How many have given TPA for massive PE?

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pinipig523 said:
How many of you guys have given tPA for massive PE?

I just did a few days ago - first one yet.
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Hemodynamically stable = 0

Actively circling the drain = 3 (2 died anyway, the remainder is one of 6 patients who have ever sought me out in the ED just to say thank you)

-d
 
I did one about a month ago. Young previously healthy patient. New onset DM put her in DKA which made her dry and immobile for days = big PEs. PEs were seen on CT and she was starting to circle. Did TPA and it seemed like it helped. She did well.
 
BoneCrusher13 said:
Whats interesting is that the original and only randomized tPA / PE study there were a total of 6 patients. 3 got tPA and survived, 3 didn't and died. There will never be another randomized study because the evidence was so overwhelming.
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I would hardly call n = 6 overwhelming evidence
 
Done it once--guy went from needing bipap in the ED to being up in the ICU eating a turkey sandwhich a few hours later.

Still, we need better RCTs, alough the MOPETT trial is a good start and pretty interesting on half dose tpa
 
you guys using alteplase for this?
 
Never tPA. Sent one guy about a month ago to open thrombectomy in the OR and he arrested on the way up. Survived surgery and walked out a week later.
 
tpa x1 in a coding PE patient, they were coding by the time I got there (floor code). no effect, but it was a ****storm by the time I got there. Of course I get a letter from my hospital committee asking to explain why I used a non-ACLS medication during a code...
 
Rendar5 said:
tpa x1 in a coding PE patient, they were coding by the time I got there (floor code). no effect, but it was a ****storm by the time I got there. Of course I get a letter from my hospital committee asking to explain why I used a non-ACLS medication during a code...
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Did you respond by sending them the ACLS PEA algorithm with "Consider H's and T's" circled?
 
I've used alteplase 2-3 times, 2 lived 1 died (not 100% sure it was a PE but was in arrest and by history that was most likely). In more stable large PEs we usually send them to the OR for thrombectomy.
 
WilcoWorld said:
Did you respond by sending them the ACLS PEA algorithm with "Consider H's and T's" circled?
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lol, didn't feel that snarky, just told them that tpa is an accepted treatment for massive PE, which is what the pt had.
 
Sooo... update on my patient. Massive saddle - gave tpa. A day later, EKG had normalized. No longer was there RBBB and rt strain, no longer was there s1q3t3. Completely normal EKG. It was phenomenal.
 
I've used it often enough I suppose.

It doesn't work if you're super sick.

I'm not sure some of the posters in this thread understand "massive" with regards to PE is defined by clinical manifestations NOT the size of the clot on imaging.

I'm also surprised to see the surgeons taking "stablish" patients to the OR. Different cultures. Now, that's a study that would be nice to see, but would be hard to make it past an IRB, especially since tPA for sub-massives is really pretty equivocal IMHO, surgery vs usual care in sub-massive PE. I'd also like to see some pooled data from the centers that just put these folks right on ECMO. I like ECMO for massive PE.
 
jdh71 said:
I've used it often enough I suppose.

It doesn't work if you're super sick.

I'm not sure some of the posters in this thread understand "massive" with regards to PE is defined by clinical manifestations NOT the size of the clot on imaging.

I'm also surprised to see the surgeons taking "stablish" patients to the OR. Different cultures. Now, that's a study that would be nice to see, but would be hard to make it past an IRB, especially since tPA for sub-massives is really pretty equivocal IMHO, surgery vs usual care in sub-massive PE. I'd also like to see some pooled data from the centers that just put these folks right on ECMO. I like ECMO for massive PE.
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Most of us don't have ECMO available. In regards to thrombolytics vs. thrombectomy, most of the ICU docs I've worked with are leery of tPA in high-clot burden/decent hemodynamics because of experience with pushing tPA and having the thrombus become occlusive as it breaks up. They seem to have similar feelings to they way we feel about giving tPA for CVA (evidence is equivocal to mildly positive with potential for rare but devastating consequences).
 
Arcan57 said:
Most of us don't have ECMO available. In regards to thrombolytics vs. thrombectomy, most of the ICU docs I've worked with are leery of tPA in high-clot burden/decent hemodynamics because of experience with pushing tPA and having the thrombus become occlusive as it breaks up. They seem to have similar feelings to they way we feel about giving tPA for CVA (evidence is equivocal to mildly positive with potential for rare but devastating consequences).
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Don't disagree with anything said here. I don't know if you're responding to the comment about send the patient to surgery? All I was saying was that the surgeons I've worked with regarding this have a similar bias about sub-massive clots . . . if they're stable, they're stable, and they're not going to the OR.
 
jdh71 said:
Don't disagree with anything said here. I don't know if you're responding to the comment about send the patient to surgery? All I was saying was that the surgeons I've worked with regarding this have a similar bias about sub-massive clots . . . if they're stable, they're stable, and they're not going to the OR.
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IR seems more interested in these cases. I agree that I've never gotten a surgeon to get excited about an open thrombectomy (either they're too well or too sick).
 
jdh71 said:
Don't disagree with anything said here. I don't know if you're responding to the comment about send the patient to surgery? All I was saying was that the surgeons I've worked with regarding this have a similar bias about sub-massive clots . . . if they're stable, they're stable, and they're not going to the OR.
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I don't think the question is the immediate mortality of a massive PE but the complications a few years down the line due to pulmonary hypertension. I agree it isn't fully clear in the literature yet whether thrombectomy or thrombolytics will have a significant effect on morbidity in submassive PEs. The current AHA guidelines give it IIb/C in submassive PEs with evidence of RV dysfunction or myocardial ischemia. There is a large RCT study underway headed by Jeff Kline who hopefully will shed some light on it (he suggests that preliminary data shows there is benefit).
 
Twice. Second time last week. 39 year old 13 days post cabg. Came in hypoxic and cyanosis with leg pain past two days. Promptly coded pea. Ed doc called STEMI, came down to help. Story from wife really fit more PE. Ed doc and cardio unsure mi/PE. Offered to do Bedside echo. huge hypo contractile RV. Everyone agreed on PE, Pushed tpa. Worked for an hour never got him back. Autopsy showed saddle embolus.
 
So you guys that are using TPA for massive PEs and having success, are you doing it on pulseless patients or on people when you think they are about to arrest? Bolus and drip or just bolus?

Considered it a couple times, but didn't pull the trigger for various reasons (usually prolonged code before I got there).

At my shop, for the big PEs that are quasi-stable, IR and CV surgery decide on thrombectomy vs catheter directed TPA.
 
I gave it a few days ago to a guy who was hemodynamically stable but hypoxic to 80s on room air and tachypneic to 60s. We had a discussion with him and the family about risks and benefits and they all wanted it. A few hours later he was off O2 and comfortable.

Unfortunately most of our medical intensivists don't feel it's indicated for PE unless CPR is in progress, but I think that's why we have to make the decision in the ED.
 
suckstobeme said:
So you guys that are using TPA for massive PEs and having success, are you doing it on pulseless patients or on people when you think they are about to arrest? Bolus and drip or just bolus?

Considered it a couple times, but didn't pull the trigger for various reasons (usually prolonged code before I got there).

At my shop, for the big PEs that are quasi-stable, IR and CV surgery decide on thrombectomy vs catheter directed TPA.
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I give it to people who fit the definition of massive PE (SBP < 90 for > 15 minutes) unless I can get surgery to take them. I usually don't give it to coding patients unless they have short down time and the story is completely clear that it is PE (did it once as a resident was discharged the day before with a large DVT, came in talking with pleuritic CP, hypotension, hypoxia and then dropped - they didn't make it). I think tpa for massive PEs is more or less the standard of care now unless there is an alternative. I wouldn't be surprised if in the future we see a wave of lawsuits from people with severe pulmonary htn who say "if only the doctor gave me tPa I'd be able to walk more than 10feet without sob"
 
pseudoknot said:
I gave it a few days ago to a guy who was hemodynamically stable but hypoxic to 80s on room air and tachypneic to 60s. We had a discussion with him and the family about risks and benefits and they all wanted it. A few hours later he was off O2 and comfortable.

Unfortunately most of our medical intensivists don't feel it's indicated for PE unless CPR is in progress, but I think that's why we have to make the decision in the ED.
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I have yet to be convinced of the benefit in submissive PE, but I agree with the use you're describing. An O2 sat in the 80's with a respiratory rate in the 60's? That's clearly on it's way to hypotension if nothing is done.
 
We had a pt with very similar presentation. Clearly PE, multiple wells criteria for DVT who had s1q3t3, rbbb and rv strain. Breathing in the 50s and sating 80s, got heparin then CT then it for focused TPA delivery with the ultrasonic catch. In 1 day was back at baseline. I believe these are the ppl jeff Klein encourages early Tpa vs ones who are coding.

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WilcoWorld said:
I have yet to be convinced of the benefit in submissive PE, but I agree with the use you're describing. An O2 sat in the 80's with a respiratory rate in the 60's? That's clearly on it's way to hypotension if nothing is done.
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shoal said:
We had a pt with very similar presentation. Clearly PE, multiple wells criteria for DVT who had s1q3t3, rbbb and rv strain. Breathing in the 50s and sating 80s, got heparin then CT then ir for focused TPA delivery with the ultrasonic catch. In 1 day was back at baseline. I believe these are the ppl jeff Klein encourages early Tpa vs ones who are coding.

Sent from my Nexus 7 using Tapatalk
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Sent from my Nexus 7 using Tapatalk
 
Shoal - the definitions of massive PE that I have read include patients with refractory hypoxia. If you look at MOPPET's inclusion criteria, I believe you'll agree that their definition of "moderate" PE includes patients who are significantly more stable than the one you describe. I suspect the patient you describe might not even be eligable for inclusion in MOPPET - they'd be considered too sick.
 
Yes the AHA definition of massive PE includes significant hypoxia or even respiratory distress. I think tPA is underused for PE (and overused for stroke).

By the way there is no benefit to catheter directed tPA for this, which makes sense because the lungs get 100% of the systemic circulation anyway.
 
I've done it once. Had 30 y.o. F h/o PE, no longer on coumadin. Came in respiratory distress. Hypoxic on bipap. EKG showed strain. I shot a quick CXR which was neg for edema, PTX, CHF. I called pulm on-call who cautioned me about giving TPA to a patient w/o a confirmed diagnosis of PE. Said I'd have no defense whatsoever if she had a bad outcome from the TPA. After the patient turned purple on me and stopped breathing midsentence, I tubed her, grabbed the TPA and started pushing it....she didn't make it.
 
only caution I'd think against empiric use is that PE and effusion/tamponade can present pretty similarly (a nice reason to bedside echo someone if you do it routinely at your place). TPA will save one of those and kill the other.
 
We crashed a 21 y/o kid onto ecmo who coded in IR suite during thrombectomy. He got ROSC, but you could not ventilate or oxygenate him after we pushed 50mg of IV tpA through his PAC his first gas was pH 6.7, PCO2 90, PaO2 50 on 30/500/100%/5 and subsequent ones similar. MAPs lowish and so we cannulated in IR. He was extubated and neurologically intact yesterday.
 
Rendar5 said:
only caution I'd think against empiric use is that PE and effusion/tamponade can present pretty similarly (a nice reason to bedside echo someone if you do it routinely at your place). TPA will save one of those and kill the other.
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This is going to seem nit-picky because it is.

Your most likely result from pushing tPA empirically (which I assume would be in a code situation) is going to be the same as pushing it for CVA: nothing. Most tamponade/effusions are not going to be hemorrhagic and most people in PEA from PE are not going to come back because you pushed the tPA.
 
Arcan57 said:
This is going to seem nit-picky because it is.

Your most likely result from pushing tPA empirically (which I assume would be in a code situation) is going to be the same as pushing it for CVA: nothing. Most tamponade/effusions are not going to be hemorrhagic and most people in PEA from PE are not going to come back because you pushed the tPA.
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This may be even more nit picky but since you opened that door...

You can give bolused tPA, specifically tenecteplase which has a 15-fold higher fibrin specificity and reduced binding affinity to plasminogen activator inhibitor PAI-1 and 6-fold prolonged plasma half-life (22 vs 3.5 minutes) when comparing alteplase and tenecteplase. Consequently, tenecteplase can be administered as a single intravenous bolus of 30-50mg over 5-10 seconds, in contrast to the 90-minute accelerated infusion regimen of alteplase.

You are correct that in general pushing tPA is not likely to result in ROSC in most patients, but it might and you should give it as a bolus if they are coding. As for comparing strokes to PE's its like apples and oranges. The revasculariation rates after tPA in stroke are supposedly better at 24 hours, yet all the benefit is seen at 90 days which neurologists have come up with a variety of reasons why immediate benefit is not demonstrated. SO bolusing tPA in CVA has no benefit because there is no benefit of improved immediate revascularization, while in PE your goal is open the main pulmonary arteries and allow distal clot migration since there is so many downstream vessels in the lungs that if you can open the main PA, patients tend to do better.

If you do get them back be ready for some wicked dead space and potential ECMO candidates as the patients intrinsic fibrinolysis system continues to break up clot.
 
Arcan57 said:
This is going to seem nit-picky because it is.

Your most likely result from pushing tPA empirically (which I assume would be in a code situation) is going to be the same as pushing it for CVA: nothing. Most tamponade/effusions are not going to be hemorrhagic and most people in PEA from PE are not going to come back because you pushed the tPA.
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Don't disagree with it at all. But it has happened to an extremely smart doc I new in residency. bad luck I suppose because it's the only case I've ever heard of it.
 
We just had a massive PE walk through the door the other day ended up getting ECMO then vascular intervention. Doing well I hear.
 
i am an ED pharmacist - I have done it probably 12 times - 3 survived (ROSC approx 10-15 min after bolus of 50mg). 1 with significant neruological damage, 1 nearly full recovery, 1 recovered only to find extensively metastasized liver ca that was newly diagnosed because of PE. Likely less than 6 months to live.
 
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