anatomy. The situs can also be totally reversed, or situs inversus, as in this patient. Then there were bilateral left-sidedness and
right-sidedness. So bilateral left-sidedness or polysplenia syndrome, is a manifestation of heterotaxy syndrome. And in these patients we can see a midline liver, mal-rotation of the bowel, and bilateral left-sidedness to the lower anatomy of the lungs. And in asplenia syndrome, generally the spleen is absent, and again, we have mal-rotation of the bowel with a central
liver. [BLANK_AUDIO] So with polysplenia syndrome, we can get multiple different findings, and none of these have to be present for diagnosis. In the spleen, generally, we can see multiple spleen or polysplenia, but sometimes it can just be lobulated or even normal appearing. The liver tends
to be midline, and there may be anomalies of the biliary tree/g. Like in our patient, with a intrahepatic gallbladder. The pancreas tends to have an absent body and tail so it's a just shortened pancreas. There is interruption of the inferior vena cava. Generally, the aorta tends to be left-sided as does the heart, and usually there are rotational anomalies affecting the bowel. [BLANK_AUDIO] This patient
This is another patient with heterotaxy syndrome. In this patient we can see a midline liver which is generally located more on the left side, the heart is also on the left side. When we look at the axial images we can see that the spleen and the liver are both left sided, okay. But also, there are bilateral adrenal masses which
are high signal intensity on T2, and which demonstrate fluid-full levels because of hemorrhage. So this patient actually has two different syndromes. Left Sided Liver, Spleen, Heart, and Stomach with rotational abnormalities of the bowel, which I didn't show you. And these are consistent with situs ambiguous, and then bilateral pheochromocytomas.
The patient also had a known medullary thyroid carcinoma, and so they also have multiple endocrine neoplasia type II. When we see
diffuse liver diseases it's important to look at the pattern of their distribution, and in this patient, we can see that these nodular cystic areas within the liver tend to be distributed in a periportal manner or area. Okay. And here on this CT scan we can see
that they follow the portal triads. And these are in fact, peri-biliary abscesses. The patient had a history of gastric carcinoma, and the question was whether these nodules are metastases or they represent abscesses, as the patient also had the fever and this distribution would be typical for for abscess. Here's the MR examination. You can see the MR
CP where there is ductile obstruction and dilatation because of tumor recurrence, and this was the cause for the peri-biliary abscesses.
[BLANK_AUDIO] This is a patient who presented to us, he was 19 years old, and he had nausea and vomiting, and abdominal pain which was chronic,
but which had worsened recently. In this patient, we can see that there is enlargement of the liver. It began with the lateral segment coming over and touching the spleen. The spleen itself is also enlarged. So there is element of portal hypertension here. And we can see that there is lobar redistribution with the right lobe of the liver relatively small, and the left lobe of the liver
being quite enlarged. There's ductal dilatation, and there is some areas of hepatic congestion, with this reticulated appearance. We perform an MRCP to look at the bile ducts a little more carefully, and we could see that there was a filling defect within the left hepatic duct, and this is nicely demonstrated also on the ultrasound as
well. So this patient actually had stool examination. And his stool was positive for eggs from three different parasites. Hepatic schistosomiasis mansoni, fasciola hepatica probably what's causing the bile duct disease, and also tapeworm disease within the intestines. [BLANK_AUDIO] There
are two different species of schistosoma that cause hepatic diseases. These are schistosomiasis japonicum and schistosomiasis mansoni.
Japonicum tends to cause more linear parenchymal areas of fibrosis because the eggs of japonicum are quite small and they tend to travel up the portal vein and deeper into the hepatic parenchyma. Schistosomiasis mansoni produces larger eggs, and these eggs get lodged in larger hepatic, sorry portal veins, and this rather causes an inflammatory reaction and fibrosis
in the central portal veins. And so we can see periportal fibrosis. And so the imaging manifestation hepatatious/g schistosomiasis really depends on where we see those areas of fibrosis, where the eggs deposit. So on a ultrasound, with schistosomiasis japonicum, we'll see radiating
echogenic septae that extend from portal triads to the hepatic capsule. And these will appear as turtoise shell areas of calcification, if they're calcified, on CT scan. And on MR we can also see the enhancing thickened capsule and the fibrous bands. With schistosomiasis
mansoni, on the other hand, on ultrasound, CT, and MR we can see the manifestation of periportal fibrosis with increased echogenicity or decreased attenuation on ultrasound and CT around the portal triads. So here
is a patient with schistosomiasis japonicum, and here we can see, on an unenhanced CT scan, that there are these linear areas of calcification extending
onto the surface of the liver. And so this is typical turtoise shell calcification seen in a schistosomiasis japonicum. Sonography also tends to be quite diagnostic in these patients. We'll see these linear bands that extend to the hepatic capsule, and you can see that they extend from the portal triads on towards
the capsule. So this is a pathognomonic appearance for hepatic schistosomiasis japonicum. With schistosomiasis mansoni, on the other hand, we can see that there is increased thickening around the portal triads manifested by increased echogenicity
on ultrasound, and decreased areas of signal intensity on the T1-weighted MR. These areas will tend to enhance on the delayed enhanced MR exam, and so on this patient we can see that there are bands of fibrosis, this black arrow is pointing to, that are going around the portal triads, and also thickening of the hepatic capsule.
This is a patient that has multiple hepatic masses, but before we look at the hepatic masses, we should also look at the backroom/g liver. And here we can see that the liver is enlarged, and has this reticular pattern of enhancement which is typical for hepatic congestion. So in this patient we can see that the hepatic masses on the arterial phase have nodular
areas of enhancement, but not only these are peripheral, as would be seen in a hemangioma, but we can also see central areas of enhancement. So this would be quite atypical for hepatic hemangioma. So then we have these masses with hypervascular regions, and in the venous phase, these areas don't tend to get larger. On the venous phase we can also appreciate the reticular pattern of enhancement that
we can see in hepatic congestion along with the enlarged hepatic veins, and prominent IVC. So putting the findings together, multiple hypervascular hepatic masses, with hepatic congestion, these will be consistent with the carcinoid hepatic metastases, and the congestion would be from right heart failure from endocardial fibrosis.
Hepatic congestion has a typical appearance, as I had mentioned,
gives you that reticular pattern of enhancement. And these are three different patients with different causes for congestion. In the first patient, she had pulmonary hypertension, second patient had dilated cardiomyopathy, and the third patient actually had a tumor within the heart which was causing obstruction of the hepatic outflow.
[BLANK_AUDIO] This is a patient that has an unusual appearance to the liver, and the liver looks a little bit bizarre in its outline. And then we provide contrast enhancement we can see that in the arterial phase there are multiple heterogeneous areas of enhancement throughout the liver, but also early in the arterial phase, we can see that
there is filling of the hepatic veins. So this is a hint to us, a clue to us, that there is shunting through the hepatic parenchyma from the hepatic artery into the hepatic veins. So multiple hepatic mass-like areas with shunting through/g the liver. This is a different patient with the same diagnosis. So when we look at the liver, we can identify these
large mass-like regions of shunting through the liver. Again these are arterial phase images with early filling of the hepatic veins. The liver is also enlarged and lobulated, and the hepatic artery is quite enlarged because of all the shunting. So this is a typical appearance for hereditary hemorrhagic telangiectasias or Osler–Weber–Rendu syndrome. So we see numerous hepatic shunts and the shunts can
be between the artery and the hepatic vein or the hepatic artery and the portal vein, and even between the veins themselves. There is also early filling of the hepatic veins, there is a manifestation of the shunting, the liver becomes enlarged as does the hepatic artery. Here is a different patient on MR examination, and we can see this
large lobulated liver with flow voids in the hepatic arteries because of the increased hepatic velocities. [BLANK_AUDIO] And this brings us to the
end of part one of diffused liver diseases. I wanna thank you, and I'd like you to join us for part two of the same topic. [BLANK_AUDIO]
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