0:02

Hello and welcome to noon conference hosted by MRI online.

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In response to the changes happening around

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the world right now and the shutting down of in

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person events, we have decided to provide free

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noon conferences to all radiologists worldwide.

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Today we are joined by Dr. Brandon Patrick Brown.

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Dr. Brown is vice chair of radiology and

0:22

associate professor at Indiana University.

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His interests include fetal imaging,

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medical ethics, and medical education.

0:30

He is chair of professionalism for the

0:32

RSNA and works as a pediatric radiology,

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radiologist at Riley Hospital for Children.

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A reminder that there will be a Q and A session at

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the end of the, at the end of the lecture, so please

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use the Q and A feature to ask your questions and we

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will get to as many as we can before our time is up.

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That being said, thank you all for joining us today.

0:51

Dr. Brown, I'll let you take it from here.

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Ah, perfect.

0:56

Well, thanks for having me.

0:57

I'm excited to be here and hopefully

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everyone can see my images.

1:02

We're going to talk today about prematurity

1:04

and unlike other topics, um, where we focus

1:09

on a disease process or an organ system.

1:12

We're going to talk about prematurity as its

1:15

own set of challenges and vulnerabilities.

1:18

Notwithstanding, uh, associated disease processes,

1:22

but every single premature infant that's

1:24

born, um, faces certain challenges and, uh,

1:30

first period of life.

1:31

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

1:35

things that anyone who's reading imaging, um, at a

1:38

hospital where there are deliveries, where there's a

1:40

neonatal intensive care unit, um, these are the types

1:43

of bread and butter things that anybody would see.

1:45

And, um, the first thing that we have to

1:48

remember is just how small these patients are.

1:52

If you look at this image over here, Uh, this

1:54

radiographic image, you can see, um, a syringe and,

1:59

uh, a syringe that's, you know, the size of my hand.

2:03

And you can see it right here

2:05

next to this chest and abdomen.

2:09

Sure, baby.

2:10

So these are quite small organs.

2:12

These are quite small patients and, uh, everything requires

2:17

a little bit more care and attention because of that.

2:21

So, uh, when we're talking about.

2:24

Such a large topic, the whole body of, you know,

2:28

a human being at the earliest part of life.

2:31

There's really an infinite number of things we could review

2:33

and since time is, is limited to one hour today I want to

2:37

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

2:42

Those are three areas that frequently

2:44

receive imaging in every premature newborn.

2:47

And, uh, in particular, I want to talk about

2:49

effects to the lungs because of prematurity, but

2:52

also because of the way we treat prematurity,

2:55

uh, with, uh, the big category of barotrauma.

2:59

And then I also want to talk about infection, um,

3:02

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

3:07

who have an immature mucosa and who are much more

3:10

susceptible to bacterial overgrowth and its complications.

3:14

And, uh, we'll also talk a little bit about the effects

3:17

of premature infants, uh, with bowel obstruction.

3:21

Uh, but finally we'll review some of the findings.

3:24

Um, in sonographic imaging of the premature brain, these

3:28

patients are often so unstable, they can't go down to

3:30

the scanner to get an MRI or even a CT, less commonly.

3:36

But at the bedside, we can always do head ultrasound.

3:38

So we end up doing a lot of imaging at

3:41

the bedside for prematurity, just because

3:44

of the instability of these patients.

3:46

So what parts of the body are adversely

3:48

affected by being born too early?

3:50

And really, this is anything.

3:52

Definitions change.

3:54

Most people would say term is 39 weeks now,

3:56

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

3:58

And I think prematurity is anything earlier than 37

4:02

weeks, according to the latest neonatology definitions.

4:05

So what's what's going to be at

4:08

risk and what's going to be safe?

4:09

Well, it turns out that the liver is one of the

4:11

first organs we can visualize in fetal imaging,

4:14

and it functions pretty well in premature infants.

4:17

Um, there's not a whole lot of prematurity associated

4:20

liver disease that we see on a routine basis.

4:22

Same thing with the gallbladder and the spleen

4:24

and the kidneys really make urine pretty well.

4:27

In fact, the kidneys have been making

4:28

urine since the sixth week of gestation.

4:31

That's about the time most people find out they're pregnant.

4:34

Uh, the only thing, the only caveat is that in the

4:37

first two weeks of life, uh, newborns, whether premature

4:40

or term, are often chronically dehydrated for one

4:44

to two weeks, and so imaging of the kidneys can be a

4:48

deceptive, because if you're dehydrated, then any kind

4:51

of renal disease you might have won't be visualized,

4:55

um, until you start having sort of normal fluid volumes.

4:59

So what's not okay in a premature infant?

5:02

Well, it turns out that the

5:04

lungs are frequently problematic.

5:07

They're hypoplastic, they're immature, and there's

5:10

also difficulties with pulmonary vasculature.

5:13

But also, The gut mucosa, the

5:16

small bowel mucosa is immature.

5:19

It's not properly developed.

5:20

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

5:23

mucosa can, and it's susceptible to super infection.

5:27

And then the brain itself is not finished

5:29

growing and developing even in its external form.

5:33

But certainly with things like myelination, with

5:36

things like involution of what are supposed to be

5:39

embryonic structures, like the germinal matrix.

5:42

And, uh, you know, there's, there's a greater

5:45

risk for injury to all of these things.

5:47

Some of the stuff that's part of risk for every

5:51

neonate that we don't really spend as much time

5:53

imaging and radiology would be retinopathy.

5:56

Uh, you know, there's a breakdown in the normal protective

5:59

barrier of the skin because it hasn't properly matured.

6:01

And, uh, I'm not going to spend any time today,

6:04

but, you know, we could focus on the topic of

6:06

functional immaturity of the colon as well.

6:09

So these are the things that every, uh,

6:11

Pediatric imager or every radiologist who

6:14

sees newborn imaging should be thinking about.

6:17

And I want to go ahead and start

6:18

off by talking about the lungs.

6:19

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

6:23

Well, it turns out that we need to worry about

6:25

whether pregnancy, uh, was going according to plan

6:30

and going according to the way it ought to go.

6:32

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

6:35

It turns out that the lungs are heavily dependent on

6:39

the influx and outflow of amniotic fluid throughout.

6:43

gestation.

6:44

It's not just a matter of practicing the

6:47

respiratory motions of intercostal muscles and

6:49

diaphragms, but the fluid itself is nourishing.

6:52

And there's a sort of synergistic relationship

6:56

between the mucosa, uh, and the, The pneumatic

7:00

sites that are developing secretions and also the

7:03

amniotic fluid and their cell signaling that goes

7:06

on when that fluid is able to nourish the lungs.

7:10

If you have, you know, oligohydramnios or an

7:14

hydramnios the lungs aren't going to develop

7:16

properly so lungs can be small, because of space.

7:20

considerations, then this is a fetal MRI image

7:23

showing narrow, almost columnar, hypoplastic lungs,

7:27

which are too small and haven't been given the

7:30

opportunity to develop because this is a fetus

7:33

with a large omphalocele and the body cavity never

7:36

had to expand because all the organs are outside.

7:38

side.

7:38

So sometimes the lungs don't develop

7:40

because of size considerations.

7:41

Sometimes they don't develop because of

7:43

insufficient amniotic fluid considerations.

7:46

And sometimes they don't develop because of mass effect.

7:48

If you think of a diaphragmatic hernia

7:50

case, uh, the other thing is it takes time.

7:53

There's just a normal process of development.

7:56

And if a You know, a delivery occurs too soon.

8:00

Then some of the cellular makeup

8:02

of the lungs isn't present yet.

8:03

Those type two pneumocytes aren't functional.

8:06

And we all know about surfactant deficiency.

8:09

And, uh, that's a big challenge for

8:12

the newborn, uh, intensive care unit.

8:14

They're trying to basically create gas exchange.

8:18

In a set of lungs that don't

8:19

have all of the necessary cells.

8:21

Uh, and finally there's pulmonary hypertension,

8:24

which is a normal process in utero.

8:26

We don't want a bunch of blood going into the fetal

8:29

lungs because it would be a waste, but we need

8:32

those lungs to be able to be nourished as soon as

8:35

delivery, as soon as that umbilical cord is cut.

8:38

And if there hasn't been proper

8:40

maturity of the lungs and the alveoli.

8:43

Then there's no cell signaling to tell the pulmonary

8:46

arterioles and, you know, the tiniest areas of

8:50

the pulmonary arteries to dilate sufficiently to

8:53

allow perfusion, uh, to match the ventilation.

8:56

So these are the things we need to worry about.

8:58

And we can see problems when there's not enough

9:01

fluid going into the lungs like this image.

9:03

We can also see problems when

9:04

there's fluid trapped in the lungs.

9:06

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

9:09

are hyperexpanded.

9:11

They're enlarged.

9:12

Look at how the diaphragms are inverted.

9:14

This is a case of congenital high airway obstruction

9:18

syndrome, or sometimes called chaos syndrome.

9:21

And you can see all this fluid

9:22

dilating the trachea and the bronchi.

9:25

Uh, this is fluid trapped in the lungs.

9:27

This is not enough fluid in the lungs.

9:30

And here is This is the happy media and this is

9:33

what we want to see normal looking fetal lungs and

9:36

this is what the lungs are going to be like when

9:37

they're delivered right because prematurity is

9:40

basically a fetus having defend for itself outside.

9:45

And this is what it looks like in a newborn we've all

9:47

seen newborn chest x rays, and we're familiar with.

9:50

Uh, the various patterns of disease and a lot of the

9:53

terms that get thrown around are a little bit imprecise

9:55

because we're not talking about discrete structures.

9:58

People use terms like hazy opacities or cloudy

10:03

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

10:07

opacities in the lungs and they tend to be diffuse.

10:10

They tend to be symmetric and this is a sign of.

10:15

the earliest stages of premature lung disease.

10:17

We've had a lot of names for this.

10:19

We've called it surfactant deficiency disease and various

10:22

other things, but basically it's the effects of prematurity.

10:25

And I like the term premature lung disease

10:27

because it's big enough to encompass

10:29

problems intrinsic to the lungs themselves.

10:32

not proper cells, problems secondary to our

10:35

treatment of this barotrauma, and also problems

10:39

due to scarring and atelectasis that develop.

10:41

So I like to use the phrase premature lung disease.

10:44

It starts out indistinct, soft and hazy like this, and

10:48

then it becomes gradually coarser and more discreet.

10:52

Now we're starting to see interspersed aerated lung

10:57

with atelectasis and coarse interstitial opacities.

11:01

throughout the lungs.

11:02

And these are both alveolar and interstitial,

11:04

um, appearance of the opacities.

11:07

And finally, as it organizes even more fully and

11:10

ventilatory support is able to get rid of some

11:13

of that atelectasis, uh, we can see even more

11:15

lucency interspersed with the scattered opacity.

11:19

So just to see all of those together, you can see

11:21

how in the earliest stages of a premature newborn's

11:25

life, there's a mild diffuse haziness, which gradually

11:28

becomes coarser and more discreet in its opacity.

11:32

This is the normal process of just the

11:35

radiographic appearance of premature lung disease.

11:38

This isn't necessarily something

11:41

that's been done right or done wrong.

11:43

This is just what happens for

11:44

every newborn that's born too soon.

11:46

And this one I think was born at 27 weeks.

11:51

So then there's the question of

11:53

what's going to happen long term.

11:55

And just by convention, I'm not sure that there's

11:57

any, um, you know, rule that's absolute, but most

12:01

neonatologists start thinking of lung disease of

12:04

prematurity as a chronic process after 30 days.

12:07

So it's an arbitrary line that we draw.

12:09

And this is a.

12:10

A neonate born at 26 weeks now at about 45 days of life

12:15

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

12:18

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

12:22

There's some more focal atelectasis.

12:24

There's definitely some scarring going on here.

12:26

This is a neonate that's been on a ventilator.

12:28

Here's the endotracheal tube, uh, for,

12:30

for, you know, a month and a half.

12:32

And so there are areas of damage to the lungs

12:35

and, uh, we can also see that there's more.

12:38

Asymmetric aeration so there are areas like this lateral

12:42

left lung base which are better aerated than maybe the upper

12:46

lobe, and it tends to be much less diffuse and symmetric

12:49

like the earliest stages as the lungs start to become

12:53

irregular due to both damage, and the fact that there's a

12:57

continual battle between the ventilator, which is using.

13:01

High pressure air, maybe even it's a jet ventilator

13:04

for our sickest babies, and it's shooting in bursts

13:07

of air, but then the lungs don't have surface

13:10

tension, the alveoli, and so they want to collapse.

13:12

And there's this battle of enough pressure

13:14

to pop those alveoli open, but not so much

13:17

pressure, you know, that we cause a pneumothorax.

13:20

And that is something that happens quite a bit.

13:23

It's not a question of will premature

13:26

infants who are intubated have barotrauma.

13:28

It's just a question of how much.

13:30

Every child with premature lungs disease has

13:33

barotrauma and it can present in various ways.

13:35

So here's a patient earlier in the process,

13:39

um, hasn't even been intubated yet.

13:42

And then we can start to see after the patient

13:45

has been intubated and then extubated this

13:47

development of these tiny leucine seeds.

13:50

in the right medial portion of the lung, and a few of

13:54

them extending down here into the lateral lung base.

13:56

And this is an area where we're starting to see

13:59

air dissect into the interstitium of the lung.

14:02

Uh, it's pretty subtle at this point, but I'm

14:04

going to show you some more dramatic examples.

14:06

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

14:08

these lucencies have expanded and developed even further.

14:12

And now there's air outside the lung in the left hemithorax.

14:16

Uh, this is kind of a classic neonatal pneumothorax.

14:19

There's also air outside of the mediastinal

14:23

structures, but within the mediastinum.

14:25

So there's pneumomediastinum, pneumothorax,

14:28

and all this interstitial air, which we

14:30

call pulmonary interstitial emphysema.

14:33

Uh, chest tubes been placed, we can get rid of the pleural

14:37

air, but sometimes it can be very hard to treat this.

14:40

And over time.

14:41

These patients can develop pneumatic seals or

14:44

trapped loculated pockets of air because the lungs

14:47

are being damaged and it creates these negative

14:49

spaces in the thorax where air can accumulate.

14:54

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

14:56

Barotrauma with air in the mediastinum.

14:59

You can see it outlining the thymus here.

15:01

You can see it over here to the left

15:03

of the superior mediastinum and maybe

15:06

just a hint of it down around the heart.

15:08

On this image, instead of air tracking up, to

15:11

the apex of the lung, like you saw on this pneumo

15:14

mediastinum case, this air is outlining the heart

15:18

and it's following the contours of the pericardium.

15:21

So this is pneumo pericardium, yet

15:24

another manifestation of barotrauma.

15:26

So why does this keep happening?

15:28

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

15:32

structures, the premature lungs, Are susceptible to injury.

15:36

They're not fully supported by the architecture,

15:39

the scaffolding of the interstitium, it's not ready

15:42

for prime time yet, but it's trapped and, uh, it

15:45

has to do a job that it wasn't quite ready to do.

15:48

So if you can imagine these tissue paper

15:51

decorations that are sometimes hung at

15:52

birthday parties, they're delicate structures.

15:55

They have an architecture to them.

15:57

And imagine then that you took compressed air

16:00

from, uh, you know, from Gas powered or an electric

16:04

powered air compressor and you started shooting

16:06

jets of air at these things rapidly and maybe you

16:08

started shooting higher and higher volumes of air.

16:12

Eventually, that tissue paper is going to start to tear

16:16

in certain places and it's going to start to deform the

16:18

architecture and shape of whatever it was supposed to

16:22

be and in the neonate of course it's a lung, and over

16:25

time, you're going to go from this highly organized

16:28

uniform ordered structure of these undamaged lungs.

16:32

Even though they're premature into something

16:34

more like this, that's irregular and amorphous

16:37

and has larger spaces and smaller spaces and

16:40

the lines aren't as crisp and sharp anymore.

16:43

And it's because we're fighting this battle.

16:44

If we don't give enough air, then atelectasis

16:48

takes over in respiratory failure.

16:50

There's not enough.

16:51

oxygen and these, these are the neonates

16:53

that end up needing to go on ECMO.

16:55

If we give too much air, then we risk damaging the

16:58

lungs, and that also can make them non functional.

17:01

So it's a, it's a very delicate balance and, you

17:05

know, for those of us who read, morning portable chest

17:08

x rays on newborns, on premature newborns, you can

17:10

see that waxing and waning of atelectasis and then

17:13

barotrauma and then atelectasis and then barotrauma.

17:16

And it's because the neonatologists

17:18

are adjusting the vent settings.

17:20

Both the PEEP, we talk about

17:22

Positive end expiratory pressure.

17:24

That's the kind of the force of the jet of air going

17:27

in, but increasing research has shown that the title

17:30

volume, the actual size of the blast of air going in

17:35

may be even more important in determining barotrauma.

17:38

So precise regulation of the title volume may be even

17:43

more necessary to keep those lungs as safe as possible.

17:47

So just a few more images showing the effects of

17:50

ventilatory support for premature lung disease

17:53

and the ways in which it can damage the lung.

17:56

So here's a large pneumothorax.

17:58

Here's a small pneumothorax with just a

18:00

subtle, uh, lucency underneath the lung.

18:03

And then here's a patient with more

18:05

of that interstitial emphysema.

18:06

You can see That the air hasn't dissected, uh, between the

18:10

lung and the body wall, but instead it's dissected into

18:13

the architectural spaces of the lung, the interstitium,

18:17

and here's a super dramatic example of pulmonary

18:20

interstitial emphysema, where there's so much air

18:22

dissected into those spaces, it's causing midline shift.

18:27

Not because the air spaces of the lung are expanded.

18:31

We would call that a hyperventilated

18:33

lung or a hyper expanded lung, or an,

18:35

you know, almost like an over inflation.

18:37

In this case, the lung isn't inflated,

18:40

the interstitium is inflated.

18:42

And that's much harder to explain.

18:43

to repair.

18:44

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

18:49

So let's shift gears a little bit and talk about

18:52

one iatrogenic cause of difficulties in premature

18:56

newborns, and that is umbilical catheters.

18:59

We use umbilical catheters because it's such a

19:01

great access for infusion of fluids and medications,

19:04

for drawing off blood, for monitoring pressures.

19:07

And you see them in almost all premature newborns

19:10

who are going to spend time in the neonatal ICU.

19:13

This is actually a fetal MRI, showing a mid sagittal

19:17

view you can see the spine nicely laid out here, and it's

19:21

just a really beautiful example of the inflow of blood.

19:25

So here of course is the umbilical

19:27

cord at the anterior body wall.

19:30

And here you can see blood going in through the

19:32

umbilical vein and coursing up the umbilical vein into

19:36

this dilated portion, just as it enters the liver.

19:39

And we call that the umbilical recess.

19:42

And it continues to travel.

19:43

At this point, the umbilical vein is

19:45

joined to the portal venous system.

19:49

But it needs to get past the liver,

19:51

because this is oxygenated blood.

19:53

Bear in mind that with umbilical vessels,

19:56

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

19:58

The vein is what's carrying the oxygen, and

20:00

the arteries are what need to go back to the

20:03

mom to be filtered by the maternal lungs.

20:06

via the placenta.

20:08

So it's this vein that carries the oxygen.

20:10

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

20:12

We want it to get straight to the heart.

20:14

So we have this embryonic vessel, the ductus venosus,

20:17

and here you can see the blood going through the

20:19

umbilical vein, the recess joining the portal venous

20:22

system, but bypassing that and going through the ductus

20:27

venosus up into the inferior cable atrial junction.

20:32

So it joins the confluence of the hepatic veins right here.

20:35

At the intra hepatic IVC, and then

20:38

straight into the right atrium.

20:39

So that's the path that our catheters are going to take.

20:42

And this is an example of a normal placement of an

20:46

umbilical venous catheter, we can see it going straight

20:49

in to the umbilicus through the umbilical vein, and

20:54

at this point right here would be that umbilical

20:56

recess that more dilated portion before traversing

21:00

the ductus venosus, and through the umbilical vein.

21:03

Intra hepatic IVC to the right atrium

21:06

at the lower cable atrial junction.

21:09

Now one of the things that can be challenging

21:11

is getting the catheter to go straight up

21:12

to the heart versus taking turns or detours.

21:15

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

21:18

placement, you'll notice that the neonatologist

21:21

will eventually pull the catheter all the way

21:23

back to this inferior margin of the liver.

21:25

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

21:28

That's that umbilical recess.

21:30

So if they do need higher flow rates for blood

21:32

draws, et cetera, it's a better place down there

21:36

than somewhere in the middle of the umbilical

21:38

vein or somewhere in the middle of the liver.

21:40

So ideally lower caval atrial junction, but

21:43

second best at the inferior margin of the liver at

21:46

that, uh, at that, recess of the umbilical vein.

21:51

Here's an example of a placement of a

21:53

catheter that didn't go according to plan.

21:55

And this is just reminding us that the umbilical

21:58

vein does join the portal venous system.

22:00

So this is a catheter that's turned right

22:02

and gone into the right portal vein.

22:04

And not only is that a problem because any infusion

22:07

of medication is going to You know, get delayed by

22:10

having to pass through the portal triads, but also

22:14

it's very narrow in there and any attempt to draw blood

22:18

is going to put the liver at risk and rapid infusions

22:22

could also overwhelm the liver and any advancement

22:25

of the catheter can create injury to the liver, even

22:29

hepatic hemorrhage or hematoma because the catheter

22:32

is capable of piercing the, the hepatic parenchyma.

22:38

Here's an example of a catheter that's been

22:40

pulled back and advanced and repositioned and

22:43

it's just coiling up within the portal vein.

22:45

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

22:47

We can also see here an example of an umbilical arterial

22:50

catheter, which characteristically has to descend, uh,

22:55

inferiorly along the bladder and join the iliac artery

22:59

before then returning, uh, superiorly into the aorta.

23:03

And the ideal location for the tip of this

23:05

catheter is somewhere between the branch vessels.

23:08

So that's kind of a wide margin of error.

23:12

Uh, you don't want it up in the aorta, there's a lot

23:15

of branch vessels there, and you don't want it down

23:17

by the celiac axis or the superior mesenteric artery.

23:20

Anywhere, the tip of that catheter could occlude

23:23

a takeoff of an artery or could potentially draw.

23:26

blood away from an organ when the catheters being

23:31

used is going to be a problem, but typically

23:34

at the level of the diaphragms are slightly

23:36

above the diaphragms is going to be a safe zone.

23:39

There's no important branch vessels

23:41

off the aorta at that level.

23:43

Finally, you can see, um, the same patient has had

23:47

a continued repositioning of their umbilical venous

23:50

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

23:53

Um, the way that the liver is positioned on a

23:56

frontal chest and abdomen radiograph often makes

24:00

the left portal vein look like it's oriented.

24:02

posteriorly, um, instead of just 90 degrees to the left.

24:07

So that's why the catheter looks like

24:08

it's headed towards the patient's spine.

24:12

And then finally, we can see that the catheter was

24:14

repositioned and has made it to the lower caval

24:17

atrial junction, which is the ideal location.

24:20

So evaluating the location of these catheters is one

24:23

of the most important things the radiologist needs

24:25

to recognize and identify on these x rays because

24:29

it can cause a lot of morbidity for patients and

24:32

missed, um, malpositioned lines and tubes is the

24:36

number one reason for medical malpractice complaints.

24:41

So lines and tubes, even though it may seem

24:43

elementary in some cases is very important.

24:47

It's probably the number one thing the neonatologists

24:49

are looking to our reports to find out.

24:52

And when we don't give adequate attention, it's the

24:54

number one reason that it can turn into a legal issue.

25:00

The one caveat I'll say to the normal trajectory.

25:03

of the umbilical venous catheter, and that tends to be

25:06

the catheter that has the hardest time getting to where

25:09

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

25:12

So everything I've just said about where the

25:14

umbilical catheter should go is predisposed

25:17

on a normal liver being in a normal location.

25:20

But if you have abdominal, you know, uh, situs inversus,

25:25

Or as in this radiograph, if you have a congenital

25:29

diaphragmatic hernia with supra diaphragmatic positioning

25:32

of the liver, the left hepatic lobe in this case is oriented

25:36

superiorly, then the orientation of your catheter is

25:40

going to have to change in order for it to be appropriate.

25:44

So that red line that I've placed on

25:46

the image is the outline of the liver.

25:48

And knowing that we can now be suspicious of this

25:51

catheter That it's in the left portal vein, an accurate

25:55

positioning of a catheter in the case of diaphragm

25:58

hernia with a malposition liver would actually curve.

26:02

up like this.

26:03

So you have to know where the liver is in

26:06

order to know where the catheter should go.

26:09

That's a rare situation, but it does occur.

26:11

And you can see that the same would hold true

26:13

for this suction catheter, which is actually

26:16

appropriately positioned in the patient's stomach.

26:18

But the patient's stomach is

26:20

inappropriately up in the chest.

26:24

And this is just a umbilical venogram revealing those

26:28

vessels that I was just describing so here's the umbilical

26:31

vein you wouldn't want to leave an umbilical venous

26:32

catheter down here look at the narrow caliber of that,

26:35

whereas the recess the umbilical recess is a much better

26:38

place for flow rates, and then the normal trajectory

26:42

to get to the heart is through this ductus venosus.

26:45

Here's the confluence of the hepatic veins and

26:48

the inferior aspect of the caval atrial junction.

26:52

So any turns this way would be a portal venous

26:55

turn or this way would be a portal venous turn.

26:58

You could even end up in some

26:59

of these branch draining veins.

27:02

So what we need to do is Be aware of the venous

27:05

anatomy be aware of the location of the liver and we

27:08

can add a lot of value on these lines and tubes cases.

27:12

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

27:17

Let's talk a little bit about necrotizing enterocolitis.

27:21

This is the most common abdominal

27:24

infection in premature infants.

27:26

It's also one of the most dangerous conditions

27:28

for a premature infant because it can rapidly

27:31

progress from bowel infection to systemic

27:35

decompensation, hypotension, and even death.

27:39

And the reason is because it can progress from

27:42

a mild infection to a severe, almost near total.

27:46

small bowel necrotic situation.

27:50

What's happening is the premature gut mucosa is not

27:54

yet sufficiently able to keep bacteria at bay and

27:58

anything that injures the bowel or the balance of

28:02

gut mucosa is going to make the infant susceptible.

28:05

A newborn at term and a child or an adult is

28:09

much better able to handle fluctuations in guts.

28:12

Uh, bacteria because they have mature mucosa

28:17

and also because they have the ability

28:20

to sustain fluctuations in perfusion.

28:24

But any kind of fluctuation of perfusion in

28:27

a newborn that's premature is going to create

28:31

ever so brief transient ischemia of the bowel.

28:34

And that's the most common type of injury that

28:36

then makes the bowel susceptible to those bacteria.

28:40

So we all have lots of bacteria in our bowel.

28:42

It's appropriate.

28:43

It's even necessary, but there's a balance.

28:46

And if there becomes a bacterial overgrowth situation

28:49

where one unhealthy type dominates all the rest,

28:52

the slightest insult to the bowel will let that

28:55

then become submucosal and infecting the bowel.

28:59

And here you can see that it dissects, not

29:02

straight through but along the mucosa of the

29:04

bowel, creating all of this submucosal pneumatosis.

29:07

It can then progress to the serosa

29:10

and create subserosal pneumatosis.

29:12

And, uh, the appearance.

29:14

can often be a thickened bowel, but the tissues themselves

29:17

aren't so much thickened as they are full of gas.

29:20

This happens a lot in the youngest patients, the

29:23

very low birth weight infants, nearly 10 percent

29:25

of them are going to encounter this situation.

29:28

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

29:34

And it happens almost always at 19, or

29:37

I'm sorry, at 29 weeks post menstrual age.

29:40

And the reason I say 29 weeks post menstrual is

29:44

It's the age adjusted age, the gestational adjusted

29:49

age, the premature adjusted age of 29 weeks.

29:53

It is the most common time to get this.

29:54

So if you're born at 29 weeks, you're at high risk.

29:58

If you're born at 25 weeks, Then around four weeks

30:02

after birth is when you're going to be at highest risk.

30:05

So once you've made the adjustment for post

30:09

menstrual age, uh, that's when you can know when

30:12

these neonates, these premature babies are most

30:16

likely to get this super infection of their bowel.

30:19

And what happens is the bacteria, the

30:22

dysbiosis, that's the overgrowth syndrome,

30:25

then takes advantage of intestinal injury.

30:27

And and dissects through the mucosa, which

30:31

has become even transiently ischemic.

30:34

And once it gets below the mucosa it runs between

30:37

the muscularis and the mucosa layers, and that

30:40

bacteria flourishes in there, it creates pockets

30:44

of air, and eventually, it creates progression

30:48

of air into the veins draining the bowel,

30:52

which become the superior mesenteric vein.

30:54

which go back to the liver, of

30:55

course, and become the portal vein.

30:57

And we see this on imaging as portal venous gas.

31:00

And I'll show you examples of this one question.

31:03

You might be wondering, why doesn't this happen in the womb?

31:06

Why doesn't this happen to a 29 week fetus?

31:09

And the simple answer is that the fetus.

31:12

inside the uterus has incredibly protected blood supply.

31:17

Everything about the maternal body protects consistent

31:21

perfusion to the fetus and the placenta almost at all costs.

31:25

So it's only when pregnant women are in a

31:28

terribly ill, maybe near death situation

31:31

that that blood flow gets compromised.

31:33

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

31:37

it's in the neonatal intensive care unit, it's subject

31:41

to fluctuations in body temperature, much more than

31:43

normal fluctuations in respiratory function, much

31:46

more than normal, and blood pressure fluctuations.

31:49

And those fluctuations are what make the bowel

31:52

susceptible to this super infected bacteria.

31:56

So this is what it looks like on radiograph.

31:59

And the most sensitive, in other words, the first thing we

32:02

see, the most sensitive sign of neck is not very specific.

32:06

It's just Focally dilated loops of bowel.

32:09

And here you can see in this, uh, this image

32:13

over here on the left side of your screen,

32:15

you can see a horseshoe shaped loop of bowel.

32:17

And a couple of hours later that same horseshoe shaped

32:20

bowel is there again even though other bowel has moved

32:23

around, and it's still there, about 36 hours later.

32:27

So the first sign is.

32:28

Focally dilated loops of bowel,

32:31

just like you see in this image.

32:33

Oftentimes it's folded over on itself

32:35

in this horseshoe shape configuration.

32:37

That's very sensitive, but of course many different

32:40

things can look like that, including normal bowel.

32:42

So it's not specific.

32:44

What's the next step?

32:45

Well, it stays fixed in that location for quite a while.

32:48

So it's focally dilated.

32:50

Then it becomes fixed in a focally dilated appearance,

32:53

and you'll see maybe one, two, three days in a row,

32:56

this loop of bowel frozen in position and appearance.

33:00

This is suspicious, but still not very specific.

33:04

And then what will happen is, The bowel,

33:08

even though we can't see it, has probably

33:10

already become damaged and is being infected.

33:15

And so we already have necrotizing enterocolitis here,

33:18

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

33:21

The things that everyone always talks about, like

33:23

pneumatosis intestinalis or portal venous gas.

33:26

Those things are coming.

33:28

The bowel is already necrotizing.

33:31

We just haven't seen it yet.

33:33

And all of a sudden it can go from this

33:36

radiograph here, which is certainly not normal.

33:39

It's got some suspicious signs, but none of those

33:42

classic, uh, findings that we're looking for.

33:46

Within a very short period of time, it

33:48

can rapidly progress to a florid case.

33:51

of portal venous gas, which you can see as these thin

33:55

lace like linear branching lucencies all over the liver.

33:58

This is quite extensive.

34:00

And florid pneumatosis intestinalis, which is

34:04

frequently seen as thin linear lucencies just outside

34:08

a thin opaque line, which represents the mucosa.

34:12

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

34:15

mucosa, and then that lucent line is the submucosal gas.

34:20

So we've got pneumatosis intestinalis here,

34:23

and we've got it here, and we've got it here,

34:26

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

34:29

Sometimes it's been described, here's

34:32

some more down here, as bubbly leucencies.

34:35

The problem with the bubbly leucencies.

34:38

A descriptor is that it has a high false

34:40

positive rate because intraluminal foamy

34:44

contents also look like bubbly lucency.

34:46

So for example, this over here kind of looks like bubbly

34:49

lucencies, but it's not pneumatosis and this over here kind

34:52

of looks like bubbly lucencies but that's not pneumatosis.

34:56

So the most Compelling evidence for pneumatosis

34:58

intestinalis is this thin submucosal lucency.

35:02

And this patient is very ill and has extensive

35:06

complications of the breakdown of bowel and

35:09

ended up having extensive amounts of small bowel

35:11

resected, uh, in order to survive this illness.

35:16

Now, what can ultimately happen?

35:17

Well, necrotizing enterocolitis can progress

35:20

to pneumoperitoneum perforation, and not

35:23

just pneumoperitoneum, but also infection and

35:27

abscess formation within the peritoneal space.

35:30

And, uh, this is the sign to the

35:32

surgeons that they need to intervene.

35:34

Many of these infants are quite ill, quite vulnerable.

35:38

They can't go to surgery without

35:39

a significant additional risk.

35:41

So, surgery will be reluctant to take this fragile,

35:45

vulnerable, premature infant to the operating room.

35:48

But once we see frank pneumoperitoneum, that's

35:51

usually the sign that something has to be done.

35:53

Surgery, or if not surgery, at least drain

35:56

placement, uh, and close surveillance.

35:59

And sometimes it's massive.

36:01

This is an example of a, of a patient with necrotizing

36:04

enterocolitis who developed such extensive pneumoperitoneum.

36:08

It's hard to point out where there's Not free

36:11

intraperitoneal air, but often it's more subtle than that.

36:14

And where we add value as radiologists is being

36:17

able to pick up on the subtleties, uh, that

36:20

that sort of describe the earliest signs that

36:24

something has progressed to the complicated phase.

36:27

So here's an image of a patient who had been x rayed

36:30

repeatedly looking for signs of necrotizing enterocolitis.

36:34

And you might squint down here and say, well,

36:37

maybe is there a little pneumatosis down there?

36:40

I don't know.

36:41

There's not really any frank portal venous gas.

36:44

There's this nice lucent stomach over here.

36:46

But for those of you who are looking carefully,

36:49

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

36:51

And remember, almost all portable, uh,

36:54

NICU radiographs are obtained supine.

36:56

So any free air will be non dependent and will

36:59

tend to layer out anteriorly over the abdomen.

37:02

It can be difficult to see.

37:04

But it should raise our suspicion.

37:06

Same thing here.

37:07

This patient is more suspicious because they have definite

37:10

pneumatosis intestinalis, and they also, in addition

37:14

to their gastric lucency, have a vague lucency here

37:18

and a little lucency there and a little lucency there.

37:21

So these are the kinds of things that are very suspicious

37:24

for perforation and, uh, What do we want to do?

37:28

Well, we want to confirm.

37:29

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

37:33

and we rely on the fact that air moves non dependently and

37:36

we want to put it up against a solid organ like the liver.

37:39

So here's that patient again with this suspicious anterior

37:42

lucency, and when we put them in the decubitus position,

37:45

sure enough, it layers between the body wall and the

37:47

liver and this is confirmed pneumatosis intestinalis.

37:51

Uh, once you've seen enough of these cases,

37:52

you may not need the decubitus and you might

37:54

just describe it and, uh, feel confident saying

37:57

this is anterior layering intraperitoneal air.

38:01

But it's never the wrong thing to

38:04

confirm if there's any uncertainty.

38:07

And so decubitus positioning can be really helpful for that.

38:10

Here's another example.

38:12

This is a patient with a lot of bubbly lucencies.

38:16

It turned out all of, almost all of this was foamy

38:19

liquid bowel contents, but a very distinctive

38:22

appearance where we can see the internal margin and

38:26

external margin of the bowel wall quite clearly.

38:29

Sometimes this is called Wrigler's sign.

38:31

Suspicious for free intraperitoneal air, but we're not

38:34

seeing the focal lucency, and so we tried the decubitus

38:38

positioning and sure enough, there's a quite large

38:40

volume of free intraperitoneal air outlining, not just

38:44

the liver, but also the entire right pericolic gutter.

38:47

And this patient needed to go to the operating room.

38:50

Note that on all of these cases, the pneumatosis

38:53

wasn't sufficient to cause portal venous gas.

38:56

So we can go from a relatively mild or

38:59

vague appearance of the complications of

39:01

neck to needing to be in the OR quickly.

39:04

So these patients require careful

39:06

attention and, and some extra scrutiny.

39:09

But what about the patient?

39:11

Who doesn't respond really well to decubitus positioning.

39:14

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

39:18

cubitus and it layers between the body wall and the liver.

39:21

That's great.

39:22

No problem.

39:23

But sometimes we see a vague lucency over

39:26

the mid abdomen, like you can see here.

39:29

And we wonder, is that free intraperitoneal air?

39:32

The patient has risk factors and we put them

39:34

into cubitus positioning and disappointingly,

39:38

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

39:40

Does that mean we're done?

39:42

We were wrong.

39:43

Well, it turns out that that sign of air moving

39:47

non dependent is only reliable in a patient

39:51

with a clean, pristine peritoneal space.

39:55

And I always think of the movement of structures

39:58

within the peritoneum like the movement

40:00

of a piece of plastic on a wet countertop.

40:03

It just glides smoothly.

40:05

All the organs are gliding against each other.

40:08

The bowel and mesentery are gliding against the organs and

40:11

the lining of the body wall with peritoneum is also smooth.

40:17

and gliding.

40:18

But if you have a sick abdomen and remember the

40:21

reason we're following these patients is because

40:24

of suspected necrotizing enrocalitis, you're

40:26

not going to have smooth gliding structures.

40:30

The inside of the peritoneal cavity gets

40:33

very sticky and everything is inflamed.

40:36

Tissues are thickened.

40:38

They don't glide well.

40:39

It's like that piece of plastic on a dry countertop.

40:42

Now it's.

40:43

not moving very well.

40:44

It's stuck together.

40:46

And if you picture a pocket of free intraperitoneal

40:49

air in the middle of the abdomen, and you

40:51

turn that patient to cubitus, it's not

40:53

going to immediately float up non dependent.

40:55

It's going to take some time.

40:57

That air is going to have to work its way through a

40:59

sticky abdomen all the way to the non dependent location.

41:02

So I always say, if my suspicion is strong and the

41:06

initial decubitus film doesn't satisfy my suspicion for,

41:10

uh, for to be extra safe, I do a 15 or 20 minute delay.

41:14

I tell the NICU, keep the patient decubitus

41:17

for 15 minutes and then obtain a radiograph.

41:20

And you can see how the immediate decubitus film was

41:23

not very satisfying, but the delayed decubitus shows

41:26

quite clearly that in fact there is a bowel perforation.

41:32

If you don't have the luxury of communicating with

41:35

a team that's going to help you with that, The

41:38

other option is to use the window level feature,

41:40

which we use much more frequently in cross sectional

41:43

imaging, but can be quite valuable in radiographs.

41:46

And all of a sudden, um, a pocket of free

41:48

intraperitoneal air layering anteriorly, that is

41:51

challenging to see on this normally windowed image.

41:54

When we window it much more harshly, now

41:57

you can see the lucency of the free air.

42:00

So that's another tool at our disposal.

42:02

If moving the patient for whatever reason is going to be.

42:06

Uh, a difficulty.

42:08

And there's that pocket of air.

42:09

Sure enough, this patient went

42:10

to surgery and had a perforation.

42:14

So just to reiterate, in these

42:16

cases, we can see a lot of things.

42:19

Focally dilated bowel that's fixed over time.

42:22

We can see free intraperitoneal air.

42:25

We can see a lot of things that we can't see.

42:26

All sorts of abnormal findings, but the most specific

42:30

sign, this is not the early sign, but the most

42:33

specific sign, of course, is pneumatosis intestinalis.

42:37

And that's that thin submucosal linear lucency, just like

42:41

you see outlining this loop of bowel right here, that is the

42:44

most specific thing and essentially there's not much else

42:47

in a premature newborn that can give you that appearance so

42:50

we consider it diagnostic of necrotizing enterocolitis and

42:55

sometimes you'll hear clinicians talk about medical neck

42:58

versus radiographic neck and that always seems a little

43:02

silly to me because There's just necrotizing enterocolitis.

43:05

Either your bowel is infected or it isn't.

43:07

What they mean is, do they have the

43:09

specific signs of neck, or don't they?

43:12

Either way, they have infection.

43:14

And you can call the ICU and they

43:15

know, Oh, this patient's sick.

43:17

Their blood pressure has given us trouble.

43:19

They have body wall edema.

43:21

They have neck.

43:22

We're just waiting to see the signs on x ray.

43:24

And this is, uh, this is essentially,

43:26

what we're adding to that diagnosis.

43:30

What about patients who have abdominal

43:32

challenges without necrotizing enterocolitis?

43:35

Because not every, uh, premature

43:38

neonate develops it, only about 10%.

43:41

And it turns out that one of our best clues of a

43:44

problem in the abdomen, other than massively dilated

43:48

bowel, is calcification because calcification

43:50

is a sign of old healed peritoneal inflammation.

43:54

So this, again, this is not smooth gliding peritoneum.

43:58

This is something that got inflamed and

44:01

thickened and sticky, and then it healed

44:03

and as it scarred down, it calcified.

44:05

So anytime you see calcifications in the peritoneal

44:08

space outlining the body wall or outlining

44:11

an organ or creating a little pseudo cyst.

44:17

lining that, that's a sign that

44:19

there was an inflammatory process.

44:21

Sometimes we jump right to the

44:22

diagnosis of meconium peritonitis.

44:25

And it turns out that the presence of meconium

44:28

in the peritoneal space from a perforated loop of

44:31

bowel is a very common cause of calcification, but

44:34

there are other ways to inflame the peritoneum.

44:36

So no matter what it was, The calcifications point to

44:40

prior inflammation, and we can see the natural progression

44:44

of this if we compare fetal and neonatal imaging.

44:47

So for example, this is a fetal MRI of a patient

44:51

who is seen to have cystic structures in the

44:53

abdomen and here you can see multiple dilated loops.

44:56

of bowel in the fetal abdomen,

44:59

suggestive of some type of obstruction.

45:02

And when we look carefully on the sagittal view, we realize

45:05

that these are actually dilated loops of small bowel, and

45:09

the colon is this tiny collapsed microstructure back here.

45:13

So that suggests that nothing is

45:15

progressing from large bowel to small bowel.

45:18

And on this final frontal view, we

45:20

can again see the dilated loops.

45:23

of bowel that are this intermediate signal

45:26

intensity as compared to these less dilated

45:28

loops that are brighter signal intensity.

45:31

And the way it works is the more recently swallowed

45:34

amniotic fluid maintains its hyper intense.

45:38

signal.

45:38

And as the fluid progresses through the bowel, especially

45:42

fluid that's sitting within obstructed bowel, it

45:44

becomes less hyper intense and more intermediate signal.

45:48

And that's a sign that this fluid

45:49

has been sitting around for a while.

45:51

So on ultrasound imaging of this not yet

45:56

delivered fetus, you can see this echogenic

45:59

strongly shadowing structure within the abdomen.

46:03

And then on subsequent fetal MRI, you can see that

46:06

there's a focal cystic structure in the anterior

46:09

abdomen and conglomerated bowel and mesentery behind

46:13

it with a large amount of ascites surrounding it.

46:16

That's the T2 weighted sequence.

46:19

the steady state, the single shot

46:21

fast spin echo sequence, I should say.

46:23

This is the gradient echo, which is showing susceptibility

46:27

all around the rim of that cystic structure.

46:30

That lets us know that there's

46:32

either blood or calcium around it.

46:34

And then here on the T1, we can see that

46:36

it's filled with T1 hyper intense signal,

46:39

which is the classic appearance of meconium.

46:41

So this by all fetal imaging is likely meconium.

46:45

pseudocyst from a case of obstruction that

46:49

progressed to ruptured bowel that progressed

46:52

to pseudocyst formation and calcification.

46:55

And after birth, here is that patient's

46:58

pseudocyst completely calcified and notice how

47:02

all the loops of bowel are clumped together and

47:05

conglomerated just under that calcified pseudocyst.

47:07

So this is a patient that required surgical

47:10

exploration and in fact there was a closed loop.

47:14

obstruction that had perforated and then sealed off

47:17

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

47:20

And this patient required ostomy formation

47:22

and then a subsequent re anastomosis.

47:27

Here's an example of a patient

47:28

with this very unique appearance.

47:31

almost like a folded appearance of calcification, a thin rim

47:35

of calcification lining the entire lower peritoneal space.

47:39

And this is a patient who had had a perforation.

47:41

You can see there's very little gas

47:43

in the abdomen except proximally.

47:45

And that perforation had never healed off properly.

47:49

So it had just spilled a lot of bowel contents.

47:52

This premature infant had a large amount of

47:56

complex societies, which had to be drained.

47:59

And ultimately the bowel had to be re anastomosed.

48:03

And here's an example of a patient again with

48:06

abnormal dilated bowel, no distal rectal gas.

48:10

And little elements of calcification here, all

48:13

pointing to the fact that not only is the bowel

48:15

obstructed, but it's been previously perforated.

48:18

And by the way, this is not the same thing

48:20

as identifying, you know, complex fluid with

48:23

ultrasound, which might suggest an acute perforation.

48:26

If there's calcification, you know that

48:28

something's been going on for a while.

48:31

This is subacute to chronic.

48:33

It's always a little silly to say chronic

48:34

in a premature newborn because they haven't

48:36

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

48:41

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

48:44

cases of either obstruction or necrotizing enterocolitis,

48:47

we can assess how the fluid balance, and overall, Vitality

48:53

of the patient are faring by looking at the tissues and just

48:57

notice what a dramatic change in the body tissues of the

49:02

chest wall and the flank coming down early after intubation.

49:07

In a patient, you can see dilated bowel.

49:09

They ended up having an obstruction and um, a perforation.

49:15

To post operatively, this patient has

49:18

developed massive body wall edema.

49:20

It almost doesn't look like the same patient.

49:22

And this can be a really important sign of

49:25

the morbidity of our patients in the NICU.

49:28

And it can be important for us to kind

49:30

of track whether there's increasingly

49:32

progressive or resolving body wall edema.

49:37

And just for the final phase of this lecture, I

49:39

want to review what we can see in the brain and

49:43

brain imaging, of course, is going to be ultrasound.

49:46

For those who are too sick to be moved to cross sectional.

49:49

So, remember that the brain goes from having almost

49:52

no, uh, complex surface development to increasingly

49:57

convolutional gyri and sulci from the fetal

50:01

period to the neonatal period to the adult period.

50:04

And most of the change in complexity occurs

50:07

between second trimester and newborn.

50:09

That's right where we're going to

50:10

be delivering premature babies.

50:12

And then the changes between.

50:15

Child and adult have more to do with size and internal

50:19

development as opposed to gyration on development

50:24

and on fetal imaging we can see that complexity by

50:27

measuring the Sylvia and Fisher which starts out as

50:29

just a little dimple and then becomes increasingly.

50:32

complex and insulated, hence our

50:35

use of the phrase, the insula.

50:36

And, uh, the insular brain is not yet insulated in

50:40

a very young 20 week, uh, fetus, but becomes, um,

50:43

the normal characteristic Sylvia and fissure in a

50:46

term infant, same parents down here on ultrasound.

50:50

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

50:53

So look at the complexity as indicated by

50:56

these echogenic markings showing us it.

50:59

tissue interfaces of the sound wave hitting the

51:03

fluid and the surface of the brain and the parenchyma

51:06

of the brain and creating all these echoes.

51:08

This is a near term infant.

51:10

Here's a premature infant and an extremely premature

51:13

infant and notice how the central cerebral parenchyma

51:16

is quite echogenic in this premature infant and there's

51:19

very little complexity to the surface of the brain.

51:21

This is not disease.

51:23

This is just the normal immature brain.

51:26

And this is the normal appearance of the lateral

51:28

ventricles and the caudal filament groove, which

51:31

is where we focus a lot of our attention right

51:33

between the head of the caudate and the thalamus.

51:35

That's where the ganglionic eminence, the germinal

51:38

matrix so called originates all the gray matter

51:41

that migrates out to the surface of the brain

51:43

starts there, and it's highly perfused with this

51:46

capillary bed that doesn't have much structure to it.

51:48

So it's just a bunch of capillaries

51:50

without anything protecting them.

51:52

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

51:54

prematurely, it hasn't involuted yet, and it's very

51:57

susceptible to those fluctuations of blood pressure,

52:00

just like we were talking about earlier with the gut,

52:04

something that would have been protected and insulated

52:06

intra uterine, once you're outside, you're much more

52:10

susceptible to fluctuations and that causes hemorrhages.

52:13

So we look for.

52:15

Echogenic material accumulating

52:17

in that caudophylamic groove.

52:18

This is a grade one intraventricular hemorrhage.

52:21

There's one again in the left caudophylamic groove that's

52:24

got some central hypoechoic appearance, which means

52:27

it's older, it's evolving, the blood is organizing.

52:30

There it is on the sagittal view, tucked right into that

52:33

space between the head of the caudate and the thalamus.

52:37

And then as it enlarges into the

52:39

ventricle, it goes up in grade.

52:41

And the important distinction is a grade one hemorrhage.

52:44

is difficult to see, but is not considered

52:47

sufficiently morbid to stop any anticoagulation.

52:51

And the most common reason in a sick premature

52:53

baby would be as if that neonate is on ECMO.

52:57

If they're on ECMO, they have to be anticoagulated.

53:00

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

53:03

anything more severe than a grade one, It's contraindicated

53:06

to anticoagulant so you're between a rock and a hard place.

53:09

Do I want this child to risk bleeding in their

53:12

brain or do I want them to not get enough oxygen

53:15

for life, because we can't put them on ecmo

53:17

these is a terrible choice we have to make.

53:20

But typically, people will say grade one.

53:22

We'll keep ECMO grade two, we need to

53:24

stop ECMO because we stop anticoagulation.

53:27

And here you can see increasing amounts of blood

53:30

filling the ventricle, now expanding the ventricle.

53:33

So this is a grade three hemorrhage, where you've got blood

53:36

visible in the ventricle and the ventricle is enlarged.

53:39

A little bit on the other side as well in this image,

53:42

and then appearance of both acute and chronic so

53:46

this is a grade three hemorrhage with these organized

53:49

spaces and also some new blood with the ecogenic

53:52

material is, and ultimately if you get enough.

53:55

Expansion of the ventricles

53:57

because of intraventricular blood.

53:59

There's a bunch of veins draining just

54:01

under the ependymal lining of the ventricle.

54:03

And if those get compressed, you get ischemia in the

54:06

adjacent brain because of impaired venous drainage.

54:09

And you develop a grade four,

54:11

an intra parenchymal hemorrhage.

54:13

So that's the severest kind.

54:15

You can also have changes to the brain without hemorrhage.

54:18

And this is an example of ischemic injury.

54:21

Okay.

54:21

In the periventricular white matter, it's sometimes

54:24

confused with the normally echogenic appearance.

54:26

So this image with two arrows is a normal

54:28

brain without ischemia, and you can see

54:31

symmetric echogenicity around the ventricles.

54:34

But on this other image, you

54:35

can see asymmetric echogenicity.

54:37

How can we tell the difference?

54:38

This can be challenging, but I think it's useful to use two

54:42

rules, heuristics, I guess you could say, rules of thumb.

54:45

One.

54:46

Is the echogenic area of the brain as bright

54:49

as or brighter than the choroid plexus?

54:52

And in this patient, I would say, yes, it's as bright

54:54

as or brighter than the adjacent choroid plexus.

54:57

Over here in this, what I know to be normal brain,

55:00

it's not, it's not as bright as the choroid.

55:03

And then my second rule of thumb, can I draw a

55:06

line around where I think the ischemic area is?

55:10

And right here, I feel like I could take

55:11

a pencil and trace the outline of this.

55:15

echogenic injury, this periventricular leukomalacia,

55:18

whoops, but over here, these are too vague.

55:21

They just kind of fade out into the surrounding parenchyma.

55:24

This is an injured, this echogenic asymmetric area is

55:28

going to eventually lead to some infarction and that

55:31

infarction is going to eventually die and disappear

55:35

because we know that the brain liquefies with necrosis

55:38

and then it just becomes absorbed by the ventricle.

55:41

So it becomes ex vacuo dilatation.

55:43

Here you can see that little expanded part of

55:46

the ventricle from periventricular leukomalacia.

55:49

In the last couple of minutes I just want to show a couple

55:52

of examples of both normal and abnormal extra axial blood.

55:56

Premature infants will frequently have extra axial fluid.

56:00

But it's subarachnoid fluid and we call it

56:03

benign because we see normal fluctuations,

56:06

especially in premature infants and newborns.

56:09

And, uh, the way we can tell that it's benign.

56:13

Subarachnoid is the presence of vessels traversing the

56:17

space between the cerebral parenchyma and the skull.

56:21

And on Doppler here, you can see

56:22

there are vessels coursing between.

56:24

So even though there's a prominent amount of

56:26

extraxial fluid here, we can feel pretty confident

56:29

that this is likely benign subarachnoid fluid.

56:32

Not so in this case.

56:35

Here you can see that there's all this material

56:38

just above the superior sagittal sinus and

56:40

the surface of the brain, but it's echogenic.

56:43

And it's different than the subarachnoid space

56:46

on this image you can see there's a little simple

56:48

subarachnoid fluid, and there's this much more

56:51

prominent ecogenic material outside the brain.

56:54

So this is unfortunately subdural blood, pretty

56:57

uncommon, but in very traumatic deliveries.

57:01

patients can get, um, you know,

57:03

subdural and even epidural hematomas.

57:06

So there's some blood here from a traumatic

57:09

delivery and these patients, even more common than

57:12

blood, um, in those spaces is blood on the scalp.

57:16

So like a cephalohematoma or less

57:18

frequently a subgaleal hematoma.

57:20

And, uh, here we've got a sagittal image.

57:22

This is the echogenic line for the skull.

57:25

And here is a hematoma under the scalp,

57:28

and you can see the contour abnormality.

57:30

And this is probably the most

57:32

common finding in birth trauma.

57:35

So just be aware of the differences there.

57:37

Subarachnoid fluid, less concerning, but

57:39

subdural or even rare epidural fluid is,

57:42

is more concerning, uh, in these neonates.

57:46

So I'm going to round out this lecture.

57:48

We're at the end of our time and

57:49

I just a few take home points.

57:51

I know that we've all seen chest x rays and KUVs and

57:54

it's easy to blow through them, but remember that

57:56

all premature lungs are going to have barotrauma.

57:58

So really scrutinize for that.

58:00

It's just a matter of how much barotrauma.

58:02

Second, don't be afraid to wait.

58:05

If you're suspicious of intraperitoneal air, give

58:07

it a delay to prove that it's there because that

58:10

sticky abdomen can make it hard for the air to move.

58:13

Number three, Neck evolves quickly and you can

58:16

go from dilated bowel loops without specific

58:19

signs to florid, you know, portal venous gas

58:23

and perforation and it can happen within hours.

58:27

Um, intraventricular hemorrhage is important not just

58:30

because of what it can do inside the ventricles but that

58:33

compressed venous drainage just outside the ependyma.

58:37

puts at risk that periventricular brain, and that's

58:40

what's going to have the greatest long term morbidity.

58:43

And finally, remember to look, if you see extraxial

58:46

fluid, look for vessels to reassure yourself that

58:49

it's the more benign, uh, subarachnoid location.

58:53

Thanks very much, everybody, for your attention.

58:56

I do have a few minutes, um, that we can

58:58

talk about questions, if there are any.

59:02

It does look like we have a few

59:03

questions in the Q and a function.

59:06

Okay.

59:07

Uh, question here is there benign

59:11

pneumatosis intestinalis in neonates?

59:13

And the answer is yes.

59:15

Uh, typically when we see submucosal pneumatosis, that's

59:20

at risk of perforation and causing necrotic bowel.

59:23

But if there's sub cirrhosis, if the air is on the

59:26

outside of the bowel, that's the benign version.

59:29

We don't see it very frequently, and it's easy to confuse.

59:33

So there are cases, especially infants with large steroid

59:37

therapy, who can get benign subserosal pneumatosis.

59:40

But I usually err on the side of caution.

59:42

And I'm willing to call it benign and leave it alone

59:45

in a teenager, but in a premature newborn, More often

59:48

than not, I continue my surveillance very closely

59:51

because I'm not always as confident I can tell

59:54

the difference between submucosal and subserosal.

59:58

Um, our next question, what intervals are x rays to

60:02

be taken in a sixth child and do I have a protocol?

60:05

Um, you know, we don't use protocols quite as much except

60:08

to say that Um, we do a lot of lateral imaging when we're

60:12

looking at lines and tubes, so frontal chest radiograph,

60:15

frontal abdominal radiograph, or very commonly in a newborn,

60:19

we do chest and abdomen altogether, like you saw in some

60:22

of my examples, but don't be afraid to do a lateral.

60:25

Usually we talk about laterals when we're looking

60:27

for pneumonia in older children and adults, but in

60:29

neonates, it can be very helpful to look at umbilical

60:32

catheters and to look for free air and other things.

60:35

Um, at what intervals?

60:37

I think that people are starting to get away from the

60:40

routine, daily portable chest x ray wherever possible.

60:44

That's not to say it doesn't happen, but there's no evidence

60:48

suggesting that every patient needs a chest x ray every day.

60:52

On the other hand, if the patient is sick and you're

60:54

seeing rapid development of pneumatosis and they

60:58

have body wall edema, I'll do x rays every six hours.

61:01

So it really depends on the patient.

61:03

If the patient's sick and unstable,

61:05

then I like to tailor my protocol.

61:07

to them.

61:08

But as a routine matter, just because

61:09

you're in the ICU, we don't believe that

61:12

you need to get an x ray every single day.

61:14

And we've been trying to get away from that.

61:18

Someone's asked what is ECMO?

61:19

ECMO is extra corporeal membrane oxygenation.

61:24

And basically, we only use it in the most

61:26

dire circumstances for really sick patients.

61:29

And it's kind of like artificial heart lung bypass.

61:32

We take all the blood out of the body.

61:34

We put it through the machine, we

61:36

oxygenate it, then we put it back in.

61:38

You can do it with catheters in the artery and the

61:41

vein, usually neck, so that's veno arterial, but

61:45

you can also do it using two veins, veno venous.

61:48

And in both cases, it does the job of

61:51

getting oxygen in the blood, but at a cost.

61:54

Very much increases your risk for thrombosis.

61:58

and clot formation and hemorrhage because

62:01

you're taking the blood out, you're running it

62:03

through, uh, you know, an artificial machine.

62:04

So we have to anticoagulate a lot of these patients

62:07

hemorrhage as a result of the anticoagulation.

62:11

Uh, someone's asked if I prefer decubitus

62:13

or lateral shoot through for catheters.

62:15

I like the lateral shoot through because I want

62:18

to know where the catheter is antero posteriorly.

62:21

But for air, I find it much more useful

62:24

to push that air against the liver.

62:26

So I like to turn the body into a lateral decubitus.

62:30

So cross table lateral for catheters,

62:33

lateral decubitus for for air.

62:36

Um, does laparoscopy help in suspected neck?

62:39

You know, our surgeons don't do that, and it's

62:42

for the reason that I suggested earlier, the

62:44

morbidity from surgery is sometimes worse than

62:48

the morbidity from necrotizing enterocolitis.

62:51

So we don't do laparoscopy unless we're, we've

62:55

gone from suspected neck to confirmed perforation.

62:58

Otherwise, we try not to operate because

63:00

the evidence that we have suggests it does,

63:03

um, in many cases more harm than good.

63:06

And someone says your subdural appeared to cross midline

63:10

superior to the sagittal suture was this epidural.

63:12

Absolutely yeah that patient turned out to have both

63:15

subdural and epidural blood, and normally, I would

63:19

really caution people to not describe epidural blood.

63:23

In a newborn, that's just who hasn't had some sort of,

63:26

you know, fall or head injury, but in rare traumatic

63:30

deliveries, especially where forceps and suction is used,

63:34

that doesn't happen as often as it used to, but it can

63:37

be sufficient to cause epidural hematoma, a good pickup

63:41

does prone positioning help immature lungs ventilate.

63:44

You know, this is really interesting.

63:46

A lot of critical care doctors is believe

63:48

that prone positioning does help, and I

63:50

think there's some evidence to support that.

63:52

I'm not a critical care physician myself, so take

63:55

what I say with a grain of salt, but what we've

63:58

seen in our imaging is that it can help, but

64:02

what helps even more is change in positioning.

64:05

So we have these patients often get rotated, and

64:10

we end up using the jet ventilator, which is going

64:12

to put in smaller volumes of air much more rapidly.

64:15

So instead of maybe like a

64:20

It's going to be

64:23

and the idea is to do anything we can to gently pop

64:26

the lungs open too much trauma and we get the damage.

64:32

Well, it looks like we've concluded all of our questions.

64:35

Thank you all very much for your attention.

64:37

I appreciated the opportunity to speak with

64:39

you and hopefully we'll do it again sometime.

64:42

Yeah, and thank you

64:43

Dr. Brown for this lecture and thanks to all of

64:45

you for participating in our noon conference.

64:48

Just a reminder to everyone that this conference

64:50

will be available on demand on MRIonline.

64:53

com in addition to all previous noon conferences.

64:57

Be sure to join us again on Friday for a lecture from Dr.

65:01

Borani on Imaging Evaluation of Living Liver Donors.

65:06

You can register for that at MRIonline.

65:09

com and follow us on social media at The MRI Online

65:14

for updates and reminders on upcoming new conferences.

65:17

Thanks again and have a great day.

65:19

Bye bye.