Sonography of the Infant Brain-Hypoxic/Ischemic Disease - SD

Periventricular Leukomalacia (PVL)

This is hypoxic ischemic disease in the premature infant.

We see an incidence of approximately four to 15% of PVL in low birth weight infants. These are infants who weigh less than 1000 grams.

There is an association of PVL with maternal chorioamnioitis. This is a condition that results in infarction and necrosis of the periventricular white matter. Typically the frontal cerebral white matter near the forter of Monroe, as well as at the level of the optic radiations adjacent to the trigones of the lateral ventricles.

It's thought to be related to the fact that the vasculature in the per ventricular regions is immature and is actually a watershed area. The junctional zone of the end arteries lacks collateral circulation in combination with a lack of cerebral vascular autoregulation in premature babies. They are at very high risk for having hemorrhage as well as necrosis.

Typical Findings of PVL

Typical findings of PVL include during the first 10 days, generally bilaterally, symmetric course globulin broadbands of bright echogenicity in the per ventricular white matter. We may see these changes in up to about 28% of patients who actually have PVL so that the sensitivity of ultrasound in the first 10 days is not high.

Babies with PVL are generally attached to life support systems and therefore are not able to be safely taken to MRI for evaluation of the brain, even though this is a more sensitive examination.

To identify the findings of periventricular leukomalacia within the first 10 days of life with PVL, there's white matter gliosis, there's hemorrhage and there is edema in the brain, particularly in the deep white matter.

Typical ultrasound findings when we can see them consist of very bright coarse increased echogenicity in the deep white matter paralleling the lateral walls of the lateral ventricles.

Here we see the choroid plexus in the right ventricular atrium, and here we see the choroid plexus in the left lateral ventricular atrium. Bright coarse echogenicity, suspicious for hemorrhagic necrosis.

Right para sagittal view shows that there is a bright area of increased echogenicity in the deep white matter in the region where we normally would see the fine lines of the expected periventricular blush. Remember that the choroid plexus is the brightest echogenicity within the brain. And when the deep white matter echogenicity is similar to the choroid plexus or brighter than that, one has to be concerned about hemorrhage.

Findings 2-3 Weeks After Insult

If we scan the brain within two to three weeks after the initial insult, what we'll see in the deep white matter are multiple small cysts due to necrosis and cavitation.

This is a mid posterior coronal view where picking up the choroid plexus within the atrium of the left lateral ventricle, there's a little bit of rotation of the baby's head, and so we're only picking up a small part of the gloss of the right lateral ventricle. But notice that there's still bright echogenicity in the deep white matter with little tiny cysts scattered throughout.

And this is the parietal occipital region in a very far posterior coronal view, showing the bright echogenicity with the superimposed tiny areas of cystic necrosis and cavitation.

Right para sagittal view shows the extent frontal parietal occipital, and we see a similar phenomenon in the left side of the brain. So this is very typical of what happens within the two to three week period after the insult.

Later Findings (1-3 Months and Beyond)

If we wait a little bit longer, somewhere between one and three months, we'll see that the cysts become larger. We may see multiple cysts or the tissue between the cysts may disintegrate, and so it will look like there are single cysts. These cysts range in size from millimeters to about two centimeters.

Over time, these small cysts may collapse and disappear and white malio scars can develop. Thus, it's important to image these babies at the two to three week interval after birth because if we have a baby in which we can't see the changes within the first two weeks of life, if we miss our opportunity to see the cystic degeneration and we wait so long that the cysts may collapse and disappear, we may never know that there were structural changes to the brain.

There may also be decrease in the cerebral myelin. The ventricles can get larger, particularly in the region of the trigone and the occipital horns. As the brain undergoes atrophy, some of the largest cysts may resolve or they can develop into non communicating porn cephalic cysts.

And here's the same baby a couple of months later in which we see that there are multiple coalesced large cystic spaces in the deep white matter that are totally separate from these prominent right and left lateral ventricles. This is the cavem septum lucidum note that there is still maintenance of the concavity of the lateral walls of the lateral ventricles, implying that this is atrophy and not increased intraventricular pressure.

Here's the para sagittal view of one of the cerebral hemispheres. The opposite side looked identical. We see that there are multiple cystic spaces in the deep white matter consistent with periventricular leukomalacia.

Neurodevelopmental Outcomes

PVL is associated with major neurodevelopmental handicaps. The babies can have developmental delay. They may develop symmetric spastic diplegia, the lower extremities more so than the upper extremities. The necrosis basically involves the descending fibers from the motor cortex, which run in the per ventricular frontal white matter. And so these babies can become quite spastic.

If they have very severe lesions, they may have spastic quadriparesis. And the sooner these babies get enrolled in physical therapy programs, the better chance they will have to reduce the spasticity.

They may also have severe visual impairment and cortical blindness intellectual deficits are less common. So this is basically the insult that leads to cerebral palsy.

Hypoxic Ischemic Encephalopathy in Full-Term Infants

Now, full term babies have a different pattern of insult when they are exposed to hypoxia or ischemia. That results in encephalopathy during the 36th to 40th week of gestation.

The watershed area of the brain moves towards the cortex by 44 weeks. The watershed is between the end fields of the anterior, the middle, and posterior cerebral arteries and is completely peripheral. And so hypoxic ischemic encephalopathy in full term infants is more likely to involve the cortex and the subcortical regions of the white matter.

There are some findings that we can look for on ultrasound. Initially, the findings are indicative of changes that could suggest cerebral edema. Remember too that patients who have encephalitis can have similar findings, but again, the gestational age, the clinical presentation and lab analysis of cerebral spinal fluid can help differentiate edema can result from encephalitis as well.

So typically what we're going to see initially are slit like ventricles where the lumen of the lateral ventricle is extremely difficult to discern. There will be obliteration of the extra axial fluid spaces, ssci and interhemispheric fissure. There will be increased cerebral echogenicity diffusely or perhaps more superimposed focal areas of increased echogenicity. And it can be seen in the subcortical areas, the periventricular white matter, the phite, and the basal ganglia.

Examples of Cerebral Edema Findings

Here's an example of cerebral edema, and I can remember the first time I saw this on ultrasound where the technologist called and said, I just can't seem to demonstrate the architecture of the brain and the normal anatomy. And they started playing with the dials of the machine to see whether or not they could clarify the image. Well, in fact, with cerebral edema, we lose the usual architectural markings.

Notice that there is increased echogenicity. There's a little bit of patchy superimposed, increased echogenicity. We don't see the interhemispheric fissure. Well, we can't really see the lateral ventricles well because of the fact that there is edema and compression of the ventricles.

This is a mid posterior coronal view, and I think you can recognize the compressed gloma of the choroid plexuses as they wrap around the atria of the lateral ventricles. But overall hazy increased echogenicity with some areas appearing somewhat more patchy.

Here's the midline view. Difficult to see the detail completely of the corpus callosum, but we can surmise that this is the corpus callosum, partial obliteration of multiple ssci. We can't really see the third and fourth ventricles. Well, here's the region of the cerebellum, and this is a very far sagittal lateral view of the insula with marked decrease in the visualization of the cerebral sulci.

And here's the para sagittal view showing the region of the lateral ventricle demonstrating that we can't see the lumen of the lateral ventricle because of the pressure of the cerebral edema causing the walls of the ventricles to be immediately contiguous with each other throughout the ventricle. This is the gloss of the choroid plexus, and there's also some obliteration of the fine lines in the periventricular blush.

Later Changes in Full-Term HIE

What happens later on is that the brain can undergo atrophy, which will be manifested by increase in the size of the ventricles and increase in the size of the extra axial fluid spaces, including the fluid around the soci and between the brain. In the region of the interhemispheric fissure, multicystic encephalomalacia can develop secondary to necrosis, and this is a baby who had had cerebral edema.

In follow-up, we see the enlargement of the lateral ventricles. Notice the maintenance of the concavity of the lateral walls, which is consistent with atrophy rather than increased intraventricular pressure. Notice the widening of the extra axial fluid spaces.

Here's the para sagittal view showing the dilatation of the lateral ventricle, as well as the increase in the extra axial fluid space consistent with atrophy that developed secondary to hypoxic ischemic disease.

Another baby, in addition to having increase in the extra axial fluid space over time and dilatation of both right and left lateral ventricles had small areas of cystic degeneration scattered throughout the cerebral hemispheres. So this is a rather extensive hypoxic ischemic insult that involved the cerebral hemispheres bilaterally.

Cerebral Cortical Infarction

Cerebral cortical infarction is uncommon in neonates in young infants. Predisposing factors include prematurity, asphyxia, congenital heart disease, polycythemia, which can result in hyperviscosity and decreased arterial perfusion, trauma, meningitis and thromboembolism.

Most often it is in a distribution of the middle cerebral artery and initially we'll see during the acute phase an absence of gyral definition, an absence of vascular pulsations, altered parenchymal echogenicity, a territorial type of distribution, possible midline shift and ventricular compression.

After there is some resolution, one may see return of the pulsations of the brain gradually and the development of cystic spaces. It's quite common for infants who have had a cerebral cortical infarction to develop seizures and hemiplegia following a stroke.

Example of Cerebral Cortical Infarction

Here's an example of a baby who was born with thrombocytopenia and petee. It was noted during intrauterine life and then on this postnatal sonogram that there is severe dilatation of the right lateral ventricle. There are areas of bright echogenicity within the frontal horn in the body, in the occipital horn within this ventricle consistent with hemorrhage and the very far para sagittal view shows that there is a large area of bright echogenicity with hypoechoic appearance somewhat more centrally implying ischemic tissue breakdown and developing poor cephalic.

Here's a coronal view that is set side by side with the CT scan showing the dilatation of the right lateral ventricle, mild dilatation of the left la I'm gonna fix that, showing the moderate to severe dilatation of the right lateral ventricle, mild to moderate dilatation of the left lateral ventricle, and the tissue breakdown in the cerebral hemisphere adjacent to the ventricle.

Summary

So in summary, we've discussed insults to the infant brain that consists of hemorrhage and hypoxic ischemic disease. Thank you very much.