Ultrasound Evaluation of Pediatric Gynecologic Emergencies - SD

Introduction

Hello, I'm Dorothy Blis from Children's National Medical Center in Washington DC.

I'll be lecturing on hypoxic ischemic injury in the neonate.

This talk will initially describe the techniques of the neonatal neuros sonographic evaluation of the brain, including doppler techniques and the mastoid view.

We'll then review the differences in preterm and term cranial anatomy.

Finally, we'll discuss the pathophysiology of hypoxic ischemic injury of the preterm and the term infant.

This will include intraventricular hemorrhage per ventricular white matter injury, and hypoxic ischemic encephalopathy.

Techniques of Neonatal Neurosonographic Evaluation

When evaluating the needy needle brain, it's important to not just review the brain via the anterior fontanel.

We classically will look via the coronal and sagittal planes via the anterior fontanel at the cranial structures, however, we'll view different viewing techniques including the posterior and mastoid fontanel and discuss how doppler using mine, cerebral artery and anti cerebral arteries, resistive indices and help to assess for hydrocephalus as well as loss of autoregulation.

When looking v the inter fontanel, it's important to use the highest resolution transducers possible.

With our improved technology, we can now even detect the optic radiations of the area per atrial regions between 26 and 36 weeks gestation.

Improved resolution allows us to better look at the deep grade matter here.

The immature GR deep grade matter becomes more genic earlier gestation become becomes more hypoechoic in later gestation.

If there is increased ethnicity in the deep great matter in a term infant one may worry that there is indeed hypoxic ischemic encephalopathy.

Higher frequency transducers, particularly the linear transducers give us beautiful detail of the cortical gray matter.

The white matter as well as the ventricles.

Higher frequency linear transducers also allow us to look at the subarachnoid space, meningeal spaces as well as with color doppler.

Looking at the superior sagittal sinus, here's a case of a 29 week gestation Using the curved transducer, we can see the ventricles cave septum, lucidum and corpus callosum quite well and there does not appear to be any evidence of a germal matrix hemorrhage.

However, with the linear transducer, we do see improved resolution of the cuddle thalamic notch with evidence of a small germal matrix bleed.

Here is another infant using both the curved and linear transducers.

We can see in both that there is indeed intraventricular blood filling and extending the ventricles.

With the linear transducer you can see somewhat better a blush in the peri ventricular white matter consistent with the peri ventricular um, area of infarction.

Besides going via the inter fontanel, it's important to remember that there are several other supplemental windows that we can use to look at the brain.

The advantages of using these different supplemental windows include the ability to use higher frequency transducers, which give us higher resolution and earlier detection of abnormalities

Posterior Fontanel View

Via the posterior fontanel. One can see the atrium and per atrial white matter better.

Here we have with a curved array transducer via the inter fontanel questionable areas of lucency along the per atrial white matter going via the posterior fontanel.

Using a linear transducer, one can clearly confirm the fact that indeed there are regions of per ventricular leal laia in the white matter.

The posterior fontanel allows us to visualize the occipital horn, Cory Plexus and basal s cisterns.

In a study by Coria etal, they found that there was a greater accuracy in detecting intraventricular hemorrhage using the posterior fontanel and was superior and distinguishing normal pergonal blush from true white matter necrosis.

It also can be used to look at the posterior fossa.

Transtemporal Approach

The transtemporal approach via the thin temporal bone allows us to look at the brain in an axial projection.

This also allows us to see the third ventricle frontal horns and occipital horns quite well.

Here we have an infant who had a posterior fossa bleed nicely demonstrated via the temporal window.

Mastoid View

The mastoid view is an important view that can demonstrate pathology in the posterior fossa, including the brainstem and cerebellum.

This deeply obliged view allows us to angle in any direction we really want in the posterior aspect and we can see the cerebellum in this plane, which looks like a bi lobe structure.

It's an axial plane, but in a steep projection

With the poid font now we see that there's improvement in visualization, not only of the cerebellum and midbrain, but also the cisterns.

In a study by Luna Etal, they showed that using the mastoid fentanyl improved visualization of the posterior fossa.

In virtually all cases increased diagnostic confidence in 75% of cases and more importantly, was the only technique to show abnormalities in the posterior fossa in 46% of cases.

Here we can see the posterior fossa with blood clot obstructing the aqueduct with dilatation of the third ventricle and lateral ventricles.

Here are several different examples of blood filling the fourth ventricle and causing hydrocephalus.

Doppler Techniques

The last technique we'll talk about before we get to the actual imaging of the neonatal brain is doppler.

We can look at the anterior cerebral artery via the sagal midline view.

With colored doppler we can see the anterior cerebral artery and then the per cosal artery as it courses along the cafa septum lucidum.

By putting the cursor on the anterior cerebral artery branches, we get a doppler signal and um, we should look at the peak systolic velocity, end diastolic velocity resistive index and or pulsatility index.

The middle cerebral artery can also be intonated.

This can be obtained via the coronal plane, both the right and left middle srebro arteries can be insin and again peak systolic and diastolic and resistive indices Measurements can be obtained.

Resistive index is a very important uh, value to obtain as we use doppler work on the neonate because it minimizes the effect of angulation.

The reive index is peak systole minus n diastole divided by peak systole.

There are age dependent values available and as you can see from what's listed here, that by H two the normal value of 0.5 is met.

It's important to remember that term infants are resistive. Index of 0.7 is normal and in preterms it's actually slightly higher with a mean of 0.77.

An increase in diastolic flow will result in a decrease in resistive index.

You will get this type of waveform pattern, which looks somewhat venous with very high flow. In diastole with a decrease in diastolic flow, you get an increase in resistive index and here you see a very pulsatile waveform.

As intracranial pressure increases above mean arterial pressure, diastolic flow may actually become reversed.

The resistant indexes will be greater than one and you can see that the diastolic flow is below baseline.

Differences in Preterm and Term Cranial Anatomy

We'll now start looking at actually the brain.

There is quite a lot of maturation that occurs from 24 weeks to 36 weeks gestation.

There's gyration myelination, glial cell migration, decrease in water content.

These images of the fetus demonstrate how smooth the cortex is at 20 weeks and you begin to start getting infolding of the sylvan fissures by about 20 weeks gestation.

As the infant matures by 36 weeks, you have a fairly more mature pattern with multiple sci and gyri and the corpus callosum nicely demonstrated here is seen on top of a cave septum with a cavem virgie getting smaller in size.

Pathophysiology of Hypoxic Ischemic Injury in Preterm and Term Infants

Germinal Matrix and Intraventricular Hemorrhage (IVH)

The germal matrix is the origin of neuronal glial development.

There are rich arterial perforators from the A-C-A-M-C-A and PCA and these will drain to the deep venous system.

The dermal matrix is present in the fetus and starts to regress from posterior to anterior between the 24th and 28th week gestation.

Typically by 32 weeks. The entire germinal matrix has involuted

because of the vascularity to this area with pore support structure and thin vessel walls. This is a very vulnerable area for hemorrhage.

It is the most common origin of hemorrhages in the preterm infant with up to 20% of preterm infants developing a germal matrix hemorrhage.

Infants less than 1500 grams are also quite vulnerable in getting germal matrix bleeds and it's felt that these bleeds are are venous in origin.

The coto thalamic notch where the last part of the germal matrix resides has a very poor stromal support and the vessels here converged to form the draining veins.

The theory is that with increased flow venous, um, rupture occurs at these convergence points and that's why it's so common to see hemorrhages in this region

with hemorrhage, oxygen deliveries reduced and there's typically a switch from aerobic to anaerobic metabolism with an increase in lactate formation.

This can also cause secondary injury to the brain.

In addition, as the blood ruptures into the ventricle, you get hemorrhage blocking CSF absorption ending up, um, causing a ventriculitis with, with hydrocephalus developing.

It's important to remember Papilla's classification as this is useful in assessing long-term outcome.

Grade one hemorrhages are simply isolated sep, dependable hemorrhages that do not extend into the ventricle.

Grade twos. There's enough blood that ruptures into the ventricles, but ventricular dilation does not occur acutely with grade threes.

There's so much hemorrhage that occurs into the ventricles that ventricular dilatation um, occurs with filling of blood.

Grade four, which we now call peri ventricular hemorrhagic infarcts, are hemorrhages in the parenchyma that are associated with a germinal matrix bleed.

Some people use a modified classification of the pape system, particularly if you do not follow the um, head ultrasounds closely and systematically.

Thus, if you see blood isolated in the subependymal hemorrhage, you will just label that as sub dependable hemorrhage.

If there is blood in the ventricle, you call it an intraventricular hemorrhage and then just add with or without hydrocephalus.

Once there is a peri ventricular hemorrhagic infarct associated with it, you'll describe it as a germal matrix bleed with a peri ventricular hemorrhagic infarct.

Here are some examples.

This is a subependymal hemorrhage isolated to the germinal matrix.

It has not extended into the ventricle and there is no ventricular dilatation.

The sagittal view is particularly helpful in identifying the cuddle thalamic notch.

So here's the thalamus, here's the caudate, here's the notch, and here's a little bit of blood.

Remember that the choroid does not extend anterior to cuddle thalamic notch.

So once you identify echogenic material anterior to this level, indeed there is an intraventricular hemorrhage.

Here we have echogenic blood at the coth thalamic notch that's extending somewhat anterior to that co thalamic notch consistent with intraventricular hemorrhage but without hydrocephalus.

Here we have a 28 week gestation where you see that there's blood extending anterior to the cau thalamic notch.

So we have blood in the ventricle with mild dilatation of the ventricle and blood also in the back of exci horn.

Once you have ventricular magaly with the blood, this can be called germinal matrix bleed with ventricular magaly or grade threes.

And here we see nicely blood filling the co thalamic notch, filling the ventricles and causing ventricular dilatation.

Here's another case where you have ventricular dilatation blood filling the ventricles and this again is a grade three.

Often you'll see blood filling the ventricles and the third ventricle here when the bleed initially occurs.

It's very important these cases to do followup ultrasounds as increasing ventricular magaly will occur within a week.

In this case you can see that there is marked dilatation of the lateral and third ventricles with increased tricity along the walls consistent with ventriculitis.

With per ventricular hemorrhagic infarcts, typically you can see a germal matrix bleed, it may extend into the ventricle and then associated with it you'll start seeing a area of increased ethnicity within the per ventricular white matter.

These are typically asymmetric and um, if they are bilateral they usually have one side larger than the other.

With these per ventricular hemorrhagic infarcts, you find them classically and the peri ventricular white matter in the dorsal lateral aspect of the lateral ventricle where the medullary veins are confluent.

Here we have blood filling the ventricle.

It's quite difficult actually to see where the ventricle ends and the white matter necrosis occurs

and here we have a large peri ventricular hemorrhagic infarct and with time this blood clot will break down.

You'll start seeing the area of poor cephalic with intraventricular hemorrhages and per ventricular hemorrhagic infarcts.

It's very common for hydrocephalus to develop several days to weeks later as the ventricles dilate.

It's useful to know whether there is increased intracranial pressure.

The neonatologist rely on this information to know how often they need to tap the infant and whether a drain needs to be placed.

If the ventricles are dilated simply be because of atrophy, tapping or drain is not necessary.

So how do you differentiate between hydrocephalus and ventricular magaly?

This is where doppler can help.

When there is increased intracranial pressure, there is decreased perfusion during diastole and you result with this very pulsitile wa pattern with very little flow. During diastole.

In this case there was no flow, so this resistive index is elevated and it's gonna measure only one.

So with goin all we saw that if there was an increase in resistive index, this is indeed sign of an increase in intracranial pressure.

And as mentioned in the neonate, typically in a premature infant the resistive index should measure about 0.77 and anything greater than 0.8 to 0.9 should be considered increased and consistent with increased intercranial pressure.

Dr. Taylor demonstrated that if you put some pressure on the an fontanel and demonstrate increasing um, resistive indices during this maneuver, this also is a sign that the infant does have hydrocephalus.

Post tapping an infant with increasing intracranial pressure with elevated resistive indices, the pressure diminishes and you start seeing improvement in diastolic flow.

If this continues in a cycle to wait a few days, see elevated resistive indices tap see normalization of resistive indices, eventually this should start stabilizing and tapping can be decreased in number.

If however, there's no change in the resistive in index after tapping, it suggests that there may need a shut.

As I mentioned, the classification grade one through grade four is useful in assessing for outcome.

Notice that infants who have a normal ultrasound and these are in premature infants, while the ultrasound may be normal still about 10% of premature infants in this subgroup will have abnormal neurologic outcome.

And this is true for infants who have grade one hemorrhages.

Those infants with grade two hemorrhages have about um, an 85% chance of doing well neurologically and the slightly higher risk of abnormalities is due to the possible requirement of a shunt.

With grade threes, the outcome is worse.

There is now up to an 8% mortality and 30 to 50% abnormal neurologic outcome.

When there's a peri ventricular hemorrhagic infarct, the outcome is quite dramatically worse.

There is up to 60% mortality.

Almost all these infants will have a major motor deficit and over 60% will have decreased cognitive function.

Why is this outcome so poor?

Well, with hydrocephalus, um, you may get some injury due to the ventricular dilatation or if they're dependent on a shunt you may get shunt related complications from infections, obstruction, seizures, but in addition there is hypoxic ischemic injury to the white matter with gliosis and axonal swelling and this is what results in your spastic hemiparesis and cognitive deficits.

Periventricular White Matter Injury (PVL)

Now question to be raised is which of the following is the current leading cause of neurologic cognitive deficits in preterm infants?

And in the past people would've said int ventricular hemorrhage, but nowadays it's actually diffuse non-cystic white matter injury.

So white matter injury previously called per ventricular leala had a quite a high prevalence up to 25%.

Nowadays the report is as low as 7%.

Yet we have noticed that premature infants that survive particularly very low birth weight preterms have an increased incidence of cerebral palsy.

The question then is raised, are we truly accurate accurately identifying white matter injury?

By ultrasound,

We know there's a changing understanding of perinatal white matter injury.

We no longer think this is purely from ischemia or hypoxia and there may be maternal and fetal factors as well even before the baby is born.

We know that ischemic pre oligodendrocytes are quite susceptible to reactive oxygen species, glutamine, cytokines, and adenosine.

As these glial cells differentiate to ostracizing oligo glia, there is active myelination occurring.

There is a lot of metabolic activity with high oxygen demands and these are quite vulnerable to hypoxia and that's why in premature infants the peri ventricular white matter is the most vulnerable to injury by ultrasound.

We may not recognize these areas of injury well because they're deep in the white matter and they tend to be symmetric and isotropic effects of the peri ventricular halo can um, mimic an injury.

So we can have both false positive and false negative readings.

An area that may look genic may actually be normal or an area that we think is normal may actually be true white matter injury.

In addition, the timing of the exam is also critical because initially you may have some subtle areas of increased ethnicity, but within a few days that ethnicity may resolve and the ultrasound may look completely normal and only after 10 to 14 days may cystic encephalomalacia develop.

So if you do the ultrasounds too early or too late, you may miss some of these findings

So acutely you might see patchy areas of increased ethnicity.

But in the subacute stage you may actually have a fairly normal looking ultrasound and in only some of these patients does cystic cavitation occur.

So initially you might see these patchy areas of increased ethnicity.

If this is not well seen, it's important to do fall exams two to three weeks after the initial event to see whether cystic cephalic omas occurs.

So thus it's quite important to use the highest frequency transducers possible to be aware that indeed these are true white matter areas of necrosis.

And on follow up you may end up seeing these areas of cystic encephalomalacia.

Here we have an infant with focal areas of increased ethnicity.

On higher resolution you can see that in fact these are scattered with multiple areas of peri ventricular leukomalacia.

Here again, with a curved, it's hard to see whether there's cystic encephalomalacia in these areas of increased ethnicity, but the linear transducer, this confirms the fact that indeed these are areas of white matter necrosis that have broken down.

With our improved resolution, higher resolution transducers, we can actually see smaller infarcts that have been confirmed by MRI.

Here we can see focal areas of infarction in the caudate secondary to infarctions of the A CA.

Here we see increased acidity in the thalamus and basal ganglio, which are secondary to infarctions of the lulu dry eight vessels.

Hypoxic Ischemic Encephalopathy (HIE) in Term Infants

It's important to remember in term infants with asphyxia the injuries are not in the periventricular white matter.

They're more vulnerable in the cortex and in the thalamus.

So here we have to look very carefully for areas of increased ethnicity, loss of architecture and asymmetry.

Here in this term infant, you look carefully for border zone cortical regions of increased ethnicity.

Many infants in the newborn period have sl like ventricles and look somewhat echogenic being delivered vaginally or by C-section.

Looking at the thalami for increased ethnicity may suggest that this is an infant who has significant hypoxic ischemic encephalopathy.

On follow-up one sees that the patchy areas of increased ethnicity are indeed real and this child did have severe hypoxic ischemic encephalopathy.

Another way to help prove that a term infant has been sophisticated is to use doppler.

Typically after asphyxia you lose cerebral autoregulation.

You get vasso dilatation with increase in flow. In diastole.

This low resistive index is typically seen in the first 48 hours of asphyxia and this strongly correlates with poor neurologic outcome.

So here we have a term infant looks somewhat genic.

Is this truly an asphyxiated infant?

When we use doppler, this is via the anterior cerebral artery.

The risk index is quite low measuring 0.5 and on follow-up, the hypoxic ischemic injury was confirmed.

Here's another term, infant. Is this normal or is it emus?

With doppler, we can see the risk index was quite low, less than 0.5.

And on follow-up MRI, we see not only injury to the thalami basal ganglia, but to the cortex as well.

Non-Hemorrhagic Infarctions

We can also use doppler to look for non hemorrhagic infarctions.

These are fairly rare and typically found in term infants.

They may present with seizures.

The etiology of these focal infarcts is not clear at times.

Emboli heart disease. Meningitis have come into play.

Here we have an infant who had suggestion of increased ethnicity in the right hemisphere.

There was decreased uh, resistive indices with increased diastolic flow on the right and it was confirmed by CT that this was a right MCA in fart.

Here's another infant.

There's an appearance of slight increased ethnicity in the left hemisphere.

Normal flow was seen in the right MCA and no flow was seen in the left MCA And by CMCA infarct was confirmed.

Posterior Fossa and Cerebellar Injuries

Now here we have a premature infant via the angio fontanel.

We see a focal area of peri ventricular hemorrhagic infarct.

So you might think that our job is done.

Notice that the cerebellum looks quite normal here.

However, on the mastoid view we identify a focal cerebellar hemorrhagic infarct as well.

It turns out that cerebellar hemorrhagic infarcts are do occur both in extreme low weight preterm infants as well as term infants, particularly those on ecmo.

There is a quite high incidence of cerebellar hemorrhagic infarcts in the extreme low birth weight preterm infants.

And their outcome is significantly affected by this finding.

Thus, because the posterior fossa hemorrhages are under recognized, it becomes quite useful to perform mastoid views routinely to look for posterior fossa lesions.

So here we have an infant.

The cerebellum looks relatively normal here we're losing the fourth ventricle and brainstem, but on the mastoid view we clearly see a focal area of hypo um, genicity.

And on ct, this was confirmed to be a posterior fossa hemorrhage.

Here's another infant where you have a heterogeneous posterior fossa.

There's actually areas of low as well as increased genicity and on ct again confirmation of the posterior fossa bleed.

One last case again on coronal imaging via the angio fontanel, the posterior FOSS abnormal.

Yet on the mastoid view we see an area of heterogeneity within the cerebellum confirmed by CT with bilateral infarcts of both cerebellar hemispheres.

Conclusion

So in conclusion, neuro synology is an integral part of the care of the neonate.

There are numerous hypoxic injuries that can be seen and these do vary with gestational age.

Ultrasound is extremely helpful in the assessment of hemorrhages within the germal matrix and in the ventricle.

It is less sensitive for the identification of white matter necrosis in FARCs and the posterior fossa.

However, with the use of high resolution transducers, supplemental views and doppler, these more subtle anomalies can be identified.

Thank you.