Sonography of the Infant Brain-Hemorrhage Grades 3-4 - SD

Grade Three Hemorrhage

In a baby who has dilatation of the lateral ventricle,
we begin to consider grade three hemorrhage.
If there's no parenchymal hemorrhage
to put it into a grade four classification, it's important
to know where the walls of the ventricle are.
Always look for the ependymal lining, which is slightly echogenic,
even in babies who don't have hemorrhage.

And here we can see that there is
essentially a normal sized frontal horn,
but as we get towards the occipital horn
and towards the temporal horn,
we see that there's dilatation.
There's also bright echogenicity that's in excess
of the echogenicity that we would normally see in the region
of the glomus of the choroid plexus.
There's some in the temporal horn,
some in the occipital horn,
and there is a bright area
of echogenicity in the germinal matrix.
So this is mild hemorrhage, mild dilatation
with germinal matrix hemorrhage consistent
with a grade three A.

Grade Three B (Moderate)

Notice the difference in the appearance
of a grade three B hemorrhage, which is moderate IVH
moderate ventricular dilatation,
and in this particular baby also includes
germinal matrix hemorrhage.
So if we outline the ventricle here, we see that there is
moderate dilatation of the ventricle.
This bright area of echogenicity represents
the germinal matrix hemorrhage,
and then there is a moderate size area
of bright echogenicity that's occupying parts
of the frontal horn
and the body even extending into the atrium
of the lateral ventricle.
And there's increased echogenicity in the occipital horn
as well as some in the temporal horn.
So this is a moderate degree of hemorrhage
and dilatation as well as a germinal matrix hemorrhage.
So this is a grade three B.

Grade Three C (Severe)

Notice the extreme difference between the mild
and the moderate degrees of intraventricular hemorrhage
and dilatation compared
with severe IVH severe ventricular dilatation
and germinal matrix hemorrhage.
Here we have a very far anterior coronal view of the brain
demonstrating large areas of bright echogenicity
with in the frontal horns right side greater than left.
Notice that instead
of the ventricle maintaining a concave lateral wall,
it's now convex, which raises the question
of increased intraventricular pressure.
And this is consistent with intraventricular hemorrhage
that is severe.

Coming a little bit more to a mid coronal view,
we see the right lateral ventricle, the left,
and here we have the third ventricle.
We could see hemorrhage extending through the foramen
of Monroe from these dilated ventricles,
which are severely dilated into the third ventricle.
A posterior coronal view shows bright echogenicity more
so than what we would expect with just the choroid plexus.
It's quite broad on the left side as well,
but not quite as extensively.
So we have bilateral grade three hemorrhage.

Notice the parasagittal view.
There is an entire cast of the lateral ventricle formed
by this huge amount of hemorrhage.
The frontal horn, the body, the atrium
of the lateral ventricle in continuity with the body,
the occipital horn, which is filled with blood as well
as the temporal horn.
In fact, the echogenicity is so bright compared to the glomus
of the choroid plexus
that it totally silhouettes out the borders
of the choroid plexus.

Resolution of Hemorrhage

Now what happens when there is a hemorrhage within
the ventricular system?
Basically the clot will undergo a process
of internal liquefaction.
The clot will retract from the ventricular walls,
it will undergo fragmentation and absorption.
At times, septations will persist
and characteristically.
There will be thickening
and brighter echogenicity in the ependymal lining
that is obvious within one to six weeks
after the hemorrhagic insult.
Sometimes there are some disruptions noted in the
region of the ependyma.

Well, here's the same baby.
As we look at the ensuing process of
attempt at resolution,
there is bright echogenicity in the region
of the germinal matrix.
Here's the caudothalamic groove,
which is also showing some central decreased echogenicity
indicating that it is beginning
to undergo early liquefaction.
And then we notice that the bright echogenicity
that was previously seen as a cast of the lateral ventricle
is no longer totally brightly echogenic,
but we see a bright line that is the outline of
where that major hemorrhage occurred.
Often people have difficulty seeing the difference
between the clot as it's undergoing resolution
and the walls of the ventricle.
So I'm gonna show you the outline
of the walls of the ventricle.
There's thickening
and bright echogenicity in the frontal horn in the body
of the lateral ventricle extending all the way out
to the occipital horn.
Here's the temporal horn,
and this is usually due to a gliosis reaction
or adherence of blood cells
to the ependymal lining of the brain.
Here is the glomus
of the choroid plexus tapering toward the caudothalamic
groove and the temporal horn.
Notice that there is preservation
of the periventricular blush,
so this is a clot undergoing liquefaction
and undergoing retraction from the ventricular walls.

Ventricular Enlargement and Post-Hemorrhagic Hydrocephalus

Well, so far as the ventricular enlargement is concerned,
initially the enlargement is due
to distention by the hemorrhage.
This enlargement may resolve,
it may persist, it may progress.
One of the problems that is always
of concern when there is a hemorrhage that is
more severe than a grade three A is
that the babies can develop post hemorrhagic hydrocephalus.
It may be obstructive, which is usually at the aqueduct,
Sylvian aqueduct, or it may be communicating.
And in this situation,
the cerebral spinal fluid is not resorbed
by the arachnoid granulations usually
because of some hemorrhage around the brain as well.
There may also be an inflammatory type of ependymitis
that can cause persistent ventriculomegaly.

When the ventricles are large, it's not uncommon
for the neonatologists if they see a enlarging head
circumference to use lumbar punctures to try
to relieve the pressure by removing some of the fluid,
at times ventricular punctures will be made
to relieve the pressure by aspirating fluid.
At times when shunts are done too early
and there is residual clot within the ventricle,
the side holes of the shunt tube can become clogged
and the shunt will be totally ineffective.

Well, here's the same baby that we looked at
with a grade three C hemorrhage.
That's severe hemorrhage dilatation,
and in this particular baby also germinal matrix hemorrhage,
and we see that approximately a month
and a half later, there is marked dilatation
of both the right and the left lateral ventricles as well
as the third and the fourth ventricles.

Here's the midline sagittal view.
We're picking up one of the ventricles,
very wide foramen of Monroe.
We see that there is an echogenic appearing third ventricle
with the cerebrospinal fluid outlining the massa intermedia.
There's also a very prominent fourth ventricle.
Here's a good example of how the third
and fourth ventricles may appear to be filled
with echogenic fluid.
When the ventricle is widened,
there are no specular reflectors that will be picked up
by the ultrasound transducer,
and so this is a very useful way of knowing
that there is in fact dilatation of the third
and fourth ventricles.

Here we can see some pressure on the cerebellum
and we're looking at this very enlarged posterior horn
of the lateral ventricle.
This is just an artifact
and notice how compressed the occipital cortex is as well
as the decreased depth of the parietal
and the frontal parenchyma.

Grade Four Hemorrhage

Now with grade four hemorrhage, in addition
to ventricular dilatation
and intraventricular hemorrhage, there may
or may not be germinal matrix hemorrhage,
but there is hemorrhage in the brain parenchyma over time.
Usually within several weeks to a couple of months,
there will be liquefaction of the infant brain.
In the area of insult with hemorrhage,
the infant brain is relatively quite liquid
and extremely vulnerable to degradation of the tissue.
In the presence of hemorrhage,
intraparenchymal hemorrhage is most often a form
of hemorrhagic periventricular infarction.
It is associated
with intraventricular hemorrhage in approximately 80%
of cases and occurs on the side
with more severe IVH.
The distribution is often frontoparietal,
but it can extend into the occipital areas as well.
Over time, the porencephalic cyst will be
demonstrated as a communicating cyst
with the associated lateral ventricle.

Example. This is a coronal view of the brain In an infant
who has moderate dilatation of the left lateral ventricle,
the right lateral ventricle is not seen distinctly
because there is a bright area of increased echogenicity,
not only in the region of the ventricle,
but in the subependymal region and in the brain parenchyma.
As we look more posteriorly,
the findings show indistinctness of the ventricle
with this huge area of hemorrhage
in the parietal occipital region.
This is the choroid plexus in the atrium
of the left lateral ventricle.
It appears that there's some hemorrhage in this ventricle
as well and hemorrhage extending into the posterior portions
of the right lateral ventricle.

The parasagittal view shows indistinctness
of the lateral ventricle.
It appears that there is a germinal matrix hemorrhage,
but in addition to hemorrhage in the region
of the ventricle, there's also a frontoparietal
occipital hemorrhage in the parenchyma.

While about one month later on this coronal view, we see
that the lateral ventricles have enlarged that there is now
convexity to the lateral walls of the lateral ventricles,
presuming increased intracranial pressure.
The third ventricle is large, the temporal horns are large,
and notice that there is bright thickened ependymal lining
bilaterally thought to be due to a gliosis reaction
or adherent blood cells.
There is also a large amount of contained
material within the ventricle in the region
of the previous hemorrhage.
It's beginning to undergo clot retraction and liquefaction,
and at first look, one might think
that the hemorrhage in the parenchyma is actually resolving
satisfactorily because it looks like there are parts
that show the same echogenicity
as the unaffected brain parenchyma.
What in fact is happening is
that this clot is undergoing dissolution,
and we can see that there's actually continuity
and communication of this clot in the parenchyma
with the intraventricular clot,
and there's still quite a bit
of bright echogenicity within the brain parenchyma.
This is the beginning of the formation
of a communicating porencephalic cyst,

parasagittal view baby's head is facing.
To our left, we see the frontal horn, the body,
the atrium of the lateral ventricle,
occipital horn, temporal horn.
Notice the thickened, the ependymal lining,
and the fact that there is now beginning destruction
of the deep white matter in the region of the
previously noted grade four hemorrhage.
Also note that the intraventricular clot
that had formed the cast of that ventricle is undergoing
retraction from the walls of the ventricle
and is undergoing internal liquefaction
intraventricular hemorrhage.

Depending on the severity may resolve within days to months,
and this is the left lateral ventricle,
we see the thickened ependymal lining,
the enlargement of the ventricle.
This is the glomus of the choroid plexus.
There's hemorrhage in the temporal horn as well
as some residual clot in this very prominent occipital horn.

Well, one month later.
This is what this unfortunate little
baby's brain looked like.
We see that there is further dilatation
of the left lateral ventricle
and that there is complete destruction of the brain tissue
in the region of the previous intraparenchymal bleed.
Parasagittal view confirms the tissue breakdown
in the frontoparietal region extending into the more
anterior portions of the occipital region,
and notice how little parenchyma there is
left in this brain.
From the pressure of the porencephalic cyst
and the dilated ventricle.

Paraventricular Hemorrhagic Infarction

A few words about periventricular hemorrhagic infarction.
It's thought that the parenchymal hemorrhage
is basically due to increased pressure
in the terminal vein in the subependymal region,
which drains the medullary veins in the
periventricular white matter.
When there is a germinal matrix hemorrhage,
intraventricular hemorrhage complex,
the pressure from the hemorrhage can obstruct the terminal
vein in the periventricular white matter.
This results in increased intraparenchymal
and periventricular pressure,
which can impair the blood flow to the brain
from the arterial side,
and ultimately infarction can occur.

This is an example from Dr. George Taylor's work
of a 26 week gestation infant
who had a germinal matrix hemorrhage.
As we see, just to the right of the cavum septum lucidum,
and below this right lateral ventricle,
there's some dilatation of the left lateral ventricle.
There's also a little hemorrhage in the germinal matrix on
the left, but notice that there is satisfactory flow
in the terminal veins as well as the
internal cerebral vein.

Here's another example.
We can see that the terminal veins are displaced
and draped over these bilateral germinal matrix hemorrhages,
but there is satisfactory flow.

Contrast that with this.
This is a baby who has a grade four hemorrhage marked
dilatation of both lateral ventricles.
We can see the more anterior parts of the ventricle here,
the temporal horn, the temporal horn, lots
of clot within the left lateral ventricle extending into the
region of the deep white matter.
There's also clot within the temporal horn
of the right lateral ventricle.
Notice what happens to the flow in the terminal veins.
On the right side, we see satisfactory flow into the
internal cerebral vein, but on the left side,
because of the pressure from this severe hemorrhage that has
afflicted this baby's left lateral ventricle
And the parenchyma, there is pressure on the vein so
that there is inappropriate venous return.

Morbidity and Mortality

There's quite a bit of morbidity
and mortality associated
with intracranial hemorrhage in the premature infant.
Once the grade of the hemorrhage is more than a grade one
and two, grade one and two hemorrhage, the risk of morbidity
and mortality is about the same as in a baby
who has no hemorrhage, which is about 12
to 18% in terms of morbidity.
Grade three and four though is associated
with a significant risk of major neurological handicaps such
as developmental delay, mental retardation,
motor disabilities,
and contralateral hemiparesis of a grade four
hemorrhage.