00:01
Now, let’s talk about treatment of intracranial hemorrhages.
00:06
So, the first thing we think about in managing patients with
intracranial hemorrhage is
what is the cause of the intracranial hemorrhage, and
knowing the cause can help us to
guide the management of those patients. When we talked about
causes, there were 5
major categories of causes of intracranial hemorrhage. We
talked about hypertensive
hemorrhage, hemorrhagic transformation of ischemic strokes,
amyloid angiopathy,
vascular lesions and tumors like metastases or primary brain
tumors. And if we can
determine the cause of the hemorrhage, that helps to guide
us in how we will manage
those patients. For patients presenting with hypertensive
hemorrhage, the most important
management is control of blood pressure. Early control of
blood pressure prevents
propagation or expansion of hemorrhage and is ultimately the
best long-term therapy
for those patients. We will consider MRIs of the brain to
evaluate for other potential
causes and confirm the most likely etiology of hypertensive
hemorrhage. For patients
presenting with a hemorrhagic transformation of ischemic
stroke, this typically occurs
within the 3 to 5 or 7 days following an initial ischemic
infarct and that presentation should
give us concern for a hemorrhagic transformation. We may
consider MRI of the brain or
additional ischemic stroke evaluation in those patients if
not already performed.
01:21
In patients with amyloid angiopathy, MRI of the brain with
susceptibility weighted image
is important. Those patients present with lobar hemorrhages,
often with small micro
hemorrhages that are only evident on the susceptibility
weighted image, and that
imaging technique really helps to guide us in the diagnosis
of those patients in long-term
management. Vascular lesions need to be evaluated by
vascular imaging and that may
include CTA or catheter angiography to evaluate the cause
location and best
intervention for an underlying cerebrovascular lesion. And
for tumors, MRI of the brain
is the diagnostic modality of choice for evaluating the type
of underlying lesion.
02:02
Unfortunately, often that hemorrhage initially obscures
evaluation of the underlying lesion
and we often need subsequent imaging at 4, 6 or sometimes 8
weeks after their initial
presentation to establish an ultimate diagnosis. Our next
question in managing these
patients is, “Is surgery needed?” Oftentimes, these
hemorrhages are emergencies
initially, some can be managed conservatively. In fact, the
vast majority of patients
will be managed conservatively but surgery may be needed to
manage the underlying
lesion or evacuate the blood in patients who have declining
clinical symptoms. Surgery
is rare in patients with intracerebral hemorrhage. It is
reserved for lesions that are
suspicious for an underlying tumor or rapid and severe
clinical deterioration. That's really
important. We will hospitalize these patients and monitor
them closely within those
first 24 to 48 hours to evaluate those patients who may
suffer clinical deterioration
and require early intervention with neurosurgery. What are
the conservative steps
that we can do to help manage patients who do not require
surgery for treatment
of their intracranial hemorrhage. Well, I like to think of 3
categories of things that
we can do. The first is to manage blood pressure. And that's
important regardless of
the cause and regardless of the underlying etiology. So,
really important for patients
with hypertensive hemorrhages but we want to manage blood
pressure in any patient
presenting with an intraparenchymal or intracranial
hemorrhage. We typically consider
a goal systolic blood pressure of less than 160 as our
target. The second goal is to
reduce re-bleeding risk. We hold antithrombotics, reverse
anticoagulants, and avoid
medications that could result in coagulopathy. We evaluate
for coagulopathy and
manage that risk in patients who may have an inherited or a
newly acquired cause of
increased hemorrhage risk or coagulopathy. And then the last
is to manage secondary
complications. Patients who are immobile may be at higher
risk of DVT. We want to
consider DVT prophylaxis initially with mechanical devices
such as sequential compression
devices and then ultimately as the hemorrhage has been
determined to be stable
we can consider chemical prophylaxis for DVT. We do need to
consider the risk of
seizures and patients with intracranial hemorrhage. That
hemorrhage on the brain and
particularly around the cortex of the brain can increase the
likelihood of seizure.
04:26
We do not prophylax all patients with intracranial
hemorrhages for seizures but in some
patients particularly those with subdural hemorrhage or
subarachnoid hemorrhage
or lobar intraparenchymal hemorrhages we may consider
seizure prophylaxis for a short
period of time ranging from 1-4 weeks after the initial
hemorrhage. Now let's talk
about the second cause and major category of
intraparenchymal hemorrhages and that's
hemorrhagic transformation of an ischemic infarct. This is a
patient that initially presented
with acute onset of a left MCA syndrome, right hemibody
weakness, and aphasia.
05:03
The patient underwent non-contrast head CT, CTA, and CT
perfusion. CT perfusion
looks at areas of low blood flow both infarcted territory
that is lost and in penumbra
territory that is at risk. Here we see CT perfusion showing
a large area of ischemic
penumbra in the left MCA territory and this is what's
resulting in this patient's symptoms.
05:29
Here we're looking at the non-contrast head CT and the CTA
that corresponds to that CT
perfusion for this patient. On the non-contrast head CT to
the left, we see early areas
of ischemia in the subcortical regions and structures. We
see blurring of the gray
white junction in the insular cortex which is consistent
with initial ischemic injury to that
area and on the CTA we see a large proximal occlusion of the
left MCA. If you look
at the right MCA territory, there is good opacification and
patency of the right MCA
and a cutoff of the left MCA that's causing this perfusion
change in the patient's
symptoms and ultimately contributed to a large area of left
MCA stroke. The MRI scan
that corresponded to this for this patient didn't show a
large area of diffusion restriction.
06:19
This was performed 24 hours into the hospitalization and we
see this heterogenous
signal. Around that same time, the patient had suffered a
clinical decline and underwent
non-contrast head CT which shows the reasons for this MRI
imaging and the patient's
clinical deterioration and that is an area of hemorrhage
into this ischemic infarct.
06:38
We see an area of hyperdensity in that same subcortical
region where we are seeing
the early ischemic changes consistent with hemorrhagic
transformation of this ischemic
infarct. And this was confirmed on susceptibility weighted
image on that same MRI scan.
06:53
On the far right, we see the susceptibility weighted image
which shows us areas of
hemorrhage and we see a large area of hemorrhage deep in
this area of ischemic insult.
07:02
Hemorrhagic transformation after and ischemic infarct
typically occurs in the first
3-5 days or sometimes out to 7 days. That's the period of
time when the blood vessels
are friable after an initial ischemic infarct. The risk of
hemorrhagic transformation is
greater in large strokes like we saw and are seeing for this
patient and in patients who are
already on pre-existing antiplatelet or anticoagulation
therapy and these patients
typically have a period of fixed deficit followed by
clinical decline in the first 3-5 or up to
7 days. Now in contrast head CT should be performed and
we'll demonstrate this area of
hemorrhage which is often managed conservatively but may
require surgical intervention.