekly

Although maybe I'm just a nihilist. I'm willing to wager, that if a proper study is ever done, hydroxychlorquine and remdesivir both end up being useless too.
My n=1 says they are both useless. My pt died of profound hypoxia after an extended course of remdesivir and 5 days HCQ.
 
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I'm highly skeptical of any of these 'magic bullet' type papers.

Remember the reports from Thailand about combining oseltamivir (no biological rationale) w/ kaletra? Cocktail of flu, HIV drugs appears to help fight coronavirus: Thai doctors | Physician's Weekly

Although maybe I'm just a nihilist. I'm willing to wager, that if a proper study is ever done, hydroxychlorquine and remdesivir both end up being useless too.

At the end of the day, I think the therapeutic window for many of these drugs, if they have any effect at all, is likely very narrow. Right med, right dose, right time. If you miss your chance, then it's left to good ICU care for ARDS and that's it. As we all know, sometimes that's enough and other times it's not.

I like the plasma intervention the best, as it could be deployed locally without as many hurdles as a medication trial. The safety profile is pretty well established, it doesn't require something new (as the Mayo news story points out "...since it relies on standard blood-banking practices"), and multiple specialties are familiar with the concept that you don't get trapped into the "who is the expert in this" driving/impeding care.
 
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Can anyone provide sources that compare the number of cases we're seeing this year in the ICU to the usual number of flu cases that are in ICU? And show evidence how our hospitals are reaching over capacity, which doesn't normally happen with the flu? There's lots of people arguing about the true mortality of this virus, but all I think that matters is to prove to them that we are seeing way higher numbers in the ICU than usual. Whether that's through high spread or high mortality (or both) doesn't matter, the answer is still to self isolate at this point.
 
Can anyone provide sources that compare the number of cases we're seeing this year in the ICU to the usual number of flu cases that are in ICU? And show evidence how our hospitals are reaching over capacity, which doesn't normally happen with the flu? There's lots of people arguing about the true mortality of this virus, but all I think that matters is to prove to them that we are seeing way higher numbers in the ICU than usual. Whether that's through high spread or high mortality (or both) doesn't matter, the answer is still to self isolate at this point.

I mean, why don't they just read the news?

Even a bad flu season doesn't lead to the kind of ****storm you're seeing in NYC right now. A bad flu season doesn't lead to residents/attendings being pulled from other specialities to cover patients because the intensivists/hospitalists/medicine residents can't handle the sheer volume of patients. A bad flu season doesn't lead to Italy literally stacking coffins up outside the hospitals. How much more proof do they need? The case fatality rate doesn't matter. What matters is right now there's obviously enough cases occurring in a short enough timeframe to lead to enough ICU admissions that lead to enough fatalities that it is overwhelming local healthcare systems.
 
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How old was your patient?
My pt who passed away was in his 60s. I have another 1 now in his 70 who was on Plaquenil but could not tolerate. He is though slowly getting better but now dealing with critical care weakness / delirium.
 
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Sorry, reflex.

I read them when they were originally published last week (not sure if they updated them 2 days ago?). I just can't believe they're still talking about gelatins.

Thank god, Covid doesn't usually cause hyperlactatemia, or we'd be forced to further drown these patients. (As it is, I'm sure a lot of pts are still getting the usual 30 cc/kg bolus just for fever and tachycardia but at lease those of us with a brain aren't going to get nastygrams and sent to peer review by admin).

An intensivist had started MIVF NS at 150 ml/hr on a patient of mine yesterday. Am I crazy for thinking this was unneccessary and counterproductive?
 
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Sorry, reflex.

I read them when they were originally published last week (not sure if they updated them 2 days ago?). I just can't believe they're still talking about gelatins.

Thank god, Covid doesn't usually cause hyperlactatemia, or we'd be forced to further drown these patients. (As it is, I'm sure a lot of pts are still getting the usual 30 cc/kg bolus just for fever and tachycardia but at lease those of us with a brain aren't going to get nastygrams and sent to peer review by admin).

An intensivist had started MIVF NS at 150 ml/hr on a patient of mine yesterday. Am I crazy for thinking this was unneccessary and counterproductive?
Yes I’m seeing this as well. Surviving sepsis campaign really set back pulmonary care like, two decades with their fluid management. Shame on the experts!
 
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Any updates on how your hospital is doing COVID therapeutics? We stopped using azithro. Now just HCQ and steroids (though they evidence seems like it’s not there). What r u guys doing in your ICUs?
 
We have our first full blown cytokine storm patient. Looking into the treatments, one of the options is a dialysis like filter (per their website, can be done alone or in line with CRRT or ECMO) specifically for removing cytokines. Supposedly good results in Italy to the point where the European Renal Association has included it in their recommendations.
Does anyone have any experience with this treatment modality?
Thanks and stay safe.
Link to guidelines: https://www.era-edta.org/…/COVID_guidelines_finale_eng-GB.p…
Picture for quick reference included.
 

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We have our first full blown cytokine storm patient. Looking into the treatments, one of the options is a dialysis like filter (per their website, can be done alone or in line with CRRT or ECMO) specifically for removing cytokines. Supposedly good results in Italy to the point where the European Renal Association has included it in their recommendations.
Does anyone have any experience with this treatment modality?
Thanks and stay safe.
Link to guidelines: https://www.era-edta.org/…/COVID_guidelines_finale_eng-GB.p…
Picture for quick reference included.

I thought cytosorb was study only, is it being used clinically in the us?
 
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I thought cytosorb was study only, is it being used clinically in the us?
It doesn't look like it's being used in the US yet, but it is approved and being used apparently in the EU. I imagine it's only a short matter of time until it's approved here...
 
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We have our first full blown cytokine storm patient. Looking into the treatments, one of the options is a dialysis like filter (per their website, can be done alone or in line with CRRT or ECMO) specifically for removing cytokines. Supposedly good results in Italy to the point where the European Renal Association has included it in their recommendations.
Does anyone have any experience with this treatment modality?
Thanks and stay safe.
Link to guidelines: https://www.era-edta.org/…/COVID_guidelines_finale_eng-GB.p…
Picture for quick reference included.
I mean, people have tried hemofiltration for overwhelming cytokinemia for decades. The small experiment studies have not been as successful in larger trials.

Seems like if you are already doing CRRT for other reasons, eg fluid overload, it’s seems like a “what could it hurt?” idea.

It is unfortunate though that according to that recommendation, patients have an increase risk of “developing clothing”
 
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If one is doing CRRT for fluid overload in Covid-19, one should wonder why the patient got fluid overloaded or AKI in the first place.

I would rather go for plasma exchange, if available. If I remember correctly, there is more evidence behind it.
 
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Fascinating thread, even though 98% of what is being discussed is over my head. The sharing of information is impressive. I have a question for you all; my kid, PGY3 peds, was infected and has recovered from covid-19 and is back at work. Symptoms were mild, comparable to a very bad cold; bad cough, fatigue, anosmia. What is the prevailing thought in regards to chance of reinfection, severity, immunity post recovery?
 
Fascinating thread, even though 98% of what is being discussed is over my head. The sharing of information is impressive. I have a question for you all; my kid, PGY3 peds, was infected and has recovered from covid-19 and is back at work. Symptoms were mild, comparable to a very bad cold; bad cough, fatigue, anosmia. What is the prevailing thought in regards to chance of reinfection, severity, immunity post recovery?
Please don't ask for medical advice on the forum.

If your kid survived his/her first infection, s/he'll probably do well even with a reinfection, as long as his/her immunity is not depressed and the virus doesn't mutate.
 
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Please don't ask for medical advice on the forum.

If your kid survived his/her first infection, s/he'll probably do well even with a reinfection, as long as his/her immunity is not depressed and the virus doesn't mutate.
I'm sorry, I was trying to word it in a way so it wouldn't come across as asking for medical advice. I was looking for information in a general sense or if there were any articles you could link that discuss this. Your reply did a good job of explaining this. Thank you.
 
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God, I love Amal Mattu. When I was in paramedic class, many years ago now, we used to watch one of his videos per week before it became a pay site (still subscribe just because it’s such great review).
 
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God, I love Amal Mattu. When I was in paramedic class, many years ago now, we used to watch one of his videos per week before it became a pay site (still subscribe just because it’s such great review).
Great speaker. I love that he's still using the exact same powerpoint template that's been around since the 1990s.
 
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We put our guy on solumedrol 62.5 BID 3 days ago and he's gone from peep of 22 to 5!
FIO2 from 100 to 40! CRP went from 30 to 2!
 
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We put our guy on solumedrol 62.5 BID 3 days ago and he's gone from peep of 22 to 5!
FIO2 from 100 to 40! CRP went from 30 to 2!
One of the podcast I listen to from the Italian Dr. couple of weeks ago. Said that even though everybody was touting no steroids, he thought steroids were helpful in keeping the lungs more pliable and less stiff.
However, I am now reading that most of these patients have very compliant lungs.
It is nice to see something work, or it could be the natural course of the disease.
 

Tons of latest Covid-19 articles.
 
God, I love Amal Mattu. When I was in paramedic class, many years ago now, we used to watch one of his videos per week before it became a pay site (still subscribe just because it’s such great review).
I think ecgweekly.com is free for the duration of the pandemic, for those interested. And it's absolutely worth the $26/year for anybody who deals with ECGs on a regular basis.

Here's an example: Amal Mattu’s ECG Case of the Week – April 6, 2020
 
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Between my group and our hospitalist team I am seeing a lot of variability in obtaining/trending the "COVID Labs" such as LD/Ferritin/Diner/CRP. I've seen some observational data from the Wuhan group detailing an association between a significantly elevated dimer as well as LDH in the non-survivors...but both were elevated in around 30-50% of the survivors as well.

Is anyone here utilizing these labs in a prognostic fashion or to any clinical utility that has a benefit patient outcome? This question does not include any who are collecting these data for research purposes.

Curious if we're just creating more iatrogenic anemia than anything else...
 
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Between my group and our hospitalist team I am seeing a lot of variability in obtaining/trending the "COVID Labs" such as LD/Ferritin/Diner/CRP. I've seen some observational data from the Wuhan group detailing an association between a significantly elevated dimer as well as LDH in the non-survivors...but both were elevated in around 30-50% of the survivors as well.
ly
Is anyone here utilizing these labs in a prognostic fashion or to any clinical utility that has a benefit patient outcome? This question does not include any who are collecting these data for research purposes.

Curious if we're just creating more iatrogenic anemia than anything else...

One of my partners is checking them. Variable among the hospitalists. It doesn't change my management so I am not checking.
 
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Off-topic, the 2019 Hospitalist and Resuscitationist conference is available on-demand, for $0.99, on Vimeo: Watch The Hospitalist & The Resuscitationist 2019 On-Demand. Online | Vimeo On Demand.
 
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Prelim paper from ISTH discussing the incidence of DIC and some recs, we're sitting down to figure out if we're going to establish thresholds for anticoagulation based on dimers and fibrinogen
 

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I think the biggest thing about the anticoagulation leads to better outcomes study (Error - Cookies Turned Off) is that they're definition of anticoagulation was DVT PPx (heparin 10,000-15,000 units/day or lovenox 40-60 mg/day). I don't know that many people in the US not advocating for DVT PPx in all patients, little less COVID patients.
 
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I think the biggest thing about the anticoagulation leads to better outcomes study (Error - Cookies Turned Off) is that they're definition of anticoagulation was DVT PPx (heparin 10,000-15,000 units/day or lovenox 40-60 mg/day). I don't know that many people in the US not advocating for DVT PPx in all patients, little less COVID patients.

When I see a patient and have the thought "it seems stupid to annoy this person with lovenox shots" I'll try to justify not doing it based on a Padua score. But the subset of adult hospitalized patients with a Padua score <4 is extremely small
 
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I think the biggest thing about the anticoagulation leads to better outcomes study (Error - Cookies Turned Off) is that they're definition of anticoagulation was DVT PPx (heparin 10,000-15,000 units/day or lovenox 40-60 mg/day). I don't know that many people in the US not advocating for DVT PPx in all patients, little less COVID patients.

Dammit. I lost interest after seeing the design and p values, and didn’t bother to read the anticoagulation dosing. I could have saved myself some headache
 
One of the reasons I haven't been jumping on any band wagons at the moment. Seems unusual that these intubated critically ill patients aren't on some kind of prophylaxis.

Little outside of my knowledge base here...the post mortems they performed demonstrated some platelet aggregation and microthrombosis in distal pulmonary vasculature, what is the likelihood that this represents coagulation intrinsic to the PV itself versus embolism from elsewhere?

Also any thoughts on this contributing to the underlying hypoxemia that is being seen? So many competing theories and people seem fairly established in their camps of HAPEish phenotype vs microthrombosis vs hemoglobinopathy vs whatever. It's some great physiologic food for thought for sure.
 
Thanks! Added to my MDCalc.
My hospital uses Cerner and we have a VTE tab that calculates it for us. That said, most patients in the ICU should be high risk anyways.
 
One of the reasons I haven't been jumping on any band wagons at the moment. Seems unusual that these intubated critically ill patients aren't on some kind of prophylaxis.

Little outside of my knowledge base here...the post mortems they performed demonstrated some platelet aggregation and microthrombosis in distal pulmonary vasculature, what is the likelihood that this represents coagulation intrinsic to the PV itself versus embolism from elsewhere?

Also any thoughts on this contributing to the underlying hypoxemia that is being seen? So many competing theories and people seem fairly established in their camps of HAPEish phenotype vs microthrombosis vs hemoglobinopathy vs whatever. It's some great physiologic food for thought for sure.

I think most of that is BS. I think the key is going to be finding something antiviral so you can stop the actual source of the pathology. Based on the SARS 1 studies, I'm looking forward to the ivermectin and INF-B studies. Indomethicin would be another possible treatment target, but I don't think I've seen anything on clinicaltrials.gov regarding it.
 
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