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what's up ninja nerds in this video
we're gonna be talking about
intracerebral hemorrhage before we get
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get into it iron engineers let's start off
off
talking about the etiology and
pathophysiology of intracerebral
hemorrhage so what causes it how do
these particular causes lead to a bleed
within the brain
so first thing by far one of the most common
common
causes of intracerebral hemorrhage is
going to be hypertension
so when we talk about intracerebral
hemorrhage it's important to remember
that there's actually kind of two
subtypes there's a non-traumatic
interest representation that's what
we're primarily going to focus on in
this lecture
and there's also a traumatic interest
reprehemous it's pretty obvious
what the etiology is if it's traumatic
there's some type of blunt force
trauma penetrating trauma that's present
let's focus on the
non-traumatic causes that most common
one being hypertension
so how does hypertension cause interest
reproduction it's really straightforward
if someone has high blood pressure right
really sustained high blood pressures
that's going to exert
a lot of forces on these blood vessel walls
walls
as you exert a lot of force on these
blood vessel walls enough
in particular areas of the brain where
the vessels may be a little bit more
weak or a little bit more susceptible to
rupturing guess what happens
these vessels will then rupture as a
result of this maybe acute
or sustained or very intensely elevated
blood pressure
and this can lead to these vessels
rupturing and blood spilling out of these
these
into the brain tissue and so that is an
important thing to remember
so very extremely elevated blood
pressure can lead to bleeds within the
brain via simple shear forces and stress
on those vessel walls
what's really important though is where
these bleeds most commonly occur that's
what i want you guys to remember
the most common locations for
hypertensive bleeds
include first your basal
ganglia so what are the different
components of the basal ganglia
so your internal capsule your putamen
your globus politus which makes up the
lentiform nucleus the caudate nucleus
the thalamus
a lot of those structures are components
of your basal ganglia
what's the next one the next one is here
in your pons
your pons is a very very important area
and it is very prone to hypertensive
bleeds as well
another one is the cerebellum the
cerebellum is
extremely sensitive and has a very high
risk of bleeds
that are secondary to hypertension and
the least
common one is going to be bleeds that
are near the actual
cortex so bleeds that are near the
cortex so
cortical we also call this
low bar and we say low bar because
we're talking about is this the frontal
lobe the parietal lobe the occipital
lobe the temporal lobe where this bleed
is occurring
so by far most common locations include
basal ganglia ponds cerebellum and low
bar with low bar being the least
likely another big thing to remember is
that this is by far
going to be one of the most
common causes
and patients usually less than 60 years
of age
okay boom roasted let's move on to the
next one
the next one is called cerebral amyloid angiopathy
angiopathy
you're probably what the heck this is actually
actually
interesting so when you hear amyloid you
probably think oh is this like dementia
stuff yeah it definitely is
amyloid proteins or amyloid beta peptides
peptides
and what happens here here we're going
to have let's say that here we have here's
here's
kind of like your proteins right so
we're going to call this a beta
amyloid peptide what happens is these
beta amyloid peptides
they deposit into the walls of these
cerebral blood vessels near the cortex
near the cortex they deposit into these
blood vessels
and when they deposit into the blood
vessels they kind of weaken the blood vessels
vessels
so imagine here i have a bunch of these
little beta amyloid plaques
that are developing within the blood
vessel this weakens the blood vessel
makes them very fragile and prone to
little micro
hemorrhages and small little ruptures
where where is the most common location
bleeds at the
cortex i need you guys to remember that
so where are these bleeds most common
most common location for these are
cortical bleeds
and this is going to be low bar bleeds
now when we talk about cortex this could
be it's important to remember this one
these bleeds we already concluded the
cerebellum as a separate one
when we talk about cerebral amyloid
angiopathy this can happen in the cerebrum
and it can happen in the cerebellum
okay so very very important thing to
remember here last but not least
this is the most common cause of ich in patients
patients
greater than 60 years of age so most common
when you're greater than 60 years of age
especially if they have
previous history of ich also
there is a a component of dementia
related to this so if the person also
has maybe some dementia present
take that into consideration as well so
there is a
dementia component present
okay all right great so we have
hypertension most common
generally the most common cause
especially in those who are usually like
less than 60 or any age really
but the most common cause greater than
60 cerebral amyloid angiopathy
the next one that i want you guys to be
thinking about here is coagulopathies
so this is a big one there's a lot of
drugs and medications that are involved
in this
so coagulopathy we particularly see this
with anticoagulation or some type of
measure that we'll talk about
anti-thrombotic anti-platelet agents
anticoagulants um fiber analytic
medications we'll talk about all these
but what happens is this coagulopathy
usually you put someone on
anticoagulants right so they're on anticoagulants
anticoagulants
let's just say here as the example
anticoagulants is basically you're decreasing
decreasing
the coagulation cascade right so when
you give someone anticoagulation
you're decreasing the coagulation
cascade if you will and if you decrease
the coagulation cascade that is a
component of what
hemostasis so you decrease hemostasis
let's say that someone has little micro
tears just from the daily wear and tear
on those blood vessels
so they develop like little you know
tiny little micro tears which is pretty common
common
in individuals usually what happens is
we have particular measures like
hemostasis and the coagulation cascade
that help to plug up those little holes
but if someone's an anticoagulation
especially if they're on super
therapeutic levels
this anticoagulants are going to affect
them being able to properly plug up
those holes
and lead to hemorrhages or a little
seeping of blood out of these blood vessels
vessels
that's really important to remember so
coagulopathy is another one
and there's a bunch of different types
of medications some that we'll talk
about are going to be warfarin
it's going to be a big one the other one
is going to be heparin
we'll talk about tpa
and there's even the uh the last one
which could be
okay which are your anti-platelet agents okay
okay
the last thing that you want to think
about is if it's not anti-quack
related is there a cirrhosis or liver
injury or there is there acute liver
failure chronic liver failure
where they can't make pro coagulants
so they can't make the coagulation
protein so you're giving drugs that are inhibiting
inhibiting
the pro-coagulants or the liver is not
making the pro-coagulants
so think about that as well if someone has
has
that could lead to what
a decrease in the pro coagulants
okay so here we'll put that like this a
decrease in
pro coagulants
like which ones factors two factor seven
factor nine vector ten
uh protein c protein has all of those
and the same kind of process here occurs
okay and so then you can get bleeds
related to that so we have hypertension
we have cerebral amyloid angiopathy and
we have coagulopathies either related to anticoagulants
anticoagulants
or severe liver failure let's move on to
the next one all right so what's another
potential cause of interest rebel hemorrhage
hemorrhage
hemorrhagic transformation is a big one
to be thinking about so we got
hypertension we got cerebral amyloid angiopathy
angiopathy
we got coagulopathies hemorrhagic transformation
transformation
what could this be do too think about it
simply someone had an ischemic stroke
they had an ischemic stroke maybe they
got tpa
and what happened is they converted that
ischemic infarct into a hemorrhagic infarct
infarct
or they had an ischemic stroke they
didn't get any intervention
but they had such a big infarct that we
re-perfused that area maybe by pushing
their blood pressure up too high and we
just converted that ischemic infarct
into a hemorrhagic infarct by bleeding
into that infarcted bed
either way there's a transformation of
an ischemic infarct
into a hemorrhage so what does this
usually do
to someone had an ischemic
into an ich
what could be the reasons for that one
is maybe they got tpa
and that tpa just was enough to kind of again
again
weaken the integrity of those blood
vessels enough that they couldn't actually
actually
uh sustain that and they cause a bleed
right so it could just be from the tpa
that caused that because again tpa is
designed to be able to make the blood
thin to break up clots
and so they have a high bleeding risk
when you give a jug like that the other
thing is that they develop a
re-perfusion injury
so what happens is let's say that maybe
they didn't get any tpa
um or maybe they did get tpa and you
just don't control their blood pressure
as well
and so what happens is the blood
pressure is maybe a little bit too high
and you push
too much blood into an area where the
vessels are already weak
because of an underlying ischemia
infarction will explain how that happens
but the blood vessel is just really weak
and you push the blood pressure a little
bit too high into those weak vessels
they rupture and cause a bleed into that
infarcted bed
so how does this kind of mechanism
happen so really what happens is
let's say here i have some neurons here
so here i'm going to have maybe some neurons
neurons
and these neurons become damaged
because they had an ischemic infarct
there what happens is they release a lot
of inflammation this basically leads to
a lot of inflammation right because of
their injury
there's a lot of inflammation
and that inflammation causes like a lot
of neutrophils to come to the area
causes a lot of reactive oxygen species
and free radicals and stuff like that to
come to the area
and that inflammation starts really
acting and wreaking havoc on these
vessel walls
and so those vessel walls just become
relatively weak
then you give someone tpa after they've
had an ischemic infarct so the ischemic infarct
infarct
right of these neurons lead to
inflammation lots of inflammation
weakens the vessels
you push the blood pressure a little bit
too high into those weak vessels
or you give them tpa and it just again
causes more weakening of the vessels
those little bad boys rupture and you
bleed into that infarcted bed
and that's where you can get a
hemorrhagic transformation okay
so we got hypertension cerebral amyloid
we got coagulopathy we got hemorrhagic
transformation the next one
is malignancy there's some type of
metastatic cause not
usually usually the most common cause of
these ichs is a metastatic cause
rather than primary so malignancy
you got to know where are these actual
where these cancer cells coming from
they started somewhere they got into the brain
brain
they broke down the blood-brain barrier
i'll explain what that means which
caused blood to seep into these areas
around the tumor
what are the tumors that you have to be
thinking about that were the original
source that spread to the brain
big one papillary thyroid cancer so
that's one
so which one is it the first one here is
going to be thinking about
thyroid so papillary thyroid cancer is
the first one
the other one is lung cancer particularly
particularly
small cell lung cancer the other one is
renal cell carcinoma so renal cell
carcinoma is another one the other one
is melanoma melanoma melanoma's a son of
a gun right so this one can
really be a nasty type of cancer that
can spread
and then the last one here is choreocarcinoma
choreocarcinoma
so let's actually write this one out choreo
choreo
carcinoma okay so this can definitely
plague like the uterus and
reproductive organs as well so what
happens is
these cancers right some of the cancer
cells spread from these different
primary locations
and what they do is they actually
infiltrate the brain tissue right so
they're going to infiltrate the brain tissue
tissue
when they infiltrate the brain tissue
what they do is they disrupt
the blood-brain barrier you guys
remember what the blood-brain barrier is
made up of you get the endothelial cells
then you get the basal lamina and then
what are those little glial cells
the astrocytes right well what these
guys do is they really
damage and disrupt that blood-brain barrier
barrier
and so now you don't have a proper
blood-brain barrier and what is the
blood-brain barrier designed to do
control things leaving the blood and
coming into the neural tissues
if you don't have good control guess
what's going to happen some things are
going to leave the blood
and enter into those neural tissues so
you start kind of destroying that
blood-brain barrier
and blood can start seeping in around so
imagine here would be the mass that came
from one of these cancers
there would be kind of a bleed that
would surround
that mass okay because of it disrupting
the blood-brain barrier so what do these
things do let's actually write that down
the blood brain barrier
okay so that gives us the next cause
which is malignancy
let's move on the next one is cerebral
venous sinus thrombosis that's a heck of
a name also abbreviated cvst
cerebral venous sinus thrombosis
it's basically a dvt of the brain that's
literally what it is
so you have different types of veins in
the brain right so you have like what's
called the superior sagittal sinus the
inferior sagittal sinus the transverse
the sigmoid the straight sinus
all of these crazy sinuses
someone can develop a clot a venous
clot within these veins and it can
literally lead to a bleed i'll explain
how that happens but generally
what is a cerebral venous sinus
thrombosis it is a
clot in the
uh the venous system
of the brain okay how does
this now okay let's talk about one more
thing before that so we know it's a clot
in the venous system
what in the heck causes the clot in the
venous system
it's really any kind of like hypercoagulable
hypercoagulable
condition whether that hypercoagulability
hypercoagulability
condition so it's any kind of
hypercoagulable condition
this hypercoagulability it could be due
to an underlying like
inherited disorder so we're not going to
write down all of them but for example
this could be things like factor 5 leiden
leiden
this could be things like
anti-phospholipid syndrome
this could be things like anti-thrombin
3 deficiency
and so on and so forth but it could also
be acquired things so sometimes if
people are on oral contraceptives
or if they're pregnant these are all
things that can also kind of make them a
little bit more hyper coagulable
and at risk for forming clots within
that venous system in the brain
now let's talk about how these clots
actually do lead to
basically a hemorrhage so if you imagine here
here
imagine there's like this arterial thing
that's eventually feeding into this vein
here right so they say that there's kind
of like you'll have a capillary network
but let's say that blood will come in
through the artery
and then leave out through the vein
right if you have a clot that's
obstructing the venous
drainage sometimes what can happen is
the blood
is actually going to have to like so you
might not be able to get blood past this
and so what happens is this may plump up
the vessels
that are proximal to wherever that clot
is in the venous system
and these suckers may plump up a little
bit enough
that they can rupture and then what can
happen is they can bleed
into the brain tissue but it's usually
near the edges of the brain tissue like
near the edges of the cortex
so usually whenever you see like a
cerebral venous sinus thrombosis it
produces a very characteristic bleed
that's usually near the edges of the cortex
cortex
so again that's kind of the basic way
that cerebral venous sinus thrombosis
leads to an ich or a basically an
intracerebral hemorrhage
there's a clot in the venous system
venous congestion can lead to hemorrhaging
hemorrhaging
of the venous system some of the
arterial system there and
bleeds near the cortical regions and
it's usually due to
some type of hypercoagulable type of
condition there
okay so that's cerebral venous sinus
thrombosis so we got hypertension we got
cerebral amyloid we got coagulopathy
we have a hemorrhagic transformation malignancy
malignancy
dvt of the brain the last one is
vascular abnormalities
you see this in younger individuals so
first things first is you see this in younger
younger
patients and this is actually a vascular
malformation referred to
as an avm so let's write this above it
so that we know that this is
in younger patients what is this thing
here called this is called an
a v m an arteriovenous malformation
so this is present in younger
individuals and it's basically this abnormal
abnormal
arterial capillary network so there's
not a
complete formation of that micro circulation
circulation
so what happens is usually you have an
arterial it branches into your
capillaries goes into the capillary bed
jane's into a venule
and then to a vein this one you kind of
have like this
abnormal connection between the arterial
and the vein and it creates like this
abnormal ball or nitis
that's just super susceptible to if
there's any kind of increase in pressure
it's going to rupture and so that can
cause a bleed there as well so usually
this is a kind of
more commonly in younger individuals and
it's basically an abnormality within
their vascular channels
okay the other abnormality here is
something i want you guys to think about
and this is what's called a microtic
aneurysm so you can have ichs that can
be due to
aneurysms in general and there so if we
had for example let's say that we had an
aneurysm there's different types of aneurysms
aneurysms
you can have saccular aneurysms fusiform aneurysms
aneurysms
and microtic aneurysms so this is one
that i really want you to remember
we'll talk about aneurysms those
rupturing and what's called subarachnoid
hemorrhages aneurysmal subarachnoid hemorrhages
hemorrhages
but for right now the big aneurysm that
i want you to remember that can cause ich
ich
is called a mycotic aneurysm
and what happens with mycotic aneurysm
is someone may have what's called
infective endocarditis
so what do we call this infective we'll
put i endocarditis
endocarditis
and in infective endocarditis they
develop these kind of like
vegetations like these little septic vegetations
vegetations
on the valves and what happens is these
little vegetations can break
off from the left atrium left ventricle
into the aortic system
go up through the carotid system so now
into this actual cerebral circulation
and go here where it kind of
nestles into these vessels and what
happens is
this is basically little septic
structures these little infective
little vegetations that get lodged into
the cerebral vessels and cause damage to
those vessels
and cause them to balloon up and then if
someone has kind of this little
ballooning and weakening of the blood
vessel what can happen if maybe there's
just a little brief rise in pressure
these little bad boys can rupture and
lead to bleeding into the brain tissue
which is going to cause their ich okay
and so usually mycotic aneurysms are
secondary to an effective endocarditis
so now let's talk about the clinical
features of intracerebral hemorrhage
so the first one and probably one of the
most common symptoms is especially if
there's a cortical bleed
right or a low bar bleed they can
present with a headache
the reason why is if the bleed's near
the cortex under the lobe like
it's involving particularly a cortical
region or a low bar region
it's close to the meninges and they can
agitate the meninges
you know the meninges are supplied by
cranial nerves like the trigeminal nerve
and so that can send signals via the
sensory fibers of the trigeminal nerve
to the trigeminal nucleus up via the
trigeminal thalamus tract and cause this pain
pain
basically within the head region so headache
headache
is a very common
clinical manifestation or clinical feature
feature
that can be seen in individuals with ich
cortical or low bar and again that
mechanism is via
agitation of the meninges activation of
the sensory fibers of particular cranial nerves
nerves
activating the trigeminal thalamic tract
now we're not going to go through
all of the different types of
neurodeficits because we talk about that
in stroke syndromes because it's the
same kind of concept if someone has a bleed
bleed
in a particular area where they also
maybe comparatively had an ischemic stroke
stroke
they can present somewhat similar so if
you guys want to know more about
these focal neural deficits go check out
our video we're gonna have a link up here
here
to go watch the stroke syndromes okay
but they will have different types of
focal neural deficits
maybe aphasia maybe weakness on one side
maybe gaze preferences maybe sensory loss
loss
so on and so forth okay
the next particular clinical feature
that i want you guys to be aware of
is that these individuals can also have
high intracranial pressure whenever you
have a bleed
there's something called the monroe
kelly doctrine where inside of the skull
the skull is kind of a fixed thing it
doesn't really expand
you have brain blood and csf if you have
more of one of those things it's going
to increase the space now crowded within
that skull
and the pressure inside of the cranium
is going to increase
if we got a lot of blood more blood than
we should have inside of that skull it's
going to increase the intracranial pressure
pressure
so you can develop symptoms from this bleed
bleed
okay so this is going to cause high
intracranial pressure
what are some of the symptoms of high
intracranial pressure they're relatively generic
generic
and vomiting okay and this may be due to
like a stimulation or compression
of things in like the the chemo trigger
zone the area post stream which is in
the brain stem
so maybe some brainstem compression this
also could lead to kind of a
decreasing level of consciousness
so l-o-c so maybe like an altered mental status
status
they're really becoming sleepy you're
trying to say hey
you know wake up wake up wake up when
you're trying to examine them
and they're just not waking up as well
the other thing
is they can start to have cranial nerve
deficits what do i mean maybe their
pupils are starting to become
ones larger than the other maybe it's
not reactive to light
maybe you're testing their corner
reflexes they're not reacting
maybe you're trying to see if they have
a cough reflex and it's not there
and the other thing is they may start
showing signs of posturing
so you have the different things like
the cerebral posturing decorticate
posturing that may become
a little bit more evident with high
intracranial pressures and the last
thing is
you guys already know this there's a
particular triad
called the cushing's triad what is the cushing's
cushing's
triad i want you guys to remember that
it's a high
bp it is a
low heart rate and it's a
low respiratory rate or irregular
respirations as well
okay that gives us the big clinical
features now that we understand
how interest reprehensive can present to
us let's now talk about how we diagnose it
it
so first thing the most
important if you only had one kind of
test that you could use to determine if
someone has
an ich it's a image a stat ct scan of
the head
so by far the most important thing to obtain
obtain
is a stat ct of the head
so stat ct generally like a non-contrast
ct scan of the head
and this will help you to identify if
there is a bleed
present so i can tell you if there's an ich
ich
it can tell you if there's any midline shift
shift
what does that mean so some of the brain
so from this bleed you start having some
of the brain tissue pushing
to the opposite side maybe causing like
herniation syndromes to be present
you also want to note is there any hydrocephalus
hydrocephalus
so sometimes when you get a lot these
bleeds you can get hydrocephalus because
some of the blood from here
starts extending into the ventricles and
so they get what's called hydrocephalus
due to ivh or intraventricular hemorrhage
hemorrhage
so that's one thing we could do you
could get a ct angio
if you want to look for like a vascular
like a cta mra something like that if
you're looking for vascular abnormalities
abnormalities
so that could be another image you could
obtain is maybe a cta
or an mra if you're looking for
particular types of like vascular causes
like you know anomalies of some form for
example you're maybe looking for
a mycotic aneurysm maybe you're looking for
for
maybe some type of avm or something like
that you can also do like angiography
as well but the cta is a pretty quick
one relatively easy
especially if you're getting a ct scan
the other thing that you can do is an
mri this is actually a relatively
significant thing that you should be
able to obtain
after you've you know pretty much you
got the first diagnosis with the ct
later on after you stabilize them you
can get an mri
and an mri also
mrv you should add on okay and we'll
explain why in a second
mri what i like to look for is i look at
pretty much
like one sequence really i look at the swi
swi
so the swi is a particular sequence that
tells me if there's any like iron
or blood that's kind of sitting in a
particular area of the brain
and so an swi will come up basically
showing like these like black spots
really so it'll show like little
black holes if you will that tell me
that there was blood there's blood in
this area there is a hemorrhage in this area
area
and that is important if you're trying
to really see okay do they have a
hemorrhage you can obviously tell that
from a ct scan but remember i told you
there was a particular thing called
cerebral amyloid angiopathy
you want to get a swi because if someone has
has
tons and i mean tons and tons and tons
of little bleeds all over their cortex
and their cerebellum and they're older
greater than 60
what do you think that could be
indicative of cerebral amyloid angiopathy
angiopathy
and the other thing we said is an mrv
why is an mrv going to be helpful for me
what was that condition so we have an
mri it just kind of gives us a look at
the brain no contrast there's no you're
not filling the vessels
cta mra you can fill the arteries to
look at those to see if there's any
abnormalities there
mrv is you're feeling contrast through
the cerebral veins
what was one of the etiologies as a
potential cause of hemorrhage
cerebral venous sinus thrombosis right
so look there to find any
cerebral venous sinus thrombosis
all right i think that's a pretty good
start when you all right let's move on
we got our imaging the big imaging next thing
thing
we found an ich we've looked for some
vascular anomalies to help us to find
the cause we did like
some other mri studies to look to see if
there is an ich cerebro amyloid cvst
all that good stuff what was another
particular cause
malignancy so sometimes what i may do
is i can obviously maybe get an
ultrasound of the thyroid
i could do that to look to see if
there's any mass there but
the common biggest thing to look for here
here
is to do what's called a ct you can do
what's called a ct
of the chest
can help you to look at the the lungs to
look to see if there is any particular like
like
lung mass there you can get a ct
and this is all one order so for example
you would get a ct at the
chest abdomen and of the pelvis
and if you see as you know a mass within
the lungs that could be a cause
a mass within the kidneys that could be
a cause a mass within the uterus or
other reproductive organs that could be
a cause of their malignancy
so if they have a bleed and they're
imaging and you go and you find a mass
somewhere else that it metastasized from
you now have a cause or
primary source and again check their
skin from melanoma
you know palpate and do ultrasound for
the thyroid as well
so i think that's a pretty good kind of
test for that
what else could we do we could get an echo
echo
you get an echo why why do i want to get
an echo zach
so remember we said infective
endocarditis you form little infective
vegetations on those valves they
bust off they get stuck in a cerebral
vessel cause a mycotic aneurysm
look for that do an echo so we can do
a trans thoracic echo
or we can do a trans-esophageal echo and
what we're looking for is is there any
kind of like septic
emboli that's present
and we'll talk later because the other
thing that we can add on to help an
aiding in our diagnosis is
did the person have a fever so what
could add to that
did they have a fever do they have any iv
iv
drug abuse and then check the blood
cultures because usually blood cultures
are positive
okay and then if they have a murmur do
they have a new murmur that you're
whenever you're auscultating them
so i think this is kind of the big stuff
to think about is
images ct you can get
arterial images venous images a big
thing is mri
looking at that swi you suspect
malignancy ct of the chest abdomen pelvis
pelvis
you suspect a septic emboli infective endocarditis
endocarditis
echo with the other associated blood
cultures that we'll talk about in a second
second
let's talk about some labs that can help
us so now we got our images let's talk
about some labs that we'd want to order
and what these things could tell us and help
help
aiding and our diagnosis and maybe more specifically
specifically
the etiology the causes of this diagnosis
diagnosis
because really the main thing about the
diagnosis we get a ct that's going to
tell us what we need
figuring out the etiology of the ich is
kind of going to be the extra things
that we can get from other images
and labs so labs what do we do well it's important
important
because you want to be holistic you want
to see cbc right start off with a cbc
why a cbc because this can tell you if
the person has any severe anemia
right anemia if they're maybe they're
bleeding a lot do they have
any thrombo cytopenia so basically do
they have any very low
platelets that's another thing that
could be important from this as well
another lab that i would obtain is a
cmp so a cmp is going to be helpful
it'll tell you remember we said that one
of the things could be coagulopathies
so coagulopathy could be due to the anticoagulation
anticoagulation
we'd have to ask them about their
history do you guys take any anticoagulation
anticoagulation
but the other thing about a cmp is it's
going to tell us is there any elevation
in their ast
their alt they're alphos and
maybe this is the reason why they have a
coagulopathy because they have severe
liver failure and they're not making pro
coagulants so something to think about
the other thing is for the most part it shouldn't
shouldn't
always determine whether or not you add
contrast in a study if you need the
contrast it's important for the study
you should get it but sometimes a cmp is
helpful because it tells you about your
renal function tells you if there's any elevated
elevated
bun tells you if there's any elevated
creatinine because that could come into
play whenever you're going to give them contrast
contrast
but again don't get too bogged down in that
that
okay the other thing is coags
we should check a pt we should check up ptt
ptt
and we should check an inr right these
are things that are important because if
someone has maybe an elevated ptt
we got to figure out why do they have an
elevated ptt or if they have an elevated inr
inr
why do they have an elevated inr is it
due to a coagulopathy
or is it due because they're taking
warfarin do they have an elevated ptt
because they're on heparin
and they were just on too much heparin
and that's why they bled
thinking about those potential causes
thinking about these from the labs can
be helpful in aiding in what the cause is
is
and how you're going to treat them okay
so we got a cbc we got a cmp we got some
coags there
it's also important remember we were
talking about someone having infective endocarditis
endocarditis
and also there's another risk factor we
didn't talk about some of the risk
factors but there is risk factors for ich
ich
any time someone is on any kind of like
drug like cocaine
any methamphetamines alcohol itself
really is a risk factor for bleeds to happen
happen
so it's important to also obtain a urine
drug screen
and someone for a couple reasons one
it's important just to make sure that
there is no thing uh
there's nothing that you're missing as
potential risk factors that way if they
do recover and they do
recover from this bleed you can try to
prevent them from
developing a bleed in the future by
addressing these issues like avoiding
things like methamphetamines and and so
on and so forth so basically looking for
any tox
stuff so for example are they on cocaine
because that is a very important risk
factor was it positive for alcohol
because that's another important risk
factor okay
the other thing that you should always
obtain it's a quick little easy test
is a point of care glucose a point of
care glucose is a
quick little easy thing to look to see
if they have any hypoglycemia
so point of care glucose it's important
to obtain to look to see if they have
any low glucose
hypoglycemia or high glucose hyperglycemia
hyperglycemia
okay what else
a blood culture that's oh that's another
reason you should get a urine drug screen
screen
because what if somebody is an iv drug
abuser and you don't actually
know it because it's not someone that's
not told to you or
the person's basically non-responsive
and they can't tell you that they use drugs
drugs
or you just can't find it maybe on the
top screen they're positive for heroin
that could maybe lead you to think oh do
they have infective endocarditis
maybe that's the cause for their bleed
and the same time you should also get
blood cultures
especially if they were fibril
especially if they have a new murmur
especially if your echoes suggest
potentially some vegetations there
so definitely doing something like that
like obtaining blood cultures
may be helpful to rule out
infective endocarditis as a cause for
those septic emboli
the other thing is remember we said that
cerebral venous sinus thrombosis we may
be able to pick it up from the mrv
but the thing that we got to think about
is what was the cause of someone
developing cerebral venous sinus
thrombosis hypercoagulable conditions right
right
and so maybe doing a hypercoagulable workup
workup
may be somewhat beneficial in this
scenario as well so
checking for hypercoagulable
work up and we are not going to go
through all of these
what you can do is we'll mention a
couple you can check the factor 5 levels
you can check their anti-thrombin 3 levels
levels
you can check their protein c and s and
there's so many other ones that you can
check we won't go through all of these
but checking some of those levels to
look to see is there hypercoagulable condition
condition
that is causing them to form a basically
a dvt in the brain and that's why they developed
developed
a bleed okay so that can aid in your
diagnosis as well
particularly the causes the other thing
and kind of the last thing we didn't
really mention it as causes because
they're really really really
relatively rare and it kind of goes
along with the vascular malformations
the two big ones that i wanted you to
know was the avms
and the kind of like aneurysms like
mycotic aneurysms barrier aneurysms
but another really low in the
differential it should really be low
is any kind of cause of vasculitis so
sometimes vasculitis are also
susceptible to
the blood vessels kind of rupturing as
well so is there
you know a suspected vasculitis
and so again autoimmune
cause what can you do for that one check
an esr
check a crp check an anchor
checking a a so on and so forth we can
do there right is it infectious
how do i determine if it's infectious
well think about the causes
look for varicella zoster virus
right so you can do like the interferon
assays you can check the vdrl rpr you
can check a pcr for vzv
and then the other one is is there like
a primary cns
vasculitis that is the cause of this one
and this actually would somewhat require
a biopsy to kind of confirm that
so these are things to be thinking about
of how you're going to go about
diagnosing ich and figuring out the
causes of
ich i hope this helps now let's move on
to the treatment
all right ninja so now let's talk about
the treatment of intracerebral hemorrhage
hemorrhage
so this is the biggest you know really
really kind of like you need to know
this stuff you have to have this part down
down
so first thing when someone has a really big
big
whopping ich that has midline shift and
increased intracranial pressures
there's always the concern can they
protect their airway especially if they
have this declining level of consciousness
consciousness
and they're not able to kind of like
follow commands and you know really
they aren't completely oriented to
person place time and things like that so
so
you should have a very low threshold for
intubating somebody especially if they
have a very very large bleed
with a declining mental status so airway
in every emergent situation abcs right
so airway breathing circulation is
always kind of the best steps here
so why is an airway a problem well think
about this you have
all these respiratory centers here in
your brain stem right
pons medulla and these basically are
important because the nerves that are
coming from here via the intercostal nerves
nerves
and the phrenic nerve supply muscles
that help to aid in breathing via your
respiratory rate and your respiratory depth
depth
if there is compression because there's
high icps maybe you have a bleed right here
here
and this bleed is causing some some
compression of that brain stem that's
going to injure these areas and decrease
your ability to generate
respiratory you know breaths
particularly rates and and depth
so important to think about that so when
someone has these large bleeds you need
to protect their airway how do we do that
that
have a low threshold for intubation so
sometimes intubation
may be a very important thing to do in
these patients
and when you intubate them and you put
them on a mechanical ventilator there's
different types of modes there's all
these different types of modes we'll
cover this in another lecture but
maybe cmv maybe asv so continuous
mechanical ventilation adaptive support ventilation
ventilation
but the biggest thing is that you want
to control their ability to breathe and so
so
we set particular things in settings
here so you set like your fio2
you set your peep and these two things
control your
oxygen saturation you can also control
your tidal volume you control your
respiratory rates which helps you to determine
determine
your co2 concentrations
so very important thing to be thinking
about whenever you're intubating somebody
somebody
also when you're intubating somebody it
helps because high intracranial pressures
pressures
you want to control their breathing and
you also want to try to sedate these
patients a little bit because
these sedation meds also help to lower
basal metabolic rates lower the actual
oxygen consumption of the brain
so sometimes intubation allows for
someone to be able to be sedated because
you can protect their airway
so allowing for sedation is also helpful
so things like propofol or
versed also known as midazolam let's
write that down here midazolam
can be helpful to kind of really sedate
the patient keep them comfortable and
help to control their uh
potentially elevated intracranial
pressures so protecting their airway
with mechanical ventilation is very important
important
what's the next thing so after we've
stabilized the airway it's kind of and
they're in their breathing
it's circulation so blood pressure is a
huge thing
it is definitely one of the big most
most important things to control
so when someone has a bleed you want to
prevent the expansion of that already
present bleed
so keeping a blood pressure goal
systolic blood pressure less than 160
millimeters of mercury
sometimes it can be even if you want to
have a more stringent goal
less than 140 millimeters of mercury but
we're controlling their blood pressure
with particular antihypertensives
so things that are going to be like what
well the best thing to be thinking about
is nicardipine
nocardipine you have very good control
over blood pressure
other things are going to be things like
libado law
so the beta law is a a so nocartipine is
a calcium channel blocker labatal is a
beta blocker
you also can use things like enalapril
okay and actually it's called a
naloprenet and this is also iv so all of
these are these iv forms
you want to use iv forms and when
someone's this sick so that you get very good
good
better blood pressure control also
there's other drugs that you can give
sometimes you can even give furosemide
especially if someone is actually volume overloaded
overloaded
that may also be helpful in iv form as
well so either way controlling the blood
pressure by whatever means you can
particularly be these iv methods and
then later
you can use oral antihypertensives so anti
anti
hypertension meds once you kind of get
them a little bit more stable
so you have a plethora of options ace inhibitors
inhibitors
arbs you have also your dihydropyridine
calcium channel blockers like amlodipine nephetipine
nephetipine
you have other drugs like beta blockers
so beta blockers things like
labetalol or other options and then you
even have alpha 2
agonists things like
clonidine so it's important to get good
control of their blood pressure less
than 160 and again you can use
iv drugs and then once able oral
antihypertensive medications for
prolonged blood pressure control is also
very important
okay what else so control their airway
intubate mechanically ventilate sedate
blood pressure control less than 160
more stringent goals say even less than 140.
140.
the next thing is do they have a coagulopathy
coagulopathy
so reversal of an underlying
coagulopathy is extremely high yield
so think about the anticoagulation right
so first thing are they taking a
particular medication
like warfarin if they're taking warfarin
you need to know the reversal
agent what is the reversal agent for warfarin
warfarin
well the first thing is you need to give
iv vitamin
k generally you give this like
10 so you're going to give 10 milligrams
of iv vitamin k
the other thing that you give is what's
called p c
c prothrombin complex concentrate
and it's important to remember that this
is based
on the inr we're not going to go and
write all of these down i'll quickly
list like
for example if the inr is between 1.5 to
1.9 you get 15 units per kg
if it's 2 to 4 you give 25 units per kg
if it's 4 to 6 you get 35 units per kg
and if it's greater than 6 inr you give
50 units per kg
of pcc another option
is that there's another other option of
what's called f
f p fresh frozen plasma but generally
pcc is preferred
so warfarin what do you do again
remember you reverse it with iv vitamin k
k
and pcc based upon their inr
the next one is heparin so if someone is
on a heparin infusion
particularly they have a hepa infusion
within the past three hours
you can give a drug called protamine
sulfate and protamine sulfate you can
give this there's a particular
conversion factor for this one
generally it's like a 50 milligram kind
of max that you can give
and that can reverse the heparin
especially if they've kind of finished
this within the past
or they've been on it with at least the
past three hours
the next one is your do axe and there's
a couple different types
of doax or no wax if you want to know
them but
and there's also a doxaband but these
two drugs
you reverse these there is no like
specific reversal agent as compared to
these other ones up here
but we've seen somewhat of a decent efficacy
efficacy
reversing these with pcc so prothrombin
complex concentrate
and again this one ranges as well this
can go anywhere from 20 to 50 units
per kg but that's one option the other
option is there is somewhat of a newer
drug there's not a ton of
evidence to support its use but indexing that
alpha is believed to be a drug that can
reverse these dough acts as well
there's one more dough act that you have
to remember because it does have a very specific
specific
type of reversal agent so the other one
is called
debigatran so uh apixaban rivaroxaban if
you really want to remember these are 10a
10a
inhibitors factor 10a inhibitors
de bigatran is a factor
2a inhibitor or also known as a thrombin
inhibitor and this one you actually
reverse with a
very specific like a monoclonal antibody
called ioda
richisumab okay
so warfarin reverse with iv vitamin k pcc
pcc
or ffp heparin protamine sulfate dox
if it's the 10a inhibitors it's pcc or
indexing at alpha
if it's the bigatran which is a thrombin
inhibitor it's idler
kisumab alright what about tpa
well if you guys watched our ischemic
stroke lecture you already know what we
do for tpa
if they're still getting the tpa
infusion you stop the tpa infusion
but you give them what's called tran
examic acid also known as txa
a one gram bolus and then maybe another
gram eight
hours later you can also give what's called
called
cryo precipitate
maybe up to 10 units plus or minus
platelets that can be transfused in
these patients okay
the next thing is if there wasn't enough
already is if someone is on
anti-platelet agents
now here's the last thing with these anti-platelet
anti-platelet
uh platelet agents include which ones
so this is your aspirin which is a
pretty common one
in clopidogrel all right which is also
so these two agents there's actually not
a lot of evidence
to support the use of
platelet transfusions okay the
only time where platelet transfusions
may be utilized is if the person is
getting a neurosurgical
intervention so neurosurgical
interventions you actually
want to have platelets that are greater
than a hundred thousand
so if they have less than a hundred
thousand they've been on anti-platelet
agents you can consider giving like a
platelet transfusion
another option besides this is also
there's what's called a ddavp
which is also known as desmopressin
so this is another option to give in
someone who is anti-platelet agents
big big big thing to remember there's
not a lot of evidence to suggest
actually using these things
if someone took an anti-platelet agent
and they developed a bleed
it's mainly the ones above that we would reverse
reverse
this one not a lot of evidence to
support okay
we've so we've supported their airway
we've controlled their blood pressure
we've reversed the coagulopathy
now what let's control the cerebral
edema and elevated intracranial pressures
pressures
all right so now let's talk about how we
treat cerebral edema elevated
intracranial pressure that's seen in
ichs so whenever someone has an ich they
have probably a big midline shift a big
old pocket of blood
it's important to know kind of the
treatment measures that we would go
about within this patient
so what do we do so the first things you
really really need to know is
is sometimes neurosurgical intervention
is the big big thing here
um intervention so what are these
neurosurgical interventions that we
could employ for this patient
so the first thing is so sometimes if
you have a pretty decent sized bleed
right sometimes what we we don't want is
we don't want this bleed causing so much
midline shift that you start trying to
push parts of the brain tissue downwards
onto the brainstem causing herniation
so what we do is is take the bone off
where that bleed maybe is near that area
so that the brain can actually swell
outside of that actual calvaria
bone flap area and not downwards onto
the brain stem
so we can do kind of a decompressive
craney okay now if the bleed is super
tentorial there's been a couple
different trials like the stitch trials that
that
look at blood within the super tintorial
so above the tentorium up in the
this portion of the cerebrum versus
impertintorial kind of
like posterior fossa where the
cerebellum and brainstem is
there's not a lot of support to say you
can you know evacuate and pull out blood
within the super tentorial region but
sometimes it's still done
there's a lot more support for saying
pull and evacuate out the blood
that is actually within the
infra-tintorial region because it's such
a small space
and it can smash on the brain stem and
cause really significant hydrocephalus
so sometimes not only you can decompress
them but you can sometimes evacuate
some of that actual blood the other
thing is if this this blood extends into
those little cavities right so you have
the different cavities let's just say i
draw a cavity here
this cavity let's just say is the fourth
ventricle some of that blood
coming from that hemorrhage can extend
into these ventricles
and block up the flow of cerebral spinal
fluid and so that
that cerebrospinal fluid can actually
back up and start causing those
ventricles to balloon up
and that can cause hydrocephalus so
sometimes putting in what's called
an external ventricular drain and evd
can help with the hydrocephalus so this
is important in situations with
ivh intraventricular hemorrhage
the next thing is we can employ
particular medical management
so there's some medical kind of like
interventions that we can employ
for these patients so one of the things
that we can do is we can make the blood
really salty and just dehydrate the crap
out of the normal healthy brain tissue
to just decrease the amount of space
inside of the brain
and so we can use different types of
salty kind of measures
so we can use drugs like three percent
hypertonic saline
or 23.4 percent
hypertonic saline and really make the
blood salty maybe you approach a sodium goal
goal
of like 150 to 155
and that's your goal to make the blood
so salty that you draw water
out of maybe this area here where
there's healthy brain tissue
and an intact blood brand barrier
another medication that we can give
besides like these hypertonic salines is
there's also the option
of mannitol okay so mannitol generally
like it's a 25
solution and this comes in various
different doses that you can give
but mannitol is another drug that you
can give to kind of again
dehydrate the brain pulling some of the
fluid away from this
healthy brain tissues to kind of
dehydrate the brain a little bit
so these are kind of the basic
measurements that you can utilize for
cerebral edema and increase icp
the next thing that i want us to talk
about here
is seizures man oh man
bleeds that are near the cortex are very
high risk for seizures
so these bleeds create a very
significant kind of epileptogenic focus
that can lead to maybe focal seizures so
these individuals can maybe develop
focal seizures and depending upon where
that is it could be very specific so for
example if it was like in the left like uh
uh
front like maybe to the frontal or
parietal lobe maybe you start developing
like some twitching on that right side
of the body or something of that nature
so that you can develop focal seizures
now sometimes these focal seizures can
actually generalize
and you can develop generalized
seizures that are full on like tonic clonic
clonic
okay another thing is sometimes
these bleeds can not only cause focal seizures
seizures
generalized tonic clonic seizures but
they can cause these types of seizures that
that
are really not that obvious they're not
just flailing around or twitching
certain parts of their body
it can lead to what's called
non-convulsive status epilepticus
and this is one where they just really
are just kind of like a decreased mental
status they're not super
involved they're not really maybe a
phasing maybe they have gaze preferences
and stuff like that
and you actually need a continuous eeg
to really kind of diagnose this type
either way
it's really important to treat these
seizures with anti-epileptic medications
okay and so there's many different types
we're not going to go through all of them
them
but i want you to know that there's some
medications that we can give such as
phenytoin phosphonotoine valproate
levitarazetam lucosamite and we can even
accelerate that to really intense
sedation agents
like propofol and midazolam and even if
we have to
uh barbiturates in those situations as well
well
okay so that covers the seizures
the last thing that i want us to well as
we get towards the last thing is kind of
the ich
prevention so there's different things
that we've talked about as potential
causes of ich
that we want to prevent from happening
in the future and what are those things
and what do we say is the most common cause
cause
of someone developing an ich hypertension
hypertension
right so we need to have better um so
control of someone's
hypertension and so it's very simple
and so that's very very important
because if you have someone who develops
a bleed
and it was due to hypertension you
really want to maximize their
antihypertensive medicines
to keep their blood pressure lower so
they don't develop another bleed somewhere
somewhere
the other thing that you want to be
thinking about here is
what if somebody had an ischemic infarct that
that
can transformed or kind of converted
into a hemorrhagic bleed
and it was due to an embolic source so
you want to be thinking about
anticoagulation sometimes in those situations
situations
so sometimes sometimes anticoagulation
may be needed
but here's the big reason why
there's really one condition that i want
us to know this for
anticoagulation there's a thrombus
that forms within your veins what was
that called cerebral venous sinus
thrombosis so cerebral venous sinus
thrombosis you have to anticoagulate
even if the person does develop a
bleedbeak from that
you have to prevent that clot from
continuing to develop
so you want to start breaking down that
clot preventing future clots
with giving them anticoagulation like
heparin or
different types of heparin there's
unfractionated there's low molecular
weight heparin
and sometimes even treating them with
different types of dough acts as well
so it's important to remember
anticoagulation is very important for
these individuals
especially if they have a hyper
coagulable condition underlying there
and then again
if they have um risk so let's say that
this person has atrial fibrillation
so they have atrial fibrillation that is
causing their ischemic infarct
you don't want to give them
that anticoagulation while they're
bleeding you want to give it time
you need to give the person time for
that bleed to heal
so for afib you might start this maybe
you know
two months to three months later you'll
start their anticoagulation but you
definitely want to restart that
and the reason why is if they go on and
develop an ischemic and fart
they're going to develop a stroke
because of that so you want to
anticoagulate them if they have some
type of cardio embolic source i'm just
putting afib
as an example here sometime later after
their bleed heals and it starts to clear
some of that clot
you want to put them back on their
anticoagulation if they were on that
okay but give it some time for that
bleed to heal and recover before you do that
that
the next thing that i want to think
about let's just keep the blue marker
here is infective endocarditis that was a potential cause right so
that was a potential cause right so infective endocarditis
infective endocarditis what do you do for this
antibiotics right so you're going to put these individuals on broad
these individuals on broad spectrum antibiotics until you obtain
spectrum antibiotics until you obtain their blood cultures and find out what
their blood cultures and find out what exactly they're on so maybe start them
exactly they're on so maybe start them on vancomycin and cefepime and then
on vancomycin and cefepime and then adjust based upon whatever comes back
adjust based upon whatever comes back from their blood cultures
from their blood cultures okay so that and then sometimes
okay so that and then sometimes infective endocarditis if it causes
infective endocarditis if it causes mycotic aneurysms
mycotic aneurysms sometimes there is potential in
sometimes there is potential in indication for coiling so coiling
indication for coiling so coiling that actual area where the mycotic
that actual area where the mycotic aneurysm is to prevent that from
aneurysm is to prevent that from continuously bleeding into that cerebral
continuously bleeding into that cerebral tissue
tissue okay last but not least is
okay last but not least is vascular abnormalities so you know that
vascular abnormalities so you know that goes back to your vasculitis that goes
goes back to your vasculitis that goes back to your avms and things like that
back to your avms and things like that the big one that i want you to remember
the big one that i want you to remember is the avm so avm sometimes you don't
is the avm so avm sometimes you don't touch them you don't even
touch them you don't even mess with them but if they're really
mess with them but if they're really becoming problematic
becoming problematic what you can do is you can actually
what you can do is you can actually develop kind of you can literally clot
develop kind of you can literally clot off the blood flow to these these avms
off the blood flow to these these avms and so cause these little avms to pretty
and so cause these little avms to pretty much like die down so they're not even
much like die down so they're not even getting
getting any blood's even going to them anymore
any blood's even going to them anymore so that way if you know if you develop
so that way if you know if you develop kind of another brief rise in pressure
kind of another brief rise in pressure sometime in the future
sometime in the future you don't rupture those anymore because
you don't rupture those anymore because again we're embolizing them so that no
again we're embolizing them so that no more blood actually goes to these
more blood actually goes to these avms so sometimes there may be an
avms so sometimes there may be an indication for what's called
indication for what's called avm embolization
and that will cover everything that we need to know about
need to know about intracerebral hemorrhage
intracerebral hemorrhage [Music]
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