Hepatic Vascular Conditions - HD

Introduction and Learning Objectives

I am Dr. Madrazo Beatrice Mado.
I'm a professor of clinical radiology at the University of Miami Miller School of Medicine.
Formally I was at Henry Ford Hospital subsequent to my trainee in radiology and William Beaumont Hospital in Royal Oak, Michigan.
I've been doing ultrasounds since 1976.
I'm sorry to admit my age, but hope that you enjoy my lecture.

Our learning objectives would be to detail the characteristics of congenital and acquired hepatic shunts, including tips de describe that the hemodynamics of hepatic venous thrombosis of either the portal or systemic veins, such as seen in Bud Chiari syndrome, and offer clues to the diagnosis of typical and atypical hepatic vascular neoplasms, including he angios Oma.

Portal Vein Flow Detection

One word regarding flow detection in the portal vein, your technique should be optimized to settings for slow flow and obtain flow measurements in quiet respiration, because deep inspiration will flatten the wave forms and diminished portal vein velocity.

Occasionally we'll find that the portal veins exhibit a pulsatile flow, and this may be seen in patients in congestive heart failure or with tricuspid regurgitation.
Occasionally the normal young, thin patients will also exhibit pulsatility of the portal flow.

Hepatic Vein Flow Patterns

The hepatic veins on the other hand, have a different flow pattern.
They will transmit the hemodynamic changes of the right atrium, and the first component is a reversal of flow towards the liver as the right atrium under goes systole and then forward flow into the right ventricle.
As the right ventricle fills during its systole, its diastole actually.
So this ity of the hepatic veins is normal and is a sign of patency of these venous structures.

Portal Vein Thrombosis: Clinical Impact and Causes

Portal vein thrombosis can result in worsening of liver functions in patients that have underlying hepatic insufficiency cirrhosis.
There can be also a onset or worsening of ascites.
Patients may experience abdominal pain or distension, or sometimes there is portal vein thrombosis, but the patient is asymptomatic.

The causes for portal vein thrombosis are variable and go from idiopathic where an explanation is never elicited.
It can be due to the cirrhotic process and diminished flow due to the fibrotic state of the liver.
Patients may have hypercoagulable states one word of caution, the port of vein thrombosis may be a tumor thrombosis due to an adjacent hep to cell carcinoma.
We have to share with you a case of exclusively hep to cell carcinoma in the portal vein.
Pancreatitis, sepsis and trauma are also associated with portal vein thrombosis.

Normal and Abnormal Portal Vein Flow on Imaging

What one we'll see during colored doppler surveillance of the portal vein is that flow is heidal to the periphery of the liver.
The flow fill completely the lumen of the portal vein.
No turbulence or dilated segments are seen.
This is normal portal flow.

Contrast that with this patient recently transplanted who experienced portal vein thrombosis of the right and its posterior branch.
You see that there is good color flow technique.
There's flow identified in the inferior nava and in the proximal portal vein, but no flow is seen in the right and the posterior branch of the right portal vein.

Compensatory Hepatic Artery Flow

As a compensatory mechanism to the diminished portal flow, the liver will have increased hepatic artery flow.
This will result in also elevated hepatic arterial blood flow elevated the velocities in the hepatic artery.
As you can see in this case, this is just a mechanism of the liver to assure that it remains profused.
As we know, the hepatic car is only supplied 25% outflow to the liver while the portal veins supplied the remainder 75%.
So this is a compensatory mechanism that occurs when there is portal vein thrombosis.
As we see here, the hepatic artery becomes hyper purified and with increased velocity to develop that extra blood to the liver.

Here we see on this MR with contrast that we have filling defects within the portal vein, both in its intra hepatic segments, its segments at the portal Haus and also in the superior mesenteric vein.

This is a case with color doppler of portal venous thrombosis of both the portal vein and portions of the splenic vein.
This patient had coagulopathy and experienced extensive thrombosis.
You can see that the liver is very heterogeneous and I wanna caution you to not only find the portal venous thrombosis, but also look in the hepatic parenchyma.
Since once there is portal vein thrombosis, the patient may develop a intra hepatic abscess.

So here we have an expanded lumen of this portal vein at the port of Haus.
And on colored doper, we noted that not only was the main portal vein thrombosis, but there was extension of the thrombosis to the superior mesenteric vein and also to the splenic vein.
Extensive portal venous thrombosis due to a hypercoagulable state.

Now sometimes our studies are followed by additional confirmation of problems and in this diffusion weighted imaging sequence of MRI, we can see that there is flow in the left portal vein and we have a higher signal where the distribution of the right portal vein would be.
But this is the edema caused by that portal venous thrombosis, and there is absence of flow in the right portal vein.

Tumor Thrombosis in Portal Vein

This is the example that I mentioned earlier that exclusively heto cell carcinoma was present within the portal venous system.
We have two cases here.
We see that a little bit of gadolinium is seen in the main portal vein as it comes into the portal Haus, but there's absence of flow in the right portal vein.
It's anterior posterior branches.
And you can see the extensive involvement of the right portal vein by this tumor thrombus, which was the exclusive site of HETO cellular carcinoma.
This patient underwent a biopsy of the thrombus.

Now we can really add to the assessment of porto venous thrombosis by noting if there are intrinsic signals and if we see intrinsic signals in the thrombus, we should sample them because if there are arterial signals, this is tumor in the venous structure.
This tumor thrombus is important to document and is essential in staging the patient's heto cellular carcinoma.

Here we see extensive tumor thrombus with enhancement on this contrast enhanced ct.
There is expansion of the portal vein and linear areas of contrast a test for the presence of enhancement within the tumor thrombus.

This is the second case of this extensive tumor thrombus in the portal vein, here is the Corona MRI demonstrating a more delayed sequence where exclusively tumor is seen in the portal vein and no associated parenchymal hap to cell carcinoma could be seen.

Intrahepatic Abscesses Secondary to Portal Vein Thrombosis

And as I mentioned earlier, portal venous thrombosis can result in the development of intra hepatic abscesses.
As you can see here, there are low hypoechoic areas in the periphery of this liver transplant.
And these were all abscesses secondary to the portal venous thrombus in this immune suppressed patient.
You can see several areas of abscess formation in the hepatic parenchyma in this transplanted patient.

Ultrasound Accuracy for Portal Vein Thrombosis

So ultrasound is very accurate in the detection of portal vein thrombosis in the 98% sensitivity, 92% specificity and its negative predictive value is very high.
So if there is presence of flow by doppler, no further workup is necessary.
The false positive examinations are due to low flow in patients with severe portal hypertension and cirrhosis.
You have to maximize your settings for slow flow and you can also use power doppler and also sample for the presence or absence of waveforms.

Confirmation is often needed because of the possibility there is an underlying process causing the portal vein thrombosis, which may have been overlooked during sonographic assessment.

Portal Vein Stenosis in Liver Transplants

Now, the portal vein is with flow, but there's a focal area of INE in its mid portion and we then decide to sample right there to look for any kind of increased velocity at this site.
In patients that have been transplanted, there's often a small increase at the anesto site between the donor's portal vein and the recipient's portal vein.
But if this becomes permanent following transplantation one or two days beyond transplantation and they if there is a increase in velocity, in other words, there is a gradient comparing the proximal segment, which was only 76 to the segment where the alias is taking place.
We can see there's a rapid rise in velocity right there.
This is very concerning for an element of stenosis.
We would be watching this portal venous anastomosis.

And here is another case, again, focal area with aliasing, and we note that this is the area that we're going to be sampling and we measure the portal vein beyond the suspected area of stenosis and it is dilated relative to the proximal segment.
So here we see that this velocity is extremely high and this gradient is important to report.
So what you do is you measure at the site where there is an elevated velocity and compare that to a proximal value where there isn't an elevated velocity.
In this case, we did also the distal segment.
So this portal venous stenosis in this liver transplant had a gradient between the right and main portal vein.

If untreated, there can be a development of a portal venous aneurysm beyond the stenosis post-traumatic dilatation with the development of a portal vein aneurysm.
This was noted on that patient approximately four weeks post transplantation.

So as we mentioned, we can survey the transplant for portal vein stenosis and if the increase in velocity identifies a three to fourfold gradient or increase in velocity across that area of stenosis, this is important to report.
And there have been patients that have had stent placed in their portal veins to alleviate the stenosis.
So that portal vein aneurysms do not develop patients may undergo angioplasty as well.
We've seen both stents and angioplasty.

Portal Vein Aneurysms

So here we have a portal vein aneurysm on gray scale.
It's a very dilated segment of the main portal.
Vein turbulent flow is present hele choal type of flow, and we can see quite chaotic on the spectral doppler and we can see that proximal to the aneurysm flow is more organized on a ct.
We could see that in this transplant, this portal vein aneurysm was exclusively of the main and the right portal vein that the left portal vein was normal in caliber.

This is another patient with a very large portal vein aneurysm involving again, the main and right portal vein and we had heco flow patterns in it.
We were obtaining signals that were arterial, but we realized that this was the proximity of this portal vein aneurysm to the hepatic artery, which we can see right on the surface of this portal vein aneurysm, there was a calcified component to this portal vein aneurysm, but we really did not appreciate that on our sonogram.
Notice that this calcified component was partially thrombose.

Cavernous Transformation of the Portal Vein

Now, subsequent to portal vein thrombosis, there can be cavernous transformation of the portal vein, and this cavernoma is seen as multiple serpiginous structures where the portal vein used to be.
These are collaterals that develop along the course of the native portal vein to reconstitute flow to the liver.
Kes are receiving a lot of attention because they can result in a recently recognized biliary orthopathy.
We'll talk about that in a minute.

Now, portal vein thrombosis in transplants is in itself a little bit rare and cavernous transformation in transplants is very rare.
Even though we have extensive experience at university of Miami with liver transplants, I only have a few cases of cavernous transformation in liver transplants.
So you can see that there are numerous collaterals where the portal vein would be expected to be present.
These always have hepato petal flow, never hepato ugal flow.
So cavans only flow towards the periphery of the liver.

Now what are we looking at?
A gallbladder with tubular structures around its surface are these areas of edema.
I want you to recognize that these are perico cystic varicosities that do occur when there is portal vein thrombosis.
It's very common to have collaterals reconstituting flow to the liver via the perico cystic veins, the veins of sappi.
The can also extend to other areas in the vicinity of the portal vein thrombosis.

In this case, a very unusual representation is that these are collaterals that follow the pancreatic veins and kind of superimposed the pancreas and we can see that the cavernoma has extended to the region of the pancreas.
And we see this both by ultrasound and by ct.
We can see the cavernous transformation of the intra hepatic segments of the portal vein, but extension of the cavernoma to the pancreatic region.
Very rare presentation.

Portal Biliopathy and Biliary Dilatation

So I mentioned to you that the caroma can compress the biliary system and we can see the dilated biliary ducts in this contrast enhanced CT that is caused by compression of the biliary three by the caroma.
This portal portal myopathy is recognized as an entity now and again, important that we search also for dilatation of the biliary three when we see cavernous transformation, approximately 50% of portal vein thrombosis results in cavernous transformation of the portal.
Vein can occur as early as four weeks subsequent to the thrombosis.
And remember we saw the periportal, but there could also be some perico assisted collaterals and they extend usually into the hepato duodenal ligament and lesser momentum.
Often this is an ineffective compress decompression in patients will have esophageal varis.

Other Collateral Flows in Portal Hypertension

Other sites of collateral flow are the ized para umbilical vein, a very common portal, systemic collateral, easy to identify, and when present is an indication the patient has portal hypertension, we can demonstrate 'em in gray scale or in color.
And of course, we have the ability to demonstrate their pattern of flow so they can also be demonstrated in CT studies and they can have a variable course not necessarily towards the umbilicus to form the cap with Medusa.
So recanalize para umbilical vein, a sign of portal hypertension.

Hepatic Embryology and Intrahepatic Shunts

Now the hepatic embryology is complex, but I summarized it so that we can understand why do we have patients that are born with the intra hepatic shunts.
The paired vilin veins have an intra and extrahepatic component, the left vilin vein involutes, and the left part of the liver redistributes its blood to the right vilin vein.
The terminal IVC hepatic veins and portal veins are derivatives of the vilin veins.
So you can see that these venous structures have a common embryological origin, so intra hepatic shunts can be spontaneous either congenital or acquired.

So again, the lene veins, the common origin to the venous structures of the liver and the intra hepatic IVC, the afferent branches formed the portal veins and the efferent branches, the hepatic veins.

I have a clip that was formed with portal and hepatic veins and cava with color doppler that demonstrates how close to each other these venous structures can be.
And actually they are of common embryological origins, so they're not too far from each other, so they're not supposed to communicate with each other.
But here we have a case of a patient with a large intra hepatic shunt who was totally asymptomatic.
Her portal vein communicates with the right hepatic vein via a aneurysm.
This would be a park type three intra hepatic shunt.

Classification of Intrahepatic Shunts

So here's the classification of intra hepatic shunts by park.
Type one would be a single large tube that connects the right portal vein with the IVC, so a direct communication without an aneurysm type two peripheral shunts within single hepatic segment.
So multiple shunts, but in exclusively in one hepatic segment.
Type three would be a portal systemic shot through an aneurysm such as we saw a few minutes ago.
I'll show it again.
And type four would be multiple communications between peripheral portal and systemic veins.

So the patient that we saw earlier on gray scale, we could see the portal vein, an aneurysm and the hepatic vein.
The patient was totally asymptomatic.
She actually was undergoing gynecological surgery and underwent a CT where we could see an unusual tubular structure at the Port of Haus.
And we could see that it was enhanced to the same degree as other vascular structures and we could sample flow and see that this is portal and this is hepatic vein and this aneurysm communicating the two structures.
So a part three, intra hepatic shunt.

This one is a little bit unusual because this one is a shunt between the right and middle hepatic veins, and you can see it's quite an exuberant shunt.
This patient had severe tricuspid regurgitation and this resulted in increased pressure in the hepatic veins.
And this int hepatic shunt, this has been described.
It's all felt to be associated with congestive heart failure and the high pressure in the hepatic venous system secondary to hepatic venous congestion is the most likely mechanism for the development of these shunts between hepatic veins.

Shunts Due to Superior Vena Cava Obstruction

Now we also know that when there is compromised venous return to the heart, collaterals will develop and in the case of brachiocephalic or superior vena cava stenosis or occlusion, hun can develop by blood returning through the liver into the right atrium and the collaterals will develop along the chest wall, and we can see some of these collaterals here and this reformatted ct and then a shunt will occur and it's usually in segment four B four A and four B.
This is called the apex of the liver.
And connections between these intrahepatic vascular structures will occur with the inferior thoracic vein and then blood can then return to the right heart.
So here we see a small such shunt, and here we see a large shunt.
And again, these are to reconstitute flow back to the heart since there's been obstruction of the brachycephalic vein or if you've superior vena cava.

Arteriovenous Malformations

This patient is interesting because she had a CT prior to the ultrasound where a hypervascular structure round was seen in segment three.
We then did the ultrasound and we could see a hypoechoic area.
Note the absence of acoustic enhancement.
That means sound is being attenuated.
Color doper demonstrated a small arterial venous malformation at the tip of segment three, and we could see a enlarged draining vein and then we could see it also on the ct.
So this was an isolated arterial venous malformation in a patient with renal cell carcinoma.

This is a rare case and an old case, but again, a hypoechoic area in the liver without acoustic enhancement because if there is flowing blood it will attenuate sound.
And then when we put the color on, we could see that it did have flow in it.
And here is the ct.

This is a rare case because it is a case of polyarthritis nodosum with hepatic involvement.
Polyarthritis nodosum we know is primary or secondary.
It is an autoimmune process and there is foid or highline necrosis of the media of medium and small size arteries.
This results in aneurysms stenosis or occlusions of these vessels.
And this can involve several organ and structures.
The primary polyarthritis nodosum is exclusively involvement of the kidney, while other sides can include the heart, gi tract, the liver, the spleen, or the pancreas.
What's important to remember is that the secondary type of polyarthritis nodosum has associated systemic conditions, and we'll talk about that in a minute.

So the diagnosis of polyarthritis nodosum is obtained via muscle or skin biopsy and anti neutrophilic cytoplasmic antibodies are present in the specimen.

So the secondary type of polyarthritis naza is associated with the mixed cryoglobulinemia and is seen in chronic active or persistent hepatitis.
Hepatitis C viral infection can have associated polyarthritis nodosum.

So the vasculopathy causes a l leukocytoclastic destruction of the vasa vasorum and ental tissues and the subsequent changes we discussed.

Intrahepatic Shunts in Cirrhosis

So when imaging a patient with underlying liver disease, you will sometimes come across tubular structures in the hepatic parenchyma that do not correspond to either the hepatic veins or portal veins.
And you know, the physiology of cirrhosis, it will, patients will develop intra hepatic shunts when there is cirrhosis.
The problem is that on contrast, enhanced CT or mr, they can be worrisome for areas of hypercellular carcinoma and you can see a cluster of hyper enhancing areas on the arterial phase here by the Port of Haus and near the intra hepatic IBC on delayed ct.
These become iso dense a characteristics for intra hepatic shunts.
They don't wash out, they don't have a capsule.

Another way we can sort out if these are just shunts is by doing diffusion weighted MRI.
And I won't extend the discussion to a great length on this technique, but you can see that the on this T two shine through on diffusion weighted imaging, we don't see those shunts and on added diffusion coefficient maps, we don't appreciate any findings at the site where those shunts were seen.

We took one step further and we did a liver specific surveillance with gatto acetate di sodium, and we don't see any signs of a hyper enhancing area.

Occasionally there is a shunt and care should be undertaken because near a shunt there can be a tumor.
This patient has decompensated cirrhosis, a large volume of ascites.
You can see the nodularity of the hepatic parenchyma.
So a patient at risk for HAP two cell carcinoma, we could see the shunt.
We could appreciate a small hypodense area immediately adjacent to the shunt and premature enhancement of the portal vein secondary to that shunt.
Here you can see a little bit more a composite showing all the findings, the shunt, the small lesion, and the premature enhancement of the portal vein.
But ultrasound was very elegant in demonstrating these findings.
We did this subsequent to the ct.
Here's the tumor, the shunt is immediately posterior to it.
There is also hepato ugal flow in the portal vein secondary to this shunt.
But the mass is readily apparent on the sonograms.

Bud Chiari Syndrome

But Chiari syndrome is the obstruction of the venous outflow of the liver.
It can occur in the hepatic veins, it can occur in the intra hepatic segment of the IVC and will result in hepatic congestion.
This congestion of the liver will result in congestion at the sinusoids of the liver at the very periphery of the liver.
All the way back pressure will build up.
This venous stasis leads to hypoxic damage and oxidative injury to the hepatocytes.
If this is not resolved, permanent hepatic injury will occur and progress to fibrosis and cirrhosis.
And as we know, fibrosis leads to cirrhosis, which leads to heto cellular carcinoma.

Classification of Bud Chiari Syndrome

The classification of Bud Chiari syndrome is according to the type of venous occlusion.
Type one is limited to the intra hepatic IVC Type two is limited to the hepatic veins.
And type three is a mixed type with involvement of both the IVC and the hepatic veins.

Now it's interesting because the liver has an interesting arrangement whereby segment one, which is also known as the car date has its own venous.
C grass does not depend on those hepatic veins that join this intra hepatic segment of the IVC.
They drain directly into the lower portion of the intra hepatic IVC rather than into the level where the other hepatic veins join the cava.
This segment will then hypertrophy sometimes excessively to the point of compressing the intrahepatic IVC due to the increase in venous drainage, the caudate veins or the veins of segment number one, our enlarged.
And when we can demonstrate that on imaging studies, there are an ancillary sign that indeed there is Bud Chiari.

Imaging Manifestations of Bud Chiari Syndrome

Now I show you these four images to emphasize that bud Chiari can have many manifestations as we look here are intra hepatic shunts.
We also have hyper enhancing nodules on the arterial phase of the ct.
We also have tumor extension into the hepatic veins.
This is hep two cell carcinoma, which we associate more with portal venous infiltration, but can also infiltrate the systemic veins as we see here.
And the thrombose hepatic vein, the more common version that we look for in cases of Bud Chiari, the absence of flow of one of the hepatic veins.

And here, although we see in gray scale the lumen of the middle and left hepatic veins in the juxta cable space.
Here's the cava.
We see that they have a little bit more increased echogenicity to their lumen and we cannot document flow on color doppler.
These findings are consistent with Bud Chiari involving the middle and left hepatic veins.

This is the unusual case of Bud Chiari, which was a very elegant display by color Doppler of these intra hepatic shunts.
The first studies obtained of this patient were really the CT and the MR and we didn't know what was going on.
So the patient was then considered for a biopsy, which we didn't wanna do because there was ascites.
But in any case, an astute sonographer was the one that said.
But Dr. Madrazo, the areas of hypodensity on CT are really shunts and there were shunts in segment three.
There were shunts elsewhere in the liver.
Throughout the liver there were numerous shunts that were both intra and extra hepatic in location.

So here we see the gray scale of that segment three.
When we put the color on, we could see all the shots and those were the areas that were heterogeneous by CT and by Mr.
The advantage of sonography was that it did not have to time the imaging with the arrival of the bolus, which CT and MR had to, so we had a lead advantage because we don't have to time the imaging with the contrast bolus.

Now some of these shunts in but Chiari are quite exuberant in this patient with a thrombose inferior cava and a calcification within the cava.
Because the cava had been used for dialysis, he not only had these enormous shunts, but a sign of caval obstruction is the dilatation of the Aus and Hemi Aus system.
And you can see a very dilated aus vein substantiating the compromise of venous return via the inferior cava and numerous shunts throughout the hepatic parenchyma in this patient with.
But chiari secondary to IVC thrombosis.

Now the hypertrophy of segment one is also a cause for additional problems to deliver because by itself the hypertrophy coate can compress on the cava further compromising the return of blood to the heart via the cava.
So sometimes this is quite a situation where the cate is so hyper purified that flow through the fu cava is diminished.
The liver is quite heterogeneous and we'll see it a little bit better in the next slide, why that happens.

So the call date is able to bring blood into the inferior vena cava so that it is enhanced hyper purified while the periphery of the liver is with edema secondary to the stasis.
And here you can see this arterial phase, corona CT and a delayed phase Corona ct.
And you can see that the central portion of the liver where the caudate is, is readily enhanced, is able to drain the venous flow into the inferior cava while the periphery of the liver remains very emus and doesn't have the ability to egress blood because of the compromise in venous outflow.

Also remember to look in the subcapsular spaces because the presence of subcapsular collaterals in bad chiari is very apparent.
So you can see a very enlarged caudate vein draining into the inferior vena cava sign of blood Chiari.

Pathophysiology and Complications of Bud Chiari

So the obstruction of hepatic venous outflow track results as we discussed in sinusoidal congestion, ischemic injury to the liver cells and eventually portal vein hypertension.
This subsequently leads to hepatic congestion with necrosis, regeneration, fibrosis and hepatic cirrhosis.

What about those regenerative nodules in Bud Chiari?
I showed you two hyper enhancing nodules.
Well, they will occur as part of the reparative changes the liver established to regenerate itself.
And if they were less than three a number and small in size, they were followed.
We wish to see them enhance and never wash out because that's a reassurance that we are not seeing about happy to sell the carcinoma in bad chiri.

So the wash out on portal venous phase is a worrisome finding that warrants a biopsy.
Changes on two successive imaging studies.
Increase in size is also a reason for biopsy, as is an increase in the serum alpha-fetoprotein levels the prevalence of hep two cell carcinoma, but Chiari syndrome is variable.
Depending in geographic locations, the incidence is high.
In Japan, 41% of the cases will eventually develop a Hep two cell carcinoma and South Africa 48%.
But in the United States 25% it is felt that it is probably because we have mainly the bad Chiari of the hepatic veins while the Orientals have in South Africa have more the bud chiri of the intra hepatic IVC.

So the incidence of Hep Toce carcinoma in patients with Bud Chiri syndrome is similar to that in patients with other chronic liver disease.

So we had a patient that we could see a nodule by ultrasound as a hypoechoic, no intrinsic flow could be seen by color doppler, but we know that color doppler may not display all the vascularity that a an area has.
This was a hyper enhancing nodule on contrast enhanced ct.
It did not exhibit washout, but we got concerned because we could see that it was increasing in size.
She had other nodules, you can see them elsewhere.
And this patient did undergo a biopsy of this nodule and this was benign.

Bud Chiari in Liver Transplants

But kera can also occur in liver transplants.
It's not a common cause of transplant complication, but at baseline we could see a nice flow into the intra hepatic IVC at the caval anastomosis.
No areas of suspicious for any elevated velocities were noted at the baseline study.

However, on follow up about 11 days subsequent to transplantation, things did change.
We could see a lot of tissue vibrations surrounding the an thematic site.
We could almost identify a narrowing of the lumen as we can see here.
And what was seen as the normal baseline study of the hepatic vein with nice modulation with the right atrium had changed completely.
And now we had a very limited pulsatility at the level of the cable anastomosis.
In the middle hepatic vein, we could see no significant transmitted pulsations by the right atrium.

MRI was undertaken.
And yes, there was a cable stenosis at the junction of the donor with the recipient inferior of ine cava, a case of Bud Keri in a liver transplant.

We can also look at this study, which was a second case of Bud Keri.
A lot of hematoma present at the caval anastomosis and often this may happen, but resolve, however, the patient did not do well.
And we had a subsequent study that confirmed that flow was not intact, that there were hepatic veins that were devoid of flow due to their thrombosis.
And this thrombosis at the junction of the recipient and CVA and the donor's cava resulted in bland thrombus building up elsewhere in the intra hepatic IVC.

So Bud Chiari and liver transplants, this represents a very low prevalence complications of the IVC and hepatic vein transplants is less or about 1%, there can be thrombosis or stenosis usually at the site of surgical anastomosis.
Sometimes the causes a discrepancy in size between the donor and recipient vessels or a kink at the supra hepatic cava as the liver may undergo slight rotation.
And this causes acute IVC stenosis.

Delayed cable stenosis can be seen due to fibrosis, chronic thrombo or chronic thrombus or neointimal hyperplasia.
Chronic cable stenosis is also prevalent if it is a retrans plantation or in the children.

So these cable anastomosis can undergo complications due to hemorrhage during surgery.
And eventual cable adhesive, which very, very low prevalence we haven't seen cable dehiscence and Bud Keri can develop with inadequate venous drainage.

Inferior Vena Cava Web in Bud Chiari

This is another case of Bud Keri.
Somewhat unusual for us because we don't have too many of these cases of if you're in a cava webs, but you can see that as you follow the cve, you try to see it past the hiatus in the diaphragm and into the right aum and in in fact we don't identify that continuation of the c We have a kind of a rounded end already, in the intra hepatic segment of the cava.
And as we looked around, we could see the cava and we could see some collaterals around the cava, but we could never follow it up to the junction with the right atrium.

In addition, there was a very diminished ity in the ca indicating that it wasn't communicating with the right atrium enough to show that it was in ready communication with the right atrium.
Notice that flow actually was retro retrograde in the inferior cava, and then it would probably flow into collaterals so it could not flow towards the heart.
We could see several collaterals int hepatic and the cava.
We could never trace it up to the right atrium.

And on this MRI, you can see a very significant engorgement of the Hemi Aus and asus veins, A sign of inferior vena cava occlusion or near occlusion.
The cava could be followed to almost the level of the diaphragmatic surface, but a web prevented any flow beyond this point.
And you can see here on the angiogram on the venina cava gram that there is no flow beyond a certain point in the cava and there is significant flow via the hepatic collateral.
The Aus and Hemi aus venous structures assigned of significant cvo cvo compromise.

So again, if you're a web, but Chiari an extensive flow via the asus and hemi asus system.

Advanced Imaging in Bud Chiari

Now we can also take advantage of some additional techniques such as MRI and on the outer phase we always look for evidence of a lower signal of the liver secondary to hepatic steatosis.
But in this case of Bud Chiari, it was an elegant display of the hepatic congestion and hemorrhage because the lowering of the signal of the liver occurred on the endphase indicative of the presence of iron in the hepatic parenchyma due to the congestion and hemorrhage.

This patient had both but Chiari and portal vein thrombosis due to extensive he two cell carcinoma.
And we can see that there are nodules in the periphery of the liver secondary to the development in this patient of but Chiari and he two cell carcinoma.
So you can see that tumor had extended into the inferior Nava and hepatic veins.
We could see portions of the hepatic veins, but, but Kia is secondary to hep to cellular carcinoma.

Extrahepatic Portal Caval Shunts

We had a chance to see several of these cases of another type of hepatic shunt, but this is a extra hepatic portal cable shunt.
The first case we saw was a child, nine years old with convulsions and he was to undergo an MRI, which he did, and it showed the deposition of magnesium and manga and manganese in the basal ganglia.
And this is an indication that there is liver dysfunction when you see those findings by MRI.

So the neuroradiologist asked that we perform an ultrasound to see if he had a normal liver, which was done, and the child was quite restless and we could see the gallbladder, but then we decided that this initial sonogram was not complete and we were going to survey for any kind of shunt based on something we had read sometime in the past.

So then we brought the patient after he had had his lunch and we could see that there were no intrahepatic portal veins.
We could just identify the grooves for the in hepatic portal veins, but portal veins were not seen.
And in addition, the orientation of the main portal vein was anomalous as it directed itself towards the inferior ne cava in the extra hepatic region.

This is a closeup of the absence of intra hepatic portal veins, completely absent as we mentioned.
And here is the anomalous origin of the main portal vein.
Instead of progressing to the right and left intra hepatic segments, the portal vein deviated towards the inferior vena cava.
And here you can see the gray scale and the color doppler.
So an anomaly at the level of the Porter Haus.

Additional scanning demonstrated a nice display of the portal cavo shunt communicating via a small aneurysm and the extra hepatic communication of the porta and the inferior Ava.
So here you can see the porta redirects posteriorly to meet up with the inferior Ava chaotic flow was seen due to this shunt.

And here's the second case.
We actually have three of these.
When you study the portal Haus, you will find some tubular structures, but you will not find the portal vein.
These are hepatic arteries and common bile duct.
And then we can see a posterior orientation of the portal vein into the intra hepatic into the inferior vena cava.

So here you see the absence of the intra hepatic portal veins on this contrast enhanced CT and the anomalous direction of the portal vein, which goes on to connect with the intra hepatic IVC.
You can see this on the coronal ct, the posterior orientation, the portal vein, and its communication with the intra hepatic IVC.

Abernethy Malformation

Now as we do more imaging, we're discovering these extrahepatic portal cable shots, and these are children and adults in some cases that have an anomaly and it's called Aber anatomy mal formation that their portal vein connects with the inferior vena cava and never enters into the liver.
So there's absence of portal flow, they have cognitive problems, they have seizures, they can also develop pulmonary hypertension, which are shared with you, the case we have because of the lack of the activation of vasoactive substances by the liver.

So here you can see that posterior orientation, so extra hepatic portal cable shunt.

This is a patient on our transplant waiting list because these patients with ABER malformation will develop HETO cellular carcinoma.
She actually had undergone already bridge therapy with the delivery of lapi do to this hep to cell carcinoma.
She had a small cyst around it.
And then she, you can see she's starting to develop another HETO cellular carcinoma, hyper enhancing region adjacent to the cyst.
And this is her new tumor, her HETO cellular carcinoma with typical features wash out and capsular perception.

So ABER Anatomy malformation is a congenital extra hepatic portal cable shunt.
Again, we've revisited the Lene veins.
It's total failure of the lene veins to establish anastomosis with the hepatic sinusoids or he hepatic veins.
This was recognized by Bernet in 1793.

There are three types, type one absent intrahepatic portal vein flow is redirected into the inferior N cava.
Females have additional compromise because they have a associated polys aria, theresia and liver tumors.
Type two is the extrahepatic connection between the main portal vein and the retro hepatic IVC males do not have associated anomalies.

So it's very detrimental to females that have e anatomy malformation because they have these associated anomalies, they frequently do not survive.

So the lack of portal oxygenation will result in hepatic remodeling, the development of hepatic masses.
They will develop focal nodular hyperplasia, nodular regenerative hyperplasia or hepatoblastoma, but they can also progress to heto cellular carcinoma with or without underlying cirrhosis.

Now, as I mentioned to you, the delivery to the systemic circulation of vasoactive substances that are not deactivated by the liver will damage the pulmonary arteries resulting in pulmonary arterial hypertension, heto pulmonary syndrome, and cardiac decompensation c on this patient with.
But ABER formation, what his pulmonary arterial circulation looks like, massive pulmonary arterial hypertension because these vasoactive substances are not cleared through the liver and arrive in the pulmonary arterial vasculature damaging the pulmonary arteries.

Signs of Portal Hypertension and Cirrhosis

And here we can see a recanalize para umbilical vein.
And color doppler demonstrates this very elegant.
This is a sign of portal systemic collaterals.
This is a sign of cirrhosis and we can see it here on ct.

And here is another sign of cirrhosis.
This is a reconstitution of the ligamentum venum, which connects the porter and the cava.
But this in the intra hepatic segment with which embryologically exists the ligament and venum, but obliterates an adult life.
But it can re constitute flow in cases of cirrhosis.

So ized ligamentum venom, somewhat seen on ct, but not as elegant and as clear as we see on color doppler.

Osler-Weber-Rendu (Hereditary Hemorrhagic Telangiectasia)

Now Oslo Weber Redu or he hereditary hemorrhagic ectasia, patients will present with epistaxis because they have these ectasia in the mucosal surfaces and they can have these recurrent nose bleeds.
These can exist also in the lips, oral cavity, fingers, nose.
There can be visceral involvement in the lungs, liver in the brain, spinal cord, GI tract, family history of first degree relative with Oslo, Weber Redu.
And these other criteria make the diagnosis established.

And hepatic involvement.
We can find these on color Doppler or CT and deliver involvement varies around 41 or a little higher.
In some series.
Family screening protocol studies range between 67 to 84%.

So these are somewhat more at risk because there is a family history of Oslo Weber Randu.
They occur more the int hepatic shunts in females and after the fourth decade.

So it is an autosomal dominant condition resulting hereditary injects with hepatic involvement causes tissue proliferation and this connective tissue proliferation results in fibrosis and cirrhosis.
They can have an arterial component to these vascular malformations that leads to cardiac failure portal hypertension and the vascular malformations can be arterial portal Arterial venous or ven venous doppler findings include the dilated hepa artery greater than 10 millimeters, and the pulsatile portal flows and shunts with waveform changes in severe cases.

So these vascular abnormalities in all Le Weber redu evolve in a continuum from tiny tele injects to substantial vascular malformations.
And as a consequence, these patients can have congestive heart failure and portal hypertension.

Very few cases of arterial portal shunts have been found in the literature, but they can exist.
And patients can again, as we mentioned, develop the full spectrum of the liver involvement, including progression to portal hypertension and cirrhosis.

Here is an isolated peripheral ven venous communication between the hepatic vein and the portal vein.
A small ov venous anastomosis or malformation.
And you can see it here on the CT and you can see that it is connecting the right hepatic vein with the right portal vein.

This is another example of Oslo Wedu.
We just see tubular structures in the hepatic parenchyma.
And of course, we would have to resurvey the patient with color doppler to demonstrate that these are vascular structures anomalous, not representing the hepatic veins, hepatic artis or portal veins.

So tremendous volume of blood is flowing through these vascular malformations and causing significant engorgement of the draining hepatic vein.
And notice the very enlarged hepa when these malformations do include the hepa, these are the ones that will result in congestive heart failure.

So the hepatic artery is so large, much larger than the portal vein at the portal.
Heus not the normal situation.

So as we look with ct, we can see some peripheral tele injected sites and we can see that the Hepa cardi is about the same caliber as the portal vein, not the normal situation.

So the intense amount, the high volume of flow through the HEPA card results in enlargement of the Hepa Cardi as we see here.
And some peripheral ic.

This is another case.
And in this case, we saw on gray scale these linear echogenic sites.
We did not have any knowledge about what the these areas may represent.
It turns out that the constant pulsation of these vascular malformation in the area causes the liver to react and develop areas of fibrosis.
And these are the sites we see as echogenic linear areas bordering on the vascular malformations.
And you can see those echogenic areas and the vascular malformations surrounding them.

So Oslo Weber Randu hepatic involvement.
Notice that the flow in the hepatic artery was so high, we could hardly identify the portal vein.
That was Alia C on colored Doppler.
And flow was very high.
We couldn't even greater than 200 centimeters per second in this hepatic cardio, which normally is about a hundred centimeters per second or less.
And again, numerous sites of vascular malformation, including the one the patient could feel herself involving.
Segment three Reconstituted images on the coronal plane, sagittal plane on this side and coronal plane.

Here we can see this network of vascular malformations in the liver due to Osler Weber du and the premature return of blood.
As we were in the arterial phase of contrast delivery, there was already vascular enhancement of the hepatic veins and returning of opacified blood to the heart.
You can see that angiography of the hepatic artery demonstrates a rapid flow through the liver and flow is already returning to the heart during the arterial angiogram.

The hepa cardia is enlarged sometimes aneurysmal due to the high flow, the very significant flow through these vascular malformations.

This is just a composite of the same case.

This is a young child, an unfortunate child born with an arterial portal communication.
And this is a very rapid hyperdynamic circulation.
And these children born with these arterial portal fistulas go into congestive heart failure.
They also have portal hypertension and they have massive episodes of bleeding.

And here is this arterial portal fistula, but notice there are numerous other fistulas and the HEPA card is very dilated and premature flow occurs into the portal vein due to this anomaly.

These arterial portal fistulas are complex and can be seen in other syndromes such as Oslo, Weber, redu, erler, and biliary atresia.
But it is a known rare cause of portal hypertension and symptoms developed within the first year of life.

Hepatic Artery Complications in Liver Transplants

This is a liver transplant and we monitor the Hepa Cho because flow in the HEPA is essential in the liver transplant because the hepatic card supplies the biliary ductal system with flow.

So you can see that there is a focal area of aliasing in this HEPA artery.
And as we know, there is an anastomosis made between the donor and recipients circulation at this level.
So we can see that there's very high velocity in the hepa cho in the area of aine sine there is Rey at the baseline and we are concerned that there might be a stenosis at this site.

All of a sudden the patients started having very diminished flow in the HEPA artery.
We could barely see any kind of flow, resistance to flow was increased and this patient ended up going back to the surgical suite where a dissection was identified at the level of the anastomosis.

So this dissection was repaired, the patient was re-scanned and now we see much better flow in the hepatic cardine.
As we have mentioned, this is an essential region for the survival of the graft and for preservation of the biliary ducts.
Because the hepa cho supplies the biliary ducts, if we don't have sufficient blood flow via the HEPA artery, there will be ischemic cholangiopathy of transplantation.

So here we see flow in the HEPA artery, but it is not a significant amount of flow.
It's very diminished on ct, we could see there was an abrupt cutoff.
The celiac artery was here.
We saw a little bit of flow and then we couldn't see any flow in the intra hepatic segments or at the port of heus.

So the patient went to angiography and it was seen that there was almost complete thrombosis of the hepatic heart.
There was thrombolysis administered and a better flow in the hepa artery was achieved.

Again, here's a focal area of increased velocity and color doppler and very low resistivity to flow, elevated diastolic flow on color doppler.
And we monitor these patients very extensively, almost every six hours on the first two or three days, and then every day the subsequent days.

So we have the portal vein here and we can see that the hepatic artery has very low resistance to flow and that we're beginning to get concern is 0.5 resistivity index.
We reassessed the patient.
The HEPA heart is 158 centimeters per second 0.63 resistivity index, and then a little bit of lowering of the resistance to flow.
And on subsequent study, the common hepatic artery is very elevated now and we are worried that something is happening at this anesto site.
And we instigated a MR, which demonstrates that there is a clamp injury to the hepa artia.

I'm sorry, the arrow is in a erroneous location, but here is the clamp injury to the HEPA artery.
That was the cause of the stenosis low velocities in the hepa artis.
And the portal veins have flow that is a little bit increased and the low velocities were due to hepatic artery thrombosis.
Complication of transplant, fortunately not very common, but when it happens is catastrophic.

Prevalence and Causes of Hepatic Artery Stenosis and Thrombosis

So hepatic artery stenosis has been reported in five to 11% of transplant Complication usually occurs at the site of anastomosis within the first three months after transplantation, if left untreated and may lead to hepa cardio thrombosis, hepatic ischemia, biliary strictures and graft loss.

And we mentioned ischemic angiopathy of transplantation is secondary to the diminished flow by the hepa cho to the transplanted liver.
There can be thrombosis due to a mismatch in caliber between the donor and the recipient Hepa.
There can also be an interpositional conduit for the anastomosis, which is more rare, but they do bring a conduit between the infrarenal aorta and the hepa artery, or it can be secondary to a preexisting stenosis of the celiac axis.

The excessive duration of cold ischemia is also a factor, a BO blood type and compatibility, infections or acute rejection.

The prevalence of hepa cardio thrombosis is higher in pediatric patients where it can be 40%, but in adults it's four to 12%.

So this hepatic artery thrombosis can occur in two to 12% of patients between the 15 and the 132 day subsequent to transplantation.
This remains a a problem and we hope to improve our doppler technology as we use more.

Now, perhaps in the future the contrast agents, the reduced blood flow can be due to spasm or low cardiac output.
So we have to keep that in mind.

The hepatic artery thrombosis, the diagnosis is established by the absence of flow in the hepatic proper or the intra hepatic arteries on color and pulse Doppler imaging.
This is a very accurate and is estimated that it is able to identify portal flow.
In 92% of the cases, an abrupt cutoff of flow in the artery is diagnostic for hepatic artery thrombosis.

I'm gonna share with you a couple of things regarding hepatic vascular tumors, but the one thing that I wanna begin our discussion in this sub-segment of the lecture is on he angios.

Hepatic Vascular Tumors: Hemangiomas

We are very familiar with hagios.
We like hagios to be of homogeneous increased echogenicity.
They should not have a peripheral halo.
There can be calcifications because LeBus can develop ingios.
They are unencapsulated, so they're gonna have irregular margins.
And if we were using contrast agent, we would see the same flow characteristics that are seen on CT M-R-N-M-R-I, which is the peripheral nodular discontinuous enhancement with centripetal fill in and retention.

So here is a typical human genoma.
We have a hyper coic area.
We can see that there is no flow on color doppler because the flow within the hemangioma itself is very slow and results in flow being below the threshold of color Doppler or power doppler on MRI hemangiomas are low signal intensity on T one, but very high bright on T two sequences.
And you can see the lobulated contours due to the lack of encapsulation of these lesions because they're fluid containing, they can exhibit acoustic enhancement.
And we see on this patient a nice example of acoustic enhancement beyond this hemangioma.

But I will tell you, not all hemangiomas give us such elegant display of acoustic enhancement.
The other thing to remember is after they're about four centimeters in size or higher in size, they will stop having the typical sonographic appearance of hyper echoic lesions.

Here is a atypical hepatic hemangioma, which is hypo echoic.
It is in the background of hepatic steatosis and you can see that it has a brief enhancement during the arterial phase.
But on the portal venous phase, it's beginning to have peripheral nodule discontinuous enhancement and is going on to fill in centripetal and retain contrast on more delayed cts.

Now this is my example of a number one exophytic, hemangioma number two with foci of calcification.
So bolus and the matrix of this heman genoma.
And you can see these calcifications on the unenhanced ct and you can see the typical peripheral nodular discontinuous enhancement of this heman genoma, which is a characteristic of these lesions.
There will be gradual filling in and retention of contrast.

So vol is on a hepatic hemangioma.

This is a hypoechoic hemangioma with the unusual peripheral halo or peripheral capsule.
Capsule like area.
Very unusual.
There is some acoustic enhancement, but the margins are delineated by a hyper coic halo.
So this is very uncommon in he angios.

This is another atypical hemangioma.
Very large heman genoma portions are echogenic, other portions are hypoechoic but no acoustic enhancement.
We see that some of the vasculature is going around this large mass, but not within it.
And on CT we can see that the lesion is predominantly low attenuation prior to the infusion of contrast.
Then it begins to exhibit the characteristic peripheral nodular discontinuous enhancement.
It goes on to fill in centripetal with the exception of this large cystic cavity that exists in this atypical hepatic he meningioma.

And on MRI similar findings are present.
The lesion begins to fill in from the periphery where it has a discontinuous, peripheral nodular enhancement fills in with the exception of the large cystic cavity, which remains unenhanced.

So this is an atypical hepatic.
He In segment three we see a lesion that has a central portion that is echogenic.
There's no intrinsic flow.
We don't wanna consider this unequivocally a hemangioma.
We wanna characterize it with other methods.
And we did because this was not convincing us that this was a he genome because of this hypoechoic halo on MRI on, I'm sorry, on ct.
The lesion did enhance and this was a single lesion in segment three.
We didn't like the fact that we were losing its intrinsic flow.
BA was becoming hypo dense.
And we did worry that it was an unusual adenoma skin lose some of the contrast.
But we wanted to make sure this woman didn't have an unusual situation.
And she did have a biopsy which demonstrated beta-catenin mutations.
In that hepatic adenoma, she underwent a lesion resection and had foci of heto cellular carcinoma.

Hemangiomas in Cirrhosis

Now be careful when calling this lesion a hemangioma because this is in a patient with cirrhosis.
The patient was told to come and have this reassessed by ct he did not.
About six to eight months later he presents now with large volume ascites.
The lesion note has become hypoechoic.
It's kind of interesting.
And here are three hypercellular carcinomas in this patient at risk.

In fact, hepatic, he mens are uncommon in the cirrhotics because of the fibrotic nature of the liver, which causes a complete obliteration of the little arterial venous malformation that is the titis of a heman genoma.

So hemangiomas and cirrhotics, very rare actually.
If you see something in a cirrhotic, be it hypo or hyper coic, call it suspicious for heto cell carcinoma, you're gonna be right more than wrong.

Hepatic Angiosarcoma

Hepatic angio sarcomas are experiencing a recurrence in prevalence.
We do not understand why they were associated with exposure to such agents as vinyl chloride and arsenic.
And thore was a contrast agent using angiography that was radioactive and caused a lot of ingios sarcomas in the liver and spleen.
This does not have a high prevalence 'cause some of the patients exposed to Thora have long expired.

The malignancies derive the spindle cells and poorly organized vessels that grow along the vascular channels.

So the reason I brought this case for us to share is because I was kind of disappointed 'cause I thought for sure these were gonna be very hypervascular lesions.
We could barely make out any flow into these peripheral areas of the liver, which were the sites of involvement by this angio sarcoma.
And I wanna caution you that this is quite typical.
The literature reflects that these are typical findings where the liver is so involved.
It's actually necrosing because of this tumor involvement.
And not only is it involved in one area, such as we see here in the right lobe, but there were other areas elsewhere in the liver where these peripheral hypodense areas were seen.
These were all causing significant restricted diffusion on the DWI and a DC images of the mr.

But also these are the cavernous spaces in the periphery of the liver that are quite typical for this angiosarcoma.
And here you can see the due cause restricted diffusion on the A DC.

So peripheral areas due to the vascular involvement.
And em neoplastic embolic events to the periphery of the liver are one of the findings that are typical for this vascular tumor.

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

Our last portion of the lecture will be on tips, and this has been developed to alleviate the consequences of portal hypertension and gastroesophageal varis and bleeding.

So Ashan is deployed between the hepatic veins and the main portal vein.
And we used to have to follow these diligently because frequently they became stenotic or occluded.
But now we have a stat that has a endo prosthesis with E-P-T-F-E, which is a substance that prevents the development of intra stent areas of neointimal hyperplasia.

So these Vitor stents are aligned with this biocompatible microporous nonthrombogenic substances and become relatively impermeable to bile and tissues and provide a good substrate for the endothelial lining.

So these patients have a high incidence of patency of these tips.

So we have a patient with exuberant gastroesophageal varis, usually prior to placing the tips, they would occlude these varis and once occluded, they then could deploy the tips by entering the jugular vein and coming into the hepatic vein, and then finding a point of where they could connect the portal vein to the hepatic vein and then achieve this portal.
Decompression tips result in significant decrease in gastroesophageal bleeding by varis.

But unfortunately because blood is shunting through the tips, the patients have a greater risk of a hepatic encephalopathy.

So there's gonna be a mark reduction in portal pressure gradient, and the absolute portal pressure will be decreased.
There will be a slight increase in the inferior cava pressure and mark reduction of portal collateral.
Blood flow, it controls varie bleeding very well, but unfortunately, as we mentioned, patients are at greater risk of hepatic encephalopathy.

So we can use it for a variety of indications to prevent varice bleeding and patients in whom sclerotherapy has failed.
In patients with refractory ascites in Bud Chiari.
And in patients that are at risk of bleeding and awaiting a liver transplant, it's relatively contraindicated to place at tips if there's port of a thrombosis.
Patients with hepatic encephalopathy, patients with a hepatocellular carcinoma are patients that have undergone already many sessions of sclerotherapy.
And in cardiovascular, severe cardiovascular compromise is contraindicated as well.
In patients with a short life expectancy of less than one year tip occlusion can occur.

And this can be done with angiography and the degree of stenosis determined by angiography or tips.

Uh, malfunction is seen when there is a portosystemic gradient to more than 15 millimeters of mercury.

So the stent is deployed and there is no gastroesophageal varis.
The stent is then left in place.

So although we had tremendous importance in the assessment of stents tips, we now have a much less prevalence of stent stenosis.

But the average velocity at the portal venous side of the tips is 82 centimeters per second, plus or minus 49, mid stents 110 plus or minus 45.
And at the hepatic side of the tips 105 plus or minus 46.

So intra shot, this normal velocity is vary between 60 and 200 centimeters per second.
And in the main portal vein, the average is 40 to 60 centimeters per second.

Remember that the shot will cause an increase in hepatic artery flow because it will be diminished portal flow.
So the normal post tips, hepatic artery blood flow is above a hundred, 135.

And when the shunt is beginning to malfunction, it starts lowering the velocity in the hepatic artery and then occluded shots.

The average velocity that Hascal saw in his extensive study on tips was 109 plus or minus 39 centimeters.

So the diminishing hepatic arterial flow is an indication of tips malfunction.

So here we see the hepatic and portal vein, and we're simply in the portal vein and we see the nice minimal variation in flow.
Then in the shun itself, the flow is continuous.
And as we approach the hepatic side of the shunt, it begins to modulate a little bit more with the right atrium.
And here we can see that there's no impediment to flow into the inferior vena cava.

And here is the hepatic artery, the main portal vein, mid shunt and distal shunt.
Remember that because there is a gradient from the main portal vein to one of the hepatic veins, the left portal vein will have hepato ugal flow.
This is normal in tips.
The gradient causes flow to reverse.
In the left portal vein, there will be, as we mentioned, increased flow through the HEPA and a normal functioning tips.

And here we can see the flow in the tips, and then we can see the hepato ugal flow in the left portal vein seen here in blue.
And we again attest for the presence and patency of the tips.
And you can see the tips displayed on the coronal ct.

So the normal tips has velocity between 60 and 200.
Here we have it as 80 and 200 centimeters per second.
The flow is documented and angle corrected obviously, 'cause we're measuring velocity.

And here is a shunt, which is patent flow is present, and here is an occluded shunt.
The patient now has, again, decompensated findings with the large volume of ascites, an indication that portal pressure is elevated.
There is no flow through the shunt, and the shunt was revised.

And here we see that the tips on the CT has no flow within the lumen of the tips.
And this is because this HETO cellular carcinoma has infiltrated the portal vein and the tips.

So we have heto cellular carcinoma, infiltration of a tips.

So tips failure in this case, the pressure in the right atrium was elevated, but the tips was deployed anyway.
So the net flow into the right atrium was near zero because as much flow went forward into the heart, as much flow went back into the tips due to the elevated atrial pressure.
Therefore, a gradient was not present, could not cause flow to go through the shunt into the right heart.

So high velocities in the tips areas of neointimal hyperplasia and return of ascites are all signs of impending tips.
Failure and the lowering of the velocities through the shunt are a difference between the baseline and the present study of 50 centimeters flow per second is an indication that the shunt is failing.

Conclusion

So in conclusion, I want you to become more aware of hepatic vascular conditions because they need to be appropriately recognized by us in ultrasound and in other imaging methods so that they can result in correct management.

Ultrasound is essential for their detection.
Due to the acute nature of the presentation of some of these vascular conditions, requiring bedside evaluation and the availability of ultrasound contrast agents will greatly impact the recognition of hepatic vascular conditions.

Thank you.