Native Liver Doppler Ultrasound - HD

Introduction

Thank you very much and good afternoon everybody.

I thank the organizers for inviting me to be here among this last telescope of speakers.

I'd like to talk to you about NA or I was asked to talk to you about Native Liver Doppler ultrasound.

I have nothing to disclose, so what I'd like to do in the next 25 minutes or so is give a very brief review of the normal vascular anatomy and then we'll look at some of more common problems that we encounter, such as portal vein thrombosis, cous transformation of the portal vein.

We'll look at some findings in B Chiari syndrome and end up with transjugular portosystemic shunts.

Normal Vascular Anatomy

So as you all know, the portal vein is the vessel that supplies most of the blood to the liver, about 70 to 75%.

It is formed by the confluence of the superior mesenteric vein.

The endo splenic vein, the portal vein divides the main portal vein divides into the right and left portal vein within the liver.

And on Doppler, it has a characteristic hept pedal, monophasic blood flow.

There is some variation with the respiratory phases and there's also something called helical flow, which is a normal variant.

So here you have the normal main portal vein as it goes into the liver.

It is het pedal with continuous forward flow, low velocity.

It's non pulsatile and there are changes with respiratory variation.

Obviously the left portal vein is also antegrade in flow displayed above the baseline, and then the right portal vein dives steep into the right lobe and therefore you have the flow displayed below baseline.

This is what you sometimes can see.

This looks like a ying yang type appearance in the portal vein.

That's the helical flow. That's a normal variant.

The di normal diameter, as we just heard already from Dr. Dogra, is 13 to 16 millimeters.

You have to remember that dia diameter varies.

If the patient is postprandial or takes a deep breath in, the diameter increases.

And if the patient has been fasting or is post-exercise, the diameter decreases.

The normal velocity is anywhere between 20 and 30 centimeters per second.

Sometimes you see a little bit of pulsitile flow in the portal vein, that can be seen in normal very muscular, athletic, young subjects.

However, if it becomes more prominent or if you see it, you should think about other conditions that can cause it, such as congestive heart, congestive heart failure, hepatic to portal vein fistula or portal cable shunts.

I think I had an image in there of the normal portal vein that's wasn't, didn't transmit.

Here. However, you see a patient where the portal here is the portal vein.

It's big, it has very marked ity to its flow.

And this was a patient with congestive heart failure.

You can also see this on the venous side, you see marked dilatation of the hepatic veins.

Here's another patient with very pulsatile portal venous flow.

And you can see in this patient this patient has tricuspid regurgitation.

Sometimes you see portal pulsitile flow in both the portal vein as here and also the hepatic veins.

And this is again, patients who have congestive failure who exhibit this pattern.

Hepatic Artery

The hepatic artery is the next the arterial supply to the liver, which accounts for about 25% of blood flow to the liver.

It arises from the celiac axis in most patients, and it runs in the in the HEPA deal, hepato duodenal ligament, anterior medial to the portal vein.

Here you can see the hepatic artery coming off of the celiac and diviv diving into the liver.

An apparent hepatic artery does exist most of the time.

It's the right hepatic artery that is replaced and arises from the superior mesenteric artery.

And the hepatic artery has a low impedance flow pattern on Doppler ultrasound with a sharp systolic up stroke and good flow throughout diastole with continuous forward flow.

And here you can see again, the normal hepatic artery sharp up stroke and continuous flow throughout diastole.

And similar to the portal vein, the right hepatic artery dives deep into the right lobe to supply the right posterior right lobe, and therefore the flow is displayed below baseline.

Hepatic Veins

The hepatic veins demonstrate aphasic hepa ugal flow pattern.

There is forward flow with right atrial filling, and there's a rapid and a slow phase of this right atrial filling.

And then there's transient reversal of flow.

When the right atrium contracts in patients who have right heart failure or tricuspid regurgitation, you can see a very pulsatile, hepatic venous pattern like I already showed you.

And this has been termed the W wave form.

Conversely, if the patient has intrinsic liver disease or cirrhosis, the flow within the hepatic veins will be dampened due to the increased peripheral resistance.

So here's your normal.

This is atrial filling, the rapid and the slow face.

And then when the atrium contracts, you see transient reversal of flow.

And you see the same thing right here and here.

And here's the transient reversal.

Now here you see the W wave form.

It's very very pulsatile flow within this patient with congestive heart failure, also seen on the gray scale as dilatation of the hepatic veins.

And look at this patient here with liver cirrhosis.

There's surface nodularity, there's a little bit of ascites.

The hepatic veins here look like portal veins.

They're completely dampened with monophasic flow.

Portal Vein Thrombosis

So what are some of the etiologies of portal vein thrombosis?

Well, there's a whole long list, but the most common ones are, you can see them in in liver cirrhosis, pof, phlebitis and emph colitis, especially in children, patients who have acute pancreatitis.

And then patients who have hepatocellular or cholangiocarcinoma hypercoagulable states, penetrating trauma can cause portal vein thrombosis and then some rare endoscopic sl uh, sclerotherapy.

And then there's also an iop, uh, pad, uh, version.

What do we see on ultrasound?

Well, portal vein thrombosis looks like thrombosis anywhere in a vein vein, you see dilated portal vein with internal echos.

You see absence of flow in the portal vein.

You have to be very careful to optimize your color doppler sensitivity because you could get false portal vein thrombosis due to very very slow flow.

And if you really cannot tell, you have optimized and done everything you can, you might have to go to another imaging modality.

And in my next version I'll put contrast in health, uh, contrast enhanced ultrasound way up here over CTA and MRA.

The thrombus in the portal vein can also be genic as it ages.

And sometimes you just can't really see the thrombus, you just don't see the portal vein or its branches, so you assume it's thrombosis.

If there's partial thrombosis, you will see a little bit of flow around the clot.

And a secondary sign of portal vein thrombosis is enlargement of the hepatic artery because the hepatic artery now has to supply more blood, blood to the liver to compensate for the missing 75% that the portal vein used to supply.

So when you see enlargement of the hepatic artery in a diffuse fashion, think immediately about could this patient have portal vein thrombosis.

But you can also see it in patients with very severe cirrhosis because again, the portal venous inflow is impeded and decreased.

And of course, large hepatocellular carcinomas, because they're fed by the hepatic artery, will lead to enlargement.

If you see focal enlargement of the hepatic artery, think about hepatic artery aneurysms or pseudo aneurysms.

So here's a patient who has portal vein thrombosis.

Here's the region of the portal vein.

We don't really see much of a normal vessel.

You see the psoriatic liver with ascites, and here when you put oncolo doppler, you see the hepatic artery is quite prominent and the portal vein is completely thrombosis.

Here's another case where you see portal vein thrombosis and looked the beautiful appearance of this large cork school-like hepatic artery with increase in flow now up to 242 centimeters per second.

This compensatory work that the hepatic artery does to accommodate for the decrease of venous flow through the portal vein, malignant portal vein thrombosis, as I just learned, I guess we call it now, tumor, uh, thrombus in vein.

Uh, so we have to change this.

Um, uh, it is, it, uh, occurs when you have non occlusive thrombus with some internal vascularity and you might think is this residual, um, you know, vein that hasn't just been caught by the thrombus.

But very important you put your spectral waveform in and you can see the characteristic arterial spectrum to this flow.

So this is, um, uh, tumor thrombus.

Here's another nice example you can see in a large portal vein here filled with hypoechoic thrombus.

And then here's this, uh, vascular structure in the center.

Again, putting on your spectral waveform.

You see this is arterial flow within this, um, thrombus in vein, this is a patient who had undergone a stab a wound to his abdomen in his portal vein and hepatic artery area looked like this.

He has the hepatic artery and there was this pseudo aneurysm, post-traumatic accounting for the focal enlargement of the portal.

Cavernous Transformation of the Portal Vein

Vein cavanaugh's transformation of the portal vein occurs in about half of the patient with portal vein thrombosis.

It is due to development of periportal and peri gallbladder collaterals within the HEPA two duodenal ligament.

It can occur as early as six to 20 days after portal vein thrombosis, and it's commonly associated with the development of esophageal varis as well.

What do you see on Cala Doppler ultrasound?

You see a tangle or a cluster of irregular vessels in the region of the porter hetus and in the gallbladder wall.

And you can also see intrahepatic collaterals or recanalization of the paraumbilical portal vein as Vikram just showed you.

So here's the gray scale appearance of cavernous transformation within the portal.

Porter Heus. You see these tangles of ous IC structures you put on kalo doppler.

You see vascular channels, but you do not see in normal portal vein.

Budd-Chiari Syndrome

Moving on to but Chiari syndrome, again, multiple etiologies.

Some of them are very similar to those of the portal vein thrombosis, so cirrhosis thrombosis of the portal vein, and then important congenital webs or bands within the veins, um, neoplasms.

And then you can read the rest of the list.

So the outflow obstruction of the veins occurs at the level of the hepatic vanes, the large hepatic veins or the inferior vena cava in.

But Chiari syndrome, these patients have a very non-specific clinical presentation.

They come in with a large liver, they have pain in the abdomen, they might present with ascites and also lower extremity edema.

So what do we see on ultrasound in but QI syndrome or findings that should clue you into this.

Within the portal vein, we can see signs of post hepatic portal hypertension.

The flow might be heed or hepato ugal in 10%.

The portal vein can be thrombo and you will see the development of portosystemic collaterals within the hepatic veins and the inferior vena cava.

You can see narrowing, you can see web formation or Fran occlusion.

Sometimes you see focal areas of calcifications.

So here's a patient with but Cary syndrome.

Look at this middle hepatic vein here.

There are all these middle hepatic vein webs.

This patient also had a very large hypertrophied Quaid lobe, which you can see in, but Qri syndrome.

Here's another patient where you look at the middle hepatic vein and there's, it's visible on gray scale, but there's no flow within it.

And in this patient we also see echogenic thrombus within the inferior vena cava.

He is a patient who had occlusion of all three hepatic veins.

This is the area where the hepatic veins should be joining the inferior vena cava.

And we see nothing on gray scale and we see nothing on color.

Doppler ultrasound.

Some of the therapeutic measures in, but qri syndrome include in, um, um, a beginning of thrombolytic therapy shunts for decompression of the hepatic vasculature.

In the past we had surgical meso atrial and meso caval shunts.

And then in the last few decades, these patients have been successfully treated with tip shunts and ultimately, um, these patients might need a liver transplantation.

Transjugular Portosystemic Shunts

So that leads me into talk.

In my last part of the presentation about portal systemic shunts, they are performed to decompress the portal system in patients with symptomatic portal hypertension and to relieve the gastroesophageal bleeding that can occur from vari disease and the development of refractory ascites.

Previously we had surgical hun shunts, the meso atrial shunt, the meso caval shunt, the Port caval shunt, and the distal, um, lenor renal or warrant shunt.

These have been replaced in the vast majority of patients by percutaneous tip shunt in the last two decades.

So transjugular inate portosystemic shunts are the now the preferred alternative to surgical shunts for complications of portal hypertension.

The co the advantages are that tips shunts avoid major surgery and they also do not alter the extra hepatic vascular anatomy.

Trans, uh, with tips shunts, you gain transjugular axis of the inferior hepatic inferior vena cava and then select the most optimal hepatic vein based on the angle and diameter to place the shunt.

Usually it is the right hepatic vein.

So then you perform a transjugular puncture between the hepatic vein and the int hepatic portal vein.

Under either ultrasound or fluoroscopy, you place a metallic expandable shunt be a stent between the hepatic vein and the portal vein to divert blood flow from the high pressure portal system into the lower pressure systemic circulation.

And you monitor portal pressure, gradients and filling of varis on portal biography.

What are some of the indications for huns varial bleeding, uh, refractory ascites, the but Qri syndrome, hepatorenal syndrome, liver failure to give the patient a chance to become a potential candidate for liver transplant by being put on the wait list, uh, uh, because of an intermediary, um, help from the tip shunt that allows the patient not to con continue to go into liver failure.

So it's kind of just a a middleman while the patient still has hope to be placed on the transplant list for definitive treatment contraindications.

Ab there are a lot of, um, um, not absolute contraindications that I'm not gonna mention, but I want to just point out the two absolute contraindications to tips.

Uh, shunt placement are inadequate liver reserve, IE if the patient has severe hepatic encephalopathy because that may worsen the encephalopathy by now dumping all that extra blood into the systemic circulation and severe right-sided heart failure because that makes aspirate the patient's condition by leading to volume overload.

Normal TIPS Shunt

So let's look at normal tips shunt.

The early experience it started in about in the early nineties.

Um, so the early experience is that one decade between 1993 and 2003, um, the, um, the shunts that were used were bare metallic shunts.

They were a great success, but they only had a patency rate of about 40 to 60% at one year.

So then, um, someone developed expanded, uh, poly tetra, poly tetra, um, Fluor ethylene PTFE covered devices, the via tour stents, stents that are still being used today, and they have been in use since 2003.

And the big advantage of the via tour PTFE covered chances were that they have a patency rate of 80 to 90% at one year on ultrasound.

The walls of the stand are brightly genic.

They should be smooth and parallel.

When you turn on your color, it should fill the entire lumen of the shunt and be very careful.

Though we have learned that in the very early, uh, phase post-placement of the PTFE covered shunts, you can get an artifact that mimics portal, uh, shunt, uh, thrombosis because there is some air embedded in the stent.

And as the stent expands, this air gets released and then causes a very bright shadowing artifact along the stent, which presents Doppler interrogation deep to it.

So here's your normal shunt.

Um, nice parallel gray scale echogenic, uh, regions put on color.

You see nice color filling through the proximal mid and distal shunt.

And he as a patient, um, this was actually resonant overnight, read this case.

They had placed the shunt the afternoon before, wanted to see if shunt, if the shunt was patent and all the sonographers could find was this one bright echo.

There was nothing distal to it.

They put on color and they saw no flow.

So they called it shunt occlusion.

Well, the patient, fortunately the interventional radiologist knew better and said, let's just repeat the patient, um, in the next, uh, 48 hour, 24 to 48 hours.

And of course the shunt was patent.

So the recommendation is do not interrogate these PTFE covered shunts or stents within the first 72 hours of placement.

If you're not aware of this artifact, if you are aware of it, you can say, well, we can do it, but it's gonna be useless because I can't really tell you much about it.

So what are the normal, um, what's the normal doppler appearance of normal tips?

There's been a lot of variability in the literature.

Um, multiple studies out of Melan quad.

I use CSF, uh, several years ago.

But people generally agree that the lower and upper limits of flow through the shunda, anywhere between 90 to 190 or a hundred to 200 centimeters per second after shunt placement, the flow in the main portal vein increases.

It should be more than 40 centimeters per second, and the flow in the hepatic artery will also increase greater than 130 centimeters per second.

Very importantly is that the flow in the main, the right and particularly the left portal vein, if the shunt is properly functioning, should now go out of the liver.

So it should be hepato, ugal towards the lower conduit, lower pressure conduit of the shunt.

So reversal of flow in the left portal vein is a normal finding in a normal tip shunt.

So here you can see normal flow in the tips and if you look at the port left portal vein here, it is coming down towards the tips shunt, uh, within a hepato ugal flow fashion, that is normal.

The velocities of across in this patient were between proximal, mid and distal, anywhere from 143 to 173.

So that is normal. This is a nice normal shunt.

Complications of TIPS

What are some of the complications?

We as, um, ultra sonographers are asked to evaluate after ship, uh, tips shun placement?

Well, there are complications related to the vascular puncture and then there are complications related to the tips itself.

So what we can see are subcapsular hematomas, he mobilia blood in the gallbladder, sometimes hepatic artery injury, pseudo rhythms or AV fistula.

But these are more common if the puncture is blind and not with guidance.

And then Frank Hemoperitoneum, uh, can also occur.

He has, he had two, it's one patient who had developed a subcapsular liver hematoma and then here in the same patient you see this is the gallbladder, it's filled with blood.

This patient, um, uh, developed a pseudo aneurysm of the hepatic artery after a tips shown placement.

And this was successfully coiled.

You see it ne nicely here on the angiography also had, uh, an associated AV fistula and after coiling, um, the uh, patient, uh, as angiogram looked good.

And you can also see the flow within that PS aneurysm is gone.

And there's just now this echogenic, um, uh, artifact that you can oftentimes see after coil placement.

The technical success is fairly high in experienced hands.

However, there is associated morbidity and mortality and all those of course depend on the patient's pretest condition.

If the patient is very sick, the morbidity and mortality are much higher.

However, it has been shown to be over 90% effective in controlling varie bleeding.

When should you worry about malfunctioning of the tips?

When you see reappearance of varis?

When the sitis recurs and when you see development of pleural effusions, and these are due to either tip stenosis or thrombosis or shunt retraction, be careful sometimes if the shunt is really, really deep in the abdomen.

If the patient's very big, you could false positively, um, identify an occlusion or thrombosis.

So complications, um, due to pseudo intimal hyperplasia or thrombosis, um, result in tip stenosis or tips occlusion.

And usually if you have tip stenosis, you will see incomplete filling of the stent and decrease in the velocities.

People have usually agreed upon if it's less than 60 centimeters per second, if you see high velocities at the site of stenosis and if there is a velocity gradient across the shunt of greater than 60 centimeters per second, that's indicative of stenosis.

Um, occlusion obviously you see no flow in the shun at all and you will in the left portal vein see reversal back into the liver.

So you now we see hepato pedal flow in the portal branches the exact cause and pathophysiology of the stenosis are unknown.

There are several etiologies and pathologies that have been speculated.

People have said there's some faulty development of that PTFE, it becomes then porous and it allows bile leaks and in corals of tissue, um, there could be propagation of neointimal or pseudo inal hyperplasia usually from the ends, particularly from the hepatic venous end more than the portal venous end into the shunt.

And then sometimes you just have diffuse laminino thrombosis without tissue in growth.

The reported criteria are all over the map.

I was once at a meeting and someone said, why don't we just even worry about giving, um, velocities and criteria.

Just say it's patent or it's not.

But I don't think that's good enough.

So what most people agree upon, um, tips to no should be suspected.

When the velocity in the main portal vein all of a sudden drops, I told you it should be more than 40 centimeters per second.

It, uh, when it's be less than 30, if the velocity in the tips itself is less than 50 or 60 centimeters per second, if there are focal shunt velocities greater than 200 and centimeters per second.

And if, if there is a temporal or longitudinal change in tips velocity across the shunt, either an increase or decrease of 50 to 60 centimeters per second.

And then as I already mentioned, if you see heed flow in the left portal vein and hepato ugal flow in the main portal vein, that means the shun is not functioning.

Couple examples here has a patient who had all of a sudden reappearance of ascites.

Um, in the left portal vein, you now see HEPA dedal flow.

It goes back into the portal vein.

The gradient across the tips between proximal and mid, um, was more than a hundred centimeters per second.

Proximally was 59.

In the mid it was 168 and this patient had a stenosis.

Here has another patient who had color aliasing at the hepatic venous end.

And that's where the intimal ingrowth occurs.

Most commonly, there's marked decreased velocity in the proximal tips.

It only measures 44 centimeters per second, so less than the 60 on the peak systolic velocity at the stenosis is 218.

And there's hept toed flow in the left portal vein.

And you can see right here there's the stenosis.

It was, um, stent, graft placement and angioplasty.

And the patient did fine.

The causes of thrombosis are also unknown.

People have speculated there's a hyperdynamic phenomenon that causes competing shunts with stasis of the flow, which leads eventually to occlusion.

Um, also there's neglected or not recognized significant stenosis that goes onto blood stasis and thrombosis.

Some people therefore, uh, recommend adequate DOPP loss surveillance.

Uh, so one can recognize the stenosis before they become critical to blood flow and cause thrombosis.

Just a couple examples of occlusion in this patient.

The main portal venous flow was 18 centimeters per second.

So markedly decreased.

The flow in the proximal tip was 29, so markedly decreased.

And then in the mid and distal flow, uh, um, tips, there was no flow.

You can also see this nicely here on the gray scale and the color doppler in even power doppler image.

Again, you wanna of course make sure you optimize all your colored, uh, doppler settings.

Here's another patient with occlusion.

You see decreased flow in the main portal vein eight centimeters per second, HEPA oral flow in the left portal vein and then complete occlusion.

Uh, actually there was also reverse flow in the main portal vein with low velocities and the entire tips was occluded.

Pitfalls in TIPS Evaluation

Couple pitfalls real quick.

Um, deep location in the abdomen can make evaluation very difficult.

And then there was a really nice paper that Dr.

Cleaver, uh, uh, published many years ago where he showed that there was actually a difference of flow velocities between in an exploration, which we know from the normal portal vein, um, that there was a 22 centimeter less, uh, uh, uh, less flow with deep inspiration compared to an expiration.

So it would be ideal if you follow these patients sequentially.

We tell our patients to do like comfortable mid respiration, so no, do no deep in, no deep out or expiration.

Uh, but it would be helpful to put that on your screen so that when you see the patient again, you know in what phase of the respiratory cycle, um, this was taken.

So he is a patient where we see good flow in the proximal and midt tips and then it dives so deeply in the distal tips that we couldn't really see it.

This was actually patent as proven by angiography afterwards.

Conclusion

So in conclusion, doppler ultrasound of the native liver is very important.

It allows assessment of physiology and pathophysiology of the vessels and associated conditions.

We have discussed the normal appearance of the vasculature.

We have looked at portal vein thrombosis, cous transformation, the but Chiari syndrome and the tip shunt.