Stroke vs stroke mimic; negative CT: give TPA?

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honmd

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So let's say a patient comes to the ER with a facial droop starting < 4.5 hours ago.

DDx is stroke, TIA, migraine, conversion disorder, seizure, etc.

Head CT negative--but it is often negative in acute stroke, right?

Do all these people get TPA? Because it seems like we'd be giving tons of non-stroke patients (TIA's, migraines, etc) TPA, which has potentially serious side effects...

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What age patient? Not a Bell's palsy?

At my ED, the patient would get TPA. The decision is made by a stroke neurologist, and they feel the benefits outweigh the risks in the vast majority of cases <4.5 hrs.
 
What age patient? Not a Bell's palsy?

At my ED, the patient would get TPA. The decision is made by a stroke neurologist, and they feel the benefits outweigh the risks in the vast majority of cases <4.5 hrs.

An isolated facial droop gets a score of 3 at the worst. NIHSS <5 at my institution doesn't usually get TPA (sometimes they do, depends on the presentation).

Is there more to the story? (slurred speech, arm/leg drift, etc.) We TPA so many patients with stroke that our ED docs (all of them) start it before the neurologist is paged. We have excellent neurology coverage, and they show up very promptly. For those outside the window, we have interventionalists that do clot retrieval.

I can tell you that we have nowhere near the number of head bleeds that some of the studies have reported.
 
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I can tell you that we have nowhere near the number of head bleeds that some of the studies have reported.

...then you're probably treating a lot of stroke mimics. 😉

No, but, seriously, the bleed rates in the trials all involve folks with relatively high NIHSS – higher than what we've tilted towards treating in normal practice. So, yes, your stroke mimics, and low NIHSS and small ischemic territories have much lower bleed rates. I don't want to re-open the tPA debate, but if you have non-disabling or mild symptoms, how do you describe the benefit of tPA to patients – let alone if you're not sure it's a stroke? They're going to be practically asymptomatic in a few months, regardless of intervention. The MS-DRG for medically managed stroke is ~$4,500 vs. ~$8,600 for the uncomplicated tPA administration. If it's not helping, it's a waste of money.
 
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This patient would not get TPA at my institution because of the NIHSS. If you're talking droop, arm/leg weakness, then the answer barring other historical factors which you do not provide here (PMH, seizure activity, warfarin therapy, etc), is yes.

Edit: Although I will say that the NIHSS is not a be-all-end-all. Someone with a complete aphasia only has an NIHSS of 3 but that is quite disabling, in which case I would have a neurologist on the phone and would be more in favor of TPA.
 
I understand that our ACEP overlords want us giving TPA to people like Tamiflu but if the patient can hear me and talk to me I still ask them if they want it...I think NIH scale cutoffs are perfectly reasonable.

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I understand that our ACEP overlords want us giving TPA ...

FWIW, from this past October ACEP Council:
Resolution 32 ACEP Clinical Policy on tPA Use in Stroke (as amended)
RESOLVED, That ACEP reconsider the current “Clinical Policy: Use of Intravenous tPA for the Management of Acute Ischemic Stroke in the Emergency Department” including opening the discussion regarding the use of tPA to the ACEP membership; and be it further
RESOLVED, That any subsequent ACEP clinical policy be open to comment by the ACEP membership for a period of at least 60 days before consideration of adoption.

http://www.acep.org/uploadedFiles/2013 Resolutions Adopted by the Council and Board.pdf
 
...then you're probably treating a lot of stroke mimics. 😉

No, but, seriously, the bleed rates in the trials all involve folks with relatively high NIHSS – higher than what we've tilted towards treating in normal practice. So, yes, your stroke mimics, and low NIHSS and small ischemic territories have much lower bleed rates. I don't want to re-open the tPA debate, but if you have non-disabling or mild symptoms, how do you describe the benefit of tPA to patients – let alone if you're not sure it's a stroke? They're going to be practically asymptomatic in a few months, regardless of intervention. The MS-DRG for medically managed stroke is ~$4,500 vs. ~$8,600 for the uncomplicated tPA administration. If it's not helping, it's a waste of money.

Don't be so naive. We TPA a lot of high stroke scales (my last TPA was for a patient with a NIHSS of 26, had a NIHSS of 1 24 hours later; MRI confirmed stroke). We aren't treating stroke mimics. Every TPA patient gets an MRI either the day of or the day following TPA administration, and unless our radiologists are making stuff up, only 1 patient this year got TPA without MRI evidence of stroke. We are averaging 1-2 TPA patients per week because we are one of the nation's busiest ED's and we're in the middle of the "stroke belt."
 
I'm not yet a physician, but I am a stroke nurse and I'm on the acute stroke team. Our bleed rate is pretty low, too. I thought the new guidelines contraindicated tpa with a patient who has an nihss greater than 25.
 
My anecdotal evidence - I haven't seen a post-TPA bleed in ~ 4 years. I give TPA maybe once a month, including to occasional stroke mimics.
 
I'm not yet a physician, but I am a stroke nurse and I'm on the acute stroke team. Our bleed rate is pretty low, too. I thought the new guidelines contraindicated tpa with a patient who has an nihss greater than 25.

It is a relative contraindication. These are the people who can be helped the most. Unfortunately, they're the riskiest group. I'd rather be dead from a bleed than eating through a tube lying in a nursing home.
 
We had a a young person come in with stroke symptoms. Consented her for tpa......when hearing the risks her symptoms magically cleared. She got up and left AMA. Lol.
 
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most likely outcome in that case would be be getting the bleed AND lying in the nursing home w/ the tpa =p You're pretty much ****ed either way. and a theoretical risk of the NIH score dropping a few points in 3 months time is still gonna keep you PEGed, and in the NH. still, I hear your point about rather dying in that case.
 
I've given it to stroke mimics before, it's just the nature of the beast. That said, if it's an obvious stroke mimc, like they just had a witnessed seizure w/ a clear jone's paralysis or Bell's, or it's their usual complex migraine, they won't get it. But I need some diagnostic certainty that it's a mimic. And if it's not, it's always down to a patient discussion.
 
Had a patient in her early 20s admitted to a nursing home recently because her family thought she was being dramatic and didn't bring her to the ER in time for treatment.
 
I've given it to stroke mimics before, it's just the nature of the beast. That said, if it's an obvious stroke mimc, like they just had a witnessed seizure w/ a clear jone's paralysis or Bell's, or it's their usual complex migraine, they won't get it. But I need some diagnostic certainty that it's a mimic. And if it's not, it's always down to a patient discussion.

Call me dumb, but what is "Jone's paralysis"? Did you mean "Todd's paralysis", or am I completely out in the weeds?
 
I've given it to stroke mimics before, it's just the nature of the beast .... I need some diagnostic certainty that it's a mimic.

tPA is not some magical, life-transforming treatment to be applied indiscriminately. If you look at the entire body of trials outside of NINDS, it's pretty shaky evidence, full of pharma damage control (ATLANTIS) and bias (IST-3, ECASS III). To take a drug where the benefit (if the evidence is taken at face value) outweighs the risks in only a subset of acute stroke patients and make the default situation "to treat" is grossly irresponsible.

Anecdotes about bleeding rates are just that – anecdotes. The largest post-marketing registries have numbers similar to the randomized controlled trials: ~7%, with severe bleeds ~2%. Not sure how you'd get numbers significantly different than that without treating a lot of not-stroke or tiny-stroke.
 
I think i should not post when i am sleep deprived is all. Lol.
 
I'd rather be dead from a bleed than eating through a tube lying in a nursing home.

Not this.

At best, this is a horrible corruption of the principle of double effect.

At worst, this thinking will influence your presentation of the "risks/benefits of tpa" to patients and may result in a patient getting tpa who may otherwise have choose not to receive the drug.

Hemorrhagic conversion rarely results in immediate death. However, there is a good chance that new deficits or complete functional collapse will occur. You may go from "eating through a tube lying in a nursing home" to eating and breathing and ****ting through a "tube lying in a nursing home".

--------

Since this is also a thread of anecdotal evidence, I will point out that I have yet to walk through our Neurovascular ICU and not encountered a patient with hemorrhagic conversion. (I am in this unit at least four days per month)

HH
 
Not this.

At best, this is a horrible corruption of the principle of double effect.

At worst, this thinking will influence your presentation of the "risks/benefits of tpa" to patients and may result in a patient getting tpa who may otherwise have choose not to receive the drug.

Hemorrhagic conversion rarely results in immediate death. However, there is a good chance that new deficits or complete functional collapse will occur. You may go from "eating through a tube lying in a nursing home" to eating and breathing and ****ting through a "tube lying in a nursing home".

--------

Since this is also a thread of anecdotal evidence, I will point out that I have yet to walk through our Neurovascular ICU and not encountered a patient with hemorrhagic conversion. (I am in this unit at least four days per month)

HH

You've seen far more then me, but I've yet to see a hemorrhagic conversion survive to discharge. So from my small sample size it really has been peg tube + Straw in bed or dead. My neurologists very rarely do not give tpa unless the pt blatantly refuses. And from my what I've seen, they describe the tpa like I do a line to a pt who really needs it...."it's a little bit bigger Iv than the one in your hand that you can rarely bleed a little bit from but will significantly help us give you the medicines you need to survive".
 
I think that the data shows ~60% of hemorrhagic conversion dont die.
 
Handy replies so far, everyone--thanks!

My impression of what most people are doing is looking at NIHSS, treating patients from roughly 5-25 (too low, probably mimic; too high, may be uncomfortable with bleed risk) with some exceptions (e.g., complete aphasia).

As for whether it's bad to treat mimics, looks like the consensus is that there will inevitably be some people that get tPA that have mimics rather than strokes, but that the NIHSS is helpful in reducing that number.

Anyone have tips on DDxing TIA vs stroke clinically, other than the NIHSS? Waiting for 24 hours to see if symptoms resolve (or until the MRI gets done the next morning) closes the tPA window, so any tips would be helpful.
 
You cant unless it resolves completely before tpa
 
If the symptoms haven't resolved - it's a stroke.
If they've resolved - it's a TIA
If they're resolving - it's a TIA or minor stroke.


Handy replies so far, everyone--thanks!

Anyone have tips on DDxing TIA vs stroke clinically, other than the NIHSS? Waiting for 24 hours to see if symptoms resolve (or until the MRI gets done the next morning) closes the tPA window, so any tips would be helpful.
 
Case:

60yo caucasian male presenting with 1 week history of dysarthria that fluctuates in intensity but has been present for approx 1 week. This gentleman simply didn't want to go see a doctor until this morning 2h PTA when he suddenly suffered abrupt and complete aphasia and severe R sided weakness. EMS called, sx resolved before they arrived but then returned en route in the ambulance, then abated prior to arrival in the ED. Now the pt has mild dysarthria and a very mild L facial droop (on re-check it now seems to be gone...imagination?). There are no other focal neuro deficits other than mild drift and str is 5/5 throughout, reflexes and sensation normal. The R sided sx have resolved entirely. He received ASA en route. The nurse says that his dysarthria is worse now than when she assessed him prior to your arrival. The pt is not so sure. At first there is a question on whether the dysarthria is new as of this morning (2h ago) versus old, but as you discuss more of the history, it appears to have been present for at least 1 week in some capacity but perhaps a little worse this morning although the pt can communicate fairly well in spite of the symptoms. The family thinks he has sounded like this all week. CT Head is negative. There are no absolute contraindications to TPA. NIHSS 3-4

PMHx: HTN, DLD, Normal VS

Would you TPA this pt?
 
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Case:

60yo caucasian male presenting with 1 week history of dysarthria that fluctuates in intensity but has been present for approx 1 week. This gentleman simply didn't want to go see a doctor until this morning 2h PTA when he suddenly suffered abrupt and complete aphasia and severe R sided weakness. EMS called, sx resolved before they arrived but then returned en route in the ambulance, then abated prior to arrival in the ED. Now the pt has mild dysarthria and a very mild L facial droop (on re-check it now seems to be gone...imagination?). There are no other focal neuro deficits other than mild drift and str is 5/5 throughout, reflexes and sensation normal. The R sided sx have resolved entirely. He received ASA en route. The nurse says that his dysarthria is worse now than when she assessed him prior to your arrival. The pt is not so sure. At first there is a question on whether the dysarthria is new as of this morning (2h ago) versus old, but as you discuss more of the history, it appears to have been present for at least 1 week in some capacity but perhaps a little worse this morning although the pt can communicate fairly well in spite of the symptoms. The family thinks he has sounded like this all week. CT Head is negative. There are no absolute contraindications to TPA. NIHSS 3-4

PMHx: HTN, DLD, Normal VS

Would you TPA this pt?
Not a chance. What's the perceived benefit?
 
Not a chance. What's the perceived benefit?

You go back in to re-assess the pt and his dysarthria seems worse, now there is an appreciable L facial droop that is mild. You repeat the neuro exam and he has no R sided deficits and the remainder of your neuro exam is essentially the same.

"Hey Doc... I heard they got those clot buster drugs. Am I having a stroke? Am I always going to talk like this? I'm a real estate agent and on the phone a lot. I don't know if I can deal with not being able to talk..."

Do you discuss TPA? Do you offer it?
 
At my shop, neurology makes the decision. If it was up to me, I'd discuss it with the patient and offer it.
 
"I'm not sure if you're having a stroke or not you probably are but we won't know for sure for about 24 hours. If f you are there a lot of treatments available the aspirin and speech therapy. There are clot busting s they have a lot of risks and benefits. If you take it 5 times out of 10 you will bleed into your brain 2 of those times you will die but 15 times out of 100 people have an improvement 3 months down the line that is greater than if it just did speech therapy and aspirin. The rest of the time there will be no difference whatsoever. Some people have full and complete recovery after speech therapy some don't and I cannot predict that in any way right now. If you want we can give you the medication if you don't want to take the rest other medicine then you don't have to take it we will do whatever you decide and feel comfortable with
 
"I'm not sure if you're having a stroke or not you probably are but we won't know for sure for about 24 hours. If f you are there a lot of treatments available the aspirin and speech therapy. There are clot busting s they have a lot of risks and benefits. If you take it 5 times out of 10 you will bleed into your brain 2 of those times you will die but 15 times out of 100 people have an improvement 3 months down the line that is greater than if it just did speech therapy and aspirin. The rest of the time there will be no difference whatsoever. Some people have full and complete recovery after speech therapy some don't and I cannot predict that in any way right now. If you want we can give you the medication if you don't want to take the rest other medicine then you don't have to take it we will do whatever you decide and feel comfortable with

"I'm not sure if you're having a stroke" – the medicine only has a chance to help you if you are having a stroke.

and

"an improvement 3 months down the line that is greater than if it just did speech therapy and aspirin" – but the difference is likely to be so slight you wouldn't notice it.

This case sounds like someone I'd only be "offering" it so I could document patient declined.
 
I wouldn't tPA this patient. Our stroke team might, depending on which staff was on, when they examined the patient, and which parts of the history they focused on.

He needs a work up for risk factors (carotid stenosis, a fib, etc) that can be modified to put an end to his escalating TIA's, not lysis.
 
This case sounds like someone I'd only be "offering" it so I could document patient declined.

Exactly. Excuse the typos on my last post, speech recog software still needs work on my phone. Had exact above case with a friend of my parents except she was a teacher. Speech therapy gave her pretty much complete recovery and a return to work within several months from a moderate aphasia but low nih score cva. I like to remind patients that tpa is not the only treatment available for the inconvenient low nih strokes.
 
I'd like to see an ECHO and CTA or angio from the ED (and MRI from the ED, depending on which center I was working at)...this might be the one of the few cases I push for urgent carotid evaluation and discuss with an interventionalist.

No tpa with a a deficit the patient has had for a week and for which he has choosen not to seek care. Given the current culture, I would very clearly review the RISKS and small potential benefits.

HH
 
I posed this case to get a few of you thinking and especially give the residents food for thought. It's not always black and white. There's not always a neurologist to talk to and sometimes you have to make the best decision. I find it very difficult to have that "TPA discussion" in a completely unbiased fashion. Inevitably, I get asked "Well, what would you do?" and even if you try to be objective, pt's can pick up on your preferences. At least, in my experience.

I had this case, not exactly... but one similar. There was much confusion on the length of the sx, and no interval deterioration of sx in the ED (but I think you always have to anticipate that scenario..). At one point, it sounded like 100% neurological sx for over a week, then suspicion on my part of intermittent TIAs, but when pressed... again, it sounded as if the pt had consistent neuro deficits. However, you still have a pt presenting within the time window with a technically unresolved neurological deficit which makes them a TPA candidate whether you "really" consider them one or not.

1) Was the complete aphasia and R sided paralysis a TIA with complete resolution revealing an underlying older CVA that would explain the 1 weeks worth of mild dysarthria?

2) Or is this a new stroke with a partial resolution?

Either way, it's tough to tease out the information and not always clear in my opinion. Personally, I don't like to consider a pt like this to be a typical TPA candidate. Prognosis is very good, especially with mild symptoms. I don't think any of us like to risk a bleed on very low NIHSS with good prognosis. I intend to do a more thorough lit search but I'm curious if "very low" NIHSS should be as much of a relative contraindication as "very high" NIHSS.

The consensus that I've found so far seems to vary. I've read some institutional guidelines that mandate NIHSS > 4 for inclusion criteria. This link provides an interesting Q/A and I thought this take was interesting...

  1. In terms of rapidly improving symptoms, what is your lowest NIHSS number where you will still go ahead and treat?

    I do not think that the absolute number is as important as the perceived disability of the deficit at hand. For example, an NIHSS score of 2 based on an isolated hemianopsia is vastly different than a similar score for minimal weakness and minimal sensory loss both in one extremity. Therefore I would make my decision to treat or not to treat a “mild” stroke or “rapidly improving” stroke entirely on the clinical deficit and trajectory of the patient when I was evaluating them. — Dr. Pancioli

In cases like this, I feel obligated to inform and offer TPA, even if I don't want to give it.
 
I posed this case to get a few of you thinking and especially give the residents food for thought. It's not always black and white. There's not always a neurologist to talk to and sometimes you have to make the best decision. I find it very difficult to have that "TPA discussion" in a completely unbiased fashion. Inevitably, I get asked "Well, what would you do?" and even if you try to be objective, pt's can pick up on your preferences. At least, in my experience.

I had this case, not exactly... but one similar. There was much confusion on the length of the sx, and no interval deterioration of sx in the ED (but I think you always have to anticipate that scenario..). At one point, it sounded like 100% neurological sx for over a week, then suspicion on my part of intermittent TIAs, but when pressed... again, it sounded as if the pt had consistent neuro deficits. However, you still have a pt presenting within the time window with a technically unresolved neurological deficit which makes them a TPA candidate whether you "really" consider them one or not.

1) Was the complete aphasia and R sided paralysis a TIA with complete resolution revealing an underlying older CVA that would explain the 1 weeks worth of mild dysarthria?

2) Or is this a new stroke with a partial resolution?

Either way, it's tough to tease out the information and not always clear in my opinion. Personally, I don't like to consider a pt like this to be a typical TPA candidate. Prognosis is very good, especially with mild symptoms. I don't think any of us like to risk a bleed on very low NIHSS with good prognosis. I intend to do a more thorough lit search but I'm curious if "very low" NIHSS should be as much of a relative contraindication as "very high" NIHSS.

The consensus that I've found so far seems to vary. I've read some institutional guidelines that mandate NIHSS > 4 for inclusion criteria. This link provides an interesting Q/A and I thought this take was interesting...

  1. In terms of rapidly improving symptoms, what is your lowest NIHSS number where you will still go ahead and treat?

    I do not think that the absolute number is as important as the perceived disability of the deficit at hand. For example, an NIHSS score of 2 based on an isolated hemianopsia is vastly different than a similar score for minimal weakness and minimal sensory loss both in one extremity. Therefore I would make my decision to treat or not to treat a “mild” stroke or “rapidly improving” stroke entirely on the clinical deficit and trajectory of the patient when I was evaluating them. — Dr. Pancioli

In cases like this, I feel obligated to inform and offer TPA, even if I don't want to give it.

This patient would get a CTA where I work. This type of presentation can often follow arterial dissections, and that must be ruled out before TPA. If there was a clot present on CTA, and the patient meets TPA criteria, then TPA would be given. If he's 4.5-12 hours out and a clot is present, then he'd go for intervention in our stroke lab.
 
This patient would get a CTA where I work. This type of presentation can often follow arterial dissections, and that must be ruled out before TPA. If there was a clot present on CTA, and the patient meets TPA criteria, then TPA would be given. If he's 4.5-12 hours out and a clot is present, then he'd go for intervention in our stroke lab.

What about a negative CTA but meets TPA criteria?

In this case:

CTA was negative. MRI with small embolic appearing infarcts. Acute vs subacute.
 
Is the data well established in any direction yet?
 
I've seen some pretty miraculous things with the solitaire procedure.
 
I've seen some pretty miraculous things with the solitaire procedure.

I've seen some pretty miraculous things with normal saline.

What does what either of us have seen matter? This kind of thinking (usually from neurology residents) bothers me even more than the "Well, gosh, I'd rather die from a tpa bleed, than live with a facial droop" thinking that I responded to above.

Maybe you were being sarcastic and I am missing the humor, but I hear comments like this enough that I suspect you were being serious...

HH
 
I've seen some pretty miraculous things with normal saline.

Yeah. Infarcted brain is irreversibly dead within minutes. Not 3 hours, not 4.5 hours, minutes. Now, thrombosis and recanalization is a dynamic process, and I have no doubt there is a tiny subset of presentations where tPA tips a low flow state over into a full flow state – the ~40% of the time it even results in sustained clot lysis – and results in the observed magical improvement. But, this should be essentially an undetectably rare event. Going after old clots with endovascular devices based on the hypothesis that any recanalization will save a penumbra of wounded tissue failed (MR RESCUE). They claim their futile results were due to "old devices", but they still had nearly 70% acute recanalization. We ought to stop doing endovascular interventions outside the bounds of clinical trials until proven effective (and not keep grandfathering in FDA approval based on PROACT-II).
 
I have a hard time getting exctited about stroke patients when in my heart I don't believe the acute treatmets we offer have any proven benefit.
 
Well, our hospital has a newish interventional radiologist. I was able to watch the first solitaire procedure at our hospital on a male patient in his late 40s who was excluded as being a tpa candidate.

He had facial droop, hemiparesis, and was completely aphasic. The radiologist removed a huge embolus and by the time we were transferring him from the cath lab table to the stretcher, he was mumbling again. A couple hours later he was moving his arm again. 3 days later he was discharged walking out of the hospital with a slight limp.

Do I think there are miracle cures for everything including strokes? No. But I do get excited when things are effective.

I've also been in the cath lab when solitaire wasn't able to remove the embolus. It sucks.

Many stroke patients die, many more become disabled; why not celebrate the small victories?
 
Mechanical embolectomy is a $20-$30k MS-DRG with no proven benefit. Lovely.

There are still ongoing studies.

It's not the infarcted area that can be salvaged. It's the watershed areas. You're right, ischemic brain tissue dies within minutes when depleted of oxygen. If it's a watershed area receiving 50% oxygen, then it takes longer than minutes to kill the cell.

The pattern of patient you describe, I would not TPA if he had a negative CTA (both for dissection as well as clot). One episode of clearing up then presenting again I would TPA. Multiple episodes, no, because that has a higher bleed risk.
 
Well, our hospital has a newish interventional radiologist. I was able to watch the first solitaire procedure at our hospital on a male patient in his late 40s who was excluded as being a tpa candidate.

He had facial droop, hemiparesis, and was completely aphasic. The radiologist removed a huge embolus and by the time we were transferring him from the cath lab table to the stretcher, he was mumbling again. A couple hours later he was moving his arm again. 3 days later he was discharged walking out of the hospital with a slight limp.

Do I think there are miracle cures for everything including strokes? No. But I do get excited when things are effective.

I've also been in the cath lab when solitaire wasn't able to remove the embolus. It sucks.

Many stroke patients die, many more become disabled; why not celebrate the small victories?

Because the pleural of anecdote is not data. This is a hugely expensive intervention that requires significant infrastructure and if you're going to blow $10s of thousands of dollars on an acute intervention without discernible benefit that's money that's not available for rehab, appropriate outpt level of care, etc.

Because taking the result of random chance and calling it a victory stifles further scientific enquiry and can make it difficult/impossible to discover the truth.

I gave IV tPA to a young guy with right hemiparesis recently. The MRI after tPA (hours later because... ICU holds) showed multiple branches of the left MCA occluded and an acute corona radiata infarct. 20 min after the MRI was done, he started moving his right side again.

Hell, I had a women in residency that had an outpt MRI done while asymptomatic that showed a complete R carotid occlusion with a dense acute MCA area infarct that developed symptoms ON HER WAY TO THE ER 30 MINUTES AFTER THE MRI WAS DONE. Stroke is not heart attack, and as much as we like to act like one is a model for the other (see: AHA folding stroke into it's purview) they're not .
 
I think this whole interventionalist "I've seen them get better in front of my face" mentality is truly ridiculous. Im not an EBM snob, and I do realize there are shades of grey, RCT's have a hard time identifying the exact patients I see in everyday practice, too old, too sick etc, too many comorbidities etc. In the end I have to make a decision based on physiology, evidence, experience and guidelines (like it or not).

Neuro IR and neurologists want an effective treatment for something they are passionate about, and I respect that, but please provide me something that I can quote as reasonable evidence that improves patient-oriented outcomes (not recanalization) so I can offer this as treatment to my patients. So far we are 0/3 (MR rescue, IMS III, synthesis). Sure the studies aren't perfect, maybe there are better devices, maybe they need to happen sooner. I'll be the first to call the neuro-IR guys when they do a well completed RCT with reproducible benefits that are plausible. But currently we have NO good data to suggests that these invasive procedures are improving peoples lives.
 
Well, our hospital has a newish interventional radiologist. I was able to watch the first solitaire procedure at our hospital on a male patient in his late 40s who was excluded as being a tpa candidate.

He had facial droop, hemiparesis, and was completely aphasic. The radiologist removed a huge embolus and by the time we were transferring him from the cath lab table to the stretcher, he was mumbling again. A couple hours later he was moving his arm again. 3 days later he was discharged walking out of the hospital with a slight limp.

Do I think there are miracle cures for everything including strokes? No. But I do get excited when things are effective.

I've also been in the cath lab when solitaire wasn't able to remove the embolus. It sucks.

Many stroke patients die, many more become disabled; why not celebrate the small victories?

I had a very similar patient a few months ago.
Completely aphasic, right sided paresis, new onset afib.
Had a bag of normal saline running while I was waiting for TPA.
All of his symptoms resolved.
If the pharmacy was faster, I would have said that the TPA treatment was a miracle.

I'm sure that there are some patients where these treatments will help.
The problem is that based on the current evidence, we don't know who these patients are currently.
As such, the treatments should only be used in clinical trials.
 
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