Whop pulls the tpa trigger?

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

Bostonredsox

Full Member
10+ Year Member
Joined
Mar 15, 2011
Messages
1,235
Reaction score
120
Who does this at your institutions? Ed alone? Ed discuss with neuro? Call of admission and let hospitalist and neuro decide? I always thought this was an Ed made decision with the pt.

Case

61 y/o female with htn and dyslipidemia, brought in by daughter for acute expressive aphasia. No motor defecits. But cannot speak. Can form words in her head, can sluggishly move tongue, but no words will come out. I am called for admission. 2:40 min into window.

Take quick history. Recognize this is very healthy young woman with obvious clinical defecit with complete aphasia that she writes out has gotten worse since it started from sluggish words to complete inability to talk. Walk out of room and ask Ed doc why she hasn't been tpad. She says she spoke with on call neurologist, who over the phone says nih scale is low, don't tpa. Does not come in to see pt. my feelings are pt should be tpad, or atleast given the option. Ed agrees. Says in her last hospital she made that decision in Ed. We agree to present tpa option to pt despite neurologists recommendation. Pt writes what is alternative. I tell her um, aspirin, rehab and um, we see what happens. She actually writes out t-p-a. So we give it to her, admit her, consult a different neurologist who comes in about 30 min later and sees her. Agrees with decision.

I get an earful on the phone later that night from initial neurologist.

Pt monitored in ICU overnight, no bleeding, spends next day on floor, goes home on day 3 with no defecit.

So. At your place...how does the tpa process get handled for said pt?

Members don't see this ad.
 
We are a stroke center. The decision for tPA is 100% by ED doc. Even if the NIHSS is 3 or 4, and the deficit is major (speech, dominant hand deficit ect ) we will tPA without hesitation.
During the stroke activation, the neurology team (only residents) are paged and usually call down to the ED to see our course of action. If they are in house, they usually walk down to do a stat consult. If they are at home, we usually talk to them on the phone and tell them what our decision is. By the time the neuro resident arrive from off site, tPA is already dripping or completed.
Once in a while, we do have borderline cases that we bounce off of neuro team. More often than not, neuro favors tPA if we are sitting on the fence about it. Also, if it's a large vessel disease, we "drip and ship" to intervention. We are so efficient at these cases that when neuro resident arrive, he or she barely has enough time for assessment before moving patient to the awaiting chopper.
 
  • Like
Reactions: 1 user
Who does this at your institutions? Ed alone? Ed discuss with neuro? Call of admission and let hospitalist and neuro decide? I always thought this was an Ed made decision with the pt.

Case

61 y/o female with htn and dyslipidemia, brought in by daughter for acute expressive aphasia. No motor defecits. But cannot speak. Can form words in her head, can sluggishly move tongue, but no words will come out. I am called for admission. 2:40 min into window.

Take quick history. Recognize this is very healthy young woman with obvious clinical defecit with complete aphasia that she writes out has gotten worse since it started from sluggish words to complete inability to talk. Walk out of room and ask Ed doc why she hasn't been tpad. She says she spoke with on call neurologist, who over the phone says nih scale is low, don't tpa. Does not come in to see pt. my feelings are pt should be tpad, or atleast given the option. Ed agrees. Says in her last hospital she made that decision in Ed. We agree to present tpa option to pt despite neurologists recommendation. Pt writes what is alternative. I tell her um, aspirin, rehab and um, we see what happens. She actually writes out t-p-a. So we give it to her, admit her, consult a different neurologist who comes in about 30 min later and sees her. Agrees with decision.

I get an earful on the phone later that night from initial neurologist.

Pt monitored in ICU overnight, no bleeding, spends next day on floor, goes home on day 3 with no defecit.

So. At your place...how does the tpa process get handled for said pt?

No deficit on day 3? How quickly did the symptoms resolve?

It sure sounds like you gave tpa to a stroke mimic.

What was the initial NIHSS?

It sounds like the first neurologist was correct.

HH

-----------

At four of my last five EDs, it was neurology who ordered and "pushed" tpa. ED docs had to "push" tpa after telemedicine or phone consult with a neurologist at the other place.

I would be very unhappy working in an ED where the decision was made primarily by the ED doc. The political and malpractice and systems (and ethical) considerations are way too high.

HH
 
Members don't see this ad :)
No deficit on day 3? How quickly did the symptoms resolve?

It sure sounds like you gave tpa to a stroke mimic.

What was the initial NIHSS?

It sounds like the first neurologist was correct.

HH

-----------

At four of my last five EDs, it was neurology who ordered and "pushed" tpa. ED docs had to "push" tpa after telemedicine or phone consult with a neurologist at the other place.

I would be very unhappy working in an ED where the decision was made primarily by the ED doc. The political and malpractice and systems (and ethical) considerations are way too high.

HH

MRI next morning was acute cortical infarct.

Although I admit was a bit nervous waiting for the MRI having overruled the neurologist. Clincher for me was I evaluated pt, and truly felt in my gut that it was acute stroke with a good candidate for tpa in the window. Ed doc felt the same. Had neurologist come in, seen pt, and then told me I would not advise tpa, I wouldn't have pushed probably. But you can't just take a phone call and be like yeah I'd say don't give it, see you in the morning. To me it's analogous to nstemi or ua with unremitting chest pain on high dose nitro drip...cardio better come into see that pt. start heparin and I'll see in the morning isn't ok to me.
 
Last edited:
  • Like
Reactions: 1 user
Most TIAs also show positive findings in MRI, particularly if symptom duration is longer.

Tia's by definition have symptoms which are, well, transient right? This pt had complete expressive aphasia which worsened over nearly three hours. That's a stroke by definition not a Tia unless I'm mistaken, which is certainly possible
 
The original definitions of TIA were symptoms <24 hrs. Still not unreasonable since that's hard to project, but it sounds like lysing a TIA.

In all the tPA literature, people just don't get better that quickly with a true strokes. We put so much effort/time/money/controversy on the time onset in order to achieve outcomes at 90 days.
 
The original definitions of TIA were symptoms <24 hrs. Still not unreasonable since that's hard to project, but it sounds like lysing a TIA.

In all the tPA literature, people just don't get better that quickly with a true strokes. We put so much effort/time/money/controversy on the time onset in order to achieve outcomes at 90 days.
Precisely. Infarcts don't resolve in 3 days either.
 
The original definitions of TIA were symptoms <24 hrs. Still not unreasonable since that's hard to project, but it sounds like lysing a TIA.

In all the tPA literature, people just don't get better that quickly with a true strokes. We put so much effort/time/money/controversy on the time onset in order to achieve outcomes at 90 days.

This is strange to me. If a Tia can last more than 3 hours, how would you differentiate unilateral weakness from a Tia vs stroke or in this case, expressive aphasia from a Tia vs expressive aphasia from a true stroke within the window? If the difference is determined after the window has expired then what was accomplished as the treatment of Asa, statin, rehab and BP control will be the treatment for both?

Put another way, if Tia is symptoms <24 hours and stroke is >24 hours, what the hell is the difference? The window is only 3 hours. After that regardless of Tia or stroke it's antiplatelet therapy, statin and BP control.
 
Had an interesting conversation with a neurologist recently, he feels that aphasia is under-represented in the NIHSS and should weigh more heavily. I mean, even if that were your only deficit, would you want to be 50 or 60 and have expressive aphasia for the rest of your life?

An analogy would be burns.... if you get 2 people with severe 1% BSA burns, but one of them has a burn to the leg and the other has burn to the genitalia, you're going to be more concerned about getting the latter to a burn center.

I don't purport to have the "right" answer here, but it's an interesting point. I also agree with above, if we are going to have TIA defined as under 24 hours but the window under 3 (or 4.5) hours, then how can one ever say whether a TIA or a CVA is being treated?
 
If you read my post, I wrote that the original definitions of TIA were less than 24 hrs but have since been shortened.

I also wrote that it's difficult to tell whether symptoms will get better with patients in the ED, so that's why there is so much pressure to treat immediately.

What I can't let go though is when neurologists write for tPA and they attribute the drug to the fact that patients are magically better within minutes to hours. I've had a few actually comment that they're "suprised a patient isn't better yet" after rounding on them the next day.

All the tPA literature looks at delayed outcomes and NINDS found that there was no difference in immediate outcomes.
 
If you read my post, I wrote that the original definitions of TIA were less than 24 hrs but have since been shortened.

I also wrote that it's difficult to tell whether symptoms will get better with patients in the ED, so that's why there is so much pressure to treat immediately.

What I can't let go though is when neurologists write for tPA and they attribute the drug to the fact that patients are magically better within minutes to hours. I've had a few actually comment that they're "suprised a patient isn't better yet" after rounding on them the next day.

All the tPA literature looks at delayed outcomes and NINDS found that there was no difference in immediate outcomes.

But is three days immediate? My pt had no recovery of function till early am on the third day. How do we define immediate? Post lytics for STEMI with reperfusion arrhythmia on EKG....to me that's immediate. Return of function three days after a cerebral infarct isn't immediate to me.

But I agree with above. Aphasia is low on the nih scale. This was a healthy highly functional 61 y/o woman with complete aphasia. If that were permanent that's as devastating an injury IMO as permanent loss of motor function in a limb, maybe more. Tpa worthy to me
 
  • Like
Reactions: 1 user
Members don't see this ad :)
Your post raises a few points:
(1) At my community hospital, we have one consulting neurologist. He is great. If he is around, he runs right in and helps make a decision along with the ED doc and the patient. He is very reasonable, and he and I tend to agree on the tough grey-zone cases. That said, he isn't always around. As such, we have access to a tele-video-neurology consultant group. Again, they will see the patient via video and make recommendations via phone. All that said, in the end it is the ED doc who either pulls the trigger or doesn't.
(2) I totally agree with above, dominate hand and severe aphasia are "underweighted" on NIHSS. That is why we don't go purely on the NIHSS number when deciding for TPA.
(3) The difference between stroke and TIA was easy prior to MRI. If it went away in 24 hours, it was a TIA. NOW, if you are liberal with your MRI, you will find all sorts of strokes that are basically asymptomatic and tiny! Of course, you cannot tell if it is a stroke or a TIA when you are 2 hours in and deciding on TPA...
To make yourself feel better, be reminded that TPA is much safer in stroke mimics! They are less likely to bleed :)

While NINDS found there is no immediate difference between TPA patients and non-TPA patients, that does not mean TPA never causes rapid improvement. The only meaningful statistical improvement was late...
 
What I can't let go though is when neurologists write for tPA and they attribute the drug to the fact that patients are magically better within minutes to hours. I've had a few actually comment that they're "suprised a patient isn't better yet" after rounding on them the next day.
Could it be confirmation bias from giving TPA to TIAs? My understanding of the nomenclature is that (as has already been covered) TIA is less than 24 hours and a stroke is more than 24 hours, however once TPA is given, if the patient gets better then it's classified as an aborted stroke, not a TIA. However, that definition would also catch patients who would have gotten better if we did nothing.
 
I definitely agree that the patient should have been offered tpa, (and make the decision themselves) but you need to do that with the understanding that rapid resolutions of symptoms are much more likely to be due to the natural evolution of the stroke than they are to the tpa. Stroke courses are extremely unpredictable. I have a family friend who had the same thing happen and she didn't receive tpa. speech therapy brought her back to a fulltime teaching position despite the stroke presenting as a severe aphasia. The overall efficacy of tpa is not that good (I mean a 15% chance of mild to moderate improvement 3 months later is not a whole lot). It's not as bad a drug as people make it out to be, but it's also not a miracle drug by any means. Speech and occupational therapy can also be excellent treatments so I stress to my patients that there are effective therapies, and the overall positive effect of tpa is not seen until a few months out.
 
I definitely agree that the patient should have been offered tpa, (and make the decision themselves) but you need to do that with the understanding that rapid resolutions of symptoms are much more likely to be due to the natural evolution of the stroke than they are to the tpa. Stroke courses are extremely unpredictable. I have a family friend who had the same thing happen and she didn't receive tpa. speech therapy brought her back to a fulltime teaching position despite the stroke presenting as a severe aphasia. The overall efficacy of tpa is not that good (I mean a 15% chance of mild to moderate improvement 3 months later is not a whole lot). It's not as bad a drug as people make it out to be, but it's also not a miracle drug by any means. Speech and occupational therapy can also be excellent treatments so I stress to my patients that there are effective therapies, and the overall positive effect of tpa is not seen until a few months out.

I agree with your post, my point was not that tpa saved this lady from lifelong debilitation, it's that she had true stroke symptoms, within the window, and should have been offered tpa by the neurologist. She might have resolved without it I totally agree, but she is definitely a candidate and I see a neurologist over the phone saying nope not a candidate scale too low as poor for. That's why I pulled the trigger and offered it with risks/benefits after seeing the pt.

I just wanted to see what the process was like at other shops
 
While NINDS found there is no immediate difference between TPA patients and non-TPA patients, that does not mean TPA never causes rapid improvement.

Huh?

That is exactly what it means.

I can't follow your reasoning here...unless you are going to say that the some of the treatment group of NINDS 1/2 improved quickly due to tpa and an equivalent number of people improved in the control group of NINDS 1/2 due to the "carrier" molecules that replaced the tpa in the placebo solution.

Please explain, as I maybe then I can understand this perspective and communicate better with the residents and nurses in the NeuroICU who often thank the tpa for resolution of "strokes" soon after tpa is given.

HH
 
(I mean a 15% chance of mild to moderate improvement 3 months later is not a whole lot).

And, remember, this is the magnitude of benefit seen specifically in one population in one study. Once you get closer and closer to NIHSS 0, the absolute difference will become vanishingly small. I am neither pro- or con- tPA, but I'm unhappy with a situation where we don't have the appropriate tools to consent individual patients – sustained recanalization with tPA is not fantastically high, stroke is an extremely heterogenous disease process, and the risk of sICH differs greatly across the treatment population. That said, there are absolutely patients where, even if our supporting evidence has holes, their level of disability merits some kind of discussion regarding rapid treatment.

Also, I agree, absolutely, that NIHSS has a non-linear relationship with disability.

Oh, and since this is a "who pulls the trigger" discussion – at tertiary stroke referral hospital (i.e., we're the place you ship when you "drip and ship"), we have a "partnership" with neurology where the in-house stroke fellow basically makes the call. The ED physician has ultimate say, but we typically defer all but the most frightening out-of-bounds cases because of the registry/research mission of the department. At our wild west county shop, ED makes the call alone and then calls a neurology resident to let them know.
 
I am neither pro- or con- tPA

I try to follow what you write, and, yet, I struggle sometimes, mostly because you refer to various studies in depth, the same studies with which I have not kept up, and, as such, when you blithely refer to some vague data point buried in there, I am lost in the weeds. However, even if this is how you feel, I quite perceive your writing to be quite anti-tPA. If that is not what you feel, the tenor of writing leads in another direction.

I freely admit that it is due to my being in the community, and not in academia - that is not an excuse, but just a reality. At my current job, I think, maybe, there is a neuro-interventionalist within 100 miles, but I am not sure. Even a neuro resident? The closest residents are 60 miles away, in an FM program that is a "rural medicine" track. Subspecialty residents and fellows are 40 minutes away - by air.

However, to give you full credit, I think the line "...even if our supporting evidence has holes, their level of disability merits some kind of discussion regarding rapid treatment" is the most positive thing I have EVER seen you write regarding (presumably) tPA for CVA.
 
We are a stroke center and the ED doc orders the TPA. For questionable cases, the ED doc can consult the neurologist. We have their cell phones and get them immediately. They admit all stroke patients getting TPA'd (those not getting TPA'd are admitted by hospitalist service and neurologist consults). If we have an iffy case we aren't sure whether to TPA, they come in to see them -- even at 3am. Usually they are there within 15 minutes since they all live nearby.
 
Who does this at your institutions? Ed alone? Ed discuss with neuro? Call of admission and let hospitalist and neuro decide? I always thought this was an Ed made decision with the pt.

Case

61 y/o female with htn and dyslipidemia, brought in by daughter for acute expressive aphasia. No motor defecits. But cannot speak. Can form words in her head, can sluggishly move tongue, but no words will come out. I am called for admission. 2:40 min into window.

Take quick history. Recognize this is very healthy young woman with obvious clinical defecit with complete aphasia that she writes out has gotten worse since it started from sluggish words to complete inability to talk. Walk out of room and ask Ed doc why she hasn't been tpad. She says she spoke with on call neurologist, who over the phone says nih scale is low, don't tpa. Does not come in to see pt. my feelings are pt should be tpad, or atleast given the option. Ed agrees. Says in her last hospital she made that decision in Ed. We agree to present tpa option to pt despite neurologists recommendation. Pt writes what is alternative. I tell her um, aspirin, rehab and um, we see what happens. She actually writes out t-p-a. So we give it to her, admit her, consult a different neurologist who comes in about 30 min later and sees her. Agrees with decision.

I get an earful on the phone later that night from initial neurologist.

Pt monitored in ICU overnight, no bleeding, spends next day on floor, goes home on day 3 with no defecit.

So. At your place...how does the tpa process get handled for said pt?

The one thing you will never know, is what would have happened if you never gave her tpa. Would she have left in 3 days without deficits, as she did with the tpa, would she have left unchanged with her aphasia as on admission, or would this event have progressed and worsened?

Because there's absolutely no way to tell with certainty the difference between a stroke and Tia at the 2-3 hr mark, is why tPA has always bothered many EPs. Add that to the fact that with this as with any treatment, you have a "number needed to harm" which refers to the inevitable non-zero number of patients with Tia's that will end up getting hemorrhagic bleeds from tpa that end up worse off, disabled or dead, who would have returned baseline if you had left them alone.
 
Huh?

That is exactly what it means.

I can't follow your reasoning here...unless you are going to say that the some of the treatment group of NINDS 1/2 improved quickly due to tpa and an equivalent number of people improved in the control group of NINDS 1/2 due to the "carrier" molecules that replaced the tpa in the placebo solution.

Please explain, as I maybe then I can understand this perspective and communicate better with the residents and nurses in the NeuroICU who often thank the tpa for resolution of "strokes" soon after tpa is given.

HH

http://www.ncbi.nlm.nih.gov/pubmed/23212169
http://www.emlitofnote.com/2012/12/predicting-immediate-improvement-after.html

The way NINDS was set up, and analyzed and re-analyzed, showed statistically significant improvement in medium/long term outcomes. Heck, some trials show TPA doesn't do much of anything. However there is in the broader literature, the thought that there ARE specific subgroups of stroke that DO have a solid chance of rapid improvement with TPA, and sustained improvement (http://stroke.ahajournals.org/content/early/2012/02/02/STROKEAHA.111.646265.short).

I DO agree with you that people give TPA too much credit when, more like, they are witnessing an auto-lysed TIA or stroke mimic that is resolving. I'm really not much of a TPA fan. My own personal take on this, when it happens and I am on duty, is to remind the very excited nursing staff that just heard their TPA'd patient is doing much better that while the studies only show moderate improved long term outcomes, that on this individual patient they did a great job with rapid triage / CT / Labs / TPA and certainly gave them the best change possible for their individual improvement.
 
http://www.ncbi.nlm.nih.gov/pubmed/23212169
http://www.emlitofnote.com/2012/12/predicting-immediate-improvement-after.html

The way NINDS was set up, and analyzed and re-analyzed, showed statistically significant improvement in medium/long term outcomes. Heck, some trials show TPA doesn't do much of anything. However there is in the broader literature, the thought that there ARE specific subgroups of stroke that DO have a solid chance of rapid improvement with TPA, and sustained improvement (http://stroke.ahajournals.org/content/early/2012/02/02/STROKEAHA.111.646265.short).

I DO agree with you that people give TPA too much credit when, more like, they are witnessing an auto-lysed TIA or stroke mimic that is resolving. I'm really not much of a TPA fan. My own personal take on this, when it happens and I am on duty, is to remind the very excited nursing staff that just heard their TPA'd patient is doing much better that while the studies only show moderate improved long term outcomes, that on this individual patient they did a great job with rapid triage / CT / Labs / TPA and certainly gave them the best change possible for their individual improvement.

These are some interesting theories -- great theories in that they may incite further RCTs -- but they are only that: theories...just more theoretical, sub-group analysis that should prompt further tpa research; not lead docs to proclaim that tpa works in the short term. There is currently no "good" evidence to claim the latter; and plenty of RCTs to proclaim the contrary.

All we KNOW from RCTs about tpa in the short term is that it hurts patients.

That said, I do agree that tpa likely -- maybe even probably -- helps some small subset of patients in the short term. If only we were allowed to discuss this openly and "research" it!

HH
 
These are some interesting theories -- great theories in that they may incite further RCTs -- but they are only that: theories...just more theoretical, sub-group analysis that should prompt further tpa research; not lead docs to proclaim that tpa works in the short term. There is currently no "good" evidence to claim the latter; and plenty of RCTs to proclaim the contrary.

All we KNOW from RCTs about tpa in the short term is that it hurts patients.

That said, I do agree that tpa likely -- maybe even probably -- helps some small subset of patients in the short term. If only we were allowed to discuss this openly and "research" it!

HH

Completely agree with your general sentiment. It does seem in the last few months there has been more open discussion of TPA, so hopefully that gets us somewhere.
Maybe we can get to tamiflu next :)
 
Xaelia isn't anti-tPA any more than he is anti-antibiotics.
There are quite a few of us who are anti-overuse of drugs that aren't shown to be beneficial, and tPA is one of those.
There is likely a population that will benefit and not have increased risk of bleeding, but we haven't found it yet.
Again, no study of tPA benefits shows improvement before 30 days. If they improve before that, it isn't tPA effect based on the literature. Period.

Neurointervention devices are even worse though.
 
Xaelia isn't anti-tPA any more than he is anti-antibiotics.
There are quite a few of us who are anti-overuse of drugs that aren't shown to be beneficial, and tPA is one of those.
There is likely a population that will benefit and not have increased risk of bleeding, but we haven't found it yet.
Again, no study of tPA benefits shows improvement before 30 days. If they improve before that, it isn't tPA effect based on the literature. Period.

Neurointervention devices are even worse though.

Agree with McNinja and Xaelia--I'm neither pro or anti-tPA. The problem, however, is that within the non-EM specialties of medicine, if you're not praying to the altar of Genentech, then you're off living with the savages somewhere in the Stone Age.

In fact, I think we're going to start using these type of drugs more, specifically for massive and sub-massive PEs with data like the MOPPET trial and others coming out. In these cases, the risks are probably less than the benefits in terms of morbidity (i.e. not being able to walk to your mailbox because of CHF secondary to your previous PE) because you're not lysing damaged brain tissue.

The biggest concern that many EPs have is that much of the data for PEs in stroke has never been fully released and the trials seems to alternate on whether they are overwhelmingly beneficial or harmful, yet neurology largely chooses to disregard the harmful ones while embracing the beneficial ones.

In addition, the consent process is often somewhat biased, in that neurologists often tell patients the odds of expected improvement with lytics, yet they frequently fail to tell them the odds of improvement if no lytics are administered. They also fail to tell them the study environments where patients received the drug (community vs academic), given that these studies have been replicated in community settings and showed worse results because they don't have the larger infrastructure in place to treat stroke patients.

Finally, there is some skepticism in the new ACEP guidelines, in that many of the writers had obvious financial conflicts of interest, yet still wrote the guidelines. This certainly could have been avoided, but alas was not ...
 
However, even if this is how you feel, I quite perceive your writing to be quite anti-tPA. If that is not what you feel, the tenor of writing leads in another direction.

Fair enough – it probably comes across as predominantly negative as reactionary to the complete loss of objectivity the sponsored puppets for alteplase perpetuate.

tPA as a treatment seems like a reasonable physiologic hypothesis. I wish I could use it confidently on patients I knew had a benefit profile exceeding harms, but the literature is of no help – and I'm not a fan of racking up a ton of collateral damage the way the "treat 'em all! even the stroke mimics! who cares!" zealots would have us do.

And, ACEP has opened their policy for feedback. This is mine:
http://www.emlitofnote.com/2014/02/my-acep-tpa-policy-critique.html
 
And yet, you can have an AAEM MD/JD come to your residency and teach your residents that every minute you wait to give tPA kills thousands of brain cells.
 
the stroke/tia definition is a clinical one that was developed prior to widespread MRI use. It is solely depend if symptoms resolve. However, you can get MRI finding with a TIA. With a TIA the clot is still there. You just improve due to intrinsic clot lysis(partial or complete) or are able to compensate with collateral circulation but the clot is still likely there
 
If I'm giving TPA, we consult neuro.
More for medicolegal reasons.

I personlly don't believe TPA is a useful drug for CVA, but the current guidelines are what they are.
That means you are stuck in a lot of cases.
I find the whole "stroke alert" somewhat funny.
We are racing to find people where the only real intervention does more harm than good.
 
  • Like
Reactions: 1 user
Bostonredsox – yes, that patient had a cerebral infarction, not TIA. The patient met the modern clinical and radiographic definition of ischemic stroke:

An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013 Jul;44(7):2064-89. This paper also goes over some of the historic definitions of stroke, which may clear up some of the confusion.

The timeline you described for recovery is about what you would expect after a cerebral infarction with early re-opening of the occluded vessel (a day or so). In a patient like yours with a Broca’s aphasia without motor symptoms, the vessel responsible was likely a superior division MCA branch and a good candidate for tPA. If the MRI the next day only showed cortical infarction, that was a win. The cortex is more sensitive to ischemia and the vessel was likely opened early enough to spare the subcortical white matter.

Btw, the NIHSS on your patient would have only been about a 4. Barely a blip numerically in the context of a clinical trial, but I am sure those 4 points meant the world to her.

Our health care community IS making stroke treatment safer and improving outcomes with tPA. This is consistent with modern literature on the subject:
Time to treatment with intravenous tissue plasminogen activator and outcome from acute ischemic stroke. JAMA. 2013 Jun 19;309(23):2480-8.
Door-to-needle times for tissue plasminogen activator administration and clinical outcomes in acute ischemic stroke before and after a quality improvement initiative. JAMA. 2014 Apr 23-30;311(16):1632-40.

Final point, before I get booed off here. I saw this thread while looking for something else and was so saddened by it that I had to sign up for the forum just to say this:

tPA should not be the end-all. Cardiology moved beyond thrombolytics decades ago. EPs and cardiologists worked together to make treatments for MI safer, faster and more successful. If the physician takes the attitude that a stroke patient is doomed – they will either do bad or get better on their own (as was once the attitude towards MIs) - this will become a self fulfilling prophecy. We should be motivated rather than discouraged that the current stroke treatments are imperfect, and see this as an opportunity where together we can find solutions to an incredibly complex problem.
 
  • Like
Reactions: 1 user
Bostonredsox – yes, that patient had a cerebral infarction, not TIA. The patient met the modern clinical and radiographic definition of ischemic stroke:

An updated definition of stroke for the 21st century: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013 Jul;44(7):2064-89. This paper also goes over some of the historic definitions of stroke, which may clear up some of the confusion.

The timeline you described for recovery is about what you would expect after a cerebral infarction with early re-opening of the occluded vessel (a day or so). In a patient like yours with a Broca’s aphasia without motor symptoms, the vessel responsible was likely a superior division MCA branch and a good candidate for tPA. If the MRI the next day only showed cortical infarction, that was a win. The cortex is more sensitive to ischemia and the vessel was likely opened early enough to spare the subcortical white matter.

Btw, the NIHSS on your patient would have only been about a 4. Barely a blip numerically in the context of a clinical trial, but I am sure those 4 points meant the world to her.

Our health care community IS making stroke treatment safer and improving outcomes with tPA. This is consistent with modern literature on the subject:
Time to treatment with intravenous tissue plasminogen activator and outcome from acute ischemic stroke. JAMA. 2013 Jun 19;309(23):2480-8.
Door-to-needle times for tissue plasminogen activator administration and clinical outcomes in acute ischemic stroke before and after a quality improvement initiative. JAMA. 2014 Apr 23-30;311(16):1632-40.

Final point, before I get booed off here. I saw this thread while looking for something else and was so saddened by it that I had to sign up for the forum just to say this:

tPA should not be the end-all. Cardiology moved beyond thrombolytics decades ago. EPs and cardiologists worked together to make treatments for MI safer, faster and more successful. If the physician takes the attitude that a stroke patient is doomed – they will either do bad or get better on their own (as was once the attitude towards MIs) - this will become a self fulfilling prophecy. We should be motivated rather than discouraged that the current stroke treatments are imperfect, and see this as an opportunity where together we can find solutions to an incredibly complex problem.

I doubt you'll change anyone's mind. Good nursing ratios and rehab help stroke patients. They're not left alone to get better or die.
 
I doubt you'll change anyone's mind.
Agreed, but the least I can do is encourage my fellow physicians to update their knowledge of the conditions they speak so passionately about. Starting with the basics, like what is a TIA.

Good nursing ratios and rehab help stroke patients. They're not left alone to get better or die.
Sometimes. But if you want to talk about prognosis, you have to understand what those statements mean for each type of stroke. You wouldn’t want to say that to a patient with an acute basilar artery occlusion. No amount of nursing or rehab will ever recover a brainstem once it is infarcted.
 
tPA is overused. 8/18 vs 6/18 recovery by 3 months is just not a whole lot. I always get consent and I never neglect to mention the NINDS data on bleeding. (1/18 chance of bleeding in your head and 45% chance of dying if you are one of those 18.) I see many, many pauses and private discussions with family prior to giving the tPA while they chew on all the information that I've just provided them. I never push it and I try not to let my bias against it on occasion (mimics), influence their decision. If they meet criteria, then they meet it. It's essentially standard of care at the moment, regardless of the data and some of the newer studies. I'll admit that I end up pushing it more than I personally would like to...

OP: Yes, tPA can be done 100% in the ED by the emergency physician but that ED physician did the right thing by trying to involve neurology early on in the process and they would be a fool to dismiss a formal opinion by the specialist to withhold tPA. Can you give it anyway with the pt's consent? Of course, but you need to document VERY carefully why you gave it anyway. Let's say the pt has a fatal head bleed... they are most certainly going to claim you did not do an adequate job of stressing the risks of bleeding and death. In that particular scenario I would clearly state to the neurologist why I was going forward with tPA and ask them specifically why they wanted to withhold. I would probably let the family know that the neurologist did not want to give it (for X,Y,Z reasons...) and make them come have a discussion with the pt/family or even talk to them by phone if they were not available in a timely manner. Either way, if you're going to tPA a pt without the support of a neurologist... you'd better document the hell out of that chart.
 
If the neurologist doesn't want to give tPA, and has a reasonable thought as to why, I'd have a very hard time giving it to the patient.
Most likely they are going to be admitted to the neurology service.
It kind of sucks to be stuck taking care of a patient when the ED went against your plan.
 
  • Like
Reactions: 1 user
tPA is overused. 8/18 vs 6/18 recovery by 3 months is just not a whole lot. I always get consent and I never neglect to mention the NINDS data on bleeding. (1/18 chance of bleeding in your head and 45% chance of dying if you are one of those 18.) I see many, many pauses and private discussions with family prior to giving the tPA while they chew on all the information that I've just provided them. I never push it and I try not to let my bias against it on occasion (mimics), influence their decision. If they meet criteria, then they meet it. It's essentially standard of care at the moment, regardless of the data and some of the newer studies. I'll admit that I end up pushing it more than I personally would like to...

We've only had 2 bleeds at our facility in the past few years according to our hospital stroke coordinator. We give out TPA a LOT.
 
Anyone else notice in the daily ACEP email that ACEP partnered with Genentech to create a stroke course for pre-hospital folks. I wonder how that "revised" clinical policy is going to look...
 
We've only had 2 bleeds at our facility in the past few years according to our hospital stroke coordinator. We give out TPA a LOT.
Being such a statistical outlier must be so hard. Using it for only MIs would have a higher bleed rate than 2.
 
ED here stopped writing tPA after IST-3. Now, if neuro wants tPA it is an automatic admission and the neurology resident has to write the order. ED no longer manages the patient, if neuro makes that decision its their patient now.
 
  • Like
Reactions: 1 user
Last edited:
  • Like
Reactions: 2 users
Do you practice in a litigious state? You would have absolutely no defense against the medical malpractice lawyers if she bled. The initial neurologist consultation would absolutely burn you.

A hospitalist pushing TPA against a neurologist's explicit orders...This case would definitely go to review at my hospital and you'ld likely get reprimanded


Who does this at your institutions? Ed alone? Ed discuss with neuro? Call of admission and let hospitalist and neuro decide? I always thought this was an Ed made decision with the pt.

Case

61 y/o female with htn and dyslipidemia, brought in by daughter for acute expressive aphasia. No motor defecits. But cannot speak. Can form words in her head, can sluggishly move tongue, but no words will come out. I am called for admission. 2:40 min into window.

Take quick history. Recognize this is very healthy young woman with obvious clinical defecit with complete aphasia that she writes out has gotten worse since it started from sluggish words to complete inability to talk. Walk out of room and ask Ed doc why she hasn't been tpad. She says she spoke with on call neurologist, who over the phone says nih scale is low, don't tpa. Does not come in to see pt. my feelings are pt should be tpad, or atleast given the option. Ed agrees. Says in her last hospital she made that decision in Ed. We agree to present tpa option to pt despite neurologists recommendation. Pt writes what is alternative. I tell her um, aspirin, rehab and um, we see what happens. She actually writes out t-p-a. So we give it to her, admit her, consult a different neurologist who comes in about 30 min later and sees her. Agrees with decision.

I get an earful on the phone later that night from initial neurologist.

Pt monitored in ICU overnight, no bleeding, spends next day on floor, goes home on day 3 with no defecit.

So. At your place...how does the tpa process get handled for said pt?
 
Do you practice in a litigious state? You would have absolutely no defense against the medical malpractice lawyers if she bled. The initial neurologist consultation would absolutely burn you.

A hospitalist pushing TPA against a neurologist's explicit orders...This case would definitely go to review at my hospital and you'ld likely get reprimanded
tPa is a med-mal lawyer's dream. If I was a med-mal lawyer, I'd scrub tPa cases all day long. I'd be a "tPa chaser." There's literature saying it works. There's literature saying it doesn't work and makes people bleed. Regardless of outcome, regardless of whether you give it or don't, you can get sued for giving it, or not giving it, and successfully so.
 
On another note....

Anyone ever given TPA and then there is 100% improvement in symptoms?? I was wondering if someone who has resolution of symptoms after bolus and shortly after the TPA gtt started, do you stop the gtt then?
 
Top