I HATE tPA for Stroke!

[docB]

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I f***ing HATE HATE HATE HATE HATE HATE it!

There's gotta be something better or we've gotta quit doing this.

 

[xaelia]

Then you're gonna have to come up with $10 million to build the AHA a new headquarters so you can write their guidelines for them.

Or publish a study like ECASS III, where 10 of the 14 authors receive consulting and lecture fees from the manufacturer and three of the authors are employees of the manufacturer, so you get whatever the hell results you want.

 

[Dwindlin]

I f***ing HATE HATE HATE HATE HATE HATE it!

There's gotta be something better or we've gotta quit doing this.

You'll have to forgive my med student ignorance but why? Based on my neuroscience lectures tPA is the best thing since holy water.

 

[la gringa]

i've given it exactly once, almost pissed my pants, then got a call from the accepting stroke center that the pt seized on arrival and had to be intubated. had hx stroke for which she had gotten tpa and no contraindications. probably not directly related, but it's my N of 1 experience, arghhhhh

 

[xaelia]

You'll have to forgive my med student ignorance but why? Based on my neuroscience lectures tPA is the best thing since holy water.

The cake is a lie.

 

[Dwindlin]

The cake is a lie.

I figured as much.

 

[Hamhock]

You'll have to forgive my med student ignorance but why? Based on my neuroscience lectures tPA is the best thing since holy water.

Just wait for your 'research methodology and ethics' lectures, review the primary lit, and then re-consider.

HH

I actually believe there is a role for this ****, but it likely will be site-directeed and lesion-specific...until then, well....

HH

 

[Tiger26]

tPa sucks and the studies are horribly flawed

 

[deleted6669]

mel herbert feels the same way:
http://www.emrap.tv/index.php?option=com_content&view=article&id=2232:EMRAPTV81-EM-Blog-Aug09

 

[WilcoWorld]

And now the AHA is recommending tPA for "submassive" PE citing a "trend" towards decreased mortality - a trend that is not statistically significant and that is pulled from a metaanalysis of seriously flawed studies.

Yes, I worry that Alteplase manufacturers may have a bit too much influence on the AHA.

 

[Dwindlin]

Just wait for your 'research methodology and ethics' lectures, review the primary lit, and then re-consider.

HH

I actually believe there is a role for this ****, but it likely will be site-directeed and lesion-specific...until then, well....

HH

I've had all that (I'm post Step I), this is just the first I've heard that I should question my neuroscience lecturer. 😎

 

[deleted77919]

…

 

[Arcan57]

And now the AHA is recommending tPA for "submassive" PE citing a "trend" towards decreased mortality - a trend that is not statistically significant and that is pulled from a metaanalysis of seriously flawed studies.

Yes, I worry that Alteplase manufacturers may have a bit too much influence on the AHA.

Talking to my intensivists, their anectdotal experience is that patients tend to crump when given IV thrombolysis because of the main clot breaking up and causing more complete obstruction slightly distally. But we also have pretty aggressive IR docs who will do mechanical thrombectomy.

 

[WilcoWorld]

Talking to my intensivists, their anectdotal experience is that patients tend to crump when given IV thrombolysis because of the main clot breaking up and causing more complete obstruction slightly distally. But we also have pretty aggressive IR docs who will do mechanical thrombectomy.

So it sounds to me like your intensivists also disagree with the AHA recommendation to lyse submassive PE?

 

[Arcan57]

So it sounds to me like your intensivists also disagree with the AHA recommendation to lyse submassive PE?

Yes. It is an actual recommendation or just a consideration at this point? Also, in keeping with clotting problems, did anyone see the recommendation that was in Annals regarding targeted thrombolysis for prevention of post-DVT syndrome. Is anyone's IR/vascular docs actually doing that?

 

[AmoryBlaine]

I agree, not a huge tPA fan. A few points that many of you probably already know.

-there was a negative study published at the same time as NINDS, why was this just ignored?

-I sometimes think of tPA in terms of people I care about. My dad is a very healthy vital guy in his 60s. If he was hemiplegic from a stroke would I give him tPA? I think so, some people definitely do get better.

-lots of people who have strokes recover functionality with no intervention.

-ER docs can DEFINITELY be sued for not giving tPA.


Argh. So many questions, no great answers.

 

[xaelia]

I'm not familiar enough with the literature for submassive PE to pick apart individual studies, but the evidence really isn't all that conclusive one way or the other - some individuals from both groups will do poorly, and they just haven't identified which patients will benefit from each strategy.

Definitely not enough to support a "recommendation", but the AHA has been known to bestow Class I guidelines upon a single piece of positive evidence....

 

[xaelia]

-lots of people who have strokes recover functionality with no intervention.

That's pretty much the bullet point that summarizes the risk/benefit to tPA.

What's funny is that people rarely talk about how often tPA doesn't recanalize the target vessel - this is well-established from all the STEMI literature that it sometimes takes quite awhile to work, and sometimes it doesn't work at all.

And, conversely, some thrombosis spontaneously recanalizes. This is why the old definition for TIA used to have such a long time frame to resolution of symptoms - because some people get better in the first 24 hours regardless.

Desperate science for a terrible disease, twisted by industry money.

 

[AmoryBlaine]

That's pretty much the bullet point that summarizes the risk/benefit to tPA.

What's funny is that people rarely talk about how often tPA doesn't recanalize the target vessel - this is well-established from all the STEMI literature that it sometimes takes quite awhile to work, and sometimes it doesn't work at all.

And, conversely, some thrombosis spontaneously recanalizes. This is why the old definition for TIA used to have such a long time frame to resolution of symptoms - because some people get better in the first 24 hours regardless.

Desperate science for a terrible disease, twisted by industry money.

Requesting permission to steal that.

 

[docB]

83 yo M BIBA 40 min after onset of slurred speech and right sided weakness that has since resolved. Initial NIH is 4. D/W neuro, joint decision is hold tPA. 30 min later after neg CTH and labs pt deteriorates. At that point had almost total expressive aphasia and significant right side weakness. NIH then 8. D/W neuro again and recommendation is for tPA. D/W family for ~20 min. 30% do better, 1/20 bleed and die. Family calls other relatives and decide to go for it. tPA started at ~1h40m in. Neuro arrives a few minutes later to consult. Patient is admitted and transferred to ICU with some improvement.

Following day patient is still on my list. I notice a stat CXR done in the ICU at 0530, always a bad sign. That CXR showed pt was tubed at that point. Stat CTH at 0550 showed the bleed.

That family agonized over that decision. We all rolled the dice and lost. I wish those drug reps could tag along on those discussions. "Hi ma'am. So your loved one blew a vessel and is in there posturing as his consciousness is squeezed through a small hole in the bottom of his skull, but don't worry, here's Thad to explain what a great f*****g drug it is that killed hem. Enjoy.

I hate it.

 

[Arcan57]

83 yo M BIBA 40 min after onset of slurred speech and right sided weakness that has since resolved. Initial NIH is 4. D/W neuro, joint decision is hold tPA. 30 min later after neg CTH and labs pt deteriorates. At that point had almost total expressive aphasia and significant right side weakness. NIH then 8. D/W neuro again and recommendation is for tPA. D/W family for ~20 min. 30% do better, 1/20 bleed and die. Family calls other relatives and decide to go for it. tPA started at ~1h40m in. Neuro arrives a few minutes later to consult. Patient is admitted and transferred to ICU with some improvement.

Following day patient is still on my list. I notice a stat CXR done in the ICU at 0530, always a bad sign. That CXR showed pt was tubed at that point. Stat CTH at 0550 showed the bleed.

That family agonized over that decision. We all rolled the dice and lost. I wish those drug reps could tag along on those discussions. "Hi ma'am. So your loved one blew a vessel and is in there posturing as his consciousness is squeezed through a small hole in the bottom of his skull, but don't worry, here's Thad to explain what a great f*****g drug it is that killed hem. Enjoy.

I hate it.

That sucks.

And I know it doesn't change the emotional impact, but 83 yo's with aphasia and hemiplegia don't do well. tPA just shifts the deaths from the pneumonia/infection axis that we don't have to deal with and to ICH in the hospital, which we do find out about. One of my partners used to be a hospitalist and his stories of how poorly most of the geriatric CVAs that leave the ED in stable condition end up doing was eye-opening.

 

[GeneralVeers]

I've personally never given it. After explaining the risks to patients, the ones who would otherwise qualify generally refuse it.

Our hospital has gone to interventional approaches on our stroke protocol. We get CT to rule out bleed, then CT angio of head and neck. If lesion is found it generally goes right to IR for thrombectomy.

 

[xaelia]

If lesion is found it generally goes right to IR for thrombectomy.

What system? The published data on neurothrombectomy devices can be pretty iffy, too, but if they ever iron out the procedural complications, that'll be better than our current strategy of washing a teacup with a shotgun.

 

[Apollyon]

What system? The published data on neurothrombectomy devices can be pretty iffy, too, but if they ever iron out the procedural complications, that'll be better than our current strategy of washing a teacup with a shotgun.

Isn't the bolded more akin to streptokinase? Wasn't the whole vaunted premise of t-PA that it WOULDN'T be wholesale, disseminated thrombolysis - that it would be a bit more directed than that of the streptokinase?

 

[alreadylernd]

You'll have to forgive my med student ignorance but why? Based on my neuroscience lectures tPA is the best thing since holy water.

Just off the top of my head: (BTW, there's a recent review article, June 2nd in NEJM that has a lot of good summary and where most of the the following comes from...)

-6-8% have significant bleeding after TPA administration.
-The first half of NINDS trial showed no benefit compared with placebo (I think someone else already mentioned that sometimes patients improve without any intervention), more patients got enrolled, the study was extended and only then was the benefit seen.
-Mind you, benefit is ONLY seen at 6 months on objective neurological testing scales. Everyone has anecdotal stories of someone getting TPA and "rapidly getting better" but if you stick to what the studies say, that is not where the benefit is actually seen. As someone else mentioned, long term outcomes for elderly stroke patients is not so hot as is, so to be a couple points higher on a neuro scale 6 months from now may be statistically significant, but not so clinically significant.
-European trials have not showed similar benefit (ECASS I think) - though in fairness, I think their window was a little longer.


TPA is an FDA approved treatment if the strict criteria are met. I think a discussion with the patient and family is always important because the complication rate is high. Additionally, it is important to explain that this isn't some magic bullet where the patient is going to instantly get better to temper patient/family expectations in the setting of high risks. I can remember at least 2 times I've given TPA, neither had a bad outcome which I am grateful for. Neither had that magical improvement I can cite as my own anecdotal evidence.

 

[The White Coat Investor]

i've given it exactly once, almost pissed my pants, then got a call from the accepting stroke center that the pt seized on arrival and had to be intubated. had hx stroke for which she had gotten tpa and no contraindications. probably not directly related, but it's my N of 1 experience, arghhhhh

My N of 1 is worse. The guy met criteria-sudden onset, within the window, reasonable NIHSS score, no contraindications. Gave TPA and transferred to stroke center. MRI after arrival showed mets that were invisible on the CT. Luckily he didn't bleed. The family later admitted maybe the onset wasn't so sudden after all.

 

[southerndoc]

I trained at a place that aggressively TPA'd strokes, and currently I work at a very busy (120,000 patients/year) ED that is a primary stroke center.

I average giving TPA every few months. I've yet to see a head bleed from it (probably TPA'd about 30-40 patients), and I've seen some impressively good outcomes from it.

Of course my experience is anecdotal, and the first head bleed will definitely taint my picture. I TPA before consultation with a neurologist in most cases because I'm comfortable with it from my training and prior experiences.

With regards to TPA for PE, there's some research that shows that people with submassive PE's develop pulmonary hypertension a few years after their PE. Their exercise tolerance is crap at 5-10 years. If it's a young person, I consider TPA. Our pulmonologists usually determine who gets it. They TPA a lot of patients to prevent pulmonary hypertension and reduced exercise capacity. Nothing sucks more than to be a 30 year old who can't walk across a room without getting winded. Those patients (young patients) tend to tolerate TPA well.

 

[wook]

studies are horribly flawed

👍

Agreed +1

 

[TysonCook]

I'm in with southerdoc. See >120,000, primary stroke center and use it multiple times a month, and see it a LOT as we get lots of transfers (via stroke network). Not had anyone bleed out on it (on my shifts etc)... doesn't mean it doesn't happen, just not any more than the published rates.

Additionally, we are a big PE center (Kline is our Chair). We have criteria sets for PE and lyse accordingly. Lots of research on it, and when it happens we get two research fellows to the bedside. For massive PE it does make a difference (in my experiences).

Just my $.02

 

[WilcoWorld]

I'm in with southerdoc. See >120,000, primary stroke center and use it multiple times a month, and see it a LOT as we get lots of transfers (via stroke network). Not had anyone bleed out on it (on my shifts etc)... doesn't mean it doesn't happen, just not any more than the published rates.

Additionally, we are a big PE center (Kline is our Chair). We have criteria sets for PE and lyse accordingly. Lots of research on it, and when it happens we get two research fellows to the bedside. For massive PE it does make a difference (in my experiences).

Just my $.02

To be clear - I'm not arguing against lysing PEs that cause hemodynamic compromise, I support that practice. I'm arguing that the data for lysing stable PE associated with RV strain is weak, and that the studies are not good enough to change practice. I'm glad that someone like Kline is doing further research on this, as it's a yet unanswered question.

It's worth noting that in the study Southern Doc mentioned, the patients who got lysed were unstable.

 

[AmoryBlaine]

My N of 1 is worse. The guy met criteria-sudden onset, within the window, reasonable NIHSS score, no contraindications. Gave TPA and transferred to stroke center. MRI after arrival showed mets that were invisible on the CT. Luckily he didn't bleed. The family later admitted maybe the onset wasn't so sudden after all.

Yikes.

 

[ORL10]

To be clear - I'm not arguing against lysing PEs that cause hemodynamic compromise, I support that practice. I'm arguing that the data for lysing stable PE associated with RV strain is weak, and that the studies are not good enough to change practice. I'm glad that someone like Kline is doing further research on this, as it's a yet unanswered question.

It's worth noting that in the study Southern Doc mentioned, the patients who got lysed were unstable.

I definitely use tPA for strokes regularly and have had similar results to the trials in terms of ICH (we use tPA often and the 2010 review had 5% ICH rate within CI of prior studies). I feel like I want to shower after I give it especially when the family thanks me when their loved one improves clinically within 30 minutes (Despite me telling them the benefit isnt for months.)

As for using tPA in PE's the way I see it is if this is an unstable pt most people will lyse. If in PEA arrest and you think this is the cause consider a bolus of tPA we do 50mg IVP (supported only by case reports).

As for stable patients with RV strain/dilation there is the Konstantindes article NEJM which suggests reduction in their primary outcome (which most of this was attributed to 2ndary thrombolysis which meant the patient had worsneing dyspnea, hemodynamic comprimise, required intubation, or worsening RV dysfunction). Somehow there were more complications in the group that got heparin> tPA????
The Hamel article in the Chest looked at this as well which included thrombolysis with alteplase, urokinase and saruplase and showed no benefit with tPA over heparin and actually showed more severe complications with tPA (not unexpceted).

So in conflicting results I tend to do what I would want done to me which is give me tPA, although Ill probably end up getting sued for giving someone an ICH even with informed consent.
There are several other articles looking at maybe "non-clinically important outcomes" like improved RV function, or improved clot burden and favored tPA.

But good discussion here two pretty controversial uses of tPA and its nice to hear what people across the country tend to do. Would love to see a large randomized study on this and if you guys need another site to increase enrollment PM me.

 

[Arcan57]

I give tPA about quarterly (including last shift). Like everywhere else, most of the strokes that present to the ED have exclusion criteria (usually time, but we have a heavily anticoagulated populace also). In my n=12, I haven't seen any ICH (one UGI bleed in someone who denied hx of ulcers, got protonix and was fine). I haven't seen any get noticeably better while in the ED or in the hospital. I still get a mild cholinergic reaction giving it, but no horror stories. The more challenging thing I deal with is people with isolated facial parasthesias or UE parasthesias wanting to know why I'm not giving them the "clot-busting drug".

On the other side of things, my boss has caused 7 fatal ICHs giving it to patients that had no exclusion criteria and Neuro gave the go-ahead on.

 

[dchristismi]

I use it as well, roughly quarterly, but it seems to come in bursts. I gave it last night as well. The vast majority at my shop don't arrive in time (we use a 4.5h cutoff) or have exclusion criteria. The 60 yo lady last night had a dense hemiparesis that initially improved, then worsened. +MCA sign on her CT, so I felt like she deserved a shot at getting better. Then her gums started bleeding... yikes.

The last unstable saddle PE I saw was in a 34 yo M who was 2-3 weeks post-spinal sx after an ATV crash with HR in 140s and sats in the 70s, somehow maintaining his BP at that point. When the rad called me with the CT result, she commented that the IR guy was sitting right there, had him look at it, at which point he asked me to call cards to meet him in the lab to place a temporary pacer and took the guy to the IR lab. Made a huge difference for him, who really wouldn't have been a candidate for systemic thrombolysis.

TPA in general scares me. I believe in it more than I believe in Xopenex, but don't think it's the end-all-be-all.

 

[AmoryBlaine]

I definitely use tPA for strokes regularly and have had similar results to the trials in terms of ICH (we use tPA often and the 2010 review had 5% ICH rate within CI of prior studies). I feel like I want to shower after I give it especially when the family thanks me when their loved one improves clinically within 30 minutes (Despite me telling them the benefit isnt for months.)

As for using tPA in PE's the way I see it is if this is an unstable pt most people will lyse. If in PEA arrest and you think this is the cause consider a bolus of tPA we do 50mg IVP (supported only by case reports).

As for stable patients with RV strain/dilation there is the Konstantindes article NEJM which suggests reduction in their primary outcome (which most of this was attributed to 2ndary thrombolysis which meant the patient had worsneing dyspnea, hemodynamic comprimise, required intubation, or worsening RV dysfunction). Somehow there were more complications in the group that got heparin> tPA????
The Hamel article in the Chest looked at this as well which included thrombolysis with alteplase, urokinase and saruplase and showed no benefit with tPA over heparin and actually showed more severe complications with tPA (not unexpceted).

So in conflicting results I tend to do what I would want done to me which is give me tPA, although Ill probably end up getting sued for giving someone an ICH even with informed consent.
There are several other articles looking at maybe "non-clinically important outcomes" like improved RV function, or improved clot burden and favored tPA.

But good discussion here two pretty controversial uses of tPA and its nice to hear what people across the country tend to do. Would love to see a large randomized study on this and if you guys need another site to increase enrollment PM me.

1. Really? I don't think that is an accurate way to interpret the literature. I don't think anyone is out there saying that tPA doesn't have any immediate benefit -- we've all seen stroke sx resolve. The studies were done with 30, 60 day end points because that is much more important than 30 seconds but that does NOT mean that there can't be immediate benefit. Just think about it pathophysiologically. If you achieve regional thrombolysis and start perfusing again there is no reason to say "we won't see any benefit for months."

2. tPA for cardiac arrest from PE: I'd rather give this than epinephrine. The thing about PEA is that you really have to search for and treat underlying causes. I can't imagine withholding it from a PEA pt who I thought had a PE.

 

[WilcoWorld]

I definitely use tPA for strokes regularly and have had similar results to the trials in terms of ICH (we use tPA often and the 2010 review had 5% ICH rate within CI of prior studies). I feel like I want to shower after I give it especially when the family thanks me when their loved one improves clinically within 30 minutes (Despite me telling them the benefit isnt for months.)

As for using tPA in PE's the way I see it is if this is an unstable pt most people will lyse. If in PEA arrest and you think this is the cause consider a bolus of tPA we do 50mg IVP (supported only by case reports).

As for stable patients with RV strain/dilation there is the Konstantindes article NEJM which suggests reduction in their primary outcome (which most of this was attributed to 2ndary thrombolysis which meant the patient had worsneing dyspnea, hemodynamic comprimise, required intubation, or worsening RV dysfunction). Somehow there were more complications in the group that got heparin> tPA????
The Hamel article in the Chest looked at this as well which included thrombolysis with alteplase, urokinase and saruplase and showed no benefit with tPA over heparin and actually showed more severe complications with tPA (not unexpceted).

So in conflicting results I tend to do what I would want done to me which is give me tPA, although Ill probably end up getting sued for giving someone an ICH even with informed consent.
There are several other articles looking at maybe "non-clinically important outcomes" like improved RV function, or improved clot burden and favored tPA.

But good discussion here two pretty controversial uses of tPA and its nice to hear what people across the country tend to do. Would love to see a large randomized study on this and if you guys need another site to increase enrollment PM me.

"Most" indeed. 32 of 34 of their primary outcomes in the control arm included secondary thrombolysis. No other outcome was significantly different in that study (Mortality, intubations, pressors, etc - no difference). And they unblinded patients after randomization, so the study only showed that if the investigators found out you didn't get alteplase, then they were more likely to give you alteplase.
Also the fact that they dared compare bleeding rates of tPA + heparin vs heparin alone even though they gave about 30% of the control arm tPA really pissed me off (and this I think should explain the complication rates that seemed strange to you).

 

[xaelia]

I don't think anyone is out there saying that tPA doesn't have any immediate benefit -- we've all seen stroke sx resolve.

We call those TIAs.

It simply doesn't make any physiologic sense for symptoms to instantly resolve due to TPA. Once you have an intracranial thrombotic event resulting in tissue hypoxia, brain tissue dies far faster than the 1-2 hours it takes for us to gear up and get to the point where we're actually giving the TPA. The theory behind TPA is to lyse the clot so that the barely viable brain on the edge of the ischemic penumbra doesn't go whole hog - which leads to a little extra brain to help with the rehab and outcomes 3 to 6 months down the road. In a true stroke (infarction), there's dead brain that TPA wouldn't fix unless it was given (and took effect) less than 15 minutes after the onset of symptoms.

That's one place where it's easy to warp the data in these stroke trials - got TPA and rapidly improved? Miracle! Didn't get TPA and rapidly improved? Oh, just a TIA.

 

[alreadylernd]

1. Really? I don't think that is an accurate way to interpret the literature. I don't think anyone is out there saying that tPA doesn't have any immediate benefit -- we've all seen stroke sx resolve. The studies were done with 30, 60 day end points because that is much more important than 30 seconds but that does NOT mean that there can't be immediate benefit. Just think about it pathophysiologically. If you achieve regional thrombolysis and start perfusing again there is no reason to say "we won't see any benefit for months."

I understand what you're saying, but with the risks of the medication, improvement within second to minutes doesn't put you out of the woods just yet (and from what I gather, in no way alters your chances of complication)...It is quite possible to start lysing the clot causing the stroke and a bunch of other clots in your GI tract/brain etc, and while your facial droop and arm weakness begins to improve, you start having other problems as well.

And Xaelia's post right above me is very astute.

 

[danielmd06]

We call those TIAs.

It simply doesn't make any physiologic sense for symptoms to instantly resolve due to TPA. Once you have an intracranial thrombotic event resulting in tissue hypoxia, brain tissue dies far faster than the 1-2 hours it takes for us to gear up and get to the point where we're actually giving the TPA. The theory behind TPA is to lyse the clot so that the barely viable brain on the edge of the ischemic penumbra doesn't go whole hog - which leads to a little extra brain to help with the rehab and outcomes 3 to 6 months down the road. In a true stroke (infarction), there's dead brain that TPA wouldn't fix unless it was given (and took effect) less than 15 minutes after the onset of symptoms.

That's one place where it's easy to warp the data in these stroke trials - got TPA and rapidly improved? Miracle! Didn't get TPA and rapidly improved? Oh, just a TIA.

*Chuckles* This is often how I argued to my stroke attendings about this drug (and cerebrovascular disease in general). After your first thousand stroke cases, you start wondering at just how unpredictable the natural history winds up being.

But remember that depending on collateral circulation (often a function of age...the younger you are the better intracranial vasculature you've got) the penumbra can be pretty darn huge - and result in rapid acute improvement due to the IVtPA administration. Not only that, but people with good collaterals can "hang in there" and have viable tissue to save long past the 3-4.5 hr window. Conversely, an aged patient with poor collaterals might have 99.5% infarction and 0.5% penumbra a mere 1 hr after stroke onset. So giving one patient IVtPA at 6 hrs might be beneficial, and giving the other tPA at 1.5 hrs might be disastrous.

Better markers for the penumbra volume and rapid vascular imaging will help. In the meantime, the drug is still the "standard of care" as they say...

 

[wook]

..the drug is still the "standard of care" as they say...

Standard of Care is a legal definition decided by a particular jury surrounding a particular set of circumstances about the particular care rendered to a particular patient. It is not a medical definition.

From ACEP (http://www.acep.org/Content.aspx?id=29834):
•There is insufficient evidence at this time to endorse the use of intravenous tPA in clinical practice when systems are not in place to ensure that the inclusion/exclusion criteria established by the NINDS guidelines for tPA use in acute stroke are followed. Therefore, the decision for an ED to use intravenous tPA for acute stroke should begin at the institutional level with commitments from hospital administration, the ED, neurology, neurosurgery, radiology, and laboratory services to ensure that the systems necessary for the safe use of fibrinolytic agents are in place.

I would argue that the drug does not necessarily need to be given. It is institutional specific and the literature supporting it is not strong. It should be something decided jointly with the team that will be caring for the patient after they leave the Emergency Department.


Thanks.


Wook

 

[roja]

Craptastic literature, repeatedly done in the same way, equals lots of crap literature.

I don't give it. At all. If stroke team wants it, I have them admit the pt and they write the orders. I will not push it.

 

[Birdstrike]

I've always hated tPA for stroke. You can get sued for giving it, sued for not giving it. The studies say it's good, the studies say it's bad. It's a great example of exactly what's destroying medicine today, politics trumps science and reason.

 

[danielmd06]

Standard of Care is a legal definition decided by a particular jury surrounding a particular set of circumstances about the particular care rendered to a particular patient. It is not a medical definition.

From ACEP (http://www.acep.org/Content.aspx?id=29834):
•There is insufficient evidence at this time to endorse the use of intravenous tPA in clinical practice when systems are not in place to ensure that the inclusion/exclusion criteria established by the NINDS guidelines for tPA use in acute stroke are followed. Therefore, the decision for an ED to use intravenous tPA for acute stroke should begin at the institutional level with commitments from hospital administration, the ED, neurology, neurosurgery, radiology, and laboratory services to ensure that the systems necessary for the safe use of fibrinolytic agents are in place.

I would argue that the drug does not necessarily need to be given. It is institutional specific and the literature supporting it is not strong. It should be something decided jointly with the team that will be caring for the patient after they leave the Emergency Department.


Thanks.


Wook

Yes. Hence the quotation marks around the words my man.

 

[Chrism611]

I've seen it pushed once on a healthy patient, I mean no history, no bleed, just the first stroke. It worked fast and I was amazed just watching how quickly it effects the patient.

The attending was excited and talked about it for about an hour because of how much he loved it so I thought it was a good thing until I saw this (It's great to see other opinions than who you see regularly).
It does seem weird that such a severe problem can be "fixed" that fast as it was discussed previously though.

Sorry if I missed this previously in the thread, but are their as many complications and stuff about tPA in the cardiac situation as well?

 

[xaelia]

There are still major bleeding complications in ~5% of the cardiac cases as well. The bleeding is sometimes different in part because the cerebral vasculature is intrinsically damaged by the hypoxic insult, and histological preparation of post-TPA brain shows diffuse microhemorrhage - leading to it being slightly more prone to major intracerebral hemorrhage as opposed to cutaneous and other sites of major bleed.

In response to danielmd06's arguments he/she has used in the past, I actually came up with my own refutation to my own supposition a few hours later (while in the shower, of course), to point out that clot formation and breakdown is not a static process - thrombosis and clot lysis by intrinsic coagulation pathways dynamically alters perfusion. It may not be so much that TPA lyses a thrombosed clot for the rapid-improvement population, but that there is a population between TIA and clot where the thrombosis is waxing/waning/incomplete, and the TPA prevents it from being complete, resulting in rapid symptom resolution.

I would never argue that TPA "does not work". I would argue that the studies are small, biased, and inconclusive regarding appropriate selection criteria so we can maximize a risk/benefit calculation when assessing an individual patient, and TPA does't not work as advertised.

 

[danielmd06]

There are still major bleeding complications in ~5% of the cardiac cases as well. The bleeding is sometimes different in part because the cerebral vasculature is intrinsically damaged by the hypoxic insult, and histological preparation of post-TPA brain shows diffuse microhemorrhage - leading to it being slightly more prone to major intracerebral hemorrhage as opposed to cutaneous and other sites of major bleed.

In response to danielmd06's arguments he/she has used in the past, I actually came up with my own refutation to my own supposition a few hours later (while in the shower, of course), to point out that clot formation and breakdown is not a static process - thrombosis and clot lysis by intrinsic coagulation pathways dynamically alters perfusion. It may not be so much that TPA lyses a thrombosed clot for the rapid-improvement population, but that there is a population between TIA and clot where the thrombosis is waxing/waning/incomplete, and the TPA prevents it from being complete, resulting in rapid symptom resolution.

I would never argue that TPA "does not work". I would argue that the studies are small, biased, and inconclusive regarding appropriate selection criteria so we can maximize a risk/benefit calculation when assessing an individual patient, and TPA does't not work as advertised.

Absolutely agree. 👍 Never denigrate the shower thought process.

It's exactly the same concept that I was alluding to but with a different mechanism in the plumbing. That penumbra is sometimes a slippery devil. These caveats are frustrating precisely because you can see fluctuations (sometimes wildly) in the neuro exam and it mucks up your thinking about the drug or makes you second guess yourself after the 3-4.5 hrs have elapsed. I agree that it also gets used erroneously (but happily) to defend giving tPA when the patient may perfectly well have improved on their own without the 6.5% risk of intracranial bleeding we just gave them.

On a different (but related) note, I found it tough that patients and their families seemed to have this iron-clad concept that giving or witholding tPA would always result in this "all or nothing" outcome. The perception was if their loved one got the drug they would be 100% unaffected and if they didn't they would be 100% affected. If only it were that easy. It was hard explaining to people that the true difference was usually a statistical one in NIHSS or Modified Rankin score at 2 months or some such (as you were saying). It made for some hard offensive comments lobbed in my direction when I told one husband his wife barely met exclusion criteria.

I hope that more advanced imaging of the penumbra will help us immensely with sorting who should and shouldn't get the drug (regardless of timeframe) and that IAtPA and thrombectomy can get more to the forefront with increasing numbers of radiologists and neurologists doing interventional work. Here's hoping the data and technology keep getting better.

 

[docB]

Pt expired on hospital day 12.
😡😡😡😡😡

 

[gramcracker]

I've seen it pushed once on a healthy patient, I mean no history, no bleed, just the first stroke. It worked fast and I was amazed just watching how quickly it effects the patient.

The attending was excited and talked about it for about an hour because of how much he loved it so I thought it was a good thing until I saw this (It's great to see other opinions than who you see regularly).
It does seem weird that such a severe problem can be "fixed" that fast as it was discussed previously though.

Sorry if I missed this previously in the thread, but are their as many complications and stuff about tPA in the cardiac situation as well?

tPA doesn't work this way. Look at NINDS1: no benefit at 24 hours. The "benefit" they "found" was at 3 months. You saw a patient with a TIA that got better.

 

[deleted65604]

I'm with DocB on this one. In the past 3 years since being out of residency, I gave it once for stroke. Very unnerving, but a guy with marked new onset right arm and leg weakness, and hypertension. No bedside neuro at my place, so medical decision making was pretty much all me, with a telephone consult. We got his pressure down and talked with neuro, who recommended lytics. Poor guy got a head bleed about 4 hours later and was brain-dead shortly after that. So my personal study with an enrollment of 1 shows 100% mortality.

I gave it several other times for STEMIs with all good outcomes and usual immediate reperfusion and improvement of symptoms.