Sam: I actually wouldn't consider that to be mild in general
practice if somebody said they were actually out for 25 minutes or so.
But 30 minutes is the general accepted guideline there.
Sam : Hi everyone, and welcome to another episode of EMPlify
I'm your host, Sam Ashoo.
Before we dive into this month's episode, I want to say thank you for joining us.
I sincerely hope that you find it to be helpful and informative for your
clinical practice, and I want to remind you that you can go to ebmedicine.net
where you will find our three journals, Emergency Medicine Practice, Pediatric
Emergency Medicine Practice, and Evidence Based Urgent Care, and a multitude of
other resources, like the EKG course, the laceration course, interactive
clinical pathways, just tons of information to support your practice
and help you in your patient care.
And now, let's jump into this month's episode.
Sam: All right.
Welcome back to the podcast everyone.
Today we have a special guest, one of the authors of the March, 2026 article
on severe traumatic brain injury.
This is Dr. Klavansky and I'm gonna let her tell you a
little bit more about herself.
Welcome to the show.
Dana: Thank you for having me.
So, yeah.
My name is Dr.
Dana Klavansky.
I'm one of the neurointensivists at the Mount Sinai Hospital.
And me and my co-fellow wrote this article to really expand our knowledge,
our group's knowledge, and to just give the emergency medicine community
also a comprehensive review of what it means to treat severe TBI patients and.
In the safest way with the latest literature review.
So we're really happy with how it turned out.
Sam: Yeah, I think it's a fantastic issue and I'm excited for everyone
listening to go and read it.
It's packed full of information tables and figures lots of images, which I love, and
, it's an excellent review of the topic.
Now you, as one of the co-authors, you have a special interest in this.
You see a lot of this in your day-to-day practice.
Dana: So we actually don't see too much of it.
At our, one of our affiliate hospitals, Elmhurst is where most
of the neuro traumas actually go to, and also to Mount Sinai Morningside.
But Mount Sinai Hospital itself and Mount Sinai West where I work,
don't really see too many of them.
So this was actually even more interesting to write in that regard
because, you know, we got to learn through this process also and learn.
What the latest practices are and things like that.
So, it was really interesting to write this.
Sam: Great.
Great.
And let's talk more about severe traumatic brain injury as an entity.
So how common is it and how often do we see it in the US?
Dana: Yeah, so every year there's almost like 2 million traumatic
brain injuries to some degree.
Severe TBIs are not as common.
Thankfully, most people do get discharged from the hospital and
they end up doing really well.
But there is a certain population, especially those
that are a bit more rogue.
You know, our 15 to 19 year olds , and then our older population who, you know,
just has a higher propensity to fall and hurt themselves, and then they're
on blood thinners and all those other things that can cause severe brain injury.
It's thankfully a smaller population, but it's in the hundreds of thousands every
year that people develop severe TBIs.
Sam: So our, our teens and then our elderly population.
And is there a gender distribution there as well?
Dana: Yeah.
So as kind of maybe anticipated men have more severe TBIs than women
Sam: That doesn't surprise me.
Dana: So there is a difference in the gender distribution as well.
Sam: Perfect.
And I noticed in the article you did a review of the literature
from the last 20 years.
Has there been a lot published on the topic in that timeframe?
Dana: Yes.
So there was a lot of literature that we combed through.
We looked for the most comprehensive literature that would actually help
people really understand the mechanisms behind TBIs and how to treat TBIs
because some of the literature was unfortunately not very conclusive.
And so we were looking for more of the conclusive literature,
like I said, how to treat it.
The most pertinent imaging when to go for surgery.
So thankfully, especially the more recent literature, has been
great about that . So we had a lot of good resources to work with.
Sam: Excellent.
And in the pathophysiology section, there is a distinction drawn
between primary and secondary TBI.
Tell me more about that.
And how that fits into our clinical practice.
Dana: Yeah.
So primary TBI is.
a direct injury and the secondary brain injury is the sequela of that initial TBI.
So, with primary TBIs, it can be an open or a closed injury.
So, you know, either smash your head against something or you.
In another way, you can get stabbed or a gunshot wound and things like that.
So there's lots of different ways that a primary TBI can happen . And then
the secondary brain injury that happens is, like I said, the sequela of it.
So increased pressure in your brain, decreased oxygenation to your brain,
decreased blood flow to your brain and then the process behind that cell injury.
So the Wallerian degeneration.
That occurs, the glutamate release that occurs which really damages
those structures in the brain.
So that's why there's a distinction between primary
and secondary brain injury.
Sam: Gotcha.
And then there is also a discussion of the various types of hemorrhage
and hematomas that can occur.
None of that though, has changed as far as definitions in the last couple of decades.
What we know as subarachnoid hemorrhage, epidurals, and subdurals
is still the standard definition.
Dana: Yes, they're still the same.
Sam: Excellent.
And the epidemiology section.
This is the part that always fascinates me the most, but you already mentioned the
number of patients per year in the US and, the male predilection versus the females.
But, I did find it interesting that there are like almost 50,000 deaths each year
attributed to isolated traumatic brain injury, which is a pretty high number
of people with significant injuries.
and half of those deaths occur just in the first few hours after injury.
And then there's a pretty significant population of them
occurring in children as well.
Dana: Yeah.
So there are several factors.
So it depends of course, on the mechanism of the injury.
Some injuries are just irreversible, catastrophic injuries, and that's
why they die in the first few hours.
And then it also depends on what resources you even have.
You know what hospital you go to and things like that.
Some hospitals are incredibly specialized at treating these traumatic brain
injuries, but unfortunately, in more remote areas, the closest hospital or any
hospital in the area just may not be as well equipped to handle these severe TBIs.
So , the treatments that a person receives will also affect it.
And unfortunately.
Yes, children also do develop these severe TBIs, and that can be from
injury from either accidental injury or injury from others and things like that.
So those do unfortunately also happen.
And there's even less literature on how to treat children with TBIs.
So, we know less unfortunately on what numbers to aim for intracranial monitoring
and all those things for children.
Sam: Gotcha.
And I saw in the issue there's a table, table one, which kind of
discusses the most common etiologies for traumatic brain injury, putting
fall at the top of that list.
for all populations, all ages and then direct trauma and motor vehicle
collisions being the third most common.
There is a distinction now between mild and the moderate to
severe traumatic brain injuries.
Tell me about that classification.
Dana: Yeah.
So between a mild, moderate, and severe, it really depends on the duration of loss
of consciousness and duration of amnesia.
So with moderate and severe, there's a loss of consciousness
that's, a greater than 24 hours.
And your GCS score is much lower on the spectrum as opposed to mild TBI where
your loss of consciousness is very brief.
It's like 30 minutes . amnesia is also less than 24 hours.
So you're transiently altered, but you essentially get back to your baseline.
But with moderate and severe TBI you do not get back to your baseline essentially.
Sam: gotcha.
It, it's funny 'cause I actually wouldn't consider that to be mild in
general practice if somebody said they were actually out for 25 minutes or so.
But 30 minutes is the general accepted guideline there.
Dana: Exactly.
Sam: Okay.
Good to know.
And then there is also in the classification, a distinction
between impact versus Non-contact or inertial loading.
which is actually not terminology I'm accustomed to using in
the emergency department.
Tell me more about that.
Dana: Yeah.
So, the way I can kind of describe it, it might not be the best, honestly.
But the way I can describe it is that, like you said, there's two kinds.
So there's impact loading and also inertial loading.
So impact loading it produces more focal injuries like local skull fractures,
epidural hematomas and inertial loading is more of a diffuse injury of the brain.
So.
Concussions are more of a diffuse injury.
Subdurals can be very large and encompass essentially the outer portion
of the entire half of the hemisphere.
So that's what the difference is.
And diffuse axonal injury, which is a secondary brain injury.
So , the difference is more focal versus more of a diffuse injury.
Sam: Gotcha.
And then when we talk about.
All things on this podcast.
We always mention the differential diagnosis, but really this is quite broad.
It's just a differential diagnosis for altered mental status.
So anything from intoxication to dehydration, to infection,
anything you can think of that might cause altered mentation even, you
know, hypoglycemia for example.
All of that is on the list.
As far as the differential is concerned.
For our colleagues who are listening who work in the pre-hospital arena
is there anything new or maybe even just critically important that
we would encourage them to do as pre-hospital providers in EMS agencies?
Dana: As you mentioned, it's a very broad differential for these patients,
so I would just keep an open mind when you're working these patients up
as to, other concurrent issues that might be going on along with the TBI
because it's very easy and I'm sure it happens very often, that people think,
oh, this person has a TBI, they were in insert blank, you know, accident.
We are going to treat them for that.
But it's also very important to correct other metabolic etiologies,
other electrolyte abnormalities, arrhythmias ensure that you're not
missing any seizures, for example.
Because a lot of other concurrent issues could have also caused this.
And if they're missed, it could, you know, prove to be pretty catastrophic later.
So having a very low threshold , for doing a broad workup for why the TBI
happen is essentially as important almost as treating the TBI itself.
Sam: Good to know.
And if they are on scene and our medics are there , the initial GCS is a critical
piece of information to gather and report along with their initial vitals and,
you know, making sure that information is relayed to our emergency providers.
I noticed that you mentioned, blood pressure, oxygen measures
taken, especially in the field.
that there is a lot of debate always about stabilizing patients
on scene, how much time you take on scene versus, you know, how quickly
you can get them to a hospital.
Is there anything new in that arena as far as evidence goes?
Or, did you find anything helpful as far as data goes?
Dana: Yeah, so there have been multiple studies that I've looked
at this, . There's for example, the Epic study which was the excellence
in pre-hospital injury care study.
So , in this study, they included over 21 patients with TBIs.
And they were separated by different categories.
And then what they looked at was, you know, pre-hospital outcomes along TBI
categories , as I said, and there was greatest benefit among stabilizing
these patients if they had severe TBIs.
There was also the OPALS study, which was done in Canada.
So this was the Ontario Pre-Hospital Advanced Life support study.
And it compared outcomes with life support.
Either the patient got life support measures on the field, including
intubation, so pre-hospital care versus while they got to the hospital and there
was really no decrease in mortality after they implemented the pre-hospital care.
But this is certainly an area that's not black and white.
It really depends on the entire situation.
So how your EMS crew is able to stabilize the patient.
How far away are you from the facility, what kind of injury
the patient has et cetera.
So there are multiple factors that always go into this.
So there is not still a clear cut answer from the literature that we saw
about stabilizing the patient before they make it to the hospital versus
when they come into the hospital.
Sam: Yeah, this always seems to be a discussion for us, depending on
the community that the agency is kind of nestled in, whether it's
rural or if they have access to a trauma center and if their transport
times are very short or long.
So Certainly there are excellent medics out there with great skills
who are able to intubate in the field.
And the debate really isn't about their skill, it's more about just the ultimate
patient outcome and whether or not they can get to a trauma center quickly.
. And what's most beneficial.
So, good to see that there's still evolving data in that field.
It sounds like it's a very heterogeneous mix of agencies and patients.
So, it'll be interesting to see over the next decade if anything
different ends up being recommended.
When they get to the emergency department and we're evaluating them and we're just
talking about history, are there any specific elements that are most helpful to
pull out in the history with the patient?
Dana: Yeah, so there's a lot of information if you are able
to get it from the patient.
So how did this injury happen?
When did this injury happen?
What medications do you take?
Do you have any prior medical history?
Like, do you have a record of this injury even happening?
So those are just the basic questions that you really wanna ask them
before you start examining them.
'Cause it's especially important when I mention medications like, are there on any
antiplatelet agents or any anticoagulants because those, you have to reverse.
Unless there's a contraindication, those need to be reversed, especially if they
have an intracranial bleed because that bleed can worsen very quickly, otherwise.
Sam: Gotcha.
And then in the physical examination portion we mentioned getting a GCS is
very important in the field, but then also important to repeat multiple times.
So we're gonna repeat it again in the ED when we go to do our physical examination.
Dana: Yeah.
Yes.
So the GCS is a nice pretty quick way of just assessing the progression of
your patient and their physical exam.
And especially their pupils, if they're talking, if they're still moving their
extremities, or if something has acutely changed, which means that intracranially,
something may have also acutely changed.
So it's a nice, fast way to continuously assess the patient.
Sam: Gotcha.
So GCS pupils your basic neuro exam, and then also dealing with the
rest of the injuries that accompany their traumatic brain injury.
Dana: Exactly.
Sam: And then diagnostics.
All of these patients are going to get a CT scan and when they get their CT, you
know, hopefully we have a radiologist there to provide a rapid interpretation.
But if not, there is an interesting schema for interpreting or making
sure you don't miss things on non-contrast CTs of the brain.
In table six, the, the A-B-B-B-C approach which I had never seen before, but seems
to be a very well articulated approach.
Tell me more about that.
Dana: Yeah, so as a neurologist, I kind of take it for granted how at this point, how
pretty easy it is to interpret CAT scans.
But of course not everyone comes with that skill.
We all do different residencies, we all have different strengths.
So as we were interpreting the literature, I found this table from this resource and
I thought it was really excellent to add because it in a really straightforward
way, really explained the different major and very important components
of what to look for on a CAT scan.
So.
For example, air.
Of course we do have air in our sinuses, but there should not be air
within our cranial vaults or anywhere else, like really intracranially and
that's associated with a fracture.
Bones.
So looking at the bone windows is very important to make sure also
that there's no fractures anywhere.
Blood is.
Decently it, it's pretty easy to pick up on the CAT scan.
And this kind of explained the way that subarachnoid hemorrhages that are
traumatic would look on the CAT scan.
And same thing with subdurals and how they're crescent shaped versus
epidurals, which are lens shaped.
So that really distinguishes the two there and also what intraparenchymal hemorrhages
look like, which is quite bright white, but not as white as the bone itself
. And also it explains , in the brain itself, how to see the differentiation
between the gray and the white matter.
And also the CSF spaces as well and how they look like, what the four
structures look like, and if there is a concern for hydrocephalus.
What you may see.
So you would see effacement in the sulci, the cisterns and the
ventricles themselves would be larger.
So I thought this was a really nice table to kind of separate and explain the
different components of a basic CAT scan
. Sam: Yeah.
Yeah.
It's a, great little resource to keep in your back pocket if you're
not accustomed to looking at CTs.
And then when it comes to the timing of repeating that CT scan are there
guidelines for what is the ideal time or is it just when their exam changes?
Dana: So when we were doing our literature review, this is not something that we
like personally practiced, but very few of the guidelines recommended up
to 24 hours from the first CAT scan.
Everyone that I have worked with, and the majority of the literature has really
supported repeating a CAT scan in about four to six hours from the initial one.
Or if there's an exam change that you do want to emergently repeat a CAT scan
before that four to six hour window.
Sam: Gotcha.
So this is if they're presenting with a moderate to severe brain injury and they
have an abnormality on the initial scan.
Then you go for a, a repeat at some set timeframe.
Dana: Exactly.
And even if they may not have initially an abnormality on their CAT scan, but
you know that they had a severe TBI and if they have an exam change, you would
still repeat the CAT scan because they may have developed a new abnormality.
Sometimes the blood in the traumatic brain injury patient
can actually blossom intracranial.
And that does not happen right away.
So that's just one example where you really need to keep a really
close eye, do very frequent neurologic checks on these patients.
And if anything changes, have a very low threshold to repeat the
CAT scan to see what's going on.
Sam: Gotcha.
And I was happy to see a discussion here about the use of bedside ultrasound
for optic nerve sheath diameter.
You know, we're always looking for things to use our ultrasound
for in the ED, so there is a role for this in this population.
Dana: Yes.
So if you don't have any kind of intracranial monitor, so an EVD
or a bolt or anything like that optic nerve sheath diameter is
really your window into the brain.
Otherwise the optic nerve is an extension into the central nerve system.
But the important thing with optic nerve sheath diameter
is that you need to trend it.
Doing just one measurement It won't really help you truthfully.
So this is something that we generally try to do at least once or twice per shift and
see if that number gets bigger, bigger.
So I think I actually, somewhere I included an example of what the
optic nerve sheath looks like.
So about 0.5 was normal, and then we can see that later became
abnormal and went to point seven.
So if that does increase, then that's an indication for the providers
that the patient may be developing higher intracranial pressures.
Sam: Gotcha.
And now there's two different measurements that can be obtained.
One is the optic nerve, sheath diameter, and the other is the actual
elevation of the optic disc as well.
You can see both of those on ultrasound.
Dana: Yes, both of those can be seen on ultrasound.
Sam: Gotcha.
And when you're doing this measurement, you are doing it with the patient's head
of bed, still elevated at 30 degrees.
Dana: Yes.
So it's important also for consistency to have the patient's
head of bed at 30 degrees for this.
Just because if you lay a patient flat, their intracranial pressure can of course
be higher than when they're sitting up.
So, consistency is key when you're doing all of these measurements.
Sam: Gotcha.
And if you are giving something for increased intracranial pressure, would
you expect to see this optic nerve sheath diameter change in real time.
Dana: If you're able to do those things simultaneously, I anticipate
that you would be able to see a decrease in intracranial pressure
with the optic nerve sheath diameter.
Yeah, it's essentially a live measurement as you would see with, you know,
like I said, like an EVD or a bolt.
Sam: That's cool.
That's very cool.
All right.
And then there was a discussion about pupillometry, which is actually, again,
not something I'm accustomed to doing, but, but seems like it should be.
Tell me about what that is and what evidence we have for that.
Dana: Yeah, so pupilometers are some of our best.
We love our pupilometers, especially in the neuro ICU just because with a
pen light, sometimes it can be a little challenging to consistently especially
between providers and things like that, to really assess what the pupillary
reactivity is what the size is, et cetera.
So what a pupilometer does, it's a non-invasive, again, technique
when it assesses the pupil size symmetry and the light reflex.
So it gives you essentially an NPI number, which.
It gives you the size of the pupil and it also gives you the percent
change of the pupil which you can't get with a regular pen light.
So that's why we prefer using a pupilometer over just using a pen light.
If you have nothing else, of course a pen light is acceptable . But
if the pupilometer is available,
that's
something that we would highly prefer that's used.
Sam: And is the pupilometer that you use, is it , a separate device or is this
an app on your phone that you can use?
Dana: It's a separate device, so it's not too big and you just hold it in your
hand and you hold it to the patient's eye.
And then we shut the lights off and then it measures the pupillary size.
So you just keep it on the patient's face for just a few seconds and then it
gives you all of those numbers on the screen that comes with the pupilometer.
Sam: That's great.
And you're doing both eyes?
Dana: Yes.
Sam: Okay, excellent.
And just out of curiosity, does it dump that information into the electronic
health record, or do you just go back and copy that down into your note?
Dana: So, as far as I know we use Epic throughout our system, but the
pupilometer does not connect to Epic.
So the nurses do have to input it every time they do it, and then we see their
numbers and trends and things like that.
And we repeat it at bedside ourselves when we assess patients.
So those numbers go into our notes as well.
So that information is also carried on in multiple ways.
Sam: And you're looking for trends as in worsening pupillary reflexes
being a surrogate marker for worsening brain injury or brain function.
Dana: Exactly.
So with the percent change and with the size of the pupil, those are
really two of the things that we look at, and also pupilary asymmetry.
So if the pupilary size starts to decrease or increase, if the percent change
starts to decrease, then those are really alarms for us that something intracranial
like either the bleed is expanding, there's a new bleed, you know, something
is acutely worse with the patient.
Sam: Gotcha.
That's pretty cool.
And then there was a discussion about biomarkers.
So where are we today as far as reliability of biomarkers , and
how we would incorporate them into clinical practice.
Dana: So biomarkers are something that can be used in conjunction with
the data that we have, but there's still a copious amount of research
that's going on in the realm of TBI as to how useful these biomarkers are.
Just because, for example, so I'll discuss like neuron specific amylase
because that's something that's been around for a very long time.
And we also use it for our cardiac arrest patients.
The concentrations do rise in about the first 12 hours after the injury.
But the specificity, it can be kind of limited because other factors
can also affect the neuron specific amylase level and can make it look
high because there are other reasons.
So if a person is undergoing hemolysis, if they're on ECMO and also.
Like , there are other factors that can kind of affect the level that
you get for neuron specifically?
Some labs even process the lab differently.
So it's something that can be used in conjunction with all of your other tests.
But it's not something that we use yet by itself to predict how a patient will
do in their course with their severe TBI.
Sam: Gotcha.
Okay, let's move on to treatment.
Once we've gotten our objective data and we know that they have a
traumatic brain injury, and maybe we've gotten some abnormal imaging
and we're moving on to treatment when we start with airway management.
It seems like our standard airway protocols, including medications like
etomidate and succinylcholine are, safe to use and there's no reason to avoid
these in this specific population.
Dana: Yeah.
So, both succinylcholine and rocuronium are fine to use and etomidate is
fine to use just the precautions with succinylcholine that we know from even,
you know, outside of our TBI population.
So if someone is hyperkalemic or they have a known neuromuscular
disorder, then I would avoid succinylcholine . But otherwise,
both are absolutely fine to use.
And there was a concern historically about using ketamine with the concern
of how it would affect the ICP but it's not supported by evidence.
So it is okay to use ketamine as well.
Sam: Great.
And then there has always been historically the notion that you
could always hyperventilate somebody in an emergency to temporarily
reduce intracranial pressure.
But there are some good published studies for where we want that measure to be and
what we want that CO2 level to reach.
Tell me more about that.
Dana: Yeah, so the latest literature really supports keeping the patient's
CO2 at about 35 to 45, just because of the long-term effects after the patient
gets intubated more than anything else.
So we really want to avoid, of course, keeping them you know, hypoxic.
We don't want them to be hypercarbic.
Because of the fact that it can cause, strokes.
So that's why we really prefer because of like the vasoconstrictive
and vasodilatory effects.
So long term we do not wanna keep them hypo capic.
So that's why we really, if feasible, would prefer an aim of
the PaCO2 to be about 35 to 45.
Sam: Perfect.
And the ideal therapy for increased intracranial pressure.
You've got a couple of options, or there was a discussion in the article about
hypertonic saline and about mannitol.
So let's start with hypertonic saline, if that's available to us.
There's good evidence that that works and it's safe to
administer , and it works quickly.
Dana: Yes.
So hypertonic saline is great.
It comes in different concentrations, anywhere from 3% to 23%.
The way that it works is that it decreases the ICP by causing an osmotic shift of
fluid from the intracellular space to the interstitial and intravascular spaces.
And this draws additional fluid in and while it helps maintain mass by
also lowering the ICP it's probably more challenging in the ED to get 23%.
So from what I saw in the literature mostly 3%, two 50 CC bolus is used
and the osmolarity for that is 1,026.
Milli Osmoles.
Hypertonic saline is far more concentrated, of course, and
it has a higher osmolarity.
It's about 8,008 milli osmoles.
There is also, and it's important to know, is there's a difference
with how this is administered . So hypertonic saline, that's 23%
is given through a central line.
Over about 10 minutes.
But two 50 ccs of 3% can be given through a peripheral iv.
But they both help with that temporizing measure of decreasing the intracranial
pressure, especially as you're initially stabilizing the patient.
Sam: Gotcha.
And if we're giving the 3%, 250 cc quantity of hypertonic saline,
, that's not a push bolus that's going in over 20 minutes or so.
Dana: Correct.
Over 20 minutes.
Sam: Okay, great.
And if for some reason we have mannitol and don't have hypertonic
saline, is it okay to use mannitol?
Does that also have a, beneficial effect?
Dana: Yes, mannitol is also really great to use.
The major caveat with mannitol is we do not use it with our end stage
renal disease patients if they're on dialysis because it can cause
the opposite effects where it can actually cause worsened cerebral edema.
But mannitol is also very good.
It works through a similar but different mechanism.
So it still does create that osmotic gradient.
It like the brain tissue volume has decreased.
It can decrease CPP.
So it's also a very useful medication to use.
The labs that we frequently monitor with mannitol, so we do check the serum
osmolality if it is greater than three 20.
And if, especially if the osmolar gap is greater than 20, then
we do tend to avoid using it.
But otherwise, if a patient doesn't have those issues and if they're not
an end stage renal disease patient, then it's fine to use manitol.
Sam: Gotcha.
And both hypertonic, saline and mannitol have a pretty rapid onset.
Dana: Yeah.
So, within 10 to 20 minutes, mostly we do see, and even at the, just
anecdotally at the bedside, we do see even faster responses in that,
but typically it's, especially with mannitol, about 10 to 20 minutes.
Sam: Fantastic.
And then we do all of this with the goal of maintaining an ideal
cerebral perfusion pressure.
Tell me more about that.
Dana: Yeah.
So there's A compliant brains and noncompliant brains.
So compliant brains are far more injured and they're not
able to self auto-regulate.
But with a compliant brain, you want your CPP to be about 60 to 70 millimeters
of mercury while keeping the ICP less than 22 millimeters of mercury.
So all of this is especially helpful if we already, of course, have
an intracranial device such as an EVD because that can tell us what
the ICP is and all those things.
So we can easily calculate what that is.
But those are the goals that we aim for when we're managing these patients.
Sam: Gotcha.
And that cerebral perfusion pressure is calculated how?
Dana: So CPP is, it's the cardinal formula in the neuro ICU.
CPP equals map minus your ICP.
So that's how you would get your numbers where you have your patient's
MAP, of course, and their ICP, and then you would get the CPP from that.
Sam: Gotcha.
And even with an ideal cerebral perfusion pressure, we still wanna
keep their systolic above a hundred just general guidelines for, recovery.
Is that right?
Dana: Yes.
So it depends a little.
In the Brain Trauma Foundation guidelines it depends just a tiny bit on what their
age is for the majority of patients.
So for those that are 50 to 69 years old it's greater than a hundred and
then it's greater than 110 for the 15 to 49 and over 70-year-old patients.
So just a slight variance.
Sam: Gotcha.
And then temperature management.
We're looking for normothermia in these patients.
Dana: Yes.
So one of the things that virtually everyone agrees on is that higher
temperatures increase cerebral metabolic demand, and they worsen
their risk for a lot of different things such as cerebral ischemia.
So that's why we prefer to keep the brain always normothermic
avoid fevers and also prophylactic hypothermia is not recommended.
Sam: Great.
And then is it common to see coagulopathies in this population?
Is that as a result of medications they're on or as a result of injury
mechanisms or, or how, common is that?
Dana: In the literature we saw it varied extensively.
It was between, I think I put in the chapters between like 7%
to like 60 something percent.
And this can vary for a lot of different reasons.
So the patients could be on medications that make them coagulopathic.
They can have disease processes, for example, like liver
disorders, cancer, et cetera.
That can also lead to coagulopathic derangement.
So that's why, as we had discussed earlier, getting that initial
history if able is very important , especially if they have any kind of
coagulopathic issues to see how it can be reversed or managed appropriately.
Sam: Gotcha.
And that comes with a significant mortality here.
I saw that you guys cited a ninefold, increased risk of mortality and a 30
fold increased risk of unfavorable outcome if they develop a coagulopathy.
Dana: Yes.
So it, of course, it depends on how easily it can be reversed, how
difficult or easy it is to treat what the initial pathology is.
But especially
if it's.
difficult to get a hold of, and the patient just continues to worsen
from a neurologic perspective.
They do have a much higher chance of mortality.
Sam: Perfect.
Okay.
So in this patient population sometimes we're worried about seizures or seizures
occurring after the brain injury.
How do we handle that?
Are we still giving prophylactic anti-epileptics, or what's
the latest data on that?
Dana: Yes.
So there should be a pretty low threshold to connect these patients to EEG, just
because, especially if they have a poor exam, they could have underlying
subclinical seizures which would otherwise be very difficult to detect, especially
if they don't have those classic like tonic-clonic types of movements.
But if they don't have that in terms of prophylaxis, the data is still not.
The best, but at least according to the Brain Trauma Foundation , Keppra
and Phenytoin are still the most common seizure medications that we use.
And , the recommendation is up to seven days.
Post-injury.
There was a pretty large meta-analysis that was done and it found no
association between early seizure prophylaxis, so that seven day
period and the 18 to 24 month risk of epilepsy all cause mortality in adults.
So it actually would be interesting to see what research in the
future can show us about this.
But it's still a little bit of a gray area, but usually the recommended
period of time for prophylaxis for seizures is about seven days.
Sam: Gotcha.
Dana: And the doses vary.
We always get asked about, especially for Keppra, do we do, for
example, 500 or a gram or seven 50?
And I have not seen anything in the literature to really distinguish
the doses and how it eventually affects the patient's outcome.
Sam: Gotcha.
And you mentioned EEG, so you're just talking about continuous EEG
monitoring if it's available, or you know, if that's not available.
Is there really any utility in SPOT EEG testing?
Dana: So, we highly prefer continuous EEGs just because Spot EEGs are only
done for about 20 to 30 minutes, which may not capture the seizure.
It's, you know, seizures come and go.
It may occur once in a blue moon, once in a day, et cetera.
So if at all feasible, we would prefer to do a continuous EEG
monitoring over a spot EEG.
Sam: Gotcha.
Perfect.
And then I like the tiered management of elevated intracranial pressure.
It's another one of those key tables in the article.
This is number 11, which kind of provides you with a do now then do next approach
Walk me through that for one second.
Dana: Yeah, so this is hopefully also kind of and this stems from the ED all the
way to when the patient goes to the ICU.
But this is kind of how we think about when we're managing these
patients because it is such a highly specialized patient population.
So just broadly with your severe TBI patients, they are gonna come
to the ICU, they will be sedated.
We do these initial measures to preliminarily decrease the ICP.
And we have sodium goals that we aim for.
We always wanna avoid cerebral edema, for example.
So we don't want to drop the patient's sodium glucose goals because either
being hypo or hyperglycemic is also dangerous for the brain hemoglobin
goal of greater than seven.
And of course, hopefully by then you have your at least initial
non-contrast CT head to understand what.
the patient's intracranial pathology looks like, and you always want to do
other basic ICP measures, like head of the bed should always be at 30.
It should be midline.
And you'll wanna do fever prevention as well with cooling
blankets, Tylenol, et cetera.
If your patient develop.
Elevated ICPs.
That's when the previously discussed hyperosmolar therapies that's when we
would like to do that in addition to keeping them more on the normocarbic side.
And what's also helpful , with this point is placing an EVD if that's
available to also relieve that elevated intracranial pressure because
hyperosmolar therapy, it's a temporizing measure, but it's not going to.
Be effective for a long time, you need something that's more permanent.
And at this point also we say to consider EEG especially 'cause the exam
is likely poor Just to make sure that seizures are not also contributing,
especially to an elevated ICP.
And if you're ICP persists, despite all of these things, repeat the CAT
scan and see if, the intracranial pathology has worsened at this point.
Tier two.
So about the same PC O2 goal, a little lower to try to temporarily decrease
that elevated intracranial pressure.
We also encourage increasing sedation.
So for example propofol is something that's useful, fentanyl, et cetera.
You give little boluses, to decrease their ICP.
Ways that we play around with the , cerebral perfusion pressure, so we can
sometimes trial pressors with that.
And you use that in conjunction with that formula that I mentioned to try to change
the cerebral perfusion pressure as well.
You can paralyze the patient to try to decrease their ICP.
And also at this point, you're speaking with the neurosurgeons way before
this anyway, but now you're really discussing decompressive surgery.
And then finally tier three, if it's really refractory mild hypothermia
can sometimes be done, but really the goal of it at this point should be
to go for decompressive craniectomy because you've tried all of these
other measures and they're not working.
So that's.
Really the next step
. Sam: Gotcha.
Well, on that note, it's always been a mystery to me at what point a
patient is supposed to go to surgery or maybe would benefit from going to
surgery based on their injury pattern.
Do we have good published data to guide that decision making?
Dana: Yeah, so especially the more recent literature that we came across
of course nothing in medicine is black and white, but it gave us nice cutoffs
on when to really pursue surgery.
I tried to outline that, especially in.
Table 12 to really help guide with that.
So if the, for example, the size of an epidural hematoma is greater than 30 ccs.
If the acute subdural is, if the thickness is greater than 10 millimeters
or if there's a shift if the hematoma volume is greater than 50, or if
there's a frontal or a temporal lesion that's greater than 30 ccs.
That's when we would highly consider surgery.
But other things also just like if their GCS decreases by more than two points,
if there's concerning pupil changes, or the measurements that I already
mentioned, and those are really reasons to highly, highly consider taking a
patient for a surgical intervention.
Sam: Gotcha.
Yeah, this is , a very helpful table, honestly, because there again, in resource
constrained areas you may not always have a neurosurgeon around, and if you've got
someone waiting for transfer, it helps to be able to include this detail in
the conversation and say, we have a CT.
It shows an epidural hematoma of this specific volume.
And then you hopefully will not be surprised with the response you get
back based on that information from
looking at this table.
So you can kind of expect,
Sam: okay, this person needs to be expedited to get to this tertiary
center to get neurosurgical intervention while this other person
maybe has time to wait and we can optimize with medical therapies.
Dana: Exactly.
Yeah,
Sam: That's great.
This is very, very helpful.
And then in general, what's the general prognosis for patients
who have moderate versus severe traumatic brain injury nowadays?
Dana: Yeah.
So it depends on which classification we use.
I try to outline some of the classifications and what
the percent mortality is.
Of course, there's always going to be some slight variation with it.
But if they really do have a catastrophic brain injury with a really poor GCS
score it can be in the range anywhere.
I believe I put between 70 to 90%.
Unfortunately, the patients may, you know, not make it.
But then again, it depends on, the extent of the hematoma, what other injury
there is you know, ventricular size.
So there's a lot of components that go into it, depending on
which CT classification and which clinical factors are present.
Sam: Gotcha.
And that's even with ideal care.
So yeah, you've done everything right.
, The mortality is still pretty high in the severely traumatic brain injury.
Okay.
Yeah.
And some special circumstances.
So we all hear a lot about sports injuries and then there is good data
about second impact syndrome and, you know, multiple head injuries.
Has there been more published on that in the recent years?
That is helpful for us clinically.
Dana: Yeah, so there's, especially in the realm of chronic traumatic encephalopathy
or CTE there has been a lot of research that's , gone into that recently,
especially with certain sports like, you know, for example, like football is
a very clear example , of, adults who develop chronic traumatic encephalopathy.
And there is research that's going into how to treat it, how
to prevent it how to optimize safety equipment for these players.
Just because it is something that doesn't occur right away, but it
happens, you know, years to decades after the initial head injury.
And it can really be devastating.
And if we can.
Find a way to prevent that, to help 'em live longer lives.
That would be excellent.
So, there's certain medical centers within the country that have entire
labs and departments, et cetera, that are working actively on this.
Sam: Good, good.
And tranexamic acid, one of those medications, again, we're very fond of.
It seems like it's always looking for an indication.
Is there benefit in giving it early in this patient population?
Dana: Very good question.
So , our study that we always talk about with this is crash three.
So just to like briefly go over that.
So it was a randomized clinical trial and they included about
12,000 patients with this.
And they included patients who had a GCS of 12 or an intracranial hemorrhage on CT.
The trial suggested a reduction, 28 day head injury related death in
patients with less severe injury.
So what they found in the end was that there was no benefit in
patients who had severe injury.
However, the other thing we worry about with TXA is DBTs, PEs, stroke, et cetera.
They found that patients who.
did receive TXA did not actually have increased rates of DVT or PE or MIs.
So with severe TBIs there was no benefit.
Sam: But if there is going to be a benefit, even for the mild ones, this
has to be given pretty early on, right?
Within the first Few hours or three hours I think it was of injury.
Dana: Yes, exactly.
Sam: Gotcha.
Okay.
All right, well that's a lot of stuff we've covered.
Thank you very much for joining us on the podcast to discuss the article.
Again, this is The March issue of emergency medicine Practice on
the ED Evaluation and Management of severe traumatic brain injury.
There's more in this article that we didn't touch on.
Lots of tables, lots of figures great pictures of the
different types of intracranial hemorrhage and injury patterns.
So I really encourage you to go look at the article, read through it, and then
of course, as always, claim your CME.
And I'll put the link to that in our show notes.
And Dr. Klavansky, I wanna say thank you so much for joining us on the show.
It's been a pleasure.
I really appreciate you taking the time to teach us and share your knowledge
with us and to author this article.
It was fantastic.
Dana: Of course.
Thank you so much again for having me.
This was awesome to write and also to be on this podcast.
Sam : And that's a wrap for this month's episode.
I hope you found it educational and informative.
Don't forget to go to ebmedicine.net to read the article and claim your CME.
And of course, check out all three of the journals and the multitude of
resources available to you, both for emergency medicine, pediatric emergency
medicine, and evidence based urgent care.
Until next time, everyone be safe.