So what can we do to lower the intracranial pressure?
Well, there’s several interventions that we commonly perform.
The easiest and quickest one
is just elevating the head of the bed
and that works by enhancing venous drainage
out of the cranium.
Basically, you know, gravity helps us.
So we put the head of the bed up
more blood flows out of the head
and decreases the amount of intracranial blood volume.
It can be safely used for anyone
and if you’re not able to sit your patient up
because their spine isn’t cleared
you can just use the reverse Trendelenburg position
to put the head up a little bit above the heart.
Another common intervention that we use is mannitol.
So mannitol is an osmotic diuretic and basically what it does
is it pulls water osmotically
out of the neurons and into the intravascular space.
So it’s actually physically shrinking the brain.
It’s dehydrating the neurons
and making the brain volume smaller.
This is a great treatment option for patients
who are normotensive or hypertensive.
However, remember, it is a diuretic,
so it’s gonna cause increased urine output
and volume depletion.
So if your patient is hypotensive to begin with,
you wouldn’t wanna give them this,
‘cause it’s gonna decrease their circulating volume.
So really only appropriate for normo or hypertensive patients.
And you wanna make sure you watch the blood pressure
after you give it
because the diuretic effect can cause hypotension as well.
Hypertonic saline works basically the same way.
So if you give saline
that is hyperosmolar relative to the intracellular space,
it’s gonna also pull water out of the neurons
and into the serum
thereby decreasing the volume of brain tissue.
The nice thing about hypertonic saline
is it can be used pretty much for any patient
unless they’re grossly hypernatremic
because it’s gonna increase you circulating volume
and increase you blood pressure.
So it’s safe for you hypertensive multi trauma patients
and it probably will be the treatment of choice for our patient
who presented in hemorrhagic shock.
Another option we can use is hyper-ventilation.
And hyper-ventilation works by constricting the cerebral vasculature.
So basically, in response to respiratory alkalosis
the cerebral vasculature clamps down
thereby decreasing the circulating blood volume in the brain.
Now, this is a great treatment option
for patients who have impending herniation.
If you really think, "Wow.
This patient’s got a blown pupil,
he’s got a massive bleed in his head
and I’ve got to keep him from herniating
until he gets up to the operating room."
Hyper-ventilation is a really good option.
But a couple of important things to remember
is one, it’s got a transient effect.
So there’s no point in doing it
unless you are bridging the patient
to a more definitive intervention.
Basically, it’s only gonna work for an hour or two
at which point the whole system resets itself
and you’re not gonna get any benefit from it.
So it’s not something that you would use
as a long term treatment alternative
for somebody who is not going to the operating room.
It would really just be used as a bridge
for somebody like our patient
who is gonna get definitive management.
The other thing to remember is that you know,
is a little bit of a double-edged sword.
So a little bit of vasoconstriction is nice
cause it’ll decrease the circulating blood volume in the brain
and decrease your pressure.
As you can imagine though,
a lot of cerebral vasoconstriction is problematic
because then that’s gonna impaire cerebral blood flow
and cause ischemia.
So you wanna be very, very careful with hyper-ventilation
that you don’t overdo it.
You wanna have your patient on continuous
end-tidal CO2 monitoring
and you wanna aim for a pCO2 of 30-35.
Do not go below 30 because if you do,
you’re gonna cause cerebral vasospasm and ischemia.
So really important to remember,
you can only use this briefly
and you have to monitor closely and not overdo it.
The last option is not really something we do
in the Emergency Department
but it’s placement of a ventriculostomy catheter.
Which basically allows one direct monitoring
of intracranial pressure,
and two manipulation of intracranial pressure
because you can pull off CSF if you need to
in order to lower the pressure.
This is used for patients with severe ICP elevation
who really aren’t surgical candidates,
who have non-surgical disease process
and it’s not done in the Emergency Department.
It’s done by a neurosurgeon,
but it is something for you to be aware of
as a potential treatment for patients who has severe ICP elevations.
Moving on to control of bleeding.
One thing you wanna make sure you do
is to check coagulation studies
and platelet levels in every single patient
with intracranial hemorrhage.
In the event that your patient is coagulopathic
or they’re on an anti-coagulating agent,
you wanna reverse that immediately.
This is one of the few situations
where you wanna just completely normalize
the coagulation status regardless of their reason for anti-coagulation.
If they are coagulopathic,
you can consider treating them with fresh frozen plasma
in order replace clotting factors
and help improve the clotting of the blood.
And if they’re thrombocytopenic,
you can give platelet transfusion.
There have been studies looking at patient
who are anti-platelet agents like aspirin,
ticagrelor or clopidogrel.
And there’s no evidence that giving those patients platelets
actually produces clinical benefits.
So it’s probably not necessary to do that,
although you will probably see it done in some cases regardless.
Last thing to talk about is blood pressure.
So both hypertension and hypotension
are problematic for patients with intracranial injuries.
Hypotension is strongly associated with poor outcomes
and that’s because of impaired cerebral perfusion.
So if your patient is hypotensive,
you need to be aggressive.
you need to treat them with fluids.
If you’re not getting good response with fluids,
you need to treat them with pressors.
And you need to identify the underlying cause.
So head injury in it of itself
would never cause hypotension.
You need to look for some other explanation
either hemorrhagic shock or some medical cause of their shock
and address that underlying problem.
So head injury does not cause hypotension.
elevated blood pressure can potentially be problematic.
Now, a little bit of hypertension is a good thing
because if you’re intracranial pressure is elevated
having a high blood pressure actually
will improve your cerebral perfusion.
But if the blood pressure is too high
that raises the hydrostatic pressure in the vasculature
and can actually make bleeding worst.
So your goal is to be judicious in your treatment of hypertension.
You generally want a goal systolic pressure of about 160.
So if your patient is much above that
you probably wanna bring them down a little bit.
But you don’t need to bring them down to normal.
In fact, normalizing their pressure rapidly can be very harmful.
So you do wanna make sure that you use agents
that you can readily titrate.
So use a continuous infusion
of the medication like Nicardipine for example,
so you can turn it up and down as needed
to attain your goal blood pressure
rather than giving them something oral
that is gonna have an unpredictable long term effect.
All right, so back to our patient.
We already talked about his large subdural hematoma.
And he actually had an anisocoria
with a blown pupil on his physical exam.
So we’re very concerned that he has signs of impending herniation.
So if he wasn’t already intubated
which I’m thinking he should have been,
we definitely would wanna intubate him at this juncture
and make sure we have adequate IV access.
We’re gonna get our neurosurgical team on board,
because he needs surgical evacuation of this hematoma.
We’re gonna reduce his ICP
by elevating the head of the bed.
We’re gonna use hypertonic saline for him.
And he is somebody that we probably would hyper-ventilate,
because we would be bridging him
to a definitive treatment
that being surgical evacuation of his hematoma.
His blood pressure right now is adequate
so we’re gonna keep an eye on it.
if he gets hypotensive again
we’re gonna wanna be very aggressive about treating that.
And then, he doesn’t have any anti coagulant user coagulopathy
but we are gonna check his coags and platelets
just to make sure that all of his levels are normal.
So just to wrap it up,
take home points from this lecture are one
that GCS is a very reliable way to quantify mental status
and it is useful for predicting outcomes at least up to a point.
Your essential neurologic primary survey
is gonna include an assessment of the GCS,
a pupillary exam,
and four extremity motor exam.
You need to obtain a non-contrast head CT
in any patient with a GCS of less than 13,
and you might consider CT in patients with higher GCS
if they have complicating factors.
The injury pattern that you observed on CT
is what’s gonna determine your management.
And your management in the ED
is gonna focus on stabilization of the ABCs,
regulating the ICP,
managing the blood pressure,
and stopping bleeding.
Thank you very much.