Fetal Gastrointestinal System - HD

Introduction

My name is Dr. Mary Frady. I'm the assistant director of ultrasound at Brigham and Women's Hospital in Boston.

And today's lecture will be on the fetal gastrointestinal system.

This will be a lecture on the fetal gastrointestinal system.

When we talk about the GI tract in the fetus, we're gonna start at the top and work our way through down to the bottom.

Fetal Stomach

Starting with the fetal stomach, that's should be seen in all fetuses after 14 weeks.

If the stomach is not seen early on in pregnancy, 50% of the time that fetus will turn out to be okay.

But once you get to 18 weeks, if the stomach's not seen, only 15% of the time will there be a normal outcome.

Here's an example of a normal stomach.

We're all used to seeing this where it's a transverse view of the abdomen and you have a nice black stomach bubble here in the left upper quadrant.

In contrast to this fetus a little bit earlier in pregnancy, this is a sagittal image and we can see the stomach here and it's got a little bit of stuff in it.

The reason for that is on this video clip you can see there's lots and lots of echoes and debris floating around in the amniotic fluid.

And since the fetus swallows the amniotic fluid, once it swallows the fluid, this debris will end up in the stomach.

In this instance, you again, you can see there's a lot of am of, echoes in the amniotic fluid and the stomach is getting hard to see because there's so much debris and material in the stomach that you lose the koic nature of the fluid.

As you move down the GI tract, the normal fetus, will display peristalsis of the small bowel and you can see lots of peristalsing loops of bowel here.

None of them are dilated. And that is a normal process.

Abnormalities of the Stomach

Let's go into some abnormalities starting at the top.

What happens when you see a big distended stomach?

The first thing you wanna think about is gastric outlet obstruction.

Alternatively, this could be normal. What are we gonna do?

We're gonna get a follow up.

Here's an example of a fetus in the third trimester who came in with this enormous stomach filling up half of the upper portion of the abdomen.

But when we saw the fetus again, 10 days later, the stomach is completely normal.

Missing Stomach

What if the stomach's missing altogether?

There's lots of explanations for why the stomach could be missing.

One, it could be normal, in which case we'll just get a follow up in, a week to 10 days.

And if the stomach's there we're good to go, severe oligohydramnios can keep the stomach from appearing because the fetus has no fluid to swallow.

A neurologic deficit or a facial deformity can interfere with swallowing and prevent the stomach bubble from showing up.

This commonly will occur in fetuses with an abnormal karyotype.

Maybe the stomach is there and normal, but it's in the wrong spot because of congenital diaphragmatic hernia or abnormal sitis.

And lastly, probably what most people think of immediately when the stomach's missing is could this be esophageal atresia without a tracheal esophageal fistula?

So here's an example of a fetus in which we didn't see a stomach.

This is the transverse view of the upper abdomen.

Here's the inter hepatic portion of the umbilical vein, and there's nothing present in the left upper quadrant where the stomach should be.

However, when we go up into the chest, we can see that there's a stomach bubble up in the left side of the chest and the heart has been displaced over to the right in this fetus with a diaphragmatic hernia.

Here's another case of a fetus where no stomach bubble is seen.

Here's the transverse view of the upper abdomen.

Once again, the int hepatic umbilical vein and no stomach in the left upper quadrant.

But look, in this instance we have at least mild and possibly moderate polyhydramnios, which leads us to the next diagnosis, which is esophageal atresia.

Esophageal Atresia

Esophageal atresia is a sporadic and complete division of the foregut.

It happens very early in gestation at under eight weeks.

The classic finding is absent stomach with associated polyhydramnios.

However, in some fetuses, secretions in the stomach can fill the stomach up enough so that you do appreciate a small stomach as we did in this fetus with esophageal atresia.

80% of the time, pa fetuses with esophageal atresia will have third trimester polyhydramnios, and over 90% of the time these fetuses have an associated tracheal esophageal fistula along with the esophageal atresia.

Now the typical or most common malformation is that the proximal esophagus ends in a blind pouch and then there's a fistula that goes from the trachea into the distal esophagus.

Now if this fistula from the distal esophagus from the bronchus to the, or the trachea to the distal esophagus is large, the fluid that is normally secreted in the chest can, be, sent through the fistula into the distal esophagus and into the stomach.

And you may see a normal stomach on the survey, in which case you won't be able to identify the esophageal atresia in utero fetuses with esophageal atresia, 40 per up to 40% can have associated intrauterine ge, growth restriction because a portion of the fetal growth is related to the protein in the swallowed amniotic fluid.

And when the fetus can't swallow the, the um, caloric content and the protein in that amniotic fluid is no longer available to the fetus to assist in growth.

30 to 70% of fetuses with esophageal atresia have associated anomalies, particularly fetuses with trisomy 18.

And this is a good time to remind you that when we see an int growth retardation and polyhydramnios, this is an ominous combination and you do wanna pay attention to this fetus.

Here's an example of what I'm talking about.

You can see the transverse view of the upper abdomen here.

Here's the stomach bubble, so everything should be fine.

We do note that we have severe oligo, severe polyhydramnios.

This fetus went to term delivered in the delivery room, was unable to be resuscitated, was unable to be oxygenated and died shortly after delivery.

Autopsy showed complete trachea esophageal atresia.

The trachea was completely blocked, so no oxygenation was possible and the esophagus was completely blocked.

That's the explanation for the severe polyhydramnios.

However, why do we have a stomach bubble?

There's a stomach bubble because there was a large fistula from the right main stem bronchus to the distal esophagus and all of the fluid that by um, traditional diagnoses should have distended the lungs and let us make the diagnosis of tracheal atresia.

All of that fluid was dumped down into the stomach and we had no ability to identify this complete tracheal esophageal atresia.

Duodenal Atresia

Moving right along through the GI tract in this fetus, we see two round fluid filled structures in the left upper quadrant and this of course is the double bubble of duodenal atresia.

This occurs in one out of 5,000 pregnancies.

About a third of the time this will be related to trisomy 21.

So when you see the double bubble and you're suspecting duodenal atresia due a good cardiac exam, 50% of the time these fetuses will have other anomalies.

And remember that it's not necessarily duodenal atresia, it could be a duodenal web or an annular pancreas causing this double bubble appearance.

What do I mean by the bubbles must connect?

Here we have the two bubbles in the upper, in the mid and left upper quadrant, and here's the image that shows that they connect because certainly you could have other cystic lesions in the abdomen that are unrelated to the stomach.

So you wanna show that here's the dilated stomach, the antrum, and the proximal portion of the duodenum to make this diagnosis and you should have associated polyhydramnios.

Small Bowel Obstruction

Moving a little farther down in this fetus, we have a very large distended stomach.

As we look for the double bubble, we see that there's not just one additional bowel loop, but several additional bowel loops in the upper quadrant.

And this is an example of a proximal small bowel obstruction.

Small bowel obstructions are typically due to bowel atresia.

There may be more than one site of atresia throughout the small bowel.

And what we see on sonography or multiple loops of dilated fluid-filled small bowel, traditionally we talk about greater than seven millimeters in diameter.

There is some, thought that maybe, greater than 10 millimeters is would be more, reasonable to use to diagnose obstruction.

If the obstruction is in the proximal small bowel, there will be polyhydramnios.

But if the site of the atresia is in the distal small bowel, the amniotic fluid volume around the fetus will remain normal because the fetus is still able to swallow and digest that fluid.

And the proximal, and mid small bowel is still functioning enough to reabsorb the fluid atresia are felt to be vascular accidents and the associated anomalies are all related to some other vascular etiology.

When you have a small bowel obstruction, the number of dilated loops will depend on the level of the obstruction.

So proximal obstruction will have a fewer number of loops and a distal obstruction will have more loops.

It's important to remember that the jejunum is easily dilated and that, proximal obstruction can have larger small bowel loops, whereas the ileum does not stretch quite as well.

And ileal obstructions tend to, result in perforations at smaller diameters.

About 7% of the time the rees will be multiple.

Here's another example of a small bowel obstruction.

We could see multiple distended dilated loops of fluid, fluid-filled bowel, which are peristalsing rapidly.

Another example of a more distal atresia.

In this instance, we can see a loop of distended bowel right across the anterior uh, abdominal wall just underneath the skin surface here with associated polyhydramnios, this fetus is at 41 weeks.

Pretty unusual to see polyhydramnios at 41 weeks, which brings you back to the fact that you do have this distended loop of bowel.

And this diagnosis was not made until the patient was the fetus was post dates.

When there is a small bowel obstruction, there's a risk of ischemia, infarction, and in utero perforation, the reason for this obstruction could be an atresia or a volvulus or meconium milus, but any one of them can have the risks of these complications.

A hydroureter should be identified by its presence posteriorly in the fetal abdomen near the spine.

About of the a third of patients with small bowel obstructions will ultimately be diagnosed with cystic fibrosis, and this diagnosis should be, especially considered if echogenic bowel was seen in the second trimester.

Here's another patient with a bowel obstruction seen at 34 weeks and we see this very large distended loop of bowel filled with these internal echoes, not peristalsing, just sitting, and, and not moving.

And if you look on the sagittal image, I think you can appreciate that we have multiple loops here that have twisted all around itself.

And this did turn out to be a ous and this bowel had infarcted and which explains the lack of peristalsis.

This child lost about a third of his small bowel after delivery.

Meconium Ileus

Another example of a small bowel process.

In this instance though, we see a short segment of bowel.

You could see rapid peristalsis, more normal appearing peristalsis all through the abdomen.

But this loop is not peristalsing, it's just sitting there and sort of, squeezing a little bit but not giving us normal peristalsis.

And this is an example of meconium ileus.

What happens in meconium ilis is the normal meconium that's present in the small bowel is abnormally thick and it becomes impacted because it is so thick and sticky once that meconium is stuck.

The result for the imagers is the typical small bowel obstruction where we see dilated bowel typically, filled with epigenic material that may or may not be peristalsing.

When we see this thick echogenic material within the bowel loop, these patients nearly always have cystic fibrosis and indeed 10 to 15% of fetuses with cystic fibrosis present with meconium ileus in this instance.

Again, another, look at that single loop of bowel which is distended and not peristalsing.

When we look closely, we can see there's a little tiny bit of fluid outlining the outside of the loop in this patient.

Once we see fluid in association with uh, a, uh, a bowel obstruction, we're can now consider that we've got the situation of meconium peritonitis.

Meconium Peritonitis

Meconium peritonitis is the result of a perforation in utero.

The meconium leaks out of the small bowel, and the result is a subsequent sterile chemical peritonitis.

Because of course there are no, bugs in a fetus.

A fetus is sterile. So this is a chemical peritonitis.

The immediate result is free fluid.

Now that perforation can occur proximal to meconium ileus to a atresia, to a volvulus, to an intussusception, or it can be idiopathic.

Often these perforations will seal spontaneously.

So if a fetus comes in with ascites, it should be considered as a possibility.

When you're trying to determine the source of the as ascites, what will happen to the fetus depends on what caused the perforation.

Most of the time, fetuses who present with ascites with their small bowel obstruction do not have cystic fibrosis.

Once the perforation has occurred, there's a reactive membrane that forms over the whole.

Typically it's incomplete, but sometimes it is complete.

So we can't predict whether there's going to be more leaking from that hole or not.

But what happens is that reactive membrane has some inflammatory process and the fetus will subsequently deposit calcifications around that inflammation.

They can be linear, they can be in clumps or they can wall off the fluid into a cyst like structure or the leak can just seal over and you'll never know what happened to it and you'll never know where it was.

So here's the fetus. With a small bowel obstruction, we can see these dilated loops of bowel, but in this instance we can see these coarse calcifications clumping along the anterior abdominal wall that gives us, confident, understanding that at some point this bowel obstruction did perforate and there was a leak and then it swelled back up again.

Here's uh, an an example of the late outcome of meconium peritonitis.

We see these scattered calcifications in the fetal abdomen.

There's some here on this view, there's some over by the stomach, there's some all around the outside edge of the liver.

And this tells us that at some point this fetus did have a small bowel obstruction with a perforation and the chemical peritonitis.

However, by the time we saw the fetus, there was no evidence of a small bowel obstruction or a gastric outlet obstruction at all.

And this fetus can be predicted to have an excellent outcome.

In this instance, however, the meconium was walled off with the calcium in what is called a meconium pseudocyst.

And it's clearly not a cyst.

There's no through transmission.

It's not koic, but it is round.

And so it's gotten the name of the pseudocyst.

And here's another example of this meconium pseudocyst.

The, the chemical peritonitis has created a wall around the extruded meconium.

In this instance on the left, we don't see any dilated bowel left behind, but on the right we can still see that the, the dilated small bowel obstruction is still present when there's uh, a meconium pseudocyst.

It's interesting to realize that the presence of calcium is very uncommon in cystic fibrosis.

There's a few theories for why this is, it's possible that the cystic fibrosis fetus meconium is so thick that it doesn't leak out when the perforation occurs.

Another thought is that the cystic fibrosis fetus lacks the enzymes that are necessary to react to the peritonitis.

If you're thinking it may be a case of cystic fibrosis with meconium ileus and meconium peritonitis, it's worth taking a look around to see if you can see the gallbladder because this cystic fibrosis patient typically will not, have a gallbladder in evidence on the ultrasound.

So if you look over in the right upper quadrant and there's a beautiful gallbladder, it probably is not cystic fibrosis.

That leads us to uh, something that I mentioned earlier, which was that if you are considering cystic fibrosis, it is important to go back and see if you had this finding earlier on in the gestation, which is the finding of echogenic bowel.

Echogenic Bowel

We have a collection of echogenic debris or material in the pelvis, lower abdomen and pelvis of the fetus, and notice that it is equivalent in echogenicity to the adjacent ileum.

So we can describe echogenic bowel in the second trimester when the bowel echogenicity is equal to bone.

In these instances, it is important to, analyze the chromosomes in these fetuses because up to 25% of fetuses with echogenic bowel may have aneuploidy and about half of those fetuses will, re will have uh, trisomy 21.

Now echogenic bowel, in addition to be associated with aneuploidy, is associated with uh, infections such as CMV.

It's associated with cystic fibrosis and it also can be an indicator of severe early onset.

IUGR. One explanation for echogenic bowel is that the fetus has swallowed intra amniotic blood.

So the mom has had a, um, intrauterine hemorrhage, uh, so-called abruption either in the first or early second trimester.

The amniotic fluid has become echogenic.

The fetus swallows all that echogenic debris, which is basically red cells in the, uh, amniotic fluid just like the fetus I showed really at the opening of the talk.

As that debris moves through the gut, it settles down into the pelvis and can become genic.

Um, now 60% of fetuses with echogenic bowel will have an or could have an adverse outcome, and those outcomes could include abnormal chromosomes, spontaneous IUFD, intrauterine growth retardation.

So these fetuses, regardless of what the source is for the echogenic bowel need close follow-up.

And one explanation for that could be that the kids who have intrauterine hemorrhages because they have a, uh, placental abruption, maybe they have a lousy placenta and therefore they're getting IUGR and IDs.

And the echogenic bowel is a side, um, effect of this bad placental hemorrhaging process that's going on through the gestation and resulting in these poor outcomes.

Here's a case that we followed.

Uh, at 18 weeks we can see the echogenic bowel, uh, down in the pelvis and at 19 weeks we can still see the echogenic bowel.

And at 25 weeks a tremendous amount of genic bowel presumably all related to swallowing of intra amniotic blood.

Here's another patient. Here's the first trimester ultrasound, and you can see when we sort of jiggle the mom's abdomen, the placenta is back here, the uterine wall is here with a big contraction and in the anterior aspect of the uterus, notice the jiggle that happens in this area because this is an coic hemorrhage.

When the patient came back in the second trimester, that iso coic low anterior hemorrhage has sort of re um, reformed itself into this hypoechoic structure along the inferior wall of the uterus.

And when we look at the fetus, indeed there's the echogenic bowel that has resulted from swallowing the intra amniotic blood that resulted from that first trimester hemorrhage.

GI Duplication Cysts

Moving on in our uh, trip through the GI tract, we're now gonna move towards GI duplication cysts.

These cysts can occur anywhere from the esophagus to the rectum.

They're usually completely cystic and the cyst can be the lead point for an intussusception or a bowel obstruction.

And on this in uh, image here, I wanna point out all the normal cystic things that you see in the upper abdomen of a fetus.

So here's the gallbladder in the right upper quadrant, here's a loop of bowel, presumably transverse colon.

Here's the umbilical vein, which I know from turning color on and following its pathway.

And here is a cyst that isn't supposed to be there.

This is the same fetus just showing you a real time clip.

You can see the gallbladder, you can see the bowel coming across here, the intra hepatic umbilical vein and the cystic structure sitting right here closely related to this loop of bowel, consistent with a small duplication cyst.

Duplication cyst can be of any size.

Here's a much larger one over four centimeters in the fetus and you can see it here just pushing the gallbladder over the gallbladders draping over this cyst, which is unrelated to the liver.

This is the postnatal image of that fetus.

And we can see when we scan from the side from the right side of the of the neonate, uh, here's the skin surface and here's the cyst and you've got this bowel signature around the back.

And um, on the clip here you can see that the um, the cyst has bowel signature all the way around it and we can see some good through transmission confirming that it's a cyst.

No air has gotten into this lesion because it is adjacent to the bowel but not part of the bowel lumen.

Liver Lesions

Moving on, uh, here's a lesion that you don't see very often.

This is a transverse view of the upper abdomen.

Here's stomach intra hepatic umbilical vein.

This is the liver and there's an echogenic lesion here seen in the left lobe of the liver.

On this coronal view, we see it's a very well-defined discrete lesion within the liver.

Now liver tumors can be seen in utero.

Typically we see a mass and we'll look for central calcifications, which may help us with the differential.

The most common lesion in a fetus would be a he, he angio endo thoma.

But we can also identify adenomas, focal nodular hyperplasia, he angios hepatoblastoma and metastatic tumors.

In addition, we can see cysts in the liver.

These can be hepatic cysts or choli doco cysts.

And these are typically at the right lower edge of the liver.

Here's the confirmatory fetal Mr on the case that I showed you earlier.

Here's the um, heart, the diaphragm, the liver is here and here's the genic.

What was on the ultrasound was an genic liver, uh, lesion in the liver corresponding to a hemangioma in this fetus.

Here's another coronal image in a different patient, uh, a hundred percent credit goes to my sonographer who identified that there was a lesion in the liver and I think it's pretty darn hard to see.

Taking pictures of the liver is not part of our protocol, but she identified on this coronal image and again for some anatomy, here's the stomach and there's the diaphragm.

Sorry, here's the, this is the heart, this is the diaphragm, this is the stomach here and the liver is here.

And in the right lobe of the liver, you can see this hypoechoic solid mass in the inferior edge of the right lobe.

Well, when we put color on, it makes the mass a lot easier to see and you can appreciate I think this typical feeding vessel with peripheral rim flow, which we see in hepatic heman endothelials

In this patient we can see, uh, on the right side, so we're looking at the liver, this koic structure right up against the rib cage.

So when something's koic, we'd like to call it a cyst, but to call it a cyst we need to have through transmission.

So what did we do? We turned the mom on her side to try and get a shot at this thing, this two centimeter thing coming from this side so we could get the through transmission.

And here's the image coming in from the right side.

You get this koic structure and you have the beautiful through transmission that let us diagnose a hepatic cyst in utero.

Gallbladder Abnormalities

What else can we see in utero?

I'm sure that most people who have done obstetrical ultrasound will have seen this.

And this is a transverse image in the upper abdomen.

And here we have the gallbladder and right in the fundus of the gallbladder, the echogenic lesion with posterior shattering.

And of course this is a little gallstone.

Now sometimes you can see the focal gallstones like this and other times the gallbladder will completely be chock full of all of this echogenic debris.

Both of them represent gallstones.

The gallbladder does start to contract in the third trimester.

So if you don't see the gallbladder in the third trimester, it could be completely normal just going through the phase of contraction.

It may be due to atresia of the gallbladder or it could be supporting evidence for cystic fibrosis.

A gallstones, as we just saw, can occur in utero.

And these resolve spontaneously usually post in the immediate postnatal period.

They do not need to be imaged in the neonate and choli doco cysts get a lot of press.

They get talked about a lot, but they're extremely rare.

So here's an example of a fetus where we could see the beautiful gallbladder in the right upper quadrant, but then we also identified this structure that also looks like a beautiful gallbladder in the right upper quadrant.

And on this image with the color, you can see there's no flow in either structure and this fetus did indeed turn out to have a duplicated gallbladder.

Splenic Abnormalities

Something else that you don't see very commonly in a fetus.

This time we're looking in the left upper quadrant.

So here's the stomach and posterior to the stomach right here we again see a well-defined an coic structure and this is completely con um, um, centered within the spleen.

And this is a splenic cyst.

So cysts of the spleen are extremely unusual.

Uh, any sort of abnormality in the spleen is very unusually seen in the fetus, but there's no reason why you can't see it.

You just have to remember to go look for it.

Once again, not one of the things on our protocol of the fetal survey, the spleen can be absent.

Typically that's related to the asplenia hetero taxii syndromes and in those instances the stomach will be located very far posteriorly or possibly anteriorly in the midline because of the hetero taxii syndrome.

Splenomegaly can occur in utero if there's severe iso immunization of the fetus with um, um, hemolytic anemia.

It can also be seen in infection and metabolic problems and neoplastic, um, instances, particularly in fetal lymphoma.

Ventral Wall Defects

A few minutes now on ventral wall defects.

These fetuses present with high a FP levels due to the skin defect and it's important to evaluate the cord insertion and the bladder in all of these fetuses.

So here we have an example of a anterior abdominal wall lesion here, seen a little better here.

And you can see these free floating loops of bowel coming out just to the right of the umbilical cord.

And these loops float around with no surrounding membrane and are very closely related to the site of the cord insertion here.

This of course is gastroschisis the defect, as I just said, it does occur to the right of the umbilicus.

This is a sporadic defect with no genetic associations and no recurrence risks.

That does tend to occur in younger mothers, meaning in particular mothers under the age of 20.

To make the diagnosis of gastroschesis, we look for free floating bowel in the amniotic fluid.

Now what that means is there is no membrane over the bowel, therefore you will never see ascites because if there's ascites in the fetus, it will be completely, easily released into the amniotic fluid.

And the presence of ascites means you're not looking at gastroschesis.

There can be an inflammatory pseudo membrane over the bowel in up to 20%, but that's typically not seen as a discreet thin, um, covering membrane.

These fetuses often have other issues with the GI tract because of the fact that when gastroschesis occurs, the bowel does not have its ability to, do its normal protrusion out into the base of the cord, the 270 degree rotation and the return to the, to the fetal abdomen where it can then lay down from the ligament of trites in the left upper quadrant all the way down to the cecum in the right lower quadrant.

That's the process that prevents volvulus and mal rotations.

And because this bowel has protruded out of the abdomen, it's at high risk for mal rotations and volvulus and other GI anomalies in these fetuses, despite the fact that the only thing they have wrong is GI tract anomalies.

They tend to have postnatal complications in a very high percentage of these fetuses.

They spend a lot of time in the hospital and a small number of these fetuses lose a lot of small bowel.

Here's another example of a patient with gastroschesis at 33 and a half weeks and you can see these fluid filled dilated loops of small bowel freely floating out in the amniotic fluid.

And notice in this instance that the stomach in this fetus, these images were done at the same time, same day.

The stomach is quite small.

So this fetus, this mom was going along and we're waiting for the, for the pregnancy to continue.

And she came back into the hospital at 35 weeks complaining of decreased fetal movement.

Now of course this was nine o'clock on a Friday night and which is of course when all of these things tend to happen and there's a radiology resident on call and he called me up and said, I don't think I can scan this patient.

I've never scanned gastroschesis.

I won't know what to do, I won't know what to look for.

So I said, that's okay, give it a try.

Go back and look at the priors and then look at today and then call me up and tell me what you think.

So he scanned today after looking at the priors and he said, you know, it's very different now.

The gastroschesis doesn't have any fluid in it.

There's no dilated loops anymore and the stomach is huge and those are really, really good observations.

And so he also noted that the biophysical profile score was two, the fetus was not moving.

So this was an unhappy fetus who is no longer putting any fluid into this gastroschesis loops and who has is now giving us evidence of a possible gastric outlet.

Obstruction. The fetus was delivered that night and indeed the bowel was navy blue, but at delivery as soon as the bowel was lifted up straight and the blood flow could, could um, be restarted.

It pinked right up every time they let go of the bowel and let it drop to the side back to navy blue.

So we were lucky enough in this instance to pick up the acute ischemia that was happening in this fetus as the gastroschesis progressed.

Omphalocele

Another anterior abdominal wall defect we need to be aware of is this one.

In this instance we see a piece of liver, this homogeneous liver sticking out from the abdominal wall.

This is the anterior surface of the chest and you have the stomach back here.

And in this instance we do see this thin membrane covering over the top of this loop of liver that's sticking out.

So now of course we're looking at um, falle and um, falle is a midline defect with a covering membrane.

And in this instance we do see the ascites because the membrane outlines it for us.

The umbilical cord inserts into this mass of the um, falle and the opposite of gastroschesis.

Um, falle occurs more often in older moms, particularly over the age of 40.

Here's an in falle that was seen as early as 13 weeks.

It's a profile sagittal view of the fetus and you can see this little tiny thing sticking out right here in the anter abdominal wall.

And here it is, uh, on the transverse view and this was a, uh, die chorionic twin gestation and the upper twin has the emale.

Another example of an emale in this instance with just bowel in it instead of just liver in it.

And you can see the covering membrane and the umbilical choroid inserting just into the side here.

Amal seals have a high association of chromosomal abnormalities if there is no liver present in the mass, like this case I just showed, if there's liver out in the emale, the risk of chromosomal abnormalities are associated is much lower regardless of whether there's a chromosomal abnormality or not.

When there's an emale present, there is a high association of other anomalies in the fetus.

You wanna be very careful that you're getting a good look at these kids.

In particular, congenital heart disease will be present in over 50%.

Another example of a fetus with a gap with a um, falle.

Here's the fetus here you can see some spine back here and notice this enormous, um, falle almost as big or even bigger than the body of the fetus itself.

And with the color doppler we can see that the umbilical cord runs right into the em falle and along the inferior edge of it.

Well we know we have to look around, up in the brain we can see a choroid plexus cyst and when we went to look at the extremities we had bilateral clenched fists and everyone should be expecting that the chromosomes would indeed come back.

Trisomy 18, Remember that emal seals can be associated with syndromes including the penology of cantrell, which is the combination of emale, ectopic cordes, sternal diaphragmatic and pericardial defects, as well as with beck with ween syndrome.

And the things we can see in beck with ween include macroglossia, big livers, spleens and kidneys, cystic placentas and macrosomian.

Here's a fetus with, again, a very large em fall.

Here's the lower portion of the chest.

You can see the ribs here and a little bit of stomach and the entire liver is out in this val seal.

Here's the sagittal view of the same fetus and you can see the liver here.

And if you're, uh, looking very carefully at one end of the clip, I wonder if you notice that a little tiny bit of the heart and I'll move my pointer out to the other side, has protruded past the anterior margin of the sternum.

Here's a magnified transverse view of the chest and I hope you can appreciate that.

The chest wall should stop right here.

But the on this four chamber view, you can see that at least a third of the ventricular chambers have protruded out through the anterior wall in this fetus with penology of Cantrell.

In contrast to this fetus, again, here's the upper abdomen, A big um, falle stomach is here, gallbladder is out, there's a loop of bowel out right here and there's a big piece of the right lobe of the liver that's out in this fetus.

Again, when you see an em falle, you look around, here's a sagittal view of the face and here's the chin and protruding from the mouth.

An enormous tongue.

This fetus had macroglossia was unable to keep its tongue in its mouth during the exam and this fetus had Beckwith Weidemann syndrome.

Conclusion

So here we are at the end of the talk on the GI tract to this fetus and I hope we've given you something to chew on.

Thank you.