Ultrasound of Liver Transplants - HD

Introduction and History of Liver Transplantation

I have no disclosures.

I'd like to thank my colleague, Tom Grant for some of these cases.

As we all know, liver transplantation is a life-saving procedure.

The first transplant was performed in 1963 and at that time, the one year survival was only 15 to 25%.

Since that first procedure, 152,000 liver transplants had been performed 7,800 in 2016 alone.

And now the current one year survival is 91%.

We've come a long way.

The problem though is that currently there are 14,148 patients on the liver transplant wait list.

And again, only 7,800 were done in 2016.

So half the people in need don't get liver transplants.

And in fact, many people die waiting for a transplant.

Demand outnumbers supply.

So identification of any reversible complications to salvage as precious commodity should be made early and accurately.

And to that end, ultrasound is the first line and best modality to do that.

Overview of Talk

In my talk today, we'll talk a little bit about surgical technique of liver transplants.

We'll talk about sonographic technique, we'll discuss normal versus abnormal findings, you'll see, and then we'll discuss some complications concentrating on vascular, biliary complications for the sake of time.

Surgical Technique of Liver Transplants

Liver transplant surgery, obviously a complex undertaking, but thanks to a lot of technical advances and experience, it's now consistently successful in a widespread basis.

If you have a liver transplant, you can have either a cadaveric transplant, which can be whole or could be a split liver where part of it goes to, usually an adult part of it may go to a child.

You can have a living donor transplant where an adult donates a portion of the liver.

And that's what we're seeing here.

One of our surgeons gave me this clip.

Whatever the transplant successful transplantation is based on four steps.

Donor hepatectomy, recipient hepatectomy, the an hepatic phase implantation of the graft with the anastomosis and hemostasis.

They're foreign anastomosis, the arterial portal venous biliary, and the hepatic Venus.

And we'll go through each of these individually.

Hepatic Arterial Anastomosis

This is the hepatic arterial anastomosis.

And what's usually done is that the donor arteries taken at the junction of the splenic artery, near the celiac axis, and in a cadaver, a little patch of the aorta is taken as well.

A Carrel patch.

The recipient hepatic artery is, ligated or resected at the branch point with the GDA and these two are, sutured together.

It's important to realize that oftentimes there is variant hepatic arterial anatomy, and the surgeons navigate this by putting in conduits.

It's very important that you realize what the anatomy is.

It's important to read the surgical reports or have a discussion with your surgeons because these anastomoses can be in different places, they can have higher complications rates as well.

Oftentimes they'll sketch a picture for us in a, the old adage, a diagram or picture is worth a thousand words is very true.

Portal Vein Anastomosis

Portal vein anastomosis is usually end to end.

IVC and Hepatic Venous Anastomosis

And now in terms of the IVC hepatic venous anastomosis, it's almost exclusively done as a piggyback technique instead of transecting the recipient IVC, what happens is that the donor supra hepatic IVC is sutured to sometimes the cuff of the hepatic veins.

What our surgeons do and what you see here is they do a little caval cavostomy so that there's a big conduit there to minimize hepato-occlusive obstruction.

And then the inferior aspect of the IVC is ligated.

Biliary Anastomosis

The biliary anastomosis usually end to end.

Sometimes a choledochocholedochostomy is done in patients with diseased CBDs as in PSC or if the CBD is too short.

Sonographic Technique

Let's go on and talk a little bit about the scanning technique.

And what's interesting is that the timing of when you should scan a transplant is not standardized.

Each center does, what they think is right.

Most people do a baseline exam, which is very important.

We scan the transplants within 24 hours and then we always scan within two weeks.

Because asymptomatic problems can happen and if that patient needs a repeat transplant, they are at the top of that wait list within that two week period.

And obviously we scan when a clinical issue arises as well.

So when we scan, again, always confirm that surgical anatomy, we do our gray scale of the liver as per typical liver protocol.

Large field of views looking for fluid collections.

We scan for collaterals and we look at the biliary system and then we look at all the vascular, connections and we'll look at those one by one.

The one thing with the hepatic artery, we march through the hepatic arterial system, extra hepatic region of the anastomosis intra hepatic, and then the branches, oftentimes you don't know exactly where the anastomosis is.

The sonographers infer the location of it because it's in the area of most aliasing, but you don't really know where it is oftentimes in terms of, normal values has covered that.

But, typically less than, a peak systolic velocity less than two to 300 centimeters per second.

It's a typical low resistance wave form.

The RI should be between 0.5 and 0.8.

And the acceleration time, which is taken from end diastole to the first systolic peak should be less than 80 milliseconds.

Abnormal hepatic artery and contrast PSV greater than 300 centimeters per second or 200.

And the classic tardus parvus waveform that you are all familiar with, again, an acceleration time greater than 80 milliseconds diminish pulsatility diminish difference between systolic and diastolic velocity.

In terms of the portal vein, again, we marched through the system.

Again, you can tell, in contrast in the portal vein where the anastomosis is oftentimes and hepatic veins the typical phasic waveform.

Early Postoperative Period

So I wanna spend some time talking about what you can see in the early postoperative period.

It's a time of tremendous change in the transplant and sometimes you get waveforms that normally would make you think that there is a complication, but these are entirely normal in the postoperative period.

Oftentimes in the hepatic artery, you'll see an elevated peak systolic velocity here, and that's oftentimes due to edema at the anastomosis.

It may be due to a persistence of increased arterial inflow in these patients that have had portal hypertension.

But oftentimes this will, this will diminish with time.

Oftentimes these transplants will also have a very elevated resistant index, as high as 46% of transplant patients in some series.

And this may be due to a hepatic artery spasm edema, increased cold ischemic time, older donor increased portal flow.

Again, the fact that the RI is also elevated in the liver parenchyma is reassuring.

It's been shown that this waveform has absolutely no significance in terms of graft function and this usually normalizes as well.

Now sometimes you can also see a decreased ri and in general that is a better indicator of hepatic artery complications, but sometimes you can't see it as a normal finding in this early postoperative period.

This also may be due to edema at the anastomosis reperfusion of the transplant.

Sometimes vessel caliber mismatch as you see here, big vessel caliber mismatch between the recipient and the donor can give you this kind of low RI waveform, but the upstrokes are usually maintained in these waveforms.

So here's an example of a patient who had a liver transplant December 20, 2011, and we see high RIs throughout the liver.

Three days later we see that the waveforms look entirely normal.

Different patient who had, who had a liver transplant one day previously.

High peak systolic velocity 314 centimeters per second lowish RIs just two days later, that peak systolic velocity's coming down and now these waveforms look completely normal.

Hegar et al did a very nice paper where they looked at 645 patients in this early postoperative period, trying to find which doppler waveforms were most predictive for hepatic artery thrombosis.

And what they found was that a normal hepatic artery waveform during this early time is actually present in only a minority of the patients.

Many patients will have this elevated ri waveform.

Some patients will have a low ri, some patients will have non visualization of hepatic artery.

Many of these though did have hepatic artery thrombosis.

So in those first 12 hours when these patients are very difficult to scan with bandages, poor acoustic windows, any hepatic arterial signal is good signal.

In terms of the portal vein early on, oftentimes we see very high peak systolic velocities.

Here I've seen velocities as high as 300 centimeters per second that come down.

Again, edema usually perhaps increased splenic flow.

And again, these patients with portal hypertension, which now have a new liver that has no resistance to flow, so you have a lot more flow coming in.

We never make the diagnosis of portal vein stenosis early on.

It usually doesn't happen early on anyway.

And in liver transplants oftentimes you can see helical flow as well.

Now you would think with all this post-surgical change, you'd see perhaps monophasic flow in hepatic veins.

What we found in our series is that that normal phasic waveform is usually maintained even in the early period in these transplants.

So an example of a patient high peak velocity in the main portal vein, not even really that high 148 centimeters per second, that goes down nicely on progressive exams.

Vascular Complications

Let's talk a little bit about complications starting with vascular and starting with the hepatic artery.

Hepatic Artery Complications

Problems with the hepatic artery are the leading cause, vascular cause of graft failure.

The liver has dual supply, but the biliary ducts have a sole supply supplied by the hepatic artery.

So if there's a problem, you'll see biliary ischemia, necrosis, stricturing stones, infection abscesses.

What's interesting also is that hepatic artery problems can occur in asymptomatic patients and cause graft failure 10% of the time.

So again, screening these patients, even if the clinical picture looks good, is very important.

Hepatic Artery Thrombosis

In terms of hepatic artery thrombosis, it's the most common vascular complication in incidences of four to 12% in adults, higher in children, and it comprises 60% of vascular complications.

It really consists of two separate entities.

Early hepatic artery thrombosis, which occurs within 15 days of the transplant and delayed hepatic artery thrombosis that can occur months, even years after the transplant.

Risk factors for HAT are numerous, including small vessels and grafts, and it's very important to have revascularization of that thrombosis either through IR surgery because if it's done before clinical or lab abnormalities, the incidence of biliary complications really decreases.

But unfortunately, 60% of these patients require repeat transplantation.

How is ultrasound in making this diagnosis?

Again, it depends on the type of hepatic artery thrombosis.

The early type we're almost a hundred percent sensitive.

The later type not so good, 73% sensitive.

With early hepatic artery thrombosis, typically you see a non visualized, hepatic artery flow.

This is the most consistent finding.

The caveat though, is that you really need to optimize for slow flow.

Again, these are sick patients, tough to scan, they may have had hypotension.

You need to optimize your doppler settings.

And ultrasound contrast I think will be very useful in this context.

Sometimes you can't see a tardus parvus waveform and there is a syndrome of impending thrombosis has been described in the literature on progressive exams, you may have a progressive decrease in diastolic flow, so increased RIs and a dampening of that systolic peak.

The arterial thump, we haven't seen that so much in our practice, but it has been described.

And false negatives. Hepatic artery thrombosis are collateral vessels and these collateral vessels oftentimes have abnormal flow.

Luckily, oftentimes you'll see low RIs in those collateral vessels.

So this is what these cases usually look like.

This was a patient who we were able to see the native hepatic artery, couldn't see anything in the region of the anastomosis, couldn't see anything intra hepatic.

This patient went to IR.

We see a big filling defect within that hepatic artery.

The patient underwent thrombolysis and stent successfully and now we have beautiful flow.

Late hepatic artery thrombosis again occurs later.

Ultrasound is less sensitive because again, you get collateral flow.

Is that collateral flow enough to sustain that transplant In pediatric patients?

It often is, and even in some adult patients it is.

In terms of the ultrasound findings, sometimes you still will see non visualized arterial flow less sensitive.

But again, these are the patients where you see low ris with tardus parvus morphology, sometimes single branch RI abnormalities.

These are tough patients.

These are patients where the case doesn't make complete sense.

So you need to be very careful and look for subtle changes in RI.

And tardus parvus.

And you need to look at progressive exams.

So this is a patient that's not so subtle, but this patient had a liver transplant, had this ultrasound one and a half years later and we see very marked abnormal tardus parvus morphology throughout the liver.

This is a CTA and this person had a conduit that actually had thrombosis of the conduit here and here.

But what we can also see are these small vessels by the hepatic hilum, which represent those collateral vessels that are providing that abnormal RI flow to the liver.

Hepatic Artery Stenosis

Hepatic artery stenosis is the second most common vascular complication.

It occurs later with a median time of 100 days.

Dal was one of the first to describe these findings in liver transplants.

High peak systolic velocity.

This alone gives you a sensitivity of 30% tardus parvus alone, a sensitivity of 73%.

If you combine them, you get a sensitivity of 97%.

Now when we're screening these liver transplants, we are a screening exam, so we wanna increase our sensitivity if we see either an elevated PSV velocity or a tardus parvus that would prompt us to do something, whether it's a re-scan or another exam.

So here's one such patient.

Patient had a liver transplant December 2nd.

The ultrasound was done on the same day.

We see a high peak systolic velocity here, 311 centimeters per second, more distally.

We have a tardus parvus waveform.

We want to re-scan within 12 hours as patient came back 10 days later for some reason.

And the RIs are worsening and there's a tight stenosis here on angio.

This underwent angioplasty different patient who just demonstrated an elevated peak systolic velocity, 303 centimeters per second distal vessels just lower, high ris, no tardus parvus morphology at all.

This person also had, hepatic artery stenosis status post stent with good flow.

And this is a patient who had a single branch, low ri, the native looks good.

The region of the hilum looks good.

Left hepatic looks good and the right looks different.

Much lower ri here, abnormal morphology.

This was the surgeon's sketch and sometimes you need a sketch to explain the sketch.

A conversation is the best thing actually, but this person did have a replaced right hepatic artery with a severe stenosis, had to go back to surgery.

And now we have nice flow over there.

Hepatic Artery Pseudoaneurysm

Hepatic artery, pseudo aneurysm, rare but potentially catastrophic.

Ultrasound findings are the typical board exam, right?

You see a cystic area in the hilum or intra hepatic and you need to be cognizant of this.

So you put color doppler flow and you see that pseudo aneurysm, disorganized flow to and fro spectral flow is classic.

And here's one such pseudo aneurysm.

This one's huge.

This one is also partially thrombosed.

We can see this on the ct and here it is on the angio.

Prior to coiling, this is a different patient.

We saw a lot of blood here.

The patient was stable, but we saw a lot of blood hepatic arteries actually looked good on CT though, a lot of acute blood.

There's active extravasation.

This was hepatic artery rupture from presumably a pseudo aneurysm.

Splenic Artery Steal Syndrome

Talk a little bit about splenic artery steal syndrome or a hepatic artery hypoperfusion syndrome.

This is shunting of the hepatic artery flow to the splenic artery.

The cause is actually a bit controversial.

Most people have thought this is a primary arterial abnormality, that it goes to the spleen because of splenomegaly.

Now people think this may be due to portal hypertension and hepatic artery.

Buffer response occurs in the early post-op period and what you see on ultrasound is high RI decrease the hepatic artery flow, sometimes a low, systolic peak.

Sometimes you can see high velocity flow in the splenic artery as well.

So this was a patient, scan them on day zero.

Pretty good.

Hepatic arterial flow for, just coming out of the OR anastomosis looks fine.

We saw some flow on the right.

We saw some flow on the left and then this was three days later.

We weren't really able to get consistent flow on the right.

The left didn't look normal.

And on angio, there is sluggish flow to the hepatic artery with preferential flow to the splenic artery here consistent with splenic artery steal.

That's how you make the diagnosis.

Patient underwent coiling and now we see good flow into the liver and nice flow on doppler ultrasound as well.

Arteriovenous Fistulas

AV fistulas are not uncommon.

Ultrasound only detects half of them, but it detects the ones that are, clinically significant often.

And classic findings, again, arterialized venous flow as ELR showed us, this is an example of some abnormal vessels here.

Very turbulent flow.

Classic arterialized venous flow here.

Early portal venous branch filling.

And here's the angio showing this AV fistula.

Different patient here.

Turbulent arterialized venous flow.

And we actually see the connection really nicely here.

Management of Early Postoperative Hepatic Artery Scenarios

So I wanna go through, the management of some of these early postoperative hepatic artery scenarios in kind of a rapid fire, way.

So let's say you see normal flow in your early liver transplant, what should you do?

You should think your lucky stars because the minority of the, the majority of the time you won't see a normal flow and that person would just go to routine screening protocol.

Let's say you see non visualization, the hepatic artery, well that's the best predictor for hepatic artery thrombosis.

If the main's not seen that patient goes straight to angio or surgery Ultrasound contrast.

Again, this is a perfect context for this.

If the right or left are not seen, oftentimes that patient will go to angio two.

But sometimes we will re-scan early within 12 to 24 hours.

What if you see a high RI throughout the liver Early on, again, normal finding, we see it very often.

This typically normalizes and this patient, with us would go to routine screening.

What if you see a high RI but a low peak systolic velocity?

Well that may be that wave form of progressive decrease in velocity, perhaps impending thrombosis could be, splenic artery steal.

We would watch this person very slowly and potentially go to angio.

What about all these low RI scenarios?

What do you do there?

Well again, these absolutely could be suspicious for a hepatic artery abnormality.

You need to have a discussion with your surgeon and see how that patient's doing.

We may follow them very closely.

Go to ultrasound contrast. MRA CTA.

What if the upstroke is sharp though again, still could be a hepatic artery abnormality, but you can also see this with reperfusion and vessel size mismatch, especially in partial liver transplants.

So we'll often re-scan these single branch RI abnormalities.

Possibilities include replaced vessels, collateral flow AVF check your surgical report and anatomy re-scan versus CTA versus MRA.

What if you have a high peak systolic velocity in hepatic artery and a normal ri again could be hepatic artery stenosis, but could be post-surgical.

We will re-scan these to and fro flow.

Pseudo aneurysm materialized flow AVF.

Both of these go straight to angio.

Okay, we have talked about the hepatic artery ad nauseum.

We're gonna talk about the other vessels.

Portal Vein Complications

Portal Vein Thrombosis

Portal vein thrombosis rare, but it's an early complication within the first month oftentimes due to technical issues.

Vessel size mismatch, has gone through all the findings of portal vein thrombosis beautifully.

But you really need the trifecta.

You need gray scale, you need color and you need spectral doppler to make this diagnosis correctly.

Here's not a subtle case.

Big portal venous thrombosis and main portal vein.

Little bit of flow.

So it's partially occlusive.

Here's the ct.

Here's another patient with non occlusive partially occlusive portal venous thrombus.

Showing that color blooming artifact.

Whereby color can obscure small defects because of the resolution is lower than that of gray scale

Portal Vein Stenosis

Portal vein stenosis is uncommon and it also may not be very clinically significant the majority of the time.

There have been a lot of papers looking at criteria for this.

What people usually use is a velocity of greater than 125 centimeters per second.

A stenotic to non stenotic ratio of three to one.

Oftentimes you can see helical flow in patients with portal venous stenosis as well.

And again, we see very high velocities.

Normally we never make this diagnosis early on.

Here's a case that just came in actually a week ago.

A little bit dilatation of the anterior and posterior branches of the right portal.

Vein helical flow in both branches.

High velocity over here, 137 centimeters per second.

Again, helical flow sometimes could be a pitfall and can look like hepatofugal flow if you, if you interrogate it at exactly the right time.

And this is the coronal MIP image from the MRA showing this tight stenosis here and they're just watching this patient.

Patient's doing well clinically.

Portal Vein Steal

Portal vein steal decreased flow in the portal vein due to preferential flow in the splenic collaterals.

We don't see that as much now because there's better preoperative planning, which would include mapping of collaterals and preemptive embolization.

On ultrasound you'll see decreased velocity of the portal vein bidirectional flow and you can see these collaterals as well.

So this was a recent case, that was a little bit tough.

It didn't make complete sense in terms of the main portal vein, portion of it was a hepatofugal portion of it was a hepatopetal, then it looked a hepatofugal but did not have an appearance of helical flow.

The main portal vein was very pulsatile though.

Here's a hepatofugal flow in the left portal vein right portal vein here looks okay.

Pulsatile left.

And then this is a spleen with a lot of collateral.

So we thought for sure there was some type of portal.

There was some kind of steal phenomenon going on into the spleen, but we couldn't really explain the pulsatility in the portal vein.

So we thought, hmm, could there be an AVF there?

Well indeed this is the angio with the hepatic artery catheterized, in the angio suite.

And there's early filling of the portal vein here in the early with when the hepatic artery is being injected.

This person had an AVF and then also had something of flow into these big collaterals.

Everything was embolized and the patient's doing well

Hepatic Venous and IVC Complications

In terms of hepatic venous IVC thrombosis and stenosis.

More common with, living donor liver transplants.

Clinically, these patients will have ascites pleural effusion, hepatomegaly an ultrasound, you'll have a loss of the pulsatility index, more monophasic flow.

You could have turbulent flow and increased peak systolic velocity within the hepatic veins or the IVC and you can have portal venous abnormalities as well that can be reflected.

This is a patient who had nice phasic flow on the initial exam one month later.

Big change.

Very monophasic ascites.

And this patient has a tight stenosis in the IVC as we see here on this MRI patient went to the OR and now has good phasic flow.

Again, different patient phasic flow.

Initially high velocity turbulence aliasing here, there was hematoma adjacent to the IVC causing compression as we can see on this clip.

And here's the cavogram.

This was surgically evacuated.

The patient's doing well.

Different patient initial ultrasound phasic flow, monophasic flow when to angiogram.

Here's the cavogram and very astutely the angiography said this orientation is not right.

This was IVC graft torsion and the patient went to the OR immediately

Biliary Complications

Biliary complications.

Common source of liver transplant morbidity.

Again, the biliary tree supplied solely by the hepatic arteries.

It's been called the achilles heel of liver transplantation and won't necessarily lead to graft failure.

But these are tenacious problems that oftentimes require a lot of interventions.

What's interesting is that the ultrasound diagnosis ability debilitation and transplants is not good sensitivity of 38 to 66%.

And there's a lack of correlation between ultrasound and ERCP size.

And it's felt that the donor ducts don't display the same degree of dilatation as native ducts.

They're less pliable for some reason.

And we found that in our series as well.

Our mean CBD diameters were about three millimeters.

So the biliary system is relatively decompressed in these transplants.

Now in terms of strictures, you can have anastomotic versus non anastomotic strictures.

In anastomotic strictures.

The dilatation emanates from the anastomosis.

It's a single stricture, thought to be due to surgical technique most likely, but there may be an ischemic element later on as well.

And these respond well to endoscopic intervention.

Here's an example of a patient, a little bit of biliary dilatation here.

This is the MRCP showing a tight stenosis here that underwent successful angioplasty.

And again, often technical, but there's some, there's some literature now showing that even these may have an ischemic component.

So in terms of non-anastomotic ischemic cholangiopathy, this is all about ischemia.

So it's hepatic arterial compromise causing biliary ischemia.

The hepatic artery abnormality usually precedes the stricture by one to three weeks.

And oftentimes the ischemic insult happens before it could be intraoperative and the hepatic arteries may be completely normal.

But you see the results of the ischemic cholangiopathy oftentimes occurs earlier than anastomotic strictures.

And what you see are multiple strictures, usually at the hilum and intrahepatically.

There's oftentimes intraluminal debris from biliary necrosis and these do not respond well to the endoscopic intervention.

This is a very unfortunate patient.

She had her liver transplant when she was a child 16 years ago.

She came in very sick and we went up and did her ultrasound.

This is her hepatic artery anastomosis, extra hepatic.

But then we could not find any flow in the left or right.

And while we were scanning, we found these hypoechoic, bizarre areas with some echogenic foci that we thought were air.

We thought this was biliary necrosis.

And indeed this is her CT scan.

Large, huge areas of biliary necrosis.

And unfortunately she died soon after all this imaging.

This is a patient where the hepatic arteries look beautiful, but we saw biliary dilatation.

This is the MRCP multifocal areas of stricturing compatible with ischemic cholangiopathy.

This is a different patient where we saw this strange echogenic area.

We really didn't know what it was at all.

Everything else looked fine.

Her, the arteries looked fine.

We did do an mr.

These are the T two weighted coronal images, ill-defined, edema, some biliary ductal dilatation.

And on the T one weighted fat sats, you see this bright area.

And this is, very consistent with biliary cast syndrome.

Sometimes some of this debris within the biliary system becomes a concretion and becomes biliary cast syndrome.

Other biliary complications include bile leaks, oftentimes in partial livers due to cut surface.

Other sites of bile leak include anastomosis, cystic duct remnant, stump T tube entry site, and we see a bile leak here.

You can have sphincter of Oddi dysfunction, you can have recurrence of PSC.

Mucoceles are very rare.

And MRCP is a great way of, looking at these.

Rejection and Malignancy

Won't talk about rejection except to say that there really is no role in ultrasound except to exclude other etiologies of graft failure.

And then lastly, touching on malignancy.

Liver transplants overall have a higher risk of cancer, almost 25%.

Skin cancer is the most common malignancy you can get

Post-transplant lymphoproliferative disorder occurring seven to 10 months after transplant, usually EBV related.

And you can see extrahepatic adenopathy and solid organ involvement.

And you can also get recurrent neoplasms.

This is a patient who had had hepatic artery thrombosis, had a second transplant in 2011.

We were doing routine screening, found a new mass here, and this was a recurrent HCC, different patient innumerable masses throughout the liver.

Mediastinal adenopathy effusion.

This was PTLD.

Whole versus Partial Living Donor Liver Transplants

And I wanna spend just two seconds talking about whole versus partial living liver, living donor transplants because you can't see different things.

You can see a higher incidence of biliary complications in these partial livers.

And the other thing you can see is those aberrations that we talked about early on are accentuated in these partial living, transplants.

And at first it was a little bit alarming, we thought, gosh, is there a higher incidence of hepatic artery, thrombosis or stenosis?

These truly are aberrations and do tend to normalize and it's probably because these vessels are smaller and shorter and there's vessel diameter mismatch.

So again, partial livers, higher biliary complication rate than whole livers.

Portal vein velocities tend to be higher in these partial liver transplants.

But again, with time, this is, this is one month.

They tend to normalize.

RIs tend to be a lot lower with these partial liver transplants.

And again, these normalize with time as well.

Conclusion

So in conclusion, liver transplant is a lifesaving technique.

Ultrasound is the way to go in terms of detecting complications.

Knowledge of surgical anatomy and technique is very important.

Many doppler aberrations occur in the early postoperative period that can normalize.

Ultrasound rescanning should be done liberally and is very important.

Have a game plan for some of these early hepatic artery scenarios and how you're gonna manage them.

And, other complications including portal and hepatic venous thrombosis and stenosis can be accurately made by ultrasound.

Biliary complications are common.

Ultrasound should be used as a screening tool, so we wanna optimize our sensitivity.

We can increase our specificity with repeat scanning and other modalities.

And partial and whole liver transplants can differ on complication rates and doppler values, but the doppler values tend to normalize with time.

Thanks so much.