CDT vs Periph. Lytics in Submassive

[Bostonredsox]

I was approached about this the other day in discussion with admin. concept of acquiring CDT and the EKOS system. I have been reading up on alot of the data. I liked Farkas' summary in Pulmcrit last year. I am wondering if their is significant benefit to running 25mg TPA over 24 hours via PA catheters vs through a standard IJ or even peripheral line. It seems to me their is probably a legit reduction in bleeding risk by giving 25mg or even 50mg over 24hr as opposed to as a bolus over 1-2 hours (my shops current protocol is a flat 100mg over like 90 minutes followed by heparin gtt without bolus once completed). I was thinking of making a continuous order set with fibrinogen level tracking as opposed to the bolus but I am not sure the benefit to CDT itself. I mean I love putting extra large pieces of plastic into peoples hearts but trying to match my resource utilization with what i have available.

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[deleted547339]

I was approached about this the other day in discussion with admin. concept of acquiring CDT and the EKOS system. I have been reading up on alot of the data. I liked Farkas' summary in Pulmcrit last year. I am wondering if their is significant benefit to running 25mg TPA over 24 hours via PA catheters vs through a standard IJ or even peripheral line. It seems to me their is probably a legit reduction in bleeding risk by giving 25mg or even 50mg over 24hr as opposed to as a bolus over 1-2 hours (my shops current protocol is a flat 100mg over like 90 minutes followed by heparin gtt without bolus once completed). I was thinking of making a continuous order set with fibrinogen level tracking as opposed to the bolus but I am not sure the benefit to CDT itself. I mean I love putting extra large pieces of plastic into peoples hearts but trying to match my resource utilization with what i have available.

I don’t think we have enough data yet to consider cartheter-directed lytics as a standard protocol. If you’re going to do it, you should randomize it and collect your data. It may work, but we just don’t know. My suspicion is that whether you put it in a PIV, CVL or PAC, it won’t matter - it all goes to the same place.

Regarding systemic lytics in submissive PE, I feel like it’s case closed - not indicated. I think you would be happy to settle out of court on your first head bleed s/p. tPA for non-massive PE. Hep gtt and time.

 

[Dr.CCM]

I don’t think we have enough data yet to consider cartheter-directed lytics as a standard protocol. If you’re going to do it, you should randomize it and collect your data. It may work, but we just don’t know. My suspicion is that whether you put it in a PIV, CVL or PAC, it won’t matter - it all goes to the same place.

Regarding systemic lytics in submissive PE, I feel like it’s case closed - not indicated. I think you would be happy to settle out of court on your first head bleed s/p. tPA for non-massive PE. Hep gtt and time.

What about the submassive PE with “impending doom” those that have syncopized, are unstable but not on pressors just tachy and Bp is a little soft, high lactates, you see a clot on Echo that’s moving on up, etc? The ones that come up with “tpa at the bedside” just in case they arrest...

We typically EKOS them but don’t know why we couldn’t do it peripherally.

It looks like the risk of ich is about as high as the risk for a heparin drip when using the lower dose tpa protocols 25-50 without a heparin bolus fwiw.

 

[deleted547339]

What about the submassive PE with “impending doom” those that have syncopized, are unstable but not on pressors just tachy and Bp is a little soft, high lactates, you see a clot on Echo that’s moving on up, etc? The ones that come up with “tpa at the bedside” just in case they arrest...

We typically EKOS them but don’t know why we couldn’t do it peripherally.

It looks like the risk of ich is about as high as the risk for a heparin drip when using the lower dose tpa protocols 25-50 without a heparin bolus fwiw.

I would argue that a PE that leads to syncope, lactic acidosis or have relative hypotension are all massive.

I think meta-stable with clot in transit is rare enough you could argue to do it and be defensible.

 

[Dr.CCM]

I would argue that a PE that leads to syncope, lactic acidosis or have relative hypotension are all massive.

I think meta-stable with clot in transit is rare enough you could argue to do it and be defensible.

I guess it’s just semantics but massive PE according to AHA has a different definition and the above description would fall into the submissive category—hence the “impending doom”

 

[deleted547339]

I guess it’s just semantics but massive PE according to AHA has a different definition and the above description would fall into the submissive category—hence the “impending doom”

I know that it’s technically not massive by the strictest of criteria, but I think with those findings you had shock and that’s what the definitions of massive are getting at.

 

[engineeredout]

Agree with the piss poor terminology we currently have for these PEs. The asymptomatic patient on room air with echo findings of possible RV dilation is lumped in the same category as the tachypnec on 6L NC, spo2 91%, BP 95/62, P 130. We know these two patients are not the same, but they are both called submassive. The former gets a NOAC, the latter gets alteplace. We need a redefinition for the low risk vs high risk.

Anyone actually had a head bleed post TPA for PE? Post stroke yea, but that's because we're throwing lytics at an injured brain.

 

[deleted547339]

Agree with the piss poor terminology we currently have for these PEs. The asymptomatic patient on room air with echo findings of possible RV dilation is lumped in the same category as the tachypnec on 6L NC, spo2 91%, BP 95/62, P 130. We know these two patients are not the same, but they are both called submassive. The former gets a NOAC, the latter gets alteplace. We need a redefinition for the low risk vs high risk.

Anyone actually had a head bleed post TPA for PE? Post stroke yea, but that's because we're throwing lytics at an injured brain.

Never seen it, but incidence is likely in the 1-ish percent range and I definitely haven’t lysed 100 PEs.

 

[Bostonredsox]

I don’t think we have enough data yet to consider cartheter-directed lytics as a standard protocol. If you’re going to do it, you should randomize it and collect your data. It may work, but we just don’t know. My suspicion is that whether you put it in a PIV, CVL or PAC, it won’t matter - it all goes to the same place.

Regarding systemic lytics in submissive PE, I feel like it’s case closed - not indicated. I think you would be happy to settle out of court on your first head bleed s/p. tPA for non-massive PE. Hep gtt and time.

I disagree very much with your premise that its case closed not indicated, but in a way I am also agreeing after reading your later posts. We agree, the non hypotensive, not on vasopressors, lactate under 4 pt (thus not massive) with a saddle clot that does have a huge RV:LV, echo evidence for hypocontractility, + trops, is hypoxic, diaphoretic and clammy, should be lysed. the difference is that that pt by current guidelines IS submassive. they are submassive with high risk for PEA arrest. that pt should be lysed. I agree, in terms of physiology, we both feel thats a massive pe. but per the literature they are not massive, they are submassive. so in terms of litigation, they are a high risk submassive PE and I think very much should be lysed. I agree with the low risk submassives or stable submassives who have been walking at home for 5 days with progressive dyspnea and have a dilated RV on CT with clot, they should not be lysed and the literature supports lysing them probably does not improve outcomes. the terminology is piss poor thats correct, but it is what it is. and high risk submassives I think have convincing evidence they should be lysed.

my question is more so looking at the concept of slow infused TPA at 1 mg/hr over 24 hours as opposed to bolus. I think we all agree, 100% of the venous return hits the PA so who cares where you dump in the tpa. i think if there was an RRT comparing CDT with peripheral lysis with the same dose of tpa over the same duration, outcomes would be identical with lower complications. regardless, many shops do not have the resources for CDT anyway. real question is should we be giving these high risk submassives 50mg of tpa over 2 hours or over 24 hours. wondering about the difference there in terms of primary outcome. I think its logical bleeding risk will be lower.

 

[deleted547339]

I disagree very much with your premise that its case closed not indicated, but in a way I am also agreeing after reading your later posts. We agree, the non hypotensive, not on vasopressors, lactate under 4 pt (thus not massive) with a saddle clot that does have a huge RV:LV, echo evidence for hypocontractility, + trops, is hypoxic, diaphoretic and clammy, should be lysed. the difference is that that pt by current guidelines IS submassive. they are submassive with high risk for PEA arrest. that pt should be lysed. I agree, in terms of physiology, we both feel thats a massive pe. but per the literature they are not massive, they are submassive. so in terms of litigation, they are a high risk submassive PE and I think very much should be lysed. I agree with the low risk submassives or stable submassives who have been walking at home for 5 days with progressive dyspnea and have a dilated RV on CT with clot, they should not be lysed and the literature supports lysing them probably does not improve outcomes. the terminology is piss poor thats correct, but it is what it is. and high risk submassives I think have convincing evidence they should be lysed.

my question is more so looking at the concept of slow infused TPA at 1 mg/hr over 24 hours as opposed to bolus. I think we all agree, 100% of the venous return hits the PA so who cares where you dump in the tpa. i think if there was an RRT comparing CDT with peripheral lysis with the same dose of tpa over the same duration, outcomes would be identical with lower complications. regardless, many shops do not have the resources for CDT anyway. real question is should we be giving these high risk submassives 50mg of tpa over 2 hours or over 24 hours. wondering about the difference there in terms of primary outcome. I think its logical bleeding risk will be lower.

I think that with the peitho followup study being released, the onus is on the physician to explain why he or she is lysing a patient. The previous argument was to keep the patient out of long-term RV failure, but that’s been relatively debunked. If you lyse a HD stable patient with marginal echo, positive trop and positive BNP, you don’t have a leg to stand on if the patient has an ICH. That just isn’t up for debate - people may not like it, but the facts are the facts. Heck, I really wanted to believe in it and I’ve given a lot of half dose lytics.

I think the only argument that can be made (and I suspect you agree) is if you think the patient is in shock but doesn’t meet traditional massive PE criteria. The categorization of massive vs sub-massive PE is what it is because it has to be simple to be studyable. As an intensivist, I feel like I have the authority to say that a patient is in shock by a criteria other than simple hypotension. I can put a guy with an NSTEMI and a map of 90 on ionotropic support because his pulse pressure is 5, he has an ScvO2 of 40 and he is cold and not peeing. I can call that cardiogenic shock easily and only a fool would argue with me. Similar arguments can be made saying that people with a PE have obstructive shock, but the argument is based on criteria of shock that you could defend in court, not simply positive trop, BNP or echo. In my mind, syncope = sustained hypotension, potential lethal arrhythmia or both.

 

[CCM-MD]

Anyone actually had a head bleed post TPA for PE? Post stroke yea, but that's because we're throwing lytics at an injured brain.

I've had a couple of patients - one had EKOS for lower extremity DVT, ended up with occipital bleed. Another with half dose TPA for submassive PE ended up with thalamic bleed and a paraspinal hematoma.

 

[Hernandez]

Anyone actually had a head bleed post TPA for PE? Post stroke yea, but that's because we're throwing lytics at an injured brain.

Yes, I’ve seen several and they tend to be devastating.

 

[Hernandez]

I disagree very much with your premise that its case closed not indicated, but in a way I am also agreeing after reading your later posts. We agree, the non hypotensive, not on vasopressors, lactate under 4 pt (thus not massive) with a saddle clot that does have a huge RV:LV, echo evidence for hypocontractility, + trops, is hypoxic, diaphoretic and clammy, should be lysed. the difference is that that pt by current guidelines IS submassive. they are submassive with high risk for PEA arrest. that pt should be lysed. I agree, in terms of physiology, we both feel thats a massive pe. but per the literature they are not massive, they are submassive. so in terms of litigation, they are a high risk submassive PE and I think very much should be lysed. I agree with the low risk submassives or stable submassives who have been walking at home for 5 days with progressive dyspnea and have a dilated RV on CT with clot, they should not be lysed and the literature supports lysing them probably does not improve outcomes. the terminology is piss poor thats correct, but it is what it is. and high risk submassives I think have convincing evidence they should be lysed. .

So convincing is the evidence, that it shows no improvement in mortality or long term outcomes because of the side affects!

 

[joeDO2]

Rebel EM has a great summary of all of the different studies of full dose, half dose, and CDT:
Treatment of Submassive Pulmonary Embolism (PE): Full Dose, Half Dose, or No Dose? - R.E.B.E.L. EM - Emergency Medicine Blog

Based on the information so far (may evolve as new data comes out), this is my strategy for submassive:

>65 yrs old (greater bleeding risk): offer CDT as option to treat after consent w/risks and benefits
<65 yrs old (less bleeding and longer life to deal with pulm residual effects): offer 1/2 dose systemic as option to treat after consent
Based on available evidence, I do not consider full dose lytics for submassive.

 

[deleted547339]

Rebel EM has a great summary of all of the different studies of full dose, half dose, and CDT:
Treatment of Submassive Pulmonary Embolism (PE): Full Dose, Half Dose, or No Dose? - R.E.B.E.L. EM - Emergency Medicine Blog

Based on the information so far (may evolve as new data comes out), this is my strategy for submassive:

>65 yrs old (greater bleeding risk): offer CDT as option to treat after consent w/risks and benefits
<65 yrs old (less bleeding and longer life to deal with pulm residual effects): offer 1/2 dose systemic as option to treat after consent
Based on available evidence, I do not consider full dose lytics for submassive.

This may be a rational framework, but is somewhat out of date.

 

[Bostonredsox]

I think that with the peitho followup study being released, the onus is on the physician to explain why he or she is lysing a patient. The previous argument was to keep the patient out of long-term RV failure, but that’s been relatively debunked. If you lyse a HD stable patient with marginal echo, positive trop and positive BNP, you don’t have a leg to stand on if the patient has an ICH. That just isn’t up for debate - people may not like it, but the facts are the facts. Heck, I really wanted to believe in it and I’ve given a lot of half dose lytics.

I think the only argument that can be made (and I suspect you agree) is if you think the patient is in shock but doesn’t meet traditional massive PE criteria. The categorization of massive vs sub-massive PE is what it is because it has to be simple to be studyable. As an intensivist, I feel like I have the authority to say that a patient is in shock by a criteria other than simple hypotension. I can put a guy with an NSTEMI and a map of 90 on ionotropic support because his pulse pressure is 5, he has an ScvO2 of 40 and he is cold and not peeing. I can call that cardiogenic shock easily and only a fool would argue with me. Similar arguments can be made saying that people with a PE have obstructive shock, but the argument is based on criteria of shock that you could defend in court, not simply positive trop, BNP or echo. In my mind, syncope = sustained hypotension, potential lethal arrhythmia or both.

I think we are still arguing scemantics here. You and I are agreeing in principal about the type of patient, in terms of their physiology, that should be offered lysis. The difference is, you are labeling that patient massive and I am labeling them submassive. The reason I am pointing out the difference is that you brought up the litigation issues of thrombolysis and poor outcomes. And in this case, the literature and guideline recommendations are what the laywers would utilize. And although the patient you are described with “massive physiology “should be offered thrombolysis, by the current literature and guidelines they are actually a “high risk submassive “. This is the fundamental reason why I disagree with your premise that the data is clear, do not thrombolyse submassive. There is a distinct difference between high risk submassive, the patient you described above who has evidence of impending arrest from developing cardiogenic shock, and low risk submassive, mildly dilated right ventricle, weakly positive troponin, marginal echocardiogram with stable hemodynamics. Both are submassive. One is high risk for progression to pulmonary arrest. One is low risk. One gets offered lytics. One does not. But by current guidelines/diagnostic criteria, they both are submassive. I agree with you, we should have the ability as physicians to determine whether not the patient is in shock and thus at risk for pulmonary arrest and thus should be offered thrombolysis. This is really all that matters. The previous argument of prevention of long-term right ventricular failure was debunked I agree with you. But the reason we are offering thrombolytics now is to prevent immediate PEA arrest. If the patient has extensive saddle embolus, markedly dilated right ventricle with hypocontractility by CT/echo, laboratory evidence of demand ischemia, lactic acidosis and a clinical exam consistent with systemic end-organ hypoperfusion at risk for arrest, that patient is offered thrombolytics. But that does not change the fact that by the current literature, that patient is still considered submassive. High risk submassive, but submassive none the less. It is for this fundamental reason that I think offering a blanket statement that we do not thrombolyse submassive is incorrect. It is misleading as in reality between all of us, we know this patient really has massive physiology so we are really offering thrombolysis to a massive PE which is a category 1a recommendation. But in terms of the lawyers, they do not have that luxury. what they have is the diagnostic criteria and guidelines offered by ACC, chest, etc. And per those as of today, that pt is high risk submassive

 

[Hernandez]

I think we are still arguing scemantics here. You and I are agreeing in principal about the type of patient, in terms of their physiology, that should be offered lysis. The difference is, you are labeling that patient massive and I am labeling them submassive. The reason I am pointing out the difference is that you brought up the litigation issues of thrombolysis and poor outcomes. And in this case, the literature and guideline recommendations are what the laywers would utilize. And although the patient you are described with “massive physiology “should be offered thrombolysis, by the current literature and guidelines they are actually a “high risk submassive “. This is the fundamental reason why I disagree with your premise that the data is clear, do not thrombolyse submassive. There is a distinct difference between high risk submassive, the patient you described above who has evidence of impending arrest from developing cardiogenic shock, and low risk submassive, mildly dilated right ventricle, weakly positive troponin, marginal echocardiogram with stable hemodynamics. Both are submassive. One is high risk for progression to pulmonary arrest. One is low risk. One gets offered lytics. One does not. But by current guidelines/diagnostic criteria, they both are submassive. I agree with you, we should have the ability as physicians to determine whether not the patient is in shock and thus at risk for pulmonary arrest and thus should be offered thrombolysis. This is really all that matters. The previous argument of prevention of long-term right ventricular failure was debunked I agree with you. But the reason we are offering thrombolytics now is to prevent immediate PEA arrest. If the patient has extensive saddle embolus, markedly dilated right ventricle with hypocontractility by CT/echo, laboratory evidence of demand ischemia, lactic acidosis and a clinical exam consistent with systemic end-organ hypoperfusion at risk for arrest, that patient is offered thrombolytics. But that does not change the fact that by the current literature, that patient is still considered submassive. High risk submassive, but submassive none the less. It is for this fundamental reason that I think offering a blanket statement that we do not thrombolyse submassive is incorrect. It is misleading as in reality between all of us, we know this patient really has massive physiology so we are really offering thrombolysis to a massive PE which is a category 1a recommendation. But in terms of the lawyers, they do not have that luxury. what they have is the diagnostic criteria and guidelines offered by ACC, chest, etc. And per those as of today, that pt is high risk submassive

I must have read different guidelines than you as that’s not the hair splitting I recall. I’d bet if one were to run the NNH and the calculate the number needed not to treat to harm (NNNTTTH), that not giving tPa to those who decompensate is a wash and doing nothing is a viable option.

 

[jdh71]

I don't use systemic lytics unless the patient is "massive".

I ageee the "submissive" category is frustrating.

These days until better data is available I'm using catheter directed lyrics against anything that smells of RV strain/struggle, especially with a reasonable troponin bump. Taking Pa pressures from the 60-70s systolic to the 20-30s in 12 hours seems like a good thing for patients and their possible long term morbidity. Again. No hard data for this but seems reasonable.

The last time I pushed lytics for massive PE killing the patient they died anyway. I have yet to see big brain bleed. My n might be 5?? Tops.

 

[deleted547339]

I don't use systemic lytics unless the patient is "massive".

I ageee the "submissive" category is frustrating.

These days until better data is available I'm using catheter directed lyrics against anything that smells of RV strain/struggle, especially with a reasonable troponin bump. Taking Pa pressures from the 60-70s systolic to the 20-30s in 12 hours seems like a good thing for patients and their possible long term morbidity. Again. No hard data for this but seems reasonable.

The last time I pushed lytics for massive PE killing the patient they died anyway. I have yet to see big brain bleed. My n might be 5?? Tops.

I don’t disagree with you, but I think your argument is funny. I’m going to X intervention that lacks data because we don’t have enough data on Y intervention.

 

[jdh71]

I don’t disagree with you, but I think your argument is funny. I’m going to X intervention that lacks data because we don’t have enough data on Y intervention.

Which is "X" and "Y" the way you think I'm suggesting treatment.

 

[Bostonredsox]

I must have read different guidelines than you as that’s not the hair splitting I recall. I’d bet if one were to run the NNH and the calculate the number needed not to treat to harm (NNNTTTH), that not giving tPa to those who decompensate is a wash and doing nothing is a viable option.

I think that depends on which patient we are specifically talking about. The data for massive is pretty good from what I have read. The NNT is not PCI for STEMI level good, but pretty good. The question is the data on submassive. And then the concept that we are all discussing right now is really a massive patient which by current guideline criteria is really submassive. If you label them as submassive I would agree, the data isn't super strong and it is probably not unreasonable to not offer them tPA. But ifif what we are really describing is a massive PE labeled as submassive because of the frustrating guidelines in terms of what qualifies for massive and what does not, then the indication for tPA is actually much stronger.

As for what TNR brought up, the litigation aspect, the data supports use of TPA in high risk submassive (which we all really believe is massive based on physiology). the problem here is how we are differentiating massive and submassive as the current system sucks IMO. I think alot of pts who probably have PA pressures in the 60s with massive physiology are not being offered tpa because "theyre not hypotensive so they are only submassive". That was my point.

But.....The actual purpose of my post if yall scroll all the way up...was the concept of CDT vs peripheral infusion AND bolus (50mg/2hr or something like that) vs slow infusion (25-50mg over 24 hours) and if there is really a difference and what yall are seeing being done.

 

[Hernandez]

I The data for massive is pretty good from what I have read. .......

As for what TNR brought up, the litigation aspect, the data supports use of TPA in high risk submassive (which we all really believe is massive based on physiology). the problem here is how we are differentiating massive and submassive as the current system sucks IMO. I think alot of pts who probably have PA pressures in the 60s with massive physiology are not being offered tpa because "theyre not hypotensive so they are only submassive". That was my point.

Eh, I don’t think the data for either subset is “great.”

 

[Bostonredsox]

Eh, I don’t think the data for either subset is “great.”

yes, hence the 'pretty good". IE in massive physiology, I look to see if their is any compelling reason NOT to offer lytics. In true submassive physiology thats not high risk, I look to see if their is any compelling reason TO offer lytics.

but still no one has offered any insight on my actual question lol

 

[Dr.CCM]

yes, hence the 'pretty good". IE in massive physiology, I look to see if their is any compelling reason NOT to offer lytics. In true submassive physiology thats not high risk, I look to see if their is any compelling reason TO offer lytics.

but still no one has offered any insight on my actual question lol

Well the EKOS Catheter prob doesn’t matter as the Ultrasonic thing doesn’t seem to add any benefit and as discussed the lung is going to get the tpa no matter the delivery.

Pulmcrit’s idea seems like the safest idea for these things given the risk of significant bleeding for low dose tpa/24 hr is equivalent a heparin drip. No need for a big catheter and saves money by not having the IR bill. That will be my practice after fellowship for these submassive PEs as defined by the AHA/ACCPs c/b syncope, high lactate, looks like crap likely 2/2 the clot etc.

 

[Bostonredsox]

Well the EKOS Catheter prob doesn’t matter as the Ultrasonic thing doesn’t seem to add any benefit and as discussed the lung is going to get the tpa no matter the delivery.

Pulmcrit’s idea seems like the safest idea for these things given the risk of significant bleeding for low dose tpa/24 hr is equivalent a heparin drip. No need for a big catheter and saves money by not having the IR bill. That will be my practice after fellowship for these submassive PEs as defined by the AHA/ACCPs c/b syncope, high lactate, looks like crap likely 2/2 the clot etc.

I think this is plausible and i am leaning towards moving to a 25-50mg over 24hours strategy if only for decrease risk of bleeding.