0:02

Hello, and welcome to Noon conferences hosted by MRI Online.

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In response to changes happening around the world

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right now and the shutting down of in-person

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events, we've decided to provide free daily

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noon conferences to all radiologists worldwide.

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Today we're joined by Dr. Glynis Sacks, who is

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a radiologist, primarily interested in obstetric

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and gynecologic ultrasound, and a professor of

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clinical radiology at Vanderbilt Medical Center.

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A quick reminder, there'll be time at the

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end of the hour for a Q&A session.

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Please use the Q&A feature to ask your questions,

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and we'll get to as many as we can before our time is up.

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We'll be using the polling feature today, so be on the

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lookout for that, and a reminder that the polling window

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can be moved on your screen if it's blocking something.

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That being said, thank you so much

0:44

for joining us today. Dr. Sacks,

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I'll let you take it from here.

0:47

Good morning.

0:48

Um, I am going to be discussing, um, an approach to

0:52

fetal anatomic evaluation in the second trimester.

0:55

And that's obviously a very, very broad topic, but it's just

0:59

the way I approach fetal anatomy and the way we sort of come

1:03

to the conclusion about what the likely, uh, problem is.

1:05

When we do encounter abnormalities, when

1:09

we're looking at fetal anatomy, it's really

1:10

important to recognize that there is.

1:13

An interconnection between the different systems that we're

1:16

looking at, and we can really get good clues as to what's

1:19

happening in the spine by looking at the head, what's

1:21

happening in the abdomen, but while looking at the chest.

1:24

So we have to kind of think about

1:26

that altogether while we are looking.

1:28

And I'll start by evaluating the fetal head,

1:30

which is the first thing we usually look at.

1:32

And there's a kind of checklist as

1:34

to what I look at in order to confirm, to

1:37

actually confirm that everything is normal.

1:39

So starting off with the premise that there

1:41

may be a problem, we kind of confirm normal

1:44

rather than con evaluating for abnormal.

1:47

So the first thing would be looking at the

1:48

cranium, and you really want to make sure that it's

1:50

there, but also look at the shape of the cranium.

1:54

The next thing we look at is the lateral ventricles.

1:56

Evaluating the size of the lateral ventricles,

1:58

which should not be more than 10 millimeters in, um,

2:01

diameter, and then should be filled with Choroid Plexus,

2:04

which you can see as this white area which should

2:07

actually fill the, uh, body of the lateral ventricle.

2:10

The next thing we look at is the posterior fossa,

2:13

where mainly looking at the cerebellum, which

2:15

should have this dumbbell figure-eight shape, and

2:18

measuring the cerebellum in the second trimester, the

2:20

cerebellar diameter, millimeters, should equal the weeks.

2:23

And then we look posterior to the cerebellum, where there

2:26

is the, um, cisterna magna, which should measure between,

2:30

usually measures between four and seven millimeters, but

2:33

the normal range would be between two and 10 millimeters.

2:36

Um, the cavum septum pellucidum is an important structure to

2:40

identify, which we see as the sort of empty box or equal

2:43

sign, and that develops together with the corpus callosum.

2:46

So seeing the cavum septum pellucidum kind

2:49

of reinforces or gives us confidence that there

2:52

is no total agenesis of the corpus callosum.

2:54

And then lastly, we look at the thalami,

2:56

which to me look kind of like an arrow, uh,

3:00

pointing posteriorly that we see over there.

3:02

So again, when you're scanning, going slowly through the

3:05

head in this image, we can nicely see a normal shape to

3:10

the, um, head with lateral ventricles filled with choroid.

3:14

Then we can clearly see the cavum septum pellucidum, the

3:16

normal thalami, the normal cerebellum, and the normal cisterna magna.

3:23

the.

3:24

Most catastrophic cerebral, um, abnormalities we're going to

3:27

see is the anencephalic fetus, where there's total absence

3:31

of the cranium and what we call the frog-like faces where

3:34

we just see the orbits and nothing developing above that.

3:38

Obviously a, a extremely, um, traumatic patient

3:43

for patient in with this lethal anomaly, but not

3:46

something that can be missed on ultrasound at all.

3:50

This is the first case that I'm going to be polling for

3:52

answers, but this shows you, um, and I've got two

3:55

images to show the, um, fetal head in this fetus.

3:58

So here we, we see this image going through

4:02

the region of the lateral ventricles.

4:05

This is kind of an oblique image looking at the posterior

4:07

fossa, and again, looking at the lateral ventricles, which

4:10

measure just above where we would like, 10.3 millimeters.

4:16

Um, kind of concentrate on the cranial

4:18

configuration and the posterior fossa.

4:22

And if you would start with your, your answer suggestions.

4:26

Um, these are the four, um, possibilities I've included.

4:29

What do you think the diagnosis is?

4:35

Well, that was a classic example

4:37

of a Chiari II malformation.

4:40

Oh, sorry.

4:42

Which I can see.

4:44

Most of you actually got right.

4:46

Um, and we can see here when we, we look at

4:52

the spine, we can see the spinal defect, but—

4:57

I'm trying to go back.

5:00

So here this is the classic lemon

5:02

configuration to the cranium with the

5:04

banana configuration to the posterior fossa.

5:07

And the way I think about, um, Chiari II malformations is

5:10

when you have a neural tube defect, every, everything gets

5:13

kind of tethered down or pulled down at the sites of the.

5:16

So your cerebellum herniates posteriorly

5:19

and effaces the cisterna magna and

5:21

assumes the shape of the occipital bone.

5:23

And that would give you the classic

5:25

banana configuration to the cerebellum.

5:27

You have less brain anteriorly, so your

5:30

frontal bones are going to cave in, which

5:31

gives you your classic lemon configuration.

5:34

So this is a classic example of a, uh, Chiari

5:37

II as a result of a neural tube defect.

5:39

I think what this shows you is that the spinal defects

5:42

are not quite as obvious as one would think, and you

5:45

have to look really closely in order to see them.

5:48

But here we see the splaying of the pedicles with

5:51

the, um, exposed meningomyelocele in this patient.

5:56

So it's almost always associated with neural

5:58

tube defects with a small or usually obliterated

6:01

cisterna magna giving rise to the banana sign

6:04

or banana configuration to the cerebellum.

6:07

The frontal bone concavities, which would be the lemon

6:09

sign, and often ventriculomegaly, which is usually mild.

6:14

Uh, this would be to contrast with

6:18

the normal appearance to the head compared

6:20

with the lemon configuration to the head.

6:23

Here the banana configuration to the posterior fossa

6:29

in a second fetus with a different neural tube defect.

6:33

Obviously when we are talking about, um, looking at the

6:37

head, we're really looking at to see are there any, is

6:41

there any indication there could be a spinal defect?

6:44

How do we evaluate the spine?

6:45

We can look at the spine in sagittal view.

6:48

In coronal, which we see here, coronal reconstruction on

6:51

3D, or in an axial plane, which is the probably the best

6:56

way to look at the spine, but the hardest to document.

6:59

So that's how we would evaluate the normal spine.

7:01

In all those three views, this would a fetus

7:04

with a kyphoscoliosis, which we can clearly

7:07

see on these, um, sort of oblique or, or.

7:10

Sagittal and oblique coronal views.

7:13

So kyphoscoliosis, the longitudinal views are going to be

7:15

best with coronal for scoliosis and sagittal for kyphosis.

7:19

Isolated vertebral anomalies are definitely

7:21

a cause, but a more rare cause, which would

7:23

be the hemivertebra, butterfly vertebra.

7:26

But there's almost always, in the vast majority,

7:28

of cases, associated anomalies, either spina

7:30

bifida or as a component of the VACTERL association.

7:35

In this fetus with a neural tube defect, we clearly

7:38

see the lemon sign, but here, when we look at the

7:40

sagittal view of the spine, we can see the intact skin

7:43

covering, and then we completely lose the skin covering.

7:47

Here on 3D reconstruction, you can see

7:49

this almost exposed, excavated type defect.

7:52

So the spina bifida classification would

7:54

include the meningocele, which contains the CSF

7:57

fluid only, the meningomyelocele, which would

8:00

contain the neural elements as well as the CSF.

8:03

And then what we see in this patient, the myelo-

8:05

schisis with exposed neural tissue, but no sac.

8:10

It's always important, um, if we see something

8:12

extending from the distal spine to consider the

8:14

possibility that this represents a sacrococcygeal teratoma,

8:18

and not a, uh, component of a meningomyelocele.

8:21

And in this fetus with a large sacrococcygeal

8:24

extending from the, uh, distal sacrum,

8:27

if you extending from the distal sacrum.

8:29

If you have any question, go and look at the head.

8:32

This fetus has a completely normal intracranial

8:35

evaluation with a normal cranial configuration.

8:38

No evidence of the lemon sign, normal posterior fossa,

8:41

normal cerebellar size, normal cisterna magna.

8:44

So we can, we know that this is not a, uh, a spina

8:47

bifida, but this is in fact a sacral teratoma.

8:51

Sacrococcygeal teratoma is an exophytic mixed cystic

8:54

and solid mass extending from the sacrum.

8:57

The size is variable, but they often vary,

8:59

large with rapid growth potential, and they

9:02

can extend into the fetal pelvis or abdomen.

9:04

The AV shunting may be significant, which

9:07

really is a significant risk for hydrops

9:09

with polyhydramnios, and the prognosis is very

9:12

poor in those fetuses that develop hydrops.

9:15

It's one of those abnormalities that really has to

9:18

be detected in utero for a good fetal outcome because

9:21

if we know that it exists in utero and a C-section is

9:24

done, many of these babies do very well with surgery.

9:27

But if it's missed during the, um, antenatal period and

9:31

a, uh, vaginal delivery is attempted, there are often major

9:34

issues, and usually death results from exsanguination

9:37

because you cannot deliver the large sacrococcygeal mass.

9:43

Now we're going to, uh, move to the second case.

9:45

And again, I have two slides.

9:47

So this would be the first image,

9:52

and this is the, uh, second image.

9:58

And I'm including the same four

10:00

possibilities as to the diagnosis.

10:05

And as again, as most of you saw, this is a Dandy–

10:08

Walker with a large posterior fossa cyst, completely,

10:12

really absence of the, um, of the cerebellum, with the

10:17

ventricles, with large ventricles, with dangling choroid.

10:21

Hallmark features would be cystic dilatation of

10:23

the fourth ventricle in a large posterior fossa with

10:25

tentorial elevation, complete or partial agenesis of

10:28

the cerebellum, with associated hydrocephalus in most

10:32

of the cases, and aplasia in about half the fetuses.

10:36

It's also important to recognize cerebellar hypoplasia

10:41

as an isolated entity, where, which we see like in

10:44

this fetus, where you can see a small cerebellum,

10:48

sort of this rectangular configuration, normal, uh,

10:51

normal-looking cisterna, no posterior fossa cyst, but

10:54

the cerebellar diameter should equal, in millimeters,

10:56

the weeks at, at 20 weeks.

10:58

This was a 16-millimeter, um, hypoplastic cerebellum.

11:02

And this fetus, uh, when karyotyped was a mosaic,

11:05

uh, Turner, triple X. Cerebellar hyperplasia may involve

11:09

the vermis, the hemispheres, or the entire cerebellum.

11:12

MRI is useful for evaluation.

11:14

If there's any question on the ultrasound, uh,

11:16

it can be seen with aneuploidy, as we saw in the

11:18

fetus, or in a variety of syndromes if isolated.

11:22

The neurologic consequences are variable, but stable.

11:26

And then, to close out the sort of major anomalies

11:29

that we can see, um, in the central nervous system,

11:32

here we see an example of an encephalocele, which

11:35

would be characterized by a defect in the skull

11:37

with protrusion of the intracranial structures.

11:40

Uh, ventriculomegaly in about 70 to 80% of cases

11:42

and microcephaly in about 25% of cases, obviously,

11:46

depending on how much brain is herniated.

11:50

Um.

11:51

Is really going to determine what the likely outcome is.

11:54

In a fetus like this, with a large defect and protrusion

11:58

of a significant amount of, uh, brain tissue, you've got

12:01

a very poor prognosis, um, with significant microcephaly.

12:04

If there is a, a smaller defect with protrusion of

12:07

only meninges, then sometimes the babies do very well.

12:12

Um, now move on to evaluation of the fetal heart,

12:14

and obviously we always start with the four-

12:17

chamber view of the heart, which is kind of our

12:19

mainstay of looking.

12:21

Um, anytime you're evaluating the fetal heart, I think

12:24

it's important to get, look at a, a, uh, static cross-

12:26

section of the chest and work out which chamber is which.

12:29

The way I do it is identify the fetal spine and

12:32

aorta, and your, uh, right ventricle, which is going to

12:36

be your most anterior structure, and your left atrium,

12:39

which is going to be your most posterior structure.

12:41

Here we see left ventricle, right ventricle, mitral

12:44

valve, tricuspid valve, which should be offset.

12:47

Intact interventricular septum,

12:49

intact interatrial septum and foramen.

12:52

So perfectly normal four-chamber view of the heart.

12:55

Um, in addition to the, um, four-chamber view

12:58

of the heart, it's important to look at the, uh,

13:01

right ventricular and left ventricular outflow

13:02

tracts, and to confirm that what you're looking at

13:05

is, in fact, the right ventricular outflow tract.

13:07

It's always important to document the bifurcation.

13:11

So we are moving to the third case and, uh, again,

13:14

I have two slides showing this abnormality.

13:16

I'll start with the four-chamber

13:17

view of the heart, which we see here.

13:24

Motion.

13:25

And

13:29

this would be a, um, and this is a classic

13:33

example of hypoplastic left heart syndrome.

13:35

Where there was no question about the, um,

13:38

abnormal four-chamber view of the heart.

13:43

So here, when we look at the four chambers, so we

13:45

identify aorta, this would be left atrium, left

13:48

ventricle, right ventricle, and right atrium.

13:52

When we look at the contractility, you can

13:54

see not only is the ventricle really small,

13:57

but the wall is really very, very white.

14:00

And that's a very important, um, finding that

14:02

we see in hypoplastic left heart, which is

14:05

something called endocardial fibroelastosis.

14:08

And when we look at the, um.

14:10

Image with the flow, we can see there is

14:12

only flow on the right side of the heart.

14:14

So again, classic example of hypoplastic left

14:17

heart syndrome characterized by the abnormal

14:19

four-chamber view, a small or non–apex-forming

14:22

left ventricle, echogenic

14:24

left ventricular endocardium.

14:26

Um, representing the endocardial fibro-

14:28

elastosis, poor left ventricular function.

14:31

The interatrial septum will be bowed to the left

14:33

because of the reversed flow across the foramen,

14:36

and there'll sometimes be a large right ventricle.

14:41

Um, and now another unknown in terms of cardiac, the image.

14:45

This image here on the bottom is for

14:46

normal, a normal comparison, and actually

14:49

it's labeling the different chambers.

14:52

So this would be the abnormal.

14:55

Um, and what do we think it is?

15:01

I'm glad to see the majority of people

15:05

recognize this as an Epstein's anomaly.

15:10

And so here we see aorta, left atrium, left ventricle.

15:15

In the left ventricle, we see this little white dot,

15:17

which is called an echogenic intracardiac focus.

15:20

It's calcification in a papillary muscle.

15:23

It can be a soft marker for Down syndrome.

15:25

Um, if multiple and bilateral, can be seen

15:27

with trisomy 13, but it's really, um.

15:31

Usually an incidental finding, but this is a

15:33

classic example of Epstein's, where we see downward

15:36

displacement of the tricuspid valve with atrialization or

15:40

incorporation of part of the, um, right ventricle.

15:46

Um, the baby kind of flipped over for us, so

15:48

we can see how it, in this view, we can see

15:51

the mass of right atrium here in this image.

15:53

The mass of right atrium on the

15:55

other side, it classically shows, um.

15:59

Epstein's anomaly.

16:00

So as I said, it's apical displacement of the septal and

16:03

posterior tricuspid valve leaflets with atrialization

16:06

of the right ventricle and marked dilatation of

16:08

the right atrium associated with tricuspid, uh,

16:12

regurgitation and a functionally small right ventricle.

16:17

I am going to just show you a couple of cardiac cases.

16:19

Um, now, and this was an example of when

16:22

anytime you're doing a cardiac evaluation, it's

16:25

always really important to determine situs.

16:27

So we start out and make sure that the heart

16:29

is on the left, as we see here, and then move

16:31

directly into the abdomen to confirm under normal

16:34

circumstances that the stomach is on the left as well.

16:38

But we see in this fetus that the heart is on the, um,

16:42

left, but the stomach is on the right.

16:45

So this is a fetus with situs inversus.

16:48

Um, we know that, um, when we have heterotaxy,

16:52

there is a very high incidence of cardiac anomalies.

16:55

So we have to look really carefully at the heart,

16:56

and actually the four-chamber and the outflow

16:59

tracts look pretty normal.

17:01

But what we notice is, instead of just seeing

17:03

the aorta, we see two vessels, a double vessel.

17:07

That's because the most common anomaly

17:09

you're going to see with, um, heterotaxy is

17:11

an interrupted IVC with azygos continuation.

17:14

So instead of just seeing the aorta, we

17:16

are seeing the azygos as well as the aorta.

17:19

So that's, this would be, again, for contrast,

17:21

you can see just a nice, normal single aorta.

17:24

So it's, it's a, anytime we see that,

17:27

it's kind of a really easy thing.

17:28

You look at the heart and just look behind

17:30

and see if you see two vessels, right?

17:32

But then one.

17:33

You know, you're dealing with an

17:35

interrupted IVC with azygos continuation.

17:39

Um, this is a case where we have intracranial

17:42

findings and, um, cardiac findings.

17:45

Um, so we're going to start out looking at the

17:47

head and, um, the next image shows the heart.

17:54

And again, it's, uh, most people recognized, um,

17:58

that this is most likely Trisomy 21, which it is.

18:03

And this.

18:04

So what we see is a classic demonstration

18:08

of endocardial cushion defect, or AV canal.

18:11

What are the findings we see?

18:13

Well, the first thing we really

18:15

notice is this fused AV valve.

18:17

The straight line going across.

18:19

I said that you should have the mitral

18:20

and tricuspid valves being offset.

18:22

And here you can see they're going straight across, and

18:25

you have both this atrial and ventricular septal defect.

18:29

Um.

18:31

This is probably one of the best demonstrations

18:33

that you'll see of this single valve going

18:36

across, sort of splaying across the large defect.

18:39

Anytime you're looking at the four-chamber

18:40

view of the heart, always concentrate and

18:42

make sure that what you're seeing is an offset

18:44

between the mitral and the tricuspid valve.

18:47

What is the second-trimester hallmark finding of Trisomy 21?

18:50

Exactly what we saw here, an endocardial cushion defect. You can

18:54

see evidence of duodenal and esophageal atresia, although these

18:57

usually manifest in the third, not the second trimester.

19:00

But there are a whole host of second-trimester soft markers

19:03

that we see with babies with Down syndrome, uh, borderline

19:06

ventriculomegaly, which we actually saw in the fetus where

19:08

the, um, ventricles were measured close to 11 millimeters.

19:12

There can be an increased nuchal fold, which is when

19:14

you measure, when you look at the axial view of the

19:16

head, you measure posteriorly from the occipital bone.

19:20

And greater than six millimeters is

19:21

considered an increased nuchal fold.

19:24

The nasal bone is often absent or hypoplastic.

19:27

They may have an echogenic intracardiac focus,

19:29

as I showed you, in that fetus with Epstein's.

19:32

The tibia and humerus are sometimes a little shorter

19:35

than you would, um, imagine, and you may have mild pyelectasis.

19:39

Many of these soft markers can be normal findings

19:44

and are seen much more commonly in normal

19:45

fetuses than in fetuses with Down syndrome.

19:48

But if we see them in combination, um,

19:50

your index of suspicion increases somewhat.

19:53

And so, um, now almost every

19:56

patient that has multiple markers

19:58

will opt to have, uh, non-invasive fetal testing or

20:01

cell-free DNA, which has an excellent, uh, 99% detection

20:06

of Down syndrome with no risk, um, to the pregnancy.

20:11

Um, many people might say, well, would you do

20:14

that if the patient says they wouldn't act on it?

20:17

And the sort of inference is that acting on it means

20:21

terminating a pregnancy, but acting on it is very different.

20:24

It's very important to actually have all the knowledge, so.

20:28

Determining whether the fetus has Trisomy 21,

20:31

whether or not, uh, it is really important to know,

20:34

even, um, if the pregnancy is going to be continued.

20:37

And now, looking at the rest of the, uh, chest,

20:40

not necessarily just the heart, we see, uh, in this

20:43

fetus with a, uh, congenital diaphragmatic hernia.

20:46

The stomach is on the left.

20:48

And actually, at the time of the second-trimester

20:50

study, the stomach was still in the abdomen.

20:52

But when we look at the cross-section of the chest, we can

20:55

see that the heart is pushed all the way over to the right.

20:58

So now we have a, a heart on the right and a

21:01

stomach on the left, but this is not because the heart

21:04

started on the right, but it's because it's been pushed.

21:06

And I think you can kind of infer

21:07

that by looking at the cardiac axis.

21:10

And also, when we look at this chest, you

21:12

can see evidence of bowel in the chest.

21:14

So if you're seeing the heart on the right

21:16

and the stomach on the left, one of the

21:18

things you have to consider is, is this heart

21:20

just being pushed over by a diaphragmatic hernia?

21:23

And when this patient came back in the third trimester,

21:26

we can clearly see at this point that now the stomach

21:28

is actually above the diaphragm, really confirming the

21:31

diagnosis that we, um, made in the second trimester.

21:35

In this fetus, we, uh, see evidence of a pleural effusion.

21:39

Now, you may see pericardial fluid

21:42

in utero as a normal variant.

21:44

Usually it's a small amount of pericardial

21:46

fluid, but it, it can be a normal finding.

21:49

Pleural fluid is never a normal finding in

21:51

utero, so if we see pleural fluid, we have to

21:53

consider that there is some pathologic process.

21:57

going on.

21:58

And it can be, um, primary chylothorax

22:01

due to, uh, pulmonary lymphatics.

22:03

Uh, it can be seen in association with, uh, chest mass,

22:06

with some kind of cardiac anomaly or cardiac arrhythmia,

22:10

with fetal anemia, with infection, or with aneuploidy.

22:13

And this fetus actually had Trisomy 21.

22:19

Um, now we have another case, um, case number six.

22:23

Uh, MR images of the chest,

22:29

and as most of you recognize, this is a very large,

22:33

complex, uh, chest mass, pretty characteristic

22:37

for a, uh, CPAM, CPAM, or congenital pulmonary

22:43

airway malformation, has a variable appearance, which can

22:46

be echogenic and solid appearing if it's microcystic.

22:50

Macrocystic with one or more cysts greater than five

22:53

millimeters, the vascular supply is from the pulmonary

22:56

arteries. Stable lesions can be watched, but there's

22:59

a very poor prognosis if, um, hydrops develops.

23:03

And this would be an example of the microcystic, which looks

23:05

really very, very echogenic, in contrast to this patient,

23:09

where we have a mixed lesion with multiple, uh, cysts.

23:13

Um,

23:16

case number seven.

23:18

Um.

23:21

I'll show you these images,

23:25

and the question is, what is the fetal gender?

23:29

And that may seem like a strange question, but this is a

23:33

classic example of a cystic hygroma from Turner syndrome.

23:37

So this would be a female fetus. So this would be your

23:40

classic cystic hygroma, where we actually see intracranial

23:43

structures look normal, but we see this very, very large,

23:47

multiseptated, uh, cystic hygroma with significant anasarca.

23:53

Um, this fetus also had some pleural

23:55

fluid and some pericardial fluid.

23:57

So this would be a cystic hygroma with

23:59

hydrops due to, uh, Turner syndrome.

24:01

And the hydrops is so, um, extensive that

24:05

you see this massive skin edema that

24:06

is sometimes referred to as peau d’orange edema,

24:09

because if you look at the fetus, it really

24:11

looks like the fetus is wearing a, a

24:13

spacesuit because of the massive, um, edema.

24:17

Uh, Turner syndrome would be a monosomy X or 45,XO.

24:21

The missing chromosome is usually paternal, and

24:23

there's no increase with advanced maternal age.

24:26

There's a very high incidence of in utero

24:29

loss, up to three-quarters in the first

24:31

trimester, and many during the second trimester.

24:34

And any fetus that, uh, presents with hydrops like we

24:36

see there, it's really a lethal anomaly with, with loss,

24:40

very soon after that.

24:42

Um, high incidence of severe lymphatic

24:44

abnormalities as we see here with a large septated,

24:47

um,

24:48

cystic hygroma and, and hydrops.

24:51

Um, the hygromas are usually septated, as we see here,

24:55

and if associated with hydrops,

24:56

it's almost uniformly lethal.

24:58

To understand hydrops is fluid in at

25:00

least two areas, so hydrops of any cause.

25:03

We have to have fluid in at least two areas.

25:05

Um, AKA pleural effusion,

25:07

ascites with the hygroma, and as I said, the

25:10

massive edema is called peau d’orange edema.

25:13

The associated cardiac anomalies include coarctation

25:16

of the aorta and, in about 15% of the cases, um,

25:20

hypoplastic left heart syndrome, and the classic

25:22

renal anomaly would be a horseshoe kidney.

25:25

Those that survive are often mosaic,

25:28

um, associated with short stature,

25:30

primary amenorrhea because of

25:31

the streak ovaries and a webbed neck.

25:34

Possibly the sort of remnant of the cystic hygroma.

25:38

Now we're going to move on to the area of the cord insertion.

25:41

And although I'm talking about second trimester, it's just

25:43

always important to, um, recognize, uh, the normal midgut

25:47

herniation that occurs between weeks nine and weeks 11.

25:51

So we very rarely call abdominal wall defects

25:55

um,

25:56

prior to week 11, unless we see

25:58

herniation of liver as well.

26:01

So here this would be the normal midgut

26:03

herniation that you see during development.

26:05

And again, a different fetus where

26:07

we see the normal midgut herniation.

26:08

This was

26:09

a component of a, um, ultrasound

26:12

nuchal translucency measurement.

26:13

And when you look at the cross-section of the normal

26:16

midgut herniation, the important thing to recognize

26:18

is it's bowel only, and you always have less bowel

26:22

herniated than you actually have in the abdomen.

26:24

So the abdominal diameter is way greater

26:26

than the diameter of the herniated, uh, bowel.

26:30

But this only occurs until, um.

26:33

So in this fetus at 14 weeks, where we can see

26:36

what looks like a small omphalocele, it's important

26:39

to recognize this is not a normal finding.

26:43

And this fetus had, uh, Beckwith–Wiedemann syndrome.

26:46

So, uh, small bowel–only omphaloceles are a common,

26:50

uh, finding that we're going to see with Beckwith–

26:53

Wiedemann, but could also be, um, Trisomy 18.

26:57

The normal cord insertion should be

26:59

documented, obviously, on every study.

27:01

And here we see perfectly normal, um, cord insertion.

27:07

What do we worry about with an abnormal?

27:08

We're really trying to differentiate between an omphalocele

27:12

and a gastroschisis in the vast majority of cases.

27:15

Um, omphalocele is a midline abdominal, um, wall defect

27:18

where the cord inserts in the apex of the defect to

27:22

front of the defect, uh, usually covered by a membrane.

27:26

Um, with herniation of the abdominal, uh, contents into

27:29

the base of the cord and covered by the membrane, which is

27:31

comprised of peritoneum and amnion. Uh, ascites is common,

27:36

which really helps outline the membrane we see on omphalocele.

27:41

It's associated with aneuploidy in up to

27:42

40% of cases and cardiac anomalies in up to

27:45

50% of cases, with GI anomalies about 40%.

27:48

And the prognosis is really going to depend on

27:51

the karyotype and the associated abnormalities,

27:53

but omphalocele, because of the very high

27:55

association of, um, associated anomalies, rarely,

27:59

um, fetal karyotype is an essential part of the,

28:02

uh, management, um, and dedicated, um, ultrasound

28:06

to make sure you don't have, um, associated cardiac

28:09

anomalies.

28:10

So here we see a large, um, abdominal

28:13

wall defect with herniation of, uh, liver.

28:16

This would be the membrane with a small amount of ascites.

28:18

So we can actually outline the membrane really

28:21

clearly for us, and we can see how the cord inserts.

28:26

Gastroschisis, in contrast, is a para-

28:29

umbilical abdominal wall defect.

28:31

Uh, greater than 95% are going to be right-sided,

28:34

no membrane, um, bowel dilatation.

28:37

Um, the extruded bowel dilatation is pretty common.

28:40

They are almost always euploid, and most people don't

28:42

recommend karyotyping for associated,

28:44

uh, for isolated gastroschisis.

28:48

But there are associated GI

28:50

complications, usually atresia and volvulus.

28:54

And this would be what a gastroschisis looks like.

28:56

So here we can see this sort of free-

28:58

floating bowel, no surrounding membrane, and

29:00

the cord inserting lateral to the defect.

29:03

So a normal cord insertion, um, with the extrusion of bowel.

29:07

So this would be a classic gastroschisis.

29:09

So it is always, when we see an abdominal wall defect,

29:13

it's imperative that we try and determine whether this

29:16

represents an omphalocele or gastroschisis,

29:19

because of significant differences in management.

29:23

And in this, um, case, um, we see these

29:26

three images, and then if you just wait a bit,

29:28

after you've looked at the images, I will give you the, um,

29:33

answer, uh, possibilities.

29:36

So what we see here is an omphalocele; we

29:38

see the large abdominal wall defect with a

29:40

membrane-covered omphalocele with, um, ascites.

29:45

How do we know it's Trisomy 18?

29:47

Or when you look at this foot, we can

29:49

see a, uh, classic rocker-bottom foot.

29:53

So the combination of the omphalocele with

29:55

the rocker-bottom foot really

29:57

increases the likelihood that what we're dealing with

30:00

is not an isolated omphalocele, but a fetus with a trisomy.

30:04

And this was Trisomy 18, uh, Trisomy 18, or Edwards syndrome.

30:08

Um, there are multiple anomalies that we usually see, um,

30:13

or a single major anomaly in association with a, a very

30:16

strong marker for, uh, Trisomy 18, which would include

30:20

a choroid plexus cyst or clenched hand with overlapping

30:25

index finger. Choroid plexus cysts are so common we

30:28

see them in about one to 3% of normal babies.

30:32

Uh, but if you look at fetuses with Trisomy 18,

30:35

about a third are going to have choroid plexus cysts.

30:38

So anytime we identify a plexus cyst in

30:40

utero, um, again, the next thing we

30:43

have to do is look for associated anomalies.

30:45

If it looks like an isolated choroid plexus cyst, it

30:49

almost never means anything.

30:51

But if we see any issues, particularly if we see what

30:54

look like clenched hands or, um, abnormalities of the

30:57

feet, we have to presume that this fetus, um, has a

31:01

likelihood of having Trisomy 18 and do karyotyping.

31:06

The next, um, area we're going to look at is the, um,

31:10

kidneys, and the AIUM, uh, requires documentation of

31:13

kidneys on all second- and third-trimester scans,

31:17

but the cortex is pretty isoechoic in the mid-trimester,

31:20

so normal kidneys are not that easy to see.

31:23

In contrast, abnormal kidneys are pretty easy to

31:26

see because they're either obstructed and filled

31:28

with fluid and they look kind of black, or they're

31:30

dysplastic and look kind of white, or they're mixed.

31:33

And, uh, so usually abnormal kidneys are pretty easy to see.

31:37

Renal arteries should be documented, and it can really help,

31:40

uh, confirm the presence or absence of normal kidneys.

31:43

Um, this is just a rule of thumb, but renal length in

31:46

millimeters approximates gestational age in weeks, and

31:49

that's going to be really a more important finding or factor

31:53

when we're really considering, uh, kidneys being too large.

31:57

Um, the other important thing we have to

31:59

evaluate is the renal pelvis.

32:02

Um, and we always measure the

32:03

renal pelvis in the axial view.

32:05

You never do it in the coronal view

32:07

because you can be oblique, you can have

32:09

an extrarenal pelvis and exaggerate it.

32:11

So we always measure it in the axial view.

32:13

Um, and it should measure less than four,

32:15

uh, millimeters prior, uh, to 27 weeks.

32:20

And we should not have ectasis.

32:22

So this would be normal.

32:22

And you can see how the normal kidneys are really pretty

32:25

isoechoic.

32:26

We could see a little bit of the

32:27

pelvis, but not that easy to see.

32:30

Um, kidneys live right next to the spine.

32:33

So whenever we look at something, we want to look

32:36

right next to the spine, and here how the renal

32:38

arteries really, um, help confirm that we have two

32:41

normal, uh, normally located kidneys in the fetus.

32:45

Um, we obviously can't look and evaluate

32:47

the kidney without looking at the bladder,

32:49

in fact, confirming that that is normal too.

32:52

And this would be a perfectly, uh, normal bladder.

32:56

The, uh, normal, um, three-vessel documentation

32:59

of the three-vessel cord around the bladder.

33:02

That is the best place to document that

33:03

you do have two, um, umbilical arteries.

33:06

So the normal cord should have two arteries

33:08

and one vein. To confirm two arteries,

33:10

that is the view that we use. Um, in

33:13

this fetus of bilateral renal agenesis,

33:15

the most striking feature is the anhydramnios,

33:19

so there is absolutely no amniotic fluid.

33:22

Um, we can see the head is significantly dolichocephalic.

33:26

No fluid at all.

33:27

And when we look at the region of the

33:30

bladder, the bladder is completely empty.

33:33

So bilateral renal agenesis, uh,

33:36

pretty obvious on this ultrasound.

33:39

In contrast, this fetus has a multicystic

33:42

dysplastic kidney, and as I said, the kidney

33:45

lives right next to the spine.

33:46

As we see here, we don't see the contralateral

33:49

kidney that well on this image, but I can infer

33:51

that that kidney is, in fact, normal because

33:53

we have a normal amount of amniotic fluid.

33:55

So this would be a classic multicystic dysplastic

33:58

kidney, and you can see the cysts of varying sizes,

34:01

um, with this sort of intervening echogenic, um, area.

34:05

And there is nothing that looks like a pelvis with calyces.

34:10

Varying sizes that do not communicate.

34:12

Absence of the normal renal parenchyma.

34:15

The cysts may change in size during gestation,

34:17

and they can get bigger or smaller, but they're

34:19

very rarely requiring utero, uh, drainage, um,

34:23

bilateral and about 20%, and very poor prognosis if

34:27

you have bilateral multicystic dysplastic kidneys.

34:30

Pretty much as poor as, uh, bilateral renal

34:33

agenesis with oligohydramnios and Potter type II.

34:37

Contralateral renal anomaly in about 40%.

34:39

But, um, uh, often it's, uh, not a, uh, lethal anomaly.

34:44

It's something like a UPJ, uh, posterior urethral

34:48

valves is another entity that has, um, an enormous.

34:52

Spectrum that we can see in ultrasound.

34:54

But this would be the, the worst part of the

34:56

spectrum where this fetus, again, has anhydramnios

34:59

with no, um, amniotic fluid at all, just massive

35:03

distension of the, uh, bladder, which we can see here.

35:07

Confirm what we are looking at in the

35:08

bladder by looking that what we're looking

35:10

at is bladder because of, um, the vessels.

35:13

So this would be a posterior urethral valves that has a, uh.

35:18

Very, uh, lethal prognosis because of

35:21

the anhydramnios, posterior urethral valves.

35:23

The urethral membrane acts as a valve, resulting

35:26

in bladder outlet obstruction to varying degrees.

35:29

Um, it's seen exclusively in males, and often you have

35:32

a keyhole appearance to the bladder because the, um.

35:36

The, the standard bladder kind of funnels

35:38

into the dilated posterior urethra.

35:40

If you see something that looks like this and what

35:42

turns out to be a fetus, then it would be urethral

35:45

atresia, um, often associated with, um, hydronephrosis,

35:51

oligohydramnios, and, uh, cases with poor prognosis.

35:53

And this is a cause of urinary ascites,

35:55

where you can get rupture of the bladder.

35:57

As I said, there's a broad spectrum of severity with overall

36:01

mortality at 25 to 50%, but if there's oligo, as high as 90%.

36:08

Uh, UPJ obstruction is going to be the most common

36:10

abnormality that we're going to see, and this is where

36:12

I'm showing you how we measure, um, the renal pelvis.

36:15

So here we can see on this coronal view, we can

36:19

clearly see that the left kidney has a dilated pelvis

36:22

with calyces. We should not normally see the calyces.

36:25

We can see mild pyelectasis as a physiologic

36:28

variant, but we don't usually see the calyces.

36:31

And this is where we would measure, um.

36:34

On, on axial view, we measure the, the left kidney is

36:37

obviously way more dilated than the right, so should not

36:40

measure more than four millimeters, uh, until 27 weeks.

36:43

And then more than seven millimeters, um, 32 weeks, and

36:47

greater than 10 millimeters is always going to be abnormal.

36:49

So here we have seven millimeters on the

36:51

left and 0.38 millimeters,

36:54

on the right, which would be normal.

36:57

So hydronephrosis without hydroureter,

36:59

the pelvis can become massive.

37:02

Uh, pelvis of greater than 10

37:03

millimeters is always going to be abnormal.

37:06

It can result in dysplasia, which

37:07

would, uh, usually, uh, be evident.

37:10

Sonographically with increased echogenicity and

37:12

or renal cysts, can be bilateral and up to 10%

37:16

with a contralateral abnormality and up to 25%.

37:20

It is sporadic, more common in

37:22

males and more common on the left.

37:24

The prognosis is excellent if it's unilateral and

37:26

isolated, poor prognosis with bilateral disease,

37:29

again, with oligohydramnios, which is going to be our,

37:32

our most important marker as to, um, outcome.

37:35

Um, or if there are other extrarenal abnormalities.

37:39

Um, if you consider that there may be, um.

37:42

UPJ in utero.

37:43

It's very important to recognize that you do

37:45

not do an ultrasound until, um, within the first

37:48

72 hours because the physiological dehydration

37:51

during that period can really, um, under, uh.

37:57

You, the, uh, degree of, um, lysis will not

38:00

be as obvious within the first 72 hours.

38:03

That can sometimes be an issue because now that

38:04

babies go home, um, so much earlier, everyone wants

38:07

to get everything done before the baby goes home.

38:09

But this is one study that needs to be then

38:11

scheduled as an outpatient, um, a little later.

38:14

'Cause you do not want to do it within the, uh, first.

38:16

72 hours.

38:18

So what is true about a UPJ obstruction,

38:22

and does it count for 40 to 60% of, uh,

38:25

prenatal urinary tract abnormalities?

38:27

Um, they don't always require, uh,

38:30

postnatal treatment, and oligohydramnios is not common.

38:32

That's what we are going to see with posterior urethral valves.

38:38

Um, this case, uh, it is going to be, and, and

38:41

there are a couple of slides that I want you

38:42

to look at before we, we do the poll question.

38:45

So here would be, uh, a, an axial image.

38:50

Um,

38:55

There's another, um, image that's going to come later.

38:58

This is looking at the area of the bladder.

39:01

This again, looking at the kidney.

39:03

And then here we have a clip going through the kidney.

39:09

Let's do it one more time.

39:15

This is the last question.

39:17

Um, what do we think it is?

39:19

So I think that, oh, I think this shows

39:23

really well when we go through the kidney,

39:25

the obstructed upper pole with the, um.

39:28

Pelvic ectasis from the reflexing lower

39:31

pole that you get with a, uh, duplex system.

39:34

Um, so, uh, where we know that the, um, upper

39:37

pole ureter will, uh, insert, um, infra uh,

39:42

medially and often be associated with an

39:44

ectopic ureteral as we saw in that, uh, patient.

39:48

Um.

39:49

I'm just gonna talk a little bit

39:51

again, talk about the mild ectasis.

39:53

As I said, greater than four millimeters at 20

39:54

weeks greater than seven millimeters at 32 weeks.

39:57

Require follow up, but might be physiologic.

40:00

Greater than 10 millimeters is always gonna be pathologic.

40:03

Caerus is abnormal.

40:04

We should not see celiacs.

40:07

It's often, uh, bilateral, but can be a little asy.

40:10

Um, a little asymmetric.

40:12

We usually recommend reevaluation at 32 weeks, unless

40:15

it looks pretty remarkable at 20 week study and it.

40:18

It can be physiologic, but might reflect reflux

40:21

and let's say soft marker for, uh, trisomy 21.

40:25

Um, but if we are talking about soft

40:27

markers in general, when they are isolated,

40:30

we just recommend follow up at 32 weeks.

40:32

But if they're associated with other abnormalities,

40:35

uh, then they may require, uh, workup, uh, sooner.

40:38

So this will say fetus with mild lysis, renal

40:41

pelvis off five millimeters on the 20 week scan.

40:45

Moving into the extremities.

40:47

When we looked at this fetus's feet, we can see a

40:50

club foot with, um, inverted, bilateral inverted feet.

40:54

We should never see the calf and the foot in the same plane.

40:57

And here we consistently on, uh, both these lower

41:00

extremities, seeing the calf and the foot in the same plane.

41:03

So now we have.

41:04

Two findings.

41:05

So we have PIIs as well as club feed, both in isolation

41:09

would probably not require a utero um, workup.

41:12

But anytime we have two findings,

41:14

we do recommend a utero workup.

41:16

And this fetus has had something called Loeys-Dietz

41:18

syndrome, which was originally described in,

41:20

uh, 2005, and really is characterized by aortic

41:23

aneurysms, which are prone to rupture at sizes smaller

41:27

than in, um, other connective tissue disorders.

41:29

So it's a very important.

41:31

Issue to know because these, um, these children require

41:35

very close monitoring with fairly early intervention.

41:39

And I'm gonna just conclude with, um, two, um,

41:43

abnormalities of the, um, MSK system that are.

41:48

Both lethal anomalies, unfortunately, but to just show

41:50

you how we can kind of come to, so here on this 19-week

41:53

scan, we can see this fetus has got a really small chest.

41:56

Look how small this chest is relative to the abdomen.

41:59

Look at the ribs.

42:00

And this is an example of short rib polydactyly,

42:03

which is characterized by, uh, short, I should say,

42:06

sorry, short tubular bones with no fractures, short

42:09

horizontal ribs with a severely constricted thorax.

42:13

It's autosomal recessive.

42:15

So, um, unfortunately this patient had two fetuses

42:18

that we scanned that both had, uh, short rib poly,

42:21

the 25% recurrence risk, and there's usually,

42:24

um, neonatal death due to pulmonary hypoplasia.

42:28

And then this final case is another

42:30

example of a, uh, lethal, um.

42:33

Short, uh, uh, a short bone or,

42:37

or multi, uh, skeletal dysplasia.

42:40

And here the interesting, this fetus has

42:42

markedly shortened limbs with hydrops.

42:45

But you really, um, the way we can actually

42:48

come to the correct diagnosis here is when you

42:50

look at this head, you really should not be

42:53

able to see intracranial structures that well.

42:55

And if you think whenever you look

42:57

at an OB ultrasound, usually the, uh.

43:00

We see the dependent hemisphere quite well,

43:02

but this hemisphere is usually filled in with

43:04

artifacts, and we kind of presume, um, symmetry.

43:06

So this, you're seeing the head way too well,

43:09

and that is the clue that what we're dealing

43:11

with is osteogenesis imperfecta because of the

43:14

poor mineralization of the, um, fetal skull.

43:16

So looking, you can actually look

43:19

at the abnormalities of the lungs.

43:21

By looking at the head, we can come to

43:23

the, um, right diagnosis at this time.

43:25

So, osteogenesis imperfecta, genetically and clinically heterogeneous

43:29

group of connective tissue disorders characterized

43:31

by osteoporosis and fractures, the multiple fractures

43:35

lead to the, uh, bone, um, angulation and shortening.

43:39

The mild to moderate severity were previously called

43:41

types one, four, and five. Progressively deforming would

43:45

be what we see here, which is prenatally lethal, formerly

43:49

called type two or progressively deforming type three.

43:53

This is a 3D reconstruction of the fetus,

43:57

showing the marked limb shortening.

44:00

Uh, so this is a whirl through, um, the evaluation of

44:04

fetal anatomy, but hopefully, um, it kind of gave you

44:07

an approach that can help you go back and have a look

44:11

at, um, what you think the likely abnormalities are.

44:14

This fetus kind of made us laugh.

44:16

It looked like a see-no-evil,

44:18

speak-no-evil, hear-no-evil.

44:20

Just stop looking at me.

44:22

It's enough now.

44:25

Okay.

44:25

Uh, as we bring this to a close, I want to thank

44:27

you, Dr. Glynis Sacks, for your time today, and I thank

44:29

you all for participating in our new conference.

44:31

Again, this new conference will be

44:32

available on demand on MRIOline.com.

44:35

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44:38

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44:41

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44:45

Um, without further ado, I guess if

44:48

you want to take away some questions.

44:50

If anyone wants to put those in

44:51

the Q&A section, feel free.

44:55

Dr. Sacks, if you can please open the Q&A feature

44:58

and answer the questions of your choosing.

45:01

Okay.

45:05

Um.

45:07

Differential for the, um, banana sign there.

45:10

Pretty much the banana sign, if you

45:12

really see the banana sign, is a Chiari II.

45:14

Uh, the lemon sign can be a normal finding in some

45:17

fetuses, but if you're truly seeing the banana

45:19

sign, I don't really think there is a differential.

45:21

I think that's Chiari II.

45:23

Um, explain heterotaxy slowly.

45:26

Um, I think we don't really have enough

45:28

time, but the way I kind of think about it.

45:31

If the heart and the stomach are both on the same

45:33

side, even if they're both on the right, most of the

45:36

fetuses are going to, most people are going to do fine.

45:40

Um, it's when you have heart on one side and intra-abdominal

45:45

structures on the opposite side that you end up with

45:48

the issues of either indeterminate situs or, um, asplenia.

45:52

And so those are the fetuses that require, or the,

45:55

the infants that really require further workup.

45:57

So it's when the heart and the

45:58

stomach are on different sides.

46:01

How early can we diagnose anencephaly?

46:03

Really quite early.

46:04

And if you look at some first-trimester studies, um,

46:08

usually the cranial configuration looks a little abnormal.

46:11

We've seen our cases early as, um, eight

46:15

and a half weeks, where it almost looked like

46:17

there was a sort of a, an abnormal almost, um.

46:22

Kind of a, a triangular cone-shaped look to

46:25

the fetal head, and, and following it up.

46:27

So what we do if we see an abnormal

46:29

cranial configuration really early is we

46:31

recommend pretty short-term follow-up around,

46:33

uh, you know, maybe, uh, I think we, you know, around

46:36

about 10 or 11 weeks, and then you can be pretty sure.

46:39

The interesting thing is when you look

46:40

early, it looks more like a cranium.

46:43

A little later, more like your classic anencephaly,

46:45

because the extruded, uh, brain contents

46:48

get kind of destroyed or broken down by the

46:52

mechanical and chemical, um, influences in utero.

46:55

But you can diagnose it pretty early if you, if

46:57

you look, um, uh, re: from, um, Ebstein's anomaly.

47:05

Um, well, Ebstein, we are going to really

47:08

the tract, tractology of flow, um.

47:11

We're going to see different findings.

47:13

Um, we're going to see the VSD, the overriding aorta,

47:16

um, usually don't see right ventricular hypertrophy

47:19

in utero, but it's not going to, you're not going to

47:22

have the massive right atrium, I don't think.

47:25

Um, when you can diagnose an omphalocele, as I said, you don't

47:28

want to diagnose a four-week, um, 11 unless you see extruded.

47:33

Um, and unless you, uh, see extruded, um.

47:41

Um, liver.

47:43

'Cause liver should not, um, be outside.

47:46

Um, the liver should be inside.

47:48

So we've diagnosed an omphalocele, and

47:50

I've seen one in a 10-week exam.

47:52

You saw a liver mass, uh, obviously

47:54

out, and there was, uh, a trisomy 18.

47:57

Um, I'm trying to go back to the, that

48:01

image, if I could find, of the outflow tracts.

48:04

Um.

48:06

Uh, but this was normal, this image.

48:11

So, I mean, I think that the aorta and, and,

48:13

um, pulmonary artery were pretty equal in size.

48:16

I'm trying to get back there.

48:20

So here, when we are looking at the aorta and we

48:23

are looking at the PA, they are pretty equal in size.

48:25

This would be, this would be normal.

48:27

This was a normal, completely normal heart.

48:29

So I think that it, it really is, is the kind of, um.

48:34

They look pretty equal in size.

48:36

Uh, once postnatal verification, it's going to look

48:38

a little bit smaller, but yeah, that looks fine.

48:40

That's normal.

48:45

See if there are any more questions.

48:49

Um, explain about keyhole.

48:51

So, what the keyhole is, is it looks like a keyhole because

48:54

the distended, uh, urethra kind of fills with fluid.

48:57

So the bladder is, is really distended.

49:00

And then there the urethra looks, so it kind

49:02

of looks like, like the wider part and the, the

49:06

more narrow part, like a, a keyhole would look.

49:13

What are the, uh, implications of an absent

49:15

nasal bone without other, uh, markers?

49:19

Um, we know that there is a, a slightly increased incidence

49:22

of anomalies with a, um, a hypoplastic nasal bone.

49:26

Um, absent nasal bone.

49:28

We are going to see sometimes, often it's really technical,

49:31

and you're not getting the, um, really good view.

49:34

Just an isolated absent nasal bone would be unusual.

49:38

Absent nasal bone, but if you really thought

49:40

nasal bone was absent, um, you could counsel

49:43

the patient about getting cell-free DNA.

49:46

Cloacal abnormality.

49:48

Um, I kind of think about, um, a low abdominal

49:52

wall defect with absence of the normal bladder.

49:54

So you look down and you see this low abdominal wall

49:56

defect, and when you look at the bifurcation, there's

49:59

no fluid-filled bladder because usually the, um,

50:01

cloacal or bladder exstrophy really just looks more

50:04

like a, sort of a solid, um, a more solid component.

50:08

Yes, the right heart can be a little

50:10

bigger than the, um, left in utero.

50:13

It's usually not that marked, but it's more usual,

50:15

under normal circumstances, for the right ventricle

50:18

to be bigger than the left.

50:21

The, um, anomalies that are delayed in onset

50:24

and occur after a normal second-trimester scan?

50:26

Well, I kind of always think about when you are looking in

50:29

the third trimester, we always have to, even if it's not an

50:32

anatomy scan, we're just looking for growth or well-being,

50:34

we always have to look at the head, heart, and kidneys

50:37

because those are the areas that rarely change.

50:39

So what are the kind of things you can see?

50:41

You can see intracranial hemorrhage,

50:42

you can see intracranial teratoma, um.

50:46

Some evidence of, uh, manifestation of

50:48

intracranial infection, um, in the heart you can

50:52

always see, um, some heart defects definitely

50:56

evolve during, um, during uterine life.

50:59

And you can have a, um, aortic issue where suddenly

51:02

the critical aortic stenosis can no longer be overcome,

51:05

and a hypoplastic left heart develops

51:08

in what looked like a, a pretty normal, um,

51:12

second trimester study.

51:13

Um, you can see things in tuberous

51:15

sclerosis like, uh, rhabdomyomas that you,

51:18

they were not manifest until the third trimester.

51:21

Duodenal atresia, esophageal atresia,

51:24

um, often not seen until the third trimester.

51:27

The, um, both are going to have polyhydramnios, classic esophageal,

51:31

um, atresia, which although you would think you

51:34

wouldn't see the stomach there, you often see the fistula.

51:36

But if you see nothing that looks like a stomach and

51:39

polyhydramnios, you have to worry about esophageal atresia.

51:42

Duodenal atresia is going to give you

51:43

your, um, double bubble appearance.

51:46

Um.

51:48

Pericardial fluid, a small amount of pericardial fluid,

51:50

we often see, um, us, we, we use four millimeters,

51:54

um, as a cutoff, but I think particularly now

51:58

that our resolution is so good on our studies,

52:00

um, we really can see some, um, pericardial fluid normally,

52:05

and we just talk about a small amount of pericardial fluid,

52:08

likely a physiologic variant. If you're

52:10

really worried because you see it earlier,

52:13

it could be the first sort of

52:14

manifestation of what might become hydrops.

52:17

So then short-term follow-up to make sure

52:18

that the fetus doesn't develop hydrops with

52:21

ascites or, um, pleural fluid is important.

52:25

Isolated polyhydramnios, I, again, I kind of think about

52:29

what gives polyhydramnios. Well, some issues with swallowing.

52:31

So there is some reason the baby can't swallow

52:34

properly because there is some CNS abnormality or

52:37

facial cleft or some kind of neuromuscular abnormality,

52:40

which makes it hard for the babies to swallow.

52:42

They can swallow, but then there is some

52:44

obstruction, which would be your esophageal and,

52:46

um, duodenal atresia that, um, could give you that.

52:50

But probably the most common cause we're going to

52:52

see of polyhydramnios now is abnormal, uh, glucose.

52:56

In, uh, in moms we will see idiopathic, but you'll

52:59

see either, frankly, gestational diabetes

53:02

or just abnormal glucose in the mom.

53:05

So the fistulas, as I said, um, I think you're

53:09

going to have polyhydramnios, but if you see a perfectly

53:12

normal filled stomach, it can be, I think, very hard.

53:15

And so I would say I have not diagnosed, um, that

53:20

in utero. You can suspect it because of the polyhydramnios,

53:22

and if you have other anomalies, then, uh, be suspicious.

53:26

But, um, I think it can be hard in isolated TEF, too.

53:30

All right, Dr. Sacks, as we bring this call to a close,

53:33

I want to thank you, Dr. Sacks, for your time today.

53:36

Thanks to all of you for

53:37

participating in our noon conference.

53:39

A reminder that this conference will be

53:40

available on demand on MRIOline.com.

53:44

In addition to all previous noon conferences tomorrow,

53:47

please join us for a noon conference with Dr. Thapa

53:50

on uniquely pediatric upper extremity injuries.

53:54

register@mrionline.com.

53:56

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53:59

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54:02

Thanks again, and have a great day.

54:05

Thank you.