tpa high-fives

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Hamhock

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To prevent derailing of the "Hat Trick" thread, I am bringing this up here.

It was mentioned in that thread that a patient was giving 'high-fives' after receiving tpa...with the implication that it was the tpa that resulted in resolution of some unmentioned neuro deficit.

I often hear nurses and doctors giving verbal 'high-fives' when a rapid recovery is made in stroke patients who receive tpa.

Do even the most pro-tpa zealots argue that tpa works in 24h? If so, what data or arguments are used?
Should I ask in the Neurology forum?


HH

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If:
1) tPA successfully lyses a clot
2) collateral circulation preserved brain function

Then, sure, you could see rapid improvement. I've no doubt this occasionally happens.

Stroke mimics also rapidly improve.
 
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I'm sure that there are situations where exactly that has happened ie: tPA dissolves the clot and they get rapid improvement. Sort of like you can get ST segments to go back down to baseline on occasion.
But no, the data from all the trials I've bothered to look at indicates improvement of MRS at months, not hours or days.
 
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I am under the impression that in the literature, tPA has no patient oriented outcome improvement outside of something like 30 days. Therefore, if you see any improvement within some arbitrary time, like 6 hours, then this is due to a mimic (most likely TIA) and not the tPA itself. I could definitely be wrong though...
 
Therefore, if you see any improvement within some arbitrary time, like 6 hours, then this is due to a mimic (most likely TIA) and not the tPA itself.

Nah. If you look at the evidence in support of endovascular therapy, patients with revascularization and small ischemic cores will start to display symptom improvement immediately following the procedure.

There are basically two big myths perpetuated about tPA. The first is that it's a "clot-buster", when in reality, response ranges from OK to minimal, depending on many factors. The second is that "time is brain", when for some patients they can have recovery in hugely extended time windows, while other patients have nothing but dead tissue within minutes.
 
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Strokes get better on their own a lot. It's called a TIA. The problem is that if a TIA is a stroke that gets better in 24 hours, you don't know if it is a TIA or a stroke for 24 hours.
 
Yep – the body also makes something called tissue plasminogen activator ... you know, the non-recombinant kind.

Sorry but the government doesn't let me bill for that
 
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I am under the impression that in the literature, tPA has no patient oriented outcome improvement outside of something like 30 days. Therefore, if you see any improvement within some arbitrary time, like 6 hours, then this is due to a mimic (most likely TIA) and not the tPA itself. I could definitely be wrong though...

Is that because the researchers didn't look for short term improvements (due to inability to determine tia vs CVA short-term, or short term gains not being important compared to 30 days out), or because they didn't find any??

Also, ED trials are done in tertiary hospitals where neuro or cards (hopefully) quickly takes the patient. Two weeks ago I TNKased a post arrest guy and watched the ST elevation resolve to near baseline in the 2.5 hours I was waiting for transport.

In the urban ED I part-time in the STEMI's usually aren't in the ED for more than 10-15 minutes.
 
To prevent derailing of the "Hat Trick" thread, I am bringing this up here.

It was mentioned in that thread that a patient was giving 'high-fives' after receiving tpa...with the implication that it was the tpa that resulted in resolution of some unmentioned neuro deficit.

I often hear nurses and doctors giving verbal 'high-fives' when a rapid recovery is made in stroke patients who receive tpa.

Do even the most pro-tpa zealots argue that tpa works in 24h? If so, what data or arguments are used?
Should I ask in the Neurology forum?


HH

No literature has ever demonstrated any early efficacy for lytics in stroke. The argument of lytics resolving a STEMI is a poor one, I think. The reason being is that you rarely ever see a STEMI resolve on its own (outside of vasospasm), whereas you frequently see CVA sx improve as the were either a TIA or a mimic. Intuitively, it makes sense that a lytic agent could resolve a clot which could allow for reperfusion and subsequent resolution of symptoms, the problem with that is that there are tons of things in medicine that "make sense" but end up being entirely wrong when actually studied clinically.

Whether you're a TPA proponent or not, one has to agree that the studies are designed to favor TPA at least somewhat. I think if there was a benefit, they would have found it by now.
 
If:
1) tPA successfully lyses a clot
2) collateral circulation preserved brain function

Then, sure, you could see rapid improvement. I've no doubt this occasionally happens.

Stroke mimics also rapidly improve.

Yes, I also bet this happens rarely.

However, if this does, there must be, with equal frequency, a deterioration (that is not due to hemorrhage) that must also occur. Such a "balancing" event would be necessary to have the groups be identical at 24h starting with NINDS "1".

HH
 
A lot of "TIA's" turn out to be actual strokes when MRI'd.

I work in a comprehensive stroke center that gives alteplase a LOT and does a TON of interventions. Our health system sees over 750,000 patients/year among all our hospitals, so we get a lot of referrals for endovascular care. All of them come through the ER and we see them to facilitate going to the vascular intervention suite. I'm not joking when I say I average giving alteplase to a stroke patient at least once per week (seriously, gotta love living in the "stroke belt").

My experience with strokes is this: alteplase works sometimes, but not all the time. Evidence is clear that clot retrieval should be done in patients receiving alteplase without improvement or with documented large clot (CT angiogram). The risk of intracranial hemorrhage in patients receiving alteplase is nowhere near what was reported in prior research (NINDS). My facility averages <0.5% intracranial hemorrhage rate in alteplase patients. We do have the benefit of a neurologist that responds to our code FAST's. We work as a team -- with the pharmacist accompanying us with the alteplase. We start alteplase while on the CT table (before labs come back -- i-STAT BMP only).

You'll never know if it was the alteplase or time that caused resolution of symptoms. One thing you can count on is that alteplase is now the standard of care, and if you don't give it in a patient with a stroke, you're risking litigation. There are expert witnesses willing to support a plaintiff on this, and you will have a hard time defending yourself. Patients expect it and the AHA now pushes it as a standard of care.
 
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You'll never know if it was the alteplase or time that caused resolution of symptoms. One thing you can count on is that alteplase is now the standard of care, and if you don't give it in a patient with a stroke, you're risking litigation. There are expert witnesses willing to support a plaintiff on this, and you will have a hard time defending yourself. Patients expect it and the AHA now pushes it as a standard of care.
There are also expert witnesses that will support a plaintiff harmed by tPA. This is becoming quite similar to steroids for spinal cord injury. Basically, you're going to get sued for a bad outcome, regardless of whether you did or did not give the drug.
 
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A lot of "TIA's" turn out to be actual strokes when MRI'd.

I work in a comprehensive stroke center that gives alteplase a LOT and does a TON of interventions. Our health system sees over 750,000 patients/year among all our hospitals, so we get a lot of referrals for endovascular care. All of them come through the ER and we see them to facilitate going to the vascular intervention suite. I'm not joking when I say I average giving alteplase to a stroke patient at least once per week (seriously, gotta love living in the "stroke belt").

My experience with strokes is this: alteplase works sometimes, but not all the time. Evidence is clear that clot retrieval should be done in patients receiving alteplase without improvement or with documented large clot (CT angiogram). The risk of intracranial hemorrhage in patients receiving alteplase is nowhere near what was reported in prior research (NINDS). My facility averages <0.5% intracranial hemorrhage rate in alteplase patients. We do have the benefit of a neurologist that responds to our code FAST's. We work as a team -- with the pharmacist accompanying us with the alteplase. We start alteplase while on the CT table (before labs come back -- i-STAT BMP only).

You'll never know if it was the alteplase or time that caused resolution of symptoms. One thing you can count on is that alteplase is now the standard of care, and if you don't give it in a patient with a stroke, you're risking litigation. There are expert witnesses willing to support a plaintiff on this, and you will have a hard time defending yourself. Patients expect it and the AHA now pushes it as a standard of care.

I have a really hard time believing 0.5%. The rate of ICH for lytics in MI or PE hovers right around 1%. I can't imagine a brain damaged patient would have a lower rate of ICH than a healthy brain. At any given time, out neuro ICU has a few people who bled after tpa. Are y'all publishing that data? Everything I've read has been much higher than that.
 
The argument of lytics resolving a STEMI is a poor one, I think. The reason being is that you rarely ever see a STEMI resolve on its own (outside of vasospasm), whereas you frequently see CVA sx improve as the were either a TIA or a mimic.

Whaaa??? What am I missing here? Big tombstone ST elevations in very sick looking person. Push TNKase and watch monitor. Watch for AIVR, then repeat 12 lead and ST elevations are improving. Repeat the 12 lead every 10 minutes or so and you can SEE the ST elevations improve. Meanwhile you can SEE the patient get better before your very eyes. I've done this numerous times...last time was 2 weeks ago with an in-the-field arrest. I read the d/c summary today...they d/c him to home 3 days ago.

I get the argument that CVA improvements may be TIA or mimic, but STEMI? You can literally watch the EKG, and the patient, improve after TNKase.
 
Whaaa??? What am I missing here? Big tombstone ST elevations in very sick looking person. Push TNKase and watch monitor. Watch for AIVR, then repeat 12 lead and ST elevations are improving. Repeat the 12 lead every 10 minutes or so and you can SEE the ST elevations improve. Meanwhile you can SEE the patient get better before your very eyes. I've done this numerous times...last time was 2 weeks ago with an in-the-field arrest. I read the d/c summary today...they d/c him to home 3 days ago.

I get the argument that CVA improvements may be TIA or mimic, but STEMI? You can literally watch the EKG, and the patient, improve after TNKase.

Re-read my post. Maybe I wasnt eloquent, but you misunderstood me. I said stemis don't get better on their own. I meant the argument that since STEMIs resolve with lytics means that CVAs can resolve with lytics is a flawed one. I mean that a STEMI doesn't just go away without treatment. Neuro symptoms often time do.

Hope that was better stated.
 
@southerndoc -- or any of the others who "see tpa" working in front of them in some cases:

Please help me understand your line of thinking. Given that it has repeatedly been shown -- and I think agreed upon!?! -- that tpa has no "sum" benefit at 24 hours, what are the negative outcomes that you "see tpa" doing in some cases?

There must be an equal frequency of negative outcomes to "balance" the positive outcomes (tpa working in front of you) that you "see"...otherwise, I see no way to explain that the ("sum") outcomes at 24h have been repeatedly shown to be EQUIVALENT for groups receiving IV systemic tpa vs. placebo.

HH
 
Whaaa??? What am I missing here? Big tombstone ST elevations in very sick looking person. Push TNKase and watch monitor. Watch for AIVR, then repeat 12 lead and ST elevations are improving. Repeat the 12 lead every 10 minutes or so and you can SEE the ST elevations improve. Meanwhile you can SEE the patient get better before your very eyes. I've done this numerous times...last time was 2 weeks ago with an in-the-field arrest. I read the d/c summary today...they d/c him to home 3 days ago.

I get the argument that CVA improvements may be TIA or mimic, but STEMI? You can literally watch the EKG, and the patient, improve after TNKase.

How do you know you're not trying to thrombolyze prinzmetal angina and risking intracranial hemorrhage and major gi bleed? Maybe those patients would have gotten better whether or not you pushed tpa.
 
How do you know you're not trying to thrombolyze prinzmetal angina and risking intracranial hemorrhage and major gi bleed? Maybe those patients would have gotten better whether or not you pushed tpa.
Try to divine the difference with H&P, and if you can't then you rely on the NNT for TNKase for STEMI vs the NNH for TNKase in Prinzmetal. Same thing we do for everything else.
 
Try to divine the difference with H&P, and if you can't then you rely on the NNT for TNKase for STEMI vs the NNH for TNKase in Prinzmetal. Same thing we do for everything else.

And what exactly on the H&P would tip you off?
 
How do you know you're not trying to thrombolyze prinzmetal angina and risking intracranial hemorrhage and major gi bleed? Maybe those patients would have gotten better whether or not you pushed tpa.

I understand that you're probably just trying to play devils advocate, but the science is entirely against you on this one.

The harm from lytics in a non-CNS indication for lytics are consistent and just below 1%. The published rate of symptomatic ICH in ischemic CVA is on average 6ish%. This is without taking into account the pretest probability of the disease you're treating.

The rate of something other than an ischemic stroke causing neuro symptoms is certainly higher than the rate of a something other than a STEMI in the right clinical setting causing ST elevation. I say this without data (although I'm sure it exists), but knowing the few times I've been fooled with a STEMI and the dozen and dozens of times I've seen focal neuro deficits caused by etiologies other than ischemic CVA.
 
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Also, tPA for STEMI is like meat tenderizer on a steak. tPA for stroke is like meat tenderizer on pate. One of these things is not like the other.
 
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I have a really hard time believing 0.5%. The rate of ICH for lytics in MI or PE hovers right around 1%. I can't imagine a brain damaged patient would have a lower rate of ICH than a healthy brain. At any given time, out neuro ICU has a few people who bled after tpa. Are y'all publishing that data? Everything I've read has been much higher than that.

I think the neurologists did report it IIRC.
 
I'm not sayin this is true at southerdoc place. But when you start tpa'ing a lot of stroke mimics your denominator increases and then leads to less "percentage" of bleeds
 
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And what exactly on the H&P would tip you off?
History of dx'd prinzmetals? Hx of this kind of recurrent, but resolving symptoms. Recent heart cath that was clear.
 
I've got a few on call neurologists at my shop who can smell bs from a mile away and have the cajones to say no tpa. Much respect to them.


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Like Southern Doc, I work at a comprehensive stroke center, we frequently administer TPA and send patients for endovascular therapy, and we have a symptomatic ICH rate less than 2%. The older studies showed that the efficacy of TPA and risk of TPA goes up dramatically starting at about 1.5 hours, it's indicated for most patients up until 3 hours, and a very select few outside that window up to 4.5 hours. In many of the older trials, systemic TPA was administered to patients 6 hours out from onset. With the correct patient selection, there is no doubt that TPA is efficacious and I think many comprehensive stroke centers have bleed rates much less than in the old trials. Our door to drug time averages about 50 minutes, which is also helpful. Mimics and TIAs (if you could predict the future and know it would resolve) also almost never bleed since there's no dead brain, although we try to avoid lysing mimics :)
 
Like Southern Doc, I work at a comprehensive stroke center, we frequently administer TPA and send patients for endovascular therapy, and we have a symptomatic ICH rate less than 2%. The older studies showed that the efficacy of TPA and risk of TPA goes up dramatically starting at about 1.5 hours, it's indicated for most patients up until 3 hours, and a very select few outside that window up to 4.5 hours. In many of the older trials, systemic TPA was administered to patients 6 hours out from onset. With the correct patient selection, there is no doubt that TPA is efficacious and I think many comprehensive stroke centers have bleed rates much less than in the old trials. Our door to drug time averages about 50 minutes, which is also helpful. Mimics and TIAs (if you could predict the future and know it would resolve) also almost never bleed since there's no dead brain, although we try to avoid lysing mimics :)

2 points:

Plenty of people have doubt that tpa works. The results are conflicting, but negative studies are ignored. It hasn't been repeated. The pre3 hour vs post 3h lacks face validity. There were many conflicts of interest in the initial positive study. I'm not saying I think tpa is a placebo, but there are plenty of MDs smarter than I who would vehemently oppose the statement "there is no doubt that tpa is efficacious."

The argument that mimics don't bleed is a crazy one. Why you are saying is that if you give a drug that is not indicated, you have about a 1% chance of having a life-ending/altering hemorrhage.....without an indication....tell that to the mimic I saw in the ICU recently that was aphasic and hemiparetic. When you're talking about a devastating complication, close isn't close enough. If vascular said they only perforate the aorta on 1% of patients that didn't need a surgery people would go insane.
 
I have a really hard time believing 0.5%. The rate of ICH for lytics in MI or PE hovers right around 1%. I can't imagine a brain damaged patient would have a lower rate of ICH than a healthy brain. At any given time, out neuro ICU has a few people who bled after tpa. Are y'all publishing that data? Everything I've read has been much higher than that.

2 points:

Plenty of people have doubt that tpa works. The results are conflicting, but negative studies are ignored. It hasn't been repeated. The pre3 hour vs post 3h lacks face validity. There were many conflicts of interest in the initial positive study. I'm not saying I think tpa is a placebo, but there are plenty of MDs smarter than I who would vehemently oppose the statement "there is no doubt that tpa is efficacious."

The argument that mimics don't bleed is a crazy one. Why you are saying is that if you give a drug that is not indicated, you have about a 1% chance of having a life-ending/altering hemorrhage.....without an indication....tell that to the mimic I saw in the ICU recently that was aphasic and hemiparetic. When you're talking about a devastating complication, close isn't close enough. If vascular said they only perforate the aorta on 1% of patients that didn't need a surgery people would go insane.

I also work at a large stroke center. I reviewed our retrospective analysis of all lytics for vascular and neuro last year, ICH was <0.5% for us as well. I haven't really done stroke neurology since I was an intern many years ago, but I probably pushed tPA on maybe 6-7 people in the span of a month. On the other hand, I have done lower extremity lysis dozens of times (and am sitting in the doctor's lounge right now waiting for the ER to send up my patient so that I can do another). tPA removes clot. I have done the before and after angios. I have also operated on patients who have gotten tPA and don't form clot. I certainly would not weigh in on whether our current stroke tPA guidelines are adequate or they need revising based on my anecdotal experience. But, as with everything, there will always be people that disagree with the guidelines or want them revised. I know that based on my experience, I would rather personally get tPA than not if I am having an ischemic stroke.
 
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I also work at a large stroke center. I reviewed our retrospective analysis of all lytics for vascular and neuro last year, ICH was <0.5% for us as well. I haven't really done stroke neurology since I was an intern many years ago, but I probably pushed tPA on maybe 6-7 people in the span of a month. On the other hand, I have done lower extremity lysis dozens of times (and am sitting in the doctor's lounge right now waiting for the ER to send up my patient so that I can do another). tPA removes clot. I have done the before and after angios. I have also operated on patients who have gotten tPA and don't form clot. I certainly would not weigh in on whether our current stroke tPA guidelines are adequate or they need revising based on my anecdotal experience. But, as with everything, there will always be people that disagree with the guidelines or want them revised. I know that based on my experience, I would rather personally get tPA than not if I am having an ischemic stroke.
Your ICH rate was less than 0.5% for what?
 
I also work at a large stroke center. I reviewed our retrospective analysis of all lytics for vascular and neuro last year, ICH was <0.5% for us as well. I haven't really done stroke neurology since I was an intern many years ago, but I probably pushed tPA on maybe 6-7 people in the span of a month. On the other hand, I have done lower extremity lysis dozens of times (and am sitting in the doctor's lounge right now waiting for the ER to send up my patient so that I can do another). tPA removes clot. I have done the before and after angios. I have also operated on patients who have gotten tPA and don't form clot. I certainly would not weigh in on whether our current stroke tPA guidelines are adequate or they need revising based on my anecdotal experience. But, as with everything, there will always be people that disagree with the guidelines or want them revised. I know that based on my experience, I would rather personally get tPA than not if I am having an ischemic stroke.

I'm not saying tPA doesn't work. I just think the data we have isn't nearly as robust as people like to believe and there seem to have been a lot of conflicts of interest initially.

I'm very surprised to hear about another area with rate of <0.5%. Rate for STEMI is commonly quoted at 0.9% (admittedly a different lytic agent) - it's just hard to believe that a CNS pathology with presumably ischemic brain matter would have a lower rate of bleeding than healthy brain tissue. If you have a decent sample size, you really should publish that data.
 
Systemic tPA for PE, systemic tPA for stroke, catheter directed tPA for leg ischemia

How does that break down (if you can say)? I would guess leg ischemia approaches 0, PE is in the 0.5-1 range and CVA is in the low single digits.
 
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I also work at a large stroke center. I reviewed our retrospective analysis of all lytics for vascular and neuro last year, ICH was <0.5% for us as well. I haven't really done stroke neurology since I was an intern many years ago, but I probably pushed tPA on maybe 6-7 people in the span of a month. On the other hand, I have done lower extremity lysis dozens of times (and am sitting in the doctor's lounge right now waiting for the ER to send up my patient so that I can do another). tPA removes clot. I have done the before and after angios. I have also operated on patients who have gotten tPA and don't form clot. I certainly would not weigh in on whether our current stroke tPA guidelines are adequate or they need revising based on my anecdotal experience. But, as with everything, there will always be people that disagree with the guidelines or want them revised. I know that based on my experience, I would rather personally get tPA than not if I am having an ischemic stroke.

I know nothing about your specific hospital, but it seems the ICH rate my hospital (also a large stroke center) is a lot lower than expected because a lot of pts get tpa that probably are just stroke mimics. And the stroke neurologist rational is that "if it is a stroke mimic...then it's unlikely to cause ICH."

And that's fine, but that does not negate the fact, that if you have a real stroke, especially one with a medium to higher NIH, you have a very real chance of bleeding a dying.

And then there is this... http://www.thennt.com/nnt/thrombolytics-for-stroke/

I would definitely withhold it for myself and family.
 
I'm not saying tPA doesn't work. I just think the data we have isn't nearly as robust as people like to believe and there seem to have been a lot of conflicts of interest initially.

I'm very surprised to hear about another area with rate of <0.5%. Rate for STEMI is commonly quoted at 0.9% (admittedly a different lytic agent) - it's just hard to believe that a CNS patho
logy with presumably ischemic brain matter would have a lower rate of bleeding than healthy brain tissue. If you have a decent sample size, you really should publish that data.

This is completely speculative, but...
Time to tPA becomes a health care metric at your institution-->Shorter decision times on stroke symptoms-->increased lytic therapy for stroke mimics --> larger denominator-->lower bleed rates for t-PA.

It's counterintuitive to conclude that thinking less about t-PA would decrease the bleeding rate, but that's exactly how it could happen.

Again, I'm totally speculating. I could be wrong and it could be that mimelim's site is just doing an excellent job with lytic use. My center describes surprisingly impressive low bleed rates as well. I really don't know.
 
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This is completely speculative, but...
Time to tPA becomes a health care metric at your institution-->Shorter decision times on stroke symptoms-->increased lytic therapy for stroke mimics --> larger denominator-->lower bleed rates for t-PA.

It's counterintuitive to conclude that thinking less about t-PA would decrease the bleeding rate, but that's exactly how it could happen.

Again, I'm totally speculating. It could be that

But how do you get to a bleed rate lower than that of STEMI? That's were you lose me.
 
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As above, giving TPA to people with no acute infarction will lower the bleed rate.

I would not be surprised if TPA works in some patients, but the sum of the data does not support it's use.
No way to ever get good studies now as it is considered standard of care.
 
I'm not saying tPA doesn't work. I just think the data we have isn't nearly as robust as people like to believe and there seem to have been a lot of conflicts of interest initially.

I'm very surprised to hear about another area with rate of <0.5%. Rate for STEMI is commonly quoted at 0.9% (admittedly a different lytic agent) - it's just hard to believe that a CNS pathology with presumably ischemic brain matter would have a lower rate of bleeding than healthy brain tissue. If you have a decent sample size, you really should publish that data.
I think there have been retrospective series published on it, but it's still the same mimics and retrospective data problem. I've heard our neurologists quote 1/200 ICH rate to patients before giving tPA for a resolved stroke (or TIA).
 
How does that break down (if you can say)? I would guess leg ischemia approaches 0, PE is in the 0.5-1 range and CVA is in the low single digits.
I haven't seen that many people get catheter directed lytics for lower extremity clot, but I have taken care of two big ICHs in the ICU after they got the catheter directed lytics.
 
I think there have been retrospective series published on it, but it's still the same mimics and retrospective data problem. I've heard our neurologists quote 1/200 ICH rate to patients before giving tPA for a resolved stroke (or TIA).

So what you're saying is that you've heard a neurologist give a drug that's not indicated.
 
All... The... Time. Had a stroke alert (called by EMS) that came in at the same time as a major trauma. When I get back from the trauma resuscitation I find the neurologist has already given TPA to this patient who had an NIHSS of 0. His "deficit" was a subjective feeling of clumsiness in his dominant hand. Neurologist cited this as an "example of how the NIHSS really fails us for some patients."

Stuff like this needs to be submitted to the board of medicine. You're literally risking a patient's life for no benefit in a clearly off-label manner. This is a slam dunk for a malpractice attorney.
 
So what you're saying is that you've heard a neurologist give a drug that's not indicated.
Heard it? I've seen it.

But her symptoms resolved completely...
"Could be another stroke about to happen."
But that's crazy talk...
"Lytics are already in, gotta go."

I'm paraphrasing of course.
 
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Heard it? I've seen it.

But her symptoms resolved completely...
"Could be another stroke about to happen."
But that's crazy talk...
"Lytics are already in, gotta go."

I'm paraphrasing of course.

Wow.

You give tPA to my dad with a NIHSS of zero, and I'm going to do SOMETHING.

Sue? If there's harm done, for sure.
Report? No question.
Raise hell such that the neurologist has credentialing problems? Guaran-damn-teed.
 
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I know nothing about your specific hospital, but it seems the ICH rate my hospital (also a large stroke center) is a lot lower than expected because a lot of pts get tpa that probably are just stroke mimics. And the stroke neurologist rational is that "if it is a stroke mimic...then it's unlikely to cause ICH."

And that's fine, but that does not negate the fact, that if you have a real stroke, especially one with a medium to higher NIH, you have a very real chance of bleeding a dying.

And then there is this... http://www.thennt.com/nnt/thrombolytics-for-stroke/

I would definitely withhold it for myself and family.

tPA can and does work in the right situations. The original tPA trials did not use vascular imaging, so data on clot length, location, and residual flow (all variable that influence recanalization) was not know. Despite this lack of vascular information, there was a time-dependent effect of tPA. Emberson et a. (2014) did a great meta-analysis stratified by onset to needle with individual patient data that shows this (see attached figure). A lot of the earlier tPA trials were negative because they were lysing after 6 hrs. Reperfusing dead brain is not beneficial, and perhaps even harmful leading to more edema. thennt.com article does not address this, which is why they conclude there is no benefit to tPA.

Lancet. 2014 Nov 29;384(9958):1929-35. doi: 10.1016/S0140-6736(14)60584-5. Epub 2014 Aug 5.
Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials.
 

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tPA can and does work in the right situations.

A simple search of this forum will find threads with far more sophisticated discussion of this topic and the totality of evidence. A meta-analysis, specifically, is also very good at obfuscating the trial-specific flaws and biases; garbage-in, garbage-out.
 
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