Linking To And Excerpting From Critical Care Time's "82. Strokes and Intro to Neurocritical Care with Dr Casey Albin"

Today, I review, link to, and excerpt from Critical Care Time‘s “82. Strokes and Intro to Neurocritical Care with Dr Casey Albin”.

All that follows is from the above resource. [Note: start at 9:30. The first part is nonclinical.]

Aug 3, 2026

We’ve heard you guys and we are ready to deliver! We are proud to bring you guys our first of several episodes on Neurocritical Care! On this episode – our introductory show – we had the pleasure of hosting Dr. Casey Albin a neurologist & neurointensivist who introduces the topic of neurocritical care with a special focus on basic tenets of stroke management. What type of imaging should you order? What do you do with anticoagulation? Who get’s seizure prophylaxis? We cover all this and more with Dr. Albin. Please take a listen and let us know what you think and what else you want to hear from us!

Transcript

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[music]

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Very frequently when we think about when does most blood get delivered to the brain most of that that flow [music]

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that profusion is going to happen incyally. So when a patient has a really high ICP, that’s actually going to impede their diastolic flow, right?

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Because the the pressure the ICP is so high that your diastolic flow or your diastolic pressure may sort of get to

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almost the same as your ICP. Therefore, even more flow is happening in cy. The brain really really relies on [music]

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that systolic profusion. So how does your how does your brain get more time in cy? it becomes teacartic and so I will tell you having done this like day

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in and day out all the time the patients who are herniating or teocartic [music] when I walk in around the unit and I see somebody who’s hypertensive and

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teacartic to me that is like a brain that’s really stressed [music] so I will see people reflexively give beta blockers like please don’t do that that

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is like the brain the brain’s asking for [music] more profusion it’s asking to have more time in cy to me that teoc

1 minute, 9 seconds

cardia is really like a that’s a that’s a [music] red flag warning situation Bradic cardia is going to be a really late finding after they’ve herniated.

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[music]

1 minute, 21 seconds

Welcome to Critical Care Time, the podcast for everyone who cares for the critically ill. I’m your host, Dr. Cyrus Saskin. I’m here with my co-host, Dr. Nick Mark. Hey, man. How’s it going?

1 minute, 30 seconds

It goes good. It’s been a little bit of a chaotic day, but uh things are settling down now, and I’m excited to be here. Excited to uh to be recording.

1 minute, 38 seconds

Nice, man. Yeah. Did you have a good Father’s Day? I did. I did have a good Father’s Day.

1 minute, 43 seconds

We watched the ultimate Father’s Day movie in my opinion, Return of the Jedi. Ah, yeah. Good one. Good one. So, we enjoyed it. It was a fun time.

1 minute, 50 seconds

Went to the pool. Life was good. How about you?

1 minute, 53 seconds

Sweet. Yeah, similar. Uh, I bunch of people I work with uh took me out for belated birthday celebration the night

2 minutes, 1 second

before. So, I had kind of a I I kind of a relaxed stay in bed Father’s Day for a little while.

2 minutes, 6 seconds

Um I see. Yeah. But it was happy belated birthday. I’m sorry I missed it. Yeah, usually the kids made me some stuff. This little

2 minutes, 14 seconds

guy that says dad that lives on my desk now. I don’t know. It was great. Awesome, man. Good stuff.

2 minutes, 21 seconds

Anyway, uh you know, turning our attention to the podcast here where where we find ourselves today. Um we’ve had a very requested topic since the

2 minutes, 29 seconds

just season one even, right? People have said, “You got to do some neuroccritical care.” And so they they talked to us and we answered or we or we will answer.

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We’ve got we got a great thing lined up today. Yeah.

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Yes. Yes. We’ve been teasing it for quite a while now. It’s finally here.

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Yes. Lots of lots of our listeners are interested in neuroccritical care content and we’re happy to bring that to uh to them today. I think it’s going to be fun, exciting, all that good stuff.

2 minutes, 56 seconds

So uh with us today, fortunately Nick and I don’t have to delve into the uh the great unknown alone here uh is Dr.

3 minutes, 2 seconds

Casey Albin. So she’s an associate professor of neurology and neurosurgery in the division of neurocritical care at Emory University. She’s interested in all aspects of neurocritical care. Uh

3 minutes, 11 seconds

and additionally she’s passionate about social mediabased medical education and simulation. Those are of course two areas that Nick and I are similarly

3 minutes, 18 seconds

passionate about which I mean I I certainly hope that doesn’t come as a surprise to our audience. Um but yeah, super excited.

3 minutes, 26 seconds

Yeah, let’s uh let’s get into it, man.

3 minutes, 31 seconds

Yeah. So, Casey, welcome to Critical Care Time. We’re excited to uh explore the mysteries of the brain with you as our guide. Um why don’t you take a

3 minutes, 39 seconds

minute and introduce yourself? Tell us your superhero origin story. Why did you uh why why did you become a neurintensivist?

3 minutes, 46 seconds

Yeah, it’s so funny. Um first of all, thanks so much for having me. I’m like super excited to be here. you know, going through medical school, I really

3 minutes, 54 seconds

knew I wanted to do critical care and kind of bounced around through all the different aspects of critical care and I didn’t really love, you know, in the

4 minutes, 2 seconds

miku you’re dealing with a lot of like mucus and like bronco spasm and I was like this is like kind of not my thing.

4 minutes, 8 seconds

And then anesthesia was just like oh so much time like sitting in the O kind of bored like that’s not really my thing either. And I eventually did my neuro

4 minutes, 17 seconds

rotation. I was like, gosh, this is so cool. Like the brain is such a mystery. It’s such a puzzle. The exam is amazing.

4 minutes, 22 seconds

You get to localize lesions. You get to see a diverse pathology. And so I after that did a rotation in the neuro and

4 minutes, 30 seconds

kind of found this synergy of like the puzzling aspects of neurology with the kind of full body care that you get with

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critical care. Um, and truly have just been in love ever since. And so here I am doing that.

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body meets mind. Great. Um, totally.

4 minutes, 48 seconds

Well, we’re we’re really excited to sort of build sort of a foundation in this topic. Um, you know, we have a couple of cases that we thought would be sort of a

4 minutes, 56 seconds

great way to explore different pathologies, the the diverse pathologies as you said. Um, yeah, I think, you

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know, we can kind of we can kind of take them one by one and, uh, you know, sidebar and talk about cool physiology

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and other stuff as it comes up. Um, Cyrus, you wanna wanna you want to lead us into case number one?

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You know, I I will, but just before I do that, I was thinking, you know, a lot of our listeners are sort of um trying to decide what they want to do with their

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their lives going forward, and I think neurocritical some of our hosts are trying to decide that, too. [laughter] That’s that’s that’s actually quite

5 minutes, 32 seconds

true. Um but we’ll we’ll focus on our on our listeners for now and I’ll say that you know neurocritical care I think is one of the paths um less traveled in the

5 minutes, 42 seconds

world of critical care. I think that’s safe to say and so I was thinking maybe before we get into the first case um Casey if you wanted to let us know like

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maybe how folks can get into neurocritical care what are the pathways and and and just like a little bit of an overview of the of the career.

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Great point.

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Yeah. No, I think that’s awesome. I think well first of all I think a lot of neurocritical care is being provided by non-neurologists and by people who have

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not specialized in neurocritical care and you know it used to be that you could kind of grandfather into being board certified in neurocritical care having taken care of those that is sort

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of more phasing out and they now want to see people having done some sort of formal training in neurocritical care to

6 minutes, 21 seconds

take the boards. Um that changed kind of a couple years ago. Um but you know there are a diverse amount of ways that people can get into neuroccritical care.

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Um myself I was a neurology trained resident and I kind of did four years of neurology did a two-year fellowship in critical care. I tacked on one

6 minutes, 39 seconds

additional year in sort of uh med research and simulation. But there are certainly people who come into it from emergency medicine and then do a

6 minutes, 47 seconds

neuroccritical care fellowship. you can do anesthesia critic care and then tack on um usually for those people it’s a one-year fellowship um to kind of

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specialize in the neuro aspects and you can actually do it through medical and like critical care miku training um and

7 minutes, 5 seconds

tack on to that that’s a little bit harder and certainly less common the three big ones are neurology the anesthesia critical care um and then ED

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uh as a sort of like the three most common and then the medical training into neurocritical care fellowship is less widely done and I think if I

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remember correctly there are some accreditation issues with like having to do that and then take the boards but um anything is possible

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and I I feel like I know a couple other random ones too like I know at least one sort of like reformed neurosurgeon term turned neurointensivist and you know I

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know another guy who does a lot of neurointerventional stuff like neuroraiology type stuff who’s also neurocritical care so I mean ju just like critical care in general it’s kind a cool diverse group.

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Yeah, absolutely. I mean, we don’t see a ton of the neurosurgeons who decide to do this way, but it is possible and you can infold that into their fellowship.

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So, usually they’re doing sort of dual dual operations like they’ll do some surgery and also care for their posttop

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patients. I I always the the times that I work in the neuroICU during the day which is not that many but you know we

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have a two attending model and so it’s it’s often like me with a real bonafide neurintensivist and I feel like the cross-pollination is always fun because

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you know I’ll be like yeah you stick the chest tube in like this and they’ll be like like oh you note this really subtle lesion here which causes a calculia

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which I’m sure you noticed on your exam and I’m like yes because obviously I make all my patients do math problems when examining them. No, it’s so true.

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I really I do love that and I love that in our group we have um an ED person, we have a person uh within our group who does Siku and is really interested in

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like transplant sort of hyperammia neurology. So he’s a siku intensivist some of the time with like liver transplant and then he is a

8 minutes, 53 seconds

neurintensivist the other half of his career. So it’s I mean his his real interest is in you know hyperammia and the encphylopathy of liver transplant.

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But it really is that bringing in the different knowledge and getting to work with different subsp specialties of critical care that makes us all better and stronger.

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Absolutely.

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Well now that we’ve done that now that you humored me Casey I think we could maybe jump into the the meat and potatoes here. I think that’s going to be helpful though for our listeners who

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are maybe thinking about a a career in neurocritical care. um the many listeners who have who have begged for this content. So, okay. Um for these

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cases, you know, sometimes we do longer form cases, but I kind of just wanted to focus on the content. So, these are relatively short, punchy cases. Um and

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so, uh away we go. We’ll start with the first one. This is a 28-year-old who uh had unfortunately had an MVC, so motor vehicle collision, coming in intubated.

9 minutes, 49 seconds

The GCS is 6T, so pretty poor. uh right pupils noted to be sluggished. The

9 minutes, 56 seconds

patient has a CT that shows traumatic subdural hematoma, contusions, compressed sisterns, and a 7 millimeter

10 minutes, 2 seconds

midline shift. So, um why don’t we just start with kind of this one of the one of the things I learned early in

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neurocritical care is this concept of the Monroe Killily doctrine and how it relates to incraanial pressure. So, so maybe you could

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wait I thought that was the no more Europeans in the continent thing. the Monroe Doctrine. Different Monroe, different Different Monroe, different doctrine. Okay.

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Um but yes, so perhaps for this one, uh Casey, you can walk us through how this differs from the um the uh you know, US history doctrine.

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Put this in the context of the Monroe presidency.

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Yes. No, none of that. Uh this is all, you know, this really is the foundation of neuroccritical care. And it’s a really simple thing. And I think the way I boil it down to trainee when they’re

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rotating with me, it’s pretty simple that the skull is a box, right? There’s only so much stuff you can fit in the box before the box explodes. And so to

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me, that’s like a pretty simple way to explain it. You know, there is CSF that goes in the box. There is blood, that’s the arterial volume that goes in the blood and the the box, our our skull.

11 minutes, 5 seconds

There is going to be the Venus blood volume. And then we’re going to have CSF. And those contents sort of exist in harmony when your brain is in its normal

11 minutes, 13 seconds

non-pathologic state. But then you know many of my patients all of a sudden have an acute pathology like this traumatic subdural that’s showing up for our guy

11 minutes, 21 seconds

and that rapidly changes the contents of what’s in the box. Right? So this guy now has a lot of blood in the brain, right? Something that’s causing 7

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millimeters of midline shift. That’s not a small subdural. And the Monro Kelly doctrine just states that like those things can’t be out of balance because

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when they’re out of balance, you ultimately get herniation. And so our job as neurintensivists is to figure out

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how do we keep those things in balance to prevent herniation.

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Excellent. Yeah. Maybe maybe that’s um the next thing we should talk about too which are like what are the sort of immediate things that can be done and

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what are the sort of more more invasive things that can be done to control uh rising in cranial pressure right yeah and I think that that’s a

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really great focus because I mean this guy you’re telling me that already his right pupil he’s got some ancoria so to me what that’s saying and we harp on

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these pupils all the time because the pupil is basically the control of it uh starts at the midbrain and runs is along

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the ocular motor nerve which is cranial nerve three and that’s coming out kind of in the center of the midbrain and then it travels down the optic tract to

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the eye and and control some of the parasympathetic pupilary constriction.

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And so when you have an expanding mass lesion that’s compressing down on the midbrain then all of a sudden that nerve

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is not communicating with the pupilary uh sphincter to cause pupilary constriction. So your pupil ends up dilated. And so like why does that all

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matter? Well, because the midbrain is so important um when we think about you know protecting the brain, protecting the brain stem is really of like the

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maximum important stuff because you know sitting right beside that pupilary signaling is our reticular activating

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system which if you remember from medical school or just because you live in a world of nerysiology like I do, you know that’s really important to like

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being awake, right? And so for us also where uh caffeine works via adenazine. So something near and dear to many of our listeners

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so many right we are just leveraging this path or this this circuitry all day every day in our usual lives. Um but

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this guy right he has a depressed level of consciousness and aniscoria and those two things are telling me that there is

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a there is clinically significant shift on the brain. He is not there’s too much compartment. There’s too [clears throat]

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much stuff in the brain and our enroll Kelly doctrine says that this is going to leave us out of balance and we’re worried already about herniation. All right, so circling back from this

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neurohysiology u what are we going to do about it? I think the first thing and what drives me crazy is I’ll walk down into the ED and the patient will be

14 minutes, 2 seconds

laying flat like first and foremost sit the patient up. That’s going to help with Venus return. The other thing that all trauma centers want to do is just

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stick a C collar on somebody and wrap it on really tight. that’s also going to contrast your um internal jugular veins which is also helping for Venus return.

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And so one of the things I go down to the ED when I’m seeing these patients, I make them sit up, make sure that you know the CC collar, fine. Like let’s protect their C-spine, but you know,

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let’s just make sure that we can stick our finger in the sea collar and like we’re not compressing our jugulars. And I think that that’s like actually two of

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the most important things that you can do at the bedside here and now before you’ve done really any pharmacological or surgical interventions.

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Nice.

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Great point. And and even if you can’t even if you can’t bend them at the waist, even if they’re on like a spine board or something, you can tilt the whole bed. Like you can make gravity work for you.

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Yeah. Yes. 100%.

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All sorts of stuff you can do. Okay. So, um let’s continue this tour uh of sort of um ICP management strategies. I like

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how we started with the least invasive, most readily accessible. Um, let’s say we’ve done those things and now we’re looking at a situation where, you know,

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we’re we’re concerned like in this patient’s case, we obviously are going to need to do more than just that. Um, so where would we go from here? Yeah, I

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think that’s a great uh you know like it’s all tiers and I think of this as in tier zero, tier one, tier two, tier three, you know, in the way that’s

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classically sort of set when we think about the brain trauma foundation guidelines which is really looking at diffuse injury. Um we’re sort of

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thinking of tier one being, you know, control their agitation. If they’re sedated and intubated, make sure that they’re comfortable in the vent. They’re

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not bucking the vent. they’re, you know, they’re not sedated to the point of being in burst suppression, but they’re just comfortable. And then you’re

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thinking about hyperosmolar therapy. And then you’re thinking about sort of these stronger interventions like sedating, paralyzing, and cooling, right? And we

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can get to those, but I think the really important thing to do before you start to go down ICP management ladders is to

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think about is this a surgical case or is this not a surgical case? Right? And this guy is a surgical case. no amount

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of my physiology uh tinkering like we can we can optimize him to get to the O but this guy he’s a 28-y old kid he’s

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got seven millimeters of midline shift he is already antisycoric this guy just needs to go to the O right and I think that that’s a really important thing for

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all of us who take care of these patients to sort of to think about is is this a surgical lesion or can I get by with medical treatment

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right and and I think that’s a really good point that like this is a situation where haste is really important Like I’ve literally seen like you put in the

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order for manitol or whatever and pharmacy hasn’t even approved it yet.

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Meanwhile, the neurosurgeons are like shaving the patient’s head as they’re going down the hall. Like you know there’s like a trail of hair leading to the operating room because they’re

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treating it so urgently. Like that that’s really important context I think.

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Yeah, I absolutely agree. I think that this is like just someone you can do the stabilizing things and we can talk through them if that’s helpful. But I think that that this kid needs to get to

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the O. I think that’s yeah that’s a really important point too because I think a lot of us are familiar with the like sick not sick paradigm that we use

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to sort of assess a patient at the at the jump. I think in the world of neurocritical care, especially if you’re doing, you know, a lot trauma patients

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as well, this is like a good example of the interface between trauma and and neurocritical care. Being able to make that assessment quickly and getting the

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right people available, getting the O spun up, so on and so forth, I think is really important as you as you outlined because your, how shall we say,

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manipulation of physiology is only going to take you so far.

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Yeah, absolutely. I mean I think that this is one of those cases where you’re also balancing you know we can talk through so when we think about again

17 minutes, 55 seconds

like sort of the tiers of ICP management you want to have the patient sitting up not compressing you then kind of move to step tier one which is making sure

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they’re comfortable on the ventilator that they’re not agitated then tier two and that the backbone of all of our sort of ICP manipulation is really hypermolar

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therapy like that’s our our go-to medication and in this case with the suburb physiology, you kind of have to balance,

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well, if I dehydrate the brain, I’m potentially increasing the potential space for that subdural to expand.

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That’s really a theoretical concept, but our sort of general what we tell our trainee is like if the patient is not

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herniating from their subdural, no hypermolers for them. Like we’re just going to talk to our neurosurgery colleagues. We’re get them to the O. If

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the patient is antisycoric and certainly if they get to the point where their pupil is blown and non-reactive then I think that the benefit of manitol

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probably outweighs this theoretical risk of expanding the subdural and that’s when we sort of say let’s get manitol let’s get 23% on board whatever you know

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you have in your wherever you’re taking care of this patient and whatever your access permits you to have um but I think it is

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important to think about the physiology that’s different when someone who has a subdural versus someone who comes in with say like diffuse exonal injury and

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they just have a really swollen brain but no surgical target to go after and that that patient and the subdural patient are a little bit different

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because one’s a surgical patient and one is going to be a surgical patient only if all medical interventions fail.

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Great point.

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Um should we should we maybe walk through like I think you did a great job sort of outlining the tier zero tier one. Should we talk about the sort of higher tiers like let’s just for the

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sake of this story um let’s imagine the neurosurgeons are busy in one case they’re going to be a little while you know we have to keep this person alive

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totally and even I think even more commonly we’ll have this patient this young guy we see this all the time this guy comes in they’ve got a surgical lesion they go to the O they do a

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decompressive hemiactomy they evacuate the lesion they do a duroplasty to give more space for the brain to expand and

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yet 2 days later you know they put in an EVD monitor just cuz you know the guy’s in a coma and so by the brain trauma

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foundation guidelines we typically monitor patients who have traumatic brain injury who are in a coma with the GCS less than 8. Um so he has an EVD

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he’s surgically decompressed and yet it still is saying ICP is 25, ICP is 25, ICP is 30, ICP is 44. Like we see this

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all the time because often these young brains not only do they have their subdural but they also have a lot of diffuse exonal injury. So they have this

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really swollen, very reactive, very adeous brain that even with a decompressive hemi craniactomy, there’s still not enough space and they’re still

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really swollen. So not at all uncommon that we get into this the situation where you know we have our hypesolar

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therapy on board. There is actually like we could talk about this all day long about how we as neurotensivists have very um deeply held beliefs about how

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hyperresolar therapy should be given without a lot of evidence to guide that deeply held religious like there’s only

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one way to do this. I will share my my sort of approach to hypermolar therapy and trauma. There is a preference to

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using 23%. Manitol is obviously a diuretic and so our trauma patients who have poly trauma like probably not the best thing to do for them.

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What what goal sodium to use is kind of like a it’s a gestalt. It’s a feeling. What I

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always tell our our trainee is like this the number doesn’t really matter to me.

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What matters to me is that the patients getting hyperosmolar therapy every time their ICP is elevated or every time you

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know they’re sort of at eligible to get so ever you know 6 hours 8 hours however often you’re sort of checking their

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sodium. So to me, for someone who’s at risk of herniation, who we’re, you know, we’re treating with sodium therapies, to

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me, it’s not so much what is the number we get to, but how often are they able to get their bull dose of sodium and making sure that if we have an EVD, what

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we’re really doing is is is using manitol or using 23% as guided by an elevated ICP.

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Let’s let’s double click on that for a second because I think you know sort of listeners may or may not be super familiar with different methods of measuring like what is it what is an EVD

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is sort of an important question thinking we might have put the the cart before the horse a little bit because we’re talking ICP maybe we should talk about how we assess and then and then we should then we

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should introduce the concept of cerebral profusion pressure as well I suppose yeah let’s do it so um EVD is obviously that’s a external ventricular drain EVD

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it is a drain that’s placed by the neurosurgeons at the bedside side or in the O. Um, usually kind of blind pass.

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It goes in through preferably the right frontal lobe because turns out your right frontal lobe is not all that important. So if you hemorrhage, it’s what they call an ineloquent part of the brain.

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It is it is less important when I don’t know I think probably you don’t want to hemorrhage anywhere in your brain but you can tolerate some some blood in the right frontal lip. So

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ideally it goes into the right frontal lobe and it’s going into sort of the intervententricular uh fammen between the two lateral ventricles and ideally

23 minutes, 19 seconds

all of those are connected. So if you you know measure the pressure at one of the ventricles you’re measuring the whole the whole system and that’s why

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it’s a this is a sort of gold standard is because it can give you an entire pressure monitor of the brain whereas something like a bolt which is just a

23 minutes, 36 seconds

parankal probe that really gives you sort of the local tissue pressure. And so bolts are kind are nice in that you

23 minutes, 43 seconds

can put other things like if you’re putting a prankal pressure in, you can put a an EEG lead in. You can put a cerebral micro dialysis catheter in. You

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can put all sorts of like, you know, fancy Moberg monitors in with the like you can do fancy stuff with with the bolts.

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I I tend to trust the number from an EVD more than I trust a number from a prankal probe. So at the end of the day an EVD is a diagnostic and a therapy as

24 minutes, 7 seconds

opposed to a both which is really just a diagnostic.

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Absolutely. And especially with people who like have subactoid hemorrhage or they have profound bacterial menitis or they have IVH for whatever reason like

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that that drainage can be really important.

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So when we’re having these conversations um again we I know we keep uh keep kicking the can down the road on the specifics of therapy but I think this is

24 minutes, 29 seconds

really important. So when we’re having these conversations with our colleagues about who does and who doesn’t get invasive monitoring, ICP monitoring, I

24 minutes, 38 seconds

know that can be a sticking point. So are there certain criteria we should be looking for for like who’s a good candidate, who can we follow more clinically? Um how do you approach that?

24 minutes, 48 seconds

Yeah, it’s again this is like a an area of active research and I don’t know that we have the correct right answer because at least in trial data, you know, when

24 minutes, 57 seconds

we put in ICP monitors, we did not change outcomes. Um, and it that to me feels like expecting the Swans catheter to change.

25 minutes, 6 seconds

I was going to say the PA catheter of the brain. Yeah.

25 minutes, 9 seconds

Yeah. Yeah. Like it’s it’s not about the catheter, it’s about what you do with the information, right? And so to me for

25 minutes, 17 seconds

from the brain trauma foundation guidelines, we’re still in most instances and when it’s available placing an invasive ICP monitor when

25 minutes, 25 seconds

patients come in in a coma and it’s not easily explained by some like other reason like we really do think it’s a swollen brain. They’re not able to wake

25 minutes, 34 seconds

up. they get an ICP monitor just because that helps us say is this an ICP problem or is this some other global issue that

25 minutes, 41 seconds

we need to take care of you know causing them to be in a coma. Um so so that’s from the brain trauma foundation guidelines that’s GCS lesson 8. Um you

25 minutes, 51 seconds

can also get them if you have like a abnormal head CT and some other physiologic parameters but mostly it’s just if you’re a comeomaos trauma

25 minutes, 58 seconds

patient right the other people who need the invasive neurom monitoring or EVD a lot of those are just driven by like

26 minutes, 6 seconds

they need treatment of obstructive hydrophilis so that’s our subacoid hemorrhage patients that’s our intraventricular hemorrhage patients

26 minutes, 14 seconds

that’s patients with profound bacterial menitis where you would need to do sort of ventricular toileting um Those patients also will end up with neurom

26 minutes, 22 seconds

monitoring and that’s very helpful for us but they’re getting the EBD primarily because it’s part of their treatment of obstructive hydrophilis therapeutic benefit.

26 minutes, 31 seconds

Yes.

26 minutes, 32 seconds

I see. Okay. So, sounds like there are some uh basic guidelines we can follow

26 minutes, 39 seconds

in terms of who needs this and who doesn’t need it, but still an area for research and an area for debate to a degree. Yeah.

26 minutes, 45 seconds

What are you what are you setting an EVD at in these patients? It’s a great question. So, EBDs are a little bit funny in that we measure the ICP in

26 minutes, 54 seconds

millimeters of mercury, right? We’re all used to that. Um, so we’re thinking about a a abnormal ICP being somewhere

27 minutes

between 20 or 22, right? Most of the time when we’re talking about trauma, we’re talking about 22. We kind of in other medical pathologies get a little nervous when the ICP is greater than 20.

27 minutes, 10 seconds

I think it’s up for debate. Right?

27 minutes, 11 seconds

Somewhere in the low 20s, your brain is probably not as happy as it would be if your ICP were lower. So, we’re measuring

27 minutes, 18 seconds

in millimeters of mercury. Now, EVDs, they’re simple drains. They’re gravitational drains. Like, when the pressure in the brain is higher than

27 minutes, 25 seconds

whatever you set the chamber that’s collecting the CSF at, then the CSF is going to flow from high pressure to low

27 minutes, 33 seconds

pressure. So, your EVD chamber can be set, it’s leveled to the tragus. It can

27 minutes, 38 seconds

be set at zero, 5, 10, 15, 20. And that’s going to be at least at my

27 minutes, 45 seconds

institution set in centimeters of water because you’re measuring out on a ruler literally in centimeters.

27 minutes, 52 seconds

Yes. Exactly. And so I mean it’s just confusing and like the EVD will have side by side. It will have centimeters of water, millimeters of mercury. And

27 minutes, 59 seconds

there are some shops around the country who who will set their EVD in millimeters of mercury by convention because it’s measuring in centimeters of

28 minutes, 6 seconds

water above the tragus. We mostly are using centimeters of water. Um, and that’s how shunts are that’s how shunts are calibrated, too. So, it’s easier for

28 minutes, 15 seconds

the surgeons to say, “Oh, well, we’ve been draining at 10 centimeters of water. We’re going to set the shunt to four or set the shunt to five or whatever it is.”

28 minutes, 23 seconds

That’s important because when we’re setting the EVD at 10, that’s a pretty nice drainage, right? Like anytime the

28 minutes, 31 seconds

the patient’s you know pressure in the brain is above 10 cm of water which is going to be about 8 mm of mercury it’s

28 minutes, 40 seconds

going to drain from the brain to the chamber which is set at 10 cm. So that’s a draining catheter right like that that that is going to remove CSF for most

28 minutes, 49 seconds

patients because most patients are spending time higher. Even if you set the EVD to 20 cm of water, that is still

28 minutes, 58 seconds

18 mm of mercury. So you are allowing it to be a pop off valve before you’re getting into the danger like the danger zone of ICP.

29 minutes, 8 seconds

Yeah. For for for our listeners, it’s 1.35 um uh centimeters of water for one millimeter of mercury, right? Like I

29 minutes, 17 seconds

always it’s it’s confusing, but I just think about it as like mercury is much denser. So, you know, absolutely. Takes a lot more to move it.

29 minutes, 25 seconds

Totally. And it’s not something that you need to memorize. Like, you can go and look at the EVD catheter and just say, “Oh, 26 years of water, dot dot dot, that’s going to be about 18 millimeters

29 minutes, 33 seconds

of mercury.” And I’ve just done this so often that I know that in my head, but like you don’t have to know that. Um, the important point is is like even said

29 minutes, 40 seconds

at 20, you’re allowing the brain to have some some pop off of CSF before you get to the danger zone.

29 minutes, 48 seconds

The other thing about EBDs is that when they are draining, you are not measuring the pressure. And so we all we all seem

29 minutes, 56 seconds

to think that like this is some sort of continual monitor. It is not. The only time it’s measuring the pressure is when you turn the EVD to off. And when you

30 minutes, 5 seconds

set it to not drain, now all of a sudden it can measure the pressure. But the nurses are only going to do that once an hour. and they’re going to record an a

30 minutes, 13 seconds

an EVD pressure like this was the the whole experience of the patient for that whole hour, which is not true. I mean, the the e that number fluctuates wildly.

30 minutes, 23 seconds

It’s also just important to know that if you walk by the room and the EVD is open, it’s still going to show you a number on the monitor. And just think of that as like a random number generator.

30 minutes, 32 seconds

Like it just it means nothing unless the EVD is closed. Unless you have a very fancy EVD that does the pressure pressure sensing while the drainage like

30 minutes, 41 seconds

something like an Irlow device, but those are expensive and and most of the time people know that they have this special device.

30 minutes, 47 seconds

Yeah, I that’s a really important really important caveat, right? Because I’ve seen people get confused by that many times. Um yeah, it’s uh it’s kind of

30 minutes, 56 seconds

like if it’s not leveled, if you haven’t if you don’t know what position the three-way stock is in, like don’t don’t react to the number.

31 minutes, 3 seconds

Don’t react to the number. And certainly if the EV is open, don’t go move the bed up and down because now we’re just changing where the, you know, the relation of the patient to the drain and

31 minutes, 12 seconds

then we’re going to dump out CSF or we’re going to stop draining CSF. So like right, you know, it’s just important to know the drain.

31 minutes, 19 seconds

It really is more like uh more like a swan gans catheter less less like an art line. Yeah. In that regard. Yes.

31 minutes, 25 seconds

Um which I think is is important.

31 minutes, 31 seconds

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31 minutes, 42 seconds

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32 minutes, 31 seconds

Nick, you’d mentioned this and um this is another area that I found can be um a source of constrnation, debate, what

32 minutes, 39 seconds

have you. But this idea of the relationship between ICP MAP and cerebral profusion pressure and you know

32 minutes, 48 seconds

which number is actually really important. I’m I I would suspect they’re all important in their own way. You know, we’re very very egalitarian here,

32 minutes, 56 seconds

but but yeah, how do you so I guess maybe the first question is what is cerebral profusion pressure? Because we hear that term all the time. And then when you’re sort of globally looking at

33 minutes, 5 seconds

these numbers and looking at a patient with increased intraanial pressure, how do you sort of rank and stack those numbers?

33 minutes, 12 seconds

Yeah, it’s so true. So I I think they’re obviously related, but I think of them separately, right? Your ICP being overly

33 minutes, 21 seconds

elevated for a long time puts you at risk of herniation eventually, and that’s really important. We want to prevent herniation. But the more

33 minutes, 28 seconds

insiduous damage or what’s happening in the background that’s putting you at risk for secondary brain injury is that

33 minutes, 35 seconds

if your ICP is high, it lowers your cerebral profusion pressure. [snorts] And so the relationship between those variables is that your cerebral

33 minutes, 43 seconds

profusion pressure is your mean arterial pressure minus your ICP. So you can imagine if your ICP goes up, you’re diminishing your cerebral profusion

33 minutes, 52 seconds

pressure. And if you don’t get blood to the brain, the brain’s going to get secondary hypoxic brain injury. And so

33 minutes, 59 seconds

the the overall time above the ICP threshold is going to put you at risk for herniation. Too much stuff in the box, stuff explodes out of the box. But

34 minutes, 9 seconds

the s I think the more insiduous and the bad thing that we’re trying to prevent is blood doesn’t get to the tissue because the pressure is high. And then

34 minutes, 17 seconds

even if you don’t herniate, you can still have bad eskeemic brain injury and that’s going to really impact your recovery. So we are egal egalitarian.

34 minutes, 27 seconds

They do all matter. They just matter in different ways. Um and certainly the ICP, you know, leading to herniation or

34 minutes, 35 seconds

to secondary brain injury, like it’s related, but I’m thinking about treating them in different ways. And specifically, you’re thinking about

34 minutes, 42 seconds

things like does this person need vasopressors or some other therapy like instead of trying to lower the ICP, raise the MAP instead to try to optimize,

34 minutes, 50 seconds

right? And there are some people who as you raise their MAP they’ll actually decrease their um their ICP because the

34 minutes, 58 seconds

brain gets the cerebral profusion it’s so desperately wanted that then all of a sudden it can sort of stop existing in

35 minutes, 6 seconds

this profound vasoddilation you know like phase and and so in some patients and again this is where it gets really confusing and you have to go to the

35 minutes, 14 seconds

bedside some patients like if you increase their MAP that just directly increases their ICP because putting more

35 minutes, 20 seconds

blood into the into the skull. And then there are some patients who they’re maximally like cerebrovascular dilation.

35 minutes, 28 seconds

And if you actually raise their map, they actually are able to vasoc constrict a little bit more because their their tissue is getting the oxygen

35 minutes, 36 seconds

at once. And then that lowers their ICP, which is like counterintuitive. Funky.

35 minutes, 44 seconds

Yeah, it’s very funky. And it’s one of those things that like I remember as a student just being like, I don’t understand that. that like that can’t happen and you just have to go to the

35 minutes, 52 seconds

bedside and we we often will give them like a little vaso pressure challenge like are you someone where we raise your blood pressure and that raises your ICP

35 minutes, 59 seconds

or you’re someone if we give you the blood pressure you need does that actually ultimately lower your ICP. So it’s really cool

36 minutes, 6 seconds

and just to put numbers to this like we’re talking like a map of 75 for example as opposed to like 65 or or what what numbers would you go up to even?

36 minutes, 14 seconds

Yeah, that’s a great question.

36 minutes, 16 seconds

Especially and especially when people don’t have an ICP monitor, right? Like we have the luxury a lot of the time of having these ICP monitors, but if you’re

36 minutes, 24 seconds

not working in a trauma ICU, like not everyone’s going to end up with an ICP monitor. So, we have patients who have like large intra cerebral hemorrhages or

36 minutes, 32 seconds

large malignant MCA strokes. They have high ICPS, but we me we don’t necessarily have a monitor for that. And

36 minutes, 40 seconds

sometimes we have to fly by like those patients need intubation. And that’s why I I kind of keep in my mind like, oh, if I’m having to intubate somebody because

36 minutes, 49 seconds

I think that there’s an ICP problem, right? Like let’s say it’s an intra cerebral hemorrhage. If I’m intubating them, it’s probably because I think that there’s some compression on the

36 minutes, 57 seconds

reticular activating system. They’re herniating, right? That probably means that their ICP is somewhere over the range of 20.

37 minutes, 6 seconds

We want to keep their profusion pressure, their cerebral profusion pressure definitely over 50, ideally over 60. So when I’m intubating that

37 minutes, 15 seconds

patient, I’m actually really thinking we cannot drop this blood pressure. The blood pressure needs to be not too high.

37 minutes, 21 seconds

We don’t want to make the IC uh ICH worse, but we actually really do want to keep someone’s map like 75 80 um so that

37 minutes, 29 seconds

they get that that profusion pressure they really need. We know somewhere between 50 and 70 is kind of the sweet spot. Definitely lower than 50 you’re

37 minutes, 36 seconds

risking eskeeia. And to kind of give myself a buffer, I I mostly tell critical care teams, let’s aim for a CPP of 60. So that so we have like uh some some buffer with a their elevated ICP.

37 minutes, 49 seconds

So that usually requires having a map of 7580.

37 minutes, 52 seconds

I think that’s a great point. I mean, usually we’re telling our listeners, you know, that uh in general lower is the same as higher with blood pressure

38 minutes

targets like in sepsis and things like that. This is not sepsis. This is a very different paradigm, right? This is the situation where like 60 is not the same

38 minutes, 8 seconds

as 65 and 65 may not be enough. You may need 75 or 80. So, very different physiology.

38 minutes, 15 seconds

It’s really important. The brain really wants like good profusion. And I I I like the way that you sort of describe that too because if you’re approaching

38 minutes, 23 seconds

this with a CPP ccentric kind of uh viewpoint or from from that vantage point, then you may miss the fact that

38 minutes, 30 seconds

like okay, sure you can drive the map up and and let’s say you’re not monitoring the ICP like you aren’t able to for whatever reason, but you know, just

38 minutes, 38 seconds

because the CPP is in the box, it doesn’t mean that you’re um you’re in the clear. you could still be dealing

38 minutes, 46 seconds

with problems related to that increased ICP even with a reassuring CPP.

38 minutes, 52 seconds

Yeah, I think so. I mean, we’d absolutely see the times where we we have optimized their CPP. Their CPP is fine, but their ICP is still 40. And I

39 minutes, 1 second

mean, that’s going to activate that Cusheen’s triad, right? Like all of a sudden, you’re really hypertensive, but your pressure is still really high. So

39 minutes, 8 seconds

even if the CPP number is fine, hanging out with an ICP of 50 is not acceptable. Right?

39 minutes, 15 seconds

Um right one one other sort of pearl to leave people with is I think we all memorize the Cusheen triad as sort of

39 minutes, 22 seconds

hypertensive bradaartic agonal respirations. One we never see the agonal respirations because these patients are all intubated right so we

39 minutes, 29 seconds

we control their agonal respirations. If you put them on pressure control, you might see them take gigantic agonal breasts, but most of the time they’re sedated enough they’re on some sort of volume assisted control method. Right?

39 minutes, 40 seconds

The other thing is that the brada cardia is sort of a late finding.

39 minutes, 45 seconds

Very frequently when we think about when does most blood get delivered to the brain, most of that that flow that profusion is going to happen incally.

39 minutes, 57 seconds

So when a patient has a really high ICP, that’s actually going to impede their diastolic flow, right? Because the the

40 minutes, 4 seconds

pressure the ICP is so high that that your diastolic flow or your diastolic pressure may sort of get to almost the same as your ICP.

40 minutes, 15 seconds

It’s probably still a little bit higher, but it it could be more approximate.

40 minutes, 18 seconds

Therefore, even more flow is happening in cy. The brain really really relies on that systolic profusion. So how does

40 minutes, 27 seconds

your how does your brain get more time in cy? It becomes teacartic. And so I will tell you having done this like day in and day out all the time the patients

40 minutes, 35 seconds

who are herniating are teacartic. When I walk in around the unit and I see somebody who’s hypertensive and teacartic to me that is like a brain

40 minutes, 43 seconds

that’s really stressed and I will see you know we want to make the numbers pretty. So I will see people reflexively give beta blockers like please don’t do

40 minutes, 51 seconds

that. That is like the brain like the brain’s asking for more profusion. is asking to have more time incally that’s a brain that’s stressed and and they

40 minutes, 59 seconds

certainly need hyperresolar therapy. We can talk next about the sedation and paralyzing and cooling them but to me that teoc cardia is really like a that’s a that’s a red flag warning situation.

41 minutes, 10 seconds

Bradic cardia is going to be a really late finding after they’ve herniated.

41 minutes, 13 seconds

Well, I was going to say so like most of these sort of classic descriptions in medicine you know this was in the era

41 minutes, 20 seconds

long before CT scanners and things like that. So this was like a an observation of people who had herniated, right? Like

41 minutes, 28 seconds

you don’t want to be waiting for Cushing’s triad to determine this person has ICP. That that means, you know, you missed your chance.

41 minutes, 35 seconds

That chip has failed. Yes. And I I really do think that’s so important because I do see people want to like reflexively normalize that number. And and again,

41 minutes, 43 seconds

like the way to normalize that number is not with beta blockers, it’s with controlling the ICP.

41 minutes, 48 seconds

Excellent. So yeah, I’m I’m really glad we covered all of that and sort of like added the foundational uh elements to this discussion. What are we looking at?

41 minutes, 58 seconds

How do we make these measurements? Why do we care about these numbers? So maybe getting back to um the original question

42 minutes, 6 seconds

from several days ago, which was, you know, how do we

42 minutes, 9 seconds

[laughter]

42 minutes, 9 seconds

um how do we No, I mean I say that tongue-in-cheekly because this was like I’m really glad we did this. I think we needed to do it this way. But um you

42 minutes, 17 seconds

know we we talked uh the question at hand was like okay so um this person’s ICP is elevated they need a neurosurgeon

42 minutes, 25 seconds

got it in the interim or or you know what you had said you know maybe post-operatively how do we approach the management of

42 minutes, 33 seconds

their ICP to the extent that we can do it medically. We talked about head position and bed position. We talked about um sea collars. We don’t want them

42 minutes, 41 seconds

tied like a neck tie. Um, you know, there’s I think sort of like, uh, the one other thing I’ll throw out there, um, which is, I think, become a little

42 minutes, 49 seconds

bit more of a myth now is the, um, central line in the neck, you know, avoiding that. I don’t I don’t know that we have to go through, um, you know, a

42 minutes, 57 seconds

bunch of hoops to avoid that. Maybe you can correct me if I’m wrong. What are your thoughts on that? Yeah.

43 minutes, 1 second

Yeah. It’s it’s really it’s awesome. um one of my colleagues like here at Emery like we really wanted to debunk this myth and we have so many subactoid

43 minutes, 9 seconds

hemorrhage patients who have central lines central lines sometimes in the subclavian in the J in the FIM like lots of subclavians lots of ICP monitoring

43 minutes, 17 seconds

and so they went through and they looked at it and they looked at all the ICP data around the timing of central line placement and it made no difference if

43 minutes, 25 seconds

you had a pick if you had an if you had a subclavian if you have ephemeral there was no impact whatsoever to your ICP And

43 minutes, 33 seconds

so put in what’sever safest like do do what you know how to do. We have really moved away from subclavians just because we had more complications with them and

43 minutes, 40 seconds

it didn’t seem to be protecting their their ICP in any meaningful way. Awesome.

43 minutes, 45 seconds

Excellent. I love busting a good myth and that that is a good myth that to to let go. Excellent.

43 minutes, 51 seconds

So we talked about the mechanical stuff then maybe we could take the next step and and get into the nitty-gritty on the medications.

43 minutes, 58 seconds

Yeah, totally. I mean really like we talked about the cornerstone of of managing brain edema is going to be your hyperresolar therapy mostly going to be

44 minutes, 6 seconds

your 23% sometimes manitol it really is center specific you’re trying to to to

44 minutes, 13 seconds

find a reason to give it and so for patients who have ICP monitors that usually can just be an elevated ICP for the patients who have like they have

44 minutes, 22 seconds

large strokes or for whatever reason they don’t have an ICP monitor you’re really looking for clinical radiographic evidence of you know midline shift of

44 minutes, 31 seconds

transenterial herniation of sleepiness as your sort of clinical guidance of like I should give hypermolar therapy I should push their sodium like we said

44 minutes, 39 seconds

it’s not the number it’s really how often you’re giving the doses but even still sometimes that just like you can

44 minutes, 47 seconds

you can make the patient salty as can be right the patient can be sodium of 155 I tend not to get to 160 because that’s just really going to make you

44 minutes, 55 seconds

hyperchlormic and your kidneys are not going to love that so Um, but let’s say your sodium is 155 and the ICP is still sitting there saying 28 28 32. You’ve checked in everything.

45 minutes, 6 seconds

It’s a good waveform. Now, we got to get into tiers where there is not great evidence to guide what you’re doing next. And it is a little bit of clinical

45 minutes, 14 seconds

gestalt and this physiologically makes sense. But the next steps are going to be we want to decrease the amount of metabolic energy that the brain needs.

45 minutes, 24 seconds

Because if you decrease the amount of metabolic energy the brain needs, you’re gonna simultaneously decrease how much arterial blood volume it’s going to

45 minutes, 32 seconds

require, right? And so there are a couple ways that we do that. First and foremost, you can deeply sedate somebody, right? Like so you’ll see a

45 minutes, 39 seconds

lot of these like ICP crisis patients, they end up on whopping doses of mazzlim. usually mazzel because it’s going to be a dayong week-long crisis

45 minutes, 48 seconds

and propall for that long just gets you into trouble and hemodynamically it’s not going to protect your CBP as well.

45 minutes, 55 seconds

Um so most of them are getting mazzlim.

45 minutes, 58 seconds

Propal does the same thing. They’re both sort of going to decrease the metabolic demand. They’re going to decrease how much blood arterial blood volume your

46 minutes, 5 seconds

brain needs. So that’s good. Um fentinyl really important. Infinel is a great drug for like controlling people’s

46 minutes, 12 seconds

agitation and if you’re agitated your ICP is going to spike. Beyond that, I do not see a reason for people to need to

46 minutes, 19 seconds

be on like 300 of fentanyl an hour. Like that to me is just creating opiate addiction. And so I am very rigorous about like when I round with the trauma

46 minutes, 28 seconds

team getting people down to like you know if they’re sedated out of their mind like I don’t think they need any fentanyl. Like if they are uncomfortable

46 minutes, 36 seconds

with the breathing tube, sure let’s get them comfortable on fentanyl so they don’t bite the tube but it is not it is not doing the same thing for your brain

46 minutes, 45 seconds

like just like the way that gabaurgic drugs like mazzlm and propal decrease your metabolic demand. So stop the 300 400 of fentanyl like not needed.

46 minutes, 54 seconds

Um so so again so that’s going to be decrease your cerebral metabolic demand.

46 minutes, 59 seconds

The other way that we think that this gets done is is by lowering your temperature, right? There’s good animal

47 minutes, 6 seconds

data for like low temperature like lowers your cerebral metabolic demand, preserves brain function. I don’t know.

47 minutes, 13 seconds

TTM one and two keep debunking this. I’m not really sure how good a treatment this is for like cerebral protection or

47 minutes, 20 seconds

ICP management. I will tell you personally, I do not see a lot of bang for my buck. and I have like really moved to just like very mild hypothermia

47 minutes, 29 seconds

that’s mostly just aimed at fever prevention. So trying like yeah this is it’s it’s fascinating because there’s there’s great

47 minutes, 37 seconds

physiologic measurements that tell us for every degree Celsius your temperature goes up your oxygen consumption goes up by like 15%. So

47 minutes, 43 seconds

running a high fever makes you much more makes you consume much more oxygen. Your V2 is much higher. But when we start

47 minutes, 51 seconds

extrapolating that in the other direction and we say like dropping your temperature will reduce it by this much.

47 minutes, 56 seconds

That might or might not be true. But I I don’t know. I mean it’s it’s funny because great physiology with canines

48 minutes, 3 seconds

and pigs that has not turned into robust survival data in good human trials.

48 minutes, 8 seconds

Yeah. Yeah. Yeah, I mean I think this really is one of the things where especially if lowering the temperature then ends up the patient is just shivering out of their mind that’s going

48 minutes, 17 seconds

to increase their metabolic demand that is undoing the good physiology that may or may not be accomplished by fever prevention. So I I really do not let

48 minutes, 26 seconds

people who have ICP crisis be febriel until there is like better data to support like you know that fever

48 minutes, 33 seconds

prevention does nothing. But short of fever retention, I have really moved away from like deeply uh cooling people.

48 minutes, 40 seconds

People in my group will still go down to 33 for ICD crisis. Like I just I just can’t convince myself that that the

48 minutes, 47 seconds

potential harm of that and the certainly the shivering complications and all the meds and the bear huggers and everything else we’re going to need to prevent their shivering is really worth it from

48 minutes, 56 seconds

the ICP standpoint. that sort of again I I will say it does seem like sometimes if your goal is to keep people under 37.5 Celsius you actually have to do a lot of stuff to do that.

49 minutes, 7 seconds

So I mean it doesn’t mean it doesn’t mean like this isn’t ICU nihilism. It doesn’t mean we’re not controlling their temperature.

49 minutes, 12 seconds

It just means that we’re using a bear hugger or we’re using uh Arctic Sun or we’re using whatever thing we’re using aggressively but with a different goal.

49 minutes, 22 seconds

Yeah, totally. And I I truly am. When people are at ICP crisis like they spike one temperature and I am very much like we are putting the arctic sun on we are

49 minutes, 29 seconds

studying normotheria if they start to shiver they need counter warming with the bear hugger you can put them on bpar demoral or whatever it is like I don’t care I don’t find them either any one to

49 minutes, 38 seconds

be more effective than the other the things that really work is is fentinel and propal and precedex

49 minutes, 45 seconds

um but fever yeah fever prevention is a real thing and it takes work um so again theoretically lowers the cerebral

49 minutes, 52 seconds

metabolic demand I will personally say I’m like sort of indifferent but fever prevention probably is still important.

49 minutes, 58 seconds

So those are sort of two lower your cerebral metabolic demand. The third thing is paralysis which just like releases any intraabdominal intramuscular intrathoracic pressure.

50 minutes, 9 seconds

Right? We’re trying to do anything that we can to promote Venus return work sometimes. There’s some people who

50 minutes, 17 seconds

are like really they like you give them a dose of racharonium and all of a sudden their ICP goes from like 34 to 22 and you’re like that that was very

50 minutes, 25 seconds

effective. And there’s some people who I find that paralytics or paralytics really don’t do much for at all. So I I

50 minutes, 33 seconds

don’t really I can’t predict who physiologically is going to respond to paralytics.

50 minutes, 39 seconds

I think, you know, like long-term paralytics are extremely detrimental to the long-term recovery and physiologically like that is not a

50 minutes, 47 seconds

normal thing to do to people. So, when I’m, you know, turning to paralytics, I really try to use them in the shortest duration as possible. I aim for a train

50 minutes, 56 seconds

of four of two out of four. I do not think that there’s any lit literature that suggests that zero out of four is more effective. And then we try to get them off as soon as possible. And so for

51 minutes, 5 seconds

me that’s like can we can we paralyze them to get them to the O? Can we paralyze them to do some other intervention that we think is going to

51 minutes, 11 seconds

have a longer term impact on their ICP because days and days of paralysis like that’s just really leading to muscle

51 minutes, 19 seconds

atrophy and a really long recovery if the person survives.

51 minutes, 23 seconds

Totally agree. I think the b the bolus rockuronium is a better strategy in most of these people than starting that long acting cyatricium infusion because it

51 minutes, 32 seconds

just stays on. You know, people if you have to decide every time to rebolish something, that’s a different sort of

51 minutes, 39 seconds

approach than like deciding to take off something that you might think is protective. And so, yeah, totally agree. Like I love it.

51 minutes, 46 seconds

More than more than 48 hours of paralytics is clearly bad and and even is even that much necessary in some cases.

51 minutes, 54 seconds

Yeah, I mean I really I I could not agree more. We are on the same page.

51 minutes, 59 seconds

Nice. So before we before we move on I think getting back to the hyperosmolar therapies we’ve talked about. So manitol

52 minutes, 7 seconds

you talked about you know 23% uh the the bullet is often what I’ve heard heard it referred to that that

52 minutes, 14 seconds

it’s like a you know not all of us can order it. I think it’s actually given like you have to have special credentiing to be able to to request it.

52 minutes, 22 seconds

There’s also, you know, 3% 7% so other kind of um concentrations of sodium

52 minutes, 29 seconds

chloride. I guess what are your thoughts on on those alternatives? You’ve mentioned manitol several times. I feel like your camp manitol.

52 minutes, 38 seconds

So, so funny. No, I actually, you know, it’s so funny where I was a resident um we were a neurologist and so training all the neurology residents to play

52 minutes, 47 seconds

central lines for their like one month in the neur ICU just was not a good use of people’s time. Um, and there was like, you know, like a bias against PICSS, which may or may not be founded.

52 minutes, 57 seconds

But either way, because we did not have central lines in all of our patients, we use a lot of manitol because manitol can be given peripherally. You have to filter the line. You have to make sure

53 minutes, 6 seconds

it’s not crystallizing. But it’s a good drug. The problem with manitol is you’re going to use the osmolar gap to guide your treatment if you’re giving repeat bololises of it.

53 minutes, 16 seconds

And that’s just a lot of math to do. And so if you’re in a unit that doesn’t use a lot of manitol and is not used to calculating like the osmoler gap which

53 minutes, 24 seconds

can be done by the nurses like I mean you can you can definitely automate this if you’re somewhere that does manl all the time. Um so we were a a unit that

53 minutes, 33 seconds

used manitol. When I came to Emery, it’s totally different philosophy. It’s an Arun service and so they are all credentialed to play central lines and

53 minutes, 42 seconds

so a lot of people had central lines which you can give 23% through. For most places um you can only run up to 3%

53 minutes, 50 seconds

through a peripheral line. So 7% or higher, you’re going to need a central access um because of the extravisation risk from there’s good safety data that

53 minutes, 59 seconds

like a one-time dose of 23% through a wellplaced peripheral IV has not had a lot of complications. But again, most most institutions are going to like put their foot down and not let you do that.

54 minutes, 10 seconds

Um either way, I came here, everyone uses salt and so now I’ve become very accustomed to like thinking in salt and everyone gets salted for like their

54 minutes, 18 seconds

osmolar, you know, gradient. It’s way easier because you’re just looking at the sodium level.

54 minutes, 23 seconds

The reflective coefficient of salt is a little bit higher than manitol and there is a phys theoretical I don’t think I’ve

54 minutes, 30 seconds

really ever seen this of like manitol rebound which can make the cerebral edema worse and more of a withdrawal. I don’t know. I think use what you have use what your unit’s comfortable with.

54 minutes, 40 seconds

Both of them are going to dehydrate the brain to the same amount. Obviously, giving someone a really salty meal is not going to be good if you’re in decompensated heart failure, but you can

54 minutes, 49 seconds

diabetes people. It’s not the end of the world. Um, and then manitol, obviously, it works because um it raises the

54 minutes, 56 seconds

osmoler gap or your gradient pulls fluid out, but then you have to pee it out.

55 minutes

So, if you’re someone who’s got renal failure, you don’t pee out the manitol and then that’s the end of that. That didn’t work very well. Um, so again, I

55 minutes, 7 seconds

think I think you can be smart about what you pick for which patients, but at the end of the day, I think it really is unit comfort and like what the what the

55 minutes, 16 seconds

culture is. I am not really convinced that physiologically there’s a huge difference between them.

55 minutes, 23 seconds

That’s super helpful. And I think it’s also really good that you mentioned, you know, the specifics about um 23%

55 minutes, 31 seconds

maybe could get away with like a crash dose in a peripheral. 3% safe to give peripherally. I think we feel all pretty

55 minutes, 38 seconds

good about that. We’ve debunked that several times on the show, but yeah, I think that’s it’s helpful to know like go with what your institution knows.

55 minutes, 46 seconds

Recognize that you’re probably not the only person taking care of this patient for the duration of their illness. So, if you’re kind of, you know, flipping back and forth between team members that

55 minutes, 55 seconds

maybe are are not comfortable with this method or that method, it’s like we talked about on our APRV episode, if you’re the APRV guy and you’re the only

56 minutes, 2 seconds

APRV guy, you’re going to have a hard time making that work. So, yeah, all all great stuff.

56 minutes, 8 seconds

What I’m taking away from this is uh Matitol versus 23% is like a Coke Pepsi thing. There’s there’s personal preference, but yeah, I I’ll also just say that

56 minutes, 17 seconds

listeners of this podcast, come on guys, you should know the formula. Twice the sodium plus glucose divided by 18 plus

56 minutes, 25 seconds

ura divided by 2.8. Unless you’re not in the US and then it’s totally different.

56 minutes, 30 seconds

Um we have a calculator on our website like you guys can calculate plasma aoms. You can do it. Yep. It does take time.

56 minutes, 37 seconds

You can do it. Um, again though, it just has to be like the whole unit is going to commit to like we’re doing the math, right? It’s easy. It really is not hard, but you have to like commit to it.

56 minutes, 47 seconds

And and by the way, like if you take your critical care boards, like there’s like a bazillion questions where you have to calculate the osmoler gap. So

56 minutes, 54 seconds

just just get comfortable doing it. It’s okay.

56 minutes, 56 seconds

There’s like there’s like one or two, but [laughter] I think like every question it’s there’s is an osmoler gap calculation. It’s hilarious.

57 minutes, 4 seconds

I love it. I love it so much. Um, yeah.

57 minutes, 6 seconds

So you can all learn to do this. You can do hard things like that. [snorts] All right. All right. Hard things.

57 minutes, 12 seconds

Yeah. All right. Well, uh let’s let’s do a different hard thing. Let’s let’s do another case. Yes.

57 minutes, 17 seconds

Um this is a this is a 72year-old with a history of atrial fibrillation who develops aphasia and right hemiplegia 70 minutes before arrival at your hospital.

57 minutes, 26 seconds

Uh the NIH stroke score is high. I don’t know. I could make up a number. 20. Uh

57 minutes, 33 seconds

CT shows no hemorrhage. the CTA shows a left M1 occlusion. So, how do you kind of walk us through your approach to this case?

57 minutes, 41 seconds

Yeah, I think this is great. Um, it used to be that like there was so much nhilism in stroke and I think that still somewhat persist in IC, but in eskeemic

57 minutes, 50 seconds

stroke we can we could do a lot to like to help this patient have a good outcome. Um, so I mean the first branch point was you know does the CT shows

57 minutes, 58 seconds

show hemorrhage or does it show no hemorrhage, right? Like that’s really important because clinically you really can’t make a determination when someone has like hemiparasis and you know a

58 minutes, 6 seconds

stroke syndrome looking at them. You know I sort of get an idea if someone’s extremely hypertensive and they’re vomiting like that’s probably going to

58 minutes, 13 seconds

be an other really reliable data. So we have to see you know is the head CT clean or is the head CT with a bleed. So now

58 minutes, 21 seconds

we’ve said this guy does not have a bleed. He’s got an M1 occlusion. So now he’s a we’re going to put him into the category of large vessel stroke. All

58 minutes, 29 seconds

right. And so the next thing that we sort of need to determine is we used to operate in this time window of his cute eskeemic stroke, right? We we’ve really

58 minutes, 37 seconds

like proceverated on like the time since lasting well. That is still going to be important. You’re still going to ask whoever’s presenting to you when were

58 minutes, 44 seconds

they last seen well. But we have really moved in the like world of es schemic stroke to sort of a tissuebased clock, right? So people can progress really

58 minutes, 53 seconds

rapidly and and complete their stroke very fast if they are someone who does not have a lot of collaterals. And then there are people who you know 24 hours

59 minutes, 3 seconds

out still have tissue to save. And so those patients are totally different and lasting well is important but we really

59 minutes, 11 seconds

have moved away from that and we’re really working now with a tissue clock.

59 minutes, 15 seconds

Right? So the way that we’re going to see that um or the way that we used to see this a lot is with CT profusion. So

59 minutes, 22 seconds

all the trials in the stroke literature that have been done in the last like really 10 year well almost 10 years eight years since like the major LVO

59 minutes, 29 seconds

trials of uh 2018 all use CTP which is like a profusion based imaging to see is their prenumbra which is like the tissue

59 minutes, 38 seconds

to save versus core infarked the tissue that’s already been infarked it.

59 minutes, 44 seconds

That’s how we got to establish that if you had tissue to spare, you would benefit from throbectomy if you had a large vessel occlusion. Right?

59 minutes, 54 seconds

It it took us a long time to get there in the acute eskeemic stroke world. But we did we got there by using the CT profusion paradigm of tissue to save.

1 hour, 3 seconds

Now we have noticed that like basically like if you are within 24 hours and you have an LVO and you’ve got any amount of

1 hour, 10 seconds

tissue to save then you’re probably going to benefit for throbectomy. So I feel like we’re now like the cardiologists were like if there’s a STEMI you go to the Kath lab. Now we’re

1 hour, 19 seconds

like if there’s an LVO you go for reprofusion.

1 hour, 22 seconds

Um it took us a long time to get there and we had to sort of demonstrate efficacy in a very subselected patients and then trial after trial after trial

1 hour, 30 seconds

has expanded on that. So now unless you have like a completely blitzed out totally eskeemic CT scan, you’re

1 hour, 39 seconds

probably going to go if you have an LVO, you’re probably going to go for a throctomy.

1 hour, 45 seconds

And and I think probably some of that reflects a a different understanding like you as you said this this um transition from a last seen well clock

1 hour, 52 seconds

to a viable tissue to save clock. But some of it’s also probably just that we’re better with interventions, right?

1 hour, 58 seconds

Like the technology for being able to go in there and do throctomies is both more effective and safer. So the calculus has shifted towards do more.

1 hour, 1 minute, 6 seconds

Yes, absolutely. I mean we used to get just like all this hemorrhagic reprofusion. We would scrape the vessels, they would get injured. That’s not good for tissue recovery and now we

1 hour, 1 minute, 15 seconds

don’t. So I mean truly this was paradigm shifting from both the technology and the mechanics of it to also just like the we got better at patient selection.

1 hour, 1 minute, 25 seconds

I think the other important thing to double click on there is that getting this done really requires that you’re at a center that can get this done. So the

1 hour, 1 minute, 33 seconds

importance of moving patients expeditiously to centers where they have that interventional capability has become more important over the last decade or so.

1 hour, 1 minute, 41 seconds

Oh my gosh. So much so like stroke stroke centers of care and that like whole network that it took to expand to get people from you know from their

1 hour, 1 minute, 49 seconds

spoke to the hub like I mean that was took massive coordination and we have over the last decade gotten a lot better at it. there’s still like room to go.

1 hour, 1 minute, 58 seconds

Like I mean it it’s really unfortunate that if you live in a rural center and you happen to have your stroke when it’s a bad no helicopter day like you’re

1 hour, 2 minutes, 8 seconds

going to have a way worse outcome than if you had your stroke on a clear sky day. Like that’s unfortunate but that is still sort of the the inequities of like

1 hour, 2 minutes, 17 seconds

living far from a reaper fusion capable hospital.

1 hour, 2 minutes, 23 seconds

So this is very exciting. Of course, it’s like um you know the idea that we could maybe do more for more people than we

1 hour, 2 minutes, 31 seconds

used to think. But Casey, so now that we we may have more uh more folks who are eligible for neurointervention,

1 hour, 2 minutes, 40 seconds

where does that leave us as far as systemic thrombolyis and sort of the interplay between systemic thrombolyis

1 hour, 2 minutes, 47 seconds

and going after these LVOs? Um help me understand what to do and when to do it.

1 hour, 2 minutes, 53 seconds

Yeah, I think it’s it’s a really important question. Um I think the patient walks in to a throbectomy capable center. Throbectomy is going to be like way more important than the TNK.

1 hour, 3 minutes, 4 seconds

Now we’ve moved from alt place to TNK and the vast majority of centers. TNK is like a onetime push. It’s very easy to get. Like TPA was such a nightmare to

1 hour, 3 minutes, 13 seconds

give. Um you had to get the pharmacist down there to mix it and they had to give the bolus and the drip and there was math involved. Whatever. Um TK it’s

1 hour, 3 minutes, 21 seconds

just a onetime push. So most of the time like I work in obviously a throbectomy capable center if the patient comes in within that typical three to four and a

1 hour, 3 minutes, 30 seconds

half hours lasting well and they’re like TNK eligible as long as it’s not going to slow down them getting to the angio

1 hour, 3 minutes, 37 seconds

suite they’ll still get the TNK and maybe that’s helping with sort of breaking up the sort of smaller things that get wedged into distal ca like distal arteries that we can’t go after

1 hour, 3 minutes, 45 seconds

with the catheter. So there is still the trend to give that. If you’re at a non-throbectomy capable center, then it

1 hour, 3 minutes, 53 seconds

definitely is important to give it, right? Like you want that TNK to be working as the patient’s transfer. So that’s called drip and shift. So we’re not dripping anymore because it’s mostly

1 hour, 4 minutes, 2 seconds

not out of place. It’s going to be just a push and push and shift.

1 hour, 4 minutes, 5 seconds

Push and shove doesn’t sound quite as good. So [laughter] no, drip and shift sounds nice. Push it push uh and shove sounds less nice. But

1 hour, 4 minutes, 12 seconds

yes, that is the idea. like you give them their their push of TNK and then you get them to the throctomy center.

1 hour, 4 minutes, 19 seconds

the the real interesting thing in the sort of thrombolyis literature has been can we expand the like the clock for TNK

1 hour, 4 minutes, 26 seconds

eligibility right a lot of people have their stroke in the middle of the night and that precludes them from this you

1 hour, 4 minutes, 34 seconds

know TNK eligibility because most of the time they’re not lasting well within 3 hours and so there were some like wakeup trials that basically showed in those

1 hour, 4 minutes, 43 seconds

those selected patients where there was you know there was a prenumbra and there was a smaller core there’s tissue to spare. Those patients who are wake up

1 hour, 4 minutes, 52 seconds

strokes can still benefit from TNK. Now, to do that, you need to be in a in a profusion capable center. Not all CTS

1 hour, 4 minutes, 59 seconds

have profusion capabilities. And so, again, if you’re in a small rural hospital, that’s going to be a little bit harder for you to get that CT

1 hour, 5 minutes, 6 seconds

profusion to determine that that, you know, the patient who woke up with their stroke is eligible for TNK in that extended window up to nine hours. And

1 hour, 5 minutes, 14 seconds

and let’s actually let’s actually back up and talk about the CT a little here because I think there’s some important important things to double click on. So when you’re ordering this, you’re

1 hour, 5 minutes, 21 seconds

ordering a non-contrast head CT. You’re ordering a contrasted CT of the head and the neck. And you’re order CT angiogram.

1 hour, 5 minutes, 30 seconds

CT and Right. And then you’re ordering um a CT profusion scan. Yes. And just to be clear, the Go ahead.

1 hour, 5 minutes, 38 seconds

Oh, no. I was going to say if you if you happen to get the let’s say you get a CT and a CTA and then you decide later you want the CTP that’s really unfortunate

1 hour, 5 minutes, 46 seconds

because now the contrast has already been exposed in their body and you can’t get a CTP anymore. So you if you’re going to do it you have to order it

1 hour, 5 minutes, 54 seconds

before the CT angiogram gets given because it it’s going to track the contrast. So you need a a good contrast naive patient to get a CT profusion.

1 hour, 6 minutes, 3 seconds

Again I’m going to say yes and no because you know we like fancy technology. we have the capabilities of doing this. Um we get a lot of CT

1 hour, 6 minutes, 11 seconds

profusions. The the field though has really moved away from CT profusion now that there has been so much evidence

1 hour, 6 minutes, 20 seconds

showing that basically you can look at the plain non-conct CT and make a decision of like how much eskeemic damage has been done using what’s called

1 hour, 6 minutes, 29 seconds

the aspects score, right? Um, so that’s that’s I don’t know if we want to get so much into the weeds, but

1 hour, 6 minutes, 37 seconds

basically, you know, you can look at the the CT scan. Seeing seeing early eskeemic changes is hard. Like you have

1 hour, 6 minutes, 44 seconds

to you have to window the CT scan correctly. You have to know what you’re looking for. It is subtle, right? If you just open a head CT and you’re just

1 hour, 6 minutes, 52 seconds

scrolling through like you would for any other normal head CT, it’s going to be very easy to miss early eskeemic changes. you don’t see that CT that that

1 hour, 7 minutes

stroke really develop for 24 hours. If you window it correctly, if you know what you’re looking for, you can see that early eskeemic changes. And that’s

1 hour, 7 minutes, 8 seconds

how people get an aspect score is they’re they’re having a sort of neuroraiology focus on detracting where

1 hour, 7 minutes, 15 seconds

there’s early eskeemic changes. The score goes from 1 to 10. 10 looks perfect. Zero looks like you’ve had a complete MCA territory infar.

1 hour, 7 minutes, 25 seconds

Basically, if you have tissue to save, if your if your aspect score is greater than three, you’re probably still going to go to to throctomy.

1 hour, 7 minutes, 35 seconds

So, again, it’s easier to use a CTP because it’s like it’s like little color map. It’ll bring up like here is the core, here is

1 hour, 7 minutes, 43 seconds

the profusion, like red, bad, blue, good. Yeah.

1 hour, 7 minutes, 47 seconds

Exactly. Like it’s way easier than trying to like detailedly scan. But there has been a focus of the stroke world of like hey we really want to

1 hour, 7 minutes, 54 seconds

increase access and not everyone can do a CTP and like we we need to make decisions of who is going to benefit from transfer and the best way to do

1 hour, 8 minutes, 3 seconds

that is just to to kind of look at you know their their plain noncon headct. So yes, where I am practicing, we often get

1 hour, 8 minutes, 10 seconds

a CT, just non-contrasted head CT, a CT angagram head and neck. That’s going to help you look for the large vessel occlusion as well as sort of help you

1 hour, 8 minutes, 18 seconds

identify the ideology of the stroke. And then often we’re getting the CTP, but if you don’t work in a CTP capable center

1 hour, 8 minutes, 25 seconds

and you’re not trying to do, you know, delayed indication for TNK, it’s all good. You can you can make a lot of acute stroke decisions just with a plain noncon.

1 hour, 8 minutes, 35 seconds

And and sometimes you can even see like the MCA dot sign like you can you can identify that without even before you even give the contrast you have a sense of what it’s going to show.

1 hour, 8 minutes, 44 seconds

Yeah. Exactly. So I think I I think again you work with the resources you got. That’s great practical practical advice.

1 hour, 8 minutes, 52 seconds

And yeah, I think the the rest of our talk is I think going to be a little quicker now that we’ve laid a great framework because I think a lot of this

1 hour, 9 minutes, 1 second

does does kind of throw back at least foundationally to some of the things we talked about in the first hour. Totally.

1 hour, 9 minutes, 7 seconds

Which is great. So, so great conversation so far uh regarding this patient and how you know we are going to manage them, what we’re going to look at

1 hour, 9 minutes, 15 seconds

um you know the conversation of TNK managing that LVO invasively but what about you know for the for the ICU team

1 hour, 9 minutes, 23 seconds

that’s actually going to be caring for this patient potentially pre and post intervention what do they need to be thinking about in terms of things like I

1 hour, 9 minutes, 31 seconds

don’t know blood pressure management, glucose management, uh those other things that are really going to help ensure a good outcome and then I don’t know if there’s anything that you’d want

1 hour, 9 minutes, 39 seconds

to comment on Casey in terms of like discharge considerations for a patient like this.

1 hour, 9 minutes, 44 seconds

Yeah, absolutely. So after a throbectomy case, you know, often uh patients are intubated for their throbectomy. Most of the time they’ll exabate them right

1 hour, 9 minutes, 52 seconds

after the procedure, right? But not every time. Sometimes they’re slow to wake up. Sometimes they’re concerned that there’s been hemorrhagic transformation. So a lot of times that’s

1 hour, 9 minutes, 59 seconds

the ICU’s job to like decide like can we excavate this patient? I will tell you that like even patients with pretty large strokes often will do well and

1 hour, 10 minutes, 8 seconds

project their airway unless there’s some other comorbid pathology going on. So our our goal is pretty much always to try to extate them and if they have to

1 hour, 10 minutes, 15 seconds

be reintubated so be it. The other things that we’re doing, you know, after you’ve gone into the blood vessel and you’ve tried to like scrape out the clot, you probably don’t want them to be

1 hour, 10 minutes, 24 seconds

like super hypertensive. And so there’s been a lot of like trials about like what is the right blood pressure after throbectomy. we’ve kind of as a field

1 hour, 10 minutes, 31 seconds

landed on less than 160 is the ideal sort of place to land. Um so you’re trying to you know prevent them from being super hypertensive. You also want

1 hour, 10 minutes, 39 seconds

to protect their CPP. The brain does not like to be recovering in sort of non-physiologic

1 hour, 10 minutes, 46 seconds

mill to say better. So you want to keep their glucose normal. You want to keep their like um their blood pressure we

1 hour, 10 minutes, 53 seconds

talked about already but anything that you can oh their temperature normal.

1 hour, 10 minutes, 56 seconds

Anything that you can do to sort of protect the normal environment for the brain is going to help it recover. So that’s like really what we do in these postroctomy patients. Honestly, it is a

1 hour, 11 minutes, 6 seconds

like gamechanging procedure. And so a lot of these patients, they come in, they look terrible, they get reprofused.

1 hour, 11 minutes, 12 seconds

Uh we watch them for a day in the ICU and they go on their merry way. Their NHR scale goes from, you know, 20 to three. Sometimes we’ll get a follow-up

1 hour, 11 minutes, 20 seconds

MRI to kind of see like, you know, do they have evidence of cardioism? Are we where where do we think the stroke came from? But this used to be like these

1 hour, 11 minutes, 27 seconds

patients would come in with these devastating hemorrhages and we’d have to worry about cerebral edema and decompressive hemi craniactomy and like

1 hour, 11 minutes, 35 seconds

the game has so changed because that subpatient population is like more rare like truly every day I think we’re doing such a better job.

1 hour, 11 minutes, 45 seconds

Excellent. Yeah. I mean I I think you know as as you said initially like this is this is a testament to like you know everything from like EMS like early

1 hour, 11 minutes, 53 seconds

recognition and transport decisions to like you know more aggressive like triage and getting people to the right hospital.

1 hour, 12 minutes, 1 second

What what are your thoughts? Is TNK better than TPA or is it just logistically easier?

1 hour, 12 minutes, 5 seconds

It’s logistically easier and so therefore yes it’s better.

1 hour, 12 minutes, 8 seconds

Okay. Fair. Yeah. Right. It’s given faster at least.

1 hour, 12 minutes, 11 seconds

Mhm. Um, and then maybe maybe do you want to comment on some of the other advantages of a stroke center? Like what are some of the other considerations because like you know in in many cases

1 hour, 12 minutes, 20 seconds

we’re doing it for these services on day one, but it’s also the services on day like 7 through 14.

1 hour, 12 minutes, 26 seconds

Totally. I mean you’re getting SLP like a lot of these patients can’t swallow because they got facial droops and so you’re getting physical therapy, occupational therapy, you’re getting speech therapy, you’re getting case

1 hour, 12 minutes, 34 seconds

managers that are going to place them in acute rehab so that they can like begin their recovery journey. Like all of that is really streamlined in an acute stroke

1 hour, 12 minutes, 41 seconds

center. And so again, like I think that’s kind of the value of the multi-disiplinary care that these patients get on a stroke service is like all the other people who are going to be

1 hour, 12 minutes, 50 seconds

part of their like PMR like that really matters to patients in their recovery.

1 hour, 12 minutes, 55 seconds

And so like that is really what a stroke center is optimized for. And then there’s just great relationships with the rehab centers and we get people to

1 hour, 13 minutes, 1 second

rehab faster which again starts their recovery journey faster. And then also you’re looking at like, you know, they get an echo pretty pretty quickly. They

1 hour, 13 minutes, 10 seconds

get their MRIs. Like most of the stroke services are like set up to like do all the diagnostic stuff that they need in sort of like a rapid time period. And is

1 hour, 13 minutes, 19 seconds

that a reason to transfer someone to a stroke service if they don’t need the like acute intervention? Probably not.

1 hour, 13 minutes, 25 seconds

But once they’re there, they can certainly get their diagnostic workup more expediently.

1 hour, 13 minutes, 30 seconds

And I think it’s worth noting that that’s probably the reason why stroke centers have lower mortality, reduced long-term disability, faster times of

1 hour, 13 minutes, 38 seconds

recovery despite having generally sicker patients.

1 hour, 13 minutes, 41 seconds

Yeah, absolutely. I mean, it’s it’s a teamwork strategy.

1 hour, 13 minutes, 45 seconds

So, I was going to ask you too, uh, Casey, you know, this patient, uh, has atrial fibrillation, so if they they,

1 hour, 13 minutes, 53 seconds

you know, presumably they weren’t on anti-coagulation, they’re going to be on anti-coagulation now. There’s always a lot of discussion I think about in

1 hour, 14 minutes, 2 seconds

this is a whole another whole podcast episode right here. We’re starting. Yeah.

1 hour, 14 minutes, 5 seconds

You just asked you just asked a stroke neurologist about like when to resume anagulation. Like now we’re going to talk for like four hours. Like the poor med student is just like burying their

1 hour, 14 minutes, 13 seconds

head like oh god here we go again. Like no one likes this conversation.

1 hour, 14 minutes, 17 seconds

I I think we have to talk at least a little bit about antilag.

1 hour, 14 minutes, 21 seconds

Can we can we do like the two-minute version? Yes we will do the two-minute version.

1 hour, 14 minutes, 24 seconds

Here’s what I’ll say. So DAP has become like super popular within like the stroke world. Everyone seems to end up on DAP. DAP is fine for patients who

1 hour, 14 minutes, 33 seconds

have small vessel disease or have incraanial aro or even who have extranial afro if they’re going to get stinted. Right?

1 hour, 14 minutes, 41 seconds

So kind of things above the neck I think of as like probably antiplatlet problems. So, if your neck has a problem, if your intra like your large

1 hour, 14 minutes, 48 seconds

vessels in the brain have plaque, if your small vessel disease like from your long-standing hypertension and diabetes, all of those things do really well with

1 hour, 14 minutes, 57 seconds

antiplatlets. And DAP is fine as long as your patient’s not going to need like a bunch of different procedures because I personally don’t like to go and argue

1 hour, 15 minutes, 4 seconds

with all the different services that are going to do procedures about like doing their procedure on DAP.

1 hour, 15 minutes, 10 seconds

Anything in the heart is going to probably more likely benefit from anocoagulation, right? Okay, so if you’ve got atrial fibrillation, if you got an LV thrombus, if you got paradoxical embolism and a DVT, like

1 hour, 15 minutes, 18 seconds

those are all going to be things that are going to require anticoagulation. So it is it is more complicated than above the neck antiplatlet, below the neck

1 hour, 15 minutes, 25 seconds

anti-coagulation. But I think that’s a pretty nice simple way to think about it. And that’s at least that’s how at least how I tell the medical students like that’s great.

1 hour, 15 minutes, 33 seconds

Yeah, there you go. Two minutes, less than two minutes.

1 hour, 15 minutes, 35 seconds

If we didn’t if we didn’t scratch the itch, we wouldn’t have revealed that awesome pearl. I mean, it’s it’s like if it’s going to work 80 to 90% of the time, that’s great. And then, you know,

1 hour, 15 minutes, 44 seconds

we can sort of um spar with intellectually spar over the [laughter] other 10%. Totally. I love it.

1 hour, 15 minutes, 50 seconds

Awesome. Okay, cool. Well, thank you for humoring me. I I just had to ask that question. I wasn’t going to I wasn’t going to let us slip through that. I love it.

1 hour, 15 minutes, 57 seconds

Um so, okay. I think now we’ve probably covered a lot of the salient points on case two. Um do you want to move on to

1 hour, 16 minutes, 5 seconds

case three, Nick? Do you think we’re ready?

1 hour, 16 minutes, 7 seconds

Yeah, I think so. So this is a 64year-old um man on a Pixaban for AIB who presents

1 hour, 16 minutes, 15 seconds

with acute left weakness, vomiting and somnolence. His blood pressure is 218 over 112. Uh CT shows a right basil

1 hour, 16 minutes, 23 seconds

ganglia with intraventricular extension and signs of early hydrophilis.

1 hour, 16 minutes, 29 seconds

So maybe maybe this is a good one to sort of compare and contrast to the last one. So how is this different? How is our management different? Yeah, I mean I

1 hour, 16 minutes, 37 seconds

think a lot of it’s almost like a foil and complete opposite, right? So in patients who have, you know, an eskeemic event, we’re trying to protect their

1 hour, 16 minutes, 45 seconds

blood pressure and keep their blood pressure elevated so that they get, you know, reprofusion around the eskeemic block. Now we’ve got somebody who’s got

1 hour, 16 minutes, 53 seconds

a basil ganglia and so one of the key points for us is going to be blood pressure lowering. There used to be a lot of nihilism around uh intra cerebral

1 hour, 17 minutes, 1 second

hemorrhage and I think some of that is justified like it is a more serious stroke subtypes and I I do worry more about the patient with ICH than I do

1 hour, 17 minutes, 9 seconds

with the you know LVO that we’re going to go pluck out right it is harder for us to treat this but that doesn’t mean that there aren’t therapies right and so

1 hour, 17 minutes, 17 seconds

sort of the cornerstone for me when I think about a patient who has ICH I’m thinking about anagulation reversal blood pressure lowering protecting their

1 hour, 17 minutes, 25 seconds

CPP right so a lot of these patients end up intubated and we don’t want to tank their blood pressure because their ICP is probably elevated

1 hour, 17 minutes, 33 seconds

and then thinking about sort of surgical interventions for patients who qualify and I think that is probably the hardest

1 hour, 17 minutes, 40 seconds

part of care is that that is constantly an evolving target and and it it gets a little complicated about what kind of

1 hour, 17 minutes, 49 seconds

surgical procedures are patients eligible and how likely is it to impact their recovery.

1 hour, 17 minutes, 55 seconds

All right. Well, let’s let’s kind of double click on each of those. So, first off, anti-coagulation reversal. That’s obviously timesensitive. Um, there used

1 hour, 18 minutes, 3 seconds

to be a really expensive way to do this and now there isn’t.

1 hour, 18 minutes, 7 seconds

So, just just last year, um, adex alpha uh, ad next adex alpha, sorry. Yes. I I

1 hour, 18 minutes, 15 seconds

can’t even I can’t even say the name was withdrawn from the market. So, now the reversal agent is just for factory PCC. Is that right?

1 hour, 18 minutes, 23 seconds

Yep. And I think that that makes things a lot simpler for us.

1 hour, 18 minutes, 26 seconds

Yeah. You don’t have to spell addex in it anymore. Just PCC. Yeah.

1 hour, 18 minutes, 31 seconds

We got it or justify why you are using it.

1 hour, 18 minutes, 34 seconds

Right. And I think you know it’s it’s it is hard when people like don’t know the last DOAC time and um you know it can be

1 hour, 18 minutes, 43 seconds

everyone is on a doack. It used to be like everyone was on war and then there was some good literature that was like sort of fixed dosing was okay for

1 hour, 18 minutes, 50 seconds

anagulation reversal and warfin. I think we’ve mostly moved to fixed dosing for antipagulation reversal for DOA if they’ve taken a dose within the last 48

1 hour, 18 minutes, 58 seconds

hours. But there there is sort of discussion and I do think that it is still a little bit hospital specific on

1 hour, 19 minutes, 5 seconds

what dose people are giving for their case entra. So we use 25 international units per kilogram as our sort of

1 hour, 19 minutes, 12 seconds

standard reversal. Um and then we do check um uh anti-10A levels although

1 hour, 19 minutes, 19 seconds

then you have to like work with pharmacy to make sure that those are sort of like normatized and you know to me they don’t often correlate

1 hour, 19 minutes, 28 seconds

directly with the level of the drug and we don’t have a great way of measuring the level of the drug. So again, I think most people are kind of giving like if

1 hour, 19 minutes, 37 seconds

if you are, you know, just a run-of-the-mill IC, you get 25 international units per kg of your PCC.

1 hour, 19 minutes, 47 seconds

If someone’s going to get an EVD, like this patient who has an intraventricular hemorrhage, I may sort of just say like, let’s just give them 50 international

1 hour, 19 minutes, 54 seconds

units per kg because like that’s the dose range, but I don’t know that there’s great evidence to support doing that. That’s just kind of my personal practice.

1 hour, 20 minutes, 3 seconds

And just because it’s it’s just really hard to measure those levels and feel confident in them. And as someone who’s going to need procedures to me, like

1 hour, 20 minutes, 11 seconds

it’s worth the extra money to give the the medication and prevent them from having sort of another bleed with the EBD placement.

1 hour, 20 minutes, 18 seconds

Absolutely. That totally makes sense.

1 hour, 20 minutes, 20 seconds

All right. So that’s kind of one pillar you laid out for us, which is the um anti-coagulation reversal. What about um blood pressure? This is kind of a complex issue.

1 hour, 20 minutes, 30 seconds

Totally. So we know too low is not good, right? Because then that’s compromising our cerebral profusion pressure. But we

1 hour, 20 minutes, 38 seconds

know that letting your blood pressure be like 200 is also going to increase the risk of hematoma expansion. And so for patients who come in with a blood

1 hour, 20 minutes, 46 seconds

pressure that’s less than 220 on admission, we’re going to try to get their blood pressure to somewhere between 130 and 150 systolic. And you

1 hour, 20 minutes, 54 seconds

want a sustained, slow, controlled, not a lot of fluctuations. We’re going to use nicardipene or whatever infusion

1 hour, 21 minutes, 1 second

that you use for clipine. Clip I can’t say that word right now.

1 hour, 21 minutes, 6 seconds

Clipitipine. Clip. Okay. We’re going to use clipitine or we’re going to use nicardipene. Whichever your center uses um to thankfully nicardipene because I can say that one.

1 hour, 21 minutes, 14 seconds

Yeah, I know. Me too. Heaven forbid I had to do the other one. Um you’re going to use that sort of like slow decrease in your blood pressure, right? And if

1 hour, 21 minutes, 22 seconds

you get to 130, you need to turn the medicine off because now we’re getting into like we’re going to create hypoxic

1 hour, 21 minutes, 29 seconds

injury and that’s our hyper limited profusion. We don’t want to we don’t want to decrease the profusion too much,

1 hour, 21 minutes, 36 seconds

right? If you come in above 220, which is like every patient I have down in the stroke belt, then you probably live

1 hour, 21 minutes, 44 seconds

really hypertensive at your normal baseline, right? So if you come in with a blood pressure of 240, hey, is that real? I don’t know. Um, and your kidneys

1 hour, 21 minutes, 54 seconds

really are gonna hate if you get to a systolic blood pressure of 140. And like that AKI, like you guys know, like the

1 hour, 22 minutes, 1 second

AKIs are like sort of like secondary injuries and like we sort of like, oh, the AKI, but like that really sets people back. Like they’re urmic, they

1 hour, 22 minutes, 9 seconds

end up intubated longer, they they have a worse outcome. Like that to me really matters. And so for those patients,

1 hour, 22 minutes, 17 seconds

we’re going to aim for maybe like a a little bit more of a modest decrease to less than 180. And honestly, that really is most of my patients. We’re kind of

1 hour, 22 minutes, 24 seconds

getting them at 240. We get them to less than 180. The next day, we try to get them to less than 160. And we’re trying to like more slowly do that. And obviously, if they develop an AKI, we

1 hour, 22 minutes, 33 seconds

pump the brakes on the blood pressure control as long as their he Yeah. Like hematoma is not expanding.

1 hour, 22 minutes, 39 seconds

Excellent. All right. Uh next pillar, uh surgical interventions. So we’ve already mentioned EVD. What what else is potentially an option for these folks?

1 hour, 22 minutes, 48 seconds

Yeah, EVD really great. If you have obstructive hydrophilis from your IVH, you need to be in a center who can do an an EVD, right? Not every patient with

1 hour, 22 minutes, 57 seconds

IVH is going to need an EVD, but they should be watched in a place that can do it if they need it. The other place we have really good data for is suboxipital

1 hour, 23 minutes, 5 seconds

cranies, right? So if you have a cerebellar bleed, sub oipital craniactomy is like a life-saving procedure and like you should be in a place that can do the sub oipital crania.

1 hour, 23 minutes, 15 seconds

Everything else gets a little murky, right? So our patient has a basil ganglia hemorrhage. Even in rich, which really moved the needle on surgical

1 hour, 23 minutes, 23 seconds

candidacy, did not show an improvement um in functional recovery for for sort of like minimally invasive surgery with

1 hour, 23 minutes, 32 seconds

hematoma evacuation for the basil ganglia.

1 hour, 23 minutes, 36 seconds

So far, none of the the minimally invasive surgeries have like really shown improvement in and functional recovery. Uh and so for those

1 hour, 23 minutes, 46 seconds

it really becomes a question of does the patient accept to live with a significant disability and if so and our

1 hour, 23 minutes, 54 seconds

goal is lifesaving procedures we’re going to just do a decompressive hemocrainiactomy um to let them expand and the switch

1 hour, 24 minutes, 3 seconds

trial really showed that there really probably is not a functional benefit of that. So it is it is a life-saving intervention. Now if someone has like a

1 hour, 24 minutes, 12 seconds

cortical bleed like the bleed is 30 to 80 cc’s and it’s sitting in the cortex and the patient has a GCS that’s you know less than 13 like they are

1 hour, 24 minutes, 20 seconds

symptomatic from this and not just have a focal deficit they’re a little sleepy.

1 hour, 24 minutes, 24 seconds

Then the enriched trial showed that like the minimally invasive surgery to clot evacuate does have a functional recovery

1 hour, 24 minutes, 32 seconds

benefit. So that was the first trial that’s ever showed functional recovery after um a minimally invasive clot

1 hour, 24 minutes, 39 seconds

evacuation procedure. So important, but a lot of our patients have basil ganglia bleeds and we have not really um moved the needle on that.

1 hour, 24 minutes, 49 seconds

So Casey, you know, Nick’s taken you through a few of the the pillars or, you know, one by one sort of put you held your feet to the fire on these, which I

1 hour, 24 minutes, 57 seconds

think is great. Um now um one thing you you mentioned this once very briefly but the idea of you know seizure risk and

1 hour, 25 minutes, 4 seconds

maybe seizure prophylaxis. So maybe we could throw that in as another pillar and and how do you um how do you decide who needs to be on you know levatoram or

1 hour, 25 minutes, 12 seconds

similar um how do you how do you make that determination?

1 hour, 25 minutes, 15 seconds

I love that question. So in this patient they have a basil ganglia hemorrhage very low risk of having cortical irregularity being active and in fact in

1 hour, 25 minutes, 24 seconds

general for all ICE seizure prophylaxis is not recommended now there there is a risk of seizures and that’s going to be

1 hour, 25 minutes, 32 seconds

exponentially higher if you have a cortical bleed but just giving everyone prophylactic levatraetam is not the way

1 hour, 25 minutes, 40 seconds

to go so the way I approach this is you know no one gets just run like no one gets just stand standing being kept

1 hour, 25 minutes, 47 seconds

if they have alterations of consciousness if they are fluctuating I have a low threshold to put people on EEG and obviously if there’s clinical

1 hour, 25 minutes, 55 seconds

seizures we’ll treat those but standing prophylactic not needed in the like interparimal bleeds that is different

1 hour, 26 minutes, 3 seconds

than our our traumatic guy from the very beginning the traumatic bleeds they get seven days of prophylaxis and I think eventually we may talk about subacoid

1 hour, 26 minutes, 11 seconds

hemorrhage and they at least get some prophylaxis until the aneurysm is secured Brain tumors, no prophylactic seizure

1 hour, 26 minutes, 18 seconds

medication. ICHS, no prophylactic anti-seizure medication. Large strokes, no prophylactic anti-seizure medications. And so really, just take it

1 hour, 26 minutes, 27 seconds

away. If it’s in your order set, uncclick it.

1 hour, 26 minutes, 30 seconds

Love it. Okay. Any um kind of final thoughts on this case? Anything else we we need to talk about? We talked about reversing anticoagulation, blood

1 hour, 26 minutes, 39 seconds

pressure lowering, we’ve talked about ICP, surgical intervention, seizure prophylaxis. Is there anything else to help us?

1 hour, 26 minutes, 45 seconds

Just to echo that like ICP management is really foundation. It’s the same thing that we talked about for the the TBI patient, but for a lot of these patients

1 hour, 26 minutes, 52 seconds

that’s going to be, you know, the life-saving medical intervention that we can give them. Um, so making that decision if I sort of think if you are

1 hour, 27 minutes

intubating someone with an usually because they’re like altered consciousness, right? And that’s usually some effective transcendental

1 hour, 27 minutes, 8 seconds

herniation. that patient, they’re getting their intubation, they’re getting a D dose of hyperasmolar therapy while we sort this out, while we get them sort of the treatment for their

1 hour, 27 minutes, 17 seconds

obstructive hydro, you know, just in my mind, that’s like an order set that goes together like intubating the CH, they get a dose of hyperosmolar therapy.

1 hour, 27 minutes, 26 seconds

Great.

1 hour, 27 minutes, 27 seconds

Awesome. So, we’re going to talk about status epilepticus and some seizure stuff. I think that’s actually going to be a great follow-up episode if if

1 hour, 27 minutes, 35 seconds

Casey’s willing to suffer us again at another time.

1 hour, 27 minutes, 37 seconds

Anytime. Um because I think that you know that’s a that’s definitely a whole another topic in and of itself. So perhaps we can wrap up with this last

1 hour, 27 minutes, 45 seconds

case. I think it’s a nice another another vascular discussion um that we can have. So this is a 51-year-old uh we’ll say it’s a 51-y old lady who’s

1 hour, 27 minutes, 53 seconds

reporting the worst headache of her life. Um and in the context of that she collapses and then improves. So kind of

1 hour, 28 minutes, 1 second

mental status fluctuation there. So after the CT scan, a CTA is obtained and that shows an ACOM aneurysm. So anterior

1 hour, 28 minutes, 8 seconds

communicating artery aneurysm. So what are we going to do with that Casey? Is that just the same as any other old bleed or do we have to approach that a little differently?

1 hour, 28 minutes, 16 seconds

We’re talking about my favorite pathology now. We saved the best for last. Um great. So this is um you know when we think about subactoid hemorrhage

1 hour, 28 minutes, 24 seconds

um these are patients who have blood outside the brain, right? Like IC we think about interprankal hemorrhage. Now the blood is coming from an arterial bleed that popped and kind of it’s

1 hour, 28 minutes, 33 seconds

usually in the circle of Willis. So ACOM is a very common spot. Peacons are another common spot. You can see them in the MCA and the ACA like they can exist

1 hour, 28 minutes, 41 seconds

in the more sort of distal arteries but mostly in the circle of Willis. So when they rupture you get that sort of what we call the star of death or the crab of

1 hour, 28 minutes, 49 seconds

death or whatever. It looks like that really angry pattern in the sisterns because that’s where the blood came from. Um, and these patients are going

1 hour, 28 minutes, 57 seconds

to be a totally different challenge because, you know, early on they’re kind of behaving like a just a regular bleed

1 hour, 29 minutes, 5 seconds

where they they need treatment of their obstructive hydro, they need blood pressure control. We are going to give these some prophylactic anti-seizure

1 hour, 29 minutes, 12 seconds

medication until that aneurysm is secured. And that really I mean their early course really does mirror any other sort of interparimal hemorrhage.

1 hour, 29 minutes, 22 seconds

the downstream consequences of these patients is is really where things get interesting and because that blood is so

1 hour, 29 minutes, 28 seconds

noxious to the brain um these patients for about 3 weeks really are at high risk of having delayed cerebral eskemia

1 hour, 29 minutes, 36 seconds

and so that’s why they spend a lot of time with us is because we are monitoring for and preventing delayed cerebral eskemia which you know is used interchangeably with the word vasospasm.

1 hour, 29 minutes, 47 seconds

It’s really not the same. Vasospasm is a biioarker of who’s at high risk for delayed cerebral eskeeia but you can have delayed cerebral eskeeia without

1 hour, 29 minutes, 56 seconds

having vasospasm and you can a lot of our patients have vasospasm and they never go on to develop that that stroke right that delayed cerebral eskeemia

1 hour, 30 minutes, 4 seconds

that that es schemic stroke so again I tell the the medical students like we should be precise about what we’re talking about are they do they have

1 hour, 30 minutes, 12 seconds

vasospasm or do they have evidence of you know actually a clinical exam change which Now we’re going to say that’s

1 hour, 30 minutes, 19 seconds

delayed cereal eskemia. So these are really really cool patients and not only do they have a bunch of like cererovascular complications but they

1 hour, 30 minutes, 27 seconds

also can develop like neurogenic pulmonary edema they can develop takasubo cardiammyopathy like these patients can be so sick. Um, and because

1 hour, 30 minutes, 36 seconds

the blood is outside the brain, you know, most of these patients are still going to be left with neurologic deficits, but I think this is really where we can see patients make a pretty

1 hour, 30 minutes, 45 seconds

miraculous recovery if we get them through their, you know, month-long hospital course, which is going to be pretty brutal.

1 hour, 30 minutes, 53 seconds

Maybe this is me being a little too teeological here, but I’ve always sort of wondered like why is it that the blood vessels spasm so much when there’s

1 hour, 31 minutes, 1 second

blood? Like is this some evolved thing that like is designed to prevent further bleeding? Like if the blood vessel detects blood outside, it spasms like is anything known about that?

1 hour, 31 minutes, 11 seconds

I don’t think we really know. And I think it’s it’s much more complicated than just the spasm that occurs. Um it is like the sort of cyto cytoine

1 hour, 31 minutes, 19 seconds

release. There’s delayed cortical deolarizations.

1 hour, 31 minutes, 23 seconds

We really don’t understand the physiology like why this vaso spasm develops and like why is it in subaract but not in other you know like we see

1 hour, 31 minutes, 31 seconds

this in traumatic subaract like but it’s way more inrisismal subaract than traumatic like I don’t know that we I don’t think we know but I

1 hour, 31 minutes, 39 seconds

it’s fascinating like it’s just really crazy that like these patients like almost by the book like they look okay after their EVD is placed after you get

1 hour, 31 minutes, 48 seconds

them to their aneurysm coiled they have like a kind of a honeymoon period of like a couple days where they look pretty good. And then day four comes

1 hour, 31 minutes, 55 seconds

around and like day four to 10 they just look awful. Like it’s just like every like their their mental status goes down. They’re not as attentive.

1 hour, 32 minutes, 4 seconds

Sometimes they require intubation and we just like you know get them through this period of like

1 hour, 32 minutes, 11 seconds

vasospasm as a biomarker of the delayed cerebral eskeemia they’re having. And you know hopefully most of them we get through without long-term delayed or like long-term u es schemic strokes.

1 hour, 32 minutes, 24 seconds

H so let’s let’s walk through this one too. Like so I mean the sort of early course you know things like airway

1 hour, 32 minutes, 31 seconds

control, blood pressure control. Um what about like securing this aneurysm because like you said this is a arterial bleed. Like what what’s done for that?

1 hour, 32 minutes, 40 seconds

Yes, totally. Um, you want to get them to a center that does this and and does this with a lot of frequency. I think that like the better your endovvascular

1 hour, 32 minutes, 47 seconds

surgeon is most of them now are are coiled invascularly.

1 hour, 32 minutes, 52 seconds

Um, which is it used to be like if you were just too sick you got coiled. Now that is the preferred method of treating these. It’s safer. There’s less

1 hour, 33 minutes

complications. Um, very rare now is it that patients go and have like an a cranottomy for an aneurysm clip. Like

1 hour, 33 minutes, 7 seconds

that’s kind of a lost art which is amazing. Um, we still do it from time to time, especially with um, those that have a really large neck that you can’t

1 hour, 33 minutes, 16 seconds

get the coils to pack into. Um, but more and more these are all done indivascularly, and you really try to get them all like

1 hour, 33 minutes, 23 seconds

you secure the aneurysm by clipping or coiling it within the first 24 hours.

1 hour, 33 minutes, 29 seconds

Okay. So, we’ve we’ve uh we’ve controlled this so that it presumably won’t bleed anymore. We’ve addressed some of the other things we’ve talked

1 hour, 33 minutes, 36 seconds

about like hydrophilis with EVD. Um what what can we do to prevent some of these delayed complications?

1 hour, 33 minutes, 45 seconds

Yeah. I mean so neimonapine is like kind of the standing medication. It prevents delayed cerebral eskemia. It has and it

1 hour, 33 minutes, 52 seconds

improves functional outcomes. We don’t know exactly how it works. U it is not that it is treating vasospasm but it is doing something in the background that pre that improves functional recovery.

1 hour, 34 minutes, 2 seconds

So everyone gets namonopene given every four hours. If it causes them to be hypotensive, we half the dose and give it every two hours.

1 hour, 34 minutes, 9 seconds

Is it? Now Casey, is it something unique about that medication or is it it’s not a class effect, right? Because you can’t just put them on like any old calcium channel. Just put them on calcium channel blocker. It has to be this one,

1 hour, 34 minutes, 18 seconds

you know? I don’t think it’s been extensively studied, but there is something about this that is like that specific beta blocker has some sort

1 hour, 34 minutes, 25 seconds

of better like I don’t know bloodb barrier penetration. There’s something unique about neotipene. And so it is expensive and we have to get that one.

1 hour, 34 minutes, 35 seconds

Okay, cool. Love it.

1 hour, 34 minutes, 36 seconds

So we can do that. Anything anything else we can do from a preventive standpoint or are we sort of just like noipene and fingers crossed?

1 hour, 34 minutes, 44 seconds

Yeah, you know, it used to be that we did like hypervalmia like and pushed people like gave them a lot of transfusions and that prophylactically

1 hour, 34 minutes, 51 seconds

does not seem to be the right strategy, right? Flooding people with fluids is not effective, right? That’s I think true across the board in critical care.

1 hour, 34 minutes, 58 seconds

We we learn this every couple of years in the ICU. like every trial like we just keep showing like fluids is not the panacea

1 hour, 35 minutes, 6 seconds

but yet we keep doing the trial over and over and over really want to just give people fluids.

1 hour, 35 minutes, 11 seconds

I don’t know. So that is not the goal here. We obviously don’t want people to be hypoalmic but like again like the brain wants to be euimic like just be

1 hour, 35 minutes, 18 seconds

normal. Um, so then I mean really prevention-wise there’s not much we’re doing. Now if people start to develop

1 hour, 35 minutes, 28 seconds

either by their transcranial dopplers they have elevated velocities or we get a CTA and it shows that they have vasospasm then we’re kind of at a point

1 hour, 35 minutes, 37 seconds

of you know do they clinically have symptoms or is it just that they’re becoming really they’re they’re becoming

1 hour, 35 minutes, 44 seconds

constricted and I don’t I don’t think that there is really a clear like I don’t think it’s scientifically known what the right strategy is in the

1 hour, 35 minutes, 52 seconds

patient who has vasospasm but clinically hasn’t deteriorated. ated yet I will tell you in our center we use a lot of intratheal nicartine

1 hour, 36 minutes

um because that’s a calcium channel that can blocker that can be given intratheally um that absolutely for a lot of patients

1 hour, 36 minutes, 10 seconds

will decrease their velocities of their transcrrenal dopplers and it will relax their arteries does it prevent delays rubil eskemia I don’t know we’ve never

1 hour, 36 minutes, 18 seconds

been able to fund a trial to to show that because subaract is rare and the NIH does not seem very keen on funding trials s to better explore it. Um you

1 hour, 36 minutes, 27 seconds

can use milinone so a phosphide diastasterase um inhibitor 3 that also has vaso relaxing properties that’s been studied in smaller trials seems

1 hour, 36 minutes, 36 seconds

promising we use it a lot so we use a lot of mil renown um the key there is that obviously some patients get vasoddilated systemically and then they

1 hour, 36 minutes, 44 seconds

get hypotensive and we got to protect their cerebral profusion so a lot of the patients who get milrenone will also end up on leviped to protect their systemic

1 hour, 36 minutes, 53 seconds

map um and then just making sure that their blood pressure stays like we allow them to autoregulate, right? So once the aneurysm is secured, we’ll let them have

1 hour, 37 minutes, 2 seconds

a map of 140. Like you want to be hypertensive, like go for it. You can do do anything. And a lot of these patients

1 hour, 37 minutes, 9 seconds

have other aneurysms and that does not seem to rupture the other aneurysm. So lucky us. So um but again, that’s a

1 hour, 37 minutes, 16 seconds

patient who’s symptomatic. We allow them to autoregulate. And if they’re symptomatic, we’ll, you know, while we’re getting them on other therapies,

1 hour, 37 minutes, 24 seconds

we may use vasopressors just to kind of push their MAP to see if that improves their exam by increasing the profusion.

1 hour, 37 minutes, 31 seconds

We try not to let people like just hang out indefinitely on vasopressors.

1 hour, 37 minutes, 35 seconds

And u just to double click on on TCDs for a second because I think this is this is something that we take for granted in the neuro, but it’s it’s pretty esoteric for people who work in

1 hour, 37 minutes, 44 seconds

other ICUs. you know, correct me if I’m wrong here, but basically the principle is you’re using the the temple as a window, you’re putting a Doppler beam

1 hour, 37 minutes, 52 seconds

in, and then you’re trying to measure flows in the MCA and other vessels, and if a vessel is getting tight, if it’s getting ready to spasm, the flows are

1 hour, 38 minutes

going to be faster because it’s squeezing the same volume through, you know, smaller area. You got it. Yeah. So, we just monitor that.

1 hour, 38 minutes, 7 seconds

And how how often are we monitoring that? So in [snorts] a center that like as a center of excellence again this is like religious like gestalt and and like

1 hour, 38 minutes, 16 seconds

tightly held like principles. So like we get daily TCDs if you go practice like at other centers like they may not rigorously hang on the TCDs like they’re

1 hour, 38 minutes, 24 seconds

like you know someone’s last communion. I don’t know. So again it really is center specific. We get TCDs every day on our

1 hour, 38 minutes, 31 seconds

vasospasm patients and we like randomly chart stock every like hour of like updating the TCDs like what this this

1 hour, 38 minutes, 38 seconds

number is so important but again like I think you know what the patient look like looks like matters so much more than the number right and so the number

1 hour, 38 minutes, 46 seconds

can be your canary in the coal mine but I think sometimes we get freaked out by a number that would never have been clinically significant and that’s like a

1 hour, 38 minutes, 54 seconds

difficult balance like when you have data to not react to it if the patient doesn’t look bad. So, you know, it’s like all monitoring.

1 hour, 39 minutes, 1 second

It’s what you do with it, not not the data.

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It’s the wizard, not the wand, as they say. I love that. Exactly.

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I like that. Anything from like an electrolyte standpoint that we need to be thinking about with these folks. Is it sort of just like trying to keep them

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quote unquote in the box? I know we don’t like to practice medicine per se, but sometimes, you know, normalizing things can be helpful. Any other pearls there?

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You know, we’ve looked at magnesium.

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Magnesium is vasor relaxative and magnesium is harmless, right? Like I think it’s fine. We actually have switched to giving magnesium althanate

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because that has a little bit more bloodb brain penetration and maybe helps a little bit more with vaso relaxation.

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I don’t know if that’s true. It’s certainly not been studied in like any meaningful number of clinical trials, but um I think it’s interesting. There

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have been trials that showed that that you know hypermag does not improve your clinical outcome. So we are not like putting people on mag drips anymore. or

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that was a thing of the past. Um, but we do try to keep people’s mag above two and you know whether or not that’s truly the beall endall is fine. I don’t know.

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Um, we used to hear put everyone on a statin. I think that’s kind of laughable and I like was a really big like I’m going to put my foot down and say we should not do that. Like I don’t think

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that there there’s there’s evidence that the statin does not make a difference.

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Um, so there was a trial that showed no benefit of statins. It stayed here forever. Um, but you know, again, like I don’t think there’s a a good enough

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anti-inflammatory benefit of the statin to justify like that then the patient’s gonna stay on it for the rest of their life and no one’s going to stop it and there’s side effects like you know it’s

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fine to be on a statin if you have a clinical reason to be on a statin but like course it shouldn’t be in the water and I think that that was like we were just putting

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people on it because we could so we have stopped doing that. Yes. Yes. Just ivormected in the water.

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Yeah. Right. [laughter] uh you mentioned that that often these patients have a very long course you know and that the uh the the stress of

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this can lead to other complications. Do you want to do you want to sort of uh double click on some of those for a second and sort of think think beyond the brain what else you worry about?

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Yeah, I mean I think we we really do not see takubas all that often. That’s like a once a year. It’s kind of an exciting thing but it does happen. um or takos in

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a meaningful way where like we actually are going to need to like you know they’re going to have like an outflow obstruction like we’re gonna do cardiogenic shock we need to do things

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like it’s rare I mean you certainly will see people have a slightly depressed EF in the setting of their subacto

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like almost everyone comes in with a prolonged QTC which I think is interesting but like clinically not all that significant and then you know

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neurogenic pulmonary edema is a thing it’s pretty easily solved by diuretics not all that exciting I mean um these patients mostly like I mean they’re just

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at risk for DBTs. They’re at risk of like ilases. They’re at risk of all the like the complications of not moving for a month.

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And then for the patients who are awake, they get Q1 hour neuro checks for way too long. Like we really need to be more like intentional about like who is being

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woken up every hour. That is justifiable for maybe the first two days, right?

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Beyond that like I think we are still trying to figure out like what’s the best way to monitor these patients. Can we look for early eskeemic changes on

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EKG or sorry EEG? Can we look for should we get CTAs more frequently? Can we use TCDs? Like you know the neuroexam is

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important and it really is sort of the pinnacle of what we do. But it is mean to wake people up even every two hours

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for three weeks. like people get like so delirious and then it’s hard to tease out is that a neuro change or is that

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just delirium. So I mean there’s an art to that too. Um these these are really they’re complicated patients. They’re

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they’re really fun to see through and I like I truly have been doing this for a while and I still learn something new from every subra I take care of.

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It’s funny because you mentioned this is rare and I I realize that my sort of mental model I I don’t think about them

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that way because they stay in the ICU so long like numerically it’s few patients but comparatively it’s a larger fraction of ICU beds. Yeah.

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Yeah. Oh yeah. Yeah. I mean they they were they were here with us for a long time. It feels like there’s a lot of them but it’s less than 5% of all um

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strokes. So it is like the rarest of stroke subtypes.

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Yeah. It’s like you’re there for a week off for a week. you come back and still there’s still there. Yeah. Um yeah.

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Awesome. Well, I think um Casey, we want to be respectful of your time. Of course, I know you got um some big fish

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to fry there in your ICU. Um but this was super fun. Thank you so much. Before we go into our conclusion, um well,

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first and foremost, we’d love to have you back and and we’ll make sure that happens if you’re if you’re a medible, but also anything that you want to plug anywhere that folks can find closing thoughts generally. Yeah.

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Yeah.

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Yeah. This has been super fun. I um you know there Well, I can say like I wrote a book. You can go get that. That’s a

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cute neurology survival guide. It’s a little outdated, but you can you can still go get it. That was like my musings as a fellow. It was kind of like

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all my thoughts of like how to survive as a neurintensivist being sort of like a no novice intensivist.

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Um you know, I I really am missing the days where Twitter was Twitter and not X. So I you won’t find me there anymore just because it just got to be a sort of

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an angry place. I’ve tried out Instagram. It just takes a lot of work to be like Instagram like algorithm recognized. Like you have to post a lot.

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So I don’t I don’t keep up with it the way that like the real Instagram influencers do. But every now and then I’ll be like I am motivated today to

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talk about some sort of neuro pearl. So um you can find me there. And yeah like I love it. I love I mean this is just my

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passion is just being able to get to talk to people like like you guys about these really cool patients that we have the privilege of taking care of.

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Love it. Well, thank you so much for joining us. Yeah, we’ll have to talk more about you know whatever other neuro conditions that we can we could think of like seizures there. There’s a lot more.

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We we only scratched the surface today.

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Yeah, we’ll get into menitis and sephilitises, seizures, all the other non-vascular stuff. Love it. Awesome.

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All right.

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All right, folks. Well, thanks again to Casey. Uh we look forward to having her back again on the show. This was a ton of fun. I think we covered a lot in the world of intro to neurocritical care.

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Talked about various uh types of stroke, hemorrhagic, eskeemic, how, you know, subacttoids differ from other types of

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stroke, so on and so forth. Just a lot of great content. Nick, I mean, I hope you had as good of a time with that episode as I Oh, yeah. This was great. Um this is

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really great uh as as somebody who you know practices neurocritical care less often it’s a great topic to review and

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the exciting thing about this topic is you know I I really think that there’s a lot of ICU nihilism about neurocritical

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care in some ways and I think that increasingly that is unjustified like the progress that we’ve made in the last decade or so is actually quite

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astounding and if you’re at a center that takes care of these folks you really do see it so I I don’t know it’s great absolutely it’s great It’s great hearing about positive trials.

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It is. It’s good. And if you want to learn more about those trials, if you want to learn more about what we discussed today, you should check out our show notes and on the uh on the website there. Uh www.criticalcaretime.com.

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Subscribe to our mailing list, leave a comment, check out our store, buy some swag. We sure appreciate it.

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Yeah, you could buy a shirt like this that says the Norepy. Uh don’t don’t sue us, Northace. Um uh we’d like to say thanks to the folks

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at Northace for not suing us. We’d also like to say thanks to our listeners for encouraging us, especially those of you who have left reviews, comments. Uh, I’d

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like to thank our team over at Podpaste, you know, people who have contributed to this episode, including Kurt Bellnap for the awesome theme music. Um, if you like

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this episode, be sure to subscribe, give us a like, share the episode with somebody else, give us a fivestar review, do all of the things that help us get the word out.

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Yes, we appreciate those fivestar reviews. And also, we appreciate talking to you guys. So if you want to reach out to us, we’re uh criticare time onx or individually nickmark askins_razer.

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We’re on Instagram, LinkedIn, blue sky threads, YouTube. Any sort of permutation of critical care time will get you to us. Yes. Uh now for disclaimers. The views expressed within

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this podcast and any associated media do not necessarily reflect the views of our employers. All references to patients or encounters have been modified to be hypocmplant. Actually, they’re just made

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up. And thus, any similarities to real world cases are purely coincidental.

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[music] And remember, this podcast is for educational and entertainment purposes only and should not be used in le of seeking medical advice. With that, thank you guys so much for listening.

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I’m Dr. Cyrus Asin. So long.

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And I’m Dr. Nick Mark. I will see you next time.

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[music]

Linking To And Excerpting From Critical Care Time’s “82. Strokes and Intro to Neurocritical Care with Dr Casey Albin”

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Linking To And Excerpting From Critical Care Time’s “82. Strokes and Intro to Neurocritical Care with Dr Casey Albin”

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