Diffuse Liver Disease Pitfalls and Hints - SD

Introduction

Hello, my name is Phil Rawles and I'm a professor of radiology at the University of Southern California Keck School of Medicine, and I work at LA County USC Medical Center.

I'm gonna be talking to you today about the diffuse liver disease and the sonographic evaluation of it.

Hello. I'm gonna talk to you today about diffuse liver disease, some of the pitfalls that you might encounter in some of the hints as well.

I'm not gonna cover a lot of the basic information, because you already know that, I'm from California, and so the obligatory surfing slide is here.

Acute Hepatitis

First talk about acute hepatitis and generally we're talking about Hepatitis A here.

Acute hepatitis is really a clinical diagnosis and we don't really require imaging to make the diagnosis.

The labs however, can be confusing and we can have elevated or normal labs, which will prompt clinical infusion and therefore an ultrasound examination.

The first thing I'd like to talk to you about is the, what I call the myth of the starry sky.

The Myth of the Starry Sky

In acute hepatitis, many people believe that increased periportal echoes coupled with decreased parenchymal. Echogenicity is virtually diagnostic for acute hepatitis, and this in fact is not true.

The, the findings with respect to the periportal echoes are related to normal anatomic variability because of the variations in the amount of periportal fat not related to the hepatitis.

And in fact, this has been shown to be, true in a blinded study that was done in Italy some time ago where they did a study of 700 and, 91 patients and only 19 of the patients with acute hepatitis had this pattern.

And in a control group, comparing normals and patients with hepatitis, there was no difference whatsoever in the, frequency of this finding.

So the starry sky is not something that you ought to pay attention to.

Here's, here's an example of the starry sky.

Of course, there is, such a thing as the starry sky, as we see in this Vincent Van Gogh painting.

Thickened Gallbladder Wall

There is one little hint that can be useful to you. However, in acute hepatitis in that, often these patients will have a very ous thickened gallbladder wall.

Some people call this a striated, gallbladder wall.

And this can actually, suggest the diagnosis of acute hepatitis.

In fact, this is usually or often the only ultrasound abnormality in acute hepatitis.

Here's an example of, hepatitis A, and I'll use the point the mouse as a pointer.

And you can see that here we have the submucosa, and this is a massively thickened wall with a small lumen.

And this is a hepatitis A patient.

Here's another hepatitis, A patient whose gallbladder essentially has no lumen.

It's totally obliterated because of the wall thickening.

One thing that is, also useful is if you have significant gallbladder wall thickening with a very small gallbladder lumen, less, less than 15 millimeters.

This suggests a non intrinsic cause of gallbladder wall thickening.

That is to say an abnormality not related to gallbladder disease itself.

There are other things, of course, that cause gallbladder wall thickening.

Here's an example of a cirrhotic patient who has a low albumin in portal hypertension, and we see the ascites and the thickened gallbladder wall, both of which are caused, by the cirrhosis.

Here's another patient who has cardiac disease and a thickened gallbladder wall with a very small lumen.

Here's a less usual cause of, gallbladder wall thickening, and that's infectious mononucleosis.

And there are other things that, that can do this too.

Of course, this small lumen rule doesn't always work.

Here's a patient who has, a lumen that's larger than 1.5 centimeters in a thick wall.

And this is a patient who's cirrhotic and has, portal hypertension in a low serum albumin.

Here's a patient who actually has acute cholecystitis that looks sort of like the cases that I've already shown you.

This patient happens to have a small gallbladder wall lumen in a thick wall, so the rules are not perfect.

Here is the same patient who has, cystic duct stone in this particular video clip.

So the rules are not perfect, but they work reasonably well.

So we do have, fires in Los Angeles, and I just put this in as, an example of that.

Fatty Liver

Alright, let's talk about fatty liver.

Fatty liver is becoming an increasingly recognized health issue, especially in the United States, and elsewhere too.

Of course, it's a common condition and has many different causes.

The actual pathway to fatty liver is poorly understood, but there are many conditions that are associated with that.

I've listed some of 'em here.

Alcohol, diabetes, obesity, malnutrition, drugs, and many others.

One concern is the so-called non-alcoholic fatty liver disease, or N-A-F-L-D.

And in the US this is the hot diagnosis in hepatology.

You can get progression from fatty liver to what's called nash, which is steatohepatitis, where you have actual liver inflammation with a fatty liver, and then NASH with fibrosis, which can lead to cirrhosis.

And in fact, fatty liver disease is, probably going to be one of the major causes of cirrhosis in the United States.

And here's an algorithm that I'll leave up for a moment or two for those of you who want to, to look at this.

Hopefully you can review it.

And there's a reference that from where this came, talking about the progression of fatty liver disease and natural history of non-alcoholic fatty liver disease.

Diagnosis of Severe Fatty Liver

Now there's no problem making the diagnosis of severe fatty liver disease.

Basically, this is the classic situation where you have markedly increased liver echogenicity and visible attenuation of the sound.

This is only seen, however, in a minority of the most severe cases in this circumstance, the diaphragms poorly seen and the vessels in the liver are indistinct.

Here's an example of such a case where there's, obvious, severe attenuation.

We can barely see the diaphragm, but this is the severe case, which is not really terribly difficult to diagnose.

Diagnosis of Mild Fatty Liver

It's more important to make the diagnosis of mild fatty liver because we wanna catch the fatty liver disease early so that perhaps something can be due to mitigate the potential complications of the illness.

The way that we make this diagnosis, there are several actually, but one is to compare the, spleen in the liver, not so much directly, but using the, the, the kidney as an internal standard.

And I'll show you what I mean by this.

Normally the spleen is more echogenic than the liver, but ordinarily you can't compare them directly.

Now here, here's the circumstance.

This is an anatomic variant where the left lobe of the liver overlaps the spleen here.

And in this, particular circumstance, you can compare them directly and it allows us to see the, the echogenicity patterns.

So this is a long exa scan in the left upper quadrant, and here's this liver overlapping the spleen.

And notice how the liver, this normal liver is more genic than the spleen, and of course, both are more genic than the renal cortex.

So that's the normal situation.

Now here's a, another patient with a, with a similar anatomic variant with liver overlapping the spleen.

But in this circumstance, the liver is more oncogenic than the spleen.

So this is fatty liver.

It would be nice if we could directly compare the spleen in the liver in all patients, but it's only possible in a minority, therefore, you have to use the kidney to help us.

Basically what we do is to compare the liver in the spleen to the kidneys.

And if the liver to right kidney echogenicity is greater than the, the difference is greater than the echogenicity of the spleen compared to the left kidney, fatty liver is present.

So if the liver looks more relatively echogenic to the kidney than does the spleen, that's abnormal.

And here's one such example.

On the right we see that there is a fairly pronounced difference in echogenicity between the liver, and the right kidney on the left.

However, the spleen is not nearly so different from the renal cortical echogenicity.

So this is diagnostic of fatty liver and is an aid to making the diagnosis in more subtle cases.

Fatty Sparing and Focal Fat

Another important thing to look at is, fatty sparing or for that matter, focal fat.

These entities can be diagnostic of, fatty liver and they can also create problems by simulating a mass.

And one needs to be aware of both of these features.

Here's an example of a patient who is very prominent sparing in this otherwise fatty liver.

And, this is often confused for a mass and you don't really want to go ahead and do additional, imaging that isn't necessary when you have a fine that it's actually typical.

It's just a question of learning how to recognize what's typical and what's not.

Here's a typical area of increased echogenicity related to focal fat, which is of course a different situation.

And this too can simulate a mass.

So variations locally in fat can simulate masses and one needs to be a bit careful about that.

Here's a combination.

Basically this patient has an area of focal fat and, peripheral hypo echogenicity, which is sparing.

So this almost looks like a, a lesion with a halo, but this is in fact just fatty focal fat and sparing around it.

There's another one, this is I think is, I think this is actually the same patient who has this central hypo coic area and peripheral increased echogenicity.

Now, not everything that contains fat is innocuous. Okay.

And here's a patient who has hepatocellular carcinoma, and we can see on this non-contrast scan that there's a definite fatty component to this.

H-C-C-H-C-C is one liver lesion that has fat in it vocally, not terribly infrequently.

And here's the corresponding ultrasound with the less affected, soft tissue area and the echogenic fatty area.

In the next, example, we see a contrast hand scan where the fatty area doesn't enhance, but the other area enhances quite prominently.

And on the color doppler, we can see that the fatty area does not enhance, but there's very prominent increased flow within the solid, more non fatty affected, component of this hepatocellular carcinoma.

So the next point I wanna make, which is germane to the diagnosis of folk of uh, fatty liver, is that if you have classic spirit areas, these are diagnostic for fatty liver, for fatty liver.

And this is true even when the overall liver echogenicity is normal.

These are some of the areas that are classically affected by sparing.

And you can see basically it is the posterior or or dorsal portion of the left lobe, ventral to the, bifurcation of the portal vein along the fi for the ligamentum, venum.

And here's an example of this ventral to the, the portal vein bifurcation.

Here's the left portal vein, right portal vein in this sort of classic parametal or triangular shaped area is very typical for sparing and it's diagnostic for fatty liver down a little bit more coddle, you see the same, dorsal left lobe sparing.

And of course the gallbladder region is another area that is commonly affected by sparing.

And here's one such gallbladder that has a very prominent spar area.

Again, don't confuse this for a mass.

This is diagnostic for fatty liver.

Here's a long axis view, and here again we have sparing adjacent to the gallbladder.

And one pitfall here that isn't, always appreciated is that people will confuse this for either thickening of the gallbladder wall or more significantly more significantly, a peric coly cystic abscess.

This is foal sparing, and should not be confused, for anything else.

Now, here's a classic s spirit area diagnostic of fatty liver, but here's a case that's more problematic and we have a, a large liver here, but it's not obviously a fatty liver from the images that we have here.

However, when we look around a little bit, we see that there is in fact a classic spared area anterior to the port of Hetus portal vein bifurcation region, and this is a, thus definitively fatty infiltration of the liver.

So sparing alone is enough to make the diagnosis of fatty liver.

Cirrhosis

Let's move on to cirrhosis.

Cirrhosis has many causes, alcohol abuse, hepatitis B, hepatitis C, and many other causes including progression of non-alcoholic fatty liver disease.

This is the wine that the patients at the county hospital in Los Angeles prefer first growth, Bordeaux, et cetera.

The primary STIC diagnostic criterion that we use for cirrhosis is a nodule liver surface.

To a lesser extent we use the shape of the liver.

The morphology where you can have a small right lobe and a large co lobe are in my view, an even more useful finding is an enlarged lateral segment of the left lobe, especially when the surfaces are by convex.

Here's an example of a 3D image of a nodular surface in a patient with ascites.

And you can see this quite nicely.

Unfortunately, we can't get images like this all the time.

The, it's easy to make the diagnosis of surface nodularity, when we have ascites as we do in this case, and this is, quite readily diagnosable, but when there's no ascites, it can be harder.

Here's a patient who has a large left lobe, small right lobe, and this is again, cirrhotic morphology and certainly suggestive of cirrhosis.

Liver Surface Nodularity

A little bit about liver surface nodularity.

A lot of people will think that, looking at the nodularity of the liver, is useless.

However, if you use this sign properly, it's quite useful.

There's no question that it is an insensitive sign.

Now what does that mean? It means basically that you'll encounter many people who have cirrhosis who do not have an apparently nodular surface.

This is largely people who are, who have micro nodular cirrhosis.

Technique is important in trying to elicit, whether or not there is nodularity.

And one thing that you don't want to do is scan between the ribs and the right lobe.

We always scan ventrally in the midline using a high resolution transducer to see the anterior surface of the, left lobe.

So one pitfall is in with regard to liver surface nodularity, is that it has a very good positive predictive value, but it's insensitive.

So that means if you have an unequivocally nodular liver surface, you can pretty much take it to the bank with some exceptions that the patient has cirrhosis.

However, it's mandatory to view this either at real time or with video clips to, make the diagnosis more secure.

Looking at still images, frozen images doesn't work very well.

So what do we do? We use a high frequency linear array transducer, although occasionally you can get away with a curved linear transducer if the resolution is good enough.

And we scan longitudinally in the midline looking for the, the ventral surface of the left lobe of the liver.

And as I said, realtime images are clips or mandatory.

In doing this, you have to be careful to hold the transducer so that the beam is at 90 degrees to the liver surface because if it's not at 90 degrees, you can get erroneous results.

Here's a, a nodule liver surface with a high resolution transducer and I don't think anyone would dispute that this is, nodular and this has a good predictive value for cirrhosis.

Now this is a patient who has, liver nodularity, but it's not seen very well because we're using our lower resolution abdominal transducer.

Here's the same patient with a high resolution transducer, and you can see how much more clearly it's seen.

So technique's important.

Sometimes you will see it with, a curved linear array if, if it's a modern transducer, and I think you can appreciate the liver surface nodularity.

We have to do this sometimes in patients who are fat or have other body habitous problems that prevents us from seeing things well with the high resolution transducer.

So next hint liver surface nodularity scan the ventral left lobe in the midline.

Look at the surface and you have to do this either scanning it at real time or with video clips.

Hold the transducer at 90 degrees to the liver surface if you want to get a reliable result.

And here is a, here's a scan that sort of shows you why don't like scanning intercos on the right.

And this doesn't really show any nodularity whatsoever, scanning over in this location.

However, there is nodularity seen.

This is very subtle, but it's real of the ventral left lobe.

So scan the ventral left lobe, not the right lobe.

The reason we don't, as I said to emphasize again scan intercostal, is that there's less sensitive and there are fewer true positives.

The exception, the one exception to this is when there's a small amount of ascites presence, sometimes you can actually see the liver surface better on the right.

So if there's ascites out laterally, that can be good and can allow you to make the diagnosis if there, especially if there's no ascites meline.

Now here's one such, some one such case that's showing us the nodularity to better advantage with the ascites.

Here's another case where the liver service looks smooth on the left lobe but looks nodular with ascites through the ribs.

So there are exceptions to this as there are to almost all rules, but in general, left lobe is where you want to be.

Now, cirrhosis is not the only cause of, nodule liver surface.

You can get this with multiple liver tumors.

Metastatic disease HCC, you can get it with peritoneal carcinomatosis where there are implants on the surface of the liver.

That can cause difficulties.

You can get it with acute massive hepatic necrosis, but this is rare and, because we don't usually get these people in ultrasound, here's a patient who has neuroendocrine metastases and nodularity because of the liver, focal liver lesions, not cirrhosis.

And here's another one. This is a nodule liver surface.

This patient does not have any, any liver disease per se, but rather has implants along the surface because of the carcinomas, carcinomatosis from breast carcinoma.

Now, just to emphasize, I think that you need to be careful to only say that the liver service is nodular.

If it is definitely nodular.

If you're not sure that it's nodular, don't, don't call it nodular because you want to have a very high predictive value for surface nodularity to predict cirrhosis.

Other Diagnostic Criteria for Cirrhosis

Alright, let's talk about other diagnostic criteria for, for cirrhosis.

And we use surface nodularity primarily.

There are the only, the only other really strong criterion that we use for cirrhosis is, the presence of port of systemic collaterals.

Other abnormalities such as portal venous flow abnormalities, flow reversal, biphasic flow, slow flow, sometimes associated with enlarged arteries are intermediate in strength.

And the least specific signs are things like splenomegaly, gallbladder, wall thickening, and ascites.

So, it's important to remember that in portal hypertension, the ultrasound may be normal.

If we see any of these abnormalities like collaterals, flow reversal, et cetera, arterial enlargement, they're suggested but not necessarily, definitive and not always present.

Here's a very large, portal venous to hepatic venous collateral.

This is seen in, cirrhosis and other conditions sometimes.

Here's a patient who has, on this longitudinal image, a large coronary vein collateral system.

And here's a sketch of this, flow reversal in the coronary vein going up to form gastroesophageal varice.

Here's that same clip shown inset.

A para umbilical recanalize para umbilical vein is another common collateral After the, the coronary vein collaterals, the left gastric vein collaterals, it is the most common.

So it's number two.

Here's a smaller recanalize paraumbilical vein, again, diagnostic for, portosystemic collateral coming off the left portal vein going through the ligamentum terries and up and out of the liver.

Another type of collateral that is somewhat less common, but when you see it is, also important is a spleen nore collateral.

To make this diagnosis, you have to actually see the splenic vein and, in the renal vein joint, just the presence of big vessels in the splenic lys is not enough.

Here's a patient who has what I call a flank collateral where there's a big collateral going out between the spleen and left kidney into the region of the flank.

This is another common type of, portosystemic collateral.

Here's an umbilical collateral related to superficial abdominal vein.

So there are a whole bunch of collaterals.

Here's an interesting collateral that we'll see several times a year.

This is an inferior epigastric vein that's being recruited to support a systemic collateral going into the external iliac vein.

And it's not unusual in this kind of patient for us to be doing a deep venous thrombosis study and to discover collaterals in the thus cirrhosis when it was previously unsuspected during a DVT study, which is surprising, I think, to a lot of people.

Portal Vein Flow Abnormalities

Okay, portal vein flow abnormalities are, less specific than portal systemic collaterals, but they can be helpful as well.

Slow flow biphasic flow flow reversal are all different manifestations of portal hypertension and the normal course of events, blood flows into the liver via the portal vein in hepatic artery, then it goes through the sinusoids into the central hepatic vein and out via the hepatic veins.

And ultimately the in vena cava when there's cirrhosis, there's a fibrotic condition which decreases this flow into the sinusoids.

It's sort of a block, if you will, as shown in the sketch.

This may lead to flow reversal and concomitant arterial enlargement.

As we see here, there is flow reversal in this part of the portal vein.

Actually in this part of the portal vein, the poster segmental vein flow is antegrade.

So these changes can be regional.

Here's another, regional abnormality.

This is a transverse image of the left portal vein and blood is flowing in an antegrade fashion here, but in this medial segmental branch, there's flow reversal and of course the enlarged arteries are prominent component in this case.

So when you have blockage of the sinusoids, you can get flow reversal because the arterial flow will come in, get blocked through this, cannot go through the sinusoids and will exit via the portal veins and generating flow reversal.

Here's another such case.

This actually bi phasing, but the mechanism's pretty much the same.

So flow reversal and antegrade flow, both in this patient who has large hepatic arteries.

Now, hepatic artur enlargement results whenever there's decreased portal flow, either from portal hypertension or portal occlusion.

There are other causes too that re result from increased arterial blood flow.

And we'll talk a little bit about those like tumors and vascular malformations.

So when there's decreased portal flow, I showed you this graphic already.

There's increased arterial flow and the blood exits the can exit the, liver via the portal vein.

Here's one such example of that.

These large vessels that are alias are arteries.

The blue is flow reversal in the, especially the right portal vein.

So this is a sign of portal hypertension.

This patient actually, we can see the nodule liver ascites.

You get corkscrew arteries in, hepatic cirrhosis.

This tortuous high flow artery that we're seeing here, however you can get other causes of arterial enlargement.

It doesn't occur just in portal, flow abnormalities and may occur with, hepatic tumors and vascular malformations.

Here's a vascular malformation that is, has resulted in increased arterial flow.

Here's a patient with Oslo wedu or hereditary hemorrhagic telangiectasia who has a large common hepatic artery and a massive AV fistula in the liver.

Conclusion

Just wanted to thank you very much for, giving me the opportunity to present this and hopefully, you've learned a few things of value to you in your practice about diffuse liver disease.

If you have any questions that you'd like to ask me, please send me an email and I'd be happy to respond.

Thank you.