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
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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.