COVID-19 and discharge anticoagulation

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end stage fibro

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What are you guys discharging with? My health system has reasonable recs for inpatient AC but nothing for discharge. I've seen anything from nothing to ASA to treat as if patient had a clot. I'm leaning towards 1 month low dose DOAC with heavy variablity depending on patient decision.

I ask because we get some discharges that bounceback worse about a week after and not sure if clot burden has something to do with it.

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To be honest, seems like we are pulling our anticoag recommendations out of thin air. I've discharged people on DOAC to baby ASA with no real guiding direction from ID/hematology.
 
On heme consults depending on age, co-morbidities etc we also do anything from ASA to prophylactic doac dose. No standardized guidelines yet
 
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What are you guys discharging with? My health system has reasonable recs for inpatient AC but nothing for discharge. I've seen anything from nothing to ASA to treat as if patient had a clot. I'm leaning towards 1 month low dose DOAC with heavy variablity depending on patient decision.

I ask because we get some discharges that bounceback worse about a week after and not sure if clot burden has something to do with it.

I don't understand your question. Are you taking about all COVID comers, or COVID+PE/VTE ? I wouldn't think to AC all COVIDers. If +PE/VTE, just AC them as you would for any PE/VTE (bearing in mind renal function, etc).
 
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If they have an indication, anticoagulated them. If they don't, then don't give them anticoagulation unless there is high quality data supporting its use.
 
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I assume he is referring to all COVID. If they have another indication for anticoagulation... well duh proceed as you would otherwise.
 
The attorneys love it.

I'm going to law school.
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What idiocy. People are AC all COVID-comers, even if no other indication for AC? We've gone mad.

lol pretty sure of yourself there hotshot considering what's said on the American Society of Hematology webpage.


Should COVID-19 patients receive post-discharge thromboprophylaxis?

Patients hospitalized for acute medical illness are at increased risk for VTE for up to 90 days after discharge. This finding should apply to COVID-19 patients, though data on incidence are not yet available. Therefore, it is reasonable to consider extended thromboprophylaxis after discharge using a regulatory-approved regimen (e.g., betrixaban 160 mg on day 1, followed by 80 mg once daily for 35-42 days; or rivaroxaban 10 mg daily for 31-39 days)1,2, 3. Inclusion criteria for the trials studying these regimens included combinations of age, co-morbidities such as active cancer, and elevated D-dimer >2 times the upper normal limit. Any decision to use post-discharge thromboprophylaxis should consider the individual patient’s VTE risk factors, including reduced mobility and bleeding risk as well as feasibility. “Home hospital” approaches for COVID-19 patients involving early discharge have been suggested to free up inpatient beds. Status at discharge should be considered in any decision to use VTE prophylaxis in these unique patients. Aspirin has been studied for VTE prophylaxis in low-risk patients after orthopedic surgery and could be considered for COVID-19 VTE prophylaxis if criteria for post-discharge thromboprophylaxis are met4. Patients should be educated on the signs and symptoms of VTE at hospital discharge.
 
Should COVID-19 patients receive post-discharge thromboprophylaxis?

Patients hospitalized for acute medical illness are at increased risk for VTE for up to 90 days after discharge. This finding should apply to COVID-19 patients, though data on incidence are not yet available. Therefore, it is reasonable to consider extended thromboprophylaxis after discharge using a regulatory-approved regimen (e.g., betrixaban 160 mg on day 1, followed by 80 mg once daily for 35-42 days; or rivaroxaban 10 mg daily for 31-39 days)1,2, 3. Inclusion criteria for the trials studying these regimens included combinations of age, co-morbidities such as active cancer, and elevated D-dimer >2 times the upper normal limit. Any decision to use post-discharge thromboprophylaxis should consider the individual patient’s VTE risk factors, including reduced mobility and bleeding risk as well as feasibility. “Home hospital” approaches for COVID-19 patients involving early discharge have been suggested to free up inpatient beds. Status at discharge should be considered in any decision to use VTE prophylaxis in these unique patients. Aspirin has been studied for VTE prophylaxis in low-risk patients after orthopedic surgery and could be considered for COVID-19 VTE prophylaxis if criteria for post-discharge thromboprophylaxis are met4. Patients should be educated on the signs and symptoms of VTE at hospital discharge.

It's true that any acute medical illness can render you hypercoagulable and thus may warrant AC, but we don't reflexively put people on AC for every acute medical illness. 35-yo with +COVID, gets a little oxygen, gets better, has no other comorbids, goes home, you're gonna put him on AC? Why don't we do this for all pneumonias? For all IBD flares? (which are probably more coagulopathic)

I don't care who recommends it. Let's use our brains.

"though data on incidence are not yet available" <---Uh yeah, some data would help. There was a time in medicine not too long ago, when first we had the data then made recommendations.
 
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Is there any evidence to support that there's some uniquely prothrombotic pathophysiologic process going on with severe covid that's above and beyond what you see with any other severe hyperinflammatory condition? There's this weird tendency I've noticed with this infection where somehow everything about it is seen as some novel paradigm-shifting peculiarity.

I think the potential to do harm is too high with this practice of recommending AC when it's not otherwise indicated and I wouldn't do it before there's evidence to suggest benefit.
 
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Is there any evidence to support that there's some uniquely prothrombotic pathophysiologic process going on with severe covid that's above and beyond what you see with any other severe hyperinflammatory condition?

Of course not. And if such evidence manifests, I'd be all about AC.

There's this weird tendency I've noticed with this infection where somehow everything about it is seen as some novel paradigm-shifting peculiarity.

That's exactly what's going on. We're seeing lots of well-intentioned but not exactly scientific ideas.

What's worse is that an official sounding 'society' makes a recommendation, and we---being the good lap dogs that we are---don't think twice and run with it.
 
Bottom line: people want to do SOMETHING.

As well intentioned that may be - first do no harm. If we get good data for AC I’m all for it. Until then, this is an experimental therapy that should be used within a study.
 
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lol pretty sure of yourself there hotshot considering what's said on the American Society of Hematology webpage.


Should COVID-19 patients receive post-discharge thromboprophylaxis?

Patients hospitalized for acute medical illness are at increased risk for VTE for up to 90 days after discharge. This finding should apply to COVID-19 patients, though data on incidence are not yet available. Therefore, it is reasonable to consider extended thromboprophylaxis after discharge using a regulatory-approved regimen (e.g., betrixaban 160 mg on day 1, followed by 80 mg once daily for 35-42 days; or rivaroxaban 10 mg daily for 31-39 days)1,2, 3. Inclusion criteria for the trials studying these regimens included combinations of age, co-morbidities such as active cancer, and elevated D-dimer >2 times the upper normal limit. Any decision to use post-discharge thromboprophylaxis should consider the individual patient’s VTE risk factors, including reduced mobility and bleeding risk as well as feasibility. “Home hospital” approaches for COVID-19 patients involving early discharge have been suggested to free up inpatient beds. Status at discharge should be considered in any decision to use VTE prophylaxis in these unique patients. Aspirin has been studied for VTE prophylaxis in low-risk patients after orthopedic surgery and could be considered for COVID-19 VTE prophylaxis if criteria for post-discharge thromboprophylaxis are met4. Patients should be educated on the signs and symptoms of VTE at hospital discharge.

do the trial. until that's done, it's heresay. this is just like MONA for MI, until we studied and found out that just about everything in MONA was either harmful or neutral except for aspirin. do the trials to prove a benefit.

and that regimen sounds awful and complex. giving half-dose anticoagulation exposes patients to all of the risks with none of the benefits.

i bet if you checked d-dimers in community acquired pneumonia, a sizable portion will have >2x the ULN, likewise, for cholecystitis, cholangitis, influenza, etc etc. it's all acute phase reactants. are we doing harm by not giving patients with cholangitis anticoagulation on discharge? do we start giving tocilizumab to all septic patients with high IL-6s?

covid has turned the medical world mad. it's not a novel virus, it's not even a novel infection!
 
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It's true that any acute medical illness can render you hypercoagulable and thus may warrant AC, but we don't reflexively put people on AC for every acute medical illness. 35-yo with +COVID, gets a little oxygen, gets better, has no other comorbids, goes home, you're gonna put him on AC? Why don't we do this for all pneumonias? For all IBD flares? (which are probably more coagulopathic)

I don't care who recommends it. Let's use our brains.

"though data on incidence are not yet available" <---Uh yeah, some data would help. There was a time in medicine not too long ago, when first we had the data then made recommendations.

If we waited for multiple RCTs in agreement to do best practice medicine then we wouldnt be using paralytics in ARDS, nitric oxide, fluid restrictive resuscitation ECMO etc etc. The majority of medicine doesnt have 1A evidence backing it up. These people are sick and dieing now, they don't have 5 years for an rct or 3 to get done.

I think the legal risk is nonsense in the COVID era, but supposing it is not--it would be just as easy to come back and say why didnt you give my young low risk for AC patient AC when there was clinical opinion that it could be warranted? Now he got a PE and died and you could have prevented it !!11one!

I only see the sickest covid patients and am very quick to use ac unless a clear contraindication exists.

I've put lots of central lines in people and the covid patients clot way faster than normal septic people. I know that isn't an rct but they are actively studying incidental pocus DVT because we saw so much of it. Something is different and that is enough for me to treat them differently than regular ards.
 
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If we waited for multiple RCTs in agreement to do best practice medicine then we wouldnt be using paralytics in ARDS, nitric oxide, fluid restrictive resuscitation ECMO etc etc. The majority of medicine doesnt have 1A evidence backing it up. These people are sick and dieing now, they don't have 5 years for an rct or 3 to get done.

I think the legal risk is nonsense in the COVID era, but supposing it is not--it would be just as easy to come back and say why didnt you give my young low risk for AC patient AC when there was clinical opinion that it could be warranted? Now he got a PE and died and you could have prevented it !!11one!

I only see the sickest covid patients and am very quick to use ac unless a clear contraindication exists.

I've put lots of central lines in people and the covid patients clot way faster than normal septic people. I know that isn't an rct but they are actively studying incidental pocus DVT because we saw so much of it. Something is different and that is enough for me to treat them differently than regular ards.
We don't have time to figure out if Xigris is beneficial or not, we have patients dying today of sepsis.

Even more poignant, we can't afford to do an RCT of antiarrhymtics after MI. It's obvious that it works. Post MI patients die of arrhythmias, ergo if you suppress the arrhythmia, you save lives. In fact, it would be unethical to randomize patients to a trial because we know it works.
 
Good luck defending yourself if you get sued for someone getting an ICH or other major bleeding. There is no good data for this.

can't get sued in my state for COVID treatment :cool:

What idiocy. People are AC all COVID-comers, even if no other indication for AC? We've gone mad.
Is there any evidence to support that there's some uniquely prothrombotic pathophysiologic process going on with severe covid that's above and beyond what you see with any other severe hyperinflammatory condition? There's this weird tendency I've noticed with this infection where somehow everything about it is seen as some novel paradigm-shifting peculiarity.

I think the potential to do harm is too high with this practice of recommending AC when it's not otherwise indicated and I wouldn't do it before there's evidence to suggest benefit.

I've read some stuff in journals here and there, most recent being in the newest NEJM here. There is a plethora of preprint stuff on medarxiv but I try not to rely on that. Is this high quality by any means? not at all. My gut tells me there is something to this prothrombotic stuff.

Bottom line: people want to do SOMETHING.

As well intentioned that may be - first do no harm. If we get good data for AC I’m all for it. Until then, this is an experimental therapy that should be used within a study.

agree. hard to practice "hurry up and do nothing" medicine, even if it frequently the most appropriate
 
We don't have time to figure out if Xigris is beneficial or not, we have patients dying today of sepsis.

Even more poignant, we can't afford to do an RCT of antiarrhymtics after MI. It's obvious that it works. Post MI patients die of arrhythmias, ergo if you suppress the arrhythmia, you save lives. In fact, it would be unethical to randomize patients to a trial because we know it works.

I'm usually on board with this train of thought. However, in the context of a worldwide pandemic whose only dedicated treatment is another -ivir drug that maybe kinda might work if you look at it right, I think it is worth trying some other treatments that might have benefit and can pave the way for trials.
 
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We don't have time to figure out if Xigris is beneficial or not, we have patients dying today of sepsis.

Even more poignant, we can't afford to do an RCT of antiarrhymtics after MI. It's obvious that it works. Post MI patients die of arrhythmias, ergo if you suppress the arrhythmia, you save lives. In fact, it would be unethical to randomize patients to a trial because we know it works.

False equivalency and you know it. How many sepsis patients need to go to ltac or are hospitalized for a month? Covid patients are a different animal in critical care land. Severe ards is a horrible disease and if we had a drug that shows any promise we use it.

If your loved one (or yourself) end up in the ICU you'd want your attending to adamantly refuse to use convalescent plasma, steroids, redemsivir etc and just give you supplemental oxygen because there aren't any good rct showing that these work yet?

I understand the criticism that it is a knee jerk to do something instead of nothing but at least ac has a clear potential therapeutic effect unlike plaquenil.
 
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False equivalency and you know it. How many sepsis patients need to go to ltac or are hospitalized for a month? Covid patients are a different animal in critical care land. Severe ards is a horrible disease and if we had a drug that shows any promise we use it.

If your loved one (or yourself) end up in the ICU you'd want your attending to adamantly refuse to use convalescent plasma, steroids, redemsivir etc and just give you supplemental oxygen because there aren't any good rct showing that these work yet?

I understand the criticism that it is a knee jerk to do something instead of nothing but at least ac has a clear potential therapeutic effect unlike plaquenil.

I expect the best supportive care. I would rather pass on being a pseudo chemo patient. So yes, spare me remdesivir, plaquenil, toci, plasma, etc etc until it's been proven to work. Sometimes, doing nothing is better than doing something.

Your argument doesn't work. It's the logic that lead to people being given flecainide post MI because "we have to do something". You get VT and die, flecainide prevents VT, ergo give flecainide.

There is no such thing as having no time. More people died from MIs than COVID and we probably did much more harm for a decade giving these drugs and not studying them instead of just doing the damn trial. If you want to do something, have some evidence it works. It doesn't need to be a 20000 person trial like cards. Take 500 people, randomize them, and do the intervention. Within 3 months, you'll have your answer. Instead we are treating hundreds of thousands of people off protocol based on anecdotes and bioplausibility. Bioplausibility gave us flecainide after MI.
 
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Dexamethasone is the only thing that has good data so far. I have done experimental therapies for patients/families that feel very strongly about it.

I think many have gone too far with trying random **** on COVID. How many poorly studied "cures" is it gonna take before we get back to practicing based on evidence.
 
I expect the best supportive care. I would rather pass on being a pseudo chemo patient. So yes, spare me remdesivir, plaquenil, toci, plasma, etc etc until it's been proven to work. Sometimes, doing nothing is better than doing something.

Your argument doesn't work. It's the logic that lead to people being given flecainide post MI because "we have to do something". You get VT and die, flecainide prevents VT, ergo give flecainide.

There is no such thing as having no time. More people died from MIs than COVID and we probably did much more harm for a decade giving these drugs and not studying them instead of just doing the damn trial. If you want to do something, have some evidence it works. It doesn't need to be a 20000 person trial like cards. Take 500 people, randomize them, and do the intervention. Within 3 months, you'll have your answer. Instead we are treating hundreds of thousands of people off protocol based on anecdotes and bioplausibility. Bioplausibility gave us flecainide after MI.

I am assuming you are a cardiologist. In critical care our trials are poorly funded, heavily confounded, and very hard to recruit for. We don't have evidence like you do for cardiology. Even some of our best trials that founded the core principles of critical care issues were later shown to be wrong or effective for reasons we didn't understand (think egdt, early ecmo studies, paralysis in ards). In ccm you have to be comfortable not being sure and using underlying physiology to guide therapy at the bedside based on an individuals response because there are very very very few absolutes in the field.

While it would be nice to know that ac benefit outweighs potential harm for sure, I don't think adequate data will ever emerge so we'll never know because of small effect size and the sheer confounding variability of people showing up. I'm not going to wait for my vented covid patient on 100% fio2 who has clotted off an HD line and a central line on crrt to get a pe (and die) before I start ac. I can fix a bleeding problem but another hit to the lungs and we're done.

I don't dispo patients home so I guess I don't have a dog in this particular fight but putting my hospitalist hat on I would absolutely do a 3 month ac course if someone was sent to me sick enough to be put on lovenox. Even moreso if they are young because the overall risk of adverse event is lower and the downside of PE with recovering trashed lungs is astronomically bad.
 
I am assuming you are a cardiologist. In critical care our trials are poorly funded, heavily confounded, and very hard to recruit for. We don't have evidence like you do for cardiology. Even some of our best trials that founded the core principles of critical care issues were later shown to be wrong or effective for reasons we didn't understand (think egdt, early ecmo studies, paralysis in ards). In ccm you have to be comfortable not being sure and using underlying physiology to guide therapy at the bedside based on an individuals response because there are very very very few absolutes in the field.

While it would be nice to know that ac benefit outweighs potential harm for sure, I don't think adequate data will ever emerge so we'll never know because of small effect size and the sheer confounding variability of people showing up. I'm not going to wait for my vented covid patient on 100% fio2 who has clotted off an HD line and a central line on crrt to get a pe (and die) before I start ac. I can fix a bleeding problem but another hit to the lungs and we're done.

I don't dispo patients home so I guess I don't have a dog in this particular fight but putting my hospitalist hat on I would absolutely do a 3 month ac course if someone was sent to me sick enough to be put on lovenox. Even moreso if they are young because the overall risk of adverse event is lower and the downside of PE with recovering trashed lungs is astronomically bad.

We don't even have those poorly funded and heavily confounded trials for AC in COVID.

Also, sending someone home on AC for COVID no longer qualifies as critical care.
 
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I'm ok with trying something if there's a plausible scientific mechanism for it---for instance, plaquenil , or dex, to suppress the immune response--even in the absence of clear cut evidence. But I'd draw the line at outpatient AC. Too risky. If the patient looks sick enough to you, and you think he's gonna clot, I'd rather you keep him inpatient and AC all you want. The last thing we need is a million well-recovering COVID patients running around in society on AC.

But to each is own....it's your license (or the license of the attending you're practicing under).
 
I'm ok with trying something if there's a plausible scientific mechanism for it---for instance, plaquenil , or dex, to suppress the immune response--even in the absence of clear cut evidence. But I'd draw the line at outpatient AC. Too risky. If the patient looks sick enough to you, and you think he's gonna clot, I'd rather you keep him inpatient and AC all you want. The last thing we need is a million well-recovering COVID patients running around in society on AC.

But to each is own....it's your license (or the license of the attending you're practicing under).

We know the risk of outpatient ac use though, about 0.3% annually for ich and they have been around long enough to be generally safe and well tolerated. Someone who is critically ill bring immunosuppressed seems way riskier to me. Why not go full bore and use cytoxan if you want to actually test that hypothesis without a trial?
 
We know the risk of outpatient ac use though, about 0.3% annually for ich and they have been around long enough to be generally safe and well tolerated. Someone who is critically ill bring immunosuppressed seems way riskier to me. Why not go full bore and use cytoxan if you want to actually test that hypothesis without a trial?

Wait, hold up. You are equating 6mg of dex/day to the risk of full dose AC on a person leaving the hospital. Let me think - fall on AC, MVA on AC. Really man Cytoxan? Why don't you just give tPA instead of full dose AC in that case?

(there is actually a 3 patient case series for tPA in COVID)
 
We know the risk of outpatient ac use though, about 0.3% annually for ich and they have been around long enough to be generally safe and well tolerated. Someone who is critically ill bring immunosuppressed seems way riskier to me. Why not go full bore and use cytoxan if you want to actually test that hypothesis without a trial?

Fair enough. I said I was ok with it, not totally agreeable with it. Your points are valid. None of the above is validated.

20 years ago, if I told you that in 2020 there would be a respiratory virus, with an overall survival rate of 96% in all comers, and a 99% survival rate in the young and no comorbid----and we were throwing immunosuppressants, AC, steroids at it with out any data, you'd tell me I was nuts.
 
Wait, hold up. You are equating 6mg of dex/day to the risk of full dose AC on a person leaving the hospital. Let me think - fall on AC, MVA on AC. Really man Cytoxan? Why don't you just give tPA instead of full dose AC in that case?

(there is actually a 3 patient case series for tPA in COVID)

I think we'cve crossed wires. Cytoxan would be inpatient only obviously and they'd recover in the hospital. I guess I've managed more ac than others because I am honestly not that afraid of prescribing it to people. You make sure they understand the risks but a new insulin start seems more dangerous and nobody blinks at doing that.

No point in tpa since that doesn't prevent clots after an hour which is what I'm trying to accomplish.
 
Fair enough. I said I was ok with it, not totally agreeable with it. Your points are valid. None of the above is validated.

20 years ago, if I told you that in 2020 there would be a respiratory virus, with an overall survival rate of 96% in all comers, and a 99% survival rate in the young and no comorbid----and we were throwing immunosuppressants, AC, steroids at it with out any data, you'd tell me I was nuts.

I agree this year has been bonkers. I think a lot of people are trying random stuff and publishing terrible retrospective reviews that don't inform us of much. I don't want to be part of the problem and do random stuff that hurts people but I do want to be proactive when possible and it always involves a discussion with family and documentation.
 
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I agree this year has been bonkers. I think a lot of people are trying random stuff and publishing terrible retrospective reviews that don't inform us of much. I don't want to be part of the problem and do random stuff that hurts people but I do want to be proactive when possible and it always involves a discussion with family and documentation.

We may disagree on the AC piece but at the end of the day, wish you and everyone the best in caring for these patients.
 
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COVID is thought to cause microthrombi in pulmonary vasculature and other places to leading to its various end effects(hence AC was thought of as a potential treatment). There is a component of heightened immune system which is thought to present in some cases like cytokine storm seen with other things we deal with in Heme Onc ( hence Anti IL-6, steroids etc). Based on these various possible presentations, therapies are tried and if they dont work they dont work

There are no solid guide lines or consensus on AC, it should be dealt with on case to case basis on assessment of various different parameters like D dimer, CRP, etc etc etc. (obvious involve an Hematologist if you think about discharging a patient on AC)

I have cases which mimic antiphospholipid like presentation and a few with a complete DIC picture.

Now we are seeing neuropsychiartric sequale as well.

We dont know this beast well, as time passes we will likely get more info on it.

As RCTs are done we get more solidified treatments, we wait and do our best to weather the storm until then.

also guidelines are just guidelines, we dont go to Med school to follow guidelines only. We are taught to think rationally and based on that take the best course of educated action which is in the best interest of our patient.

Good luck with the patients
 
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