Treating COVID pre and post intubation

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Why? The ventilator isn’t going to kill them, the disease will. I mean, it’s probably okay to watch people in the 80s (maybe even 70s... maybe) temporarily if they have a static trajectory, but for that patient in the 40s, waiting till they are less than that just seems dangerous.

This seems like the antithesis of the Italian experience of intubating early. To me, if seems less of an early versus late and more of a question of optimal safety.

In a healthy person, I agree, the vent probably won't harm/kill them. But with the type of chronically unhealthy patient population I deal with, the vent could seriously harm some of them. Put an old person with bunch of comorbid conditions on the vent for a week - can definitely cause some serious harm.

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In a healthy person, I agree, the vent probably won't harm/kill them. But with the type of chronically unhealthy patient population I deal with, the vent could seriously harm some of them. Put an old person with bunch of comorbid conditions on the vent for a week - can definitely cause some serious harm.
Well, so could saturations in the 40s.
 
Well, so could saturations in the 40s.

Those were extreme examples. And as I already said, I am not advocating for that.

Most of my colleagues are still "intubating early" - >60-80% FiO2 = tube. I have been doing the same and seeing these reports makes me question whether that is still the right strategy.
 
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Those were extreme examples. And as I already said, I am not advocating for that.

Most of my colleagues are still "intubating early" - >60-80% FiO2 = tube. I have been doing the same and seeing these reports makes me question whether that is still the right strategy.
Well, it’s gonna be hard to know cause no one is gonna create a trial of moderate hypoxemia versus severe hypoxemia to see if intubation changes outcomes. If they did, my hunch is that it probably would be unfavorable not intubating the severe hypoxemia group but maybe not statistically significant for all comers. That being said, I don’t think it’s ever wrong to intubate patients if you don’t think they can handle or you can’t safely manage the hypoxemia non-invasively. I get the second guessing oneself though.
 
Well, it’s gonna be hard to know cause no one is gonna create a trial of moderate hypoxemia versus severe hypoxemia to see if intubation changes outcomes. If they did, my hunch is that it probably would be unfavorable not intubating the severe hypoxemia group but maybe not statistically significant for all comers. That being said, I don’t think it’s ever wrong to intubate patients if you don’t think they can handle or you can’t safely manage the hypoxemia non-invasively. I get the second guessing oneself though.
There is one VERY easy situation that calls against intubation. It's the patient who's at 45% O2 sat while checking her phone (there is an image of her on this forum).

This disease comes with a right shift of the dissociation curve, meaning that we should not treat O2 sat numbers blindly. If one is nervous, the mental status is a good surrogate for PaO2.
 
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There is one VERY easy situation that calls against intubation. It's the patient who's at 45% O2 sat while checking her phone (there is an image of her on this forum).

This disease comes with a right shift of the dissociation curve, meaning that we should not treat O2 sat numbers blindly. If one is nervous, one should put in an a-line and monitor the peripheral PaO2.
Ha... I saw that. Hopefully she’s not texting her last will and testament and instead doing Candy Crush because she’s bored.
 
Ha... I saw that. Hopefully she’s not texting her last will and testament and instead doing Candy Crush because she’s bored.
My trainees are usually surprised when I spend time chatting with my (non-Covid) ICU patients about their last night and symptoms, instead of blindly examining them, looking at the numbers and listening to the team. I recommend more people do that. The best monitor is the patient.

I trained in a fellowship where even intubated patients were kept as awake as possible. Nothing beats being able to have a conversation with the patient; it can be incredibly reassuring when the numbers are bad.
 
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My trainees are usually surprised when I spend time chatting with my (non-Covid) ICU patients about their last night and symptoms, instead of blindly examining them, looking at the numbers and listening to the team. I recommend more people do that. The best monitor is the patient.

I trained in a fellowship where even intubated patients were kept as awake as possible. Nothing beats being able to have a conversation with the patient.
Doesn’t really apply to pediatric critical care but I agree the number is only relevant in context.
 
Doesn't apply in dementia either. :D
People still try to label pediatric ICU patients as delirious though all the time. The 6 month old is sleeping off cycle and can’t stare at flash cards and the 6 year old is awake and ticked at 1 am. I’m like... do you people even have children?!
 
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It seems we are not the only ones thinking about delaying intubation:

 
Agreed it’s very strange, I’ve seen pts on fiO2 100%, desatting, but they’ll be texting on their phone. It doesn’t feel right intubating them.

Once intubated, they go through the whole barrage of iatrogenic harm: induced, sedation, get hypotensive, give fluids, need aline + central line, too many blood draws, inappropriate vent settings, sedated very heavily to reduce vent asymchrony. Maybe just tolerating a lower sat and watching mental status, labs as markers of organ injury (trops, LFTs, Cr, lactate) may be safer for these pts...
 
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Agreed it’s very strange, I’ve seen pts on fiO2 100%, desatting, but they’ll be texting on their phone. It doesn’t feel right intubating them.

Once intubated, they go through the whole barrage of iatrogenic harm: induced, sedation, get hypotensive, give fluids, need aline + central line, too many blood draws, inappropriate vent settings, sedated very heavily to reduce vent asymchrony. Maybe just tolerating a lower sat and watching mental status, labs as markers of organ injury (trops, LFTs, Cr, lactate) may be safer for these pts...
And maybe we shouldn't be so afraid of HFNC or CPAP in neg pressure rooms? Speaking from the outside looking in, so no first hand experience. I do understand the fear of aerosolization.
 
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I'm seeing a lot of differing, very anecdotal reports on recommended management. Most people saying to run these patients dry, this guy above saying that's leading to AKI. Initial rec's were to avoid NIV, as patients always ended up failing. Then this got conflated w/ the need to avoid aerosol generation. Then, once vents became limited, the idea was to use cpap in order to decrease the total number of required vent days. Now, we should be leaving patients on NC w/ sats in the 70s, despite the earlier warnings about silent hypoxia leading to sudden clinical deterioration and arrest.

I think there's a lot of confirmation bias, both positive and negative, with regard to these anecdotal treatment recs. Not saying they're necessarily incorrect, I just think people shouldn't be too forceful in their recommendations.

This is an interesting powerpoint on treatment recs. If you notice, they cite "promising results" of a (then) unpublished trial for kaletra. However, in all likelihood that was in regard to the negative nejm article. Oddly enough, there were 1 or 2 chinese remdesivir trials which haven't been published yet. Why?
 
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I'm seeing a lot of differing, very anecdotal reports on recommended management. Most people saying to run these patients dry, this guy above saying that's leading to AKI. Initial rec's were to avoid NIV, as patients always ended up failing. Then this got conflated w/ the need to avoid aerosol generation. Then, once vents became limited, the idea was to use cpap in order to decrease the total number of required vent days. Now, we should be leaving patients on NC w/ sats in the 70s, despite the earlier warnings about silent hypoxia leading to sudden clinical deterioration and arrest.

I think there's a lot of confirmation bias, both positive and negative, with regard to these anecdotal treatment recs. Not saying they're necessarily incorrect, I just think people shouldn't be too forceful in their recommendations.

This is an interesting powerpoint on treatment recs. If you notice, they cite "promising results" of a (then) unpublished trial for kaletra. However, in all likelihood that was in regard to the negative nejm article. Oddly enough, there were 1 or 2 chinese remdesivir trials which haven't been published yet. Why?
Is there any data at all on remdesivir?
 
Is there good data for anything?
No but I mean even a tiny bit of actual data on it.

I also just can't see how antivirals are being sold at the promising option for when a patient has gotten really sick. If your mechanism is stopping viral replication, then you need to give it on day 1.
 
I'm seeing a lot of differing, very anecdotal reports on recommended management. Most people saying to run these patients dry, this guy above saying that's leading to AKI. Initial rec's were to avoid NIV, as patients always ended up failing. Then this got conflated w/ the need to avoid aerosol generation. Then, once vents became limited, the idea was to use cpap in order to decrease the total number of required vent days. Now, we should be leaving patients on NC w/ sats in the 70s, despite the earlier warnings about silent hypoxia leading to sudden clinical deterioration and arrest.

I think there's a lot of confirmation bias, both positive and negative, with regard to these anecdotal treatment recs. Not saying they're necessarily incorrect, I just think people shouldn't be too forceful in their recommendations.

This is an interesting powerpoint on treatment recs. If you notice, they cite "promising results" of a (then) unpublished trial for kaletra. However, in all likelihood that was in regard to the negative nejm article. Oddly enough, there were 1 or 2 chinese remdesivir trials which haven't been published yet. Why?

There is a lot of voodoo out there about how to manage the hypoxia associated with COVID-19. One emergency department that I’m familiar with has effectively banned everything except intubation for all ED patients requiring more than 6L nasal out of fear of generating aerosols. This is backed by their CCM groups and admin. The logic being anyone with cough or respiratory distress is a PUI, it takes 1-2 days to get a SARS-CoV-2 test back, and the sensitivity of a single test is not that awe inspiring. That, couple with the fact that negative pressure room are far fewer than vents, and you have a recipe where CHFers and COPDers are are getting tubed as soon as their FIO2 requirements exceed what can be delivered with 6L when they likely would have done fine on NIPPV.

Then, there is the issue of vent settings. Reports out of Europe are that most patients with COVID-associated ARDS have surprisingly high compliance and shunt-fractions > 0.5. This has people screaming on YouTube that we are killing people with too high of “pressures” and insinuating that we should be using much higher FiO2s with minimal PEEP. Meanwhile, other people are touting their case series with APRV which is glorified CPAP on steroids.

My bottom line is that the optimal method is unknowable at this point. What seems certain is that COVID-SARS is very similar to other flavors where the sickest patients tend to die of multisystem organ failure (most places will run out of CRRT before vents). Thus, I’m sticking to the basics of lung protective ventilation with AC-V or PRVC until we have more institutional guidance. That means that I’ll start with TVs of 6-8 cc/kg PBW and get that down to 6 while incrementally adjusting PEEP and FiO2 to to the minimal settings to keep SaO2 88-94%. I may prone early but I’m not moving toward questionable therapies like pulmonary vasodilators, APRV, etc. without some compelling reason.
 
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There is a lot of voodoo out there about how to manage the hypoxia associated with COVID-19. One emergency department that I’m familiar with has effectively banned everything except intubation for all ED patients out of fear of generating aerosols. This is backed by their CCM groups and admin. The logic being anyone with cough or respiratory distress is a PUI, it takes 1-2 days to get a SARS-CoV-2 test back, and the sensitivity of a single test is not that awe inspiring. That, couple with the fact that negative pressure room are far fewer than vents, and you have a recipe where CHFers and COPDers are are getting tubed as soon as their FIO2 requirements exceed what can be delivered with 6L when they likely would have done fine on NIPPV.

Then, there is the issue of vent settings. Reports out of Europe are that most patients with COVID-associated ARDS have surprisingly high compliance and shunt-fractions > 0.5. This has people screaming on YouTube that we are killing people with too high of “pressures” and insinuating that we should be using much higher FiO2s with minimal PEEP. Meanwhile, other people are touting their case series with APRV which is glorified CPAP on steroids.

My bottom line is that the optimal method is unknowable at this point. What seems certain is that COVID-SARS is very similar to other flavors where the sickest patients tend to die of multisystem organ failure (most places will run out of CRRT before vents). Thus, I’m sticking to the basics of lung protective ventilation with AC-V or PRVC until we have more institutional guidance. That means that I’ll start with TVs of 6-8 cc/kg PBW and get that down to 6 while incrementally adjusting PEEP and FiO2 to to the minimal settings to keep SaO2 88-94%. I may prone early but I’m not moving toward questionable therapies like pulmonary vasodilators, APRV, etc. without some compelling reason.



The fact that 85% of intubated Covid-19 Americans are dying, despite the infamous "guidelines" and "protocols", is proof that we are doing something VERY wrong. It's not rocket science. Persisting in the mistakes won't lead to a different outcome.

To me, "voodoo medicine" is when the patient dies despite (or because) of all the "scientific" and "institutional" guidelines., and real medicine is when s/he survives because of a physician who wouldn't just blindly apply recipes, and wouldn't accept that a treatment can be right if the patient is getting worse.

Hospitals like yours make me more afraid of American healthcare than of the Chinese virus. If the virus doesn't kill me, my colleagues will.

As I've said before: the doctors who treated Spanish flu used to rationalize that patients were getting more tachypneic and febrile from the disease, not from Aspirin toxicity. Even the fact that patient survival was 30 times higher with homeopathy only didn't ring a bell, because there was too much space between the ears.

High PEEP ARDSnet protocol is probably good if the patient has ARDS. If the patient has something else (e.g. pulmonary microthromboses or hemoglobinopathy), it's probably about as good as treating flu with 30 g of Aspirin per day. So, yeah, I think one should intubate later, and one should try those pulmonary vasodilators before blasting the lung with 20 of PEEP, just so that one's sat/vent numbers look good, especially with an unconvincing CT.
 
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If people are thinking this isn’t traditional ARDS, and we shouldn’t be using higher PEEPs, what PEEPs do you think are dangerous? Most of my patients I’m able to wean PEEP to the teens (12-18), do you think this number is dangerous and I could be causing harm? I’m not in PEEP 20s unless if I’m on 100%.

I’m trying to read everyday on COVID and ask all the consultants and experts I can, but no one can give me a definite answer and I’m doing a lot of things I’m not sure about (abx, vent settings, anticoag, steroids, toci). It’s distressing to me I could be harming pts and I can’t get an answer to what I should be doing. I think in a year or two, its possible we may find out we were causing a lot of harm with how we r now treating COVID and that sucks.
 
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The fact that 85% of intubated Covid-19 Americans are dying, despite the infamous "guidelines" and "protocols", is proof that we are doing something VERY wrong. It's not rocket science. Persisting in the mistakes won't lead to a different outcome.

To me, "voodoo medicine" is when the patient dies despite (or because) of all the "scientific" and "institutional" guidelines., and real medicine is when s/he survives because of a physician who wouldn't just blindly apply recipes, and wouldn't accept that a treatment can be right if the patient is getting worse.

Hospitals like yours make me more afraid of American healthcare than of the Chinese virus. If the virus doesn't kill me, my colleagues will.

As I've said before: the doctors who treated Spanish flu used to rationalize that patients were getting more tachypneic and febrile from the disease, not from Aspirin toxicity. Even the fact that patient survival was 30 times higher with homeopathy only didn't ring a bell, because there was too much space between the ears.

High PEEP ARDSnet protocol is probably good if the patient has ARDS. If the patient has something else (e.g. pulmonary microthromboses or hemoglobinopathy), it's probably about as good as treating flu with 30 g of Aspirin per day. So, yeah, I think one should intubate later, and one should try those pulmonary vasodilators before blasting the lung with 20 of PEEP, just so that one's sat/vent numbers look good, especially with an unconvincing CT.


I wouldn’t treat the lungs in that picture the same, but I’m also the guy pushing for lower PEEPs (5 in most; 8-10 in obese) at the outset and dialing it up in response to the patient. To be fair, our COVID lungs do NOT look as pretty as pictured.

I think that one of the best ways to determine if the patient has recruitable lung units is to see how they respond to a gentle rise in PEEP. If their oxygenation is not improving with more PEEP, I think that is the patient telling me something and more of the same is probably not a good thing. That means we need a short feedback loop on how individual patients respond and flexibility in our approach rather than a one size fits all model of thinking. Thus, I’m cautious of people claiming to know that these patients need APRV, pulmonary vasodilators, or other unproven therapies at the outset early in their course; I’m not throwing the kitchen sink until I’ve thrown the knives first.

Another important consideration is the degree of hypoxia that we are willing to tolerate in these patients. Historically, I’d be happy with SaO2 88-94% in an attempt to limit hyperoxia-induced lung injury. Recent data suggests that SaO2 > 96% is the way to go in these patients.


My takeaway is that we may need to tell our RTs to leave them on 5-10 of PEEP and 0.7 FiO2 rather than driving that PEEP up higher to get the FiO2 below 0.5 which seems to the the life’s quest of every RT I meet.

Finally, while the lung mechanics of these COVID patients seems unexpected, one thing is strikingly similar to yesterday’s ARDS - the tendency to die from multisystem organ failure. We are seeing tons of AKI, shock liver, hypotension, and cardiomyopathy. One side of me thinks that the high PEEP approach (more than 18) probably isn’t helping oxygen delivery to those failing organ systems as we are robbing Peter (cardiac output) to pay Paul (SaO2). The other side of me is saying that using 5 or 20 of PEEP is not going to make a lick of difference in an elderly or obese patient who arrives with a new Crt of 3, EF of 20%, AST of 500, and MAP of 60 on 50 mcg of Levo. These seem to be the ones who are disproportionately dying.
 
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Not as far as I'm aware.

It was developed for ebola, and didn't work for that. Plus, my understanding is that the biochemical mechanism is less likely to work with a coronavirus.

Although there is this:

How New Jersey’s First Coronavirus Patient Survived
I can't grasp how an antiviral is making a big difference when a patient is very sick on day 9. If you want to stop viral replication, you need to do it on day 1 when the test is positive.
 
Apparently the OxyHgb dissociation curve is shifted much to the right, because it's "poisoned" by the virus. That's one of the hypotheses for using HCQ, which supposedly blocks this in vitro. Hence OxyHgb can offload much more O2 in the periphery, despite the O2 sat.

I'm really hoping to see more of this:

Yea, but if it was just an issue loading the oxygen trucks, why is the PaO2 still extremely low on ABG?
 
Why? The ventilator isn’t going to kill them, the disease will. I mean, it’s probably okay to watch people in the 80s (maybe even 70s... maybe) temporarily if they have a static trajectory, but for that patient in the 40s, waiting till they are less than that just seems dangerous.

This seems like the antithesis of the Italian experience of intubating early. To me, if seems less of an early versus late and more of a question of optimal safety.

The argument is that people with SARS-CoV-2 don't come off vents (which I've had a few extubations). I don't buy it because the vent doesn't kill people. On the other hand, the 70 year old who flipped off her HFNO, removed her pulse ox, and then went into brady PEA would have been better off for everyone if she had just been intubated early (we were going back and forth as her SpO2 went from 50 on room air to high 80s when she was keeping her HFNO on).

The pathology of this virus is weird.
 
The argument is that people with SARS-CoV-2 don't come off vents (which I've had a few extubations). I don't buy it because the vent doesn't kill people. On the other hand, the 70 year old who flipped off her HFNO, removed her pulse ox, and then went into brady PEA would have been better off for everyone if she had just been intubated early (we were going back and forth as her SpO2 went from 50 on room air to high 80s when she was keeping her HFNO on).

The pathology of this virus is weird.
Since this has spared pediatrics, I can’t have direct comments other than we’ve probably all had patients whose hypoxemia seems out of proportion to their compliance. In those cases that I’ve encountered, the treatment and cause is usually the same 1) increased PVR —> iNO, 2) increased West zone 3 —> proning, 3) bad genetics in response to a typically less virulent pathogen —> ECMO, or if not a candidate... priest. I mean, sure there’s the anti-inflammatory/PRISMAFLEX trials, but their effect seems random/lucky at best.

But again, I have not had experience with this particular virus, so I’ll defer.
 
Yea, but if it was just an issue loading the oxygen trucks, why is the PaO2 still extremely low on ABG?
That is a good point, and you're not the only one wondering.




A possible explanation for such severe hypoxemia occurring in compliant lungs is the loss of lung perfusion regulation and hypoxic vasoconstriction. Actually, in ARDS, the ratio between the shunt fraction to the fraction of gasless tissue is highly variable, with mean 1.25 ± 0.80(1). In eight of our patients with CT scan, however, we measured a ratio of 3.0 ± 2.1, suggesting remarkable hyperperfusion of gasless tissue. If so, the oxygenation increases with high PEEP and/or prone position are not primarily due to recruitment, the usual mechanism in ARDS(2), but instead, in these patients with a poorly recruitable pneumonia(3), to the redistribution of perfusion in response to pressure and/or gravitational forces.

If this is true, inhaled pulmonary vasodilators are the way to go. I am not on Covid-19 ICU service, so I can't confirm.
 
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1586698290922.jpeg
 
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Multiple opthalmologists on that paper, interesting research team.
 

Should be nearly useless inpatient regardless. Lots of patients have undetectable viral loads during advanced disease stages, in the tissues that are susceptible to penetration to these drugs.
Will turn out to have Tamiflu like efficacy and probably have an even smaller window of opportunity to use it - during the very early mild disease stages.
 
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Should be nearly useless inpatient regardless. Lots of patients have undetectable viral loads during advanced disease stages, in the tissues that are susceptible to penetration to these drugs.
Will turn out to have Tamiflu like efficacy and probably have an even smaller window of opportunity to use it - during the very early mild disease stages.
So essentially none?

 
That is a good point, and you're not the only one wondering.






If this is true, inhaled pulmonary vasodilators are the way to go. I am not on Covid-19 ICU service, so I can't confirm.


Just coming off a couple week in the COVID-ICU. I am not taking care of ECMO patients, but here's what I have noticed:

-almost all patients have good lung compliance. Have been using no more than 5-10 of PEEP. High PEEP doesn't seem to be helping their oxygenation.
-extubated several. Our hospital (and other hospitals I have talked to) have at this point, a mortality much lower than 85% for intubated patients. Not sure if that's just because we are intubating earlier/less sick or what.
-I don't think HCQ did anything for anyone who was already tubed, agree w/ Henry Ford data. Gave Toci to a couple, it made their inflammatory markers look better but didn't actually make the patents any better. Probably wouldn't give it again.
-High fevers for several days is pretty routine. It actually seems to be the body's way of halting viral replication. I've just been letting people fever and treating insensible losses. Occasionally we have had pts get superinfected so we are still culturing.
-Haven't had much luck with Veletri, it is clogging filters on vent and requiring that they be changed often so we've ditched it
-Have used nitric oxide in a couple non-tubed patients with success
-Nearly every COVID pt on the vent has developed renal dysfunction or needed dialysis. If they need dialysis they are also needing heparin gtts for clotting

Would love to hear other's experiences. I'm finding it hard to generalize the management of COVID, no two patients are alike and there clearly seem to be ethnic/racial differences as well. All African-American pts on the vent seem to need hemodialysis.
 
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Just coming off a couple week in the COVID-ICU. I am not taking care of ECMO patients, but here's what I have noticed:

-almost all patients have good lung compliance. Have been using no more than 5-10 of PEEP. High PEEP doesn't seem to be helping their oxygenation.
-extubated several. Our hospital (and other hospitals I have talked to) have at this point, a mortality much lower than 85% for intubated patients. Not sure if that's just because we are intubating earlier/less sick or what.
-I don't think HCQ did anything for anyone who was already tubed, agree w/ Henry Ford data. Gave Toci to a couple, it made their inflammatory markers look better but didn't actually make the patents any better. Probably wouldn't give it again.
-High fevers for several days is pretty routine. It actually seems to be the body's way of halting viral replication. I've just been letting people fever and treating insensible losses. Occasionally we have had pts get superinfected so we are still culturing.
-Haven't had much luck with Veletri, it is clogging filters on vent and requiring that they be changed often so we've ditched it
-Have used nitric oxide in a couple non-tubed patients with success
-Nearly every COVID pt on the vent has developed renal dysfunction or needed dialysis. If they need dialysis they are also needing heparin gtts for clotting

Would love to hear other's experiences. I'm finding it hard to generalize the management of COVID, no two patients are alike and there clearly seem to be ethnic/racial differences as well. All African-American pts on the vent seem to need hemodialysis.

One more thing:
2-3 weeks on the vent is pretty typical. I've yet to see anyone (who really needs it) get a tube and come off a couple days later.
 
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Just coming off a couple week in the COVID-ICU. I am not taking care of ECMO patients, but here's what I have noticed:

-almost all patients have good lung compliance. Have been using no more than 5-10 of PEEP. High PEEP doesn't seem to be helping their oxygenation.
-extubated several. Our hospital (and other hospitals I have talked to) have at this point, a mortality much lower than 85% for intubated patients. Not sure if that's just because we are intubating earlier/less sick or what.
-I don't think HCQ did anything for anyone who was already tubed, agree w/ Henry Ford data. Gave Toci to a couple, it made their inflammatory markers look better but didn't actually make the patents any better. Probably wouldn't give it again.
-High fevers for several days is pretty routine. It actually seems to be the body's way of halting viral replication. I've just been letting people fever and treating insensible losses. Occasionally we have had pts get superinfected so we are still culturing.
-Haven't had much luck with Veletri, it is clogging filters on vent and requiring that they be changed often so we've ditched it
-Have used nitric oxide in a couple non-tubed patients with success
-Nearly every COVID pt on the vent has developed renal dysfunction or needed dialysis. If they need dialysis they are also needing heparin gtts for clotting

Would love to hear other's experiences. I'm finding it hard to generalize the management of COVID, no two patients are alike and there clearly seem to be ethnic/racial differences as well. All African-American pts on the vent seem to need hemodialysis.
Definitely agree 85% mortality for intubated pts seems way too high (based on my ~3wks of ICU experience). Where is Henry Ford data re HCQ? Would love to see it.
You get to use iNO? So jealous! My RTs say I’m not allowed (I think our pulm docs set that policy).
 


The thing that @CCM-MD posted was withdrawn from publication, will have a complete change of the conclusion... and got destroyed on Facebook on top of that.

Also, we really should focus most studies on outpatient and not inpatient use.

And keep in mind, so many institutions are debating things like early vs delayed intubation based solely on loose and contradictory anecdotal data. Now that is a huge and very risky decision to make. Using an extremely harmless medication should not be held to some insanely high standard, solely for the purpose of opposing Trump (which in reality, is why most people are opposing it).
 
The thing that @CCM-MD posted was withdrawn from publication, will have a complete change of the conclusion... and got destroyed on Facebook on top of that.

Also, we really should focus most studies on outpatient and not inpatient use.

And keep in mind, so many institutions are debating things like early vs delayed intubation based solely on loose and contradictory anecdotal data. Now that is a huge and very risky decision to make. Using an extremely harmless medication should not be held to some insanely high standard, solely for the purpose of opposing Trump (which in reality, is why most people are opposing it).
You're all over the place on this one, so let me just make my points very clearly.

First, I can count on 1 hand the number of "extremely harmless medications" that exist. HCQ is not one of them (nor is azithromycin). Both have known cardiac problems and we're giving it for a disease that it turns out can cause cardiac problems on its own. Now if the data strongly supported this regimen, then the risk could be worth it. We use high-risk meds all the time because the benefit outweighs the risk. At this time, we don't know that's the case here. I'm not saying don't give it (nor am I saying give it to everyone) because I just don't have the experience with this to come to a conclusion either way. That said, historically speaking, outside of vaccines we suck at dealing with viruses. I can count on that same 1 hand from earlier the number of viral infections we can actually treat. Lots of things work on viruses in vitro, very few work clinically.

Second, HCQ is politicized on both ends. Its actually quite disturbing how strongly pro-Trump people are talking about this drug. You'd think that anyone who is skeptical was actively murdering patients if they don't give it to everyone. Interestingly, the anti-Trump physician crowd is really more just conservative about it. Its worth looking at, but let's not call it an effective treatment yet. Its the anti-Trump muggles who are super against it. And to further shatter your narrative I routinely defend Trump (just ask @FFP ) and am skeptical about this. Same with the majority of the doctors I know (and living in SC most of them are either pro-Trump or at least anti-TDS).
 
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I haven't noticed, which hopefully suggests that neither of us is too biased. :)
Slightly tangential, but something I've noticed is that most of the folks actually taking care of COVID patients at the moment seem to be overwhelmingly in the "we can try it but I don't expect HCQ to really do much and it has real potential for harm". The physicians who are super gung-ho "this is a miracle drug and will cure everyone" are in fields like me where we don't set foot in the ICU ever.
 
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Slightly tangential, but something I've noticed is that most of the folks actually taking care of COVID patients at the moment seem to be overwhelmingly in the "we can try it but I don't expect HCQ to really do much and it has real potential for harm". The physicians who are super gung-ho "this is a miracle drug and will cure everyone" are in fields like me where we don't set foot in the ICU ever.
N=1. Rita Wilson (wife of Tom Hanks) said this morning that they got chloroquine in Australia and didn't feel an improvement (even cautioned against its risks). But they are democrats, so it's a hoax.

 
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Definitely agree 85% mortality for intubated pts seems way too high (based on my ~3wks of ICU experience). Where is Henry Ford data re HCQ? Would love to see it.
You get to use iNO? So jealous! My RTs say I’m not allowed (I think our pulm docs set that policy).

The Henry Ford/Wayne state data is mentioned above, it was submitted to NEJM but not published yet, I don't think.

NO is being used here in limited amounts as part of a small clinical trial. Otherwise we probably wouldn't be using it either.
 
The thing that @CCM-MD posted was withdrawn from publication, will have a complete change of the conclusion... and got destroyed on Facebook on top of that.

Also, we really should focus most studies on outpatient and not inpatient use.

And keep in mind, so many institutions are debating things like early vs delayed intubation based solely on loose and contradictory anecdotal data. Now that is a huge and very risky decision to make. Using an extremely harmless medication should not be held to some insanely high standard, solely for the purpose of opposing Trump (which in reality, is why most people are opposing it).

You created this thread in the critical care forum. You know critical care typically happens in the inpatient setting, right?

And oh no, not on Facebook! The pinnacle of clinical research discussion.
 
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You created this thread in the critical care forum. You know critical care typically happens in the inpatient setting, right?

And oh no, not on Facebook! The pinnacle of clinical research discussion.
So we should compartmentalize a drug because of the subforum's name? It's an appropriate place to put it since this medication was triaged into inpatient use with the belief that it'll carry more value for sicker patients. Doesn't necessarily mean that's how it should be used though.
And doctors posting on SDN vs Facebook are literally no different. The latter you can actually verify they're real :) And you posted an article that the authors themselves withdrew lol.
 
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Facebook is to SDN as Dr. Oz is to Dr. Fauci. ;)

You wear a pretty big mouth for a PGY-1, @MedicineZ0Z.

This is priceless, and I need to quote it. :lol:
I think this whole "asymptomatic carrier" or "how we're all positive" is utter nonsense.
This disease WILL make almost everyone who gets it sick. And the asymptomatic carrier thing is very likely just the incubation period. And what's even more silly is suggesting that this has been around since the Fall (like chris Cuomo tried to suggested last night).

More:
I can't grasp how an antiviral is making a big difference when a patient is very sick on day 9. If you want to stop viral replication, you need to do it on day 1 when the test is positive.

Just replace "antiviral"/"viral" with "antibiotic"/"bacterial".


1587387350500.jpeg
 
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Facebook is to SDN as Dr. Oz is to Dr. Fauci. ;)

You wear a pretty big mouth for a PGY-1, @MedicineZ0Z.

This is priceless, and I need to quote it. :lol:





View attachment 302899
Love this graph. My Mt Stupid was CA3 year. Valley of despair is first attending year. Hope to climb out of it soon towards expertise-dom!
 
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Facebook is to SDN as Dr. Oz is to Dr. Fauci. ;)

You wear a pretty big mouth for a PGY-1, @MedicineZ0Z.

This is priceless, and I need to quote it. :lol:


More:


Just replace "antiviral"/"viral" with "antibiotic"/"bacterial".

Didn't you also say that myocarditis leads to torsades? lmao
 
As a side note I feel like people are forgetting basic things like early physical therapy, incentive spirometry, encouraging OOB... I have 15-16 COVID+ patients on my team every day. Some coming out of the ICU have none of the above.

Eventually these patients need to leave the hospital and they need to be prepared to do so
 
As a side note I feel like people are forgetting basic things like early physical therapy, incentive spirometry, encouraging OOB... I have 15-16 COVID+ patients on my team every day. Some coming out of the ICU have none of the above.

Eventually these patients need to leave the hospital and they need to be prepared to do so
Any evidence PT/OT makes a difference?
 
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