Traumatic ICH - An Interview with Erin D'Agostino, MD

Hi, everyone, and welcome back to another episode of Amplify. I'm your host, Sam Michu. Thank you for joining us. Today's episode is an interview with the author of the February 2025 emergency medicine practice article on traumatic intracranial hemorrhage, and I think you're going to find this to be an outstanding interview. I can't wait for you to hear it. Before we dive into that, just a quick reminder, ebmedicine.net is your one stop shop for all of

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Just write us at the email in the show notes, and we'll make sure that you and everyone in your entire program gets free access. Access. And now let's jump into this interview. My name is Erin D'Agostino. I'm currently a neurology resident at the University of Vermont. My background is maybe a a little bit unusual because, before my career started in neurology, I'm now two years into that residency. I did a brief four year stint in the neurosurgery world.

It took me just a little bit of time to realize that that wasn't exactly the direction that I wanted to go in, but I still I love the content. I'm interested in neurocritical care, so there's a ton of overlap. And this kind of content, especially traumatic intracranial hemorrhage and the managements are pretty near and dear to my heart. So I'm pretty excited about this article. I hope that it's helpful. Yeah. Now you're one of three authors for this February 2025

issue of Emergency Medicine Practice. The other two, doctor Reyes Zargosa and doctor Siket. And this article is focused on traumatic intracranial hemorrhage, but, really, this thing is like an encyclopedia of all things bleeding in the brain. You covered a lot of information, and it's quite heavy, like, meaty. There is no fluff in this article at all. It's, like, all things you need to know regardless of your practice

setting. Is that right? I'm hoping that it doesn't come across as too nitty gritty heavy. I love this stuff. I feel like it's a great example of understanding pathophysiology. It translates really nicely into the clinical management of these conditions. I think what I did try to dive into a little bit is how not every brain bleed is, the same. And if you understand where they come from and why they happen, you can appreciate what to expect from them and how to treat them differently.

The treatments for different types of leads are totally different, and the expectations for them are different. So I'm I'm hoping that some of that comes across and isn't too heavy. Or Oh, yeah. Oh, yeah. For sure. I I wasn't saying that it's a criticism. I'm just impressed that you were able to synthesize all of

that information into one article. I really think it's helpful to see them side by side, different injury patterns, different pathophysiology for different injuries altogether in one article really gives me an appreciation for more of a spectrum instead of just, oh, this is how we treat this, and then I've gotta go find some other resource for how we treat some other injury because it's completely different and unrelated. It's nice to see them all in one article together

and related, but it's rare. I think very few authors take that approach, and I really like it. I enjoyed it. I thought it was very well written. I I appreciate that. I think it's part of the big thing that I was trying to tackle is that, I think there is somewhat of a misconception on the medical community that medical management of these kinds of injuries is a temporizing measure to get to the definitive treatment of surgery. And far in a way, that's actually not

really the case. The medical management is the definitive treatment. Surgery is if all else fails, and there are actually plenty of caveats to when surgery does not work depending on what the injury is and how the pathophysiology is evolving. So I think that was maybe why I tried to dive a little bit deeper into how some of this transpires because the medical management is in many, many cases, the management. So it's not just a

temporizing intervention in the ED. That's what gets continued in the neuro ICU as well, and surgery is only in the situations that, the medical management fails and in the right clinical context. And I did have fun with I mean, it's jumping a little bit ahead in the article, but I I also do some illustration stuff, and I had fun trying to simplify what some of the surgical procedures are and what they actually do address because it's actually fairly

I don't wanna say limited. There are specific indications for what actually is going to be helpful for a patient. Alright. Well, before we get into all that, tell me about some of the epidemiology of traumatic intracranial hemorrhage. Is it common? I mean, working in the ED, obviously, we see it, but do we have any numbers about how common it is every year in The US? It's exceptionally common, especially if you're considering the

mild range of traumatic brain injury. It's about two point five million Americans, that are seen in the emergency department every year. I mean, it's an exceptionally common thing that practitioners are gonna see in the ED. The number that actually are going to evolve into critical intracranial pressure patients that need surgery

is obviously far, far fewer than that. But the ability to be able to assess those patients where every ED practitioner is going to see and be able to decide who is at high risk and who is at low risk is a skill that every ED practitioner obviously needs. So when you were doing research for this article, where are we in terms of literature or body of evidence for these kinds of injuries? Is it pretty voluminous, or is it pretty, like, guideline driven? How is that?

The the research on this topic is tricky. I would describe it as messy. There's a lot of it. Is it is voluminous. The problem is that the ability to do a randomized controlled trial in this kind of population is really limited. The size and scope of different studies, the demographics are different, what you're qualifying as the level of injury, what you're qualifying as level of outcome, All of those things vary and make it pretty challenging to draw real guideline driven conclusions.

So a lot of it is based on expert consensus. It's in combination with evidence based research. Some of the data is controversial. I mean, it's a challenging thing to be able to do a deep dive and come out with really confident conclusions. But there are certainly some things that come through as clear, and I'm hoping that in this article, we were able to define what those elements

are. And are there organizations that stand out as kind of the big players when it comes to guidelines for these kinds of injuries? Yes. The Brain Trauma Foundation guidelines are probably among the most helpful. The CIVIC guidelines, s I b I c c, are also fairly clear cut. The major trauma organization, I'm blanking on what acronym they go by, also has some pretty clear guidelines on their page. I would say those are probably the most concise ones to be able

to go to. Alright. So let's dive in a little bit of the pathophysiology of these injuries. What do we know generally about the morbidity from traumatic intracranial hemorrhage? So a lot of this comes back to the basics of what's referred to as the Monroe Kelly hypothesis, which is simple. It's just that there are three elements within the skull. There's blood, brain, and cerebrospinal fluid, and, it's a pressure volume curve depending on how much you have of those three things.

So if you have too much blood, that's going to cause you to escalate on the pressure volume curve, and it is notable that that's an exponential curve. So adding a little bit more volume is going to, at some point, escalate pressure generated by a huge amount. And that's where we run into the situation of just a little bit of extra, for instance, blood prompting something like herniation clinically because the intracranial pressure escalates to a critical point really quickly.

So in some ways, it's simple. And then if you dive into the weeds, it gets more complicated, but it does come back to that basic element of intracranial pressure. I don't wanna neglect here that it's there are three elements of this equation. It's the medial arterial pressure minus the intracranial pressure gives you the cerebral perfusion pressure. And I think sometimes when we think about intracranial pressure, we forget about cerebral perfusion pressure as being a really

fundamental element here. Because, for instance, if you drop the blood pressure in a patient, sure, you can reduce the intracranial pressure as well. But at some point, if the blood pressure is too low, you're just not going to send any blood to the brain, and then the cerebral perfusion pressure is also going to drop to a critical low. And that's going to mean that not enough blood is getting to the brain. That's critical hypoxic injury, and you're going to globally stroke the whole

brain. So in our battle against the evils of intracranial pressure, I think it is really important to remember that our ultimate goal is sure to keep the intracranial pressure below a critical limit, but also to make sure that the brain is getting enough perfusion. The classic mistake that happens here is, for instance, hyperventilation because that will allow for vasoconstriction, and that will reduce intracranial pressure because less blood flow and less blood are getting to

the brain. So by Monroe Kelly doctrine, that will reduce the pressure. However, if you're reducing the amount of blood getting to the brain, you're also risking ischemic injury by not getting enough perfusion. And that is why one of the clearest guidelines that exists now is that hyperventilation should really only be used in a very transitory setting.

Namely, I think that as an intervention to get someone to the OR, like a half an hour intervention just to keep someone from her needing for a very short period of time. Yeah. Yeah. That's a critical concept, and I I really appreciate the figure. This is figure one on page four, basic principles of mean arterial pressure, intracranial pressure, cerebral perfusion pressure has got three images there. One showing the logarithmic increase as the decompensation occurs and intracranial pressure

goes up, One showing the relative volumes. You've got brain volume, 80%, blood volume, about 10%, and CSF, about 10%. So it doesn't it's not a whole lot of blood in there to start with, and it doesn't take much to push you to that right end of the curve to increase the pressure. It's a it's a good illustration. And if you're listening and have access to the article, that's figure one. I think that solidly explains the concept in three images, which I love.

Well, and a fun thing that you that you can even look at, for example, the the venous volume is signif it's not nothing. And for instance, if a cervical collar is too tight, the venous outflow is gonna be limited. You're going to increase the amount of venous back pressure in the brain, and you're gonna spike ICP that way, and you can resolve it by loosening the cervical collar. Wow. Now does this make intracranial pressure monitoring a critical part of treatment for intracranial hemorrhage?

Oh, that's an excellent question. The guidelines in this have actually gotten less specific over time. I think that the data has shown that it is helpful in the population of patients that are less than 65 and with, GCS of less than eight in the setting of traumatic intracranial hemorrhage. It's really a little bit more challenging than that. It depends on what kind of lead we're talking about and what kind of exam the patient has. The reality is it's helpful to have a number if you

don't have an exam to follow. If a patient has a followable neurologic exam, then that's actually potentially even more helpful than having a strict number to be able to make decisions based on. But if your patient has such a low GCS, such an unfollowable exam, Or, for instance, if they're going to the Operating Room and they're gonna be under general anesthesia, there are indications separately to have a number to follow just to make sure that the patient isn't having a critical decline

while you can't follow an exam. So I think that it certainly has its role, but it's in specific context. Alright. Let's talk about types of injuries. So when we're talking about traumatic intracranial hemorrhage, what types of injuries specifically, and categories would these injuries fall into? Sure. I I end up dividing it into a few different basically based on location of bleed. The category of traumatic subarachnoid hemorrhage, I think of as sort of the most benign phenotype.

I should note that I'm qualifying traumatic subarachnoid hemorrhage primarily as peripheral subarachnoid hemorrhage. And when you're looking at a scan, the easiest way to be able to look at that is, are we looking at just on the superficial surface of the brain along the sulci and gyri, or are we looking at blood that goes deeper into the Sylvian fissure, into the basal cisterns?

If you're seeing blood going deep down into the brain, it can happen with traumatic injury, but it would make me suspicious that it's not truly a traumatic subarachnoid hemorrhage. And I think that's probably the biggest takeaway from subarachnoid hemorrhage. Peripheral traumatic subarachnoid hemorrhage largely is not a terribly concerning finding. But subarachnoid that goes deeper than that should prompt suspicion for there being an underlying aneurysm or vascular malformation.

And that begs the question, was this spontaneous with some peripheral trauma? Like, did they have hemorrhage first and then fall over and hit their head as opposed to they hit their head and then blood? Exactly. The first question that any ED provider can be asking themselves with a brain trauma that comes in is, was it a fall then bleed or a bleed then fall? And, largely, it's that they fell and hit their head, and they have blood

related to it. But it's a it's a critical thing to be able to pick up that there's something funny about the story. And I've seen subarachnoid hemorrhages from an aneurysm cause a car crash. I've seen people have seizures as a result of, an aneurysm rupture. Certainly, you can get those presentations in the mix as well. And that distinction is important because that treatment algorithm is very different than the traumatic type. Yes. Totally different. And that

is not what we're talking about today. So if you're listening and you've got a patient with a spontaneous subarachnoid hemorrhage or intracranial hemorrhage, this is not the correct podcast. Go listen to one of our other ones. Definitely not a traumatic injury. That's a very important distinction. So good to know. Alright. So that's the traumatic subarachnoid hemorrhage. What's next? Subdural hematoma, I would broadly categorize into, is it acute or is it chronic?

And then where is it? Those are also different entities. So an acute subdural is a much more concerning entity than a chronic subdural. I mean, it's a venous bleed. It's bridging veins that are spanning from the parenchyma into the dura. And so generally speaking, it's a slower bleed. An acute one can absolutely be a life threatening injury. But chronic bleeds, especially in the elderly population where you've got brain atrophy, that's gradually putting more and more tension on those poor little

bridging veins. I've seen people with a coughing fit rupture, a bridging vein, and they get little oozing that gradually accumulates into a chronic subdural. They can even eventually have mass effect associated with it. But because there's so much time, and that's kind of a big concept in, you know, the pathophysiology of brain dynamics that if your brain has time to adapt to something, generally speaking, it can adapt better as opposed to an acute change is going

to cause an acute problem. So a chronic subdural, I worry about far less. It doesn't mean it doesn't need an intervention, but I worry about it less. An acute subdural can evolve much more quickly. And then where it is also matters hugely. If it's at the convexity, anywhere along the periphery, that worries me a lot more. It's much easier to build pressure and to cause a big problem. Falcine and tentorial subdurals tend to be much more benign entities.

It doesn't mean that they can't ever cause a problem, but it's less likely. So I worry about those ones less. Now the subdural population can also have a mixed density, so acute on chronic. Do you just treat those and worry about those like they're acute, or is that a whole separate category? I kind of put them somewhere in between because they do have an acute component. You don't know exactly how much blood is going

to accumulate there. So I guess for the most part, you treat them like an acute subdural, but you know that this is someone based on the imaging that you're seeing that repeatedly has leads like this. And if they're presenting only now, then the previous ones weren't too symptomatic. So I I would say I put it kind of somewhere in between, but because there's the acute element and you don't know exactly that that bleed has stopped, you do have to treat it more along the acute end.

Alright. Epidural hematomas, this is the one we seem to be most concerned about, the the football shape, the double convexity. What about these? Yeah. I feel like this is the board's question. And and I I do think that when people think brain bleed, this is the one that people think of, which isn't necessarily a bad thing. It is probably better for us to on the side of caution and want to treat patients as conservatively as possible.

But the reality is epidural lymphomas are actually fairly rare. It it takes a fairly big trauma typically to the temporal bone at surface referred to as the terrier on. And the classic is that it causes a rupture of the middle meningeal artery as it exits the foramen spinosum. It's a part of the temporal bone that's fairly thin, and the vessel is right there. So it is sort of classically in that area.

And it's a different animal because it's arterial and because that blood is going into an area that's bounded by the cranial sutures, and so it actually can't expand the same way that a convexity subdural hematoma can go all the way around. It has room to be able to expand before it compresses down on the brain. An epidural hematoma doesn't have that luxury. It's confined into this one space, so it's a much more focal pressure that it's going to insert on the brain.

So the reason that people worry so much about it is because someone who's young and otherwise healthy can look there's referred to as lucid interval. They can look fine while that arterial bleed is still in its early stages. And then classically, they, you know, drop half an hour, forty five an hour later as that blood reaches a critical level and the compression gets severe.

From the, you know, neurosurgical perspective, it's, I don't know, one of the most addictive cases in the surgical world because often it's a young, otherwise intact person who just had the trauma like this. They can come in very, very sick. They rapidly decline. Maybe even have a blown pupil.

And if you get them to the Operating Room fast enough, this is the situation where you can actually have and I think as a medical student, I had a young guy who came in nearly dead and the following warnings asking why he was in the ICU. Wow. And the thought is that that can occur in part because there is the dura separating this bleed from parenchyma. And so the amount of irritation and injury that happens from contact of the brain with blood directly is minimized.

So there is some thought that if you can resolve the pressure fast enough, you can actually prevent there being really much of any substantial neurologic sequela. So the epidurals are their own animals to be excited about. That said, you actually can get them from other sources. You actually can get them from Venus bleeds. I love this little pathophysiologic example. There was historically a time where we didn't have areas for kids to sit in shopping carts, and so kids would be in

the cart. And it was referred to as a shopping cart injury if a kid flipped backwards out of a shopping cart and landed on the back of their head. And the first thing that a kid does when they hit their head is cry, and that might be a little bit different than the adult's pathophysiology. The reason it's relevant is because if you land on the back of your head, you have a posterior fracture. It can injure the sinus as it travels around.

And then if the next thing that you do is cry and have a whole bunch of intrathoracic pressure, that's going to decrease the amount of xenus outflow, back it up into that same sinus that just got injured. And, actually, that does bleed into the epidural space. So you do sometimes see posterior fossa, small epidural hematomas that are actually venous, not arterial, tend not to cause as much of an issue. And it it's just a different way that you can get an epidural hematoma that doesn't

follow the classic logic. You can also get them directly from bony bleeding if you have a significant enough fracture, and that would also be in the epidural space and wouldn't cause as much of a problem. So there are also epidural hematomas that don't need intervention. It's probably not good to memorize that as the direct correlation. Far and away, epidurals are highly concerning, just not always. Okay. And there are some great images, CT scans of each of these injury patterns in

the article. So, again, if you've got access, go take a look. The last one, intraparenchymal hemorrhage. So this is kind of deep hemorrhage within the meat of the brain. Yeah. Intraparenchymal hemorrhage is I also think of differently because when you have bleeding actually, within the parenchyma, blood is actually pretty irritating to the brain. And so classically, when you have a contusion and intraprancyal hemorrhage that's traumatic, the first image that you see of it,

you know that it's actually not completed. There's still an active process going on. So you actually expect contusions or interprincal hemorrhages to blossom, meaning that the first image that you see within six hours, I'd actually expect it to be worse. I expect there to be edema around it. I expect there to be more cortical irritability.

And a lot of that has to do with there's some complicated cytokine release and pathophysiology that I don't know is necessarily relevant, but they are going to behave differently. They generate more pressure than just a simple volume of blood that's there is going to. Good. And then there's a discussion about skull fractures and penetrating trauma. Tell me a little bit more about these injury patterns. So skull fractures, I kind of divide them into, are they closed and non depressed, and

are they anything else? Most of the time, they're closed and non depressed, and they don't need much of anything, especially if they don't have underlying injury associated with them. That's actually a fairly common injury in kids. I do worry about them if the fracture line crosses, for instance, across midline at the occipital region because, as I mentioned earlier, you can cause some venous injury, and so that would warrant something like a CTB to make sure that the veins underneath are okay.

And if the fracture is depressed beyond the thickness of the bone, then that may in and of itself warrant intervention. Usually, that ends being associated with some underlying injury, and there's also the reality of the cosmetic deformity of, you know, the crater in your head. Penetrating trauma, I guess, a couple of notes on this. Obviously, these are very severe injuries. There isn't necessarily a role for going after

bits of something in someone's brain. You can actually cause a lot more damage than what has already even happened. One notable statistic that I found helpful clinically is that a biventricular trajectory of something like a gunshot wound is universally associated with mortality, with death. So that can be helpful prognostically in the emergency department setting.

And one last phenomenon that I've seen happen and I think is notable prognostically, Sometimes if you have bad enough skull fracturing, it can actually serve the same role that a surgical decompression can. If the skull is not actually in continuity, then it will auto decompress itself. And I think it's an important thing to think about as far as

the timeline. I mean, those injuries are very, very severe, probably almost universally catastrophic, and it would change what I would expect from, for instance, the number of hours of survival if the brain is auto decompressed. Intraventricular hemorrhage. So I think the most important tidbit with these is if you're seeing a lot of intraventricular hemorrhage, that's not really that common in a traumatic injury.

That is something that would make me suspect that there might be a spontaneous bleed underlying it, like an aneurysm rupture, like an arteriovenous malformation. A small amount can happen with the trauma, but a large amount would make me suspicious. In this section of the article, there's a table, table two, determining the risk level for critical intracranial pressure, which I find to be

a concept I wasn't aware of before. I I love this table, but this is taking a patient who has an intracranial hemorrhage and trying to determine low risk versus high risk. This is typically something I just deferred to my neurology or neurosurgery colleagues anyway. But I think if you're in a critical resource restrained area working in rural medicine or perhaps you have an ICU but no neurosurgery available, this is a concept that might actually be very helpful, and it's beautifully laid

out in this table. You can actually risk stratify someone to being low risk, and that low risk category, for treatment, when we get into it later, might actually be someone you could hang on to and just monitor as opposed to having to transfer them from, you know, Alaska to your nearest neurosurgical center? That was my goal to try and make it practically useful, and this was probably the thing that I agonized the most over because,

obviously, you don't wanna misguide anyone. So I did try to be on the more conservative side with these recommendations. But if there's any element of a higher categorization, it will be categorized as a more concerning finding. It's not the average of I've got some factors in low risk and some factors in high risk that averages out to low risk. If there's any feature of higher risk, then it would get qualified as higher risk.

Lower risk patients clinically are gonna have, non vocal examination, meaning no neurologic deficits. The GCS is going to be somewhere between thirteen and fifteen, so into the mild traumatic brain injury category. Minimally symptomatic, meaning maybe they have a little headache, a little nausea, not more than that. And it's an important one here that it's a stable examination. If they're clinically stable, that

is very reassuring. If you have a few hours to be able to say that they're not decompensating, that's a very reassuring thing. Radiographically, as I mentioned earlier, isolated traumatic, meaning peripheral subarachnoid hemorrhage, I do not find as concerning. Salcine and tentorial subdural hematoma, which I'm categorizing differently as convexity subdural hematoma, a chronic subdural hematoma without shift. Again, we

know that that's not a new finding. That's something that they've been dealing with for, you know, weeks or months. A small volume of intraventricular hemorrhage is really rarely gonna do anything. And maybe most significantly, if you have stability of findings on repeat imaging, maybe six hours later, that is also very reassuring. You know that it's not likely to change at that point. And from the laboratory findings perspective, there does have to be no coagulopathy.

The higher risk category, I would put for patients who are clinically showing signs of moderately impaired consciousness, which is a GCS qualified as nine to 12. And if you have any asymmetric examination, that implies that there's focal effect in the brain that's having clinical ramifications, and there's a more concerning finding. Yeah. So if they're weak on one side, if you're seeing a facial droop, if you're seeing anything that's asymmetric, that would make me more concerned.

And into the radiographic category here, acute convexity subdural hematoma isn't an entity that can certainly change. Intra parenchymal hemorrhage or contusion, as we mentioned, is something that you expect to actually get worse before it gets better and before it stabilizes. Epidural hematoma classically is a concerning finding. Any kind of multicompartmental hemorrhage that indicates enough brain injury that I

would be concerned about it. And if the findings are worsening on repeat imaging, you know that you haven't seen the end of whatever decline could happen. And any laboratory, if they're showing any signs of coagulopathy, that also put in the higher risk category. You don't know that that bleed is stable yet. And then finally, the signs of critical ICP, I categorize separately because this is your indication that you should be starting medical management

for critically elevated intracranial pressure. These are the folks who come in clinically with a GCS of less than or equal to eight, a declining examination. And that can mean somebody who starts at a 13, and then you check back in a couple of hours later and they're at a 10. It doesn't matter that they're not at eight yet. If they're showing that kind of decline, that's highly concerning.

If they've got a pupillary defect, I mean, the classic long pupil is sort of an obvious one, but any other cranial nerve deficits implies that there's, brain stem pressure. And vital sign of abnormalities. The classic sign here is Cushing Triad. It actually takes quite a lot to have that effect that is someone who is, you know, bordering on herniation.

Occasionally, I've been called to the bedside for somebody who's awake and alert with high blood pressure and bradycardia and maybe some irregular respiration. That is not the Cushing Triad that is being referred to in this setting. This is somebody who is comatose and very injured. It's pretty rare to actually see in clinical practice. Radiographically, midline shift is sort of a an easy

one to be able to look for. Cisternal effacement, which can be a little bit more challenging in the younger population where their brain is just fuller. Socal effacement, again, somebody with this who's starting with a full brain, it can be a little bit more challenging to look for. And herniation, and, generally, we're talking about uncle or transcentorial herniation in this setting. And the coagulopathy is kind of irrelevant here.

This is you know, we're sort of beyond the stage of treating based on these. Great. Yeah. And that's table two, page nine, a fantastic reference, I think, to keep in your pocket. I mean, obviously, if I think if you're in a resource constrained area, this is very handy. But even if you're a tertiary center and you've got someone with a hemorrhage, this helps kinda guide the decisions that you're going to see from your neurosurgical and neurological colleagues, so it's not a surprise to you.

You can even prep family members. Oh, okay. I've got a low risk person. I'm gonna call my neurosurgical colleague. They're probably gonna say there's nothing to do here. Or I've got someone who, you know, is awake, alert, has maybe not a very worrisome radiographic finding, but is anticoagulated. So we're gonna bump them into the high risk category, and this is why we're getting

all excited about it. It's helpful to understand that decision making process that goes on for my neurosurgical colleagues. There is a great section also following this table three to try and differentiate the spontaneous

versus traumatic. We don't have to read through it, but it's a few points of information to help you differentiate spontaneous from traumatic etiology because, again, the spontaneous hemorrhage is a whole different pathway, and I think that table nicely outlines some of the characteristics of those types of patients and how you can tell them apart from the traumatic.

Next is the section for prehospital care, and I know we've got some colleagues who listen to the podcast who work in prehospital medicine, some EMTs and paramedics. What are some of the critical things that we can do in the prehospital setting for someone we suspect might have a hospital setting for someone we suspect might have, traumatic brain injury? So a lot of it is actually the same as what we're targeting in the emergency department.

I think the critical things to be bearing in mind are and and maybe it sounds a little silly, but maintaining normal thresholds is actually really, really important. Normoxia, normocarbia, normotension, normoglycemia. And they've actually had studies where they've shown that even a single reading of an oxygen saturation less than 90% or a single systolic blood pressure less than 90 has been associated with increased mortality.

So those sound like simple things, but they're actually very important things, both prehospital and in the hospital. Some other things that I think are important to remember, there's significant caution reserved against hyperventilation. As I mentioned previously, it is something that's going to reduce the cerebral perfusion pressure.

And so while it can be an excellent temporizing measure just to get someone maybe twenty, thirty minutes from the ED to the OR and prevent herniation, it's otherwise a pretty dangerous thing to do to a brain because you are restricting the amount of blood flow that gets to the brain and you can cause ischemia. So in the prehospital setting, it's typically not advised. Another important thing that the prehospital providers can be doing is having an accurate on scene neurologic assessments,

namely the GCS score. Having the trend there is actually incredibly valuable. Knowing whether someone is stable or declining changes the paradigm of how much concern you have. So having accurate trends there is really critical.

Kind of on the same level, if the patient is intubated in the field, which would be indicated for a GCS of less than nine, knowing which paralytic was given, which sedating agents were given, and when is also a critical thing for the providers later to be able to assess how this might be affecting the neurologic exam later. And any notable elements from on scene can be very helpful in the determination of was this spontaneous or

not. If it's a really low mechanism appearing car accident, but the patient is really neurologically compromised, that's concerning for there being something else that caused a crash. So elements like that from the scene can actually be very, very helpful. Other elements here, TXA, there have been actually a few decent studies that have shown that essentially in the long term, it does not improve emotional outcome at six months in the TBI setting.

There are some in the hospital settings that it seems to improve, but long term, it does not seem to make a difference. So that's not a standard recommendation in the TBI setting. I think those are the most significant things from there. Good. And that's nicely summarized. Again, table four, the Brain Trauma Foundation prehospital guidelines, really covering all of those items in one table, mostly hemodynamics, but also critically important in history gathering and in obtaining

a baseline exam for monitoring the trend. So those are some critical pieces for our prehospital personnel. Once they arrive in the ED and it's our turn to obtain a history and then perform a physical examination. Let's start with a history. Is there anything really critically important when it comes to history assuming that the patient's able to give me one? Yeah.

So, I mean, it's a good sign that the patient can give you, but but if you're also getting it from EMS, establishing those things that we just mentioned about were any alertness altering sedating medications given if the person was paralyzed, what were they paralyzed with and when. Any information you have from on scene that might help you determine whether or not you think this could be a spontaneous etiology.

And the big piece from the patient history would be, is there any reason to suspect a coagulopathy? And that includes things like liver disease as well. It doesn't have to be just medication induced coagulopathy. Yeah. Is there any reason you'd suspect thrombocytopenia? And then physical examination, obviously, we're looking for the neurological deficits and level of alertness. Anything else specifically we need to be focused on? I guess so. This is a lot of

sort of following basic ACLS algorithms. I didn't go into a ton of detail here. I think some of the things to note in the setting of traumatic brain injury, look for facial trauma that you think could compromise the airway either at the present or if you suspect that's gonna be an issue, for instance, going for imaging. That's something to be mindful

of. And maybe this is a little bit more of a subtle thing, but if your patient is already intubated, I think that this is a unique scenario where a, quote, neurologic code in that setting can be silent. If you don't have intracranial pressure monitoring, there aren't going to be any alarms or, you know, there's gonna be nothing that tells you necessarily that the patient is nearing

brain death. And so I think sometimes I've seen there be maybe less concern than is warranted because the patient, you know, appears comfortable. We don't see anything dramatically wrong with the vital signs. That doesn't mean that the patient isn't a critical neurologic patient. So just keeping that in mind if you've got a patient that's intubated and appears stable, that doesn't necessarily mean that they're stable until you've proven that neurologically.

And if they're already intubated, you're relying a lot there on brain stem function and reflexes for exam findings? Depends on what agents they've already had on board. And this is one where, I guess, knowing what paralytic was used and when, succinylcholine versus rocuronium essentially, is critical. And if they did get rocuronium in the last sixty to ninety minutes, you may well not have an exam at all. You will still have pupils

because rockeronium does not affect that. But beyond that, you're not gonna have much of anything, and that is a scenario where, let's say, it's been two hours, and now you don't know, is it the rockeronium, or is this patient really, you know, very, very impaired? And this is where I actually do advocate for use of something called a four twitch monitor or a peripheral nerve stimulator. They're really commonly used in the OR by anesthesiology after elective cases to ensure that paralytic is

off before they extubate a patient. And it's a simple tool, and, essentially, it's a shocking device that it will use the train of four feature, which is just a simple click of the button and put it generally, people do it right here at the eyebrow. It will work on any muscle, and you're just watching for each shock should cause a muscle twitch. So four shocks should

get you four muscles switches. If you are not seeing that, it means that they're still paralytic on board, and that can help you tailor what you'd expect from your neurologic exam and whether you should be giving reversal to be able to actually uncover what neurologic exam is there. So that is the risk that I worry about with rocuronium, but it's not insurmountable. You have those tools that are available to be able to determine how much an effect it still has. Great. Yeah. That's

a great point. And a good pearl there, your anesthesia colleagues are going to have those tools available. So if you've got an OR, you could probably get one pretty quickly. Yeah. I I actually grabbed one from the OR at some point and hid it in the ED so that I had it available. And Sugamadex is also really easy to get in the OR. They use it all the time. So Yeah. Swinging by there and grabbing it. Yes. In your airway cart, probably something

you should have stocked. Yeah. Alright. And then there's a whole section in this article about brain stem function and how important it is when we're talking about reflexes. Tell me a little bit more about that. Okay. So while brain stem function is not typically something that's assessed in detail in the emergency department, I do think that there is a role for it in severely impaired patients with, let's say, a GCSF three.

And part of what you're trying to be able to assess and communicate to your neurosurgical colleagues is how close this person is to herniation or have they already herniated. Mhmm. And sometimes that's the best exam that you're going to be able to give, and so you're just trying to trend something. If you have one blown pupil, and by the time they get to their neurosurgeon, they have two blown pupils, that's a very

helpful thing. Or if they had a cough or a gag or were over breathing the vent initially and now are not, those are actually really helpful things to be able to trend to and one pearl there that I think can be helpful prognostically is if someone has had bilaterally fixed and dilated pupils for six hours or more, that's universally associated with brain death.

So these elements, while we don't necessarily always associate them with something that's checked in the emergency department, there is a role for them. Yeah. That's a a really good point, actually. You know, I think of these as critically sick patients, lots of high anxiety levels, and we get to the point where we figure out, okay. This person is dying in front of me. I'm just going to call for help. And we forget about the subtleties in differentiating all of these findings and maybe even

in writing them down. Like, oh, yeah. But, you know, what exactly what time did I call you and what was the exam at that point versus what it is now? So that includes things here listed like doll's eyes, corneal reflex, the cough, the gag reflex, and, you know, spontaneous respirations and whatever motor exam there is. So those are critical things to both write down and time stamp for your colleagues who are then going to take over patient care so they can trend.

Yeah. There is a role. I have seen decisions made about whether or not someone goes for a surgery based on whether or not they still have any intact brainstem reflexes or how recently they lost them, especially in young people who are really injured. So there is a role for keeping track of those items. Okay. So laboratory studies. Tell me about labs

in this patient population. Anything important? Sure. Some there are certainly the basic labs that you wanna be the biggest thing looking for coagulopathy.

But then there is actually some new and kind of exciting research on some elements that I'd still qualify as exploratory in The US, but I think up and coming, the big three being s one hundred b testing, GFAP testing, and UHC L one testing, all of which in other countries have actually some of them are even incorporated into standard TBI algorithms to be able to assess who is low enough risk that they, for instance, may not even warrant a head CT. So I think that they could be clinically

quite useful. They're just not quite ready for prime time in The US yet, but I think that they'll need to keep an eye on. I think those will be in clinical practice in the coming years. And this is specific to intracranial hemorrhage or just traumatic brain injury in general? So this is in the traumatic brain injury in general category because these are often patients who the decision is whether or not you actually need to pursue further imaging.

Gotcha. So it it is in the broader population, not people that you know have intracranial hemorrhage. Gotcha. Alright. And then imaging studies, you know, in most emergency departments, hopefully, we have CT available. But you already mentioned that in some cases, a CT venogram might be important. We have CT arteriograms also or angiograms at our disposal. How are we gonna differentiate which population needs which study?

Yeah. I think the basic study that hopefully everyone has access to is a nonconhead CT, and that is quite good to be able to see intracranial hemorrhage. Nuance studies include a CTV, which is an appropriate study if there is an occipital fracture crossing the midline and you're worried about venous injury underlying it, or if there's a skull base fracture that in infringes on the jugular foramen. That's another situation that having a CTV to rule out vascular injury would be helpful.

CTA is going to be your go to study if you suspect any reason there's a spontaneous coverage because you'll be able to see aneurysms, vascular malformations, Or if you have a bony fracture that is, for instance, infringing on really any of the skull base elements, but specifically the carotid canal, if you're looking for a lung cerebral vascular injury, the CTA is gonna be your best

bet to be able to find it. The other element that you can use CTA for, and this is maybe a little bit more on the practically useful, but not research based prognostically useful, CTA in the setting of really, really severe brain injury with, let's say, someone who has no exam or close to no exam, CTA can be something that shows you, assuming that it's appropriately timed, if there is no intracranial blood flow, that is a situation where you can assume the intracranial pressure is so

high, there is no blood that is able to access the brain. And that can be a helpful thing in, for instance, talking to a family member about how severe an injury is. Gotcha. Alright. And what about bedside ultrasound? There's a discussion there about optic nerve sheath diameter on ultrasound. Is that a helpful imaging modality? You know, I don't see it in practice in the ED often, but I think it's kind of a cool thing that I hope starts to take more of the spotlight.

There's pretty good data to be able to suggest that if you have an optic nerve sheath diameter of greater than 4.8 millimeters, that is something that's consistently associated with an intracranial pressure of greater than 20. And the sensitivity and specificity are pretty good. So I actually think that's something that could have more of a role even now for providers who are comfortable with using ultrasound, which I think is most of my ED colleagues.

Yeah. And it's pretty quick measurements and certainly one that we can repeat at the bedside without having to take the patient back to CT every time. So Yeah. Quick, noninvasive. So I think that there is a role for that even now. I'm wondering if that's something you have to do bilaterally. If you're suspecting intracranial pressure increase, say they have a blown pupil then, do you have to do this in both eyes?

It should be a proxy for the universal intracranial pressure unless you have something really focal behind the eye, but it's probably something that's better to check on both sides. It's actually the same issue that you can run into with an intracranial pressure monitor. For instance, if you put the monitor directly into a contusion, you're gonna get a really high pressure that's not necessarily

representative of the brain as a whole. So that that's an issue that wouldn't even just be with an ultrasound. MRI imaging, again, this is not something we can typically get in the emergency department in any kind of rapid fashion, but there are some EDs that can task this to occur pretty quickly. Are there instances where an MRI would be more helpful than a CT? So I primarily have MRI mentioned here as something that I would be very cautious about using in the setting of acute brain injury.

And that's largely because for an MRI to happen, you're going to have to lie the patient flat, which is going to increase intracranial pressure, and you're gonna put them for forty minutes, sixty minutes in an unmonitored environment, and you don't necessarily know how they're gonna look when they come out. Mhmm. Yeah. In these patients, I would be very hesitant.

Even if I had an MRI at my disposal readily, I would be hesitant until I really knew that they were stable to pursue that, especially because a CT actually gets you pretty much all the information that you need. The only element the that MRI is really going to help you with is if there's DAI, diffuse axonal injury, which certainly can be helpful prognostically. It doesn't really guide initial management. So I think there are very few roles to really be considering MRI in this acute setting.

And then EEG monitoring, is that universal for all of these patients, or when would you consider that necessary? Really, I would only consider that if the it seems like their exam is so disproportionate to the amount of injury you see on imaging that you're worried about non convulsive status epilepticus. So it's a reasonable thing to throw on someone to rule that out in that setting, but certainly not something that I would expect to need for garden variety traumatic brain injury patients.

Gotcha. Alright. Let's get into treatment. So we're in the ED. We've got somebody with a traumatic brain injury. And now you have already mentioned how a lot of these injuries can be treated nonsurgically, and that treatment begins really in the prehospital setting, but we definitely wanna make sure we're giving appropriate treatment in the ED. Let's begin with just some of the basics.

There's a great table, on page 16, table seven, the summary of actions to consider for patients with traumatic brain injury that kinda walks you through all of these elements. Obviously, they we're gonna get IV access. When it comes to hemodynamics, what are some of the parameters when it comes to blood pressure? Say we don't have an intracranial monitor. The what are the kinds of parameters we're looking for for normal tension?

Yeah. So this is probably one of the biggest takeaways, as far as specific numbers, and vital signs to be thinking about in the traumatic brain injury population. Because I think there's a tendency with brain bleeds to worry about hypertension. And the bigger thing in the traumatic brain injury section is actually to worry about hypotension. And I mentioned this earlier, but I'll mention it again because I think it's pretty significant.

A single systolic blood pressure of less than 90 is associated with worse mortality. There isn't a clearly defined upper limit for what blood pressure is safe in the setting of traumatic brain injury and intracranial hemorrhage. So it's normal tension that you're shooting for, and it does vary a little bit by age. For the fifty to sixty nine year old population, you're aiming for a systolic greater than a hundred. And basically, in everybody else, you're aiming for greater than one ten.

And the research does not clearly define an upper limit. I would put it somewhere around a systolic of one sixty, but there really isn't good evidence to support that in the traumatic intracranial hemorrhage literature. You're aiming for normoxia. You're aiming normothermia, and this is where Allegan mentioned prolonged hyperventilation is something to avoid. Hyperventilation is a temporizing measure. It is not something that I would use in any kind of long term setting. Gotcha.

And those blood pressure parameters, again, in distinction to the spontaneous intracranial hemorrhage, which is a completely different population. So we're just talking about traumatic intracranial hemorrhage. That's correct. Because there because there is good evidence in the spontaneous intracranial hemorrhage category for strict systolic parameters to avoid hypertension. So this is one of the big differences between spontaneous and traumatic intracranial hemorrhage. Gotcha.

Coagulopathy, obviously, if they have a coagulopathy and they're on some agent and we can reverse it, that's indicated in all of these patients? I would actually say it's not necessarily indicated for everyone.

For example, especially if you're considering something like PCC, which maybe some places only have in access in small amounts, or if you've got somebody, for instance, with a thin chronic subdural who is also anticoagulated, You can consider, for instance, something like vitamin k. You can consider slower reversals or waiting for something to titrate off if somebody is really very stable with a minimally concerning ridge. Good to know. Positioning is important as well. Tell me about that.

So positioning, I think it sounds maybe simple, but raising the head of bed to 30, that can look like a 10 or 15 difference in somebody's intracranial pressure. It is not a small thing. And if you're worried about spinal precautions, which often in this situation you are, reverse Trendelenburg will get you there too. So it doesn't mean that you can't do it. You still can. You can just maintain spinal precautions at the same time.

And something that is maybe easy to miss, if the cervical collar is too tight, that can also have a significant effect on intracranial pressure by preventing venous outflow. So making sure that it fits the patient and that their head is square in it actually can have a significant effect as well. Good. Yeah. That's great. Those are easy things to do. Yeah. Also circumferential ET tube tape.

Anything that's going to come across here and prevent I mean, there are things that we can make sure are not causing a problem. That's right. No ligatures around the neck. Correct. Okay. Good to know. Alright. How about sedation medication? So if they're intubated and we're sedating them, you know, I'm always reaching for propofol in the emergency department, but there is an indication for not overly sedating these patients so that you can continue to perform examinations

and track reflexes. So where are we in recommendations for that? Yeah. Propofol is a safe bet. Obviously, you're walking the line here where you wanna make sure that the patient is comfortable, but that you also need to be able to trend a neurologic exam. Propofol has a pretty short half life, so being able to titrate it off and get an exam, I mean, there's a reason that it's so commonly used, and it is a good option.

I would argue fentanyl is also a decent option because it is, pretty short off. Others in eating, especially benzodiazepines, I would avoid because those really those have a much longer half life, and you'll lose your exam for longer. Good to know. Antiepileptic medications. So is this only if they have obvious seizures or have an abnormal EEG, or is this kinda prophylactic for everybody? This is a particularly messy section of the research. There isn't great data on especially prophylactic

use as anti epileptic medications. If somebody is obviously seizing, absolutely, by all means, treat it. I think the combination of the concern over possible post traumatic seizures and the fact that especially Capra, levatoracitam is so available and such a benign medication overall. Mhmm. It's given a lot. And, I don't really necessarily have a problem with it because it is a pretty benign medication to add on. But the way that I would think of it is it's not necessarily critical

unless you actively see someone seizing. For instance, I would not opt for Keppra before three percent if you've only got access in one spot. The Keppra can be put on the back burner in the emergent setting unless you see that they're actively seizing. Overall, the literature does say prophylactic, antiepileptic for seven days after a head trauma is reasonable. Even if there isn't phenomenal evidence to support it, it's pretty annoying.

And this is necessary to give in the ED on presentation, or this is kinda it's great to have an antiepileptic on board in the first twenty four to forty eight hours? Again, there isn't great data on it. I would say it's nice to have it in there in the first day or so. But unless someone is actively seizing, it's not one of my top priorities initially. Gotcha. Okay. And then medications to temper intracranial pressure. And you mentioned hypertonic saline, and, we

also have mannitol in the emergency department. Is there evidence between one or the other, or is it just kinda whatever you have available? Oh, boy. This is another really messy area. No one has ever been able to clearly show that three percent or mannitol is one better than the other. They both work. And especially mannitol, I will say, just sort of from my own experience in the OR, mannitol, you can actually watch the effect on

the brain. I mean, in the course of a minute or two, you can watch swelling decrease. So it mannitol tends to be the medication that's reached for as the, you know, can I curse on here or no? No. Okay. As the oh, damn. As the oh, damn medication. Because it works fast. That said, three percent is probably more readily available in the ED in general. And generally speaking, like we talked about, we're worried about hypotension. As a volume expander, three percent is not

going to risk that. So if you've got somebody who is borderline or hypotensive, I would certainly reach for three percent before mannitol and then he'll dieretic. You're going to risk actually dropping their blood pressures. Likewise, if they're very hypertensive, you could consider reaching for mannitol to drop the blood pressure. And similarly, if their volume status is, you know, grossly fluid overloaded, sure, mannitol is maybe a better

option where they have terrible heart failure. But that said, a volume of two fifty of three percent probably isn't going to throw off even somebody with bad heart failure. Baseline sodium is certainly something to think about. Sometimes you have that data, sometimes you don't. The only patients that I would really worry about are people who are severely hyponatremic at baseline, and you worry about central pontine myelinolysis.

That said, it's actually pretty rare in clinical practice, and there's never been a case report of somebody with normonatremia who develops central pontine myelinolysis independent of how much 3% they're given. So if you know that you're starting anywhere in the normal ish range, it's not something that I'd really worry about, especially if your leading concern is intracranial pressure. And the last one to think about is

patients with kidney disease. I would not use Manasol if you know that people have bad kidney disease. Gotcha. Alright. And then there is a section here about managing the airway. Obviously, if their GCS is eight or lower and we're worried about the airway, we're going to intubate these patients. Is there something in that process or in that management that is more neuroprotective?

Yeah. The medications that have the most evidence behind them prior to rapid sequence intubation, fentanyl or remifentanil probably have the best evidence. Induction agents, propofol, etomidate, or ketamine should all be fine. And paralytic, there is debate between rocuronium and succinylcholine. One has not been definitively proven to be better than the other. The thing to keep in mind with rocuronium is obviously that it's going to be in effect much longer.

So that is where noting the dose and the time that it was given is going to be critical to be able to pass on that information as far as when we can expect that the effects are going to wear off and whether something like secantinibex is indicated. Yeah. That debate in paralytics has only been going on my entire career, so it's okay. I wish I had clarification. I do not. I'm very disappointed you did not come up with an answer just during this article.

Okay. Managing intracranial pressure. So we talked about medications which can be given. We talked about hyperventilation as something that is only done very intently for a very short period of time, perhaps on the way to the OR. Anything else? There's a discussion here about shivering, so patients' shivering and shivering control. That's important because that can increase intracranial pressure?

Yes. Shivering absolutely can. It increases intrathoracic pressure, decreases venous outflow, increases intracranial pressure. So sometimes, paralytic is actually used in that setting. This is more of the neuro intensive care setting. Paralytic can actually be used to prevent shivering in the ICP escalations related to it. And then I like that there's on page nineteen nineteen there, a description of kinda tier one, tier two, tier three interventions for continued

in elevated intracranial pressure. This is getting more into that kinda longer neurocritical care, and this is certainly something you're doing in consultation with your colleagues. But there's an excellent description of that in the article as well. I also like that you included the surgical management. So table nine there is sort of a picture of the different types of surgical approaches, things like craniotomies, decompressive craniectomy,

burr holes, and how they're done. That's a fantastic image and I think helpful to know. Again, hopefully, you're not doing this in the ED, but, you know, burr holes are certainly something that can be done by emergency medicine physicians in a disaster scenario.

But I like that this is outlined in here, again, for completeness' sake so you can see what your neurosurgical colleagues may be doing in the OR and some of the reasons behind them, like, you know, if someone has an epidural or someone has intractable elevated intracranial pressure. This is helpful to know. Yeah. I think my primary reason for having it there, I think that it can be a little bit of a mystery for people

on the other side of it. And a lot of it is actually fairly simple, and a lot of it has to do with identifying what the source of the pressure is and how you can best address it. And I think this is where the limitations of surgery also become a little bit more evident maybe because it all depends on how accessible the lesion is. An epidural hematoma, right at the surface, very easy to access.

Contusions, especially ones that are deeper in the brain, multicompartmental hemorrhage causing kind of generalized edema, those are not things that you can really easily address surgically. And the ultimate measure that neurosurgeons can use is even a bilateral hemicraniacomy. So that would be, as you see in figure nine, not just on one side of the head, but decompress both sides, open up the dura.

And those situations are really reserved for terrible, terrible brain injury that is causing so much pressure that is not in an accessible region. There is no focal lesion to be able to evacuate, and you're just trying to give the brain more space by breaking the Monroe Kelley doctrine. The interesting thing is that the evidence does actually not support doing bilateral craniotomies.

That has never shown a long term outcome benefit, and it's probably because the brain is so injured at that point that independent of whether or not you decompress it, it is beyond recovery. So I think one of the things to be mindful of with these interventions is just that they cannot resolve every problem. And there are certainly people who you even do bilateral crani, and they still herniate Mhmm. Because there's just

too much pressure. And even just the skin at some point becomes a bounding feature, and they can still generate enough pressure to herniate. So as much as I would like to say that neurosurgery can cure everything, I mean it when I say that the medical management is often the definitive management that you're trying to do for these patients.

Yeah. Yeah. That's good to know. On the same kind of wavelengths, external ventricular drains, it's kind of an institution dependent practice whether or not they use them for trauma because intraventricular hemorrhage is fairly rare in the traumatic setting, and hydrocephalus is fairly rare in the acute traumatic setting. An external ventricular drain is an excellent intervention for hydrocephalus. That's not typically the problem in the setting of trauma.

So, yes, it's one of the three elements of the Monroe Kelley doctrine, CSF, that you're taking off and you can lower pressure that way. But I think it's also important to note that it ends up not being immensely helpful because there's often so much pressure from the brain and the blood itself. CSF is not the problem. Often, the ventricles are really tiny to begin with. You're gonna get

off some pressure. Sure. Maybe it's enough to temporize through the critical period, but it's by no means a definitive intervention. And it can also be higher risk because the ventricles are often collapsed under pressure. It's a procedure that's often done blindly at the bedside by your neurosurgical colleagues. So I think it's an intervention that can be considered, but it's also not a definitive management in the setting. Okay. What about bedside burr holes for these

patients in the emergency department? Is that actually a thing? People perform those in the ED as opposed to taking them to the OR, assuming the emergency physician isn't the one doing it? So there are actually a couple of case reports of ED physicians doing bedside burr holes for specifically epidural hematoma when they are in a critical access location. I think, in those situations, they were several hours from definitive neurosurgical care with someone with

blown pupil and a critical exam. So in the literature, there are a couple of reports where this was done successfully. I will say, I think the biggest reason that this is something that there's almost no indication for is that it just doesn't work very well. You have a tiny hole, and I think something that people don't necessarily think about is that it's clotted blood underneath it. It's not actually necessarily

liquid. It's like Jell O. And so you're just blindly suctioning in through your tiny hole to try to evacuate whatever you can blindly. And it's also not addressing the underlying bleeding, which is typically from the middle meningeal artery. So you've got active extra filling up the space that you just tried to suction out. And so the two case reports that I'd seen of it both reactumulated their epidural within,

I think, an hour or two. And I think in one situation, they were repeatedly suctioning while they were in transport trying to get to neurosurgical intervention. Wow. And both required neurosurgical intervention at some point. So, I mean, sure, there are very, very few cases where this has ever been done successfully, and it's a very limited intervention. So while I think it maybe sounds exciting in clinical practice, I think there are very few indications where it would be successful.

And temporizing at best. And and temporizing at best. Lastly, tell me about goals of care. When is it appropriate maybe to start having these conversations with patients and family members? Yeah. I think this is maybe one of the scariest things that ED providers can be occasionally tasked with because, no, it doesn't necessarily mean that you're an expert in neuroprognostication, and these injuries are really challenging.

But I do think that there is a role for at least starting the conversation in situations where you do suspect severe injury in somebody who you think may well not do very well. And so even asking some simple questions to family members just to start the thought process

can be incredibly beneficial down the road. Even when neurosurgery is speaking to the family an hour later, if they've even had a little bit of time to think about questions like, what does a worthwhile day look like for this patient? What level of functioning would be necessary to make life worth living? If they've even had a little bit of time to think about that for the patient, it can really help them make better informed

decisions. So I think there is a role for at least starting that conversation in the emergency department. Yeah. Yeah. That's a great point. And certainly something that can be quite uncomfortable to do for me, especially in these settings where I'm like, hey. I'm not a neurosurgeon. I don't know what your outcome's gonna be, but I think it's an important point to at least start that conversation and get an understanding of who the patient is and what they would have wanted.

Yeah. Even for those of us who know at least something about neuroprognostication, it's still somewhat of a black box. And we do the best that we can, and we just try to help patients make informed decisions. Fantastic. Alright. Well, that's a lot of information. Again, this is the February 2025 emergency medicine practice article on traumatic intracranial hemorrhage. We have covered almost all of it, but believe it or

not, there is more in this article. It is just jam packed, and it's a wonderful write. I really love it. So I think all three of you did an outstanding job with this article. There is a clinical pathway in it for newly discovered traumatic intracranial hemorrhage. It'll walk you through who needs to be observed, when to get your neurosurgical consult, the critical pieces you need to do at the

bedside. And there's also a clinical pathway for elevated intracranial pressure, both of which will convert into interactive formats to help you at the bedside, and it'll, I think, greatly inform your practice. I wanna say thank you for being one of the authors and for coming on the podcast to explain the voluminous amount of information contained in here. It's a wonderful, wonderful article. I highly encourage our listeners to go download it, read it, and get your CME.

I mean, that's four hours of trauma and neurocritical CME that will be well earned and, definitely inform your practice. Thank you so much for being on the podcast. Thank you so much for having me. And that's a wrap. Thanks for joining us for this episode of Amplify. As always, I wanna remind you of ebmedicine.net, your one stop shop for emergency medicine and urgent care continuing medical education.

That's three journals, the emergency medicine practice, pediatric emergency medicine practice, and evidence based urgent care journals along with a multitude of courses like the laceration course, the abscess course, the EKG course, all available to you at ebmedicine.net. Until next time, everyone. I'm Sam Ashoo.