Transcranial Doppler: How To Do It Applications From Fetal Life to Brain Death - HD

Introduction

Hi, I'm Dorothy Blis.

I work at Children's National Medical Center
in Washington, dc.

Today I'll be talking about transcranial Doppler
pediatric applications.

The objectives
of this talk includes reviewing the technique
of transcranial doppler, recognizing
what normal blood PA flow patterns are,
recognizing alterations in these blood flow patterns
and identifying applications
for transcranial doppler extending from its earliest fetal
life to brain death.

Alterations of blood flow occur following asphyxia trauma,
subarachnoid hemorrhage,
and there are many clinical indications including sickle
cell disease, vasculitis, hydrocephalus,
vasospasm, AV malformations, and brain death.

Fetal Applications

We'll start first with the fetal applications
of transcranial doppler.

The technique includes obtaining axial images of the brain
and with color doppler,
putting the cursor on the middle cerebral artery,
you can get various measures including peak sal velocity,
pulsatility index, resistive index,
and a cerebral placental ratio,
which includes the middle cerebral artery PI divided
by the umbilical artery pi.

What occurs during mammalian diving reflex, the heart slows,
peripheral vasoconstriction occurs
and there is central nervous system vaso dilatation.
All these occur thus when a fetus is in distress.

You may also see cerebral redistribution
where you see increase in MCA diastolic flow
and this ends up increasing velocity
in decreasing the pi.

Looking at the MCA one can assess fetal anemia
with an increase in peaks of velocity
and assess for intrauterine growth retardation by looking at
cranial to umbilical ratios which decrease
when there is cerebral redistribution.

With fetal anemia, pxi solic velocity can
increase when there is significant anemia.
And this is quite sensitive though there is approximately a
12% false positive rate.

There are numerous studies have demonstrated the reliability
of looking at peak cell velocities to assess
for field anemia.

For intrauterine growth retardation,
one sees a decreased perfusion to the fetus,
thus there is a redistribution of blood flow
with increasing diastolic flow to the brain.

When we deal with the cerebral placenta ratio,
we're looking at the ratio of the MCA flow
to the umbilical arterial flow.
Typically the ratio is over 1.45.
This drops to one at about term.
If the cerebral placenta ratio is less than one,
the suggestion of placental insufficiency should be raised.

Neonatal Technique

We'll now move on to the neonatal technique
of transcranial doppler with the open font.

Now we have the advantage of directly looking at the vessels
as well as looking at the brain.

Here we have a case of a vein of Galen aneurysm,
beautifully seen by ultrasound.

We can put the cursors on demonstrating very high diastolic
flow with multi multiple feeders into the vein
of Galen aneurysm.

Ultrasound can also be very useful after therapy.
In this case, the infant has been embolized
and we have successful, obliteration of the vein
of Galen aneurysm.

We can also look not only at abnormal arteries,
we can also look at the normal venous sinuses
with the linear transducer via the Anil.

One can see the straight sinus, the vein of galin.

In this case, we do not see flow in the straight sinus
and this turned out to have
a sal sinus thrombosis secondary to dehydration.

Venous sinus thrombosis can occur in several different
veins, including the vein of labbe, vein of Galen.

And these can develop hemorrhage therapy
tends to be supportive.
Rarely anticoagulation is recommended.

In this infant on the right, we do not see
any flow in the straight sinus, so it's important to know
what normal looks like.

Beware when we see vessels that do not have flow in them
and that it may not necessarily mean there's thrombosis.

You have to be very careful with your technique to make sure
that we're not simply seeing a very dilated,
slow flowing vessel.

It's also useful with transcranial doppler in the neonate
to look at the subar space.

Typically there are crossing vessels
and this can help
to differentiate simply extra axial collections
that are subarachnoid versus subdural.

With a subdural hemorrhage
or fluid collection,
the vessels are gonna be plastered along the
convexity of the brain.

You will not see any crossing vessels
and the gyr may be flattened.

We'll now look at the intracranial arteries via
the anterior fontanel.

In the sagittal plane,
one can see the anterior cerebral artery.

The pulsatility can be again assessed with peak systolic
and diastolic parameters
with which then can result in ratios including the resistive
index In the
anterior fonte.

Moving to the right and left in the Corona plane,
one can intonate the middle cerebral arteries.

Here's a case where you see no flow
on the left with normal flow on the right
and on CT we demonstrate
that there was an acute left MCA in
fart after font.

Acoustic Windows Post-Fontanel Closure

Now closure, we no longer have the luxury
of visualizing the vessels directly via the fontanels.

However, there are several windows that are available
to us even in the adult population.

This includes the transtemporal window, the orbital window,
the submandibular window, and the foramen magnum window.

Transtemporal Window

The transtemporal window can be utilized either
with the imaging or non-imaging transducers.

With the non-imaging transducer, one can place
the transducer directly over
where the MCA is coursing with sound.

One can establish various
velocity patterns including establishing the peak systolic
and diastolic and time average maximum mean velocities.

Advantages of the non-imaging transducers are
that they are relatively inexpensive.

The probe is small, so it's easy to manipulate.

There's high quality sound, which is critical
in making sure you're in the center of the vessel.

These are made specifically for transcr doppler.

So there are taco buttons from moving every two millimeters.

There's summary data sheets
and can be actually quite fast in experienced hands.

Problems with the non-imaging technique are
that it does require intensive training.

It may be hard to find the vessel simply by listening
for it, and many centers do not have this machinery
available With imaging
where most radiologists now have, ultrasounds
that can give us both color
and gray scale top doppler via the transtemporal approach.

By throwing the color on,
we often can see a beautiful circle of Willis.

The first arrow is porting
to the left middle cerebral artery.

One can see the anterior cerebral artery,
the posterior cerebral artery.

When you put the cursors on, you can get a doppler signal
that again gives us information including peak
sto velocities and diastolic velocities.

Resistive indices,
pulsatility indices time average maximum mean velocities
with the vessel coursing towards the transducer.

The strongest signal comes from the middle cerebral artery
and you can march down this vessel every two millimeters
to make sure that there are no areas of stenosis
or narrowing throughout the vessel.

At the level of the bifurcation, one gets
flow away from the transducer,
which is the anterior cerebral artery, as well
as flow towards the transducer,
which is the middle cerebral artery.

This gives you a biphasic wave pattern,
which in this case is the bifurcation
angling slightly anteriorly and a little more distally.

One gets flow in a reverse direction
and this is the anterior cerebral artery.

If you angle the transducer inferiorly slightly,
one can get portions of the distal internal cerebral artery,
which has a slightly harsher pattern and sound.

And when you angle posteriorly one can get portions
of the posterior cerebral artery.

The velocity of the posterior cerebral artery tends
to be somewhat lower than the middle cerebral artery.

Going from the posterior approach,
one can identify the basilar artery
and the vertebral arteries.

Orbital Window

One can also view an orbital window
and get ophthalmic doppler.

The ophthalmic artery also gives a
typical waveform pattern.

It's a slightly a higher resistant vessel.

However, when there's collateralization,
one has increased flow in diastole
and can help support the diagnosis
of an internal cerebral artery stenosis.

In this case, we have MR documentation
that the ophthalm artery is being used as a collateral due
to narrowing of the distal ICA.

Advantages of the imaging approach?

One can actually see the vessel
so quickly place the gate with higher confidence of
what vessel you're seeing.

It is a shorter learning curve
and most radiology departments have these,
transducers, available.

One can auto trace and if necessary can angle correct.

Resistive Indices

Let's talk a little bit about our resistive indices.

Now this is a ratio of peak systole minus N diastole divided
by peak systole.

This helps minimize the effect of angulation.

There are age dependent values in the preterm population,
the normal RI is typically around 0.77
and term infants just drops to about 0.7.

And by age two to adulthood
the normal resistive index is 0.5.

What does the resistive index mean?

An increase in diastolic flow
results in a decrease in the resistive index.

This becomes, starts looking more like a venous pattern.

A decrease in diastolic flow will result in an increase in
resistive indices and you may have actually no flow in
diastole as intracranial pressure increases
above mean arterial pressure.

Diastolic flow may actually reverse
and you'll have an RI greater than one.

Factors that impact intracranial flow include stenosis
vasospasm, complete occlusion
head injury with increased intracranial pressure
changes in CO2, including simply crying or sleeping.

And as I mentioned, age where flow velocities can decrease
with age and your resistive indices can change.

Clinical Applications of TCD

What are the applications of TCD for the next
half an hour I'll be discussing its use in assessing
for hydrocephalus, asphyxia, vasculitis,
sickle cell disease, trauma and brain death.

The first question is why should we use it?

What is the actual clinical question?

What are the presenting symptoms
and are there other studies
that can help provide information?

Do we need baseline exams for reference?

Can this be done portably or neovascular lab
and should we be using imaging
or non-imaging transducers And
how experienced are the examiners
who are performing this study?

Hydrocephalus

For infants with hydrocephalus, turns out
that resistive indices can be quite useful in
differentiating hydrocephalus from atrophy.

When ventricles are large,
they could be large simply from atrophy,
but very often the neonatologist wants
to know if there is hydros hydrocephalus which will benefit
from lumbar puncture, tapping,
or even a reservoir or shunt.

In this infant, you can see there is no flow in diastole
suggesting that there is an increase in intracranial
pressure as increased
intracranial pressure, goes higher, you get less
and less diastolic flow.

If there's atrophy,
the resistive disease will be in the normal range.

When they're elevated it implies the need for tapping
or shunting goin all
demonstrated that infants with
resistive indices greater than 0.8 used,
were an advantage of getting tapped or shunted
because they did have increased intercranial pressure.

What happens after a tap is the diastolic flow increases
with a normalization of the resistive index.

If there is continued hydrocephalus,
you may not see response to the taps
and that may imply a need
to actually get a ventricular perino shunt.

Here we have a case of severe ventricular magaly
with reversal flow and diastole.

After tapping, there is marked improvement
in the diastolic flow.

George Taylor went a little step further
and noted that if you put compression on the anterior
fontanel in infants who have
slight increase intracranial pressure, you will
actually demonstrate changes in resistive index.

If there is normal just mild ventricular magaly,
there'll be no change in the resistive index.

Here we have an example of an infant who with compression
develops some reversal of diazo flow suggesting
that there is increased intracranial pressure.

One problem with the transcranial doppler is you need
to be aware of what the rest of the body is going through.

Yes, the head is indeed connected to the body
and we need to be aware.

Here we have an infant who has reversal flow
and diastole, yet the ventricles do not look
particularly dilated.

In this case, the infant had a patent ductus arteriosis,
nothing to do with the ventricles.

Here's another infant
who had very elevated resistive indices.

This turned out to have a he angioli.

It's important to know the
clinical history of the patient.

Some studies have looked at hydrocephalus in adults.

Unfortunately there is a water variation of normal
and it's more useful if baseline values are available,
which typically are not
and you do need to have closer correlation
with clinical findings.

Joanna Art has done several studies looking at adults
with shunt failure
and did note that as in this case there was evidence
of shunt failure with low diastolic flow.

After the shunt was repaired,
there was increase in the diastolic flow
with the normalization of the resistive index.

In this case the resistive indices
or in the normal range, suggesting
that there was no increased inial pressure.

We can also sometimes actually visualize abnormally
high diastolic flow, which may be secondary
to an arterial venous malformation.

Asphyxia

Let's move on to asphyxia.

Asphyxia can result in impaired cerebral autoregulation.

This will end up with an increase in diastolic flow.

This has become a very powerful tool in the assessment
of a term infant following asphyxia.

As I'd mentioned, normal resistive in disease should measure
approximately 0.7.

When one encounters a low recessive index,
which should within 48 hours of an as associated event,
this correlates with poor neurologic outcome.

Here we have a diffusely, a emus cranial ultrasound.

The RIS are low.

This helps us to distinguish this from your typical brain
just after delivery
and on follow-up, this indeed was an infant
with hypoxic ischemic encephalopathy.

Here's another infant with a low resistive index ct,
again confirmed the severe HIE
here the SCI appear a little bit blurred.

The thalami perhaps slightly echogenic,
but this findings are quite subtle.

The fact that the resistive indices were low helps
to suggest that this is indeed hypoxic ischemic
encephalopathy and was confirmed with mr.

This has also been associated in children
after head injury or cardiac arrest.

This loss of autoregulation can again cause
increase in diastolic flow
and suggests impairment of the cerebral autoregulation
and can be used to predict cerebral injury.

One also notes that with lower eyes, hyper
ventilation may fail to alter the waveform pattern
and that also suggests vasomotor paralysis also a poor
prognostic sign.

Vasospasm

Let's move on to ruptured and cran intracranial aneurysms.

Looking for vaso spasm is something
that is used quite routinely in the adult population
with TCD, not as commonly in p the pediatric population
as this is more rare, we know
that after a arachnoid hemorrhage,
vasospasm can start developing as early as two days
after the bleed and may peak two weeks later
by about three weeks this should subside.

The first clinical of application
of TCD was in fact assessing for vasospasm.

Here's a 17-year-old who has evidence of narrowing
of both the a CA and the MCA.

What happens as the vessels narrow,
you get increase in velocity
and it turns out that TCD can be highly specific
in identifying who is developing vasospasm
before clinical symptoms develop.

This can help guide optimal timing of surgery and therapy
and one can follow the velocities as they decrease helping
to time the appropriate occurrence
of stopping therapy.

Elevated velocities, as I mentioned, often precede the onset
of the neurologic symptoms
and many centers now study the resistive indices
and peak systolic velocities
of the MCA daily In these patients,

what should the protocol include?

There is mild.
There's mild increase in your velocities,
and as the stenosis, as the vasso spasm increases,
this becomes moderate and then severe.

If the peak of salt velocities rise
to over 200 centimeters per second,
there's a high risk for ischemia.

A rapid change within a day
or so of more than 50 centimeters per second also
bodes for poor outcome.

One should perform both the right
and left middle cerebral arteries daily
identifying the highest velocities and compare day to day.

The proximal and middle cerebral artery is the most accurate
in assessing for a vasospasm.

And as mentioned, rapid increase
of over 50 centimeters per second per day
or an actual peak systolic velocity
of over 200 centimeters per day, centimeters per second.
Bows for evasive spasm.

Remember however that there are other etiologies
that can cause increased peak systolic velocity.

This can include, increased
intracranial pressures.

You can have abnormally low systolic velocities due
to low volume flow
and there can sometimes be peripheral vasospasm.

So it is critical to combine your clinical data
and lab data with the actual TCD results.

Vasculitis

One can also use transcranial doppler to assess
for cerebral vasculitis.

This small vessel vasculopathy is somewhat rare in children
but can cause acute stroke using transcranial doppler,
one can try to prevent further stroke by treating
with prednisone or cyclophosphamide.

One can also follow progression of stroke with TCD,

Sickle Cell Disease

a whole talk can be given on sickle cell disease.

We know that children are at risk for cerebral infarction
and we know that stenosis
of the internal cerebral artery middle
and anterior cerebral artery can progress
for years prior to stroke.

So it's wonderful that we can indeed assess
for a stenosis risk prior to the actual stroke occurring.

This screening includes looking at the peak
systolic velocities and mean peak systolic velocities
of the MCA distal ICA and a CA.

The stop criteria uses the mean peak velocity
of the middle cerebral artery and distal cerebral artery.

If they range over 200 centimeters per second,
the stop study has demonstrated children
that have abnormal TCDs had an abnormal risk of stroke
of over 10%.

With transfusion stroke risk decreased
to less than 1% per year.

So there is now recommendations that we scan our trans,
our sickle cell patients every six to 12 months.

Let's show you an example of a child
with sickle cell disease in the right MCA.

The time average peak velocity
or time average maximum mean was 78 centimeters per
second on the left.

Notice how high it is?

It's over 280
and indeed this child did have a stenosis.

Another 10-year-old came in for screening, was asymptomatic
and one can see that the peaky a velocities are over 300.

The actual time average maximum mean velocity measured 370
centimeters per second.

And one notices
that actually on the right the
velocities were unusually low.

Mr demonstrated absent flow in the right ICA
with proximal stenosis of the left MCA.

The patient was immediately started on transfusion therapy
and has remained stroke free.

One does need to worry about low transcranial doppler
velocities progressing to occlusion.

So beware if the velocities are less than 70 centimeters per
second in the mca in the time average maximum meanses,
that could suggest a tight stenosis
as we see in this patient.

We can also suggest moyo disease on transcranial doppler
when we do not see a normal middle cerebral artery
and a cluster of vessels.

Traumatic Brain Injury

We'll now move on to traumatic brain injury.

There are pathologic processes
that result in significant changes in cerebral
hemodynamics after trauma.

Timely diagnosis is crucial in head injury management.

Acutely there may be a decrease in the resistive index due
to loss of autoregulation.

The vessels may vasodilate
after, cerebral blood velocities can start increasing
due to vasospasm because of subarachnoid hemorrhages
or hypervolemia.

When cerebral edema develops,
resistive index will continue to rise.

As edema increases, you get less flow and diastole
and you may actually get reversal flow when the intracranial
pressure increases above mean arterial pressure.

Here we can see a pattern of trauma
where initially there's some vasodilatation
with increased flow and diastole.

You then get a drop in the diastolic flow
and as a cerebral edema worsens, you actually get reversal
of flow and diastole.

This can progress to brain death when there's such an arrest
of cerebral blood flow at the micro circulatory level,
the large vessels distend, thrombose and then collapse.

Eventually you get virtually no antegrade flow in either
systole or diastole
and you have complete circulatory arrest.

Let's look at this again.

Following trauma resistive indices can be separated
into four categories.

There may be no change.

You may get an increase in ri with no flow in diastole.

You may actually get a reversal of flow
with the diastolic flow below baseline
or you may see no flow at all.

Here is an infant, sorry, it was,
this is actually a child who had no flow
in the intracranial vessels.

Those this is already equal to brain death
when there's reversal of flow.

If the fentanyl is closed, this pattern typically progresses
to brain death in the next 24 hours.

And here you can see confirmation with a nuclear scan
in children after trauma
where there is elevated resistive indices where,
very little diastolic flow,
they may be cerebrally significantly
neurologically devastated.

But survival is, usually typical.

And if someone comes in with a normal recessive indices,
again, there may be neurologic deficits,
but survival is most likely.

Cerebral TC serial TCD readings can evaluate
how severe the edema is and follow the course of therapy.

We can see if there's vaso reactivity, if there's reaction
to hyperventilation that bodes
for a better prognosis than those who do not react to
the hyperventilation tactics.

RI increases as the vessels vasoconstrict due
to decreasing CO2.

This suggests, reactivity if there's reduced
or absent CO2 re reactivity within 24 hours of an injury.

This has a very poor outcome.

Again, cerebral edema can increase, resistive indices.

So you have to correlate with clinical and lab findings.

Brain Death

So here we have severely injured child is this brain death.

Nuclear medicine has been used to assess for brain death,
but needs to be repeated.

If some subflow is shown
and needs to wait 24 to 48 hours to repeat this exam,

we can use other modalities such as CT or an angiogram,
but they're quite invasive.

Ultrasound is a quick way of seeing whether any
of these additional studies need to be performed.

Establishing brain death, can be problematic.

And we have apnea tests, EEG, brainstem evoked potentials,
nuclear blood flow studies that all can be used
to help the condition determine brain death.

TCD can add another non-invasive method
of determining brain death
and it is not affected by phenobarbital.

It's non-invasive, repeatable, portable,
inexpensive, easy to perform.

Here we have a patient who, who has to
and fro reversal in diastole severe brain injury.

Reversal of dsoc flow can be characteristic
of essentially absent effective cerebral circulation in the
adult and older child.

Remember, however, that there are cases
where mild diastolic reversal flow have recovered.

Cur kimm suggested using a direction of flow index.

In this, the formula is one minus p systolic velocity
divided by peak diastolic velocity.

If the DFI is negative, the area
of reverse flow is greater than forward flow
and bodes for poor outcome.

If there's a negative DFI
and this is repeated over 30 minutes, all
of them died without brainstem function recovery.

Let's look at some brain death patterns.

In these cases you have very small early systolic spikes.

So there is rest of antegrade flow as well as reversal
of diastolic flow.

Here there is virtually no flow documented in the
intracranial vessels.

Here's some additional examples.

Very high spiked, minimal flow in systole
with reversal flow and diastole
with the velocities dropping over time.

Here again, some additional examples with very low
systolic velocities
and reversal in diastole

infant brain death is of particular problem in assessing
and TCD also doesn't work as well as
with the pediatric population
and adult population when the fontanel is already closed

in the neonate, low resistive indices have been described in
clinically dead patients
and in the other extreme infants
with extremely high RIS have survived.

So again, careful clinical correlation is crucial
in determining brain death.

We are looking at secreterial blood flow.

This is not synonymous for brain death,
rather it is confirmatory.

So when we think about using transcranial doppler
for brain tests, it's not to be used in isolation
and it should not be used
to supplant clinical neurologic findings.

However, it does provide data
that can help indicate the severity
of the cerebrovascular arrest.

If there is any question repeating the study can help
to confirm that there has been sufficient irreversible
damage to the super tentorial structures.

Conclusion

In conclusion, I hope I've shown to you
that transcranial doppler can be used to monitor children
with severe head injury
because it's portable, non-invasive, rapid
and can be repeated often

it provides useful adjunct in many clinical assistance
of not only the injured patient but the patient
after vasospasm, after hydrocephalus
and after stroke.

Remember that transcranial doppler is your friend.

Try to use it as o as you can. Thank you.