0:00

Well, thanks for having me.

0:02

I'm excited to be here and hopefully everyone can see my images.

0:07

We're gonna talk today about prematurity and unlike other topics, um,

0:13

where we focus on a disease process or an organ system,

0:16

we're gonna talk about prematurity as its own set of challenges

0:21

and vulnerabilities, not withstanding, uh,

0:25

associated disease processes, but every single premature infant that's born, um,

0:30

faces certain challenges. And, uh,

0:33

imaging is pretty important in first period of life.

0:36

And so what I want to do is review the types of things that anyone

0:41

who's reading imaging, um, at a hospital where there are deliveries,

0:44

where there's a neonatal intensive care unit. Um,

0:47

these are the types of bread and butter things that anybody would see. And, um,

0:51

the first thing that we have to remember is just how small these patients are.

0:56

If you look at this image over here, uh, this radiographic image, you can see,

1:02

um, a syringe and, uh, a syringe that's, you know,

1:06

the size of my hand.

1:08

And you can see it right here next to this chest and abdomen,

1:12

radiographic of this premature baby. So these are quite small organs,

1:17

these are quite small patients, and, uh,

1:20

everything requires a little bit more care and attention because of that.

1:26

So, uh, when we're talking about such a large topic,

1:31

the whole body of, you know, a, a human being at the earliest part of life,

1:36

there's really an infinite number of things we could review. And since time is,

1:40

is, uh, limited to one hour today,

1:42

I wanna try to focus in on the chest and the abdomen and the brain.

1:46

Those are three areas that frequently receive imaging in every premature

1:50

newborn. And, uh, in particular,

1:53

I want to talk about effects to the lungs because of prematurity,

1:57

but also because of the way we treat prematurity, uh, with, uh,

2:01

the big category of barrow trauma. And then I also want to talk about infection,

2:06

um, because bowel infection is a big problem in, uh,

2:11

newborns who have an immature mucosa and who are much more susceptible to

2:16

bacterial overgrowth and its complications. And, uh,

2:20

we'll also talk a little bit about the effects of premature infants, uh,

2:24

with bowel obstruction. Uh, but finally we'll review some of the findings, um,

2:29

in sonographic imaging of the premature brain.

2:32

These patients are often so unstable, they can't go down to the scanner to get,

2:36

uh, an MRI or even a CT less commonly. Uh,

2:41

but at the bedside we can always do head ultrasound.

2:43

So we end up doing a lot of imaging at the bedside for prematurity, uh,

2:48

just because of the instability of these patients.

2:50

So what parts of the body are adversely affected by being born too early?

2:55

And really this is anything definitions change.

2:58

Uh, most people would say term is 39 weeks. Now,

3:01

although in the past it's been less than that,

3:03

and I think prematurity is anything earlier than 37 weeks according to the

3:08

latest neonatology definitions. So what's, uh, what's gonna be, uh,

3:12

at risk and what's gonna be safe? Well,

3:14

it turns out that the liver is one of the first organs we can visualize in fetal

3:18

imaging, and it functions pretty well in premature infants. Um,

3:22

there's not a whole lot of prematurity associated liver disease that we see on a

3:27

routine basis.

3:27

Same thing with the gallbladder and the spleen and the kidneys really make urine

3:31

pretty well. In fact,

3:32

the kidneys have been making urine since the sixth week of gestation.

3:36

That's about the time most people find out they're pregnant. Uh, the only thing,

3:40

the only caveat is that in the first two weeks of life, uh, newborns,

3:44

whether premature or term,

3:46

are often chronically dehydrated for one to two weeks.

3:50

And so imaging of the kidneys can be a deceptive because if

3:55

you're dehydrated,

3:55

then any kind of renal disease you might have won't be visualized, um,

4:00

until you start having sort of normal fluid volumes.

4:04

So what's not okay in a premature infant? Well,

4:07

it turns out that the lungs are frequently, uh, problematic.

4:12

They're hypoplastic, they're immature. And there's also, um,

4:17

difficulties with pulmonary vasculature and, but also the gut mucosa.

4:20

The small bowel mucosa is immature. It's not properly developed.

4:25

It can't handle bacteria and the same way mature gut mucosa can,

4:29

and it's susceptible to super infection.

4:31

And then the brain itself is not finished growing and developing even in its

4:37

external form. But certainly with things like myelination,

4:41

with things like involution of what are supposed to be embryonic structures like

4:45

the germinal matrix and, uh, you know, there's,

4:48

there's a greater risk for injury to all of these things.

4:52

Some of the stuff that's part of risk for every neonate that we don't really

4:57

spend as much time imaging in radiology would be retinopathy. Uh, you know,

5:01

there's a breakdown in the normal protective barrier of the skin because it

5:05

hasn't properly matured. And, uh, I'm not gonna spend any time today. But,

5:09

you know,

5:10

we could focus on the topic of functional immaturity of the colon as well.

5:14

So these are the things that every pediatric imager or every radiologist who

5:19

sees newborn imaging should be thinking about.

5:21

And I want to go ahead and start off by talking about the lungs.

5:24

What exactly do we need to worry about with the lungs? Well,

5:28

it turns out that we need to worry about whether pregnancy, uh,

5:32

was going according to plan and it going according to the way it ought to go.

5:37

And the first thing is, was there sufficient amniotic fluid? It,

5:40

it turns out that the lungs are heavily dependent on the influx and

5:45

outflow of amniotic fluid throughout gestation.

5:49

It's not just a matter of practicing the respiratory motions of intercostal

5:54

muscles and diaphragms, but the fluid itself is nourishing.

5:57

And there's a sort of, um,

6:00

synergistic relationship between the mucosa, uh, and the,

6:04

the pneumatic cytes that are developing secretions and also the amniotic fluid.

6:09

And there's cell signaling that goes on, um,

6:12

when that fluid is able to nourish the lungs. Uh, if you have, you know,

6:16

oligohydramnios or anhy amnios, the lungs aren't gonna develop properly.

6:21

So lungs can be small because of space

6:26

considerations.

6:26

And this is in fetal MRI image showing narrow almost column or

6:31

hypoplastic lungs, which are too small and haven't, uh,

6:35

been given the opportunity to develop because this is a fetus with a large em

6:39

falle.

6:39

And the body cavity never had to expand because all the organs are outside.

6:43

So sometimes the lungs don't develop because of size considerations.

6:46

Sometimes they don't develop because of insufficient amniotic fluid

6:50

considerations, and sometimes they don't develop because of mass effect.

6:53

If you think of a diaphragmatic hernia case. Uh,

6:56

the other thing is it takes time. There's just a normal process of development,

7:01

and if a, you know, a delivery occurs too soon,

7:05

then some of the cellular makeup of the lungs isn't present yet.

7:08

Those type two pneumocytes aren't functional.

7:10

And we all know about surfactant deficiency. And, uh,

7:14

that's a big challenge for the newborn, uh, intensive care unit.

7:19

They're trying to basically create gas exchange in a set of

7:23

lungs that don't have all of the necessary cells. Uh, and finally,

7:27

there's pulmonary hypertension, which is a normal process in utero.

7:31

We don't want a bunch of blood going into the fetal lungs because it would be a

7:35

waste,

7:36

but we need those lungs to be able to be nourished as soon as delivery,

7:40

as soon as that umbilical cord is cut.

7:43

And if there hasn't been proper maturity of the lungs and the alveoli,

7:48

then there's no cell signaling to tell the pulmonary arterials and, you know,

7:53

the tiniest areas of the pulmonary arteries to dilate sufficiently to

7:58

allow perfusion, uh, to match the ventilation.

8:01

So these are the things we need to worry about,

8:03

and we can see problems when there's not enough fluid going into the lungs like

8:07

this image. We can also see problems when there's fluid trapped in the lungs.

8:11

You can see how these lungs are in this fetal MRI are hyper expanded.

8:15

They're enlarged. Look at how the diaphragms are inverted. This is a case, uh,

8:20

of congenital high airway obstruction syndrome or sometimes called chaos

8:25

syndrome. And you can see all this fluid dilating the trachea and the bronchi.

8:30

Uh, this is fluid trapped in the lungs. This is not enough fluid in the lungs,

8:35

and here is the happy median. This is what we wanna see,

8:38

normal looking fetal lungs,

8:40

and this is what the lungs are gonna be like when they're delivered, right?

8:43

Because prematurity is basically a fetus having to fend for itself

8:48

outside. Uh, and this is what it looks like in a newborn.

8:51

We've all seen newborn chest x-rays, and we're familiar with, uh,

8:55

the various patterns of disease.

8:57

And a lot of the terms that get thrown around are a little bit imprecise because

9:01

we're not talking about discreet structures.

9:03

People use terms like hazy opacities or cloudy

9:07

opacities or, you know, vague, uh, you know,

9:12

mild opacities in the lungs. And they tend to be diffuse.

9:15

They tend to be symmetric.

9:17

And this is a sign of the earliest stages of premature lung disease.

9:22

We've had a lot of names for this.

9:23

We've called it surfactant deficiency disease and various other things.

9:27

But basically it's the effects of prematurity.

9:30

And I like the term premature lung disease because it's big enough to encompass

9:33

problems intrinsic to the lungs themselves,

9:37

not proper cells problems secondary to our treatment of this barrow trauma.

9:42

And also problems due to scarring and atelectasis that develop.

9:46

So I like to use the phrase premature lung disease.

9:48

It starts out indistinct soft and hazy like this,

9:53

and then it becomes gradually coarser and more discreet.

9:57

Now we're starting to see interspersed aerated lung with

10:02

atelectasis and coarse interstitial opacities throughout the lungs.

10:06

And these are both alveolar and interstitial, um, appearance of the opacities.

10:11

And finally,

10:12

as it organizes even more fully and ventilatory support is able to get rid of

10:17

some of that ectasis, uh,

10:19

we can see even more lucency interspersed with the scattered opacities.

10:23

So just to see all of those together,

10:26

you can see how in the earliest stages of a premature newborn's life,

10:30

there's a mild diffuse haziness,

10:32

which gradually becomes coarser and more discreet in its opacities.

10:36

This is the normal process of just the radiographic appearance of

10:41

premature lung disease. This isn't, um,

10:44

necessarily something that's been done right or done wrong.

10:47

This is just what happens for every newborn that's born too soon. And, uh,

10:52

this one I think was born at 27 weeks.

10:55

So then there's the question of what's gonna happen long term and just

11:00

by convention, I'm not sure that there's any, um, you know,

11:04

rule that's absolute. But most neonatologists start thinking of lung disease,

11:09

of prematurity as a chronic process after 30 days. So,

11:12

so arbitrary line that we draw, and this is a,

11:15

a neonate born at 26 weeks now at about 45 days of life.

11:19

And you can see how the lungs have organized even more.

11:23

There's patchy areas where just overlying the thymus here,

11:26

there's some more focal ectasis. There's definitely some scarring going on here.

11:31

This is a neonate that's been on a ventilator. Here's the endotracheal tube, uh,

11:35

for, for, you know, a month and a half.

11:37

And so there are areas of damage to the lungs and uh,

11:41

we can also see that there's more asymmetric aeration.

11:45

So there are areas like this lateral left lung base,

11:48

which are better aerated than maybe the upper lobe,

11:51

and it tends to be much less diffuse and symmetric, like the earliest stages,

11:56

um,

11:57

as the lungs start to become irregular due to both damage and the fact that

12:02

there's a continual battle between the ventilator,

12:04

which is using high pressure air,

12:07

maybe even it's a jet ventilator for our sickest babies,

12:10

and it's shooting in bursts of air,

12:12

but then the lungs don't have surface tension, the alveoli.

12:16

And so they want to collapse,

12:17

and there's this battle of enough pressure to pop those alveoli open,

12:21

but not so much pressure, you know, that we cause a pneumothorax.

12:25

And that is something that happens quite a bit.

12:28

It's not a question of will premature infants who are intubated have

12:32

barrow trauma?

12:33

It's just a question of how much every child with premature lung disease has

12:37

barrow trauma. And it can present in various ways.

12:40

So here's a patient earlier in the process, um,

12:44

hasn't even been intubated yet,

12:46

and then we can start to see after the patient has been intubated and then

12:51

extubated this development of these tiny lucencies in the

12:56

right medial portion of the lung,

12:58

and a few of them extending down here into the lateral lung base.

13:01

And this is an area where we're starting to see air dissect into the

13:05

interstitium of the lung. Uh, it's pretty subtle at this point, um,

13:09

but I'm gonna show you some more dramatic examples.

13:11

So here's a more dramatic example where you can see these lucencies have

13:15

expanded and developed even further.

13:17

And now there's air outside the lung in the left hemothorax, uh, uh,

13:21

this is kind of a classic neonatal pneumothorax.

13:24

There's also air outside of the mediastinal structures,

13:28

but within the mediastinum. So there's pneumo, mediastinum, pneumothorax,

13:32

and all this interstitial air, which we call pulmonary interstitial emphysema.

13:38

Uh, chest tube's been placed, we can get rid of, uh, the pleural air,

13:42

but sometimes it can be very hard to treat this. And over time,

13:46

these patients can develop pneumatic seals or trapped ated

13:50

pockets of air because the lungs are being damaged,

13:53

and it creates these negative spaces in the thorax where air can accumulate.

13:58

Uh, here's another example of the same type of thing,

14:01

barotrauma with air in the mediastinum.

14:04

You can see it outlining the thymus here.

14:06

You can see it over here to the left of the superior mediastinum.

14:10

And maybe just a hint of it down around the heart on this image,

14:13

instead of air tracking up to the apex of the lung,

14:17

like you saw on this PMO mediastinum case,

14:20

this air is outlining the heart and it's following the contours of the

14:25

pericardium. So this is pneumo pericardium,

14:28

yet another manifestation of barrow trauma. So why is this keep happening?

14:33

Well, what we're dealing with are very delicate friable structures.

14:37

The premature lungs are susceptible to injury.

14:40

They're not fully supported by the architecture,

14:43

the scaffolding of the interstitium. It's not ready for prime time yet,

14:48

but it's trapped. And, uh, it has to do a job that it wasn't quite ready to do.

14:53

So if you can imagine these tissue paper decorations that are sometimes hung at

14:57

birthday parties, they're delicate structures.

15:00

They have an architecture to them.

15:02

And imagine then that you took compressed air from a, you know,

15:06

from a gas powered or an electric powered air compressor,

15:09

and you started shooting jets of air at these things rapidly,

15:13

and maybe you started shooting higher and higher volumes of air,

15:17

eventually that tissue paper is gonna start to tear in certain places,

15:22

and it's gonna start to deform the architecture and shape of whatever it was

15:27

supposed to be. And in the neonatal course it's a lung. And over time,

15:31

you're gonna go from this highly organized,

15:33

uniform ordered structure of these undamaged lungs,

15:36

even though they're premature into something more like this that's irregular and

15:41

amorphous and has larger spaces and smaller spaces,

15:44

and the lines aren't as crisp and sharp anymore.

15:47

And it's because we're fighting this battle. If we don't give enough air,

15:51

then ectasis takes over in respiratory failure,

15:54

there's not enough oxygen. And these,

15:57

these are the neonates that end up needing to go on ecmo. Uh,

16:00

if we give too much air, then we risk damaging the lungs,

16:03

and that also can make them non-functional. So it's a,

16:07

it's a very delicate balance. And you know,

16:10

for those of us who read morning portable chest X-rays on newborns,

16:14

on premature newborns,

16:15

you can see that waxing and waning of atelectasis and then barotrauma,

16:19

and then atelectasis and then barotrauma.

16:21

And it's because the neonatologists are adjusting the vent settings. Um,

16:25

both the peep we talk about positive expiratory pressure,

16:29

that's the kind of the force of the jet of air going in.

16:32

But increasing research has shown that the tidal volume,

16:36

the actual size of the blast of air going in may be even more

16:40

important in determining barotrauma.

16:43

So precise regulation of the tidal volume may be even, uh,

16:48

more necessary to keep those lungs as safe as possible.

16:52

So just a few more images showing the effects of ventilatory support for

16:56

premature lung disease and the ways in which it can damage, uh, the lungs.

17:00

So here's a large pneumothorax. Um,

17:03

here's a small pneumothorax with just a subtle, uh, lucency underneath the lung.

17:08

And then here's a patient with more of that interstitial emphysema.

17:11

You can see that the air hasn't dissected, uh,

17:14

between the lung and the body wall,

17:16

but instead it's dissected into the architectural spaces of the lung,

17:20

the interstitial.

17:22

And here's a super dramatic example of pulmonary interstitial emphysema where

17:26

there's so much air dissected into those spaces, it's causing midline shift,

17:32

not because the air spaces of the lung are expanded.

17:35

We would call that a hyperventilated lung or a hyper expanded lung or an,

17:40

you know, almost like an overinflation in this case. The lung isn't inflated,

17:44

the interstitium is inflated, and that's much harder, uh, to repair.

17:49

It's not as simple as sticking in a chest tube.

17:54

So let's shift gears a little bit and talk about one iatrogenic cause of

17:59

difficulties in premature newborns. And that is umbilical catheters.

18:03

We use umbilical catheters because it's such a great access for infusion of

18:07

fluids and medications for drawing off blood, for monitoring pressures. Uh,

18:12

and you see 'em in almost all premature newborns who are gonna spend time in the

18:16

neonatal ICU.

18:18

This is actually a fetal MRI showing a mid sagittal view.

18:22

You can see the spine nicely laid out here. And this just a really, uh,

18:27

beautiful example of the inflow of blood.

18:30

So here of course is the umbilical cord at the anterior body wall.

18:34

And here you can see blood going in through the umbilical vein and coursing up

18:39

the umbilical vein into this dilated portion just as it enters the liver.

18:44

And we call that the umbilical recess. And it continues to travel.

18:48

At this point, the umbilical vein is joined to the portal venous system,

18:53

but it needs to get past the liver because this is oxygenated blood.

18:58

Bear in mind that with umbilical vessels,

19:00

it's the opposite of what we've learned.

19:02

The vein is what's carrying the oxygen and the arteries are what need to go back

19:07

to the mom to be filtered by the maternal lungs via the

19:12

placenta. So it's this vein that carries the oxygen.

19:15

We don't want it to waste time going through the liver.

19:17

We want it to get straight to the heart. So we have this embryonic vessel,

19:20

the ductus osis,

19:21

and here you can see the blood going through the umbilical vein, the recess,

19:26

joining the portal venous system,

19:28

but bypassing that and going through the ductus osis up into the

19:35

inferior caval atrial junction.

19:36

So it joins the confluence of the hepatic veins right here at the int hepatic

19:41

IVC and then straight into the right atrium.

19:44

So that's the path that our catheters are gonna take. And, uh,

19:47

this is an example of a normal placement of an umbilical venous

19:52

catheter.

19:53

We can see it going straight in to the umbilicus through the umbilical

19:58

vein. And at this point right here would be that umbilical recess,

20:02

that more dilated portion before traversing the ductus osis

20:06

and through the intrahepatic IVC to the right atrium at the lower

20:11

caval atrial junction. Now,

20:14

one of the things that can be challenging is getting the catheter to go straight

20:17

up to the heart versus taking turns or detours.

20:20

And so a lot of times if there's a very difficult placement,

20:23

you'll notice that the neonatologist will eventually pull the catheter all the

20:28

way back to this inferior margin of the liver.

20:30

And the reason is that's where the vein is quite dilated.

20:33

That's that umbilical recess.

20:34

So if they do need higher flow rates for blood draws, et cetera,

20:38

it's a better place down there than somewhere in the middle of the umbilical

20:43

vein or somewhere in the middle of the liver.

20:45

So ideally lower caval atrial junction,

20:48

but second best at the inferior margin of the liver at that. Uh,

20:52

at that recess of the, uh, umbilical vein,

20:56

here's an example of a placement of a catheter that didn't go according to plan.

21:00

And uh,

21:00

this is just reminding us that the umbilical vein does join the portal venous

21:05

system.

21:05

So this is a catheter that's turned right and gone into the right portal vein.

21:09

And not only is that a problem because any infusion of medication is gonna,

21:13

you know, get delayed by having to pass through the, the portal triads,

21:17

but also it's very narrow in there. And, uh,

21:20

any attempt to draw blood is going to put the liver at risk. And, uh,

21:25

rapid infusions could also overwhelm the liver, uh,

21:29

and any advancement of the catheter can create injury to the liver,

21:33

even hepatic hemorrhage, uh,

21:35

or hematoma because the catheter is capable of piercing the,

21:40

the hepatic parenchyma out.

21:43

Here's an example of a catheter that's been pulled back and advanced and

21:47

repositioned and it's just coiling up within the portal vein.

21:49

That's not gonna work in the way that we intend.

21:52

We can also see here an example of an umbilical arterial catheter,

21:55

which characteristically has to descend, uh,

22:00

inferiorly along the bladder and join the iliac artery before then

22:04

returning, uh, superiorly into the aorta.

22:08

And the ideal location for the tip of this catheter is somewhere between the

22:12

branch vessels. So that's kind of a wide margin of error. Uh,

22:17

you don't want it up in the aorta, garch,

22:19

there's a lot of branch vessels there and you don't want it down by the celiac

22:23

axis or the superior mesenteric artery anywhere.

22:25

The tip of that catheter could occlude a takeoff of an artery or could

22:30

potentially draw blood away from, uh,

22:33

an organ when the catheter's being used, uh, is gonna be a problem.

22:37

But typically at the level of the diaphragms or slightly above the diaphragms is

22:42

gonna be a safe zone. Uh,

22:43

there's no important branch vessels off the aorta at that level.

22:48

Finally, you can see, um,

22:50

the same patient has had a continued repositioning of their umbilical venous

22:55

catheter, which now is going into the left portal vein. Um,

22:59

the way that the liver is positioned on a frontal chest and abdomen radiograph

23:04

often makes the left portal vein look like it's oriented posteriorly,

23:09

um, instead of just 90 degrees to the left.

23:12

So that's why the catheter looks like it's headed, uh,

23:14

towards the patient's spine. And then finally,

23:17

we can see that the catheter was repositioned and has made it to the lower caval

23:22

atrial junction, which is the ideal location.

23:25

So evaluating the location of these catheters is one of the most important

23:28

things the radiologist needs to recognize and identify on these x-rays,

23:33

uh, because it can cause a lot of morbidity for patients and mist, um,

23:39

malpositioned lines and tubes is the number one reason, uh,

23:42

for medical malpractice complaints. Imaging. So lines and tubes,

23:47

even though it may seem elementary in some cases, is very important.

23:52

It's probably the number one thing the neonatologists are looking to our reports

23:55

to find out. And when we don't give adequate attention,

23:58

it's the number one reason, um, that it can turn into a legal, uh, issue.

24:05

The one caveat I'll say to the normal trajectory of the umbilical venous

24:10

catheter,

24:10

and that tends to be the catheter that that has the hardest time getting to

24:13

where it needs to go, is you've gotta know where the liver is.

24:17

So everything I've just said about where the umbilical catheter should go is

24:21

predisposed on a normal liver being in a normal location.

24:25

But if you have abdominal, you know, uh, citus,

24:29

inversus or as in this radiograph,

24:32

if you have a congenital diaphragmatic hernia with supra diaphragmatic

24:37

positioning of the liver,

24:38

the left hepatic lobe in this case is oriented superiorly,

24:42

then the orientation of your catheter is going to have to change in order for it

24:47

to be appropriate.

24:49

So that red line that I've placed on the image is the outline of the liver and

24:53

knowing that we can now be suspicious of this catheter that it's in the left

24:58

portal vein,

24:59

an accurate positioning of a catheter in the case of diaphragm hernia with a

25:04

malpositioned liver would actually curve up like this.

25:08

So you have to know where the liver is in order to know where the catheter

25:12

should go. It's a rare situation,

25:14

but it does occur and you can see that the same would hold true for this suction

25:19

catheter, which is actually appropriately positioned in the patient's stomach,

25:23

but the patient's stomach is inappropriately up in the chest.

25:29

And this is just a umbilical venogram revealing those vessels that I was just

25:34

describing. So here's the umbilical vein.

25:35

You wouldn't wanna leave an umbilical venous catheter down here.

25:38

Look at the narrow caliber of that. Whereas the recess, the umbilical recess,

25:42

is a much better place for flow rates.

25:45

And then the normal trajectory to get to the heart is through this duct dys

25:49

osis. Here's the confluence of the hepatic veins and the inferior aspect

25:54

of the caval atrial junction.

25:57

So any turns this way would be a portal venous turn or this way would be

26:01

a portal venous turn.

26:02

You could even end up in some of these branch draining veins. Um,

26:07

so what we need to do is be aware of the venous anatomy,

26:10

be aware of the location of the liver, and we can add a lot of value, um,

26:14

on these lines and tubes cases.

26:17

So moving from the vessels of the abdomen into the bowel,

26:22

let's talk a little bit about necrotizing enterocolitis.

26:25

This is the most common abdominal infection in premature

26:30

infants.

26:31

It's also one of the most dangerous conditions for a premature infant because it

26:35

can rapidly progress from bowel infection to systemic

26:40

decompensation, hypotension and even death.

26:44

And the reason is because it can progress from a mild infection to a

26:48

severe almost near total small bowel necrotic

26:54

situation.

26:54

What's happening is the premature gut mucosa is not yet sufficiently

26:59

able to keep bacteria at bay.

27:03

And anything that injures the bowel or the balance of gut mucosa

27:08

is going to make the infant susceptible A newborn at term and a child

27:13

or an adult is much better able to handle fluctuations in gut, uh,

27:18

bacteria because they have mature mucosa and also

27:23

because they have the ability to sustain fluctuations in

27:27

perfusion.

27:29

But any kind of fluctuation of perfusion in a newborn that's premature

27:34

is going to create ever so brief transient ischemia of the bowel.

27:39

And that's the most common type of injury that then makes the bowel susceptible

27:43

to those bacteria. So we all have lots of bacteria in our bowel,

27:47

it's appropriate, it's even necessary, but there's a balance.

27:51

And if there becomes a bacterial overgrowth situation where one unhealthy type

27:56

dominates all the rest,

27:57

the slightest insult to the bowel will let that then become submucosal and

28:02

infecting the bowel.

28:03

And here you can see that it dissects not straight through,

28:07

but along the mucosa of the bowel, creating all of this submucosal pneumatosis,

28:12

it can then progress to the cirr Rosas and create subserosal pneumatosis.

28:17

And uh, the appearance can often be of thickened bowel,

28:21

but the tissues themselves aren't so much thickened as they are full of gas.

28:25

This happens a lot in the youngest patients, the very low birth weight infants,

28:29

nearly 10% of them are gonna encounter this situation.

28:33

And this happens at a very particular time, uh, in life.

28:38

And it happens almost always at 19, or I'm sorry,

28:43

at 29 weeks post menstrual age.

28:45

And the reason I say 29 weeks post menstrual is it's the age

28:50

adjusted age, the the gestational adjusted age,

28:54

the premature adjusted age of 29 weeks.

28:57

That is the most common time to get this. So if you're born at 29 weeks,

29:01

you're at high risk. If you're born at 25 weeks,

29:05

then around four weeks after birth is when you're gonna be at highest risk.

29:10

So once you've made the adjustment for Postmenstrual age, uh,

29:16

that's when you can know when these neonates,

29:19

these premature babies are most likely to get this super infection of their

29:23

bowel. And what happens is the bacteria,

29:27

the dysbiosis, that's the overgrowth syndrome,

29:30

then takes advantage of intestinal injury and dissects through the

29:35

mucosa, which has become even transiently ischemic.

29:39

And once it gets below the mucosa,

29:41

it runs between the muscularis and the mucosa layers and that bacteria

29:46

flourishes in there.

29:48

It creates pockets of air and eventually it creates

29:53

progression of air into the veins draining the bowel,

29:56

which becomes the superior mesenteric vein,

29:58

which go back to the liver of course, and and become the portal vein.

30:02

And we see this on imaging as portal venous gas.

30:05

And I'll show you examples of this. Uh, one question you might be wondering,

30:09

why doesn't this happen in the womb? Why doesn't this happen to a 29 week fetus?

30:14

And the simple answer is that the fetus inside the uterus

30:19

has incredibly protected blood supply.

30:22

Everything about the maternal body protects consistent perfusion

30:27

to the fetus and the placenta almost at all costs.

30:30

So it's only when pregnant women are in a terribly ill maybe near death

30:35

situation that that blood flow gets compromised.

30:38

But if that fetus is born prematurely, it's stressed,

30:42

it's in the neonatal intensive care unit,

30:45

it's subject to fluctuations in body temperature,

30:48

much more than normal fluctuations in respiratory function,

30:51

much more than normal and blood pressure fluctuations.

30:54

And those fluctuations are what make the bowel susceptible, uh,

30:58

to this super infected bacteria.

31:01

So this is what it looks like on radiograph and the most sensitive.

31:06

In other words,

31:06

the first thing we see the most sensitive sign of neck is not very specific,

31:11

it's just fally dilated loops of bowel.

31:14

And here you can see in this, uh,

31:17

this image over here on the left side of your screen,

31:19

you can see a horseshoe shaped loop of bowel. And a couple of hours later,

31:23

that same horseshoe shaped bowel is there again,

31:26

even though other bowel has moved around.

31:29

And it's still there about 36 hours later.

31:32

So the first sign is fally dilated loops of bowel,

31:36

just like you see in this image.

31:38

Oftentimes it's folded over on itself in this horseshoe shape configuration

31:42

that's very sensitive, but of course many different things can look like that,

31:46

including normal bowel. So it's not specific. What's the next step? Well,

31:50

it stays fixed in that location for quite a while, so it's focally dilated,

31:55

then it becomes fixed in a focally dilated appearance.

31:58

And you'll see maybe 1, 2, 3 days in a row this loop of bowel frozen

32:03

in position and appearance. This is suspicious, uh, but still not very specific.

32:09

And uh, then what will happen is the bowel,

32:13

even though we can't see it, has probably already become, uh,

32:17

damaged and is being infected.

32:20

And so we already have necrotizing enterocolitis here,

32:23

even though we haven't seen any of the specific signs,

32:26

the things that everyone always talks about,

32:27

like pneumatosis intestinalis or portal venous gas. Those things are coming,

32:33

the bowel is already necrotizing, we just haven't seen it yet.

32:38

And all of a sudden it can go from this radiograph here,

32:42

which is certainly not normal. It's got some suspicious signs,

32:46

but none of those classic, uh,

32:49

findings that we're looking for within a very short period of time.

32:52

It can rapidly progress to a fluoride case of portal

32:57

venous gas,

32:58

which you can see as these thin lace like linear branching lucencies all over

33:03

the liver. This is quite extensive.

33:05

And fluoride pneumatosis intestinalis,

33:08

which is frequently seen as thin linear lucencies just outside a

33:13

thin opaque line, which represents the mucosa.

33:16

So you're seeing this is intraluminal bowel, this is bowel mucosa.

33:21

And then that lucent line is the submucosal gas.

33:25

So we've got pneumatosis intestines here and we've got it here

33:30

and we've got it here and we've got it here and it's over here.

33:34

Sometimes it's been described.

33:36

Here's some more down here as bubbly lucencies.

33:40

The problem with the bubbly lucencies uh,

33:43

descriptor is that it has a high false positive rate because

33:47

intraluminal foamy contents also look like bubbly lucency. So for example,

33:52

this over here kind of looks like bubbly lucencies, but it's not pneumatosis.

33:56

And this over here kind of looks like bubbly luc disease,

33:59

but that's not pneumatosis.

34:00

So the most compelling evidence for pneumatosis intestinalis is this thin

34:05

submucosal lucency.

34:07

And this patient is very ill and has extensive complications, uh,

34:12

of the breakdown of bowel and ended up having extensive amounts of small bowel

34:16

resected, uh, in order to survive this illness.

34:21

Now what can ultimately happen? Well,

34:22

necrotizing enterocolitis can progress to pneumoperitoneum perforation

34:27

and not just pneumoperitoneum,

34:29

but also infection and abscess formation within the peritoneal

34:34

space. And uh, this is the sign to the surgeons that they need to intervene.

34:39

Many of these infants are quite ill, quite vulnerable.

34:42

They can't go to surgery without a significant additional risk.

34:45

So surgery will be reluctant to take this fragile,

34:50

vulnerable premature infant to the operating room.

34:53

But once we see frank pneumoperitoneum,

34:55

that's usually the sign that something has to be done surgery,

34:59

or if not surgery, at least drain placement, uh, and close surveillance.

35:03

And sometimes it's massive. This is an example of a,

35:07

of a patient with necrotizing enterocolitis who developed such extensive

35:11

pneumoperitoneum.

35:12

It's hard to point out where there's not free intraperitoneal air,

35:17

but often it's more subtle than that.

35:19

And where we add value as radiologists is being able to pick up on the

35:22

subtleties, uh,

35:24

that that sort of describe the earliest signs that something

35:29

has progressed to the complicated phase.

35:32

So here's an image of a patient who had been x-rayed repeatedly looking for

35:37

signs of necrotizing enterocolitis. And you might squint down here and say,

35:41

well, maybe is there a little pneumatosis down there? I don't know.

35:45

There's not really any frank portal venous gas.

35:48

There's this nice lucin stomach over here.

35:51

But for those of you who are looking carefully,

35:53

there's a vague lucency over the midline as well. And remember,

35:56

almost all portable, uh, NICU radiographs are obtained supine.

36:01

So any free air will be non-dependent and will tend to layer out anteriorly

36:06

over the abdomen. It can be difficult to see, but it should raise our suspicion.

36:10

Same thing here.

36:11

This patient is more suspicious because they have definite pneumatosis

36:15

intestinalis and they also, in addition to their gastric lucency,

36:20

have a vague lucency here and a little lucency there and a little

36:25

lucency there.

36:26

So these are the kinds of things that are very suspicious for perforation.

36:30

And uh, what do we wanna do? Well, we want to confirm.

36:34

So the classic thing that we try to do is change positioning and we rely on the

36:39

fact that air moves non independently and we wanna put it up against a solid

36:42

organ like the liver.

36:43

So here's that patient again with this suspicious anterior lucency.

36:47

And when we put them in the decubitus position,

36:49

sure enough it layers between the body wall and the liver.

36:52

And this is confirmed pneumatosis intestine analysis. Uh,

36:56

once you've seen enough of these cases,

36:57

you may not need the decubitus and you might just describe it and uh,

37:01

feel confident saying this is anterior layering intraperitoneal air. Uh,

37:06

but it's never the wrong thing to confirm if there's any

37:10

uncertainty. And so decubitus positioning can be really helpful for that.

37:15

Here's another example.

37:16

This is a patient with a lot of bubbly lucencies.

37:21

It turned out all of, almost all of this was foamy liquid bowel contents,

37:25

but a very distinctive appearance where we can see the

37:30

internal margin and external margin of the bowel wall quite clearly.

37:33

Sometimes this is called riggler sign,

37:36

suspicious for free intraperitoneal air, but we're not seeing the focal lucency.

37:41

And so we tried the decubitus positioning and sure enough there's a quite large

37:45

volume of free intraperitoneal air outlining not just the liver,

37:49

but also the entire right paracolic gutter.

37:52

And this patient needed to go to the operating room.

37:55

Note that on all of these cases,

37:57

the pneumatosis wasn't sufficient to cause portal venous gas.

38:00

So we can go from a relatively mild or vague appearance of

38:05

the complications of neck to needing to be in the or quickly.

38:09

So these patients require careful attention and, and some extra scrutiny.

38:14

But what about the patient who doesn't respond really well to decubitus

38:19

positioning?

38:19

So we'd love it if we see the bubbles and we put them into cubitus and it layers

38:24

between the body wall and the liver. That's great, no problem.

38:27

But sometimes we see a vague lucency over the mid abdomen like you can see

38:32

here, and we wonder, is that free intraperitoneal air?

38:36

The patient has risk factors and we put them into cubitus positioning and

38:41

disappointingly, it doesn't really layer out like we'd expect.

38:45

Does that mean we're done, we were wrong?

38:48

Well it turns out that that sign of air moving

38:52

non-dependent is only reliable in a patient with a clean,

38:57

pristine peritoneal space.

39:00

And I always think of the movement of structures within the peritoneum,

39:04

like the movement of a piece of plastic on a wet countertop.

39:07

It just glides smoothly. All the organs are gliding against each other.

39:13

The bowel and mesentery are gliding against the organs and the lining of the

39:17

body wall with peritoneum is also smooth and gliding.

39:23

But if you have a sick abdomen,

39:25

and remember the reason we're following these patients is because of suspected

39:29

necrotizing and R colitis, you're not gonna have smooth gliding structures.

39:34

The inside of the peritoneal cavity gets very sticky

39:39

and everything is inflamed. Tissues are thickened, they don't glide well.

39:44

It's like that piece of plastic on a dry countertop now it's not moving very

39:49

well. It's stuck together.

39:51

And if you picture a pocket of free intraperitoneal air in the middle of the

39:55

abdomen and you turn that patient to cubitus,

39:57

it's not gonna immediately float up non-dependent. It's gonna take some time.

40:02

That air's gonna have to work its way through a sticky abdomen all the way to

40:05

the non-dependent location.

40:07

So I always say if my suspicion is strong and the initial decubitus

40:11

film doesn't satisfy my suspicion for a for to be extra safe,

40:16

I do a 15 or 20 minute delay. I tell the nicu,

40:20

keep the patient decubitus for 15 minutes and then obtain a

40:24

radiograph.

40:25

And you can see how the immediate decubitus film was not very satisfying,

40:29

but the delayed decubitus shows quite clearly that in fact there is a bowel

40:34

perforation

40:37

if you don't have the luxury of communicating with a team that's gonna help you

40:41

with that. The other option is to use the window level feature,

40:45

which we use much more frequently in cross-sectional imaging,

40:48

but can be quite valuable in radiographs. And all of a sudden, um,

40:52

a pocket of free intraperitoneal air layering anteriorly that is challenging to

40:57

see on this normally windowed image when we window it much more harshly.

41:02

Now you can see the lucency of the free air.

41:04

So that's another tool at our disposal.

41:07

If moving the patient for whatever reason is going to be, uh,

41:11

a difficulty and there's that pocket of air, sure enough,

41:15

this patient went to surgery and had a perforation.

41:18

So just to reiterate,

41:21

in these cases we can see a lot of things fally dilated bowel

41:26

that's fixed over time. We can see free intraperitoneal air,

41:30

we can see all sorts of abnormal findings.

41:33

But the most specific sign, this is not the early sign,

41:37

but the most specific sign of course is pneumatosis intestinalis.

41:41

And that's that thin submucosal linear lucency,

41:45

just like you see outlining this loop of bowel right here.

41:48

That is the most specific thing.

41:50

And essentially there's not much else in a premature newborn that can give you

41:54

that appearance. So we consider it diagnostic of necrotizing enterocolitis.

41:59

And uh,

41:59

sometimes you'll hear clinicians talk about medical neck versus radiographic

42:04

neck.

42:05

And that always seems a little silly to me because there's just necrotizing

42:09

enterocolitis. Either your bowels infected or it isn't.

42:12

What they mean is do they have the specific signs of neck or don't they?

42:16

Either way they have infection and you can call the ICU and they know, oh,

42:21

this patient's sick, their blood pressure has given us trouble,

42:24

they have body wall edema, they have neck,

42:26

we're just waiting to see the signs on x-ray. And this is, uh,

42:30

this is essentially what we're adding to that diagnosis.

42:35

What about patients who have abdominal challenges without necrotizing

42:39

enterocolitis? Because not every, uh,

42:42

premature neonate develops it only about 10%.

42:46

And it turns out that one of our best clues of a problem in the abdomen

42:51

other than massively dilated bowel is calcification because calcification is a

42:56

sign of old healed peritoneal inflammation. So this, again,

43:00

this is not smooth gliding peritoneum.

43:02

This is something that got inflamed and thickened and sticky and then it

43:07

healed. And as it scarred down, it calcified.

43:10

So anytime you see calcifications in the peritoneal space outlining the body

43:15

wall or outlining an organ or creating a little pseudo cyst,

43:21

uh, and lining mat, that's a sign that there was an inflammatory process.

43:25

Sometimes we jump right to the diagnosis of meconium peritonitis and

43:30

it turns out that the presence of meconium in the peritoneal space from a

43:35

perforated loop of bowel is a very common cause of calcification.

43:39

But there are other ways to inflame the peritoneum. So no matter what,

43:43

it was the calcifications point to prior inflammation.

43:47

And we can see the natural progression of this if we compare fetal and neonatal

43:51

imaging. So for example,

43:53

this is a fetal MRI of a patient who is seen to have cystic structures in the

43:58

abdomen.

43:58

And here you can see multiple dilated loops of bowel in the fetal

44:03

abdomen suggestive of some type of obstruction.

44:07

And when we look carefully on the sagittal view,

44:09

we realize that these are actually dilated loops of small bowel.

44:13

And the colon is this tiny collapsed microstructure back here.

44:18

So that suggests that nothing is progressing from large bowel to small bowel.

44:23

And on this final frontal view,

44:25

we can again see the dilated loops of bowel that are this intermediate

44:30

signal intensity as compared to these less dilated loops that are brighter

44:34

signal intensity.

44:35

And the way it works is the more recently swallowed amniotic fluid maintains its

44:40

hyperintense signal and as the fluid progresses through the

44:45

bowel, especially fluid that's sitting within obstructed bowel,

44:49

it becomes less hyperintense and more intermediate signal.

44:53

And that's a sign that this fluid's been sitting around for a while.

44:56

So on ultrasound imaging of this not yet delivered

45:01

fetus,

45:02

you can see this echogenic strongly shadowing structure within the abdomen.

45:07

And then on subsequent fetal MRI,

45:11

you can see that there's a focal cystic structure in the anterior abdomen and

45:15

conglomerated bowel and mesentery behind it with a large amount of ascites

45:20

surrounding. That's the T two weighted sequence. Uh, the uh, steady state,

45:25

the uh,

45:26

single shot fain echo sequence I should say this is the gradient echo,

45:30

which is showing susceptibility all around the rim of that cystic structure that

45:36

lets us know that there's either blood or calcium around it.

45:38

And then here on the T one we can see that it's filled with T one hyperintense

45:43

signal, which is the classic appearance of meconium.

45:46

So this by all fetal imaging is likely meconium

45:50

pseudocyst from a case of obstruction that progressed to ruptured

45:55

bowel that progressed to pseudocyst formation and calcification.

46:00

And after birth here is that patient's pseudocyst completely

46:05

calcified and notice how all the loops of val are clumped together and

46:09

conglomerated just under that calcified pseudocyst.

46:13

So this is a patient that required surgical exploration and in fact there was a

46:17

closed loop obstruction that had perforated and then sealed off

46:22

in a way that was a continuing to obstruct the bowel.

46:25

And this patient required ostomy formation and then it subsequently anastomosis.

46:31

Here's an example of a patient with this very unique appearance,

46:36

almost like a folded appearance of calcification,

46:39

a thin rim of calcification lining the entire lower peritoneal space.

46:44

And this is a patient who had had a perforation.

46:46

You can see there's very little gas in the abdomen except approximately and that

46:51

perforation had never healed off properly.

46:54

So it had just spilled a lot of bowel contents. This, uh,

46:57

premature infant had a large amount of complex societies

47:02

which had to be drained and ultimately the bowel had to be re anastos.

47:08

And here's an example of a patient, again with abnormal dilated bowel,

47:13

no distal rectal gas and little elements of calcification here all pointing

47:18

to the fact that not only is the bowel obstructed,

47:20

but it's been previously perforated. And by the way,

47:23

this is not the same thing as identifying, you know,

47:27

complex fluid with ultrasound, which might suggest an acute perforation.

47:31

If there's calcification, you know that something's been going on, uh,

47:35

for a while. This is subacute to chronic.

47:37

It's always a little silly to say chronic in a premature newborn 'cause they

47:40

haven't been alive that long, but it's not brand new.

47:45

And uh, the last thing that I'll bring up is in a lot of these cases of either

47:50

obstruction or necrotizing enterocolitis,

47:52

we can assess how the fluid balance and overall

47:57

vitality of the patient are faring by looking at the tissues.

48:01

And just notice what a dramatic change in the body tissues of

48:06

the chest wall and the flank coming down early after

48:11

intubation. In a patient you can see dilated bowel,

48:14

they ended up having an obstruction and um,

48:18

a perforation to postoperatively.

48:21

This patient has developed massive body wall edema.

48:24

It almost doesn't look like the same patient.

48:27

And this can be a really important sign, uh,

48:29

of the morbidity of our patients in the nicu and it can be important for us to

48:34

kind of track whether there's increasingly progressive or resolving body wall

48:39

edema. And just for the final phase of this lecture,

48:44

I wanna review what we can see in the brain and uh,

48:48

brain imaging of course is gonna be ultrasound for those who are too sick to be

48:52

moved to cross-sectional.

48:54

So remember that the brain goes from having almost no, uh,

48:58

complex surface development to increasingly convolutional

49:04

gyr salsi from the fetal period to the neonatal period to the adult period.

49:09

And most of the change in complexity occurs between second trimester and

49:14

newborn. That's right where we're gonna be delivering premature babies.

49:17

And then the changes between

49:20

child and adult have more to do with size and internal, uh,

49:24

development as opposed to gyration development.

49:28

And on fetal imaging we can see that complexity by measuring the Sylvie and

49:33

fissure,

49:33

which starts out as just a little dimple and then becomes increasingly complex

49:37

and insulated. Hence our use of the phrase the insula. And uh,

49:42

the insular brain is not yet insulated in a very young 20 week, uh, fetus,

49:47

but becomes, um, the normal characteristic.

49:50

Sylvia and fissure in a term infant, same appearance down here on ultrasound.

49:55

And uh, we can see that in neonatal head ultrasound.

49:58

So look at the complexity as indicated by these echogenic markings

50:02

showing us tissue interfaces of the sound wave hitting

50:07

the fluid and the surface of the brain and the parenchyma of the brain and

50:12

creating all these echoes. This is a near term infant.

50:14

Here's a premature infant and an extremely premature infant.

50:18

And notice how the central cerebral parenchyma is quite echogenic in this

50:22

premature infant and there's very little complexity to the surface of the brain.

50:26

This is not disease,

50:28

this is just the normal immature brain and this is the normal appearance of

50:33

the lateral ventricles and the coth thalamic groove,

50:35

which is where we focus a lot of our attention,

50:38

right between the head of the caudate and the thalamus.

50:40

That's where the ganglionic eminence the germinal matrix. So-called originates.

50:45

All the gray matter that migrates out to the surface of the brain starts there

50:48

and it's highly perfused with this capillary bed that doesn't have much

50:52

structure to it.

50:53

So it's just a bunch of capillaries without anything protecting them.

50:57

It should involute by term, but if you're born prematurely,

50:59

it hasn't involuted yet.

51:01

And it's very susceptible to those fluctuations of blood pressure,

51:05

just like we were talking about earlier with the gut,

51:08

something that would've been protected and insulated, intrauterine,

51:13

once you're outside,

51:14

you're much more susceptible to fluctuations and that causes hemorrhages.

51:18

So we look for echogenic material accumulating in that coth thalamic groove.

51:23

This is a grade one intraventricular hemorrhage.

51:26

There's one again in the left coth thalamic groove that's got some central

51:31

hypoechoic appearance, which means it's older, it's evolving,

51:33

the blood is organizing there it is on the sagittal view,

51:37

tucked right into that space between the head of the,

51:39

the caudate and the thalamus.

51:41

And then as it enlarges into the ventricle, it goes up in grade.

51:46

And the important distinction is a grade one hemorrhage is difficult to see,

51:51

but is not considered sufficiently morbid to stop any anticoagulation.

51:56

And the most common reason in a sick premature baby would be as if that, uh,

52:00

neonate is on ecmo. If they're on ecmo, they have to be anticoagulated.

52:04

But if they have more blood in their brain than a grade one,

52:08

anything more severe than a grade one, it's contraindicated to anticoagulate.

52:12

So you're between a rock and a hard place.

52:14

Do I want this child to risk bleeding in their brain or do I want them to not

52:19

get enough oxygen for life because we can't put them on ecmo. These,

52:22

this is a terrible choice we have to make. Uh,

52:24

but typically people will say grade one, we'll keep ecmo grade two,

52:29

we need to stop ECMO because we stop anticoagulation.

52:32

And here you can see increasing amounts of blood filling the ventricle. Uh,

52:37

now expanding the ventricle.

52:38

So this is a grade three hemorrhage where you've got blood visible in the

52:42

ventricle and the ventricle is enlarged a little bit on the other side as well

52:46

in this image. And then, uh, appearance of both acute and chronic.

52:51

So this is a grade three hemorrhage with these organized spaces and also some

52:55

new blood, what the echogenic material is.

52:58

And ultimately if you get enough expansion of the ventricles because of

53:02

intraventricular blood,

53:04

there's a bunch of veins draining just under the append lining of the ventricle.

53:08

And if those get compressed,

53:09

you get ischemia in the adjacent brain because of impaired venous drainage and

53:14

you develop a grade four, an intraparenchymal hemorrhage.

53:18

So that's the severest kind.

53:19

You can also have changes to the brain without hemorrhage.

53:22

And this is an example of ischemic injury in the per ventricular white matter.

53:28

It's sometimes confused with the normally echogenic appearance.

53:31

So this image with two arrows is a normal brain without ischemia and you can see

53:36

symmetric echogenicity around the ventricles.

53:38

But on this other image you can see asymmetric echogenicity.

53:42

How can we tell the difference? This can be challenging,

53:45

but I think it's useful to use two rules. Heuristics,

53:49

I guess you could say rules of thumb.

53:50

One is the echogenic area of the brain as bright as or brighter than the

53:55

choroid plexus. And in this patient I would say yes,

53:58

it's as bright as or brighter than the adjacent choroid plexus over here

54:03

in this what I know to be normal brain, it's not,

54:06

it's not as bright as the choroid. And then my second rule of thumb,

54:10

can I draw a line around where I think the ischemic area is?

54:14

And right here I feel like I could take a pencil and trace the outline of this

54:19

echogenic injury. This paraventricular leukomalacia. Whoops.

54:23

But over here these are too vague.

54:25

They just kind of fade out into the surrounding parenchyma. This is an injured,

54:31

this echogenic asymmetric area is going to eventually lead to some

54:35

infarction and that infarction is gonna eventually die and disappear

54:40

because we know that the brain liquefies with necrosis and then it just becomes

54:44

absorbed by the ventricle. So it becomes X vacu dilatation.

54:47

Here you can see that little expanded part of the ventricle from periventricular

54:52

leukomalacia. In the last couple of minutes,

54:55

I just want to show a couple of examples of both normal and abnormal,

54:59

extra axial blood. Uh,

55:01

premature infants will frequently have extra axial fluid,

55:05

but it's subarachnoid fluid and we call it benign because we see normal

55:10

fluctuations, especially in premature infants and newborns. And uh,

55:15

the way we can tell that it's subarachnoid is the

55:20

presence of vessels traversing the space between the cerebral parenchyma and

55:25

the skull. And on doppler here, you can see there are vessels coursing between.

55:29

So even though there's a prominent amount of extractive fluid here,

55:32

we can feel pretty confident that this is likely benign subarachnoid fluid

55:37

not.

55:37

So in this case here you can see that there's all this

55:42

material just above the superior sagittal sinus and the surface of the brain,

55:46

but it's echogenic and it's different than the subarachnoid space.

55:50

On this image,

55:51

you can see there's a little simple subarachnoid fluid and there's this much

55:55

more prominent echogenic material outside the brain.

55:59

So this is unfortunately subdural blood pretty uncommon.

56:03

But in very traumatic deliveries, uh, patients can get, um, you know,

56:08

subdural and even epidural hematomas.

56:11

So there's some blood here from a traumatic delivery. And these patients,

56:16

even more common than blood, um, in those spaces is blood on the scalp,

56:20

so like a cephalohematoma or less frequently a subgaleal hematoma. And uh,

56:25

here we've got a sagittal image. This is the echogenic line for the skull,

56:30

and here is a hematoma under the scalp.

56:33

And you can see the contour abnormality.

56:35

And this is probably the most common finding in birth trauma.

56:39

So just be aware of the differences there. Subarachnoid fluid, less concerning,

56:44

but subdural or even rare epidural fluid is, is more concerning, uh,

56:49

in these neonates. So I'm going to round out this lecture.

56:52

We're at the end of our time and I just a few take home points.

56:56

I know that we've all seen chest x-rays and ubs and it's easy to blow through

57:00

'em, but remember that all premature lungs are gonna have barrow trauma.

57:03

So really scrutinize for that. It's just a matter of how much barrow trauma.

57:07

Second, don't be afraid to wait. If you're suspicious of intraperitoneal air,

57:11

give it a delay to prove that it's there because that sticky abdomen can make it

57:16

hard for the air to move. Number three,

57:19

neck evolves quickly and you can go from dilated bowel loops without

57:24

specific signs to fluoride, you know,

57:26

portal venous gas and perforation and it can happen within hours.

57:31

Um,

57:32

intraventricular hemorrhage is important not just because of what it can do

57:37

inside the ventricles,

57:38

but that compressed venous drainage just outside the append puts at risk

57:43

that per ventricular brain. And that's what's gonna have the,

57:45

the greatest long-term morbidity. And finally, remember to look, if you see,

57:50

extract eal fluid,

57:51

look for vessels to reassure yourself that it's the more benign, uh,

57:56

subarachnoid location.